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Showing posts with label Medical Science. Show all posts
Showing posts with label Medical Science. Show all posts

Friday, 24 January 2020

Snakes are believed to be the cause of reported coronavirus disease in China



Since late December, a new coronavirus respiratory disease has emerged in China. It has already caused several hundred victims. Now, the new strain of coronavirus baptized 2019-nCoV by the WHO, has spread to several other countries. To better understand the virus, virologists must trace its origin and the animal host through which it first passed before infecting humans. A recent study shows that 2019-nCoV was transmitted to humans in the Wuhan market from snakes.

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Snakes - Chinese krait and Chinese cobra - may be the initial source of the newly discovered coronavirus that triggered the onset of a deadly infectious respiratory disease in China this winter. The disease was first reported in late December 2019 in Wuhan, a large city in central China, and quickly spread. Since then, sick travelers from Wuhan have infected people in China and other countries, including the United States.

Using samples from the virus isolated from patients, Chinese scientists determined the genetic code of the virus and observed it. The pathogen responsible for this pandemic is a new coronavirus. It belongs to the same family of viruses as the well-known severe acute respiratory syndrome coronavirus SARS-CoV, and the Middle East respiratory syndrome coronavirus (MERS-CoV), which have killed hundreds of people in the past 17 years. The World Health Organization (WHO) has named the new coronavirus “2019-nCoV”.


What is coronavirus?

The name of the coronavirus comes from its shape, which resembles a crown or a solar crown when imaged using an electron microscope. The coronavirus is transmitted by air and mainly infects the upper respiratory and gastrointestinal tracts of mammals and birds.

Although most members of the coronavirus family cause only mild flu-like symptoms during infection, SARS-CoV and MERS-CoV can infect the upper and lower respiratory tract, causing severe respiratory illness and other complications in humans.

The 2019-nCoV coronavirus observed under the electron microscope. Credits: CDC Chine

2019-nCoV causes symptoms similar to those of SARS-CoV and MERS-CoV. People infected with these coronaviruses suffer from a severe inflammatory reaction. Unfortunately, no approved antiviral vaccine or treatment is available for coronavirus infection. A better understanding of the 2019-nCoV life cycle, including the source of the virus, how it is transmitted and how it replicates is necessary to prevent and treat the disease.

2019-nCoV: an initial transmission from animals to humans

SARS and MERS are classified as zoonotic viral diseases, which means that the first infected patients acquired these viruses directly from animals. This was possible because, in the host animal, the virus had acquired a series of genetic mutations which allowed it to infect and multiply inside humans.

These viruses can now be transmitted between humans. Field studies have revealed that the original source of SARS-CoV and MERS-CoV is the bat and that masked palm civets (a mammal native to Asia and Africa) and camels , respectively, are used intermediate hosts between bats and humans.

This graph shows the origins of the different coronaviruses. The initial strains all come from bats. Credits: Science

In the case of this coronavirus epidemic in 2019, reports indicate that most of the patients in the first hospital group were workers or customers of a local wholesale seafood market which also sold processed meats and consumable animals living.

Including poultry, donkeys, sheep, pigs, camels, foxes, badgers, bamboo rats, hedgehogs and reptiles. However, as no one has ever reported finding a coronavirus infecting aquatic animals, it is plausible that the coronavirus may have originated from other animals sold in this market.

A disease transmitted by bats?

The hypothesis that nCoV 2019 comes from an animal on the market is strongly supported by a new publication in the journal Journal of Medical Virology . Virologists have analyzed and compared the genetic sequences of 2019-nCoV and all other known coronaviruses.

Study of the 2019-nCoV genetic code reveals that the new virus is most closely linked to two samples of bat SARS-type coronavirus from China, initially suggesting that, like SARS and MERS, the bald -mouse could also be behind 2019-nCoV.

The authors further found that the DNA coding sequence for the 2019-nCoV peak protein, which forms the crown of the viral particle that recognizes the receptor on a host cell, indicates that the bat virus may have mutated before infecting people. But when the researchers performed a more detailed bioinformatic analysis of the 2019-nCoV sequence, it suggested that this coronavirus could have come from snakes.

2019-nCoV: it would have gone from the bat to the snake

The researchers used an analysis of the protein codes favored by the new coronavirus and compared it to the protein codes of the coronaviruses found in different animal hosts, such as birds, snakes, marmots, hedgehogs, manis, bats and humans. Surprisingly, they found that the 2019-nCoV protein codes are most similar to those used in snakes.



Snakes often hunt bats in the wild. Reports indicate that the snakes were sold in the local seafood market in Wuhan, raising the possibility that 2019-nCoV has passed from the host species - bats - to snakes, and then to humans at the start of this. coronavirus epidemic. However, how the virus could adapt to both cold-blooded and warm-blooded hosts remains a mystery.

The authors of the report and other researchers must verify the origin of the virus by laboratory experiments. The first thing to do is to find the 2019-nCoV sequence in snakes. However, since the epidemic, the seafood market has been disinfected and closed, making it difficult to trace the source animal of the new virus.

DNA sampling from market animals and wild snakes and bats is necessary to confirm the origin of the virus. However, the results reported will also provide information on the development of prevention and treatment protocols.


Bibliography:

RESEARCH ARTICLE:  Homologous recombination within the spike glycoprotein of the newly identified coronavirus may boost cross‐species transmission from snake to human

Wei Ji  Wei Wang  Xiaofang Zhao  Junjie Zai  Xingguang Li

First published: 22 January 2020

https://doi.org/10.1002/jmv.25682

Thursday, 23 January 2020

Alzheimer's disease: a crucial mechanism in the fight against the disease has been identified



Alzheimer's disease is a neurodegenerative disease that affects tens of millions of people worldwide today. It is characterized by two lesions: amyloid deposits and tangles of tau protein. Several treatments have been developed in recent years, targeting one or other of these lesions in order to delay the progression of the disease. But recently, researchers have identified a crucial mechanism of the disease: the process by which beta-amyloid causes tau tangles. A discovery that could lead to treatments far more effective than current therapies.

