Category Archives: Physiology

University stages photo shoot with skeleton in empty library as ‘he waits for campus to reopen and students to return’ – Yahoo News

April 23, 2020 medical

Mandy the Skeleton looks over the empty UNLV Library while students complete coursework from home. (Photo: Aaron Mayes)

A Las Vegas university is making people smile after staging a photo shoot with a figure well-known to students and alumni at one of its empty libraries on campus.

The University of Nevada Las Vegas (UNLV) is one of many universities across the country that have transitioned to online learning amid coronavirus pandemic. With students and most staff still home, UNLV officials decided to stage a photo shoot with Mandy the Skeleton, who is known to help students prepare for anatomy and physiology exams.

In a Facebook post on Monday, UNLV Libraries shared the pictures.

Mandy has a lot of free time on his hands since the COVID-19 pandemic sent the campus into a remote instruction mode. Heres a peek at how hes spending his days, following social distancing guidelines and wearing a mask out in public, as he waits for campus to re-open and students to return, the post reads.

As of Wednesday afternoon, the post has been shared at least 6,000 times, with messages from commenters who said the pictures brought a smile to their faces.

He looks good for his age, one person noted.

I love these. What a perfect laugh. I keep thinking of the person taking the pictures. I bet they were having fun and laughing, someone else commented.

These are the best....thanks for the laughs, a commenter said.

Maggie Farrell, the dean of UNLV Libraries, tells Yahoo Life that as the school has made the transition to online learning in March, they have tried different ways to keep students, staff and faculty engaged, and energized.

Humor is one way to connect in a stressful time, she says. This photo project seemed like a unique way to let students know we miss them and are supporting them during this time, while also giving them something to laugh about.

Aaron Mayes, who took the pictures of Mandy, works as a curator for visual materials in the librarys Special Collections and Archives department. Mayes tells Yahoo Life that the idea for photo shoot came from Sean Kennedy, who is the director of communications at the library.

Story continues

Mayes hoped this could bring joy during this uncertain time.

I have been working on a photograph collection for futureresearchers showing Las Vegas' response to the COVID-19 pandemic, he says. Those images can be a bit depressing. Being able to create something completely different, something humorous, something that can make people smile and laugh, if only for a minute, made it worth the effort.

Mayes notes that the response to the pictures has been positive and has helped to connect students and the rest of the UNLV community.

Some have noted the places in the library they can't wait to get back to enjoying, he recalls. Others remember using Mandy while finishing their studies. We've had requests for Mandy to be greeting students when we reopen. And, surprisingly, Mandy has fans now from all over the world. My favorite comment though is one that just says, Miss you Mandy! It reminds me that good libraries are not buildings, they are places for people to connect, learn, grow and laugh.

Farrell hopes this gesture shows students to know how much they mean to the school and its resident skeleton.

We hope students know how much we miss them and we are thinking of their academic and health needs, she says.And that Mandy will welcome students back with joy with his skinny outstretched arms when it is safe to be together again.

For thelatest coronavirus news and updates, follow along athttps://news.yahoo.com/coronavirus. According to experts, people over 60 and those who are immunocompromised continue to be the most at risk. If you have questions, please reference theCDCs andWHOsresource guides.

Can You Improve Your Mental Health By Eating Healthier? – Theravive

April 23, 2020 medical

A recent review published in the Journal of European Neuropsychopharmacology looked at nutritional psychiatry and whether mental health can be improved by what you eat.

Thepopular press often provide advice tothegeneral public about recommendations on how to improve ones mental health by changing what we eat specific diets, supplements or foods, review author Suzanne L Dickson told us.We are a group of researchers with much diverse yet collective knowledge on nutrition and brain health. We know when facts are clearly wrong, when they are right and alltheshades of grey in between. We wanted to settherecord straight and explain in an informed balanced manner,theactual data behind common claims and misconceptions.

Dickson is a professor in the Depart of Physiology/Endocrine at the Institute of Neuroscience and Physiology at the the Sahlgrenska Academy attheUniversity of Gothenburg in Sweden.

We addressed many different aspects of nutrition and brain health for some of these quite a lot is known and sotheevidence pretty much aligned to current theories proposed by scientists, Dickson told us. However, for other areas, even scientists are drawn in by assumptions, for example, that eating too much sugar exacerbates symptoms observed in children with Attention Deficit Hyperactivity Disorder (ADHD). Actually,theevidence for this is very slim indeed.

The review notes that the brain requires certain nutrients in order to function properly including minerals, vitamins, lipids, and amino acids.

We read as much possible literature onthevarious topics and summarizedthekey components. We wanted to provide an explanation as to why it is difficult for scientists and nutritionists to provide proof that any dietary ingredient or food really does improve brain health, Dickson told us.We also want to explain likely ways that we can make better progress inthefuture.

In addition to nutrients the brain requires, other elements such as gut hormones, neurotransmitters, and neuropeptides.

There are so many different topics inthearticle, some relating to cognitive function, some to ADHD and others to depression and anxiety disorders, Dickson told us. Essentially, for most disease areas, nutrition can have beneficial effects but oftentheeffects are marginal and we lack knowledge regarding howthenutritional change could causetheproposed effect on mental health.

There are scientific studies do show that proper nutrition is a benefit for ones mental health. Some studies link a higher intake of fresh vegetables and fruits with increased happiness.But more research is needed.

As scientists we were surprised at how scarcetheevidence is to back dietary advice for mental health, Dickson told us.We need to battle on to sort out fact from fiction regarding dietary advice for mental health and this can only be done by rigorous investigation.We need well controlled clinical studies as well as basic mechanistic studies examiningtheimpact of nutrients onthebody, on metabolism and brain.

Another study showed how depression could be reduced with a higher intake of not only fruits and vegetables but also whole grains and fish, or otherwise popularly known as the Mediterranean diet. Studies have also shown that a lack of vitamin B12 can cause lethargy, poor memory and depression. Studies have shown that adequate intake of vitamin D has a beneficial effect on memory and attention.

