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Patients are more likely to experience preventable harm during perioperative care than in any other type of healthcare encounter.1 2 For cenforce 100 vs viagra several decades, a hallmark of surgical quality and safety has been the use of checklists to prevent errors (eg, wrong site surgery) and assure that key tasks have been or will be performed. The most widely used approach globally is the Surgical Safety Checklist (SSC) recommended by the WHO.3 It is divided into preinduction (or sign in, consisting of seven items performed by anaesthesia and nursing), preincision (timeout, 10 items performed by the cenforce 100 vs viagra entire team) and postsurgery (sign out, five items by the entire team).4 5 Most hospitals in the developed world perform the SSC or an equivalent timeout prior to surgical incision. However, preinduction briefings, and postcase debriefings in particular, are much less commonly performed.6 7There are widely disseminated arguments recommending the use of checklists in healthcare8 but also recognised limitations.9 Checklist-based preincision timeouts appear to improve surgical outcomes in many settings,4 5 yet, in other hospitals, the introduction of the SSC failed to improve outcomes.10 Like all tools or processes intended to improve safety, ineffective implementation will reduce the desired benefits. For example, there is appreciable evidence showing that surgical teams skip or do not meaningfully respond to timeout checklist items.11 12 Even cenforce 100 vs viagra with a robust implementation, effectiveness can be weakened by contextual factors, failure of leadership or deficient safety culture.Despite numerous studies, gaps in the evidence to guide optimal checklist use persist. For example, we do not know whether checklist-based timeouts only decrease the occurrence of the undesirable events targeted by the checklist or, as many hypothesise, whether their use also facilitates teamwork and interprofessional communication.

Although there is increasing guidance on how to optimally implement cenforce 100 vs viagra checklists at the local level, many questions remain.13 Moreover, we still do not understand the circumstances in which checklist use facilitates the detection, reporting and correction of errors.In this issue of the journal, Muensterer and colleagues14 describe a clever study in which the attending surgeon intentionally introduced errors during the preincision timeout while a medical student in the operating theatre surreptitiously noted whether the error was detected and reported by one or more members of the surgical team. If the error was not verbalised, the attending surgeon corrected the error before the timeout was complete. The single error embedded cenforce 100 vs viagra in each of 120 of 1800 paediatric operations was randomly chosen from among wrong patient name, age, gender, allergy or surgical procedure, side or site. Overall, only about half (65. 54%) of cenforce 100 vs viagra all errors were detected and reported by a team member prior to surgeon correction.

Of these, errors were most commonly reported by the anaesthesiologist (64%) and almost never by residents in training (6%) or medical students (1%).This study also has important limitations. Because the investigators were leading the timeouts as part of a research study, adherence to all cenforce 100 vs viagra of the checklist items was reportedly 100%. Yet, few organisations consistently attain timeout adherence above 90%.11 Since you are less likely to catch an error if you do not address that item during the timeout, in institutions with lower adherence, the proportion of missed errors may be even higher.The authors, with input from their institutional review board, designed the study to be feasible and compliant with established human subjects protection principles. As such, the attending surgeon always corrected the error after the anaesthesiologist’s component of the timeout but before cenforce 100 vs viagra the nurses’ component. By excluding the part of the timeout when the nurses address their checklist items (eg, instruments are sterile,) followed by a final opportunity as the timeout ends to note any errors or concerns, the study may have underestimated the rate of error reporting.Because the study did not query team members individually after the timeout, we also do not know how many errors were detected but not annunciated.

For example, recognised errors that were attributed to ‘misspeaking’ and/or had no clinical significance may not have been cenforce 100 vs viagra verbally challenged. Moreover, as is discussed by the authors, there was an unequivocal hierarchy effect—individuals with the least ‘power’ (ie, low in hierarchy within the current healthcare culture) were the least likely to report the error.This study highlights two important safety relevant questions on which I will elaborate. First, why and how cenforce 100 vs viagra should we change healthcare culture to facilitate ‘speaking up’?. Second, how can we best design and implement checklists and other safety interventions to yield more consistent and sustained clinician behaviour change?. The continued problem of hierarchical culture in healthcareThe significant influence of hierarchy on the incidence of error reporting in Muensterer et al’s14 study is consistent with substantial prior evidence that lower hierarchy clinical providers are less likely to ‘speak up’, even when they are aware of major safety violations.15–17Failure cenforce 100 vs viagra of a subordinate copilot to challenge or speak up to the captain in the 1977 Tenerife disaster was the impetus for the aviation industry’s adoption of crew resource management (CRM).

Healthcare team-training initiatives like the Agency for Healthcare Research and Quality’s TeamSTEPPS now include tools such as the ‘two-challenge rule’ and emphasise speaking up.18 Flattened hierarchies and reliance on expertise rather than seniority, especially during crisis or stress, are an integral component of high-reliability organisations. In contrast, the persistent cenforce 100 vs viagra hierarchical culture of healthcare is anathema to positive safety attitudes and behaviours. This is particularly problematic in operating theatres where surgeons view themselves as ‘captain of the ship’ and where uncivil behaviour is tolerated.19 The insidious effects of hierarchy will impair effectiveness of checklist use and predispose to safety issues in all aspects of routine and emergency care.20 While team-oriented training designed to enhance the ability of lower hierarchy clinicians to ‘speak up’ can be effective,21 22 evidence to guide the design and implementation of these interventions is still sparse. Single training exposures have generally had limited effects,17 23 in part likely due to inadequate ‘potency’ to achieve the desired effect24 in a clinical environment contaminated by the hierarchical culture and in part because most interventions have focused on ‘assertiveness’ training for the less powerful members of the team rather than, or in addition to, sensitivity or receptivity training of the most powerful (eg, surgical attendings).17Discussions of cenforce 100 vs viagra power hierarchy to date have largely focused on clinicians’ professional roles (ie, nurse vs physician) and level of experience (eg, resident vs attending). Even with two attending physicians, for example, a surgeon and anaesthesiologist, power dynamics can degrade communication and decrease team performance.

In a multicentre study of experienced anaesthesiologists managing simulated crisis events, the anaesthesiologists’ failure to challenge the surgeon to initiate life-saving interventions (eg, to open the abdomen in the presence of an enlarging retroperitoneal cenforce 100 vs viagra haematoma during laparoscopic surgery, or to halt surgery to cardiovert an unstable patient) was associated with lower overall scenario performance scores as determined by trained blinded anaesthesiologist video raters.25In fact, hierarchy is much more complex and this may explain in part the variable and generally weak results seen in ‘speaking up’ intervention studies to date. When considering hierarchical effects on communication assertiveness, one must also consider individual characteristics including gender, race/ethnicity, language, personal cultural background and personality, as well as the personality of those in higher power roles, microclimate factors of the team and care unit, and overall organisational culture.17 22 An interesting direction for future study is the facilitation of more positive communication (eg, expressions of gratitude or encouragement).26In a single-site intervention study to improve the quality of handovers from anaesthesia professionals to postanaesthesia care unit (PACU) nurses,27 simulation-based training emphasised specific dyadic communication behaviours—assertiveness for the nurses when their needs were not being met and ‘sensitivity’ (or receptiveness) for the anaesthesia professionals when the nurses raised concerns. In poststudy interviews, this behavioural focus was considered an important contributor to the resulting sustained improvement in the quality of actual cenforce 100 vs viagra handovers. As part of this study, we explicitly taught participants to CUSS. CUSS is a graduated approach to cenforce 100 vs viagra facilitate speaking up.

The acronym stands for ‘I’m Concerned’, ‘I’m Uncomfortable’, ‘This is a Safety issue’ and ‘Stop!. €™. The intended learners were taught these ‘triggers’ for eliciting desired behaviours (ie, to stop what they are doing and have a conversation with the initiator) and this approach creates an environment where the initiating individual can receive support from others who overhear the conversation—‘Doctor, I hear that Maria is CUSSing at you?. How can I help to resolve this situation?. €™ Such a graded assertiveness approach to ‘stop the line’, developed in other industries, is increasingly being used throughout healthcare.28Designing and implementing more effective safety tools and processesSSCs are just one tool used to advance overall perioperative system safety.

Similarly, in commercial aviation, checklists are one tool used as part of CRM to assure operational safety. CRM is a philosophy or construct that includes explicit values and principles, procedures supported by purpose-designed checklists and other tools, and regularly scheduled mandatory simulation-based training and assessment that together contribute to an existing safety culture in pilots and across the organisation.29 CRM and most of the existing aviation safety system were iteratively designed by pilots (the front-line workers) in collaboration with other stakeholders (including regulators). Healthcare must employ similar human-centred design approaches to re-engineer our safety systems.For commercial aviation to be completely safe, no planes would fly. Similarly, safety will never be the foremost system objective in healthcare. The primary goal is to efficiently deliver cost-effective care.

Instead, in any high-consequence industry, safety is a desirable by-product (an ‘emergent feature’) of a system designed to achieve primary operational goals. In healthcare, sick patients must be treated and there is inherent risk in doing so.30 Achieving societally acceptable levels of safety will stem from a deliberately designed system founded on a strong safety culture and truly committed leadership.With this as background, it is not surprising that so many hospitals struggle to garner reliable and sustained benefit from the use of checklists and other safety tools. To understand what is required, I would like to draw parallels with anaesthesiology’s experience of implementing another type of checklist.The Food and Drug Administration Anesthesia Machine Pre-Use ChecklistThe earliest checklist used in healthcare to reduce adverse events is the anaesthesia equipment preuse checklist, developed in 1987 by the US Food and Drug Administration (FDA) in collaboration with the Anesthesia Patient Safety Foundation and the American Society of Anesthesiologists.31 After more than three decades of use, lessons learnt from the use of the FDA checklist parallel more recent experiences with SSCs, and are instructive to a more general understanding of the role of safety tools in healthcare (see table 1).View this table:Table 1 Lessons learnt from 30 years of personal experience with and reflection about the Anesthesia Equipment Pre-Use Checklist*A checklist alone is insufficient to achieve optimal resultsHospitals that get the best results from an SSC implementation are often well-resourced organisations that already have safety-oriented committed leadership, a strong safety culture, educated and engaged front-line clinicians and an established track record of successfully implementing other safety interventions.32 That said, any hospital, given adequate commitment, resources and expertise, can implement an SSC or other substantive safety intervention successfully. In doing so, it will educate and engage its workers, improve its safety culture and set the stage for further safety and quality improvements.A multimodal approach to safety interventions is more effective. Hospitals that were able to successfully implement all three components of the SSC saw greater reductions in postoperative complications.33 Similarly, the combination of the SSC with a complementary approach that more fully addresses preoperative and postoperative issues, the Surgical Patient Safety System, was associated with better postoperative outcomes than use of the WHO SSC alone.34 The most effective interventions are those that are based on an integrated conceptual framework and follow human factor principles, especially when the safety goals are multiple or diverse.35In our PACU handover improvement project mentioned earlier,27 the multimodal intervention produced a fourfold improvement in observed clinician behaviours (ie, conduct of actual handovers) that was sustained for at least 3 years after the intervention ceased.

The project began by getting perioperative leadership buy-in, conducting observations of the current handover process and engaging front-line clinicians in all phases of study development. The criteria for an ‘acceptable handover’ were chosen by an independent team of clinicians. Front-line clinicians first completed a multimedia introductory webinar that included key principles and a knowledge assessment. To attend the 2-hour simulation training session, both anaesthesia professionals and PACU nurses were relieved from regular clinical duties (a strong message that this was an organisational priority). A custom patient-specific electronic form was available at every bedside in the PACU to reinforce the training during actual handovers.

Performance feedback was provided to individuals, units and perioperative leadership. The number of components needed for successful safety interventions will depend on the behaviour change desired, the existing safety culture, current experience and expertise of the intended end users and the priority articulated by organisational leaders. Regardless, design and implementation must be based on a solid conceptual framework, consider the full life-cycle of the intervention (from conceptualisation to obsolescence) and employ human factors engineering and implementation science principles and tools.13ConclusionChecklists and other safety tools are potentially valuable tools to advance perioperative safety. However, when used in isolation or implemented incorrectly, checklists have significant limitations. Safety initiatives that take a systems-oriented multimodal approach to design and implementation can, with organisational leadership and determination, produce both targeted and more general safety improvement.Ethics statementsPatient consent for publicationNot required.Many patients admitted to hospital require venous access to infuse medications and fluids.

The most commonly used device, the peripheral venous catheter, ranges from 2.5 to 4.5 cm in length, and is typically used for less than 5 days. The midline, a relatively newer peripheral venous catheter, is up to 20 cm in length, but does not reach the central veins, and may be used for up to 2 weeks. A peripherally inserted central venous catheter (PICC) is a longer catheter that is placed in one of the arm veins and extends to reach the central veins. The PICC is used for longer periods of time compared with peripheral intravenous devices, and initially gained popularity as a convenient vascular access device used in the outpatient and home settings. Its premise has been to provide access that lasts for weeks, that is fairly safe and easily manageable.

Patients often require central venous access when hospitalised, with more than half of patients in intensive care, and up to 20% in those cared for in the non-intensive care wards.1 Common indications for PICC use in the acute care setting include the requirement for multiple and frequent infusions (eg, antibiotics, parenteral nutrition), the administration of medications incompatible with peripheral infusion, invasive haemodynamic monitoring in critically ill patients, very poor venous access and frequent need for blood draws.2 Specially trained healthcare workers place PICCs, often nurses from a vascular access team (VAT), or interventional radiologists. The VAT is comprised of skilled nurses, with either medical/surgical, emergency department or intensive care unit backgrounds. Contrary to other healthcare workers that place PICCs, the VAT’s primary function is to place PICCs, and optimise the infusion delivery, through a safe and effective process. Its scope includes assessment for need, peripheral and central device insertion, monitoring of use and removal.3In their study of five hospitals within the Veterans Administration (VA) healthcare systems in the USA, Krein et al4 underscore the importance of a formal VAT to formulate and implement explicit appropriateness criteria, ensure timely insertion and safe management and direct patient education around PICC use. They found that team structures supporting line placement vary across hospitals from a dedicated team, to individual nurses trained in placement, to hospitals where only interventional radiologists insert PICCs.

The presence of a VAT was associated with more defined criteria for PICC use, but a recurrent theme was inadequate interdisciplinary dialogue. Although qualitative data were gathered at five VA hospitals only, the study’s findings reflect the variation in PICC placement and use, whether in academic or community, small or large hospitals.An important factor in variation in the approach to PICC line placement and management is the availability of resources and expertise at the hospital site. For example, if healthcare workers have suboptimal skills to place peripheral venous catheters, including midlines,5 clinicians may resort to ordering more PICCs unnecessarily to fill that void. Furthermore, as revealed in Krein’s study, a hospital that does not have the expertise to learn about alternative devices, such as those with lower risks and shorter dwell times (eg, midlines), may resort to using more PICCs than necessary. Similarly, hospitals without clinicians skilled or comfortable placing other central lines6 may rely more on using PICCs.

In addition, the lack of an available VAT to place PICCs using uasound guidance may result in more referrals to interventional radiology for placement, potentially exposing the patient to avoidable radiation during fluoroscopy.7We propose an approach to improve the appropriate and safe use of PICCs by focusing on three elements that address the findings by Krein and colleagues. Establishing a structure powered by a VAT. Anchoring a standardised process for line selection, insertion and care. And promoting adoption by engagement with the key stakeholders.Establishing a structure to support placement and management of PICCs depends on whether the number of devices placed is enough to support the creation of a dedicated vascular access programme. Leadership plays a critical role to invest the resources for a functional VAT, understanding the financial and quality benefits associated.8 Not realising its value, hospital leaders may view the VAT as a non-revenue-generating service, putting it at risk when considering cost reduction strategies.