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Alzheimer's disease has long been characterized by the accumulation of two separate proteins in the brain: first beta-amyloid, which builds up in plaques, then tau, which forms toxic tangles that lead to cell death. . However, the way in which beta-amyloid leads to the toxicity of the tau protein has never been precisely known. Now a new study at the University of Alabama in Birmingham seems to describe this missing mechanism.

Published in the journal Science Translational Medicine , the study details a cascade of events. The accumulation of beta-amyloid activates a receptor which responds to a chemical signal from the brain called noradrenaline, commonly known to mobilize the brain and the body for action. Activation of this receptor by both beta-amyloid and norepinephrine stimulates the activity of an enzyme that activates the tau protein and increases the vulnerability of brain cells.


The role of norepinephrine in the virulence of Alzheimer's disease

Essentially, beta-amyloid bypasses the norepinephrine pathway to trigger a toxic build-up of tau, says Qin Wang, a neuropharmacology researcher in the Department of Cell, Developmental and Integrative Biology at the University of Alabama in Birmingham. " We really show that this norepinephrine is a missing piece of the whole Alzheimer's puzzle ."

This cascade explains why so many previous treatments for Alzheimer's disease have failed. Most of the drugs developed in recent decades have targeted the elimination of beta-amyloids. But new research suggests that norepinephrine amplifies the damage caused by this protein. Beta-amyloid itself can kill neurons, but only in very high doses.

Alzheimer's disease is characterized by two types of lesions: the amyloid plaques between the neurons and the tau neurofibrilar lesions (tangles) inside the neurons. Biologists have long missed the link between beta-amyloid and tau. But Wang's team has shown that norepinephrine plays the main role in this process. Credits: Dr Holland


Add norepinephrine and only 1-2% beta-amyloid is needed to kill brain cells in a laboratory can. So with treatments that targeted beta-amyloid but left the norepinephrine pathway intact, there was enough beta-amyloid left to do significant damage. But if the norepinephrine pathway is really crucial for the development of Alzheimer's disease, it suggests new ways of treating the disease.

Towards the development of a drug targeting the norepinephrine pathway

A drug that was developed to treat depression, but too ineffective to be approved, seems to work in this same direction. The drug, idazoxan, which has also been studied in schizophrenia, has already undergone the first clinical tests and has been shown to be safe. Wang is now looking to promote larger clinical trials of idazoxan to see if it can be used to effectively treat Alzheimer's disease at an early stage.

She hopes that in the long term, a drug which will act on this path linked to Alzheimer's disease in a more targeted manner can be developed, in order to minimize the side effects and maximize the effectiveness. Stephen Salloway, professor of psychiatry and neurology at Warren Alpert Medical School at Brown University, says he doesn't think Alzheimer will give in so easily to a new drug targeting the norepinephrine pathway.



“I doubt there is anything simple that will come out of it. I would be shocked if it works . ” Such a drug, however, could be part of a "therapeutic package" of treatments that could potentially advance Alzheimer's disease, he said. “ The goal is to gain a foothold on the biological level, then to develop it. The more goals we have, the greater the impact.”

The binding of beta-amyloid to norepinephrine would be responsible for the toxicity of the tau protein

Wang has a long history of norepinephrine because of its role in complex thinking and behavior. She came across the link with Alzheimer as part of this research. In two strains of mice and in human tissue in their new study, she and her colleagues showed that small pieces of beta-amyloid bind to a norepinephrine receptor, activating the enzyme GSK3-beta and causing the toxicity of tau.

Graphs and microscopic images showing the efficacy of idazoxan (inhibitor of the enzyme GSK3-beta) on the activity of beta-amyloid; it is blocked and cannot bind to norepinephrine, greatly reducing the toxicity of the tau protein. Credits: Fang Zhang et al. 2020

They confirmed this relationship by blocking the receptor with idazoxan in two strains of middle-aged mice for eight weeks. This deactivated the enzyme and prevented tau from becoming toxic. For years, researchers have wondered how beta-amyloids and tau are linked, says Rudolph Tanzi, an expert in molecular genetics of Alzheimer's disease at Massachusetts General Hospital.

Scientists basically assumed that beta-amyloid had caused tau tangles through a complicated chain of events. Then in a 2014 article in Nature , Tanzi and colleagues used cultured human brain cells to reveal a problem with the theory: mice - the main source of research information on Alzheimer's disease - do not have the right form of tau which becomes entangled in humans.

Block the GSk3-beta enzyme to neutralize inflammation

Instead, researchers have shown that in human cells, beta-amyloid directly causes tangles of tau. Tanzi and his colleagues blocked a variety of different enzymes called kinases to try to stop the process. They found two, both of which blocked the GSK3-beta enzyme - the same one that Wang and his colleagues identified in their research.

In 2014, Wang and his team had already shown that 1-Azakenpaullone, an inhibitor of the GSK3-beta enzyme, neutralizes the formation of beta-amyloid responsible for the induction of tau toxicity (in yellow). Credits: R. Tanzi et al. 2014

Tanzi believes that inflammation is a key player in Alzheimer's disease, triggering the cascade that leads to the disease. He previously described beta-amyloid as the match and tangles of tau as brushwood that catches fire. Tanzi says he has unpublished data on dozens of drugs that prevent beta-amyloid from triggering tangles, many of which support what Wang and his colleagues found in their new document.


Bibliography:

ฮฒ-amyloid redirects norepinephrine signaling to activate the pathogenic GSK3ฮฒ/tau cascade

Fang Zhang, Mary Gannon, Yunjia Chen, Shun Yan, Sixue Zhang3, Wendy Feng1, Jiahui Tao1, Bingdong Sha, Zhenghui Liu, Takashi Saito, Takaomi Saido, C. Dirk Keene, Kai Jiao, Erik D. Roberson, Huaxi Xu and Qin Wang

Science Translational Medicine  15 Jan 2020:
Vol. 12, Issue 526, eaay6931
DOI: 10.1126/scitranslmed.aay6931

Wednesday, 22 January 2020

Everything you need to know about coronavirus spreading from China

Wuhan hospital staff in protective gear, where patients were treated.

Recently, a new coronavirus causing a mysterious illness similar to SARS has spread to China and three other Asian countries since its first appearance in the central city of Wuhan. Initially, the authorities excluded human-to-human transmission, but according to the latest news and following the report of several deaths, it turns out that the virus can indeed be transmitted between humans.