Be kind to your brain by making healthier food choices, Dickson told us. Theeffects of diet on mental health are likely real. Since most data on nutrition and brain health is provisional, it is important not to follow dietary advice that is not evidence-based.

Categories: Alternative Mental Health Treatment , Anxiety , Depression , Wellness | Tags: nutrition, mental health, depression

Patricia Tomasi is a mom, maternal mental health advocate, journalist, and speaker. She writes regularly for the Huffington Post Canada,focusing primarily on maternal mental health after suffering from severe postpartum anxiety twice. You can find her Huffington Post biography here. Patricia is also a Patient Expert Advisor for the North American-based,Maternal Mental Health Research Collectiveand is the founder of the online peer support group -Facebook Postpartum Depression & Anxiety Support Group - with over 1500 members worldwide. Blog:www.patriciatomasiblog.wordpress.com Email:tomasi.patricia@gmail.com

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Can You Improve Your Mental Health By Eating Healthier? - Theravive

Physiology

Non-invasive, low-cost ventilator developed for regions with limited means – News-Medical.Net

April 23, 2020 medical

Researchers from the Biophysics and Bioengineering Unit of the UB have created a non-invasive low-cost ventilator, to support patients with respiratory diseases in areas with limited means.

Researchers published the results of the study in the European Respiratory Journal together with open source technical features to build it.

Non-invasive ventilators are usually used to treat patients with respiratory failure: for instance, those with severe symptoms with COVID-19.

Non-invasive ventilation is administrated through facial masks that bring pressured air to the lungs. This support to the natural breathing process, when the disease causes the lungs to fail, enables the body to fight the infection and therefore improve.

The study was carried out in the Biophysics and Bioengineering Unit of the Faculty of Medicine and Health Sciences of the University of Barcelona, led by Ramono Farr, professor of Physiology and member of the August Pi i Sunyer Biomedical Research Institute (IDIBAPS) and the Respiratory Diseases Networking Biomedical Research Centre (CIBERES).

Considering the growing need for ventilator support devices everywhere due to the COVID-19 pandemic, we designed a ventilator that can be built with commercial elements at a low cost. The ventilator is aimed at hospitals and health systems to help cover the demand of respiratory equipment due to the coronavirus and other severe lung diseases."

Ramono Farr, Professor of Physiology, University of Barcelona.

The article describes how to build the ventilator in open code, and it can be copied in areas with limited means.

The research team has designed, built and carried out the tests for the ventilator using a small high-pressure turbine, two pressure transducer and a monitor with digital screen.

In order to build it one needs a basic knowledge on engineering, but no previous knowledge on ventilation, although the application in patients requires a medical supervision.

To assess the efficiency of the prototype of the ventilator compared to a commercial device, the research team tested it in twelve healthy volunteers.

The participants' breathing was obstructed to simulate different levels of lung rigidity and respiratory obstruction.

Participants wore facial masks over their nose to ease breathing and marked their feeling of comfort or discomfort, both with and without a respiratory support.

The tests showed the ventilator adapted to the spontaneous breathing rhythm and provided a feeling of breathing relief similar to a commercial ventilator.

The team carried out a respiratory test bank, in which they used lung simulators to assess the response of the ventilator in patients with different levels of air flow obstruction and lung rigidity.

The test was carried out in sixteen different simulation situations, covering conditions of real life in which non-invasive ventilation is usually used in clinical practices.

In all the simulated cases, the prototype of the ventilator was efficient so that lungs could efficiently breath.

"Our tests showed the prototype could behave similarly to a high-quality conventional device providing support to patients who, with difficulties, can try to breathe by themselves", notes Farr.

The prototype is a non-invasive ventilator that provides respiratory support; therefore, it is not aimed at those patients with severe cases who are intubated and need a mechanical ventilator in the intensive care unit.

The Biophysics and Bioengineering Unit of the UB has experience on instrumentation to treat respiratory diseases, specially in the field of sleep apnoea.

Recently, Farr and his team provided advice on the design of emergency ventilator device prototypes from Protofy.xyz, GPA Innova and GAS N2.

The three devices, built with the support from the Hospital Clnic and Can Ruti, and the UB, are under clinical studyu with patients, after the initial approval to conduct the study given by the Spanish Agency of Medicines and Medical Products (AEMPS).

Farr's team has also provided support to the device carried out by the Technical University of Valencia, now in its final phase of development.

Source:

Journal reference:

Garmendia, O. et al. (2020) Low-cost, easy-to-build non-invasive pressure support ventilator for under-resourced regions: open source hardware description, performance and feasibility testing. European Respiratory Journal. doi.org/10.1183/13993003.00846-2020.

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Non-invasive, low-cost ventilator developed for regions with limited means - News-Medical.Net

Physiology

Opening up the conversation on female athlete health – Athletics Weekly

April 23, 2020 medical

Understanding our body is key if we are to get the most out of it, but some natural functions still dont get discussed so how do we know if what were experiencing is normaland use it to our advantage?

Athletes Dr Jess Piasecki and Dr Georgie Bruinvels have come together with journalist Lucy Lomax to launch theFemale Athlete Podcast a place for conversation and education ontopics relating to the female body, sport and exercise.

As well as being a lecturer in exercise physiology at Nottingham Trent University, Piasecki is one of the UKs top marathon runners, havingstormed to a 2:25:28 Florence Marathon win last November.

The 30-year-oldhasspoken openly about her struggles with injuries related to RED-S (relative energy deficiency in sport)in the past and is passionate about passing on her knowledge and experience.

I just want to raise awareness and enhance that communication amongst all females, says Piasecki. Weve called it theFemale Athlete Podcast but for me a female athlete is anyone who is female and who exercises and the majority of those will have some kind of menstrual cycle, whether its through an oral contraceptive or not, and they will have their own stories and experiences.

If we can open up that conversation then hopefully we can keep more women in sport and promote females competing at recreational right the way through to elite level.

READ MORE |RED-S: Jessica Piasecki shares her story

Bruinvels is an applied physiologist and research scientist for sport science and data analytics companyOrreco and is also an accomplished marathoner with a PB of2:37:03 andGreater Manchester Marathon wins on her CV.

