All posts by medical

Immunology

Some cells serve as unlikely heroes to defend the brain from viral invaders – STAT

Scientists have discovered the important role of microglia cells in protecting a mouse brains central nervous system from viral infections that entered the brain through the nose.

Despite entering the body through the nose which gives a pathogen a direct route to the brain via olfactory neurons many viruses rarely manage to cause fatal damage in the brain. Researchers at the National Institute of Neurological Disorders and Stroke at the National Institutes of Health wanted to figure out why thats the case. In a new study published recently in Science Immunology, they infected mice with a respiratory virus called vesicular stomatitis virus to track the immune systems response.

Youre not trying to find out why the system [is] broken the system usually works, said Ashley Moseman, an assistant professor at Duke University School of Medicine and a co-author of the study. Past studies have shown that the brain can expel a virus without killing many of its own finite number of neurons, but they wanted to pinpoint how that process occurs.

advertisement

Their research found an unlikely hero: microglia. Microglial cells in the brain are not infected themselves by invading viruses. Rather, the study found that microglia actually find antigens the toxins a virus gives off in the brain and present them to the T cells that need to kill them.

We dont want T cells to go into the brain and kill things that they arent supposed to kill, said Moseman. So, he said, the microglia acquire antigen in a way that allows them to present antigen in the area, but avoid some of these tricky situations.

advertisement

The team observed the process between microglia and T cells by using a virus that would leave a stain to show everywhere its been, allowing them to see all the cells that survived infection. They used microscopes to observe the live cells interacting red-colored T cells flashed green when they came in contact with microglia and killed the antigen.

Later in the study, the team infected mice again, this time after reducing microglia in their brain. Under the microscope, they observed that T cells were less likely to recognize antigens when microglia were fewer. The mice also had reduced survival rates with lower counts of microglia, demonstrating how critical a role this cell type plays in the brains protection.

The researchers do not know how microglia are affected after a T cell kills the antigen. The encounter might kill microglia, too, but the stakes are lower, according to Moseman. Microglia can regenerate in ways that central nervous system neurons cannot. But its still an important question to ask, Moseman said, because what happens to microglia could have implications about how in control they are of T cells during this process.

The research has no immediate clinical implications, but scientists hope it will spark more study of how the brain protects itself and how those natural defenses could be enhanced. Many researchers are particularly interested in a possible connection to SARS-CoV-2, the virus that leads to Covid-19.

Loss of smell and taste are major symptoms of Covid-19, demonstrating a potential interference in the brain when infected. But experts said its also still unclear whether SARS-CoV-2 can enter the brain through neurons in the nose and, if so, how that might be prevented.

The findings are an important step toward researching possible interventions for when the brains defense system doesnt work, said Ari Waisman, chair and professor of immunology at University Medical Center of the Johannes Gutenberg University of Mainz, who wasnt involved in the research. He said there is now a question of whether the mechanism this study revealed, which occurs after the virus has infected the central nervous system, could be manipulated to happen earlier to protect the brain from other pathogen invasions.

Microglia has a lot of roles in antiviral infection that were not appreciated before, said Waisman.

While the study sheds light on the brains successful self-defense, its important to emphasize that this process occurs when the virus is already in the body and in the brain, Moseman said.

If youre trying to prevent invasion in the first place, you should consider the surface that is going to be invaded, he said. Once you get infected, you have to deal with the consequences one way or the other.

Read more from the original source:
Some cells serve as unlikely heroes to defend the brain from viral invaders - STAT

Immunology

Bold Therapeutics Expands COVID-19 Consortium – PharmiWeb.com

VANCOUVER, BC, June 11, 2020 /PRNewswire/ --Bold Therapeutics, a clinical-stage biopharmaceutical company, has expanded its COVID-19 collaborations to include four more academic researchers: Francois Jean, PhD and Ted Steiner, MD, both researchers from the University of British Columbia; Stephen Barr, PhD, a researcher at Western University; and Len Seymour, PhD, a researcher at the University of Oxford in the United Kingdom. These new collaborations significantly expand Bold Therapeutics' COVID-19 consortium. In April, the company announced a collaboration with Marc-Andr Langlois, Faculty Professor of Medicine at the University of Ottawa and Canada Research Chair in Molecular Virology and Intrinsic Immunity.