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On December 31, 2019, the World Health Organization (WHO) was alerted by the Chinese authorities to a series of cases of pneumonia in Wuhan, a city of 11 million inhabitants. The patients had been quarantined and research into identifying the origin of the pneumonia had started.

The Centers for Disease Control and Prevention (CDC) in the United States had identified the potential origin of the virus: a seafood market in Huanan (Wuhan), China.


New coronavirus

On January 9, WHO said the Wuhan epidemic was caused by an unknown type of coronavirus , responsible for a wide range of illnesses, from colds to more serious conditions like SARS. The new coronavirus is currently called “Wuhan coronavirus”, or 2019-nCoV.

According to an official report, to date, 59 people have been infected, including seven who are in serious condition.

First Death

Chinese health officials said a first patient died of the virus on January 11. Shortly thereafter, the total number of patients was revised downwards to 41 cases.

Spread beyond China

On January 13, the virus spread beyond the borders of China for the first time, with a case emerging in Thailand, according to the WHO. The victim is a Chinese woman suffering from mild pneumonia, who was returning from a trip to Wuhan.



On January 15, the Chinese health commission said that no human-to-human transmission of the virus that caused the Wuhan epidemic had been confirmed, but that the possibility "could not be excluded."

The following day, a first case of virus was confirmed in Japan, in a person who had stayed in Wuhan in early January.

American controls

On January 17, a second victim, a 69-year-old man, died in Wuhan, authorities said.

On the same day, the CDC announced that it would start screening passengers from Wuhan at three airports: San Francisco, JFK (New York) and Los Angeles.

Confirmation of human-to-human transmission

On January 20, a third death and more than 100 new cases are announced in China, causing concern before the annual Lunar New Year (or Chinese New Year) vacation, which begins on January 25 and sees hundreds of millions of Chinese traveling Across the country.

The virus is present in Beijing to the north, east of Shanghai and south of Shenzhen. More than 200 cases have been recorded. The virus has also been detected in South Korea in a Chinese man arriving by plane from Wuhan.

Chinese President Xi Jinping said during his first public comments on the epidemic that the virus must be "resolutely contained". Human-to-human transmission is "affirmative," Zhong Nanshan told state-run CCTV, a Chinese infectious disease specialist, on public television.


First case in the United States

The first case in the United States was reported a few days ago. It concerns a person in Washington State, near Seattle. The patient was hospitalized last week after a recent trip to Wuhan.

This article will be updated regularly.


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Tuesday, 21 January 2020

Cancer: discovery of new cell receptor could revolutionize T-cell therapies



Some current cancer therapies involve the use of genetically engineered T cells to destroy cancer cells. These particular white blood cells are able to recognize and neutralize any intruder in the body. However, these therapies are extremely restrictive and must be fully personalized due to the variability of the HLA receptor, allowing T cells to detect cancer cells. However, the discovery of a new invariant cellular receptor, which can neutralize different types of cancer, could revolutionize this therapy.

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The researchers behind the discovery note that the tests are still in their infancy, as they have only been performed on mice and human cells in the laboratory, not yet in living patients. But the preliminary results, published in the journal Nature Immunology , are promising and suggest that we may be on the verge of significant progress in T-cell therapies.

T cells are a type of white blood cell involved in the functioning of our immune system. When activated when they come into contact with defective or foreign cells in the body, they attack them, which helps us fight infection and disease.


T-cell therapies and HLA receptor variability

In T-cell therapy - the most common form of which is called CAR-T (for chimeric T cells of antigen receptors), scientists divert and increase this natural function of T cells to direct them to tumor cells in particular.

In CAR-T treatments, doctors extract T cells from patients' blood and genetically modify them in the laboratory to allow them to identify and specifically target cancer cells. The edited T cells are then multiplied in the laboratory before being administered to patients.

Diagram explaining the functioning of a CAR-T anticancer therapy. Credits: cancer.gov

Some of the limitations of the CAR-T technique are that edited T cells are only able to recognize a few types of cancer, and the whole therapy has to be personalized for different patients because of a T cell receptor (TCR) called “ human leukocyte antigen ”(HLA). HLA is what allows T cells to detect cancer cells, but it varies from person to person. And this is where this new discovery comes in.

MR1 receiver: an invariant and more suitable receiver

In the new study, led by biologists from Cardiff University in the UK, the researchers used CRISPR-Cas9 to discover a new type of TCR in T cells: a receptor molecule called MR1.

MR1 works similarly to HLA in terms of detecting and recognizing cancer cells, but one big difference is that, unlike HLA, it does not vary - which means that it could potentially form the basis of therapy for T cells that would work for a much wider range of people.

Diagram showing how new genetically engineered T cells use the MR1 receptor to identify and kill cancer cells. Credits: University of Cardiff

Preliminary laboratory experiments involving MR1 are indeed promising, even if the researchers point out that the results must be reproduced safely in clinical trials before they can confirm that it is a treatment suitable for humans.

In laboratory tests using human cells, T cells equipped with MR1 killed the multiple cancer cell lines tested (lung, melanoma, leukemia, colon, breast, prostate, bone and ovaries) that did not share common HLA. Tests on mice with leukemia - in which the animals were injected with MR1 cells - revealed signs of cancer regression and led the mice to live longer than the control mice.


Towards a new T cell therapy?

At the moment, we do not yet know how many types of cancer a technique based on this receptor could treat. That said, the first results certainly suggest that a varied range could be sensitive to it. If these types of effects can be replicated in humans - something scientists hope to start testing this year - T-cell therapies could take a big step.

To this end, the team's next step - in addition to organizing future clinical trials - will be to learn more about the mechanisms that allow MR1 to identify cancer cells at the molecular level.