My real aim and passion is to drive education, drive awareness and break down barriers across the board, says Bruinvels. That was a massive motivation for doing this.

I really feel that a lot of the reasons why people dont want to talk about it and feel embarrassed to talk about it is because they dont really understand. I think that is because the education that you might get in schools around this is relatively limited.

Some work I have done has found that 82% of exercising women have never been educated around their menstrual cycle. If they dont have the understanding about it, they dont know why they might feel as they do, why are they going to suddenly start talking to their coach or other people about it if they feel almost embarrassed, they are almost internalising it.

I think theres a large part of us as women who just think its normal and think okay, Im a really heavy bleeder, thats normal or I experience loads of pain, well its my period, thats just me. Because we dont share that information, we dont know that it might be abnormal.

I definitely think the education side is so important to help break those taboos.

Lomax is ajournalist andcommentator who is also on her own running journey as she prepares for an autumn marathon.

Its so embarrassing how little research there is out there and how little female athletes actually know about their own bodies, she says. This is a great platform to be able to talk about things and have a question time at the end for people to ask questions.

Our mantra is breaking down the taboos and opening up conversation and helping women learn more about their bodies. But we want to have males learn about what were talking about as well and have an awareness.

On her own experiences, Piasecki adds:I dont want anyone to go through what I went through in terms of athletics and I want people to have a healthy, successful career. By just making my story available and also through the means of this podcast, we just again raise the awareness.

I didnt know at a younger age that never having started a period from the age of 12 to 18 naturally was not a normal thing. There are other things that could have been addressed perhaps at that time but we didnt have that education.

The full 40-minute interview is available to watch below and via the AW YouTube channel, as Piasecki, Bruinvels and Lomax give an introduction to theFemale Athlete Podcast and discuss the importance of shining light on topics that usually go under the radar.

They highlight the biggest misconceptions they have needed to address, the impact of stress and other factors, the key lessons learned and how athletes can use the menstrual cycle to their advantage, as well as sharing insight into their own running journeys and how they are coping given the current coronavirus restrictions.

Find theFemale Athlete Podcastat femaleathletepodcast.buzzsprout.com as well as via Apple Podcasts,Google Podcasts and Spotify. Follow@female_pod on Twitter andfemaleathletepod on Instagram for updates

For more on the latest athletics news, athletics events coverage and athletics updates, check out theAW homepageand our social media channels onTwitter,FacebookandInstagram

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Opening up the conversation on female athlete health - Athletics Weekly

Physiology

Physicians Push Back on Treating COVID-19 as HAPE – Medscape

April 23, 2020 medical

Editor's note: Find the latest COVID-19 news and guidance in Medscape's Coronavirus Resource Center.

For Luanne Freer, MD, an expert in high-altitude pulmonary edema (HAPE) and founder and director of Everest ER, a nonprofit seasonal clinic at the Mt. Everest base camp in Nepal (elevation, 17,600 ft), a sudden flurry of messages and questions she received about a possible COVID-19/HAPE link was startling.

"That's why it kind of poked me in the eye," she said, referencing her extensive experience treating HAPE, which she described as a pressure-related phenomenon. "My goodness, they are so completely different."

Dr Luanne Freer

Dr. Freer, an emergency physician, reached out to several pulmonary intensivists with experience treating both HAPE and COVID-19 to gauge their reactions, and within 36 hours, they had drafted their response. In the commentary, published in High Altitude Medicine & Biology, the clinicians note that the comparison between HAPE and COVID-19 is potentially risky.

"As a group of physicians who have in some cases cared for patients with COVID-19 and in all cases cared for patients with HAPE and studied its pathophysiology and management, we feel it important to correct this misconception, as continued amplification of this message could have adverse effects on management of these patients," they wrote.

The suggestion that COVID-19 lung injury sometimes looks more like HAPE than like acute respiratory distress syndrome (ARDS) appeared in a journal review article in late March and was put forth by medical professionals on social media where it gained traction in recent weeks and was amplified in multiple media outlets, including this one.

"With COVID, we don't understand everything that's going on, but we know for sure it's an inflammatory process not a pressure-related problem," Dr. Freer said. "I thought ... this could be so dangerous to load the medicines that we use when we're treating HAPE onto patients with COVID-19."

The pathophysiological mechanisms in HAPE are different than those in other respiratory syndromes, including those associated with COVID-19, said Andrew M. Luks, MD, of the UW Medicine, Seattle, and the first author on the commentary.

"HAPE is a noncardiogenic form of pulmonary edema, as are ARDS due to bacteria or viral pneumonia, re-expansion pulmonary edema, immersion pulmonary edema, negative pressure pulmonary edema, and neurogenic pulmonary edema," Dr. Luks, Dr. Freer, and colleagues wrote in the commentary, explaining that all of these entities cause varying degrees of hypoxemia and diffuse bilateral opacities on chest imaging. "Importantly, in all of these cases, edema accumulates in the interstitial and alveolar spaces of the lung as a result of imbalance in Starling forces."

A difference between these entities, however, is "the mechanism by which that imbalance develops," they noted.

The excessive and uneven hypoxic pulmonary vasoconstriction that leads to a marked increase in pulmonary artery pressure, subsequent lung overperfusion, increased pulmonary capillary hydrostatic pressure, and leakage of fluid from the vascular space into the alveolar space as seen in HAPE, is a "fundamentally different phenomenon than what is seen in COVID-19-related ARDS, which involves viral-mediated inflammatory responses as the primary pathophysiological mechanism," they added.

The authors described several other differences between the conditions, ultimately noting that "understanding the distinction between the pathophysiological mechanisms of these entities is critical for patient management."

In HAPE, supplemental oxygen alone may be sufficient; in COVID-19, it may improve hypoxemia but won't resolve the underlying inflammation or injury, they explained, adding that "only good supportive care including mechanical ventilation, quite often for long periods of time, allows some patients to survive until their disease resolves."