The value of the VAT expands from mitigating preventable events (eg, deep venous thrombosis, ) to enhancing patient experience (eg, less attempts to place a peripheral device).9 In addition, better outcomes help curb the financial risks (eg, hospital-acquired condition penalties)8 and improve hospital ratings. The VAT’s role encompasses placing PICCs and guaranteeing the proper selection of the intravascular device and its appropriate use.2The second element involves standardising processes for line selection and care, regardless of who is taking care of the device. Implementing policies to address indications, placement and maintenance and using standardised kits help minimise variation. The creation of policies should be achieved through a multidisciplinary approach with VAT, nurses and physicians. The VAT can act as the ‘gate keeper’ evaluating whether the reason for PICC placement is aligned with indications.

In addition, the VAT plays a critical role supporting nurses’ competencies for venous catheter use (eg, aseptic access and maintenance, addressing complications and mitigating risk)10 to reduce mechanical11 and infectious complications.12 The VAT performs regular rounds to mitigate process gaps (eg, dressing site intactness) and to identify complications (eg, PICC site erythema or drainage, arm swelling), and provides timely feedback on clinical performance. The VAT can also serve as subject matter experts to the ordering physicians for the appropriate device type, based on vessel size and indications for use, how many lumens, site selection and a de-escalation plan for the patient prior to discharge. It also provides services should a device-related complication occur (eg, clotting), and works with clinicians to remedy the issue and salvage the device, thereby preventing a patient from losing their vascular access and/or having to replace it.The last element, and perhaps most significant, is to enhance the adoption of best practices through a partnership with the key stakeholders. PICC-associated outcomes are not only owned by the VAT, rather it is the responsibility of the clinicians, physicians and nurses to achieve those goals (table 1). Physicians are an essential stakeholder group to engage as they are the ones responsible for ordering the PICC.

An identified physician champion who partners and empowers the VAT will help resolve any barriers and be a liaison with the local physician community.13 The ideal physician champion should have the respect of peers, understand process optimisation and promote quality improvement. They need to be well versed on the appropriate indications for PICC use, the associated complications and risks and alternatives to the device. The physician champion engages the leaders of the key disciplines responsible for requesting a PICC, educating them on the appropriate indications for use, the outcomes associated with PICC use, inviting them to be partners and responding to any of their concerns.View this table:Table 1 Disciplines and their support to mitigate PICC harmWhat about the key physician disciplines to engage?. Physicians can play an active role in enhancing PICC use through avoiding the unnecessary use of infusions. The consultation of infectious diseases specialists for intravenous antibiotic use appropriateness has been associated with less PICC use and lower complications.14 Similarly, having a surgeon support the decision for whether enteral or parenteral nutrition is needed will help reduce unnecessary device use.15 Disciplines like hospitalists or general internists care for a large number of patients and often order PICCs for venous access,16 while nephrologists may advocate avoiding the use of PICCs in the chronic kidney disease population in an effort for vein preservation.17 In hospitals with teaching programmes, the VAT and its physician champion may educate physicians in training on device choice, placement and duration of use, and address with their faculty competencies for line management.18 Engaging these disciplines, elucidating the indications for appropriate use and providing feedback and local data on the potential harm ensure accountability and further attention to PICC safety.In summary, the PICC is one of the primary solutions to achieve vascular access.

With up to one in five patients at risk for developing complications,19 it is incumbent on us to ensure that these devices are properly used and maintained. Identifying and overcoming system barriers are key to delivering sustainable safe outcomes. As a first step, clinical and administrative leaders, realising the financial and quality benefits, need to support the structure reflected by the VAT to enhance PICC care. Second, the VAT must partner with disciplines (particularly nursing) to promote and ensure adequate competencies for placement and maintenance. Finally, clinical disciplines caring for the patient should instil a collaborative environment for better decision-making on when central access is required, and what device provides the safest and most effective delivery of care.Ethics statementsPatient consent for publicationNot required..

Patients are more likely to experience preventable harm during perioperative care than in any other type of healthcare encounter.1 2 For several decades, cheap viagra a hallmark of surgical quality and safety has been the use of checklists to prevent errors (eg, wrong site how much does generic viagra cost surgery) and assure that key tasks have been or will be performed. The most widely used approach globally is the Surgical Safety Checklist (SSC) recommended by the WHO.3 It is divided into preinduction (or sign in, consisting of seven items performed by anaesthesia and nursing), preincision (timeout, 10 items performed by the entire team) and postsurgery (sign out, five items by the entire team).4 5 Most hospitals in the developed world perform the SSC or an equivalent timeout prior to surgical cheap viagra incision. However, preinduction briefings, and postcase debriefings in particular, are much less commonly performed.6 7There are widely disseminated arguments recommending the use of checklists in healthcare8 but also recognised limitations.9 Checklist-based preincision timeouts appear to improve surgical outcomes in many settings,4 5 yet, in other hospitals, the introduction of the SSC failed to improve outcomes.10 Like all tools or processes intended to improve safety, ineffective implementation will reduce the desired benefits.

For example, there is appreciable evidence showing that surgical teams skip or do not meaningfully respond to timeout checklist items.11 cheap viagra 12 Even with a robust implementation, effectiveness can be weakened by contextual factors, failure of leadership or deficient safety culture.Despite numerous studies, gaps in the evidence to guide optimal checklist use persist. For example, we do not know whether checklist-based timeouts only decrease the occurrence of the undesirable events targeted by the checklist or, as many hypothesise, whether their use also facilitates teamwork and interprofessional communication. Although there is increasing guidance on how to optimally implement checklists at the local level, many questions remain.13 Moreover, we still do not understand the circumstances in which checklist use facilitates the detection, reporting and correction of errors.In this issue of the journal, Muensterer and colleagues14 describe a clever study in which the attending surgeon intentionally introduced errors during the preincision timeout cheap viagra while a medical student in the operating theatre surreptitiously noted whether the error was detected and reported by one or more members of the surgical team.

If the error was not verbalised, the attending surgeon corrected the error before the timeout was complete. The single error embedded in each of 120 of 1800 paediatric operations was randomly chosen from among wrong cheap viagra patient name, age, gender, allergy or surgical procedure, side or site. Overall, only about half (65.

54%) of all errors cheap viagra were detected and reported by a team member prior to surgeon correction. Of these, errors were most commonly reported by the anaesthesiologist (64%) and almost never by residents in training (6%) or medical students (1%).This study also has important limitations. Because the investigators were leading the timeouts as part of a research cheap viagra study, adherence to all of the checklist items was reportedly 100%.

Yet, few organisations consistently attain timeout adherence above 90%.11 Since you are less likely to catch an error if you do not address that item during the timeout, in institutions with lower adherence, the proportion of missed errors may be even higher.The authors, with input from their institutional review board, designed the study to be feasible and compliant with established human subjects protection principles. As such, the attending surgeon always corrected the error after the anaesthesiologist’s component of the timeout but cheap viagra before the nurses’ component. By excluding the part of the timeout when the nurses address their checklist items (eg, instruments are sterile,) followed by a final opportunity as the timeout ends to note any errors or concerns, the study may have underestimated the rate of error reporting.Because the study did not query team members individually after the timeout, we also do not know how many errors were detected but not annunciated.

For example, recognised errors that were attributed to ‘misspeaking’ and/or had no cheap viagra clinical significance may not have been verbally challenged. Moreover, as is discussed by the authors, there was an unequivocal hierarchy effect—individuals with the least ‘power’ (ie, low in hierarchy within the current healthcare culture) were the least likely to report the error.This study highlights two important safety relevant questions on which I will elaborate. First, why and how should we change healthcare cheap viagra culture to facilitate ‘speaking up’?.

Second, how can we best design and implement checklists and other safety interventions to yield more consistent and sustained clinician behaviour change?. The continued problem of hierarchical culture in healthcareThe significant influence of hierarchy on the incidence of error reporting in Muensterer et al’s14 study is consistent with substantial prior evidence that lower hierarchy clinical providers are less likely to ‘speak up’, even when they are aware of major safety violations.15–17Failure of a subordinate copilot to challenge or cheap viagra speak up to the captain in the 1977 Tenerife disaster was the impetus for the aviation industry’s adoption of crew resource management (CRM). Healthcare team-training initiatives like the Agency for Healthcare Research and Quality’s TeamSTEPPS now include tools such as the ‘two-challenge rule’ and emphasise speaking up.18 Flattened hierarchies and reliance on expertise rather than seniority, especially during crisis or stress, are an integral component of high-reliability organisations.

In contrast, the persistent hierarchical culture cheap viagra of healthcare is anathema to positive safety attitudes and behaviours. This is particularly problematic in operating theatres where surgeons view themselves as ‘captain of the ship’ and where uncivil behaviour is tolerated.19 The insidious effects of hierarchy will impair effectiveness of checklist use and predispose to safety issues in all aspects of routine and emergency care.20 While team-oriented training designed to enhance the ability of lower hierarchy clinicians to ‘speak up’ can be effective,21 22 evidence to guide the design and implementation of these interventions is still sparse. Single training exposures have generally had limited effects,17 23 in part likely due to inadequate cheap viagra ‘potency’ to achieve the desired effect24 in a clinical environment contaminated by the hierarchical culture and in part because most interventions have focused on ‘assertiveness’ training for the less powerful members of the team rather than, or in addition to, sensitivity or receptivity training of the most powerful (eg, surgical attendings).17Discussions of power hierarchy to date have largely focused on clinicians’ professional roles (ie, nurse vs physician) and level of experience (eg, resident vs attending).

Even with two attending physicians, for example, a surgeon and anaesthesiologist, power dynamics can degrade communication and decrease team performance. In a multicentre study of experienced anaesthesiologists managing simulated crisis events, the anaesthesiologists’ failure to cheap viagra challenge the surgeon to initiate life-saving interventions (eg, to open the abdomen in the presence of an enlarging retroperitoneal haematoma during laparoscopic surgery, or to halt surgery to cardiovert an unstable patient) was associated with lower overall scenario performance scores as determined by trained blinded anaesthesiologist video raters.25In fact, hierarchy is much more complex and this may explain in part the variable and generally weak results seen in ‘speaking up’ intervention studies to date. When considering hierarchical effects on communication assertiveness, one must also consider individual characteristics including gender, race/ethnicity, language, personal cultural background and personality, as well as the personality of those in higher power roles, microclimate factors of the team and care unit, and overall organisational culture.17 22 An interesting direction for future study is the facilitation of more positive communication (eg, expressions of gratitude or encouragement).26In a single-site intervention study to improve the quality of handovers from anaesthesia professionals to postanaesthesia care unit (PACU) nurses,27 simulation-based training emphasised specific dyadic communication behaviours—assertiveness for the nurses when their needs were not being met and ‘sensitivity’ (or receptiveness) for the anaesthesia professionals when the nurses raised concerns.

In poststudy interviews, this behavioural focus was considered cheap viagra an important contributor to the resulting sustained improvement in the quality of actual handovers. As part of this study, we explicitly taught participants to CUSS. CUSS is a graduated approach to cheap viagra facilitate speaking up.

The acronym stands for ‘I’m Concerned’, ‘I’m Uncomfortable’, ‘This is a Safety issue’ and ‘Stop!. €™. The intended learners were taught these ‘triggers’ for eliciting desired behaviours (ie, to stop what they are doing and have a conversation with the initiator) and this approach creates an environment where the initiating individual can receive support from others who overhear the conversation—‘Doctor, I hear that Maria is CUSSing at you?.

How can I help to resolve this situation?. €™ Such a graded assertiveness approach to ‘stop the line’, developed in other industries, is increasingly being used throughout healthcare.28Designing and implementing more effective safety tools and processesSSCs are just one tool used to advance overall perioperative system safety. Similarly, in commercial aviation, checklists are one tool used as part of CRM to assure operational safety.

CRM is a philosophy or construct that includes explicit values and principles, procedures supported by purpose-designed checklists and other tools, and regularly scheduled mandatory simulation-based training and assessment that together contribute to an existing safety culture in pilots and across the organisation.29 CRM and most of the existing aviation safety system were iteratively designed by pilots (the front-line workers) in collaboration with other stakeholders (including regulators). Healthcare must employ similar human-centred design approaches to re-engineer our safety systems.For commercial aviation to be completely safe, no planes would fly. Similarly, safety will never be the foremost system objective in healthcare.

The primary goal is to efficiently deliver cost-effective care. Instead, in any high-consequence industry, safety is a desirable by-product (an ‘emergent feature’) of a system designed to achieve primary operational goals. In healthcare, sick patients must be treated and there is inherent risk in doing so.30 Achieving societally acceptable levels of safety will stem from a deliberately designed system founded on a strong safety culture and truly committed leadership.With this as background, it is not surprising that so many hospitals struggle to garner reliable and sustained benefit from the use of checklists and other safety tools.

To understand what is required, I would like to draw parallels with anaesthesiology’s experience of implementing another type of checklist.The Food and Drug Administration Anesthesia Machine Pre-Use ChecklistThe earliest checklist used in healthcare to reduce adverse events is the anaesthesia equipment preuse checklist, developed in 1987 by the US Food and Drug Administration (FDA) in collaboration with the Anesthesia Patient Safety Foundation and the American Society of Anesthesiologists.31 After more than three decades of use, lessons learnt from the use of the FDA checklist parallel more recent experiences with SSCs, and are instructive to a more general understanding of the role of safety tools in healthcare (see table 1).View this table:Table 1 Lessons learnt from 30 years of personal experience with and reflection about the Anesthesia Equipment Pre-Use Checklist*A checklist alone is insufficient to achieve optimal resultsHospitals that get the best results from an SSC implementation are often well-resourced organisations that already have safety-oriented committed leadership, a strong safety culture, educated and engaged front-line clinicians and an established track record of successfully implementing other safety interventions.32 That said, any hospital, given adequate commitment, resources and expertise, can implement an SSC or other substantive safety intervention successfully. In doing so, it will educate and engage its workers, improve its safety culture and set the stage for further safety and quality improvements.A multimodal approach to safety interventions is more effective. Hospitals that were able to successfully implement all three components of the SSC saw greater reductions in postoperative complications.33 Similarly, the combination of the SSC with a complementary approach that more fully addresses preoperative and postoperative issues, the Surgical Patient Safety System, was associated with better postoperative outcomes than use of the WHO SSC alone.34 The most effective interventions are those that are based on an integrated conceptual framework and follow human factor principles, especially when the safety goals are multiple or diverse.35In our PACU handover improvement project mentioned earlier,27 the multimodal intervention produced a fourfold improvement in observed clinician behaviours (ie, conduct of actual handovers) that was sustained for at least 3 years after the intervention ceased.

The project began by getting perioperative leadership buy-in, conducting observations of the current handover process and engaging front-line clinicians in all phases of study development. The criteria for an ‘acceptable handover’ were chosen by an independent team of clinicians. Front-line clinicians first completed a multimedia introductory webinar that included key principles and a knowledge assessment.

To attend the 2-hour simulation training session, both anaesthesia professionals and PACU nurses were relieved from regular clinical duties (a strong message that this was an organisational priority). A custom patient-specific electronic form was available at every bedside in the PACU to reinforce the training during actual handovers. Performance feedback was provided to individuals, units and perioperative leadership.

The number of components needed for successful safety interventions will depend on the behaviour change desired, the existing safety culture, current experience and expertise of the intended end users and the priority articulated by organisational leaders. Regardless, design and implementation must be based on a solid conceptual framework, consider the full life-cycle of the intervention (from conceptualisation to obsolescence) and employ human factors engineering and implementation science principles and tools.13ConclusionChecklists and other safety tools are potentially valuable tools to advance perioperative safety. However, when used in isolation or implemented incorrectly, checklists have significant limitations.

Safety initiatives that take a systems-oriented multimodal approach to design and implementation can, with organisational leadership and determination, produce both targeted and more general safety improvement.Ethics statementsPatient consent for publicationNot required.Many patients admitted to hospital require venous access to infuse medications and fluids. The most commonly used device, the peripheral venous catheter, ranges from 2.5 to 4.5 cm in length, and is typically used for less than 5 days. The midline, a relatively newer peripheral venous catheter, is up to 20 cm in length, but does not reach the central veins, and may be used for up to 2 weeks.