BOLD-100 is a first-in-class anti-resistance ruthenium-based small molecule drug which selectively inhibits stress-induced upregulation of GRP78 an important resistance, survival and proliferation pathway common across cancers. In addition, there is extensive and rapidly growing literature suggesting that GRP78 plays a critical role in host recognition, viral entry and viral replication.

"Our research team, supported by some of the brightest scientific minds in the space, continue to generate data elucidating the potentially broad antiviral utility of BOLD-100," added E. Russell McAllister, CEO of Bold Therapeutics. "In the past couple of months, we have engaged with numerous potential COVID-19 development and commercialization partners and generated significant positive feedback on our innovative antiviral program. BOLD-100 appears to have potentially broad application not only against SARS-CoV-2, but against other single-strand RNA viruses such as Dengue, West Nile, and Zika and, potentially other yet-to-be-discovered pathogens."

In collaboration with Franois Jean, PhD, Associate Professor in the Department of Microbiology and Immunology and founder of the UBC Facility for Infectious Disease and Epidemic Research (FINDER), one of the largest university-based containment level-3 (CL3) facilities in the world, Bold Therapeutics has initiated a Mitacs Accelerate project entitled: "Antiviral properties and mechanism of actions of BOLD-100 against SARS-CoV-2 in 2D and 3D cell culture systems."

Bold Therapeutics has also initiated a parallel Mitacs Accelerate project with Theodore Steiner, MD, Professor and Division Head, Division of Infectious Diseases at UBC entitled: "Cellular inflammatory and antiviral effects of BOLD-100, a novel therapeutic agent in development for COVID-19."

Bold Therapeutics also established a collaboration with Stephen Barr, PhD, Associate Professor in the Department of Microbiology and Immunology at Western University. Dr. Barr is testing BOLD-100 against SARS-CoV-2 isolates using in vitro assays, with initial data expected later this month.

Extending its consortium of COVID-19 researchers outside of North America, Bold Therapeutics is also collaborating with Len Seymour, PhD, Director of Clinical Pharmacology at the University of Oxford, who will be testing BOLD-100 against different isolates of SARS-CoV-2 using in vitro assays.

"We are focused on a data-driven COVID-19 development strategy, and this impressive international network of collaborators allows us to generate the data necessary to support our further clinical development of BOLD-100 as an antiviral," stated Jim Pankovich, Executive Vice President, Clinical Development. "We expect initial data from these partnerships in the next month, and, in parallel, we are working to secure funding so that BOLD-100 can progress rapidly into human clinical trials."

For more information, please visit the COVID-19 section on Company's website at http://www.bold-therapeutics.com/covid-19.

Media contact: E. Russell McAllister 241540@email4pr.com(604) 262-9899

View original content to download multimedia:http://www.prnewswire.com/news-releases/bold-therapeutics-expands-covid-19-consortium-301074459.html

SOURCE Bold Therapeutics Inc.

Go here to read the rest:
Bold Therapeutics Expands COVID-19 Consortium - PharmiWeb.com

Immunology

Researchers are developing statistical tools to analyze the spread and evolution of coronavirus – News-Medical.Net

For as much as the scientific community has learned about the novel coronavirus, SARS-CoV-2, since it emerged in China last year, many key aspects of the pandemic remain a mystery.

And for that reason, COVID-19 has been an especially tricky disease to contain.

For example, how did the virus travel from country to country, or region to region? Do weather patterns affect its ability to spread? What demographic or socioeconomic factors put certain populations at higher risk?

The problem is that existing tools for analyzing infectious diseases cant see how all of these factors are interconnected, says Kristian Andersen, PhD, professor in the Department of Immunology and Microbiology at Scripps Research.

Even the most advanced tools either arent capable of dealing with the amount of data we have today or arent appropriate for the types of questions were trying to answer.

Thats why Andersen and his collaborators Lauren Gardner, PhD, of Johns Hopkins University and Marc Suchard, MD, PhD, of University of California, Los Angelesare now working to develop better statistical models and visualization software.

The project has won a $1.3 million grant from the National Institutes of Health, with operations based out of the Scripps Research-led Center for Viral Systems Biology.

The funding supplements an initial $15 million NIH grant that enabled Andersen to launch the center in 2018, with the goal of helping eradicate infectious diseases such as Ebola and Lassa.