Bibliography:

Genome-wide CRISPR–Cas9 screening reveals ubiquitous T cell cancer targeting via the monomorphic MHC class I-related protein MR1

Michael D. Crowther, Garry Dolton, Mateusz Legut, Marine E. Caillaud, Angharad Lloyd, Meriem Attaf, Sarah A. E. Galloway, Cristina Rius, Colin P. Farrell, Barbara Szomolay, Ann Ager, Alan L. Parker, Anna Fuller, Marco Donia, James McCluskey, Jamie Rossjohn, Inge Marie Svane, John D. Phillips & Andrew K. Sewell

Nature Immunology (2020)

doi:10.1038/s41590-019-0578-8

Sunday, 15 December 2019

Major research shows that certain common genes are linked to the majority of psychiatric disorders



A large-scale study has shown that the development of certain psychiatric illnesses can originate from the same gene. A discovery that could lead to the development of new treatments.

Psychiatric disorders affect more than 25% of the population each year. The numerous studies carried out in this field have made it possible to link variants (or mutations) of certain genes in the appearance of these disorders. But recently, scientists from Massachusetts General Hospital (MGH), in association with an international consortium of scientists specializing in genomic analyzes for psychiatric disorders, have shown that some of these variants can cause more than one disorder. psychiatric.

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In order to identify these genes, they gathered genomic data from around 500,000 healthy people, as well as from 230,000 others suffering from at least one of the eight most common psychiatric disorders. Result: 109 gene variants would increase the risk of developing more than one psychiatric illness.

They also found that the expression of the latter is greatly increased during the second trimester of pregnancy, a crucial phase for the development of the fetal brain.

The researchers then separated into three groups the different psychiatric pathologies, according to the gene variants that they have in common: mood and psychotic disorders (schizophrenia, bipolar disorder and depression), disorders responsible for compulsive behaviors (disorders obsessive compulsive, or anorexia nervosa), and developmental disorders of the nervous system (autism, attention deficit, or Tourette syndrome).



"  Understanding how specific genetic variations can contribute to a broad spectrum of diseases could tell us something about the degree to which these disorders can have a shared biology ," says lead study author Jordan Smoller.

Although this type of large-scale research has never been done in the past, the large number of variants identified was predictable for scientists. Indeed, most genes are pleiotropic, that is, they can have many roles in the body. It was therefore highly likely that a significant number of variants whose role is the proper development and functioning of the nervous system could be involved in more than one disease.

"Understanding how disorders are linked biologically can shed light on how we classify and diagnose mental health problems, " says bioinformatician Phil H. Lee of MGH. He also adds that this discovery could help characterize the biological pathways contributing to the development of these pathologies.

The researchers are confident that their study will allow the development of clinical trials in the future in order to develop new diagnoses and treatments that can be used for more than one disorder.



"  To the extent that these genes can have far-reaching effects, they could be potential targets for the development of new treatments that could benefit multiple conditions, " says Smoller.


Bibliography:

Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Cross-Disorder Group of the Psychiatric Genomics Consortium 1

Jordan W. Smoller

DOI:https://doi.org/10.1016/j.cell.2019.11.020

Friday, 13 December 2019

A key process of human cognition has been identified


Human behavioral patterns are based on such parameters as motivation, trust, anxiety, risk assessment, and so on. Although these personality traits are relatively well understood psychologically, their cerebral origin is much less so. Professor Adam Kepecs, of the Cold Spring Harbor Laboratory, answered some of these questions in a new study published in Nature . The results could lead to the development of more effective treatments for obsessive-compulsive disorder, gambling addiction and other psychiatric disorders.

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The team studied the orbitofrontal cortex, a critical area for decision making in humans and animals. The damage of this area of ​​the brain is detrimental to decision-making. In a famous example, Phineas Gage, a railway worker, survived extreme damage in this area when an iron rod pierced his skull during an explosion. Gage survived, but his personality and decision-making skills were profoundly altered.

Kepecs and his lab have sought to clarify how neurons in the orbitofrontal cortex encode mental variables such as motivation or confidence. " We wanted to understand how neurons code for these mysterious entities, what is the logic behind that, what is the architecture of the orbitofrontal cortex, " says Kepecs.

By monitoring neural activity in the brains of rats making complex decisions, the team identified a new, unexpected structure in the functional organization of the orbitofrontal cortex.


The role of orbitofrontal neurons in behavioral management

The key idea was to use mathematical models of decision-making behavior to calculate "confidence in decision". This approach produced fairly accurate predictions of what a representation of confidence in observed variables looks like, such as the difficulty of the decision or the choice that was made. It turned out that many orbitofrontal neurons were consistent with these predictions, their activity increasing or decreasing with a formally defined decision confidence.

Previous studies on the orbitofrontal cortex have identified similar mental variables, but unlike other brain regions such as the visual cortex, there was no order in their responses and the coding complexity was confusing.

Junya Hirokawa, of Doshisha University in Kyoto, recorded large populations of neurons in the orbitofrontal cortex and used sophisticated machine learning techniques to understand their activity patterns.

Orbitofrontal cortex. This area of ​​the brain is heavily involved in decision making. Credits: Jonathan D. Wallis

The team discovered that the neurons belonged to distinct functional groups. And each group of neurons has coded for different mental variables, like decision confidence or reward value, revealing a highly structured organization hitherto unsuspected.

Towards new psychiatric treatments

Finally, Kepecs wondered whether these functional groups were supported by a specialized anatomical structure. To do this, the team used artificial viruses to target a specific group of neurons, those that send connections to the striatum, an important part of the brain to update or rethink the value of a choice. They monitored the activity of these neurons and found that they were coding for another mental variable, the reward value, increasing activity when the expected reward was low.

Deconstructing this logical relationship between the functioning of neurons during different tasks and their physical structure in the brain could also open up possibilities such as the treatment of psychiatric disorders, for example by means of more precise stimulation of the brain of patients suffering from severe depression, Parkinson's and other types of illness.




Bibliography:

Frontal cortex neuron types categorically encode single decision variables

Junya Hirokawa, Alexander Vaughan, Adam Kepecs

Nature (2019)

http://dx.doi.org/10.1038/s41586-019-1816-9

Wednesday, 11 December 2019

Mysterious and Shocking: After receiving a bone marrow transplant, a patient's seminal fluid contains only the donor's DNA


Four years ago, Chris Long, a computer scientist from Reno, Navada, received a bone marrow transplant from a European foreign donor. At the time, he did not suspect that it could have an unexpected impact: his seminal fluid is now that of the donor, containing only the DNA of the latter.