A peripherally inserted central venous catheter (PICC) is a longer catheter that is placed in one of the arm veins and extends to reach the central veins. The PICC is used for longer periods of time compared with peripheral intravenous devices, and initially gained popularity as a convenient vascular access device used in the outpatient and home settings. Its premise has been to provide access that lasts for weeks, that is fairly safe and easily manageable.

Patients often require central venous access when hospitalised, with more than half of patients in intensive care, and up to 20% in those cared for in the non-intensive care wards.1 Common indications for PICC use in the acute care setting include the requirement for multiple and frequent infusions (eg, antibiotics, parenteral nutrition), the administration of medications incompatible with peripheral infusion, invasive haemodynamic monitoring in critically ill patients, very poor venous access and frequent need for blood draws.2 Specially trained healthcare workers place PICCs, often nurses from a vascular access team (VAT), or interventional radiologists. The VAT is comprised of skilled nurses, with either medical/surgical, emergency department or intensive care unit backgrounds. Contrary to other healthcare workers that place PICCs, the VAT’s primary function is to place PICCs, and optimise the infusion delivery, through a safe and effective process.

Its scope includes assessment for need, peripheral and central device insertion, monitoring of use and removal.3In their study of five hospitals within the Veterans Administration (VA) healthcare systems in the USA, Krein et al4 underscore the importance of a formal VAT to formulate and implement explicit appropriateness criteria, ensure timely insertion and safe management and direct patient education around PICC use. They found that team structures supporting line placement vary across hospitals from a dedicated team, to individual nurses trained in placement, to hospitals where only interventional radiologists insert PICCs. The presence of a VAT was associated with more defined criteria for PICC use, but a recurrent theme was inadequate interdisciplinary dialogue.

Although qualitative data were gathered at five VA hospitals only, the study’s findings reflect the variation in PICC placement and use, whether in academic or community, small or large hospitals.An important factor in variation in the approach to PICC line placement and management is the availability of resources and expertise at the hospital site. For example, if healthcare workers have suboptimal skills to place peripheral venous catheters, including midlines,5 clinicians may resort to ordering more PICCs unnecessarily to fill that void. Furthermore, as revealed in Krein’s study, a hospital that does not have the expertise to learn about alternative devices, such as those with lower risks and shorter dwell times (eg, midlines), may resort to using more PICCs than necessary.

Similarly, hospitals without clinicians skilled or comfortable placing other central lines6 may rely more on using PICCs. In addition, the lack of an available VAT to place PICCs using uasound guidance may result in more referrals to interventional radiology for placement, potentially exposing the patient to avoidable radiation during fluoroscopy.7We propose an approach to improve the appropriate and safe use of PICCs by focusing on three elements that address the findings by Krein and colleagues. Establishing a structure powered by a VAT.

Anchoring a standardised process for line selection, insertion and care. And promoting adoption by engagement with the key stakeholders.Establishing a structure to support placement and management of PICCs depends on whether the number of devices placed is enough to support the creation of a dedicated vascular access programme. Leadership plays a critical role to invest the resources for a functional VAT, understanding the financial and quality benefits associated.8 Not realising its value, hospital leaders may view the VAT as a non-revenue-generating service, putting it at risk when considering cost reduction strategies.

The value of the VAT expands from mitigating preventable events (eg, deep venous thrombosis, ) to enhancing patient experience (eg, less attempts to place a peripheral device).9 In addition, better outcomes help curb the financial risks (eg, hospital-acquired condition penalties)8 and improve hospital ratings. The VAT’s role encompasses placing PICCs and guaranteeing the proper selection of the intravascular device and its appropriate use.2The second element involves standardising processes for line selection and care, regardless of who is taking care of the device. Implementing policies to address indications, placement and maintenance and using standardised kits help minimise variation.

The creation of policies should be achieved through a multidisciplinary approach with VAT, nurses and physicians. The VAT can act as the ‘gate keeper’ evaluating whether the reason for PICC placement is aligned with indications. In addition, the VAT plays a critical role supporting nurses’ competencies for venous catheter use (eg, aseptic access and maintenance, addressing complications and mitigating risk)10 to reduce mechanical11 and infectious complications.12 The VAT performs regular rounds to mitigate process gaps (eg, dressing site intactness) and to identify complications (eg, PICC site erythema or drainage, arm swelling), and provides timely feedback on clinical performance.

The VAT can also serve as subject matter experts to the ordering physicians for the appropriate device type, based on vessel size and indications for use, how many lumens, site selection and a de-escalation plan for the patient prior to discharge. It also provides services should a device-related complication occur (eg, clotting), and works with clinicians to remedy the issue and salvage the device, thereby preventing a patient from losing their vascular access and/or having to replace it.The last element, and perhaps most significant, is to enhance the adoption of best practices through a partnership with the key stakeholders. PICC-associated outcomes are not only owned by the VAT, rather it is the responsibility of the clinicians, physicians and nurses to achieve those goals (table 1).

Physicians are an essential stakeholder group to engage as they are the ones responsible for ordering the PICC. An identified physician champion who partners and empowers the VAT will help resolve any barriers and be a liaison with the local physician community.13 The ideal physician champion should have the respect of peers, understand process optimisation and promote quality improvement. They need to be well versed on the appropriate indications for PICC use, the associated complications and risks and alternatives to the device.

The physician champion engages the leaders of the key disciplines responsible for requesting a PICC, educating them on the appropriate indications for use, the outcomes associated with PICC use, inviting them to be partners and responding to any of their concerns.View this table:Table 1 Disciplines and their support to mitigate PICC harmWhat about the key physician disciplines to engage?. Physicians can play an active role in enhancing PICC use through avoiding the unnecessary use of infusions. The consultation of infectious diseases specialists for intravenous antibiotic use appropriateness has been associated with less PICC use and lower complications.14 Similarly, having a surgeon support the decision for whether enteral or parenteral nutrition is needed will help reduce unnecessary device use.15 Disciplines like hospitalists or general internists care for a large number of patients and often order PICCs for venous access,16 while nephrologists may advocate avoiding the use of PICCs in the chronic kidney disease population in an effort for vein preservation.17 In hospitals with teaching programmes, the VAT and its physician champion may educate physicians in training on device choice, placement and duration of use, and address with their faculty competencies for line management.18 Engaging these disciplines, elucidating the indications for appropriate use and providing feedback and local data on the potential harm ensure accountability and further attention to PICC safety.In summary, the PICC is one of the primary solutions to achieve vascular access.

With up to one in five patients at risk for developing complications,19 it is incumbent on us to ensure that these devices are properly used and maintained. Identifying and overcoming system barriers are key to delivering sustainable safe outcomes. As a first step, clinical and administrative leaders, realising the financial and quality benefits, need to support the structure reflected by the VAT to enhance PICC care.

Second, the VAT must partner with disciplines (particularly nursing) to promote and ensure adequate competencies for placement and maintenance. Finally, clinical disciplines caring for the patient should instil a collaborative environment for better decision-making on when central access is required, and what device provides the safest and most effective delivery of care.Ethics statementsPatient consent for publicationNot required..

What should I watch for while taking Viagra?

If you notice any changes in your vision while taking this drug, call your doctor or health care professional as soon as possible. Call your health care provider right away if you have any change in vision. Contact you doctor or health care professional right away if the erection lasts longer than 4 hours or if it becomes painful. This may be a sign of a serious problem and must be treated right away to prevent permanent damage. If you experience symptoms of nausea, dizziness, chest pain or arm pain upon initiation of sexual activity after taking Viagra, you should refrain from further activity and call your doctor or health care professional as soon as possible. Using Viagra does not protect you or your partner against HIV (the viagra that causes AIDS) or other sexually transmitted diseases.

Is viagra a blood thinner

After watching a parent succumb to the deleterious effects of Alzheimer's disease, it's why not try these out only natural to wonder if you might is viagra a blood thinner be doomed to the same fate. The good news?. That's not necessarily is viagra a blood thinner the case. The bad news, however, is that the disease is so prevalent your overall risk is still relatively high — especially as you age.

At 65, you have a roughly 3 percent chance is viagra a blood thinner of contracting Alzheimer's disease each year. This bumps up to a 17 percent chance after your 75th birthday, and increases to a roughly one in three chance you'll develop Alzheimer's after the age of 85. Experts agree that family history elevates the risk, particularly if you have more than one parent or sibling with the disease, but they disagree on how much. Some studies indicate the risk hovers at around 30 percent, while others estimate an up to two or four times increased risk is viagra a blood thinner.

Early onset Alzheimer's — which typically strikes individuals between the ages of 40 and 65 — has a more easily understood genetic link, with a 50 percent chance the child of an Alzheimer's patient will also be diagnosed with the disease. Read More:Why Do Women is viagra a blood thinner Get Alzheimer’s More Than Men?. How Did Alzheimer's Disease Get Its Name?. Are We Close to Curing Alzheimer’s Disease?.

However, a combination of genetic and environmental factors come into play is viagra a blood thinner for the more common late-onset variation, says Rita Guerreiro, a neurogeneticist at the Van Andel Institute. Which makes things even more difficult to predict. €œMany people who have relatives with [Alzheimer's] never develop the disease, and many without a family history of the disease do develop it,” says Guerreiro.Interested in tipping the odds in your favor? is viagra a blood thinner. Some scientists think keeping your mind active, consuming a diet low in red meat and sugar and exercising regularly could help keep the memory-zapping disease at bay.Late fall and early winter typically mean a flurry of holiday travel and get-togethers for a lot of people.

But this year will be anything but normal. Making plans is more than a matter of is viagra a blood thinner shopping around for flight prices or car rental fees. Many of us are probably also asking ourselves whether to stay home or see loved ones, and how to stay safe at holiday gatherings. For the lowest risk of spreading or becoming sick with erectile dysfunction treatment, not traveling is is viagra a blood thinner the way to go.

However, there might be loved ones who desperately need companionship in the coming months. €œThere are situations where people will choose, and choose correctly, to go and support those family members,” says Lin H. Chen, director of the Travel is viagra a blood thinner Medicine Center at Mount Auburn Hospital and president of the International Society of Travel Medicine. No matter if you’re going cross-country to see siblings or staying at home with your dog, experts say, remember two things.

Plan ahead and stay flexible.Tackle Logistics FirstFor those interested in interstate travel, first is viagra a blood thinner assess whether or not those plans are feasible. The states you’re going to (and coming back to) might have rules about isolating yourself for two weeks once you arrive. If you live in one of those states but a two-week is viagra a blood thinner isolation period isn’t feasible — because you have to go to work or send kids to school, for example — then traveling for the holidays won’t work for you, says Gabriela Andujar Vazquez, an infectious disease doctor at Tufts Medical Center. Some states say that isolation requirements don’t apply if you get a negative erectile dysfunction treatment test.

But testing you or your whole family may lie outside your budget if the exams aren’t covered by insurance, Andujar Vazquez says. Factor those financial decisions into your travel plans, too.If you do decide to travel, choose is viagra a blood thinner driving over flying if you can. Busy rest stops might mean confronting crowds of other highway travelers, Chen says. However, compared to the entire process of flying is viagra a blood thinner — getting to an airport and waiting in lines repeatedly — driving likely means fewer crowds overall.

€œThink about precautions through this journey,” Chen says, “not just on the plane, train, bus or car.”Airplanes themselves receive a lot of attention as potential viagra spreaders. But Chen says there are three instances of infected individuals spreading the disease to two or more people on a flight. Those transmissions happened before any airline required passengers is viagra a blood thinner to wear masks. Since then, other interventions like leaving seats open, disinfecting often and updated air filtration have been introduced on airplanes, too.

Though there’s no data yet on how effective these combined intervention strategies are, “the fact that we haven’t heard about is viagra a blood thinner masked transmission on recent flights is also reassuring,” Chen says. On the Big DayOdds are you’re debating travel plans for the sake of a big family meal. Or even if you’re staying local, you might try and work something out with friends and relatives nearby. Both Chen and Andujar Vazquez emphasize that no matter which you choose, keep up the erectile dysfunction treatment precautions is viagra a blood thinner once you’re all together.

Generally, the smaller the gathering (and the fewer number of households), the better. Keep activities outdoors is viagra a blood thinner if you can, seat groups apart, and keep masks on while not eating. You might also consider new ways to keep everyone fed. The typical buffet serving style can mean a lot of utensil sharing, so maybe opt for single-serving portioning or have everyone wash or sanitize hands before and after touching communal dishes.

And as fun as it might be to play bartender, is viagra a blood thinner maybe choose a BYOB policy as well. Oh, and “no one should be coming sick,” Andujar Vazquez says. €œYou cannot say that enough.”These might sound like a lot of holiday modifications, which is why it’s important to discuss what the situation will look like before coming together is viagra a blood thinner. €œPeople have to feel comfortable talking about these things, because it’s part of our daily life now,” Andujar Vazquez says.

€œHave that conversation before the event happens so people don’t have unexpected surprises or feel unsafe with some sort of behavior.”At the same time, acknowledge that even the most careful planning might fall apart. Your destination might become a erectile dysfunction treatment hotspot days before you’re set to is viagra a blood thinner arrive, or you or someone in your gathering might start feeling unwell ahead of time. Though it’s easier said than done, accept that plans will change whether you want them to or not — and that celebrations in the coming months will look different than they used to. €œRealistically, this holiday season is viagra a blood thinner is going to be difficult for a lot of people,” says Jonathan Kanter, psychologist and director of the Center for the Science of Social Connection at the University of Washington.

In individuals coping with significant life changes, one of the best predictors of depression is whether or not people can leave former goals behind and adopt new ones, Kanter says. Letting go of old expectations — like how you normally gather with is viagra a blood thinner family, for example — can involve a kind of grieving process. But recalibrating what you want to get out of a situation is an essential coping skill. €œYou won’t be able to get there unless you breathe and accept that you’re in a new context,” Kanter says.

€œWith that acceptance, hopefully there's is viagra a blood thinner a lot of creativity and innovation and grace about how to make it as successful as possible.” The prospect of not seeing loved ones in the coming months might make some people nervous, for themselves and for others. What's important to remember is that it's possible to make it through — and that future holidays will get better.As flu season creeps up on the Northern Hemisphere, cold and flu relief medications will inevitably fly off store shelves. A natural remedy that shoppers might reach is viagra a blood thinner for is elderberry, a small, blackish-purple fruit that companies turn into syrups, lozenges and gummies. Though therapeutic uses of the berry date back centuries, Michael Macknin, a pediatrician at the Cleveland Clinic, hadn’t heard of using elderberry to treat the flu until a patient’s mother asked him about it.

Some industry-sponsored research claims that the herbal remedy could cut the length of the symptoms by up to four days. For a comparison, Tamiflu, an FDA-approved treatment, only reduces flu duration is viagra a blood thinner by about a single day. €œI said, 'Gee, if that’s really true [about elderberry], it would be a huge benefit,'” Macknin says. But the effectiveness and safety of elderberry is viagra a blood thinner is still fairly unclear.

Unlike the over-the-counter medicines at your local pharmacy, elderberry hasn't been through rigorous FDA testing and approval. However, Macknin and his team recently published a study in the Journal of General Internal Medicine, which found that elderberry treatments did nothing for flu patients. This prompts a need for further studies into is viagra a blood thinner the remedy — work that unfortunately stands a low chance of happening in the future, Macknin says. Looking For ProofElderberries are full of chemicals that could be good for your health.