The team has already started its effort to build tools that can show how SARS-CoV-2 is moving around the world and what factors may be driving its spread and evolution. The idea is to be able to analyze everything at the same time, Andersen says.

Everything encompasses diverse factors such as airline traffic patterns, socioeconomic and demographic data, and weather conditions. It also includes genomic data from virus genomes sequenced from COVID-19 patients. "

"Every day, hundreds of new genomes are shared openly on research databases; Andersen and others use that data to look for mutations, or slight changes in the genetic sequence, that show how the virus moved from person to person. "

Once the new tools are developed, the genomic data and the other information will build on the Johns Hopkins COVID-19 Dashboard data and Scripps Researchs Outbreak.info website, both of which are available to the public. The Johns Hopkins dashboard, developed by Lauren Gardner, has become the worlds most accessed resource for real-time COVID-19 information.

For this project, Gardner draws from her expertise in epidemiological risk and mathematical modeling to integrate new layers of information, such as climate, land use and mobility.

Our goal is to weave together rich data layers that we will continuously analyze, creating real-time updates on the rapidly evolving pandemic. From a public health perspective, its essential to see how the virus is really spreading and how mitigation efforts are working.

Lauren Gardner, PhD., Associate Professor, Department of Civil and Systems Engineering, Johns Hopkins Univresity

Another key collaborator is statistician Marc Suchard, a professor in UCLAs Departments of Biomathematics and Human Genetics. He is the senior developer of an open-source software program thats used by more than 1,000 research groups worldwide to understand, on a genomic level, how infectious diseases spread.

Through the creation of new, scalable statistical models, well be able to more clearly identify the factors that affect viral transmission and virulence for SARS-CoV-2, Suchard says.

Not only will this allow us to understand whether certain public health measures are working, but it also will help predict how the disease could spread under different circumstances.

At its highest level, the project seeks to make complex information easier to understand, revealing patterns that would otherwise go unnoticed.

By fostering a greater understanding of the virus among researchers and the public, the team hopes that governments around the world can improve their response to the COVID-19 pandemic and minimize future outbreaks.

See the original post:
Researchers are developing statistical tools to analyze the spread and evolution of coronavirus - News-Medical.Net

Immunology

Quell Therapeutics strengthens its Board with the appointments of Dr Dhaval Patel and Sir Robert Lechler and hires Dr Natalie Belmonte as SVP Research…

London June 11th 2020 Quell Therapeutics, a biotechnology company developing engineered T regulatory (Treg) cell therapies, today announced the appointments of seasoned industry expert, Dr Dhaval Patel, Executive Vice President and Chief Scientific Officer UCB S.A. (Brussels, Belgium), and Senior Clinical Academic, Professor Sir Robert Lechler, Senior Vice President/Provost (Health) and Executive Director of King's Health Partners Academic Health Sciences Centre, to its Board of Directors.

Additionally, the Company announced today, the appointment of Dr Natalie Belmonte as SVP Research & Translation. Dr Belmonte has extensive R&D experience in the fields of Treg cell and Mesenchymal Stem Cell based therapies.

Both Dhaval and Robert are highly experienced leaders who bring a wealth of drug development and translational immunology expertise to Quell Therapeutics, said Iain McGill, Chief Executive Officer of Quell Therapeutics. We have made great progress as we work towards building out a pipeline of cell therapies leveraging our engineered Treg platform. We have already selected our first product candidate targeting tolerance in liver transplantation and Natalie, in her role as SVP Research & Translation, will play a pivotal role in helping us broaden our pipeline in auto-immune and inflammatory disorders.

I speak for both myself and Robert when I say how pleased we are to be joining the Board of Quell Therapeutics, said Dhaval Patel. The Company is at an exciting stage in its evolution as it develops CAR-Treg products in autoimmune and inflammatory diseases, which could offer patients transformative therapies to resolve chronic diseases.

Dr Dhaval Patel is Executive Vice President and Chief Scientific Officer of UCB where he is a member of the UCB Executive Committee and leads the Companys research organisation with the main goal of bringing scientific innovation to patients. He joined UCB from Novartis, where, over a period of 11 years he led various biomedical research teams in areas of neurology, autoimmunity, transplantation, and inflammation. In 2010, he became the Head of Research for the Novartis Institutes for BioMedical Research (NIBR) Europe. For 12 years prior to crossing into industry, Dhaval made a strong mark in the halls of academia and research, specifically at Duke University Medical Center and the University of North Carolina (UNC) at Chapel Hill in North Carolina in the US. Dhaval is a medical doctor and holds a PhD in Microbiology and Immunology.

