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Cell Biology

As the First Smallpox Vaccine Turns 224, A Look at How It Started – The Great Courses Daily News

By Jonny Lupsha, News Writer

The website The History of Vaccines said that the first smallpox inoculation came about as a test of a hypothesis that a cowpox infection could protect someone from getting the smallpox disease. On May 14, 1796, [Edward] Jenner inoculated eight-year-old James Phipps with matter from a cowpox sore on the hand of milkmaid Sarah Nelmes, the website said. Phipps suffered a local reaction and felt poorly for several days but made a full recovery. In July 1796, Jenner inoculated Phipps with matter taken from a fresh human smallpox sore, as if he were variolating the boy, in an attempt to challenge the protection from cowpox. Phipps remained healthy.

The 18th-century history of inoculating against smallpox also includes a young George Washington.

In 1776, the colonies that would become the United States of America faced an enemy that George Washington considered to be more dangerous than the British army.

Smallpox had ravaged General Horatio Gatess American Northern Army, said Dr. David Sadava, Adjunct Professor of Cancer Cell Biology at the City of Hope Medical Center. Of 10,000 troops, over half of them got smallpox, and the military campaign had to be suspended for a month.

Dr. Sadava said that Washington spoke of smallpox from experience. In his teenage years, Washington took his half-brother Lawrence to Barbados to help with Lawrences tuberculosis. Although the trip failed to help Lawrence, George contracted smallpox and learned of its dangers. By the time of the Revolutionary War, he had come to appreciate how serious smallpox could be. He chose to order his troops to be inoculated against the illness the following year.

The 1777, inoculation ordered by Washington was the first-known inoculation of an army, and it worked pretty well, Dr. Sadava said. Casualties to smallpox were greatly reduced and history tells us that the colonists, of course, won the Revolutionary War.

George Washington contracted smallpox when he was a teenager, but he obviously lived for a long time afterward due to his bodys vigilant immune system.

Washingtons immune system, the system that fights disease, fought off the infection in several steps, Dr. Sadava said. After the smallpox virus entered Washingtons body, some white blood cells called phagocytes engulfed the virus. They digested it to small pieces, chopped it up, and they presented some of these protein fragments of the virus on their cell surface.

After this, Dr. Sadava said, other white blood cells flagged the smallpox virus and set a series of events in motion that saved Washingtons life. These events included sending cells called killer T-cells into the fight which targeted any cell in Washingtons body that carried smallpox.

Still other white blood cells, called B-cells, made antibodiesthese are blood proteins that would bind up any viruses that were outside Washingtons cells, that hadnt infected a cell but were in the bloodstream, for example, Dr. Sadava said. So these B-cells made a whole army that would make antibodies that would bind them up. This two-pronged attackcells to kill infected tissue and antibodies to bind up free virusesswiftly reduced the infection to a mild one in Washingtons case.

Dr. Sadava said that once smallpox was eradicated from Washingtons body, the remaining cells that stood guard to watch for smallpox were called memory cells, and they were the same types of cells that were key to inoculating the army. He said that when dead smallpox viruses from the pus of smallpox victims was put into the cut skin of Continental Army soldiers, the viruses looked enough like their live counterparts to spur the immune system into producing the T- and B-cells required to fight the virus.

Today, smallpox has mostly been eradicated through vaccination. It wouldnt have been possible without Edward Jenners cowpox experiment and George Washingtons caution over the disease.

Dr. David Sadava contributed to this article. Dr. Sadava is Adjunct Professor of Cancer Cell Biology at the City of Hope Medical Center and the Pritzker Family Foundation Professor of Biology, Emeritus, at The Claremont Colleges. He earned a B.S. with first-class honors in biology and chemistry from Carleton University and a Ph.D. in Biology from the University of California, San Diego.

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As the First Smallpox Vaccine Turns 224, A Look at How It Started - The Great Courses Daily News

Cell Biology

Study finds different types of human white fat cells – Medical News Today

Discovering that white fat cells are not all the same may help researchers better understand the role of fat cells in disease.

The risks associated with white adipose tissue, or white body fat, depend to some extent on where that fat is.

For example, intra-abdominal fat (belly fat) is more likely to lead to diabetes and other metabolic conditions than white fat deposits located just beneath the skin (such as in the hips and thighs).

Now, however according to a new paper from the Joslin Diabetes Center in Boston and Boston University, both in Massachusetts it appears that there is more to it than that: There are at least two distinct classes of subcutaneous white fat cells.

A central question in our research on metabolic disease is whether white fat cells in different parts of the body, and even within a single part of the body, are different enough that some might predispose you to disease and some might not, says co-senior author C. Ronald Kahn, a physician and scientist.

Immature white fat cells do not follow a single, universal trajectory to maturity. They can develop different patterns of gene expression.

Kahn is hopeful that determining the mechanisms for these differences could lead to development of novel therapies for diabetes, obesity, and related conditions.

The paper now appears in the journal Nature Communications.

Although previous research had identified multiple types of white fat cells in mice, this is one of the first to have done so in humans.

The paper is the product of an unusual collaboration, says Kahn. According to senior co-author Simon Kasif, a biomedical engineer, The study highlights the potential of bringing interdisciplinary expertise from four laboratories to integrate biology, artificial intelligence, systems biology, and data obtained from clinical samples to catalyze discovery.

Although the study identified two different types of white fat cells, that may just be the beginning. We think this research is the tip of the iceberg if we study more samples of human fat, we will find more subtypes, says Kahn.

Single-cell RNA sequencing allows scientists to track the genetic development of single fat cells from their precursor, or preadipocyte, stage to their mature patterns of gene expression.