Further, HAPE can be prevented or treated with pulmonary vasodilators such a nifedipine or sildenafil, which decrease pulmonary artery pressure and, as a result lower pulmonary capillary hydrostatic pressure, they said.

Use of such medications for COVID-19 might decrease pulmonary artery pressure and improve right ventricular function in COVID-19, but "by releasing hypoxic pulmonary vasoconstriction and increasing perfusion to nonventilated regions of the lung, they could also worsen ventilation-perfusion mismatch" and thereby worsen hypoxemia, they explained, adding that the treatments can also cause or worsen hypotension.

Efforts to share observations and experience are important in medicine, but sometimes, as in this circumstance, "they get out there, spread around like a brushfire almost and get [unwarranted] face validity," Dr. Luks said, noting that in response to information circulating about COVID-19 and HAPE, he has already heard medical professionals floating the idea of treating COVID-19 with treatments used for HAPE.

It's true that some COVID-19 lung injury cases are behaving differently than typical ARDS, he said, adding that presentation can vary.

"But trying to equate HAPE and COVID-19 is just wrong," he said. "HAPE and COVID-19 may share several features ...but those are features that are shared by a lot of different forms of respiratory failure."

In a recent video interview, WebMD's chief medical officerJohn Whyte, MD, spoke with a New York City physician trained in critical care and emergency medicine, Cameron Kyle-Sidell, MD, who raised the need to consider different respiratory protocols for COVID-19, noting that standard protocols were falling short in many cases.

"What we're seeing ... is something unusual, it's something that we are not used to," Dr. Kyle-Sidell of Maimonides Medical Center said in that interview, stressing that the presentation differed from that seen in typical ARDS. "The patterns I was seeing did not make sense."

Like others, he noted that COVID-19 patients were presenting with illness that clinically looked more like HAPE, but that the pathophysiology is not necessary similar to HAPE.

At around the same time, Luciano Gattinoni, MD, of the Medical University of Gttingen in Germany and colleagues, published a letter to the editor in the American Journal of Respiratory and Critical Care Medicine stressing that the ARDS presentation in COVID-19 patients is atypical and requires a patient physiologydriven treatment approach, rather than a standard protocoldriven approach. Dr. Gattinoni and colleagues suggested that instead of high positive end-expiratory pressure (PEEP), physicians should consider the lowest possible PEEP and gentle ventilation.

Dr. Luks agreed that "some patients with COVID-19 do not have the same physiologic derangements that we see in a lot of other people with ARDS."

"[Dr. Gattinoni] is making the point that we need to treat these people differently ... and I think that's a valid point, and honestly, that's a point that applied even before COVID-19," he said. "Most of the things that we see in clinical practice there's a lot of heterogeneity between patients, and you have to be prepared to tailor your therapy in light of the differences that you're picking up from your observations at the bedside and other data that you're getting on the patient."

The main concern Dr. Luks and his coauthors wanted to convey, they said, is making sure that the anecdotal experiences and observations of clinicians struggling to find answers don't spiral out of control without proper vetting, thereby leading to patient harm.

"In this challenging time, we must identify the best means to care for these critically ill patients. That approach should be grounded in sound pulmonary physiology, clinical experience and, when available, evidence from clinical studies," they concluded.

Dr. Luks and Dr. Freer reported having no financial disclosures.

This story originally appeared on MDedge.com.

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Physicians Push Back on Treating COVID-19 as HAPE - Medscape

Physiology

$1.6 million NIH-funded study focuses on gut-brain clues to disease cures – Rowan Today

April 23, 2020 medical

A National Institutes of Health grant secured this month by Rowan University School of Osteopathic Medicine researcher Dr. Howard Chang could help unlock some of the biggest mysteries facing modern science including the connection between healthy gut flora and diseases like ALS.

Chang, who came to Rowan from the State University of New York Binghamton in December, said ALS, more commonly known as Lou Gehrigs Disease, is a progressive neurodegenerative condition in which patients lose muscle control and are ultimately rendered unable to move, eat, even breath on their own.

The NIH funding, $1.6 million over five years, enables Changs study, The role of superoxide dismutase SOD-1 in microbe-gut-brain interaction, to examine the role of an intestinal gene that can mutate and affect the normally healthy relationship between the human gut and the neural system. That mutation that can lead to the development of diseases like ALS, Parkinsons and Alzheimers, for which there are no cures.

With a personal connection to ALS his uncle died of the disease and he believes others in his family may carry the unexpressed mutated gene Chang hopes that a cure to it and similar diseases may one day develop, at least in part, through his research.

A healthy gut microbiome helps maintain immunity but in addition to the immune system a healthy microflora improves your psychological status, helps influence aging and can influence the development of dementia and neurodegeneration, Chang said. Were trying to figure out how a microbe in the gut influences the physiology in the brain.

He said though the gene, superoxide dismutase SOD-1, was discovered in the 1990s, his research into the connection between gut microbiomeand brain diseases could be transformative.

We hope to identify new layers, different genes and proteins, that will hopefully lead to some kind of therapeutic target to improve the condition of ALS, he said.

Chang said the mutated gene is present in a small segment of the general population but the number of people affected by ALS is determined not by the presence of that mutation, which may be tested for, but through a clinical evaluation of symptoms.

It is estimated that at least 16,000 Americans may be living with ALS at any given time, he said. Familial ALS, a hereditary form of the disease caused by SOD-1 and other mutations, accounts for ten percent of cases, whereas the remaining sporadic cases have no clearly defined etiology.

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$1.6 million NIH-funded study focuses on gut-brain clues to disease cures - Rowan Today

Physiology

Interdisciplinary Physiology Graduate Program

April 20, 2020 medical

Physiology is an integrative area in the biological sciences that employs a systems-based approach. It is important for students to integrate information about the entire biological system from across all the biological-related sciences.

Admissions Update Amid COVID-19 Pandemic:

We are still accepting applications for the Summer and Fall 2020 semesters, as well as semesters beyond(Spring 2021, etc.).