Professor Sir Robert Lechler is currently Provost and Senior Vice-President (Health) at Kings College London, Executive Director of Kings Health Partners and President of the Academy of Medical Sciences. His clinical and research career have been focused on the pursuit of clinical transplantation tolerance. Prior to his roles at Kings College London, Robert was Head of the Division of Medicine, Imperial College London, Dean of the Hammersmith Campus of Imperial College, and Professor and Director of Immunology. In 2012 Robert was awarded a Knighthood for Services to Academic Medicine and in 2015 was elected as the President of the UK Academy of Medical Sciences. Robert graduated in Medicine at Manchester University and was awarded his PhD by the University of London. He continues to direct a research group in transplantation immunology, with a primary focus on transplantation and immune tolerance.

Dr Natalie Belmonte has over 15 years of experience working in the field of cell therapy in both academic and biotech environment and has extensive experience with the development of Treg cell and Mesenchymal Stem Cell based therapies. Before joining Quell Therapeutics, Nathalie served as Chief Operating Officer at Promethera Biosciences. Prior to that, she served as VP R&D at TxCell developing Treg cell-based therapy for autoimmune and inflammatory diseases. She also has experience working with stem cells in a number of academic institutes including the San Raffaele Hospital at the Telethon Institute for Gene Therapy (TIGET) in Milan. She holds a PhD in Cellular and Molecular Biology from the University of Nice Sophia Antipolis.

Original post:
Quell Therapeutics strengthens its Board with the appointments of Dr Dhaval Patel and Sir Robert Lechler and hires Dr Natalie Belmonte as SVP Research...

Immunology

What will it take to produce a COVID-19 vaccine? – University of California

Immunology and infectious disease expert Joel Ernst, M.D., addresses key questions about how vaccine development works and why vaccines are especially important in the case of COVID-19.

First, this disease is highly transmissible. Its transmitted by the respiratory route, so people spread it easily in crowded places. Obviously, its incapacitating and deadly. Finally, effective vaccines are the most economical means to control a transmissible infectious disease.

Another reason that vaccines have a particularly special role is that this disease can be transmitted by asymptomatic and presymptomatic individuals. In other words, somebody doesnt have to have a fever or be coughing in order to infect the people around them.

Without a vaccine and without broad immunity in a population, COVID-19 could very well become an endemic infection. That means it remains steady in the population, like chicken pox, and unlike other pathogens that cause outbreaks and then recede, such as Ebola or Zika.

Finally, as were experiencing, the economic and human impacts of COVID-19 are huge.

Thats pretty unlikely. There would be a lot of lives lost before we achieved a percentage of immune people in the population sufficient to prevent community transmission. In so-called herd immunity, if a high proportion (70 percent to 95 percent) of the population is immune, then a person with the disease is unlikely to cause an outbreak. To achieve that level of immunity to COVID-19 in a community through natural infection, it would mean that nearly everyone in the community would need to be infected, and with a 1 percent mortality rate for COVID-19, thats unacceptable.

Part of what we know or what we think we know is derived from the experience with SARS, which is the most closely related coronavirus to SARS-CoV-2, the virus that causes COVID-19.

It would probably be safe to extrapolate a few things from SARS.

The first is that the protective immunity that results from infection may be transient. In people who were infected with the first SARS coronavirus, their protective immunity began waning between one and two years postinfection, as indicated by repeated checking of their antibody levels. Unlike diseases like measles or smallpox, where infection confers lifelong protective immunity, coronavirus infections may not confer long-lasting immunity.

The second thing we think we know is that neutralizing antibodies are likely to contribute to protection.

When we get an infection, our immune systems respond to fight off that is, neutralize that specific invading virus or bacteria. These responses generally protect us against future infections from the same pathogen, unless the pathogen mutates to avoid recognition by those immune responses.