For this project, the researchers used white subcutaneous fat cells from a biobank of specimens that scientists had previously collected from healthy individuals.

Scientists at the Broad Institute of MIT and Harvard in Cambridge, MA, and the Joslin laboratory of Yu-Hua Tseng then performed single-cell RNA sequencing on these samples.

Researchers performed an integrated analysis of both datasets using a novel mathematical technique that helped reveal the cells patterns of gene expression. It revealed that the datasets depicted two distinct white fat cell subtypes.

To begin with, as preadipocytes, one subtype expressed much higher levels of zinc nuclear finger genes. This is a set of master regulator genes, the function of which researchers do not yet understand. However, they may help control cells maturation, say the papers authors.

In addition, at maturity, the two cell subtypes exhibited very different patterns of gene expression.

The patterns in one subtype, for example, indicated a significantly higher intake of glucose, which is an important metabolic resource.

Body fat is linked to many different conditions beyond diabetes. This research could be important for understanding the risk factors for other metabolic diseases, such as fatty liver disease and atherosclerosis, and even non-metabolic diseases that are increased by obesity, such as cancer and Alzheimers disease.

C. Ronald Kahn

That white fat cells can be different from each other also fits with another growing area of research.

According to Kasif: Metabolic diseases are highly associated with environmental factors. This work supports the relatively understudied hypothesis that environmental factors may modify the trajectory of how cells develop and our understanding of how this process may influence biology and metabolic disease.

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Study finds different types of human white fat cells - Medical News Today

Biochemistry

Why the ACE2 receptor could be key to treating Covid-19 – ThePrint

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In the search for treatments for COVID-19, many researchers are focusing their attention on a specific protein that allows the virus to infect human cells. Called the angiotensin-converting enzyme 2, or ACE2 receptor, the protein provides the entry point for the coronavirus to hook into and infect a wide range of human cells. Might this be central in how to treat this disease?

We are scientists with expertise in pharmacology, molecular biology and biochemistry, with a strong commitment to applying these skills to the discovery of novel therapies for human disease. In particular, all three authors have experience studying angiotensin signaling in various disease settings, a biochemical pathway that appears to be central in COVID-19. Here are some of the key issues to understand about why theres so much focus on this protein.

ACE2 is a protein on the surface of many cell types. It is an enzyme that generates small proteins by cutting up the larger protein angiotensinogen that then go on to regulate functions in the cell.

Using the spike-like protein on its surface, the SARS-CoV-2 virus binds to ACE2 like a key being inserted into a lock prior to entry and infection of cells. Hence, ACE2 acts as a cellular doorway a receptor for the virus that causes COVID-19.

ACE2 is present in many cell types and tissues including the lungs, heart, blood vessels, kidneys, liver and gastrointestinal tract. It is present in epithelial cells, which line certain tissues and create protective barriers.

The exchange of oxygen and carbon dioxide between the lungs and blood vessels occurs across this epithelial lining in the lung. ACE2 is present in epithelium in the nose, mouth and lungs. In the lungs, ACE2 is highly abundant on type 2 pneumocytes, an important cell type present in chambers within the lung called alveoli, where oxygen is absorbed and waste carbon dioxide is released.

ACE2 is a vital element in a biochemical pathway that is critical to regulating processes such as blood pressure, wound healing and inflammation, called the renin-angiotensin-aldosterone system (RAAS) pathway.

ACE2 helps modulate the many activities of a protein called angiotensin II (ANG II) that increases blood pressure and inflammation, increasing damage to blood vessel linings and various types of tissue injury. ACE2 converts ANG II to other molecules that counteract the effects of ANG II.

Of greatest relevance to COVID-19, ANG II can increase inflammation and the death of cells in the alveoli which are critical for bringing oxygen into the body; these harmful effects of ANG II are reduced by ACE2.

When the SARS-CoV-2 virus binds to ACE2, it prevents ACE2 from performing its normal function to regulate ANG II signaling. Thus, ACE2 action is inhibited, removing the brakes from ANG II signaling and making more ANG II available to injure tissues. This decreased braking likely contributes to injury, especially to the lungs and heart, in COVID-19 patients.

Also read: Study suggests HCQ does not significantly reduce risk of severe infection in Covid patients

No. ACE2 is present in all people but the quantity can vary among individuals and in different tissues and cells. Some evidence suggests that ACE2 may be higher in patients with hypertension, diabetes and coronary heart disease. Studies have found that a lack of ACE2 (in mice) is associated with severe tissue injury in the heart, lungs and other tissue types.

This is unclear. The SARS-CoV-2 virus requires ACE2 to infect cells but the precise relationship between ACE2 levels, viral infectivity and severity of infection are not well understood.

Even so, aside from its ability to bind the SARS-CoV-2 virus, ACE2 has protective effects against tissue injury, by mitigating the pathological effects of ANG II.

When the amount of ACE2 is reduced because the virus is occupying the receptor, individuals may be more susceptible to severe illness from COVID-19. That is because enough ACE2 is available to facilitate viral entry but the decrease in available ACE2 contributes to more ANG II-mediated injury. In particular, reducing ACE2 will increase susceptibility to inflammation, cell death and organ failure, especially in the heart and the lung.

The lungs are the primary site of injury by SARS-CoV-2 infection, which causes COVID-19. The virus reaches the lungs after entry in the nose or mouth.

ANG II drives lung injury. If there is a decrease in ACE2 activity (because the virus is binding to it), then ACE2 cant break down the ANG II protein, which means there is more of it to cause inflammation and damage in the body.

The virus also impacts other tissues that express ACE2, including the heart, where damage and inflammation (myocarditis) can occur. The kidneys, liver and digestive tract can also be injured. Blood vessels may also be a site for damage.