All admissions interviews will be conducted via Skype or Zoom and we will still evaluate applications submitted by April 15, 2020. We will also add a new application evaluation date of May 15, 2020. As of today, our final applicationdeadline is June 15, 2020 for Fall 2020.

Important Note for Summer 2020 and Fall 2020 Applicants:

We have recently updated our testing requirementsand will now accept an MCAT or DAT score report in lieuof the GRE. A practice test score for the GRE, MCAT or DAT will not count as meeting this requirement.

NC State is the best college for the money in North Carolina, according to a national ranking of more than 700 schools.Moneymagazines annual survey,2017 Best Colleges for Your Money, is based on enrollment data and student outcomes collected from the top colleges and universities in the United States.

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Interdisciplinary Physiology Graduate Program

Physiology

Physiology of the Kidneys | Boundless Anatomy and Physiology

April 20, 2020 medical

Overview of Urine Formation

Urine is formed in three steps: filtration, reabsorption, and secretion.

Summarize the steps in urine formation

Urine is a waste byproduct formed from excess water and metabolic waste molecules during the process of renal system filtration. The primary function of the renal system is to regulate blood volume and plasma osmolarity, and waste removal via urine is essentially a convenient way that the body performs many functions using one process.Urine formation occurs during three processes:

During filtration, blood enters the afferent arteriole and flows into the glomerulus where filterable blood components, such as water and nitrogenous waste, will move towards the inside of the glomerulus, and nonfilterable components, such as cells and serum albumins, will exit via the efferent arteriole. These filterable components accumulate in the glomerulus to form the glomerular filtrate.

Normally, about 20% of the total blood pumped by the heart each minute will enter the kidneys to undergo filtration; this is called the filtration fraction. The remaining 80% of the blood flows through the rest of the body to facilitate tissue perfusion and gas exchange.

The next step is reabsorption, during which molecules and ions will be reabsorbed into the circulatory system. The fluid passes through the components of the nephron (the proximal/distal convoluted tubules, loop of Henle, the collecting duct) as water and ions are removed as the fluid osmolarity (ion concentration) changes. In the collecting duct, secretion will occur before the fluid leaves the ureter in the form of urine.

During secretion some substancessuch as hydrogen ions, creatinine, and drugswill be removed from the blood through the peritubular capillary network into the collecting duct. The end product of all these processes is urine, which is essentially a collection of substances that has not been reabsorbed during glomerular filtration or tubular reabsorbtion.

Urine is mainly composed of water that has not been reabsorbed, which is the way in which the body lowers blood volume, by increasing the amount of water that becomes urine instead of becoming reabsorbed. The other main component of urine is urea, a highly soluble molecule composed of ammonia and carbon dioxide, and provides a way for nitrogen (found in ammonia) to be removed from the body. Urine also contains many salts and other waste components. Red blood cells and sugar are not normally found in urine but may indicate glomerulus injury and diabetes mellitus respectively.

Normal kidney physiology: This illustration demonstrates the normal kidney physiology, showing where some types of diuretics act, and what they do.

Glomerular filtration is the renal process whereby fluid in the blood is filtered across the capillaries of the glomerulus.

Explain the process of glomerular filtration in the kidneys

Glomerular filtration is the first step in urine formation and constitutes the basic physiologic function of the kidneys. It describes the process of blood filtration in the kidney, in which fluid, ions, glucose, and waste products are removed from the glomerular capillaries.

Many of these materials are reabsorbed by the body as the fluid travels through the various parts of the nephron, but those that are not reabsorbed leave the body in the form of urine.

Glomerulus structure: A diagram showing the afferent and efferent arterioles bringing blood in and out of the Bowmans capsule, a cup-like sac at the beginning of the tubular component of a nephron.

Blood plasma enters the afferent arteriole and flows into the glomerulus, a cluster of intertwined capillaries. The Bowmans capsule (also called the glomerular capsule) surrounds the glomerulus and is composed of visceral (simple squamous epithelial cellsinner) and parietal (simple squamous epithelial cellsouter) layers.

The visceral layer lies just beneath the thickened glomerular basement membrane and is made of podocytes that form small slits in which the fluid passes through into the nephron. The size of the filtration slits restricts the passage of large molecules (such as albumin) and cells (such as red blood cells and platelets) that are the non-filterable components of blood.

These then leave the glomerulus through the efferent arteriole, which becomes capillaries meant for kidneyoxygen exchange and reabsorption before becoming venous circulation. The positively charged podocytes will impede the filtration of negatively charged particles as well (such as albumins).

The process by which glomerular filtration occurs is called renal ultrafiltration. The force of hydrostatic pressure in the glomerulus (the force of pressure exerted from the pressure of the blood vessel itself) is the driving force that pushes filtrate out of the capillaries and into the slits in the nephron.

Osmotic pressure (the pulling force exerted by the albumins) works against the greater force of hydrostatic pressure, and the difference between the two determines the effective pressure of the glomerulus that determines the force by which molecules are filtered. These factors will influence the glomeruluar filtration rate, along with a few other factors.

Regulation of GFR requires both a mechanism of detecting an inappropriate GFR as well as an effector mechanism that corrects it.

List the conditions that can affect the glomerular filtration rate (GFR) in kidneys and the manner of its regulation

Glomerular filtration rate (GFR) is the measure that describes the total amount of filtrate formed by all the renal corpuscles in both kidneys per minute. The glomerular filtration rate is directly proportional to the pressure gradient in the glomerulus, so changes in pressure will change GFR.

GFR is also an indicator of urine production, increased GFR will increase urine production, and vice versa.

The Starling equation for GFR is:

GFR=Filtration Constant (Hydrostatic Glomerulus PressureHydrostatic Bowmans Capsule Pressure)(Osmotic Glomerulus Pressure+Osmotic Bowmans Capsule Pressure)

The filtration constant is based on the surface area of the glomerular capillaries, and thehydrostatic pressure is a pushing force exerted from the flow of a fluid itself; osmotic pressure is the pulling force exerted by proteins. Changes in either the hydrostatic or osmotic pressure in the glomerulus or Bowmans capsule will change GFR.