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According to an article in The New York Times, the purpose of the transplant was to treat acute myeloid leukemia , a type of cancer that prevents the body from producing blood normally.

After the procedure, the donor's healthy hematopoietic cells replaced the damaged Long cells, allowing his body to resume normal blood production. It is therefore logical that Long's blood also contains the DNA of his donor.



Guinea pig…
But a colleague of Long (who works at the Washoe County Sheriff's Office), Renee Romero, who runs the office's forensic lab, suggested that bone marrow transplants could affect DNA elsewhere in her body. She had therefore encouraged Long to take DNA samples before the procedure so that the team could compare them to the post-operative samples. In other words, the office team wanted to use Long as a guinea pig (of course, after acceptance by him).

Since then, the sheriff's office team has collected many more DNA samples from various parts of the body, and at regular intervals over the years.

After analysis, they were able to identify both Long's DNA and that of its donor in some samples, including from his lips, cheeks and tongue (saliva). The samples taken from his chest and hair, in turn, reveal only the DNA of Long.

What was surprising for everyone is that four years after the procedure, Long's seminal fluid samples only reveal his donor's DNA, whereas a year later his semen contained both DNA. " I think it's pretty unbelievable that I can disappear and someone else can appear ..., " Long told NYT.

As the image on the computer screen shows, four years after the bone marrow transplant, Long's seminal fluid contains 100% of his donor's DNA, compared to 64% a year later. Credits: Tiffany Brown Anderson / The New York Times


Three bone marrow transplant experts, interviewed by the NYT, all agreed that it is normally impossible in such a procedure for a recipient to produce seminal fluid containing the donor's DNA.

But Mehrdad Abedi, the doctor who treated Long at the University of California at Davis, said the surprising seminal fluid of his patient was probably due to the fact that he had a vasectomy after the birth of his second child. However, the mechanism behind this seminal fluid DNA change remains mysterious.

Yet Long's situation raises all sorts of new questions about the use of DNA as evidence in court cases. Forensic scientists and forensic scientists now need to address the issue of the DNA of innocent people appearing at crime scenes because of bone marrow transplants.



If someone in Long's situation commits a sexual crime and the investigators collect seminal fluid samples, the bone marrow donor could be charged with the crime in the absence of any other DNA on the scene ... A comparison of DNA from several parts of the accused's body would therefore be necessary. A special case that the police must now consider.

Source

Friday, 6 December 2019

Microgravity Brings New Hope For the Cancer Patients



Practical medical examinations of astronauts in recent years have revealed that space travel involves a number of health risks: osteoporosis, reduced lung volume, loss of muscle density, exposure to radiation, and so on. However, conversely, space can also bring unexpected therapeutic solutions. This is what biologists have discovered by observing that, immersed in microgravity, the cancer cells are unable to recognize and assemble, and eventually become neutralized.

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Since 2014, Joshua Choi, a biomedical engineering researcher at the University of Technology Sydney, has been studying the effects of microgravity on the physiology and cells of the human body. Early next year, he and his research team will visit the ISS to test a new method of treating cancer based on microgravity.

According to Chou, his research was inspired by a conversation he had with the late Stephen Hawking. During the conversation, Hawking noticed that nothing in the Universe defies gravity. Later, when a friend of Cabbage was diagnosed with cancer, he remembered what Hawking said and began to wonder, " What would happen to cancer cells if we removed them from gravity? ".


Cancer cells accustomed to evolve in a classical gravitational environment

In simple terms, cancer is a disease in which cells begin to divide uncontrollably and spread to certain parts of the body. Cancer cells do this by coming together to form a solid tumor in the body, which then develops until cells invade healthy tissues - such as the heart, lungs, brain, liver, pancreas, etc.

The process by which cancer develops and spreads would seem to indicate that there is a way in which cells are able to detect and gravitate together to form a tumor. However, researchers in biomedicine know that mechanical forces are the only way for cancer cells to detect each other, and that these forces have evolved to operate in a gravitational environment.

Immerse cancer cells in microgravity to block their evolution

This prompted Chou to think of ways in which the absence of gravity could prevent cancer cells from dividing and spreading. He and his team have tested the effects of microgravity on cancer cells in their laboratory. To do this, one of his students created a device that essentially consists of a container the size of a tissue box with a small centrifuge inside.

The researchers used a rotating arm centrifuge to recreate microgravity conditions. Credits: Sascha Kopp et al.

The cells of different cancers are contained in a series of tubes inside the centrifuge, which then rotates them until they experience the sensation of microgravity. As Chou said, the results have been rather encouraging. " Our work has shown that, in a microgravity environment, 80 to 90% of the cells of the four types of cancer tested - ovary, breast, nose and lung - were deactivated and then killed ."

a) Under the effect of microgravity, thyroid cancer cells are forced to rearrange their cytoskeleton. b) Culture of cancer cells under normal conditions; the cancerous tissue formed is dense. c) Cultivation of cancer cells in microgravity; the cancerous tissue formed is loose, porous and weakly bound. Credits: Sascha Kopp et al.

When subjected to microgravity conditions, the cancer cells were unable to detect themselves and therefore had a hard time getting together.

Towards in situ confirmation of results ... And the development of new cancer therapies

The next step, which will take place early next year, will be for the team to send their experience in the ISS aboard a space module specifically designed for this purpose (SpaceX will provide launch services). Chou and his colleagues will spend the duration of the experiment (seven days) in the field, where they will follow the progress of the experiment and will perform live cell imaging via data sources.

Joshua Chou, holding the experimental prototype that will be sent to the ISS next year. Credits: Sissy Reyes

Once the experiment is over, the cells will be frozen for their return trip to Earth. Chou and his colleagues will then examine them to look for genetic modifications. If the results on board the ISS confirm what Chou and his team discovered in the laboratory, he hopes they will be able to develop new treatments that can have the same effect as microgravity and neutralize the ability of cancer cells to to detect oneself.

Ideally, these treatments would not be a cure but could complement existing cancer treatment regimens. Combined with drugs and chemotherapy, treatments derived from this research would effectively slow the spread of cancer in the human body, making conventional treatments more effective and short-lived (and less expensive as well).