In a recent research paper, we argued that a key factor that determines severity of damage in patients with COVID-19 is abnormally high ANG II activity.

Angiotensin converting enzyme (ACE, aka ACE1) is another protein, also found in tissues such as the lung and heart, where ACE2 is present. Drugs that inhibit the actions of ACE1 are called ACE inhibitors. Examples of these drugs are ramipril, lisinopril, and enalapril. These drugs block the actions of ACE1 but not ACE2. ACE1 drives the production of ANG II. In effect, ACE1 and ACE2 have a yin-yang relationship; ACE1 increases the amount of ANG II, whereas ACE2 reduces ANG II.

By inhibiting ACE1, ACE inhibitors reduce the levels of ANG II and its ability to increase blood pressure and tissue injury. ACE inhibitors are commonly prescribed for patients with hypertension, heart failure and kidney disease.

Another commonly prescribed class of drugs, angiotensin receptor blockers (ARBs, e.g., losartan, valsartan, etc.) have similar effects to ACE inhibitors and may also be useful in treating COVID-19.

Evidence for a protective effect of ACE inhibitors and angiotensin receptor blockers in patients with COVID-19 was shown in recent work co-authored by one of us Dr. Loomba.

No evidence exists to suggest prophylactic use of these drugs; we do not advise readers to take these drugs in the hopes that they will prevent COVID-19. We wish to emphasize that patients should only take these drugs as instructed by their health care provider.

In collaboration with a multidisciplinary group of investigators, Dr. Loomba has initiated a multicenter (randomized, double-blinded, placebo-controlled) clinical trial to examine the efficacy of ramipril an ACE inhibitor compared to a placebo in reducing mortality, ICU admission or need for mechanical ventilation in patients with COVID-19.

[Get facts about coronavirus and the latest research. Sign up for The Conversations newsletter.]

Krishna Sriram, Postdoctoral Fellow, University of California San Diego; Paul Insel, Professor of Pharmacology and Medicine, University of California San Diego, and Rohit Loomba, Professor of Medicine, University of California San Diego

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Also read: Ashwagandha the new HCQ? Modi govt begins study to see if herb keeps coronavirus away

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Why the ACE2 receptor could be key to treating Covid-19 - ThePrint

Biochemistry

What is the ACE2 receptor, how is it connected to coronavirus and why might it be key to treating COVID-19? The experts explain – TheStreet

Courtesy of Krishna Sriram, University of California San Diego; Paul Insel, University of California San Diego, and Rohit Loomba, University of California San Diego

In the search for treatments for COVID-19, many researchers are focusing their attention on a specific protein that allows the virus to infect human cells. Called the angiotensin-converting enzyme 2, or ACE2 receptor, the protein provides the entry point for the coronavirus to hook into and infect a wide range of human cells. Might this be central in how to treat this disease?

We are scientists with expertise in pharmacology, molecular biology and biochemistry, with a strong commitment to applying these skills to the discovery of novel therapies for human disease. In particular, all three authors have experience studying angiotensin signaling in various disease settings, a biochemical pathway that appears to be central in COVID-19. Here are some of the key issues to understand about why theres so much focus on this protein.

ACE2 is a protein on the surface of many cell types. It is an enzyme that generates small proteins by cutting up the larger protein angiotensinogen that then go on to regulate functions in the cell.

Using the spike-like protein on its surface, the SARS-CoV-2 virus binds to ACE2 like a key being inserted into a lock prior to entry and infection of cells. Hence, ACE2 acts as a cellular doorway a receptor for the virus that causes COVID-19.

ACE2 is present in many cell types and tissues including the lungs, heart, blood vessels, kidneys, liver and gastrointestinal tract. It is present in epithelial cells, which line certain tissues and create protective barriers.

The exchange of oxygen and carbon dioxide between the lungs and blood vessels occurs across this epithelial lining in the lung. ACE2 is present in epithelium in the nose, mouth and lungs. In the lungs, ACE2 is highly abundant on type 2 pneumocytes, an important cell type present in chambers within the lung called alveoli, where oxygen is absorbed and waste carbon dioxide is released.

ACE2 is a vital element in a biochemical pathway that is critical to regulating processes such as blood pressure, wound healing and inflammation, called the renin-angiotensin-aldosterone system (RAAS) pathway.

ACE2 helps modulate the many activities of a protein called angiotensin II (ANG II) that increases blood pressure and inflammation, increasing damage to blood vessel linings and various types of tissue injury. ACE2 converts ANG II to other molecules that counteract the effects of ANG II.

Of greatest relevance to COVID-19, ANG II can increase inflammation and the death of cells in the alveoli which are critical for bringing oxygen into the body; these harmful effects of ANG II are reduced by ACE2.

When the SARS-CoV-2 virus binds to ACE2, it prevents ACE2 from performing its normal function to regulate ANG II signaling. Thus, ACE2 action is inhibited, removing the brakes from ANG II signaling and making more ANG II available to injure tissues. This decreased braking likely contributes to injury, especially to the lungs and heart, in COVID-19 patients.

No. ACE2 is present in all people but the quantity can vary among individuals and in different tissues and cells. Some evidence suggests that ACE2 may be higher in patients with hypertension, diabetes and coronary heart disease. Studies have found that a lack of ACE2 (in mice) is associated with severe tissue injury in the heart, lungs and other tissue types.

This is unclear. The SARS-CoV-2 virus requires ACE2 to infect cells but the precise relationship between ACE2 levels, viral infectivity and severity of infection are not well understood.