One of the immune responses that can provide protection is the production of antibodies, proteins that recognize an infectious pathogen, with the goal of eliminating the infection. Antibodies are generally easy to measure, but the presence of antibodies does not guarantee protection. That is because the routine tests we have dont measure the quantity or quality of antibodies.

By quality, I mean that some antibodies bind to the pathogen, but they dont contribute to protection. They can be there, they can be detected, but they dont possess the activities needed to eliminate the pathogen. For example, people infected with HIV generate antibodies to HIV proteins, but the HIV infection still persists.

At the extreme end, some antibodies can actually be harmful. For example, in the case of another viral disease, dengue, which is transmitted by mosquitoes, people can have antibodies that make the infection more severe and the symptoms more critical.

What all this means is: The right antibodies are needed. Thats the goal of vaccination to confer immunity that is superior to what is conferred by infection itself.

Multiple approaches to developing a COVID-19 vaccine are underway. Some are based on inactivating the virus, essentially making it noninfectious while preserving its ability to provoke an immune response; other approaches modify the virus so it can grow but not cause severe disease. Another alternative is to use a purified pathogen protein to stimulate the immune system to provoke immune responses that block the disease an approach thats been successful with tetanus, diphtheria, and hepatitis B vaccines.

Finally, some approaches use more advanced techniques. They work at the genetic level, embedding instructions in DNA or RNA, or they use benign viruses, called viral vectors, to deliver an antigen the pathogen protein that induces a protective immune response directly to cells in our immune system.

The goals of vaccine development are first of all, safety, and second, to induce the kind of immune response that is necessary to prevent infection and disease due to the specific pathogen; distinct pathogens can require different mechanisms to provide protective immunity.

And especially in a pandemic, rapid, large-scale production is absolutely essential. We need billions of doses of any COVID-19 vaccine. For the same reason, we need them to be economical on a global scale.

Another goal, especially in the case of COVID-19, is a vaccine that blocks the infection where the virus enters the body. Since we know that SARS-CoV-2 ordinarily enters through the respiratory tract, via the mouth or nose, we want immunity that operates right there at the portal of entry and not just in the bloodstream.

Vaccines need to generate long-lived immunological memory. Ideally, vaccines will induce immune responses that recognize viral targets that cant mutate to escape, like the flu virus does, which forces us to modify the flu vaccine every year.

Finally, vaccines need to be stable enough for distribution to clinics worldwide. In other words, a vaccine that requires refrigeration is not going to reach everyone.

There are at least 90 groups worldwide working to develop COVID-19 vaccines. Roughly 20 of them are working on DNA- or RNA-based vaccines, about 25 groups are working on viral-vector vaccines, and numerous groups are working on protein-based vaccines. A smaller number of groups are working on viruslike protein particles, which are a bit more difficult and expensive to produce. Here at UCSF, there are many experts in immunology and virology working to assure that new COVID-19 vaccines have the properties that are most important.

To have a global impact, a vaccine needs to work in large, diverse populations. And those steps can only be combined or rushed to a limited extent.Joel Ernst, M.D.

The next stage is human studies. They address the question, Is the new vaccine safe? Can you give it to people without causing undue toxicity? The next question is, Does the vaccine stimulate immune responses in humans? Next, Does the vaccine protect humans from disease in a so-called efficacy trial? Finally, Does the vaccine protect humans in the real world? That is called vaccine effectiveness. The difference between efficacy and effectiveness is that in efficacy studies, the conditions and subjects are chosen to be ideal for the study. Effectiveness means that the vaccine protects people who arent preselected, who might have medical conditions that could make it more challenging for a vaccine to work. To have a global impact, a vaccine needs to work in large, diverse populations. And those steps can only be combined or rushed to a limited extent.

A recent clinical trial led by the pharmaceutical company Moderna showed promising but very preliminary results. Can you interpret their findings?

This was a safety trial of an RNA vaccine. It was designed to test how well 45 healthy volunteers tolerated different doses of the vaccine. But supplemental data showed that the volunteers produced antibodies similar to those in people who have recovered from the virus, suggesting the vaccine achieved the sought-after immune response. While finding antibodies is good news, it does not tell us if the vaccine is effective.

An expanded safety trial. In 45 subjects, youre only going to see the most common side effects things like pain at the injection site, a fever. To capture rare side effects, its necessary to expand the number of study participants. It would also be expanded into different groups, including older people. The upper age cutoff of these volunteers was 55 years. We know that older people are more susceptible to bad outcomes from COVID-19, so its important to determine whether the same vaccine at the same dose also produces an immune response in them.