Many factors can change GFR through changes in hydrostatic pressure, in terms of the flow of blood to the glomerulus. GFR is most sensitive to hydrostatic pressure changes within the glomerulus. A notable body-wide example is blood volume.

Due to Starlings law of the heart, increased blood volume will increase blood pressure throughout the body. The increased blood volume with its higher blood pressure will go into the afferent arteriole and into the glomerulus, resulting in increased GFR. Conversely, those with low blood volume due to dehydration will have a decreased GFR.

Pressure changes within the afferent and efferent arterioles that go into and out of the glomerulus itself will also impact GFR. Vasodilation in the afferent arteriole and vasconstriction in the efferent arteriole will increase blood flow (and hydrostatic pressure) in the glomerulus and will increase GFR. Conversely, vasoconstriction in the afferent arteriole and vasodilation in the efferent arteriole will decrease GFR.

The Bowmans capsule space exerts hydrostatic pressure of its own that pushes against the glomerulus. Increased Bowmans capsule hydrostatic pressure will decrease GFR, while decreased Bowmans capsule hydrostatic pressure will increase GFR.

An example of this is a ureter obstruction to the flow of urine that gradually causes a fluid buildup within the nephrons. An obstruction will increase the Bowmans capsule hydrostatic pressure and will consequently decrease GFR.

Osmotic pressure is the force exerted by proteins and works against filtration because the proteins draw water in. Increased osmotic pressure in the glomerulus is due to increased serum albumin in the bloodstream and decreases GFR, and vice versa.

Under normal conditions, albumins cannot be filtered into the Bowmans capsule, so the osmotic pressure in the Bowmans space is generally not present, and is removed from the GFR equation. In certain kidney diseases, the basement membrane may be damaged (becoming leaky to proteins), which results in decreased GFR due to the increased Bowmans capsule osmotic pressure.

Glomeruluar filtration: The glomerulus (red) filters fluid into the Bowmans capsule (blue) that sends fluid through the nephron (yellow). GFR is the rate at which is this filtration occurs.

GFR is one of the many ways in which homeostasis of blood volume and blood pressure may occur. In particular, low GFR is one of the variables that will activate the reninangiotensin feedback system, a complex process that will increase blood volume, blood pressure, and GFR. This system is also activated by low blood pressure itself, and sympathetic nervous stimulation, in addition to low GFR.

Tubular reabsorption is the process by which solutes and water are removed from the tubular fluid and transported into the blood.

Describe the process of tubular reabsorption in kidney physiology

The fluid filtered from blood, called filtrate, passes through the nephron, much of the filtrate and its contents are reabsorbed into the body. Reabsorption is a finely tuned process that is altered to maintain homeostasis of blood volume, blood pressure, plasma osmolarity, and blood pH. Reabsorbed fluids, ions, and molecules are returned to the bloodstream through the peri-tubular capillaries, and are not excreted as urine.

Tubular secretion: Diagram showing the basic physiologic mechanisms of the kidney and the three steps involved in urine formation. Namely filtration, reabsorption, secretion, and excretion.

Reabsorption in the nephron may be either a passive or active process, and the specific permeability of the each part of the nephron varies considerably in terms of the amount and type of substance reabsorbed. The mechanisms of reabsorption into the peri-tubular capillaries include:

These processes involve the substance passing though the luminal barrier and the basolateral membrane, two plasma membranes of the kidney epithelial cells, and into the peri-tubular capillaries on the other side. Some substances can also pass through tiny spaces in between the renal epithelial cells, called tight junctions.

As filtrate passes through the nephron, its osmolarity (ion concentration) changes as ions and water are reabsorbed. The filtrate entering the proximal convoluted tubule is 300 mOsm/L, which is the same osmolarity as normal plasma osmolarity.

In the proximal convoluted tubules, all the glucose in the filtrate is reabsorbed, along with an equal concentration of ions and water (through cotransport), so that the filtrate is still 300 mOsm/L as it leaves the tubule. The filtrate osmolarity drops to 1200 mOsm/L as water leaves through the descending loop of Henle, which is impermeable to ions. In the ascending loop of Henle, which is permeable to ions but not water, osmolarity falls to 100200 mOsm/L.

Finally, in the distal convoluted tubule and collecting duct, a variable amount of ions and water are reabsorbed depending on hormonal stimulus. The final osmolarity of urine is therefore dependent on whether or not the final collecting tubules and ducts are permeable to water or not, which is regulated by homeostasis.

Reabsorption throughout the nephron: A diagram of the nephron that shows the mechanisms of reabsorption.

Hydrogen, creatinine, and drugs are removed from the blood and into the collecting duct through the peritubular capillary network.

Describe the purpose of tubular secretion in kidney physiology

Tubular secretion is the transfer of materials from peritubular capillaries to the renal tubular lumen; it is the opposite process of reabsorption. This secretion is caused mainly by active transport and passive diffusion.

Usually only a few substances are secreted, and are typically waste products. Urine is the substance leftover in the collecting duct following reabsorption and secretion.

The mechanisms by which secretion occurs are similar to those of reabsorption, however these processes occur in the opposite direction.

Renal secretion is different from reabsorption because it deals with filtering and cleaning substances from the blood, rather than retaining them. The substances that are secreted into the tubular fluid for removal from the body include:

Tubular secretion: Diagram showing the basic physiologic mechanisms of the kidney and the three steps involved in urine formation.

Many pharmaceutical drugs are protein-bound molecules thatDiagram showing the basic physiologic mechanisms of the kidney and the three steps involved in urine formation. amely filtration, reabsorption, secretion, and excretion. are easily secreted, which is why urine testing can detect the exposure to many types of drugs. Tubular secretion occurs throughout the different parts of the nephron, from the proximal convoluted tubule to the collecting duct at the end of the nephron.

The tubular secretion of H+ and NH4+ from the blood into the tubular fluid is involved in blood pH regulation. The movement of these ions also helps to conserve sodium bicarbonate (NaHCO3). The typical pH of urine is about 6.0, while it is ideally 7.35 to 7.45 for blood.

pH regulation is primarily a respiratory system process, due to the exchange of carbon dioxide (a component of carbonic acid in blood), however tubular secretion assists in pH homeostasis as well.