Even so, aside from its ability to bind the SARS-CoV-2 virus, ACE2 has protective effects against tissue injury, by mitigating the pathological effects of ANG II.

When the amount of ACE2 is reduced because the virus is occupying the receptor, individuals may be more susceptible to severe illness from COVID-19. That is because enough ACE2 is available to facilitate viral entry but the decrease in available ACE2 contributes to more ANG II-mediated injury. In particular, reducing ACE2 will increase susceptibility to inflammation, cell death and organ failure, especially in the heart and the lung.

The lungs are the primary site of injury by SARS-CoV-2 infection, which causes COVID-19. The virus reaches the lungs after entry in the nose or mouth.

ANG II drives lung injury. If there is a decrease in ACE2 activity (because the virus is binding to it), then ACE2 cant break down the ANG II protein, which means there is more of it to cause inflammation and damage in the body.

The virus also impacts other tissues that express ACE2, including the heart, where damage and inflammation (myocarditis) can occur. The kidneys, liver and digestive tract can also be injured. Blood vessels may also be a site for damage.

In a recent research paper, we argued that a key factor that determines severity of damage in patients with COVID-19 is abnormally high ANG II activity.

Angiotensin converting enzyme (ACE, aka ACE1) is another protein, also found in tissues such as the lung and heart, where ACE2 is present. Drugs that inhibit the actions of ACE1 are called ACE inhibitors. Examples of these drugs are ramipril, lisinopril, and enalapril. These drugs block the actions of ACE1 but not ACE2. ACE1 drives the production of ANG II. In effect, ACE1 and ACE2 have a yin-yang relationship; ACE1 increases the amount of ANG II, whereas ACE2 reduces ANG II.

By inhibiting ACE1, ACE inhibitors reduce the levels of ANG II and its ability to increase blood pressure and tissue injury. ACE inhibitors are commonly prescribed for patients with hypertension, heart failure and kidney disease.

Another commonly prescribed class of drugs, angiotensin receptor blockers (ARBs, e.g., losartan, valsartan, etc.) have similar effects to ACE inhibitors and may also be useful in treating COVID-19.

Evidence for a protective effect of ACE inhibitors and angiotensin receptor blockers in patients with COVID-19 was shown in recent work co-authored by one of us Dr. Loomba.

No evidence exists to suggest prophylactic use of these drugs; we do not advise readers to take these drugs in the hopes that they will prevent COVID-19. We wish to emphasize that patients should only take these drugs as instructed by their health care provider.

In collaboration with a multidisciplinary group of investigators, Dr. Loomba has initiated a multicenter (randomized, double-blinded, placebo-controlled) clinical trial to examine the efficacy of ramipril an ACE inhibitor compared to a placebo in reducing mortality, ICU admission or need for mechanical ventilation in patients with COVID-19.

[Get facts about coronavirus and the latest research. Sign up for The Conversations newsletter.]

Krishna Sriram, Postdoctoral Fellow, University of California San Diego; Paul Insel, Professor of Pharmacology and Medicine, University of California San Diego, and Rohit Loomba, Professor of Medicine, University of California San Diego

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Here is the original post:
What is the ACE2 receptor, how is it connected to coronavirus and why might it be key to treating COVID-19? The experts explain - TheStreet

Biochemistry

May: Prof Cullen Fellow announcement | News and features – University of Bristol

Peter Cullen, Professor of Biochemistry and Wellcome Trust Senior Investigator, has been elected to a Fellowship by the Academy of Medical Sciences.

The new Fellows have been chosen for their exceptional contributions to advancing biomedical science via world-leading research discoveries, running national science communication and engagement programmes and translating scientific advances into benefits for patients and the public.

Professor Cullen is internationally recognised for his identification and characterisation of the molecular mechanisms that orchestrate protein and lipid transport through the endosomal network, a complex intracellular maze found in all human cells.

His world-leading research has laid the foundations for understanding how altered function of the network contributes to an array of human diseases, ranging from cardiovascular disease and neurological disorders, most notably Alzheimer's disease and Parkinson's disease, through to metabolic disorders such a type 2 diabetes, hypercholesterolemia and non-alcoholic fatty liver disease, and subversion of the network by a wide range of viruses and bacteria.

Professor Cullen said: "This accolade really reflects the talent, endeavour and friendship of the current and past members of my laboratory and the amazingly stimulating and supportive research environment within the School of Biochemistry and the Faculty of Life Sciences. I must also express my extreme gratitude to the Medical Research Council, the Lister Institute of Preventive Medicine and, in particular, the Wellcome Trust for their continued and long-term funding of our research".

Indeed, the Cullen laboratory was recently awarded a prestigious 1.8-million Wellcome Trust Investigator Award to continue its groundbreaking research into 2026.

The value of medical science has never been more apparent than during the current COVID-19 global health crisis. From testing and vaccine development, public health and behavioural science to addressing the impacts of lockdown measures on mental health, biomedical and health scientists are helping to guide the UK through unprecedented challenges. Many of the Academys newly elected Fellows are at the forefront of the efforts to tackle coronavirus.

Professor Sir Robert Lechler PMedSci, President of the Academy of Medical Sciences said:This year our new Fellows announcement happens amidst a global health crisis. Some will face the challenge of how to continue to lead on some of the most pressing health challenges our society faces beyond coronavirus, such as heart disease, diabetes or cancer. Others have joined the global research effort to tackle the coronavirus pandemic, whether that be through working out how to treat those with the virus, joining efforts to develop a vaccine, or looking to limit the impact of the pandemic more broadly on our physical and mental health.

Never has there been a more important time to recognise and celebrate the people behind ground-breaking biomedical and health research, working harder than ever to further knowledge and protect patients and the public.