Through efficacy studies, which follow safety studies. Efficacy studies can be done in one of two main ways. They can be done in very large populations at risk you vaccinate some and dont vaccinate others and compare the rates of infection in the two groups. Those are expensive, they take a long time, and they can be complicated by fluctuations in the frequency of the disease in question. For example, if a flu vaccine trial was started after the peak of flu season, the rate of infection in both groups might be too low to find a difference in infection rates.

The other alternative is a human challenge study. In that case, people are vaccinated or not and then actually challenged with the pathogen of interest. Challenge studies are generally done with pathogens for which theres curative therapy malaria, for example. You watch for evidence that a person develops a fever and treat them immediately with that therapy. We dont have that advantage in the case of the new coronavirus, since we dont currently have a highly effective treatment.

I think were roughly 12 to 18 months from being able to roll out a vaccine thats accessible to a significant slice of the population.

See the rest here:
What will it take to produce a COVID-19 vaccine? - University of California

Immunology

CSL Behring Buys Vitaeris, Picks Up Transplant Rejection Therapeutic – BioSpace

CSL Behring, based in King of Prussia, Pennsylvania, is acquiring Vancouver, British Columbia-based Vitaeris. The two companies inked a strategic partnership in 2017 to accelerate the development of Vitaeriss clazakizumab. At that time, CLS Behring also had an option to acquire Vitaeris, the therapeutic, and the rest of Vitaeriss assets.

No financial details were disclosed. In the 2017 deal, Vitaeris retained control of projects through the end of Phase III development. There was an upfront cash payment of $15 million, with research-and-development milestone payments over that period, which included future sales-related payments, as well as a royalty to Alder BioPharmaceuticals, who originated clazakizumab.

Clazakizumab is an anti-interleukin-6 (IL-6) monoclonal antibody for the treatment of chronic active antibody-mediated rejection (AMR), which is the top cause of long-term rejection in kidney transplant patients. There are currently no treatments approved for transplant recipients who develop antibody-mediated rejection.

Clazakizumab will join CLS842 and CSL964 as part of CSL Behrings late-stage program related to transplants.

Clazakizumab has been a promising monoclonal antibody in the Transplant therapeutic area since we started working with Vitaeris several years ago, said Bill Mezzanotte, executive vice president, Head of R&D, CSL Behring. Acquiring Vitaeris and their associate expertise helps us to continue to grow our strategic scientific platform of recombinant proteins and antibodies. We look forward to continuing to advance this treatment candidate as a potential option for people experiencing rejectionan area where current treatment options for transplant recipients are limited, at best.

Also today, CSL Behring announced results from a Phase II clinical trial of garadacimab (formerly CSL312), an investigational novel Factor XIIa-inhibitory monoclonal antibody to prevent hereditary angioedema (HAE). The company presented results at the European Academy of Allergy and Immunology (EAACI) Digital Congress 2020.

The trial met the primary endpoint, showing a decreased number of attacks compared to placebo in patients with HAE. HAE is a rare, genetic and potentially life-threatening disease. HAE is one of two types of bradykinin-mediated angioedema, with the other being nonhereditary or acquired angioedema. HAE is the result of deficient or dysfunctional C1-INH, a blood protein that helps control inflammation.

Last month, the U.S. Food and Drug Administration (FDA) granted garadacimab orphan drug designation for bradykinin-mediated angioedema.

The attacks that HAE patients experience can be very frightening, and clinicians want to do anything in their power to reduce the frequency of these attacks, lessen the need for rescue medicine and simplify treatment, said Timothy Craig, lead study investigator with Allergy, Asthma and Immunology, Department of Medicine and Pediatrics, Penn State Hershey, Hershey, Pennsylvania. The findings of this study are very encouraging and we look forward to further research assessing the safety and efficacy of garadacimab.

CSL Behring has been quite busy recently. On June 2 the company announced a strategic alliance with Seattle Childrens Research Institute to develop stem cell gene therapies for primary immunodeficiency diseases. The initial focus will be on Wiskott-Aldrich Syndrome and X-linked Agammaglobulinemia.