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Researchers has developed the artificial brain cells

The chip in the center (the small green square) contains 120 artificial neurons. | University of Bath

The field of electronic circuits inspired by the brain has made a big leap forward. For the first time ever, researchers have been able to decode the complex behaviors of brain cells in order to recreate them in tiny computer chips. They demonstrated that a piece of silicon could behave exactly like a biological neuron.

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These tiny neurons may well change the way we design and build medical devices because they reproduce healthy biological activity, but only require one billionth of the energy needed by microprocessors.



It should be known that neurons behave in the same way as the electrical circuits of the body, but their behavior is less predictable, especially as regards the analysis of the relationship between their electrical input and output pulses. But these new artificial brain cells successfully mimic the behavior of rat neurons in two specific regions of the brain.

Professor Alain Nogaret (left) and research associate Kamal Abu Hassan (right) in the University of Bath laboratory. Credits: University of Bath

"Until now, the neurons looked like black boxes, but we managed to open them and examine the inside, " said Bath physicist Alain Nogaret. "  Our work is changing paradigms because it provides a robust method for reproducing the electrical properties of real neurons in great detail,  " he added.

For scientists, the ultimate goal is to use these neurons to design medical devices that are better adapted to patient needs, such as a smarter pacemaker, able to respond to new stressors and the demands of the person's heart. which essentially consists in improving the devices to better adapt them to the body.

Julian Paton, a physiologist at the Universities of Auckland and Bristol, said in his press release that recreating a biological activity was an interesting challenge because it "would offer tremendous opportunities for smarter medical devices that lead to personalized medicine approaches. for a range of diseases and disabilities.



In their work published in Nature Communications (see link below), researchers accurately reproduced the complete dynamics of hippocampal neurons and rat respiratory neurons.


Bibliography:

Optimal solid state neurons

Kamal Abu-Hassan, Joseph D. Taylor, Paul G. Morris, Elisa Donati, Zuner A. Bortolotto, Giacomo Indiveri, Julian F. R. Paton & Alain

Nature Communications volume 10, Article number: 5309 (2019)

https://doi.org/10.1038/s41467-019-13177-3

Thursday, 5 December 2019

Researchers identify the protein that controls the self-renewal of blood stem cells


Blood cells - red blood cells, white blood cells and platelets - are all initially derived from hematopoietic stem cells (HSCs). During hematopoiesis, these multipotent stem cells then differentiate into several progenitors that will give the final blood cells. In many blood disorders, bone marrow disorders can significantly reduce the production of HSC. But recently, researchers have discovered a protein mechanism that allows HSCs to self-renew, opening the door to new therapeutic solutions.

UCLA scientists have discovered a link between a protein and the ability of human blood stem cells to self-renew. In a study published in the journal Nature , the team reports that the activation of the protein causes the automatic renewal of blood stem cells at least twelve times under laboratory conditions.

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The multiplication of blood stem cells in conditions outside the human body could dramatically improve treatment options for blood cancers such as leukemia and for many inherited blood diseases. Blood stem cells, also known as hematopoietic stem cells, are found in the bone marrow where they are renewed and differentiated to create all types of blood cells.

Overcome rejection problems in bone marrow transplants

Bone marrow transplants have been used for decades to treat people suffering from certain diseases of the blood or immune system. However, they have significant limitations: it is not always possible to find a donor compatible with bone marrow, the immune system of the patient may reject foreign cells and the number of transplanted stem cells may not be sufficient to effectively treat disease.

In many blood diseases, bone marrow is reached, impacting the renewal of hematopoietic stem cells. Grafts are therefore performed, with risks of rejection generally high. Credits: Sophie Jacopin

When blood stem cells are removed from the bone marrow and placed in lab boxes, they quickly lose their ability to self-renew and they die or differentiate into other types of blood cells. Mikkola's goal of allowing the automatic renewal of blood stem cells under controlled laboratory conditions would open up many new possibilities for the treatment of many blood diseases, including the safer genetic engineering of blood stem cells. patients.


MLLT3: a gene involved in the renewal of blood stem cells

It could also allow scientists to produce blood stem cells from pluripotent stem cells, which can create any type of cell in the body. In the lab, researchers analyzed genes that go out when human blood stem cells lose their ability to self-renew, noting genes that are turned off when blood stem cells differentiate into specific blood cells, such as white or red blood cells.

They then placed the blood stem cells in lab boxes and observed which genes were inactivated. Using pluripotent stem cells, they made cells resembling blood stem cells that were unable to renew themselves and monitored which genes were not activated.

They found that the expression of a gene called MLLT3 was closely related to the potential for self-renewal of blood stem cells and that the protein generated by the MLLT3 gene gave the blood stem cells the necessary instructions to maintain its ability to self-renew. To do this, he collaborates with other regulatory proteins to ensure that important parts of the blood stem cell machinery remain operational during cell division.

A higher multiplication of HSCs thanks to the MLLT3 gene

The researchers wondered whether maintaining the level of MLLT3 protein in blood stem cells in lab boxes would be enough to improve their self-renewing abilities. Using a viral vector - a specially modified virus, capable of transmitting genetic information to the nucleus of a cell without causing disease - the team inserted an active gene MLLT3 into blood stem cells and observed that blood stem cells functional were able to multiply at least twelve times more.

The researchers found that activation of the MLLT3 (orange) gene allowed for greater turnover of hematopoietic stem cells. Credits: CurioCity

Other recent studies have identified small molecules - organic compounds often used to create pharmaceutical drugs - that help multiply stem cells from human blood in the laboratory. When Mikkola's team used these small molecules, she found that self-renewal of the blood stem cells generally improved, but that the cells could not maintain the appropriate MLLT3 levels and that they did not function properly. not as well when transplanted to mice.

Self-renewal of blood stem cells without side effects

Importantly, MLLT3 has allowed blood stem cells to self-renew at a reasonable pace; they have not acquired any dangerous characteristics such as excessive multiplication or mutation and the production of abnormal cells that can lead to leukemia.

The next steps for the researchers are to determine which proteins and which elements of the blood stem cell DNA influence the on-off switch for MLLT3, and how this can be controlled using the ingredients contained in the boxes. laboratory. With this information, they could eventually find ways to turn on and turn off MLLT3 without using a viral vector, which would be safer for use in a clinical setting.