Urine that is formed via the three processes of filtration, reabsorption, and secretion leaves the kidney through the ureter, and is stored in the bladder before being removed through the urethra. At this final stage it is only approximately one percent of the originally filtered volume, consisting mostly of water with highly diluted amounts of urea, creatinine, and variable concentrations of ions.

Physiology

What are the effects of COVID-19 on the lungs? – Medical News Today

April 20, 2020 medical

How does the body respond when the SARS-CoV-2 virus infects it? Which physiological processes help or hinder us in getting rid of the virus, and which processes ensure that we have a mild form of COVID-19, the disease that the virus causes? In this Special Feature, we investigate.

The more we learn about COVID-19, the more we have to question our assumptions about it.

Early on in the COVID-19 pandemic, our information about the disease came from clinical case reports of COVID-19 and what we knew about influenza pandemics and the severe acute respiratory syndrome (SARS) resulting from SARS-CoV.

SARS-CoV is a coronavirus that shares 82% of its genome with SARS-CoV-2. In 2003, it caused an international SARS epidemic.

Stay informed with live updates on the current COVID-19 outbreak and visit our coronavirus hub for more advice on prevention and treatment.

It quickly became clear that COVID-19 was very different than seasonal influenza, with higher mortality and infectivity, but it took longer to realize that there were important differences and similarities with SARS.

For instance, COVID-19 is infectious even during the presymptomatic phase. Also, physiological processes that are harmful in one phase of the disease may become helpful later. For example, the angiotensin converting enzyme 2 (ACE2) receptor, which allows the virus to enter the body, may also be key to the protection of the lungs in the later phases of the disease.

This feature describes what we know so far about COVID-19. To explain the different processes that occur within the body, we have split the disease into four separate phases that roughly match the different levels of severity: mild, moderate, severe, and critical.

However, in reality, the physiological processes underlying these phases overlap. People with COVID-19 may or may not show features of earlier or later phases.

Both SARS-CoV-2 and SARS-CoV gain entry via a receptor called ACE2.

More commonly known for their role in controlling blood pressure and electrolytes, these receptors are also present in the lungs, back of the throat, gut, heart muscle, and kidneys.

In 2004, researchers from the University Medical Center Groningen in the Netherlands reported that ACE2 receptor cells were not present on the surface layer of cells in the nose and were, therefore, not an important site for SARS-CoV viral replication.

In SARS, there are hardly any upper respiratory tract symptoms, and viral units are rarely present outside the lungs. This fact initially took the focus away from continuing to look for ACE2 receptors in the nose.

Recently, an international team of researchers has found the ACE2 receptors on goblet (secretory) cells in and on ciliated (hairy) cells in the nose.

More recently, scientists have found ACE2 receptors in the mouth and tongue, potentially indicating a hand-to-mouth route of transmission.

Researchers also found a plentiful supply of a protease called TMPRSS2, which chemically splits off the top of the coronavirus spike to allow the SARS-CoV-2 RNA to enter into the nasal cells.

Once inside the cell, the viruss genetic material directs the cell to manufacture millions of new copies of itself.

According to a paper that has not yet undergone peer review, the protease TMPRSS2 can act more easily to remove the top section of the coronavirus spike because a genetic difference between SARS-CoV and SARS-CoV-2 means that there is now an easily broken section known as the furin-cleavage site.

As a result, SARS-CoV-2 can bind 10 times more tightly to insert its RNA into the cell, starting to explain why COVID-19 spreads so rapidly.

A small but very careful study of viral samples from nine people admitted to hospital following contact tracing as part of a cluster of COVID-19 cases in Germany has shown the importance of replication in the nose for the early spread of the virus.

On average, there were 676,000 copies of the virus per swab from the upper respiratory tract during the first 5 days of symptoms. The levels of the virus in six out of the nine participants were undetectable in the nose and throat by day 10. Samples were available from day 1 of symptoms.

In all but one of the nine individuals, the viral load in the upper respiratory tract swabs was dropping from day 1, suggesting that the peak preceded the onset of symptoms. This has clear implications for preventing the transmission of the virus.

In a preliminary report by Menni and colleagues, which has yet to go through peer review, loss of sense of smell occurred 6.6 times more commonly in people with other symptoms of COVID-19 who went on to have a positive COVID-19 PCR test (59%) than in those who had symptoms of COVID-19 but tested negative (18%).

The ACE2 receptors and the protease TMPRSS2 have also been found in the supporting structures for the sheet of nerve cells in the upper part of the nose, which transmit signals about smell to the brain.

This is the first research to provide a potential explanation for this important symptom of COVID-19. However, this study is also awaiting peer review.

According to Mennis study, loss of smell was the most commonly reported upper respiratory tract symptom in those testing positive for COVID-19, affecting 59% of people. It was more common than a persistent cough (58%) or a hoarse voice (32.3%).

Interestingly, data from the first description of 99 people who tested positive for COVID-19 in Wuhan, China, suggests that some symptoms you might expect to see from a respiratory virus are not that common in COVID-19. For instance, only 4% had a runny nose, and 5% had a sore throat.

The viral load study in Germany showed that active viral replication occurs in the upper respiratory tract. Seven out of nine participants listed a cough among their initial symptoms.

In contrast to the falling numbers of viral units in the upper respiratory tract, numbers in sputum rose for most of the participants.

In two individuals with some signs of lung infection, the virus in sputum peaked at day 1011. It was present in the sputum up to day 28 in one person. Across all participants, there was an average of 7 million units in 1 milliliter (about 35 million units in a teaspoon). This amount is about 1,000 times more than that in people with SARS.

In the lung, the ACE2 receptor sits on top of lung cells called pneumocytes. These have an important role in producing surfactant a compound that coats the air sacs (alveoli), thus helping maintain enough surface tension to keep the sacs open for the exchange of oxygen and carbon dioxide.