Like similar fruits, the berries contain high levels of antioxidants, compounds that shut down reactions in our bodies that is viagra a blood thinner damage cells. But whether or not elderberry's properties also help immune systems fend off a viagra is murky. There are only a handful of studies that have examined if elderberries reduced the severity or duration of the flu. And though some of the work prior to Macknin’s was well-designed and supported this herbal remedy as a helpful flu aid, at least some — and potentially all — of those studies were funded by elderberry treatment manufacturers.Macknin says an elderberry supplement company is viagra a blood thinner provided his team with their products and a placebo version for free, but that the company wasn’t involved in the research beyond that.

Macknin's study is the largest one conducted on elderberry to date, with 87 influenza patients completing the entire treatment course. Participants in is viagra a blood thinner the study were also welcome to take Tamiflu, for ethical reasons, as the team didn’t want to exclude anyone from taking a proven flu therapy. Additionally, each participant took home either a bottle of elderberry syrup or the placebo with instructions on when and how to take it. The research team called participants every day for a symptom check and to remind them to take their medication.By chance, it turned out that a higher percentage of the patients given elderberry syrup had gotten their flu shot and also chose to take Tamiflu.

Since the is viagra a blood thinner vaccination can reduce the severity of in recipients who still come down with the flu, the study coincidentally operated in favor of those who took the herbal remedy, Macknin says. Those patients could have dealt with a shorter, less-intense illness because of the Tamiflu and vaccination. €œEverything was is viagra a blood thinner stacked to have it turn out better [for the elderberry group],” Macknin says, “and it turned out the same.” The researchers found no difference in illness duration or severity between the elderberry and placebo groups. While analyzing the data, the team also found that those on the herbal treatment might have actually fared worse than those on the placebo.

The potential for this intervention to actually harm instead of help influenza patients explains why Macknin thinks the therapy needs further research.But, don't expect is viagra a blood thinner that work to happen any time soon. Researchers are faced with a number of challenges when it comes to studying the efficacy of herbal remedies. For starters, there's little financial incentive to investigate if they actually work. Plant products are challenging to patent, making them less lucrative prospects for pharmaceutical companies or research organizations is viagra a blood thinner to investigate.

Additionally, investigations that try and prove a proposed therapy as an effective drug — like the one Macknin and his team accomplished — are expensive, Macknin says. Those projects need FDA oversight is viagra a blood thinner and additional paperwork, components that drive up study costs. €œIt’s extraordinarily expensive and there’s no money in it for anybody,” Macknin says.Talk To Your DoctorUltimately, research on elderberry therapies for flu patients is a mixed bag, and deserves more attention from scientists. However, if you still want to discuss elderberry treatments for the flu with your doctor, that’s a conversation you should feel comfortable having, says Erica McIntyre, an expert focused on health and environmental psychology in the School of Public Health at the University of Technology Sydney.

Navigating what research says about a particular herbal medicine is challenging for patients and health is viagra a blood thinner practitioners alike. The process is made more complex by the range of similar-sounding products on the market that lack standardized ingredients, McIntyre says. But when doctors judge or shame patients for asking about non-conventional healthcare interventions, the is viagra a blood thinner response can distance people and push them closer to potentially unproven treatments. Even worse, those individuals might start to keep their herbal remedies a secret.

€œIt is that fear about being judged for use of that medication,” McIntyre says, that drives up to 50 percent of people taking herbal treatments to withhold that information from healthcare practitioners. That’s a dangerous choice, as some herbal and traditional medications can interact and cause health problems.If a physician shames someone for asking about alternative medicines, it’s likely time to find a new is viagra a blood thinner doctor, McIntyre says. Look for someone who will listen to your concerns — whether it's that you feel traditional treatments haven’t worked for you, or that you didn’t like the side effects, the two common reasons people pursue herbal treatments in the first place. €œYou’re not necessarily looking for a doctor that will let you do whatever you want,” McIntyre says, “but that they actually consider you as a patient, your treatment choices and your treatment priorities, and communicate in a way that’s supportive.” And if a is viagra a blood thinner doctor suggests that you avoid a treatment you’re interested in, ask why.

They generally have a good reason, McIntyre says.For now, know that even if your doctor doesn’t support you taking elderberry, there are other proven preventative measures that are worth your while — like the flu shot. Anyone six months or older should get it, Macknin says, and stick to the protocols we’re used to following to prevent erectile dysfunction treatment s, like social distancing, mask-wearing and hand-washing. Those measures also help prevent flu transmission, too — something, so far, no elderberry supplement package can claim.The yearly influenza season threatens to is viagra a blood thinner make the erectile dysfunction treatment viagra doubly deadly, but I believe that this isn’t inevitable.There are two commonly given treatments – the pneumococcal treatment and the Hib treatment – that protect against bacterial pneumonias. These bacteria complicate both influenza and erectile dysfunction treatment, often leading to death.

My examination of disease trends and vaccination rates leads me to believe that broader use of the pneumococcal and Hib treatments could is viagra a blood thinner guard against the worst effects of a erectile dysfunction treatment illness.I am an immunologist and physiologist interested in the effects of combined s on immunity. I have reached my insight by juxtaposing two seemingly unrelated puzzles. Infants and children get erectile dysfunction, the viagra that causes erectile dysfunction treatment, but very rarely become hospitalized or die. And case numbers and death rates from erectile dysfunction treatment began varying greatly from nation to nation and city to city even before lockdowns began is viagra a blood thinner.

I wondered why.One night I woke up with a possible answer. Vaccination rates is viagra a blood thinner. Most children, beginning at age two months, are vaccinated against numerous diseases. Adults less so is viagra a blood thinner.

And, both infant and adult vaccination rates vary widely across the world. Could differences in the rates of vaccination against one or more diseases account for differences in erectile dysfunction treatment risks?. As someone who had previously investigated other viagras such as the Great Flu viagra of 1918-19 and AIDS, and who has worked with treatments, I had a strong background for tracking down the relevant data to test my hypothesis.Pneumococcal Vaccination Rates Correlate With Lower erectile dysfunction treatment Cases and DeathsI gathered national and some local data on vaccination rates against influenza, polio, measles-mumps-rubella is viagra a blood thinner (MMR), diphtheria-tetanus-pertussis (DTP), tuberculosis (BCG), pneumococci and Haemophilus influenzae type B (Hib). I correlated them with erectile dysfunction treatment case rates and death rates for 24 nations that had experienced their erectile dysfunction treatment outbreaks at about the same time.

I controlled for factors such as percentage of the population who were obese, is viagra a blood thinner diabetic or elderly.I found that only pneumococcal treatments afforded statistically significant protection against erectile dysfunction treatment. Nations such as Spain, Italy, Belgium, Brazil, Peru and Chile that have the highest erectile dysfunction treatment rates per million have the poorest pneumococcal vaccination rates among both infants and adults. Nations with the lowest rates of erectile dysfunction treatment – Japan, Korea, Denmark, Australia and New Zealand – have the highest rates of pneumococcal vaccination among both infants and adults.A recent preprint study (not yet peer-reviewed) from researchers at the Mayo Clinic has also reported very strong associations between pneumococcal vaccination and protection against erectile dysfunction treatment. This is especially true among minority is viagra a blood thinner patients who are bearing the brunt of the erectile dysfunction viagra.

The report also suggests that other treatments, or combinations of treatments, such as Hib and MMR may also provide protection.These results are important because in the U.S., childhood vaccination against pneumococci – which protects against Streptococcus pneumoniae bacteria – varies by state from 74% to 92%. Although the CDC recommends that all adults 18-64 in high risk groups for erectile dysfunction treatment and all adults over the age of 65 get a pneumococcal vaccination, only 23% of high-risk adults and 64% is viagra a blood thinner of those over the age of 65 do so.Similarly, although the CDC recommends at all infants and some high-risk adults be vaccinated against Haemophilus influenzae type B (Hib), only 80.7% of children in the U.S. And a handful of immunologically compromised adults have been. Pneumococcal and Hib vaccination rates are significantly lower in minority populations in the U.S.

And in countries that have been hit harder by erectile dysfunction treatment than the U.S.Based on these data, I advocate is viagra a blood thinner universal pneumococcal and Hib vaccination among children, at-risk adults and all adults over 65 to prevent serious erectile dysfunction treatment disease.Left. Combined rates of childhood and adult (over 65) pneumococcal vaccination (out of a possible 200). Right. Cases (per million) population of erectile dysfunction treatment at about 90 days into the viagra for 24 nations.

Nations with high pneumococcal vaccination rates have low erectile dysfunction treatment case rates. (Credit. CC BY-SA)How Pneumococcal Vaccination Protects Against erectile dysfunction treatmentProtection against serious erectile dysfunction treatment disease by pneumococcal and Hib treatments makes sense for several reasons. First, recent studies reveal that the majority of hospitalized erectile dysfunction treatment patients, and in some studies nearly all, are infected with streptococci, which causes pneumococcal pneumonias, Hib or other pneumonia-causing bacteria.

Pneumococcal and Hib vaccinations should protect erectile dysfunction patients from these s and thus significantly cut the risk of serious pneumonia.I also found that pneumococcal, Hib and possibly rubella treatments may confer specific protection against the erectile dysfunction viagra that causes erectile dysfunction treatment by means of “molecular mimicry.”Molecular mimicry occurs when the immune system thinks one microbe looks like another. In this case, proteins found in pneumococcal treatments and, to a lesser degree, ones found in Hib and rubella treatments as well look like several proteins produced by the erectile dysfunction viagra.Two of these proteins found in pneumococcal treatments mimic the spike and membrane proteins that permit the viagra to infect cells. This suggests pneumococcal vaccination may prevent erectile dysfunction . Two other mimics are the nucleoprotein and replicase that control viagra replication.

These proteins are made after viral , in which case pneumococcal vaccination may control, but not prevent, erectile dysfunction replication.Either way, these treatments may provide proxy protection against erectile dysfunction that we can implement right now, even before we have a specific viagra treatment. Such protection may not be complete. People might still suffer a weakened version of erectile dysfunction treatment but, like most infants and children, be protected against the worst effects of the .Fighting Influenza-related Pneumonias During the erectile dysfunction treatment viagraWhile the specific protection these other treatments confer against erectile dysfunction treatment has not yet been tested in a clinical trial, I advocate broader implementation of pneumococcal and Hib vaccination for one additional, well-validated reason.Pneumococcal and Hib pneumonias – both caused by bacteria – are the major causes of death following viral influenza. The influenza viagra rarely causes death directly.

Most often, the viagra makes the lungs more susceptible to bacterial pneumonias, which are deadly. Dozens of studies around the world have demonstrated that increasing rates of pneumococcal and Hib vaccination dramatically lowers influenza-related pneumonias.Similar studies demonstrate that the price of using these treatments is balanced by savings due to lower rates of influenza-related hospitalizations, intensive care unit admissions and deaths. In the context of erectile dysfunction treatment, lowering rates of influenza-related hospitalizations and ICU admissions would free up resources to fight the erectile dysfunction, independent of any effect these treatments might have on erectile dysfunction itself. In my opinion, that is a winning scenario.In short, we need not wait for a erectile dysfunction treatment to slow down erectile dysfunction treatment.I believe that we can and should act now by fighting the erectile dysfunction with all the tools at our disposal, including influenza, Hib, pneumococcal and perhaps rubella vaccinations.Preventing pneumococcal and Hib complications of influenza and erectile dysfunction treatment, and perhaps proxy-vaccinating against erectile dysfunction itself, helps everyone.

Administering these already available and well-tested pneumococcal and Hib treatments to people will save money by freeing up hospital beds and ICUs. It will also improve public health by reducing the spread of multiple s and boost the economy by nurturing a healthier population.Robert Root-Bernstein is a Professor of Physiology at Michigan State University. This article was originally published on The Conversation under a Creative Commons liscense Read the original here.This story appeared in the November 2020 issue as "Bacteria and the Brain." Subscribe to Discover magazine for more stories like this.It’s not always easy to convince people that the human gut is a sublime and wondrous place worthy of special attention. Sarkis Mazmanian discovered that soon after arriving at Caltech for his first faculty cheap viagra online job 14 years ago, when he explained to a local artist what he had in mind for the walls outside his new office.The resulting mural greets visitors to the Mazmanian Lab today.

A vaguely psychedelic, 40-foot-long, tube-shaped colon that’s pink, purple and red snakes down the hallway. In a panel next to it, fluorescent yellow and green bacteria explode out of a deeply inflamed section of the intestinal tract, like radioactive lava from outer space.The mural is modest compared with what the scientist has been working on since. Over the last decade or so, Mazmanian has been a leading proponent of the idea that the flora of the human digestive tract has a far more powerful effect on the human body and mind than we thought — a scientific effort that earned him a $500,000 MacArthur Fellowship “Genius Grant” in 2012. Since then, Mazmanian and a small but growing cadre of fellow microbiologists have amassed a tantalizing body of evidence on the microbiome’s role in all kinds of brain disorders, including schizophrenia, Alzheimer’s disease, Parkinson’s disease and depression.But the results they’ve seen in autism could, in the end, prove the most transformative.

Autism affects about 1 in 59 children in the U.S., and involves profound social withdrawal, communication problems, and sometimes anxiety and aggression. The causes of the brain disorder have remained speculative. Now, Mazmanian and other researchers are finding that autism may be inextricably linked to — or even caused by — irregularities in the gut microbiome.A Biology StoryAt 47, Mazmanian — with his shaved head, flannel shirt and skinny jeans — resembles a young, urban hipster on his way to write at the local café. Originally, literary life was his plan.

Born in Lebanon to two Armenian refugees, neither of whom had more than a first-grade education, Mazmanian landed in the class of an energetic high school English teacher in California’s San Fernando Valley, where his family first settled. The teacher recognized his gift for language and encouraged him to pursue a career in literature. Mazmanian enrolled at UCLA in 1990, planning to major in English.Everything changed when he took his first biology class. Hunched over his new, thick textbook in the library, reading about basic biological concepts like photosynthesis, Mazmanian felt a vast new world opening up to him.Sarkis Mazmanian, shown in front of a mural that celebrates the human gut, is part of a group of microbiologists researching the effects of the digestive tract on a range of disorders.

(Credit. Caltech)“For the first time in my life, I wanted to turn the page and see where the story was going to go,” he says. €œI think I decided that minute to become a scientist.”Mazmanian was most fascinated by the idea that tiny organisms, invisible to the naked eye, could function as powerful, self-contained machines — powerful enough to take over and destroy the human body. After graduating with a degree in microbiology, Mazmanian joined a UCLA infectious diseases lab and began studying bacteria that cause staph s.As his dissertation defense approached, Mazmanian read a one-page commentary penned by a prominent microbiologist, highlighting the fact that our intestines are teeming with hundreds, if not thousands, of different species of bacteria.

But it was still largely unknown what they are and how they affect the human body.When Mazmanian dug further, he found that no one had yet answered what seemed to him to be the most obvious question. Why would the human immune system, designed to attack and destroy foreign invaders, allow hundreds of species of bacteria to live and thrive in our guts unmolested?. To him, the bacteria’s survival implied that we had evolved to coexist with them. And if that were so, he reasoned, there must be some benefit to both the microbes and the human body — a symbiotic relationship.

But what was it?. Gut InvadersMazmanian set out to study the link between gut microbes and the immune system. As a postdoctoral researcher, he joined the lab of Harvard University infectious disease specialist Dennis Kasper.To start, Mazmanian examined how the immune systems of germ-free mice — lab mice completely protected, starting at birth, from all microbes — differed from those of mice with either few or normal levels of microbes. He expected this initial census would be just a first step in a long and arduous quest for scientific pay dirt.

But when he went to examine a printout of his results in the lab, he realized immediately he might already be onto something big. The germ-free mice had a 30 to 40 percent reduction in a specific type of immune cell known as helper T-cells.This colorized close-up of a mouse’s gut reveals the tight relationship between the gut microbe Bacteroides fragilis (red) and the epithelial surface of the colon (blue). (Credit. Caltech)Since helper T-cells play a key role in coordinating attacks against invading pathogens, the finding suggested that the immune systems of the germ-free mice were far less robust than those found in peers with normal levels of microbes.“That was exciting, right?.