Bibliography:

MLLT3 governs human haematopoietic stem-cell self-renewal and engraftment

Vincenzo Calvanese, Andrew T. Nguyen, Hanna K. A. Mikkola

Nature (2019)

https://doi.org/10.1038/s41586-019-1790-2

Friday, 29 November 2019

Discovery: tendon stem cells could revolutionize wound healing


Researchers have discovered, for the first time ever, tendinous stem cells. These undifferentiated cells could help us revolutionize the way we treat tendon injuries, while avoiding surgery.

Following an injury, the accumulation of scar tissue causes the recovery of a damaged rotator cuff, a knee of the jumper (patellar tendon injury), as well as other tendon injuries becomes a painful and difficult process , which can also (often) lead to secondary rupture of the tendons.

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" Tendons are connective tissues that bind our muscles to our bones. They improve our stability and facilitate the transfer of force that allows us to move. But they are also particularly susceptible to injury, "said Fan.

Unfortunately, once the tendons are injured, they rarely recover completely, which can limit mobility and require long-term pain management, or even surgery. Why ? Because of fibrous scars, which disturb the tissue structure of the tendon.



Working with Tyler Harvey and Sara Flamenco from Carnegie-Mellon University, USA, Fan has revealed all types of cells found in the patellar tendon, located beneath the patella, including the stem cells of the United States. tendon (previously undefined).

" Since tendon injuries are only rarely completely cured, it was thought that the stem cells of the tendon might actually not exist,  " said lead author Harvey. "  Many researchers have looked for them in vain, but our work has defined them for the very first time,  " he added.

You should know that stem cells are so-called "virgin" (or undifferentiated) cells, associated with almost all types of tissues. They are not yet (or not entirely) "programmed" to fulfill a specific function. These cells can also self-renew, creating a real pool from which different types of newly differentiated cells can be formed, in order to support the function of a specific tissue.

For example, muscle stem cells can differentiate into muscle cells. But until now, the stem cells of the tendon remained unknown.

But today, the team's research has shown that the cells of the scar tissue (fibrous) and tendon stem cells have a similar origin: indeed, they come from the same place, or the protective cells that surround them. tendons. In addition, these tendon stem cells are part of a so-called competitive system, with precursors of fibrous scars, which explains why the healing of the tendons is so complicated.



The research team has demonstrated that stem cells and stem cells of scar tissue are stimulated by a protein known as platelet-derived growth factor. When tendon stem cells are modified so that they do not respond to this growth factor, only scar tissue (and no new tendon cells) will form after injury. Such behavior could be replicated in order to improve healing of tendon tissues.

" Tendinous stem cells exist, but they must supplant precursors of scar tissue to prevent the formation of fibrous and difficult scars. Finding a therapeutic way to block scar cells and improve tendon stem cells could be a game changer for treating tendon injury  , "said Fan.


Bibliography:

Article: A Tppp3+Pdgfra+ tendon stem cell population contributes to regeneration and reveals a shared role for PDGF signalling in regeneration and fibrosis

Authors: Tyler Harvey, Sara Flamenco & Chen-Ming Fan

Nature Cell Biology (2019)

https://doi.org/10.1038/s41556-019-0417-z

Thursday, 28 November 2019

Study shows extra virgin olive oil could prevent many forms of dementia


Improving brain function is essential to counter the effects of aging. And according to a study by researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) in the United States, if there is one more thing that every person should consider doing to keep his brain "young" is to add extra virgin olive oil to his diet.

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Extra virgin olive oil (or EVOO) is a superfood rich in antioxidants protecting the cells and known for its multiple health benefits, particularly to help curb related diseases. aging, such as cardiovascular diseases.

Previous research, also done at LKSOM, showed that EVOO preserves memory and protects the brain against Alzheimer's disease.

And in a new study conducted on mice, LKSOM researchers show that it is possible to add to this list another group of diseases related to aging, tauopathies, characterized by the progressive formation of an abnormal form of 'a specific protein linked to dementia, tau protein, in the brain.

This process leads to a decline in mental function, or dementia. The results obtained are the first to suggest that EVOO can help the brain defend itself against a specific type of mental decline associated with tauopathy, called frontotemporal dementia. The results of the study were published in the journal Aging Cell.


Extra virgin olive oil to fight against different forms of dementia

Alzheimer's disease itself is a form of dementia. It mainly affects the hippocampus, the storage center of memory in the brain. Frontotemporal dementia affects areas of the brain near the forehead and ears. Symptoms typically appear between the ages of 40 and 65 and include changes in personality and behavior, language and writing difficulties, possible memory impairment, and the ability to learn from experience.

Dr. Domenico Praticรฒ, Scott Richards North Star Foundation Chair in Alzheimer's Disease Research, Professor in the Departments of Pharmacology and Microbiology and Director of the LKSOM Alzheimer Center, describes this new work as additional evidence showing the ability of EVOO to prevent cognitive decline and to protect the points of convergence of neurons, synapses, crucial elements of information sharing in the brain.

" EVO has been part of human nutrition for a very long time and has many health benefits, for reasons we do not yet fully understand ," he said. " The realization that EVOO can protect the brain against different forms of dementia gives us the opportunity to learn more about the mechanisms by which it acts to promote brain health. "

In earlier research on a mouse model, in which mice were modified to develop Alzheimer's disease, the Praticรฒ team showed that the EVOO provided in the diet protected young mice from memory and learning disabilities as they age.


Improvement of memory and learning and decrease of amyloid plaques

More particularly, when the researchers examined the brain tissue of EVOO-fed mice, they did not observe the typical characteristics of cognitive decline, particularly amyloid plaques, sticky proteins that saturate the communication pathways between neurons. In other words, the animal brain seemed normal.

In the case of this new study , similar consequences could be observed. Indeed, the team shows that it is the same for mice designed to develop a tauopathy.

In the latter, the normal tau protein becomes defective and accumulates in the brain, forming harmful tau protein deposits, also called "entanglements". Tau deposits, similar to amyloid plaques in Alzheimer's disease, block neuronal communication and thus interfere with thought and memory, leading to frontotemporal dementia.