It brings me great pleasure to congratulate the new Fellows, and see our Fellowship grow to even greater heights of evidence-based advice, leadership and expertise.

The Academy of Medical Sciencesis the independent body in the UK representing the diversity of medical science. Their mission is to advance biomedical and health research and its translation into benefits for society.

The Academy is working to secure a future in which the UK and global health is improved by the best research; the UK leads the world in biomedical and health research and is renowned for the quality of its research outputs, talent and collaborations; independent, high-quality medical science advice informs the decisions that affect society and more have a say in the future of health and research.

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May: Prof Cullen Fellow announcement | News and features - University of Bristol

Human Behavior

No, you don’t have a "lizard brain": Why the Psychology 101 model of the brain is all wrong – Salon

Every so often an academic article liberates itself from the bonds of turgidity that characterize scholarly prose, and instead welcomes readers with a refreshing gust of literary flair. Such is the case with a recent piece published in Current Directions in Psychological Science,and co-authored by Joseph Cesario and Heather L. Eisthen of Michigan State University and David J. Johnson of the University of Maryland.

The title? "Your Brain Is Not an Onion With a Tiny Reptile Inside."

No, this isn't an article debunkingfringe conspiracy theories about how the world's leaders are a bunch of literal lizard people. Rather, it addresses (and debunks)one of the most commonly-used metaphors in evolutionary psychology, the idea that the human brain evolved from lower life forms and hence has evolutionary remnants from those animals akin to an onion with layers.

If you've ever heard someone speak of you possessing a "lizard brain" or "fish brain" that operates on some subconscious,primallevel, you've heard this metaphor in action. This is called the triune-brain theory;as the authors write, the basic crux of it is that"as new vertebrate species arose, evolutionarily newer complex brain structures were laid on top of evolutionarily older simpler structures; that is, that an older core dealing with emotions and instinctive behaviors (the 'reptilian brain'consisting of the basal ganglia and limbic system) lies within a newer brain capable of language, action planning, and so on."

Even respectable science magazines frequently fall back on this metaphor of the triune-brain theory.ADiscover article from 2010, titled "You Fall in Love Because Your Brain is a Jellyfish, Lizard, and Mouse Ice Cream Cone," is a prime example of triune-brain theory in action. As writer Kyle Munkittrick wrote then:

Feel that pebble in your shoe? Thank a jellyfish. Ever duck before a rogue Frisbee collides with your noggin? Thank a lizard. Remember where you left your keys? Thank a mouse. Hamiltoninterviewed David Linden from John Hopkins University whoexplained that our brain is the way it is because evolution is "the ultimate tinkerer and cheapskate." Evolution built our brain by taking simpler brains and just piling more brains on top - like adding scoops of ice cream to an ice cream cone. Hence, the pieces of our brain inherited from these other creatures are largely unchanged.

The problem, though, is that it just isn't true. Or, as the coauthors of the aforementioned paperput it:"this belief, although widely shared and stated as fact in psychology textbooks, lacks any foundation in evolutionary biology."

As they explain, thetriune-brain theorypromoted the overly-simplistic idea that animals can be easily organized from "simplest" to "most complex," and implies that evolution "is a linear progression in which one organism became another and then another." The authors explain that "the correct view of evolution is that animals radiated from common ancestors"; another implication of the assumption, "that structural complexity endows functional complexity," is in fact still up for debate.

"Perhaps mistaken ideas about brain evolution persist because they fit with the human experience: We do sometimes feel overwhelmed with uncontrollable emotions and even use animalistic terms to describe these states," the authors conclude. "These ideas are also consistent with such traditional views of human nature as rationality battling emotion, the tripartite Platonic soul, Freudian psychodynamics, and religious approaches to humanity. They are also simple ideas that can be distilled to a single paragraph in an introductory textbook as a nod to biological roots of human behavior. Nevertheless, they lack any foundation in our understanding of neurobiology or evolution and should be abandoned by psychological scientists."

It is worth noting that the "lizard brain" metaphor appears often in science journalism as well. Last month Elon Musk discussedhow he believes the lower brain is the "boss" and issues directives to the upper brain during an YouTube interview on a MIT Lex Friedman podcast episode. In March,Mike Lofgren of BillMoyers.com used the analogy to explain why conservatives tend to be more motivated by fear than liberals, arguing that "MRI tests have shown that different centers of the brain light up more robustly in these persons than others, and their amygdala the so-called 'lizard brain'that controls the threat response is larger than average. To what extent this characteristic is an inherited tendency and to what extent socialization alters the highly adaptable components of the brain is debatable." (Not to say thatMusk and Lofgren were wrong about the larger points they were trying to make, merely that they used a misleading scientific analogy to express it.)

Unfortunately, the triune-brain theory remains a staple of introductory science textbooks. The study's coauthors sampled 20 introductory psychology textbooks, published from 2009 and 2017. "Of the 14 [textbooks] that mention brain evolution, 86% contained at least one inaccuracy along the lines described above," they said."Said differently, only 2 of the field's current introductory textbooks describe brain evolution in a way that represents the consensus shared among comparative neurobiologists."

That means ifyou're clinging to a neurobiological misconception and feeling angry about it, you can no longer blame your lizard brain for those strong emotions. You have only your own human brain to blame.

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No, you don't have a "lizard brain": Why the Psychology 101 model of the brain is all wrong - Salon

Human Behavior

Restorers of Xumishan Grottoes prove to be picture of dedication –

Relic restoration experts repair murals in the No 48 cave of Yuanguang Temple at the Xumishan Grottoes in Ningxia on April 27. It's the first repair and recovery project carried out at the 1,500-year-old grottoes since the Qing Dynasty.[Photo/Xinhua]

Even during the scorching summer, the team of seven had to wear layers of thick clothes and knee pads to stay warm in a freezing and damp grotto. The dark space is dimly illuminated by their headlights and is home to wall paintings dating back hundreds of years.