The company is also working on several fronts to develop treatments and preventions for COVID-19. The company is part of the CoVIg-19 Plasma Alliance, which is working to develop an unbranded anti-SARS-CoV-2 polyclonal hyperimmune immunoglobulin therapy. The Alliance is also working with the U.S. National Institute of Allergy and Infectious Diseases (NIAID) to test the hyperimmune therapy in adult patients with COVID-19. CSL Behring Australia is developing an anti-SARS-COV-2 plasma product for the Australian market. CSL Behring is also partnered with the Coalition for Epidemic Preparedness Innovations (CEPI) and The University of Queensland (UQ) to speed the development, manufacture and distribution of a COVID-19 vaccine, as well as other initiatives in this space.

And on May 27, 2020, CSL Limited entered into a strategic partnership with Thermo Fisher Scientific to meet the growing demand for biologic therapies while also accelerating CSLs broader manufacturing objectives. Thermo Fisher will leverage its pharma services network to support CSLs product portfolio, and via a long-term lease deal, will operate a new state-of-the-art biologics manufacturing facility in Lengnau, Switzerland, which is being built now and is expected to be completed in mid-2021.

Of the acquisition by CSL Behring, Kevin Chow, president and chief executive officer of Vitaeris, stated, Were pleased to become part of CSL Behring, a well-established, global industry leader, and know that the future of clazakizumab is in excellent hands. Together, we have already achieved much progress through our partnership over the past few years and are now in an even stronger position to realize our collective goal of addressing one of the greatest unmet needs in the organ transplant community.

Originally posted here:
CSL Behring Buys Vitaeris, Picks Up Transplant Rejection Therapeutic - BioSpace

Physiology

With an internet of animals, scientists aim to track and save wildlife – Minneapolis Star Tribune

The International Space Station, orbiting 240 miles above the planet, is about to join the effort to monitor the worlds wildlife and to revolutionize the science of animal tracking.

A large antenna and other equipment aboard the orbiting outpost will soon be able to relay a wider range of data than previous tracking technologies, logging not just an animals location but also its physiology and environment. This will provide much more detailed information on the health of the worlds ecosystems.

The new approach, known as ICARUS short for International Cooperation for Animal Research Using Space will be able to track animals across far larger areas than other technologies. It will allow researchers to track flocks of birds as they migrate over long distances, for instance, instead of monitoring only one or two birds at a time, as well as far smaller creatures, including insects. And, as climate change and habitat destruction roil the planet, ICARUS will allow biologists and wildlife managers to quickly respond to changes.

Its a new era of discovery, said Walter Jetz, a professor of ecology and evolutionary biology at Yale. We will discover new migration paths, habitat requirements, things about species behavior that we didnt even think about.

As an added bonus, people all over the world will one day be able to log on with a smartphone app to follow their favorite bird or tortoise or fish as it migrates.

This space-based approach is led by Martin Wikelski, director of migration research at the Max Planck Institute for Animal Behavior in Germany. ICARUS combines such technology as solar and GPS units with technology specifically designed for tracking small animals.

On the ground, researchers will attach solar-powered bio-loggers that are far smaller than other technology the size of two fingernails. The advanced design will allow them to collect far more data by monitoring an animals physiology, including skin temperature and body position, and external conditions like weather metrics.

The technology can also be used to accomplish a range of goals beyond wildlife studies, such as picking up behavioral changes among animals prior to earthquakes and volcanic eruptions that could provide an early warning.

It also could keep tabs on species of bats, pangolins and other animals that have played a role in epidemics. With skin temperature we can see in the ducks in China whether the next avian influenza is starting, Wikelski said.

The power of this approach is partly based on the fact that the space station can pick up the signals of these animals almost anywhere on the planet. And while other projects have tracked sharks, birds and other migratory species with satellites, this one aims to be useful for any species that researchers wish to examine.

Excerpt from:
With an internet of animals, scientists aim to track and save wildlife - Minneapolis Star Tribune

Physiology

Researchers identify two brain phenomena that may explain the side-effects of ketamine – News-Medical.Net

Researchers have identified two brain phenomena that may explain some of the side-effects of ketamine. Their measurements of the brain waves of sheep sedated by the drug may explain the out-of-body experience and state of complete oblivion it can cause.