The sick mice of the experiment were then subjected to a diet supplemented with EVOO at a young age, comparable to about 30 or 40 years in humans.

Six months later, when the mice had the equivalent of 60 years in humans, the harmful tau deposits were reduced by 60% in animals at risk of tauopathy, compared to other non-fed animals. extra virgin olive oil. The EVOO diet mice also showed better performance in memory and learning tests than those without EVOO.


Healthier functioning of synapses

When Dr. Praticรฒ and his colleagues examined the brain tissue of mice fed EVOO, they found that improved brain function was probably facilitated by healthier functioning of the synapses, which was associated with higher levels of brain function. higher than the normal of a protein called Complexin-1. Complexin-1 is known to play a critical role in maintaining healthy synapses.

The research team is now exploring what happens when EVOO is given to older animals, who have started to develop tau deposits and signs of cognitive decline, which is more closely related. to the clinical scenario in humans.

" We are particularly interested in whether EVOO can reverse the damage caused by tau protein and ultimately treat tauopathies in older mice ," added Dr. Praticรฒ.


Bibliography:

Extra virgin olive oil improves synaptic activity, short-term
plasticity, memory, and neuropathology in a tauopathy model

Elisabetta Lauretti1 | Miroslav Nenov1 | Ozlem Dincer1 | Luigi Iuliano2,3 |
Domenico Praticรฒ1

DOI: 10.1111/acel.13076

Following a radiograph of the hips, doctors find that the penis of a patient is literally transformed into bone


The human body is a very complex machine ... Sometimes strange things can happen and we discover it by accident. This is particularly the case here: a 63-year-old man went to a New York emergency department for left knee pain after falling ill. Leaving the hospital, the man ended up with an alarming and rare diagnosis: ossification of the penis.

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The doctors found this case extremely rare when they performed a radiograph of the pelvis, in order to look for signs of bone fracture. But instead, they spotted a bone-like calcification in a most unexpected place ...

Calcium salts have accumulated in soft tissues and have hardened to form an "  extended plaque  " along the penis stem, as you can see on the radiograph below:

Credits: Hasbani et al./Urology Case Reports, 2019

Except for some pain, the patient has no other symptoms of this condition in the form of discharge or swelling. According to the doctors, ossification of the penis can cause a loss of flexibility and also cause erectile problems. But before the doctors could do further examinations, including to determine the cause of this ossification, the man decided to leave ignoring all the medical advice he had received from the doctors ...

Known that penis ossification was first described in humans in 1827. However, it remains rare, with fewer than 40 cases documented so far.



The most common cause is Lapeyronia Disease, a fibrosis affecting the penis. Ossification may also be due to trauma, end-stage kidney disease or other diseases that cause excess calcium in the body.

Georges El Hasbani of the American University of Beirut and his colleagues, explain the treatment of penis ossification in their case report, published in the journal Urology Case Reports . " The treatment of penis ossification depends on the extent of body ossification and the patient's symptoms  ."

Credits: Hasbani et al./Urology Case Reports, 2019

The case involving an uncomfortable acute pain or mild chronic pain can be managed with oral analgesics, topical agents, intralesional injections, mechanical stretching or vacuum devices, and extracorporeal shock wave therapy. . Serious cases of extreme chronic pain or erectile dysfunction are usually treated surgically, "they added.

Ossification of the penis is usually seen in older dogs, however, dogs already have a bone in their penis at first. In fact, this is the case for most mammal species.

Doctors explain that: "  The human body is able to form bone tissue or cartilage in places affected by pathologies, when connective tissue is present. Bone tissue is known to form even in places that have nothing in common with the skeleton, including the mammary gland, salivary glands and testicles "




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Wednesday, 27 November 2019

FDA grants "revolutionary therapy" status to psilocybin in the treatment of depression


Psilocybin is an alkaloid, active principle of certain hallucinogenic mushrooms. In addition to its illicit recreational uses, the molecule has shown some potential for the treatment of certain psychological disorders and conditions by modifying brain chemistry. In order to accelerate the development and marketing of psilocybin-based therapeutic solutions, the FDA has declared the revolutionary treatment. It will be used especially in the context of major depressive disorders (MDD).

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For the second time in a year, the US Food and Drug Administration (FDA) has designated psilocybin therapy - currently tested in clinical trials - as a revolutionary therapy, an action to accelerate slow process of development and testing. It is usually requested by a pharmaceutical company and granted only when preliminary evidence suggests that the drug could represent a significant improvement over the treatment already available.

Last year, the FDA granted psilocybin treatment as a breakthrough therapy in Compass Pathways' ongoing clinical trials investigating the potential of psilocybin to treat treatment-resistant severe depression. or depression in unimproved patients after two different antidepressant treatments.


A single dose of psilocybin to fight depression

At present, the FDA has granted this status to psychedelic treatment, this time for a US-based clinical trial conducted by the non-profit institution Usona Institute. This clinical trial, which includes 80 participants from seven different sites in the United States, focuses on the efficacy of treating patients with MDD with a single dose of psilocybin.

Synthetic route and structure of psilocybin. Credits: FDA

In the United States, more than 17 million people suffer from major depressive disorder or severe depression lasting more than two weeks. Psilocybin, in a single dose, could have a profound impact on the brain and have lasting effects after the elimination of depressive symptoms. The Phase 2 trial is expected to be completed early in 2021 and, with this status, Usona expects to move quickly to a larger Phase 3 trial.

Approximately one in three treatments that had previously received revolutionary therapy status was approved. " What is truly innovative is the FDA's legitimate recognition that MDD, and not just the smallest treatment-resistant depressive population, represents an unmet medical need and that the available evidence suggests that psilocybin may substantial clinical improvement over existing treatments, "says Charles Raison, director of clinical research at Usona.

Towards the use of psychedelics in the treatment of depressive disorders

This is not the first time that a psychedelic has been studied for its potential in the treatment of depression. In March, the FDA approved nasal spray treatment with Esketamine , a ketamine-related substance for treatment-resistant patients, an anesthetic that was also used as an illicit drug.



But we still know a lot about this approved drug. Although acting quickly, it is unclear how Esketamine modifies the brain, and therefore what its effects will be in the long term.

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