They are not adventurers, but seven restorers who are helping to bring back the luster of the artwork found in more than 160 grottoes that dot the red cliffs of Xumishan in Northwest China's Ningxia Hui autonomous region.

The Xumishan Grottoes, first built in the late period of the Northern Wei Dynasty (386-534), house 162 caves and more than 1,000 statues, along a main stretch of the ancient Silk Road.

The murals, which total 185 square meters, are now in dire need of repair due to destructive human behavior and natural factors such as erosion that have occurred over the course of a millennium.

"I got goosebumps when the whole pattern of the painting showed up clearly after we had spent some 20 days cleaning it," says 60-year-old Wang Minquan, an expert in the group who has been participating in the year-long repair program-the largest of its kind since the Qing Dynasty (1644-1911)-since April.

The work can be tedious and demanding, Wang says, adding that young people these days do not have the patience to climb up and down the scaffolds, fix cracks and clean flaky walls all day.

On some steep rocky slopes, the team has to scramble a few dozen meters to reach a higher stone statue, with ropes tied around their waist like a climber.

Years of work in the freezing and dark grottoes has resulted in cervical spondylosis and cold legs for Wang and his colleagues.

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Restorers of Xumishan Grottoes prove to be picture of dedication -

Human Behavior

DEM Offers Tips on Preventing Conflicts with Coyotes – Portsmouth Press

PROVIDENCE, R.I. Keenly intelligent, extraordinarily adaptable, and willing to eat almost any available food whether natural, including small animals, birds, insects, and fruits; scavenged roadkill; or easily obtainable human-provided sources such as garbage, pet food, birdseed, and compost Rhode Islands coyotes are on the move again.

Typically, adult male and female coyotes breed in late winter and the female gives birth to a litter of 4 to 8 pups in April. Consisting of the adult pair and the pups, this social unit will be maintained until the pups become yearlings and disperse on their own or get booted out by their parents. Noisy, hungry pups must be fed.

That means adult coyotes will be seen and heard foraging and hunting for food in rural, suburban, and even urban Rhode Island neighborhoods over the next several months. As daylight hours increase, adult coyotes may spend more time actively foraging during daytime than they would at other times of the year.

The Rhode Island Department of Environmental Management (DEM) advises Rhode Islanders that the No. 1 key to minimizing interactions and conflicts with coyotes is reducing food sources available to them, either intentionally or unintentionally around our homes and neighborhoods. Coyotes that rely on natural food sources remain wild and wary of humans. Feeding coyotes or any wild animal however, makes them less fearful of people and they can become casual or even bold when encountering people.

If you see coyotes that are bold and brazen, its often directly related to intentional feeding or easy and reliably available food sources associated with human activities, said DEM wildlife biologist Charles Brown.

Intentionally feeding wild animals habituates them, causes them to lose their inherent fear of humans, and may lead to brazen behavior. It also leads to a whole series of problems, including frequenting areas close to homes and preying on domestic animals such as chickens, cats, and small dogs.

Coyotes play an important ecological role by controlling populations of rodents, resident geese, and in some cases white-tailed deer, Brown said. Shy and elusive by nature, most coyotes usually make every attempt to avoid interactions with people.

Coyote attacks on people are very rare. On the other hand, more than 4.5 million people are bitten by dogs each year in the United States, over half of dog bite injuries occur at home with dogs that are familiar to us, and over 800,000 receive medical attention for dog bites, according to the U.S. Centers for Disease Control.

HOW TO CUT DOWN ON COYOTE CONFLICTS

Remove attractants from your yard. This means removing all food and water sources like pet food dishes and birdfeeders and keeping barbecue grills clean of grease. Dont put meat or sweet food scraps in your compost pile, and keep compost in secure, vented containers. Put your trash in containers with secure lids and store them in sheds and garages away from doors if possible. Put garbage for pickup outside on the morning of collection, not the night before. If you have fruit trees, pick up fallen fruit.

Cut back brushy edges and dense weeds from around your yard and structures like sheds. These areas provide cover for coyotes and their prey.

Chase coyotes off your property. Keep coyotes wild by hazing them, which means doing things to scare them or chase them away. According to the website CoyoteSmarts.org (or here on Facebook), the following actions are effective hazing tactics:

Protecting pets. Keep pets, particularly cats, indoors. Coyotes dont distinguish between domestic and wild animals and are likely to view cats and small dogs as potential food and larger dogs as competition. For the safety of your pets, always keep them leashed when outdoors and feed them indoors. Outdoor feeding can attract many wild animals. Do not leave small dogs outside unattended, especially at night.

When confronted by a coyote. Stand up and look big. Wave your arms. Yell loudly. Dont lose your head. Keeping an assertive posture and making eye contact will convey a message of authority that coyotes will typically respect. Maintain eye contact. If the coyote does not retreat, walk slowly away toward the house. Do not turn your back on the animal.

Report aggressive behavior. Coyotes that exhibit bold or aggressive behavior towards humans should be treated with caution and reported to authorities. Also, animals that appear or act aggressively or are noticeably sick should be reported to the DEM Division of Law Enforcement (222-3070) or to your local animal control officer. Also, any contact between a coyote and a dog or other domestic animal should be immediately reported to your veterinarian and animal control officer.