As soon as the body recognizes a foreign protein, it mounts the first response. One part of the bodys immune response the lymphocytes begin to produce the first defense IgM-type antibodies and then the longer term specific neutralizing antibodies (the IgG type).

In the German viral study, 50% of the participants had IgM or IgG antibodies by day 7, and they all had these antibodies by day 14. The amount of antibodies did not predict the clinical course of the disease.

80% of people with COVID-19 will have mild or asymptomatic disease, with common symptoms including fever, cough, and loss of sense of smell. Most will only have phase 1 or 2 physiological responses to SARS-CoV-2 infection.

Approximately 13.8% of people with COVID-19 will have severe disease and will require hospitalization as they become short of breath. Of these individuals, 75% will have evidence of bilateral pneumonia.

Pneumonia in COVID-19 occurs when parts of the lung consolidate and collapse. Reduced surfactant in the alveoli from the viral destruction of pneumocytes makes it difficult for the lungs to keep the alveoli open.

As part of the immune response, white blood cells, such as neutrophils and macrophages, rush into the alveoli. Meanwhile, blood vessels around the air sacs become leaky in response to inflammatory chemicals that the white blood cells release.

This fluid puts pressure on the alveoli from outside and, in combination with the lack of surfactant, causes them to collapse.

As a result, breathing becomes difficult, and the surface area in the lung where oxygen transfer usually takes place becomes reduced, leading to breathlessness.

The body attempts to heal itself by promoting inflammatory and immune responses. The World Health Organization (WHO) advise against the use of glucocorticosteroids during this phase, as they could prevent the natural healing response. The evidence seems to refute this position, but this is a fast developing field, and findings are subject to change.

Most patients will recover at this stage with supportive intravenous fluids and oxygen via a mask or an external positive pressure mask.

The most common time for the onset of critical disease is 10 days, and it can come on suddenly in a small proportion of people with mild or moderate disease.

In severe acute respiratory distress syndrome (ARDS), the inflammation stage gives way to the fibrosis stage. Fibrin clots form in the alveoli, and fibrin-platelet microthrombi (small blood clots) pepper the small blood vessels in the lung that are responsible for gas exchange with the alveoli.

There is hope that drugs already licensed for anticlotting action in strokes could be helpful at this stage.

Cytokines are chemical mediators that white blood cells such as macrophages release, and they can engulf infected cells. These cytokines which have names such as IL1, IL6, and TNF have actions that include dilating the vessel walls and making them more permeable. In extreme circumstances, this can lead to a collapse of the cardiovascular system.

Estrogen in mouse cells suppresses the release of cytokines from macrophages. Although animal studies often fail to translate into important findings in humans, this could be one explanation for worse outcomes from COVID-19 in males.

While smaller numbers of ACE2 receptors are protective in phase 1, as there are fewer landing sites for the virus, by the time we reach phase 4, these receptors may become protective.

ACE2 receptors in health play an important regulating role for the activities of angiotensin converting enzyme 1 (ACE1).

In response to infection, ACE1 creates excess angiotensin 2 from angiotensin 1.

Angiotensin 2 directly damages the lungs, causes blood vessel constriction, and makes the blood vessels leaky. Drugs that doctors typically use in the treatment of hypertension (ACE inhibitors and ARBs) may be helpful at this stage.

The role of ACE2 inhibitors in treating COVID-19 is a complex one. As some authors note, on the one hand, using them may lead to a higher risk of SARS-CoV-2 infection. On the other hand, ACE inhibitors may reduce the lung damage that this infection causes.

Furthermore, it is noteworthy that the protective role of ACE2 in the respiratory system is supported by ample evidence, whereas the increased danger of infection is still a hypothesis.

This is why more research is necessary to understand the physiology of this challenging new disease.

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.

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What are the effects of COVID-19 on the lungs? - Medical News Today

Physiology

Wild Turkey Anatomy and Physiology – OutdoorHub

April 20, 2020 medical

Turkeys are always a challenge to hunt, but their anatomy and physiology is just as intriguing. Some think they are ugly, while others appreciate the array of colors and behavior. Heck, they were almost our national bird. So, as you gear up to chase these illusive birds in their natural habitat, take some time to familiarize yourself with some basic wild turkey anatomy and physiology.

The head of a turkey is a colorful cornucopia. Composed of the caruncles, wattles, snood and dewlap, all are used for different purposes. The changing of color and shape in males emanates aggression, sexual arousal and overall mood. It is a signpost for other turkeys. There are also tiny hairs and feathers around the ear to aid in hearing.

The main fighting tool of a tom is the spur. Since they do all the fighting for the right to breed, they are only present in males. Gobblers jump and use their spurs as daggers to attempt to injure the competition. Spur length is good teller of age, too. Toms with spurs longer than an inch are mature birds, while toms with spurs an inch or less are usually two-year old birds.

A turkeys beard is made from the same material as a rhinoceros hornkeratin. Keratinized epithelial cells are cells filled with the protein keratin. In this case, feathers in toms (and in some hens) keratinize and form the beard. So, a beard is essentially a collection of specialized feathers.

Archibald Rutledge once said, the turkeys eyes are such that he can see a bumblebee turn a somersault on the verge of the horizon. Turkeys can see as a human would while using 8-10x zoom on a pair of binoculars. They also do not have to focus in on objects. If they can see it, it is always in focus. Being able to see in a 300-degree range helps, too. The only spot they cannot see without turning their heads is directly behind them.

Oh, and unlike deer they can see color very well. Good luck.

A turkeys breast is what we call white meat, while its thighs and legs are dark meat. Why is this? White meat is made of light muscle. These muscles are meant for short burst of energy and lack a lot of hemoglobin to sustain activity for too long. Dark meat is composed of dark muscle, which contains high levels of hemoglobin and help sustain a lot of activity for long periods of time. Turkeys walk way more than they fly, so that is why the meat of the legs is dark and the breast is white. (This is why the breast of migratory birds like ducks is dark, FYI).

What interesting things have you noticed about a turkeys anatomy and physiology?

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Wild Turkey Anatomy and Physiology - OutdoorHub