€ Mazmanian recalls. €œObviously I repeated it and tested it in a number of different ways. Then I asked the next question. €˜Can I restore the [immune] function in an adult animal?.

€™â€‰â€Mazmanian colonized the guts of the immunocompromised, germ-free mice with microbes from standard lab mice. After receiving the fecal transplant, their T-cell counts shot up. Within a month, their numbers were identical to mice raised outside the germ-free bubble.Resolving to identify the microorganisms causing this transformation, Mazmanian resorted to trial and error. One by one, he added strains of bacteria found in the guts of mice to the guts of germ-free mice.He got nowhere with the first five or six species he examined.

Then, simply because it was convenient, he decided to test one more that was readily available in his lab. Mazmanian’s adviser, Kasper, had been studying a gut microbe called Bacteroides fragilis. When Mazmanian implanted one of Kasper’s specimens into the gut of his germ-free mice, the results were dramatic. The T-cell numbers spiked to normal.

Eventually, Mazmanian demonstrated he could reproduce this effect simply by adding a single molecule that these bacteria produce, called polysaccharide A, to their guts.“There was no logic in the choice whatsoever,” Mazmanian recalls. €œ[B. Fragilis] was available, it came from the gut.” In other words, he got lucky.Mazmanian dug deeper and discovered that the biggest impact B. Fragilis had was on the population of a subtype of helper T-cells called regulatory, or suppressor, T-cells.

These cells play a key role in preventing the immune system from attacking its host body, protecting against autoimmune or inflammatory diseases. It was the first time any scientist had demonstrated that a single compound from a single microbe could reverse a specific problem with the immune system.To Mazmanian, the finding, published in 2005 in the journal Cell, alluded to new approaches to treating a wide array of autoimmune, inflammatory and allergic disorders. What if it were possible to help a faulty immune system by tweaking a patient’s microbiome?. It was with this exploration in mind that he arrived in Pasadena in 2006 to set up his lab at Caltech.A Convenient CollaborationA few years later, Mazmanian was having lunch on campus with neuroscientist and colleague Paul Patterson.

Patterson had been preoccupied with a mystery that had, for years, confounded those studying autism in humans. When pregnant mothers have a severe in the second trimester, their babies are much more likely to develop autism.As Mazmanian tells it, Patterson was a man of few words, and at lunch Mazmanian was “going on and on” about his own work.“You know,” Patterson interjected thoughtfully, “I think kids with autism have GI issues.”Patterson recalled reading that something like 60 percent of children with autism had some form of clinical GI problem, such as bloating, constipation, flatulence or diarrhea. Was it possible, he wondered, that there was a microbiome connection?. As they talked, Mazmanian’s excitement grew.A few years earlier, Patterson had discovered that when he exposed pregnant mice to pathogens like the influenza viagra, they gave birth to pups that grew up more likely to be startled by loud noises, to shy away from social contact and to groom themselves repetitively — symptoms that resemble those of autism.

Patterson was in the process of comparing the brains of these autism-mimicking mice with their neurotypical cousins to see if he could detect any differences that might explain how the maternal immune system was somehow interfering with the pups’ brain development.Mazmanian had a suggestion. The next time Patterson sacrificed one of his autistic mice to study their brains, what if he set the intestines aside for his colleague down the hall?. When the guts arrived in Mazmanian’s lab, he found that the intestines of the neurotypical mice looked normal. But the guts of the autism-mimicking offspring were almost uniformly inflamed.

Could it be that the microbiome was the cause of this inflammation?. And could that, in turn, be somehow connected to the behavioral symptoms?. Throughout the winter and spring of 2012, Mazmanian and Patterson continued their conversation. Mazmanian found distinct differences in the microbiomes of the mice.

And, they noticed, the mice with the features of autism had leaky gut syndrome, an increased permeability of the gut lining that can allow pathogens and allergens to leach out. This condition had also been reported in children with autism.So Mazmanian and Patterson turned their attention outside the gut. They took blood samples to see if any gut microbes, or the compounds they produce, were circulating in the rest of the body. They homed in on one molecule in particular, called 4-ethylphenyl sulfate, which was roughly 45 times as abundant in the mice that had symptoms of autism.

And it looked familiar. Structurally, it was almost identical to a molecule recently found to be significantly elevated in human children with autism.It was enough to take the next step. Every day for three weeks, Mazmanian injected the molecule, harvested from the mice with autism-like symptoms, directly into the bloodstream of 5-week-old normal lab mice (the age at which the autistic mice normally developed leaky gut). Then Mazmanian and his team gave them a series of behavioral tests.

The mice were far more easily startled and were less comfortable in large empty spaces than their untreated peers, indications of an increase in anxiety-related behaviors commonly seen in the mice with autism-like symptoms. The researchers published their results in Cell in 2013.Though surprising, the data made sense in some ways. Many drug companies rely on small-molecule drugs that can be taken orally, but still manage to cross the blood-brain barrier and affect behavior. It seemed entirely possible that small molecules, created by bacteria in the gut, could enter the bloodstream and reach the brain.

And they don’t even have to leak out of the gut to do so.Of Mice and MenPatterson died in 2014, at age 70, just six months after the publication of the duo’s groundbreaking Cell paper. Around the same time, a series of parallel experiments in a clinic hundreds of miles away was already paving the way forward. While Patterson and Mazmanian had been working in mice, Rosa Krajmalnik-Brown, a microbiologist at Arizona State University, had teamed up with Jim Adams, who directs the university’s autism and Asperger’s research program, to study humans.The researchers were conducting a detailed analysis of the microbiome of human autism patients and found that the bacteria were far less diverse in the children with autism. Notably, several important species involved in the digestion of carbohydrates were severely depleted.Krajmalnik-Brown and Adams launched a preliminary trial to test the effects of fecal transplants on 18 children between the ages of 7 and 16 with severe autism, who also had severe GI issues.

The researchers administered powerful antibiotics to kill off the microbiomes of the children and followed them with a bowel cleanse. They then replaced the microbes with transplanted flora taken from the guts of healthy neurotypical adult volunteers.The results were better than anyone could have expected. The procedure resulted in a large reduction in GI symptoms and increased the diversity of bacteria in the children’s guts. But more significantly, their neurological symptoms were reduced.

At the onset of the study in 2017, an independent evaluator found 83 percent of participants had severe autism. Two years after the initial trial, only 17 percent were rated as severely autistic. And 44 percent were no longer on the autism scale.“[My child] did a complete 180,” says Dana Woods, whose then-7-year-old son Ethan enrolled in the initial study five years ago. €œHis ability to communicate is so much different now.

He’s just so much more present. He’s so much more aware. He’s no longer in occupational therapy. He’s no longer in speech therapy.

After the study, he tested two points away from a neurotypical child.”In their first report on the trial in 2017, the team highlighted a number of distinct changes in the microbiome after the transplants, in particular a surge in the populations of three types of bacteria. Among them was a four-fold increase in Bifidobacterium, a probiotic organism that seems to play a key role in the maintenance of a healthy gut.But figuring out what was happening on a cellular level — to really look inside some guts — would require another vehicle. The ASU team needed Mazmanian’s mice.“At the end of the day, what we care about is healing people and how the microbiome affects people,” explains Krajmalnik-Brown. €œThat’s why we work with people.

But with mice you can do things that are more mechanistic.”The Great Mouse Detective(Credit. Caltech)Together, Krajmalnik-Brown, Mazmanian and their collaborators would uncover some tantalizing new insights that go a long way to solving the mystery. In May 2019, the team published another high-profile paper in Cell, after they transplanted stool samples from Krajmalnik-Brown’s severely autistic patients into the guts of Mazmanian’s germ-free mice. The offspring of these mice showed the autism-like symptoms, such as repetitive and compulsive behavior.This time, the team dug even deeper into the biochemical processes playing out in the brain, looking not just at behavior but at the chemicals involved in creating it.

The mice that developed autism-like behaviors had measurably lower levels of two substances called taurine and 5-aminovaleric acid (5AV). When they dug into the literature, the team learned that these two substances are known to mimic activity of a key signaling agent in the brain called gamma-aminobutyric acid (GABA) — a neurotransmitter that other studies have found is deficient in the brains of children with autism.What’s more, some have speculated that the tendency of children with autism to experience sensory overstimulation may stem from the inability to tamp down overexcited neurons. A lack of GABA could lead to just that.The scientists next orally administered high levels of taurine and 5AV to pregnant mice with the autistic children’s microbiomes. When their pups were born, the researchers continued to feed the young the substances until they reached adulthood.

Compared with untreated animals, the second-generation mice had significantly fewer behavioral symptoms. Taurine reduced repetitive behavior, as measured by marble burying, increased the level of social interaction, and relieved anxiety. Mice administered 5AV were more active and social.“We healed humans with behavioral problems,” says Krajmalnik-Brown. €œ[And we] transferred some of those deficits and behaviors to mice — basically the opposite.

It’s huge.”Mazmanian hopes to take the next step in the months ahead.“I can flip a switch, turn on a light, I know that switch turns on that light. I don’t know the circuit, I don’t know where the wire is,” Mazmanian says. €œExactly how that’s happening … we just don’t understand that.”This most recent study, by itself, hardly proves that dysregulated microbiomes cause the brain disorder — a point that plenty of other scientists skeptical of Mazmanian’s work are happy to make.“The paper made a big splash, but trying to model psychiatric-related human conditions in mice, in my view, is a little bit of a stretch,” says Sangram Sisodia, a neurobiologist at the University of Chicago who studies the microbiome. €œA mouse with autism?.

€Nor was that the only criticism. Several researchers have suggested that the group didn’t give proper attention to one of their tests ­— one whose results conflicted with their thesis ­— while others found flaws in the statistical methods they used to assess their results. Mazmanian downplays these criticisms, but agrees the work is not yet conclusive.Meanwhile, the ASU trial has also engendered skepticism, mainly due to its tiny sample size, the lack of a control group and the methods by which the children were assessed for autism severity. Krajmalnik-Brown and Adams say they stand by their results, but agree more research is needed.

In recent months, they have launched two new studies that will address these issues.Adams insists the work is already changing lives. €œWe followed up with every one of our 18 participants,” he says, referring to the children who received fecal transplants. €œSure enough, we found that most of the GI benefits had remained. And family after family said their child just slowly, steadily continued making more improvement.” They published the update in Scientific Reports in spring 2019.“I’m not ready to say the case is closed,” says Mazmanian.

€œHealthy skepticism is a good thing. I believe the preclinical data, I believe the mouse data. But there’s a lot of studies that still need to be done.” A Healthy Gut, A New OutlookEthan Woods had GI issues and symptoms of autism until researchers introduced new microbes to his gut. His mother says the treatment changed everything.

(Credit. Dana Woods)Prior to his fecal transplant at age 7, Ethan Woods suffered from chronic and severe diarrhea, constipation and cramping, symptoms so extreme that to his mother, Dana, he sounded like “a bit like a woman in labor when he was trying to have a bowel movement.” “It was just awful watching your child go through this,” she says, explaining that when she enrolled her autistic son in the Arizona State study, her “only goal was to fix his gut.”Remarkably, Ethan’s agony began to disappear just a few weeks into the trial. But that was not the most dramatic difference. Before the transplant, Ethan’s speech was drawn out and slow, his language skills rudimentary.

He seemed to live in his own bubble. He had frequent outbursts. For as long as Dana could remember, her mornings with Ethan had been marked by arguing, fighting, pushing and anger. But then one morning, something shocking happened.“He woke me up one morning with his face right in my face with this big smile and he said, ‘Morning, Mom!.

€™â€‰â€ she recalls. €œAnd he was just excited and happy and ready to go about his day with this big smile. It choked me up to the point where I teared up because I had never experienced a happy kid in the morning.”Later, Ethan carried over an iPad and opened an app with a talking cat that repeats back the words children speak aloud. He played back a video recording of himself from just a few weeks earlier.“[He] looks me in the eye and says, ‘Mom, why did I talk like that?.

What is wrong with me?. €™ And as soon as he did that, I caught my breath. I had to compose myself and say, ‘I don’t know. But do you feel better?.

Do you feel different?. Why do you think?. €™â€‰â€Ethan’s communication skills had already begun to improve. Within a year of the study, his speech therapist graduated him from speech therapy because he had met all his goals.“He went from one end of the rainbow all the way to the other end of the rainbow,” she says.

€œPrior to the study, I was very afraid. My biggest fear was ‘how is he going to navigate the world when I’m not here?. €™ And I think I have a lot of hope now that he is going to be OK now on his own.”.

After watching a parent succumb to the deleterious effects of Alzheimer's disease, it's only natural to wonder if you might cheap viagra be doomed to the same fate. The good news?. That's cheap viagra not necessarily the case.

The bad news, however, is that the disease is so prevalent your overall risk is still relatively high — especially as you age. At 65, you have a roughly cheap viagra 3 percent chance of contracting Alzheimer's disease each year. This bumps up to a 17 percent chance after your 75th birthday, and increases to a roughly one in three chance you'll develop Alzheimer's after the age of 85.

Experts agree that family history elevates the risk, particularly if you have more than one parent or sibling with the disease, but they disagree on how much. Some studies indicate the risk cheap viagra hovers at around 30 percent, while others estimate an up to two or four times increased risk. Early onset Alzheimer's — which typically strikes individuals between the ages of 40 and 65 — has a more easily understood genetic link, with a 50 percent chance the child of an Alzheimer's patient will also be diagnosed with the disease.

Read More:Why Do Women cheap viagra Get Alzheimer’s More Than Men?. How Did Alzheimer's Disease Get Its Name?. Are We Close to Curing Alzheimer’s Disease?.

However, a combination of cheap viagra genetic and environmental factors come into play for the more common late-onset variation, says Rita Guerreiro, a neurogeneticist at the Van Andel Institute. Which makes things even more difficult to predict. €œMany people who have relatives with [Alzheimer's] cheap viagra never develop the disease, and many without a family history of the disease do develop it,” says Guerreiro.Interested in tipping the odds in your favor?.

Some scientists think keeping your mind active, consuming a diet low in red meat and sugar and exercising regularly could help keep the memory-zapping disease at bay.Late fall and early winter typically mean a flurry of holiday travel and get-togethers for a lot of people. But this year will be anything but normal. Making plans is more than a matter of shopping around for flight cheap viagra prices or car rental fees.

Many of us are probably also asking ourselves whether to stay home or see loved ones, and how to stay safe at holiday gatherings. For the lowest risk of spreading or becoming sick with erectile dysfunction treatment, not traveling is the cheap viagra way to go. However, there might be loved ones who desperately need companionship in the coming months.

€œThere are situations where people will choose, and choose correctly, to go and support those family members,” says Lin H. Chen, director of the Travel Medicine Center at cheap viagra Mount Auburn Hospital and president of the International Society of Travel Medicine. No matter if you’re going cross-country to see siblings or staying at home with your dog, experts say, remember two things.

Plan ahead and stay flexible.Tackle cheap viagra Logistics FirstFor those interested in interstate travel, first assess whether or not those plans are feasible. The states you’re going to (and coming back to) might have rules about isolating yourself for two weeks once you arrive. If you live in one of those states but a two-week isolation period isn’t feasible — because you have to go to work or send kids to school, for example — cheap viagra then traveling for the holidays won’t work for you, says Gabriela Andujar Vazquez, an infectious disease doctor at Tufts Medical Center.

Some states say that isolation requirements don’t apply if you get a negative erectile dysfunction treatment test. But testing you or your whole family may lie outside your budget if the exams aren’t covered by insurance, Andujar Vazquez says. Factor those financial decisions into your travel plans, too.If you do decide to travel, choose driving over flying if you can cheap viagra.