Never feed coyotes. Feeding coyotes or other wild animals causes behavioral changes that will almost certainly cause unintended problems for neighbors and the animals that were meant to benefit. Report neighbors that are feeding coyotes to the DEM Division of Law Enforcement (222-3070) or to your local animal control officer.

Adult female coyotes typically weigh 33-40 pounds, while males typically weigh 34-47 pounds. They often look heavier because of their thick fur. The first appearance of coyotes in Rhode Island occurred in the mid-1960s, part of a range expansion into the eastern United States that began at the end of the 19th century.

Coyotes can currently be found in all Rhode Island communities except New Shoreham. They may hunt and travel alone or sometimes will travel as a group, usually an adult pair with their offspring from the most recent litter. In our area, coyotes are mostly nocturnal, mainly to avoid interactions with people. They remain active year-round and do not hibernate. Coyote pairs are territorial and will exclude other coyotes from their established territory.

Coyotes are now well established as part of our native fauna and unless you live on Block Island, you can expect that coyotes occur in your town or neighborhood and at some point, you may actually see one in your yard, on the bike path, or crossing a farm field, said DEM wildlife biologist Charles Brown. Not all coyotes exhibit bad traits and those that do have likely been encouraged or conditioned to behave that way because of human behavior.

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DEM Offers Tips on Preventing Conflicts with Coyotes - Portsmouth Press

Human Behavior

Mary E. Fissell: Pandemics come and go. The way people respond to them barely changes. – Greensboro News & Record

Pandemics have been afflicting humans for millennia, probably for as long as weve lived in large groups. Outbreaks struck the ancient Greeks, the Byzantines, the Incas and the Native Americans, among others. A century ago, the so-called Spanish flu, which as you probably know by now didnt actually originate in Spain, killed about 50 million people, and perhaps many more, around the world.

Im a historian who studies medicine in 17th-century England, and lately Ive been thinking about one particular pandemic: the bubonic plague that struck England in 1665, killing at least 200,000 people, including about 15% of the population of London. As we struggle to deal with the novel coronavirus pandemic, what strikes me most is how similar our experiences and responses are to those of the people living in England more than three centuries ago. No Zoom, no Instacart, no Tiger King, but human behavior in the face of plague seems remarkably familiar.

Just as today, a global economy was a key driver of the English epidemic. Bubonic plague, which is bacterial rather than viral, is typically spread to humans by fleas who have fed on the blood of infected rats. Earlier plague epidemics such as the Black Death of the 1300s, which may have wiped out half the population of Europe came to Europe via merchants traveling back from Asia along the Silk Road. In the same way, contemporary observers reported that the 1665 epidemic may have been brought to London by Dutch trading ships; the epidemic had already spread there a year earlier. In the months before it reached England, authorities had tried, obviously without success, to quarantine ships from the Netherlands and other plague-affected places.

Another conspicuous resemblance is socioeconomic. In the United States, weve seen that COVID-19 is disproportionately affecting poor people, as well as blacks and Latinos. Overall, these groups tend to have poorer health and less access to health care, and they are more likely to live in crowded, unhealthy conditions and to work in jobs that require them to come into close contact with others who may be infected.

In New York, for example, the death rate among blacks is twice as high as it is for whites; for Latinos, it is 60% higher. In Louisiana, blacks make up a third of the population but so far account for almost 60% of COVID-19 deaths. About 5,000 meatpacking workers, and perhaps many more, have tested positive for the virus to date, largely because of a lack of safety measures and the industrys cramped and grueling working conditions.

The situation 350 years ago in London was similar. During the epidemic, the London city government counted the dead, tracking how many people died of plague in each parish. This work was performed by searchers of the dead, who were often older poor women. These parish lists, known as Bills of Mortality, were printed up and sold weekly, a kind of early version of ZIP-code-by-ZIP-code health reports from state health departments.

Examining these lists, both 17th-century readers and historians have found that, no surprise, the poorest neighborhoods tended to have the highest death rates from the plague. The reasons for this are probably similar to the causes of todays disparities the poor were already less healthy, lived in dense, unsanitary neighborhoods and did the citys dirty work.

They also could not leave. Even without our current scientific knowledge, people knew that the disease moved from place to place. And once it reached English shores, people practiced social distancing as best they could, by getting away from the worst disease hot spots. Just as we are seeing today, those who could afford it left the cities for the countryside, where there was less disease; the classic medical advice of the time was leave quickly, go far away and come back slowly.

Even King Charles II left London, for Salisbury; when the disease showed up there, he went to Oxford. The poor, though, were largely stuck. They had no place to go, and they needed the work they were doing to survive.

And just as they are now, rumors flourished. In recent weeks, hydroxychloroquine, diluted bleach and bananas have all been promoted as treatments, with little or no evidence backing them up. Conspiracy theories have proliferated, including the false claim that Bill Gates is somehow behind the pandemic. In 17th-century England, wigs became the focus of rumor. At the time, this was a big deal; elaborate powdered wigs were the height of fashion for both men and women. During the epidemic, however, people came to fear them as a source of disease they were made from human hair, and who knew where it came from?

Other rumors spread, too: Perhaps the two comets seen a few months apart had presaged the plague. Stories of women taken to plague hospitals against their will, and houses suddenly shut up, spread rapidly. All the while, city church bells rang incessantly to mark the passing of parishioners.

Over the past few months, weve also seen officials and others use scapegoats to explain the pandemic. In the United States, China, where the virus originated, has been the most common target. Unsubtly, some leaders and media figures have called the pandemic the Chinese virus, or the Wuhan virus, after the city in which it first appeared. In recent months in the United States, there has been a sharp increase in anti-Asian bias, and 30% of people in a recent survey said they had witnessed an incident of such bias.