Busy rest stops might mean confronting crowds of other highway travelers, Chen says. However, compared to the entire process of flying — getting to an airport and waiting in lines repeatedly — cheap viagra driving likely means fewer crowds overall. €œThink about precautions through this journey,” Chen says, “not just on the plane, train, bus or car.”Airplanes themselves receive a lot of attention as potential viagra spreaders.

But Chen says there are three instances of infected individuals spreading the disease to two or more people on a flight. Those transmissions happened before any airline required passengers to wear masks cheap viagra. Since then, other interventions like leaving seats open, disinfecting often and updated air filtration have been introduced on airplanes, too.

Though there’s cheap viagra no data yet on how effective these combined intervention strategies are, “the fact that we haven’t heard about masked transmission on recent flights is also reassuring,” Chen says. On the Big DayOdds are you’re debating travel plans for the sake of a big family meal. Or even if you’re staying local, you might try and work something out with friends and relatives nearby.

Both Chen and Andujar Vazquez emphasize that no matter which you choose, cheap viagra keep up the erectile dysfunction treatment precautions once you’re all together. Generally, the smaller the gathering (and the fewer number of households), the better. Keep activities cheap viagra outdoors if you can, seat groups apart, and keep masks on while not eating.

You might also consider new ways to keep everyone fed. The typical buffet serving style can mean a lot of utensil sharing, so maybe opt for single-serving portioning or have everyone wash or sanitize hands before and after touching communal dishes. And as fun cheap viagra as it might be to play bartender, maybe choose a BYOB policy as well.

Oh, and “no one should be coming sick,” Andujar Vazquez says. €œYou cannot say that enough.”These might sound like a lot of holiday modifications, which is why it’s cheap viagra important to discuss what the situation will look like before coming together. €œPeople have to feel comfortable talking about these things, because it’s part of our daily life now,” Andujar Vazquez says.

€œHave that conversation before the event happens so people don’t have unexpected surprises or feel unsafe with some sort of behavior.”At the same time, acknowledge that even the most careful planning might fall apart. Your destination might become a erectile dysfunction treatment hotspot days cheap viagra before you’re set to arrive, or you or someone in your gathering might start feeling unwell ahead of time. Though it’s easier said than done, accept that plans will change whether you want them to or not — and that celebrations in the coming months will look different than they used to.

€œRealistically, this holiday cheap viagra season is going to be difficult for a lot of people,” says Jonathan Kanter, psychologist and director of the Center for the Science of Social Connection at the University of Washington. In individuals coping with significant life changes, one of the best predictors of depression is whether or not people can leave former goals behind and adopt new ones, Kanter says. Letting go of old expectations — like how you normally cheap viagra gather with family, for example — can involve a kind of grieving process.

But recalibrating what you want to get out of a situation is an essential coping skill. €œYou won’t be able to get there unless you breathe and accept that you’re in a new context,” Kanter says. €œWith that acceptance, hopefully there's a lot of creativity and innovation and grace cheap viagra about how to make it as successful as possible.” The prospect of not seeing loved ones in the coming months might make some people nervous, for themselves and for others.

What's important to remember is that it's possible to make it through — and that future holidays will get better.As flu season creeps up on the Northern Hemisphere, cold and flu relief medications will inevitably fly off store shelves. A natural remedy that shoppers might reach for is elderberry, a small, blackish-purple fruit that companies turn into syrups, lozenges cheap viagra and gummies. Though therapeutic uses of the berry date back centuries, Michael Macknin, a pediatrician at the Cleveland Clinic, hadn’t heard of using elderberry to treat the flu until a patient’s mother asked him about it.

Some industry-sponsored research claims that the herbal remedy could cut the length of the symptoms by up to four days. For a comparison, cheap viagra Tamiflu, an FDA-approved treatment, only reduces flu duration by about a single day. €œI said, 'Gee, if that’s really true [about elderberry], it would be a huge benefit,'” Macknin says.

But the effectiveness and safety of elderberry is still fairly cheap viagra unclear. Unlike the over-the-counter medicines at your local pharmacy, elderberry hasn't been through rigorous FDA testing and approval. However, Macknin and his team recently published a study in the Journal of General Internal Medicine, which found that elderberry treatments did nothing for flu patients.

This prompts a need for further studies into the remedy — work that unfortunately stands a low chance of happening in cheap viagra the future, Macknin says. Looking For ProofElderberries are full of chemicals that could be good for your health. Like similar fruits, the berries contain high levels of antioxidants, compounds that shut down reactions in our bodies cheap viagra that damage cells.

But whether or not elderberry's properties also help immune systems fend off a viagra is murky. There are only a handful of studies that have examined if elderberries reduced the severity or duration of the flu. And though some of the work prior to Macknin’s was well-designed and supported this herbal remedy as a helpful flu aid, at least some — and potentially all — of those studies were funded by elderberry treatment manufacturers.Macknin says an elderberry supplement company provided his team cheap viagra with their products and a placebo version for free, but that the company wasn’t involved in the research beyond that.

Macknin's study is the largest one conducted on elderberry to date, with 87 influenza patients completing the entire treatment course. Participants in the study were also welcome to take Tamiflu, for ethical reasons, as the team didn’t want to cheap viagra exclude anyone from taking a proven flu therapy. Additionally, each participant took home either a bottle of elderberry syrup or the placebo with instructions on when and how to take it.

The research team called participants every day for a symptom check and to remind them to take their medication.By chance, it turned out that a higher percentage of the patients given elderberry syrup had gotten their flu shot and also chose to take Tamiflu. Since the vaccination can reduce the severity of in recipients who still come down with the flu, cheap viagra the study coincidentally operated in favor of those who took the herbal remedy, Macknin says. Those patients could have dealt with a shorter, less-intense illness because of the Tamiflu and vaccination.

€œEverything was stacked to have cheap viagra it turn out better [for the elderberry group],” Macknin says, “and it turned out the same.” The researchers found no difference in illness duration or severity between the elderberry and placebo groups. While analyzing the data, the team also found that those on the herbal treatment might have actually fared worse than those on the placebo. The potential for this intervention to actually harm instead of help influenza patients cheap viagra explains why Macknin thinks the therapy needs further research.But, don't expect that work to happen any time soon.

Researchers are faced with a number of challenges when it comes to studying the efficacy of herbal remedies. For starters, there's little financial incentive to investigate if they actually work. Plant products are challenging to patent, making them less cheap viagra lucrative prospects for pharmaceutical companies or research organizations to investigate.

Additionally, investigations that try and prove a proposed therapy as an effective drug — like the one Macknin and his team accomplished — are expensive, Macknin says. Those projects need FDA oversight and additional paperwork, components that drive up study cheap viagra costs. €œIt’s extraordinarily expensive and there’s no money in it for anybody,” Macknin says.Talk To Your DoctorUltimately, research on elderberry therapies for flu patients is a mixed bag, and deserves more attention from scientists.

However, if you still want to discuss elderberry treatments for the flu with your doctor, that’s a conversation you should feel comfortable having, says Erica McIntyre, an expert focused on health and environmental psychology in the School of Public Health at the University of Technology Sydney. Navigating what cheap viagra research says about a particular herbal medicine is challenging for patients and health practitioners alike. The process is made more complex by the range of similar-sounding products on the market that lack standardized ingredients, McIntyre says.

But when doctors judge or shame patients for asking about non-conventional healthcare interventions, the response can distance people and push them closer to potentially cheap viagra unproven treatments. Even worse, those individuals might start to keep their herbal remedies a secret. €œIt is that fear about being judged for use of that medication,” McIntyre says, that drives up to 50 percent of people taking herbal treatments to withhold that information from healthcare practitioners.

That’s a dangerous choice, as some herbal and traditional medications can interact and cause health problems.If a physician shames someone for asking about alternative cheap viagra medicines, it’s likely time to find a new doctor, McIntyre says. Look for someone who will listen to your concerns — whether it's that you feel traditional treatments haven’t worked for you, or that you didn’t like the side effects, the two common reasons people pursue herbal treatments in the first place. €œYou’re not necessarily looking for a doctor that will let you do whatever you want,” McIntyre says, “but that they actually consider you as a patient, your treatment choices and your treatment priorities, and communicate in a way that’s supportive.” And if a doctor suggests cheap viagra that you avoid a treatment you’re interested in, ask why.

They generally have a good reason, McIntyre says.For now, know that even if your doctor doesn’t support you taking elderberry, there are other proven preventative measures that are worth your while — like the flu shot. Anyone six months or older should get it, Macknin says, and stick to the protocols we’re used to following to prevent erectile dysfunction treatment s, like social distancing, mask-wearing and hand-washing. Those measures also help prevent flu transmission, too — something, so far, no elderberry supplement package can claim.The yearly influenza season threatens to make the erectile dysfunction treatment viagra doubly deadly, but I believe that this isn’t inevitable.There cheap viagra are two commonly given treatments – the pneumococcal treatment and the Hib treatment – that protect against bacterial pneumonias.

These bacteria complicate both influenza and erectile dysfunction treatment, often leading to death. My examination of disease trends and vaccination rates leads me to believe that broader use of the pneumococcal and Hib treatments could guard against the worst effects of a erectile dysfunction treatment illness.I am cheap viagra an immunologist and physiologist interested in the effects of combined s on immunity. I have reached my insight by juxtaposing two seemingly unrelated puzzles.

Infants and children get erectile dysfunction, the viagra that causes erectile dysfunction treatment, but very rarely become hospitalized or die. And case numbers and death rates from erectile dysfunction treatment began varying greatly cheap viagra from nation to nation and city to city even before lockdowns began. I wondered why.One night I woke up with a possible answer.

Vaccination rates cheap viagra. Most children, beginning at age two months, are vaccinated against numerous diseases. Adults less so cheap viagra.

And, both infant and adult vaccination rates vary widely across the world. Could differences in the rates of vaccination against one or more diseases account for differences in erectile dysfunction treatment risks?. As someone who had previously investigated other viagras such as the Great Flu cheap viagra viagra of 1918-19 and AIDS, and who has worked with treatments, I had a strong background for tracking down the relevant data to test my hypothesis.Pneumococcal Vaccination Rates Correlate With Lower erectile dysfunction treatment Cases and DeathsI gathered national and some local data on vaccination rates against influenza, polio, measles-mumps-rubella (MMR), diphtheria-tetanus-pertussis (DTP), tuberculosis (BCG), pneumococci and Haemophilus influenzae type B (Hib).

I correlated them with erectile dysfunction treatment case rates and death rates for 24 nations that had experienced their erectile dysfunction treatment outbreaks at about the same time. I controlled for factors such as percentage of the population who were obese, diabetic or elderly.I found that only pneumococcal treatments cheap viagra afforded statistically significant protection against erectile dysfunction treatment. Nations such as Spain, Italy, Belgium, Brazil, Peru and Chile that have the highest erectile dysfunction treatment rates per million have the poorest pneumococcal vaccination rates among both infants and adults.

Nations with the lowest rates of erectile dysfunction treatment – Japan, Korea, Denmark, Australia and New Zealand – have the highest rates of pneumococcal vaccination among both infants and adults.A recent preprint study (not yet peer-reviewed) from researchers at the Mayo Clinic has also reported very strong associations between pneumococcal vaccination and protection against erectile dysfunction treatment. This is especially true cheap viagra among minority patients who are bearing the brunt of the erectile dysfunction viagra. The report also suggests that other treatments, or combinations of treatments, such as Hib and MMR may also provide protection.These results are important because in the U.S., childhood vaccination against pneumococci – which protects against Streptococcus pneumoniae bacteria – varies by state from 74% to 92%.

Although the CDC recommends that all adults 18-64 cheap viagra in high risk groups for erectile dysfunction treatment and all adults over the age of 65 get a pneumococcal vaccination, only 23% of high-risk adults and 64% of those over the age of 65 do so.Similarly, although the CDC recommends at all infants and some high-risk adults be vaccinated against Haemophilus influenzae type B (Hib), only 80.7% of children in the U.S. And a handful of immunologically compromised adults have been. Pneumococcal and Hib vaccination rates are significantly lower in minority populations in the U.S.

And in cheap viagra countries that have been hit harder by erectile dysfunction treatment than the U.S.Based on these data, I advocate universal pneumococcal and Hib vaccination among children, at-risk adults and all adults over 65 to prevent serious erectile dysfunction treatment disease.Left. Combined rates of childhood and adult (over 65) pneumococcal vaccination (out of a possible 200). Right.

Cases (per million) population of erectile dysfunction treatment at about 90 days into the viagra for 24 nations. Nations with high pneumococcal vaccination rates have low erectile dysfunction treatment case rates. (Credit.

CC BY-SA)How Pneumococcal Vaccination Protects Against erectile dysfunction treatmentProtection against serious erectile dysfunction treatment disease by pneumococcal and Hib treatments makes sense for several reasons. First, recent studies reveal that the majority of hospitalized erectile dysfunction treatment patients, and in some studies nearly all, are infected with streptococci, which causes pneumococcal pneumonias, Hib or other pneumonia-causing bacteria. Pneumococcal and Hib vaccinations should protect erectile dysfunction patients from these s and thus significantly cut the risk of serious pneumonia.I also found that pneumococcal, Hib and possibly rubella treatments may confer specific protection against the erectile dysfunction viagra that causes erectile dysfunction treatment by means of “molecular mimicry.”Molecular mimicry occurs when the immune system thinks one microbe looks like another.

In this case, proteins found in pneumococcal treatments and, to a lesser degree, ones found in Hib and rubella treatments as well look like several proteins produced by the erectile dysfunction viagra.Two of these proteins found in pneumococcal treatments mimic the spike and membrane proteins that permit the viagra to infect cells. This suggests pneumococcal vaccination may prevent erectile dysfunction . Two other mimics are the nucleoprotein and replicase that control viagra replication.

These proteins are made after viral , in which case pneumococcal vaccination may control, but not prevent, erectile dysfunction replication.Either way, these treatments may provide proxy protection against erectile dysfunction that we can implement right now, even before we have a specific viagra treatment. Such protection may not be complete. People might still suffer a weakened version of erectile dysfunction treatment but, like most infants and children, be protected against the worst effects of the .Fighting Influenza-related Pneumonias During the erectile dysfunction treatment viagraWhile the specific protection these other treatments confer against erectile dysfunction treatment has not yet been tested in a clinical trial, I advocate broader implementation of pneumococcal and Hib vaccination for one additional, well-validated reason.Pneumococcal and Hib pneumonias – both caused by bacteria – are the major causes of death following viral influenza.

The influenza viagra rarely causes death directly. Most often, the viagra makes the lungs more susceptible to bacterial pneumonias, which are deadly. Dozens of studies around the world have demonstrated that increasing rates of pneumococcal and Hib vaccination dramatically lowers influenza-related pneumonias.Similar studies demonstrate that the price of using these treatments is balanced by savings due to lower rates of influenza-related hospitalizations, intensive care unit admissions and deaths.

In the context of erectile dysfunction treatment, lowering rates of influenza-related hospitalizations and ICU admissions would free up resources to fight the erectile dysfunction, independent of any effect these treatments might have on erectile dysfunction itself. In my opinion, that is a winning scenario.In short, we need not wait for a erectile dysfunction treatment to slow down erectile dysfunction treatment.I believe that we can and should act now by fighting the erectile dysfunction with all the tools at our disposal, including influenza, Hib, pneumococcal and perhaps rubella vaccinations.Preventing pneumococcal and Hib complications of influenza and erectile dysfunction treatment, and perhaps proxy-vaccinating against erectile dysfunction itself, helps everyone. Administering these already available and well-tested pneumococcal and Hib treatments to people will save money by freeing up hospital beds and ICUs.

It will also improve public health by reducing the spread of multiple s and boost the economy by nurturing a healthier population.Robert Root-Bernstein is a Professor of Physiology at Michigan State University. This article was originally published on The Conversation under a Creative Commons liscense Read the original here.This story appeared in the November 2020 issue as "Bacteria and the Brain." Subscribe to Discover magazine for more stories like this.It’s not always easy to convince people that the human gut is a sublime and wondrous place worthy of special attention. Sarkis Mazmanian discovered that soon after arriving at Caltech for his first faculty job 14 years ago, when he explained to a local artist what he had in mind for the walls outside his new office.The resulting mural greets visitors to the Mazmanian Lab today.

A vaguely psychedelic, 40-foot-long, tube-shaped colon that’s pink, purple and red snakes down the hallway. In a panel next to it, fluorescent yellow and green bacteria explode out of a deeply inflamed section of the intestinal tract, like radioactive lava from outer space.The mural is modest compared with what the scientist has been working on since. Over the last decade or so, Mazmanian has been a leading proponent of the idea that the flora of the human digestive tract has a far more powerful effect on the human body and mind than we thought — a scientific effort that earned him a $500,000 MacArthur Fellowship “Genius Grant” in 2012.

Since then, Mazmanian and a small but growing cadre of fellow microbiologists have amassed a tantalizing body of evidence on the microbiome’s role in all kinds of brain disorders, including schizophrenia, Alzheimer’s disease, Parkinson’s disease and depression.But the results they’ve seen in autism could, in the end, prove the most transformative. Autism affects about 1 in 59 children in the U.S., and involves profound social withdrawal, communication problems, and sometimes anxiety and aggression. The causes of the brain disorder have remained speculative.

Now, Mazmanian and other researchers are finding that autism may be inextricably linked to — or even caused by — irregularities in the gut microbiome.A Biology StoryAt 47, Mazmanian — with his shaved head, flannel shirt and skinny jeans — resembles a young, urban hipster on his way to write at the local café. Originally, literary life was his plan. Born in Lebanon to two Armenian refugees, neither of whom had more than a first-grade education, Mazmanian landed in the class of an energetic high school English teacher in California’s San Fernando Valley, where his family first settled.

The teacher recognized his gift for language and encouraged him to pursue a career in literature. Mazmanian enrolled at UCLA in 1990, planning to major in English.Everything changed when he took his first biology class. Hunched over his new, thick textbook in the library, reading about basic biological concepts like photosynthesis, Mazmanian felt a vast new world opening up to him.Sarkis Mazmanian, shown in front of a mural that celebrates the human gut, is part of a group of microbiologists researching the effects of the digestive tract on a range of disorders.

(Credit. Caltech)“For the first time in my life, I wanted to turn the page and see where the story was going to go,” he says. €œI think I decided that minute to become a scientist.”Mazmanian was most fascinated by the idea that tiny organisms, invisible to the naked eye, could function as powerful, self-contained machines — powerful enough to take over and destroy the human body.

After graduating with a degree in microbiology, Mazmanian joined a UCLA infectious diseases lab and began studying bacteria that cause staph s.As his dissertation defense approached, Mazmanian read a one-page commentary penned by a prominent microbiologist, highlighting the fact that our intestines are teeming with hundreds, if not thousands, of different species of bacteria. But it was still largely unknown what they are and how they affect the human body.When Mazmanian dug further, he found that no one had yet answered what seemed to him to be the most obvious question. Why would the human immune system, designed to attack and destroy foreign invaders, allow hundreds of species of bacteria to live and thrive in our guts unmolested?.

To him, the bacteria’s survival implied that we had evolved to coexist with them. And if that were so, he reasoned, there must be some benefit to both the microbes and the human body — a symbiotic relationship. But what was it?.

Gut InvadersMazmanian set out to study the link between gut microbes and the immune system. As a postdoctoral researcher, he joined the lab of Harvard University infectious disease specialist Dennis Kasper.To start, Mazmanian examined how the immune systems of germ-free mice — lab mice completely protected, starting at birth, from all microbes — differed from those of mice with either few or normal levels of microbes. He expected this initial census would be just a first step in a long and arduous quest for scientific pay dirt.

But when he went to examine a printout of his results in the lab, he realized immediately he might already be onto something big. The germ-free mice had a 30 to 40 percent reduction in a specific type of immune cell known as helper T-cells.This colorized close-up of a mouse’s gut reveals the tight relationship between the gut microbe Bacteroides fragilis (red) and the epithelial surface of the colon (blue). (Credit.

Caltech)Since helper T-cells play a key role in coordinating attacks against invading pathogens, the finding suggested that the immune systems of the germ-free mice were far less robust than those found in peers with normal levels of microbes.“That was exciting, right?. € Mazmanian recalls. €œObviously I repeated it and tested it in a number of different ways.

Then I asked the next question. €˜Can I restore the [immune] function in an adult animal?. €™â€‰â€Mazmanian colonized the guts of the immunocompromised, germ-free mice with microbes from standard lab mice.

After receiving the fecal transplant, their T-cell counts shot up. Within a month, their numbers were identical to mice raised outside the germ-free bubble.Resolving to identify the microorganisms causing this transformation, Mazmanian resorted to trial and error. One by one, he added strains of bacteria found in the guts of mice to the guts of germ-free mice.He got nowhere with the first five or six species he examined.

Then, simply because it was convenient, he decided to test one more that was readily available in his lab. Mazmanian’s adviser, Kasper, had been studying a gut microbe called Bacteroides fragilis. When Mazmanian implanted one of Kasper’s specimens into the gut of his germ-free mice, the results were dramatic.

The T-cell numbers spiked to normal. Eventually, Mazmanian demonstrated he could reproduce this effect simply by adding a single molecule that these bacteria produce, called polysaccharide A, to their guts.“There was no logic in the choice whatsoever,” Mazmanian recalls. €œ[B.

Fragilis] was available, it came from the gut.” In other words, he got lucky.Mazmanian dug deeper and discovered that the biggest impact B. Fragilis had was on the population of a subtype of helper T-cells called regulatory, or suppressor, T-cells. These cells play a key role in preventing the immune system from attacking its host body, protecting against autoimmune or inflammatory diseases.

It was the first time any scientist had demonstrated that a single compound from a single microbe could reverse a specific problem with the immune system.To Mazmanian, the finding, published in 2005 in the journal Cell, alluded to new approaches to treating a wide array of autoimmune, inflammatory and allergic disorders. What if it were possible to help a faulty immune system by tweaking a patient’s microbiome?. It was with this exploration in mind that he arrived in Pasadena in 2006 to set up his lab at Caltech.A Convenient CollaborationA few years later, Mazmanian was having lunch on campus with neuroscientist and colleague Paul Patterson.

Patterson had been preoccupied with a mystery that had, for years, confounded those studying autism in humans. When pregnant mothers have a severe in the second trimester, their babies are much more likely to develop autism.As Mazmanian tells it, Patterson was a man of few words, and at lunch Mazmanian was “going on and on” about his own work.“You know,” Patterson interjected thoughtfully, “I think kids with autism have GI issues.”Patterson recalled reading that something like 60 percent of children with autism had some form of clinical GI problem, such as bloating, constipation, flatulence or diarrhea. Was it possible, he wondered, that there was a microbiome connection?.

As they talked, Mazmanian’s excitement grew.A few years earlier, Patterson had discovered that when he exposed pregnant mice to pathogens like the influenza viagra, they gave birth to pups that grew up more likely to be startled by loud noises, to shy away from social contact and to groom themselves repetitively — symptoms that resemble those of autism. Patterson was in the process of comparing the brains of these autism-mimicking mice with their neurotypical cousins to see if he could detect any differences that might explain how the maternal immune system was somehow interfering with the pups’ brain development.Mazmanian had a suggestion. The next time Patterson sacrificed one of his autistic mice to study their brains, what if he set the intestines aside for his colleague down the hall?.

When the guts arrived in Mazmanian’s lab, he found that the intestines of the neurotypical mice looked normal. But the guts of the autism-mimicking offspring were almost uniformly inflamed. Could it be that the microbiome was the cause of this inflammation?.

And could that, in turn, be somehow connected to the behavioral symptoms?. Throughout the winter and spring of 2012, Mazmanian and Patterson continued their conversation. Mazmanian found distinct differences in the microbiomes of the mice.

And, they noticed, the mice with the features of autism had leaky gut syndrome, an increased permeability of the gut lining that can allow pathogens and allergens to leach out. This condition had also been reported in children with autism.So Mazmanian and Patterson turned their attention outside the gut. They took blood samples to see if any gut microbes, or the compounds they produce, were circulating in the rest of the body.

They homed in on one molecule in particular, called 4-ethylphenyl sulfate, which was roughly 45 times as abundant in the mice that had symptoms of autism. And it looked familiar. Structurally, it was almost identical to a molecule recently found to be significantly elevated in human children with autism.It was enough to take the next step.

Every day for three weeks, Mazmanian injected the molecule, harvested from the mice with autism-like symptoms, directly into the bloodstream of 5-week-old normal lab mice (the age at which the autistic mice normally developed leaky gut). Then Mazmanian and his team gave them a series of behavioral tests. The mice were far more easily startled and were less comfortable in large empty spaces than their untreated peers, indications of an increase in anxiety-related behaviors commonly seen in the mice with autism-like symptoms.

The researchers published their results in Cell in 2013.Though surprising, the data made sense in some ways. Many drug companies rely on small-molecule drugs that can be taken orally, but still manage to cross the blood-brain barrier and affect behavior. It seemed entirely possible that small molecules, created by bacteria in the gut, could enter the bloodstream and reach the brain.

And they don’t even have to leak out of the gut to do so.Of Mice and MenPatterson died in 2014, at age 70, just six months after the publication of the duo’s groundbreaking Cell paper. Around the same time, a series of parallel experiments in a clinic hundreds of miles away was already paving the way forward. While Patterson and Mazmanian had been working in mice, Rosa Krajmalnik-Brown, a microbiologist at Arizona State University, had teamed up with Jim Adams, who directs the university’s autism and Asperger’s research program, to study humans.The researchers were conducting a detailed analysis of the microbiome of human autism patients and found that the bacteria were far less diverse in the children with autism.

Notably, several important species involved in the digestion of carbohydrates were severely depleted.Krajmalnik-Brown and Adams launched a preliminary trial to test the effects of fecal transplants on 18 children between the ages of 7 and 16 with severe autism, who also had severe GI issues. The researchers administered powerful antibiotics to kill off the microbiomes of the children and followed them with a bowel cleanse. They then replaced the microbes with transplanted flora taken from the guts of healthy neurotypical adult volunteers.The results were better than anyone could have expected.

The procedure resulted in a large reduction in GI symptoms and increased the diversity of bacteria in the children’s guts. But more significantly, their neurological symptoms were reduced. At the onset of the study in 2017, an independent evaluator found 83 percent of participants had severe autism.

Two years after the initial trial, only 17 percent were rated as severely autistic. And 44 percent were no longer on the autism scale.“[My child] did a complete 180,” says Dana Woods, whose then-7-year-old son Ethan enrolled in the initial study five years ago. €œHis ability to communicate is so much different now.

He’s just so much more present. He’s so much more aware. He’s no longer in occupational therapy.

He’s no longer in speech therapy. After the study, he tested two points away from a neurotypical child.”In their first report on the trial in 2017, the team highlighted a number of distinct changes in the microbiome after the transplants, in particular a surge in the populations of three types of bacteria. Among them was a four-fold increase in Bifidobacterium, a probiotic organism that seems to play a key role in the maintenance of a healthy gut.But figuring out what was happening on a cellular level — to really look inside some guts — would require another vehicle.

The ASU team needed Mazmanian’s mice.“At the end of the day, what we care about is healing people and how the microbiome affects people,” explains Krajmalnik-Brown. €œThat’s why we work with people. But with mice you can do things that are more mechanistic.”The Great Mouse Detective(Credit.

Caltech)Together, Krajmalnik-Brown, Mazmanian and their collaborators would uncover some tantalizing new insights that go a long way to solving the mystery. In May 2019, the team published another high-profile paper in Cell, after they transplanted stool samples from Krajmalnik-Brown’s severely autistic patients into the guts of Mazmanian’s germ-free mice. The offspring of these mice showed the autism-like symptoms, such as repetitive and compulsive behavior.This time, the team dug even deeper into the biochemical processes playing out in the brain, looking not just at behavior but at the chemicals involved in creating it.

The mice that developed autism-like behaviors had measurably lower levels of two substances called taurine and 5-aminovaleric acid (5AV). When they dug into the literature, the team learned that these two substances are known to mimic activity of a key signaling agent in the brain called gamma-aminobutyric acid (GABA) — a neurotransmitter that other studies have found is deficient in the brains of children with autism.What’s more, some have speculated that the tendency of children with autism to experience sensory overstimulation may stem from the inability to tamp down overexcited neurons. A lack of GABA could lead to just that.The scientists next orally administered high levels of taurine and 5AV to pregnant mice with the autistic children’s microbiomes.

When their pups were born, the researchers continued to feed the young the substances until they reached adulthood. Compared with untreated animals, the second-generation mice had significantly fewer behavioral symptoms. Taurine reduced repetitive behavior, as measured by marble burying, increased the level of social interaction, and relieved anxiety.

Mice administered 5AV were more active and social.“We healed humans with behavioral problems,” says Krajmalnik-Brown. €œ[And we] transferred some of those deficits and behaviors to mice — basically the opposite. It’s huge.”Mazmanian hopes to take the next step in the months ahead.“I can flip a switch, turn on a light, I know that switch turns on that light.

I don’t know the circuit, I don’t know where the wire is,” Mazmanian says. €œExactly how that’s happening … we just don’t understand that.”This most recent study, by itself, hardly proves that dysregulated microbiomes cause the brain disorder — a point that plenty of other scientists skeptical of Mazmanian’s work are happy to make.“The paper made a big splash, but trying to model psychiatric-related human conditions in mice, in my view, is a little bit of a stretch,” says Sangram Sisodia, a neurobiologist at the University of Chicago who studies the microbiome. €œA mouse with autism?.

€Nor was that the only criticism. Several researchers have suggested that the group didn’t give proper attention to one of their tests ­— one whose results conflicted with their thesis ­— while others found flaws in the statistical methods they used to assess their results. Mazmanian downplays these criticisms, but agrees the work is not yet conclusive.Meanwhile, the ASU trial has also engendered skepticism, mainly due to its tiny sample size, the lack of a control group and the methods by which the children were assessed for autism severity.

Krajmalnik-Brown and Adams say they stand by their results, but agree more research is needed. In recent months, they have launched two new studies that will address these issues.Adams insists the work is already changing lives. €œWe followed up with every one of our 18 participants,” he says, referring to the children who received fecal transplants.

€œSure enough, we found that most of the GI benefits had remained. And family after family said their child just slowly, steadily continued making more improvement.” They published the update in Scientific Reports in spring 2019.“I’m not ready to say the case is closed,” says Mazmanian. €œHealthy skepticism is a good thing.

I believe the preclinical data, I believe the mouse data. But there’s a lot of studies that still need to be done.” A Healthy Gut, A New OutlookEthan Woods had GI issues and symptoms of autism until researchers introduced new microbes to his gut. His mother says the treatment changed everything.

(Credit. Dana Woods)Prior to his fecal transplant at age 7, Ethan Woods suffered from chronic and severe diarrhea, constipation and cramping, symptoms so extreme that to his mother, Dana, he sounded like “a bit like a woman in labor when he was trying to have a bowel movement.” “It was just awful watching your child go through this,” she says, explaining that when she enrolled her autistic son in the Arizona State study, her “only goal was to fix his gut.”Remarkably, Ethan’s agony began to disappear just a few weeks into the trial. But that was not the most dramatic difference.

Before the transplant, Ethan’s speech was drawn out and slow, his language skills rudimentary. He seemed to live in his own bubble. He had frequent outbursts.

For as long as Dana could remember, her mornings with Ethan had been marked by arguing, fighting, pushing and anger. But then one morning, something shocking happened.“He woke me up one morning with his face right in my face with this big smile and he said, ‘Morning, Mom!. €™â€‰â€ she recalls.