Past outbreaks have been no different. During the bubonic plague of the 1300s, Jews were accused of poisoning wells and food supplies, and pogroms destroyed thousands of communities across Europe. Other European cities blamed prostitutes and ran them out of town when a plague threatened. In 1665 in England, those Dutch ships were all too easy to blame because the English were at war with the Dutch at the time. Its worth noting that these ways of thinking have recurred more recently: At the turn of the 20th century in the United States, tuberculosis was called the Jewish disease, and Italian immigrants were blamed for outbreaks of polio.

By early 1666, the outbreak had abated, to the point that the king and other well-off Londoners returned. Life slowly returned to normal. For reasons that remain mysterious, this was the last large outbreak of bubonic plague in England.

Today, as we face another disease, one that we still dont understand very well, 17th-century England reminds us that despite the enormous leaps weve made in science and technology, humans themselves remain in many ways the same: imperfect, not always rational and still deeply vulnerable to novel nasty microbes.

Excerpt from:
Mary E. Fissell: Pandemics come and go. The way people respond to them barely changes. - Greensboro News & Record

Human Behavior

Where Is The 100 Filmed? The CW Show Filming Locations – The Cinemaholic

The 100 is a post-apocalyptic sci-fi drama that follows the story of the people who are sent to Earth to find out what it looks like now for the continuation of humanity. Ninety-seven years ago, a nuclear disaster had wiped out most of the people. The survivors fled and lived in the space station orbiting the Earth. But now, the makeshift home is running out of space, and they need to get their feet back on the ground.

One of the key points about the version of Earth that the show presents is that it strays away from the urbanity of the current world, and lays emphasis on the basic ferality of human nature by posing it with the wildness of nature. With the social structures as we know them out of the picture, the mercurial nature of human behavior is brought to the fore.

In the form of the Grounders, the Reapers, and the Mountain Men- the series presents a complex web of human thought-process and their basic instinct of cruelty and survival. To reflect the same danger in their surroundings, the series relied on a lot of outdoor locations. Here are all the places where it has been filmed.

The 100 follows the story of 100 juvenile detainees who are sent to a post-apocalyptic Earth to find out if the planet is ready to be habitable again. These young people have to survive the harsh environs of the Earth, which is still recuperating from the nuclear apocalypse that had happened some 100 years ago. The 100 offers a captivating world to us and presents our planet in a new light. Despite a lot of cultural and scientific differences between our world and that of The 100, it still looks a lot like ours, though less populated. All these beautiful backdrops for The 100 can be found in Canada. Vancouver, British Columbia serves as the central filming location for the series.

Throughout seven seasons, The 100 has extensively employed locations in and around Vancouver. Some scenes have been filmed in the Vancouver Film Studios and Aja Tan Studios. However, the story requires a lot of outdoor locations, throwing the characters into dangerous situations that Earths new surroundings impose on them.

Filming under water is a challenge. Fortunately, our camera man is up to it, putting on his swim trunks to get the perfect shot. #the100 pic.twitter.com/M7jhi0dSGh

The 100 Writers Room (@The100writers) May 11, 2017

#the100 BTS: Here's a shot of the mystery room still being completed before filming the next day. pic.twitter.com/aczjdX6Ur5

Shawna Benson (@shawnabenson) March 3, 2016

Vancouver locals will find a lot of places familiar with the world of The 100. Seymour Mainline and the Lower Seymour Conservation Reserve appear in a lot of episodes in the series. The Spur 4 Bridge is also a familiar sight in the show, along with the Spur 7 Beach. The tunnels of the Britannia Mine Museum have appeared in the earlier seasons of The 100. The lush surroundings of several parks have been used to portray the picture of an uninhabited Earth. These places include Lynn Canyon Park, Twin Falls, Upper Coquitlam River Park, Widgeon Valley National Wildlife Area, and Stawamus Chief Provincial Park.

NEWS | #The100 cast and crew was filming at BC place in Vancouver yesterday. pic.twitter.com/LczvTyjvvf

Bellarke News (@InfoBellarke) September 15, 2017

Gibsons Mansion and The Vancouver Club serve as the exterior and interior setting for Alies Mansion. The series has also been shot on location at Surrey City Hall, Oceanic Plazza, Annacis Island Wastewater Treatment Plant, West Cordova Street, Guinness Tower, Blieberger Farm, Canada Place & Burrard Street.

The cast and crew of #The100 begin filming the final season today lets send them some love! pic.twitter.com/lijYPwgwRw

Eliza Taylor Daily [Fan Account] (@dailyejt) August 26, 2019

The Gravel Pit near Mid-Valley Viewpoint has also been used as a critical location in several episodes. Apart from this, the Coal Harbour Seawall, Gillies Quarry, Minaty Bay, and Widgeon Slough North Dock also feature throughout several seasons. The infamous Riverview Hospital also serves as one of the filming locations for the sci-fi series. All the places near the water bodies in The 100 have been filmed in places like Britannia Beach, Steve Falls Dam, Watts Point Beach, and Lighthouse Beach.

Filming of the season finale of #The100 #The100Season3 @yvrshoots pic.twitter.com/ezvkVZaJbg

@Sandra (@SandraOlsson) January 22, 2016

NEWS | From the beginning to the end today marks the last day of filming of #The100. A heartfelt thank you to Bob and Eliza for being the best Bellamy and Clarke we could have asked for. #BellarkeForever pic.twitter.com/AFStnWMhJ1

Bellarke Buzz (@BellarkeBuzz) March 14, 2020

Read More: TV Shows Like The 100

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Where Is The 100 Filmed? The CW Show Filming Locations - The Cinemaholic