€œAnd he was just excited and happy and ready to go about his day with this big smile. It choked me up to the point where I teared up because I had never experienced a happy kid in the morning.”Later, Ethan carried over an iPad and opened an app with a talking cat that repeats back the words children speak aloud. He played back a video recording of himself from just a few weeks earlier.“[He] looks me in the eye and says, ‘Mom, why did I talk like that?.

What is wrong with me?. €™ And as soon as he did that, I caught my breath. I had to compose myself and say, ‘I don’t know.

But do you feel better?. Do you feel different?. Why do you think?.

€™â€‰â€Ethan’s communication skills had already begun to improve. Within a year of the study, his speech therapist graduated him from speech therapy because he had met all his goals.“He went from one end of the rainbow all the way to the other end of the rainbow,” she says. €œPrior to the study, I was very afraid.

My biggest fear was ‘how is he going to navigate the world when I’m not here?. €™ And I think I have a lot of hope now that he is going to be OK now on his own.”.

Benefits of taking viagra daily

For the first time, researchers have used human data to quantify the speed of different processes that lead benefits of taking viagra daily to Alzheimer’s disease and found that it develops in a very different way than previously thought. Their results could have important implications for the development of potential treatments.The international team, led by the University of Cambridge, found that instead of starting from a single point in the brain and initiating a chain reaction which leads to the death of brain cells, Alzheimer’s disease reaches different regions of the brain early. How quickly the disease kills cells in these regions, through the production of toxic protein clusters, limits how quickly the disease progresses overall.The researchers used post-mortem brain samples from Alzheimer’s patients, as well as PET scans from living patients, who ranged from those with mild cognitive impairment to those with full-blown Alzheimer’s disease, to track the aggregation of tau, one of two key proteins benefits of taking viagra daily implicated in the condition.In Alzheimer’s disease, tau and another protein called amyloid-beta build up into tangles and plaques – known collectively as aggregates – causing brain cells to die and the brain to shrink.

This results in memory loss, personality changes and difficulty carrying out daily functions.By combining five different datasets and applying them to the same mathematical model, the researchers observed that the mechanism controlling the rate of progression in Alzheimer’s disease is the replication of aggregates in individual regions of the brain, and not the spread of aggregates from one region to another.The results, reported in the journal Science Advances, open up new ways of understanding the progress of Alzheimer’s and other neurodegenerative diseases, and new ways that future treatments might be developed. advertisement For many years, the processes within the brain which result in Alzheimer’s disease have been described using terms like ‘cascade’ and benefits of taking viagra daily ‘chain reaction’. It is a difficult disease to study, since it develops over decades, and a definitive diagnosis can only be given after examining samples of brain tissue after death.For years, researchers have relied largely on animal models to study the disease.

Results from mice benefits of taking viagra daily suggested that Alzheimer’s disease spreads quickly, as the toxic protein clusters colonise different parts of the brain.“The thinking had been that Alzheimer’s develops in a way that’s similar to many cancers. The aggregates form in one region and then spread through the brain,” said Dr Georg Meisl from Cambridge’s Yusuf Hamied Department of Chemistry, the paper’s first author. €œBut instead, we found that when Alzheimer’s starts there are already aggregates in multiple regions of the brain, and so trying to stop the spread between regions will do little to slow the disease.”This is the first time that human data has been used to track which benefits of taking viagra daily processes control the development of Alzheimer’s disease over time.

It was made possible in part by the chemical kinetics approach developed at Cambridge over the last decade which allows the processes of aggregation and spread in the brain to be modelled, as well as advances in PET scanning and improvements in the sensitivity of other brain measurements.“This research shows the value of working with human data instead of imperfect animal models,” said co-senior author Professor Tuomas Knowles, also from the Department of Chemistry. €œIt’s exciting to see benefits of taking viagra daily the progress in this field – fifteen years ago, the basic molecular mechanisms were determined for simple systems in a test tube by us and others. But now we’re able to study this process at the molecular level in real patients, which is an important step to one day developing treatments.”The researchers found that the replication of tau aggregates is surprisingly slow – taking up to five years.

€œNeurons are surprisingly good at stopping aggregates from forming, but we need to find ways to make them even better if we’re going to develop an benefits of taking viagra daily effective treatment,” said co-senior author Professor Sir David Klenerman, from the UK Dementia Research Institute at the University of Cambridge. €œIt’s fascinating how biology has evolved to stop the aggregation of proteins.” advertisement The researchers say their methodology could be used to help the development of treatments for Alzheimer’s disease, which affects an estimated 44 million people worldwide, by targeting the most important processes that occur when humans develop the disease. In addition, the methodology could be applied benefits of taking viagra daily to other neurodegenerative diseases, such as Parkinson’s disease.

“The key discovery is that stopping the replication of aggregates rather than their propagation is going to be more effective at the stages of the disease that we studied,” said Knowles.The researchers are now planning to look at the earlier processes in the development of the disease, and extend the studies to other diseases such as Frontal temporal dementia, traumatic brain injury and progressive supranuclear palsy where tau aggregates are also formed during disease.The study is a collaboration between researchers at the UK Dementia Research Institute at the University of Cambridge, University of Cambridge and Harvard Medical School. Funding is acknowledged from the Sidney Sussex College Cambridge, the European Research benefits of taking viagra daily Council Grant Number, the Royal Society, JPB foundation, the Rainwater foundation, the NIH and the NIHR Cambridge Biomedical Research Centre which supports the Cambridge Brain Bank.Researchers in the U.S. And Japan have demonstrated the first experimental cross-sectional medical image that doesn't require tomography, a mathematical process used to reconstruct images in CT and PET scans.

The work, benefits of taking viagra daily published Oct. 14 in Nature Photonics, could lead to cheaper, easier and more accurate medical imaging.The advance was made possible by development of new, uafast photon detectors, said Simon Cherry, professor of biomedical engineering and of radiology at the University of California, Davis and senior author on the paper."We're literally imaging at the speed of light, which is something of a holy grail in our field," Cherry said.Experimental work was led by Sun Il Kwon, project scientist in the UC Davis Department of Biomedical Engineering and Ryosuke Ota at Hamamatsu Photonics, Japan, where the new photon detector technology was developed. Other collaborators included research groups led by Professor Yoichi Tamagawa at the University of Fukui, and by Professor Tomoyuki Hasegawa at Kitasato University.The process of tomography is required to mathematically reconstruct cross-sectional images from the benefits of taking viagra daily data in imaging that uses X-rays or gamma rays.

In PET scans, molecules tagged with trace amounts of a radioactive isotope are injected and taken up by organs and tissues in the body. The isotope, such as fluorine-18, is unstable and emits positrons as it decays.Uafast photon detectionWhenever one of these positrons encounters an electron in the body, they annihilate each other benefits of taking viagra daily and simultaneously give off two annihilation photons. Tracking the origin and trajectory of these photons theoretically creates an image of the tissues tagged with isotopes.

But until now, researchers were unable to do that without the extra step of tomographic reconstruction, because detectors were too slow to precisely determine the arrival times of two photons and thus pinpoint their location based on their time difference.When the annihilation photons strike benefits of taking viagra daily the detector, they generate Cherenkov photons that produce the signal. Cherry and his fellow researchers figured out how to detect these Cherenkov photonså with an average timing precision of 32 picoseconds. This meant they could determine where benefits of taking viagra daily the annihilation photons arose with a spatial precision of 4.8 millimeters.

This level of speed and accuracy enabled the research team to produce cross-sectional images of a radioactive isotope directly from the annihilation photons without having to use tomography.In their paper, the researchers describe various tests they conducted with their new technique, including on a test object that mimics the human brain. They feel confident that this procedure is ultimately scalable benefits of taking viagra daily to the level needed for clinical diagnostics and has the potential to create higher quality images using a lower radiation dose. Images can also be created more quickly with this method, potentially even in real time during the PET scan, as no after-the-fact reconstruction is needed.PET scans are currently expensive and are technically limited in some ways, as the full information present in the travel time of the annihilation photons is not captured by current clinical scanners.

This new discovery involves a compact equipment setup and could lead to inexpensive, easy and accurate scans of the human body using radioactive benefits of taking viagra daily isotopes.Additional coauthors are. Eric Berg at UC Davis. Fumio Hashimoto and Tomohide Omura, Hamamatsu Photonics benefits of taking viagra daily.

Kyohei Nakajima and Izumi Ogawa, University of Fukui.The study was partly supported by grants from the NIH. Story Source. Materials provided by University of California - Davis.

Original written by Cristina Deptula. Note. Content may be edited for style and length..

For the first time, cheap viagra researchers have used human data to quantify the speed of different processes that lead to Alzheimer’s disease and found that it develops in a very where to buy cheap viagra different way than previously thought. Their results could have important implications for the development of potential treatments.The international team, led by the University of Cambridge, found that instead of starting from a single point in the brain and initiating a chain reaction which leads to the death of brain cells, Alzheimer’s disease reaches different regions of the brain early. How quickly the disease kills cells in these regions, through the production of toxic protein clusters, limits how quickly cheap viagra the disease progresses overall.The researchers used post-mortem brain samples from Alzheimer’s patients, as well as PET scans from living patients, who ranged from those with mild cognitive impairment to those with full-blown Alzheimer’s disease, to track the aggregation of tau, one of two key proteins implicated in the condition.In Alzheimer’s disease, tau and another protein called amyloid-beta build up into tangles and plaques – known collectively as aggregates – causing brain cells to die and the brain to shrink.

This results in memory loss, personality changes and difficulty carrying out daily functions.By combining five different datasets and applying them to the same mathematical model, the researchers observed that the mechanism controlling the rate of progression in Alzheimer’s disease is the replication of aggregates in individual regions of the brain, and not the spread of aggregates from one region to another.The results, reported in the journal Science Advances, open up new ways of understanding the progress of Alzheimer’s and other neurodegenerative diseases, and new ways that future treatments might be developed. advertisement For many years, the processes within the brain which result in Alzheimer’s disease have been described using terms like ‘cascade’ and ‘chain cheap viagra reaction’. It is a difficult disease to study, since it develops over decades, and a definitive diagnosis can only be given after examining samples of brain tissue after death.For years, researchers have relied largely on animal models to study the disease.

Results from mice suggested that Alzheimer’s disease cheap viagra spreads quickly, as the toxic protein clusters colonise different parts of the brain.“The thinking had been that Alzheimer’s develops in a way that’s similar to many cancers. The aggregates form in one region and then spread through the brain,” said Dr Georg Meisl from Cambridge’s Yusuf Hamied Department of Chemistry, the paper’s first author. €œBut instead, we found that when Alzheimer’s starts there are already aggregates in multiple regions of the brain, and so trying to stop the spread between regions will do little to slow the disease.”This is the first time that human data has been used to track which processes control the development cheap viagra of Alzheimer’s disease over time.

It was made possible in part by the chemical kinetics approach developed at Cambridge over the last decade which allows the processes of aggregation and spread in the brain to be modelled, as well as advances in PET scanning and improvements in the sensitivity of other brain measurements.“This research shows the value of working with human data instead of imperfect animal models,” said co-senior author Professor Tuomas Knowles, also from the Department of Chemistry. €œIt’s exciting to see the progress in this field – fifteen years ago, the basic molecular mechanisms were determined cheap viagra for simple systems in a test tube by us and others. But now we’re able to study this process at the molecular level in real patients, which is an important step to one day developing treatments.”The researchers found that the replication of tau aggregates is surprisingly slow – taking up to five years.

€œNeurons are surprisingly cheap viagra good at stopping aggregates from forming, but we need to find ways to make them even better if we’re going to develop an effective treatment,” said co-senior author Professor Sir David Klenerman, from the UK Dementia Research Institute at the University of Cambridge. €œIt’s fascinating how biology has evolved to stop the aggregation of proteins.” advertisement The researchers say their methodology could be used to help the development of treatments for Alzheimer’s disease, which affects an estimated 44 million people worldwide, by targeting the most important processes that occur when humans develop the disease. In addition, the methodology could be applied to other neurodegenerative cheap viagra diseases, such as Parkinson’s disease.

“The key discovery is that stopping the replication of aggregates rather than their propagation is going to be more effective at the stages of the disease that we studied,” said Knowles.The researchers are now planning to look at the earlier processes in the development of the disease, and extend the studies to other diseases such as Frontal temporal dementia, traumatic brain injury and progressive supranuclear palsy where tau aggregates are also formed during disease.The study is a collaboration between researchers at the UK Dementia Research Institute at the University of Cambridge, University of Cambridge and Harvard Medical School. Funding is acknowledged from the Sidney Sussex College cheap viagra Cambridge, the European Research Council Grant Number, the Royal Society, JPB foundation, the Rainwater foundation, the NIH and the NIHR Cambridge Biomedical Research Centre which supports the Cambridge Brain Bank.Researchers in the U.S. And Japan have demonstrated the first experimental cross-sectional medical image that doesn't require tomography, a mathematical process used to reconstruct images in CT and PET scans.

The work, published Oct cheap viagra. 14 in Nature Photonics, could lead to cheaper, easier and more accurate medical imaging.The advance was made possible by development of new, uafast photon detectors, said Simon Cherry, professor of biomedical engineering and of radiology at the University of California, Davis and senior author on the paper."We're literally imaging http://jbnaturopathy.com/portfolio-slider-devices/ at the speed of light, which is something of a holy grail in our field," Cherry said.Experimental work was led by Sun Il Kwon, project scientist in the UC Davis Department of Biomedical Engineering and Ryosuke Ota at Hamamatsu Photonics, Japan, where the new photon detector technology was developed. Other collaborators included research groups led by Professor Yoichi Tamagawa at the University of Fukui, and by Professor Tomoyuki cheap viagra Hasegawa at Kitasato University.The process of tomography is required to mathematically reconstruct cross-sectional images from the data in imaging that uses X-rays or gamma rays.

In PET scans, molecules tagged with trace amounts of a radioactive isotope are injected and taken up by organs and tissues in the body. The isotope, cheap viagra such as fluorine-18, is unstable and emits positrons as it decays.Uafast photon detectionWhenever one of these positrons encounters an electron in the body, they annihilate each other and simultaneously give off two annihilation photons. Tracking the origin and trajectory of these photons theoretically creates an image of the tissues tagged with isotopes.

But until now, researchers were unable to do that without the extra step of tomographic reconstruction, because detectors were too slow to precisely determine the arrival times of two photons and thus pinpoint their location based on their time difference.When the annihilation cheap viagra photons strike the detector, they generate Cherenkov photons that produce the signal. Cherry and his fellow researchers figured out how to detect these Cherenkov photonså with an average timing precision of 32 picoseconds. This meant they could determine where the annihilation photons arose with a spatial precision of cheap viagra 4.8 millimeters.

This level of speed and accuracy enabled the research team to produce cross-sectional images of a radioactive isotope directly from the annihilation photons without having to use tomography.In their paper, the researchers describe various tests they conducted with their new technique, including on a test object that mimics the human brain. They feel confident that this procedure is ultimately scalable to the level needed for clinical diagnostics and has the cheap viagra potential to create higher quality images using a lower radiation dose. Images can also be created more quickly with this method, potentially even in real time during the PET scan, as no after-the-fact reconstruction is needed.PET scans are currently expensive and are technically limited in some ways, as the full information present in the travel time of the annihilation photons is not captured by current clinical scanners.

This new discovery involves a compact equipment setup and could lead to inexpensive, cheap viagra easy and accurate scans of the human body using radioactive isotopes.Additional coauthors are. Eric Berg at UC Davis. Fumio Hashimoto and cheap viagra Tomohide Omura, Hamamatsu Photonics.

Kyohei Nakajima and Izumi Ogawa, University of Fukui.The study was partly supported by grants from the NIH. Story Source cheap viagra. Materials provided by University of California - Davis.

Original written cheap viagra by Cristina Deptula. Note. Content may be edited for style and length..

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