In a study aimed at understanding the effect of therapeutic drugs on the brains of people living with Huntington's disease, researchers used electroencephalography (EEG) to measure immediate changes in the animals' brain waves once ketamine - an anaesthetic and pain relief drug - was administered.

Low-frequency activity dominated while the sheep were asleep. When the drug wore off and the sheep regained consciousness, the researchers were surprised to see the brain activity start switching between high and low-frequency oscillations.

The bursts of different frequency were irregular at first but became regular within a few minutes.

"As the sheep came round from the ketamine, their brain activity was really unusual," said Professor Jenny Morton at the University of Cambridge's Department of Physiology, Development and Neuroscience, who led the research.

The timing of the unusual patterns of sheep brain activity corresponded to the time when human users report feeling their brain has disconnected from their body."

Jenny Morton, Study Lead and Professor, Development and Neuroscience, Department of Physiology, University of Cambridge

She added: "It's likely that the brain oscillations caused by the drug may prevent information from the outside world being processed normally,"

The findings arose as part of a larger research project into Huntington's disease, a condition that stops the brain working properly.

The team want to understand why human patients respond differently to various drugs if they carry the gene for this disease. Sheep were used because they are recognised as a suitable pre-clinical model of disorders of the human nervous system, including Huntington's disease.

Six of the sheep were given a single higher dose of ketamine, 24mg/kg. This is at the high end of the anaesthetic range. Initially, the same response was seen as with a lower dose.

But within two minutes of administering the drug, the brain activity of five of these six sheep stopped completely, one of them for several minutes - a phenomenon that has never been seen before.

"This wasn't just reduced brain activity. After the high dose of ketamine, the brains of these sheep completely stopped. We've never seen that before," said Morton. Although the anaesthetised sheep looked as though they were asleep, their brains had switched off.

"A few minutes later their brains were functioning normally again - it was as though they had just been switched off and on."

The researchers think that this pause in brain activity may correspond to what ketamine abusers describe as the 'K-hole' - a state of oblivion likened to a near-death experience, which is followed by a feeling of great serenity. The study is published today in the journal Scientific Reports.

Ketamine abusers are known to take doses many times higher than those given to the sheep in this research. It is also likely that progressively higher doses have to be taken to get the same effect.

The researchers say that such high doses can cause liver damage, may stop the heart, and be fatal.

To conduct the experiment sheep were put into veterinary slings, which are commonly used to keep animals safe during veterinary procedures. Different doses of ketamine were given to 12 sheep and their brain activity recorded with EEG.

Ketamine was chosen for the study because it is widely used as a safe anaesthetic and pain-relief drug for treating large animals including dogs, horses and sheep.

It is also used medically and is known as a 'dissociative anaesthetic' because patients can appear awake and move around, but they don't feel pain or process information normally - many reports feeling as though their mind has separated from their body.

At lower doses ketamine has a pain-relieving effect, and its use in adult humans is mainly restricted to field situations such as frontline pain-relief for injured soldiers or victims of road traffic accidents.

"Our purpose wasn't really to look at the effects of ketamine, but to use it as a tool to probe the brain activity in sheep with and without the Huntington's disease gene," said Morton.

"But our surprising findings could help explain how ketamine works. If it disrupts the networks between different regions of the brain, this could make it a useful tool to study how brain networks function - both in the healthy brain and in neurological diseases like Huntington's disease and schizophrenia."

Ketamine has recently been proposed as a new treatment for depression and post-traumatic stress disorder. Beyond its anaesthetic actions, however, very little is known about its effects on brain function.

"We think of anaesthetic drugs as just slowing everything down. That's what it looks like from the outside: the animals basically go to sleep and are unresponsive, and then they wake up very quickly. But when we looked at the brain activity, it seems to be a much more dynamic process," said Morton.

Source:

Journal reference:

Nicol, A. U & Morton A. J. (2020) Characteristic patterns of EEG oscillations in sheep (Ovis aries) induced by ketamine may explain the psychotropic effects seen in humans. Scientific Reports. doi.org/10.1038/s41598-020-66023-8.

The rest is here:
Researchers identify two brain phenomena that may explain the side-effects of ketamine - News-Medical.Net

Physiology

What Is Early Life Stress? – WTOP

The coronavirus pandemic represents a significant stress to youth and adults alike. Moreover, the images of police brutality, looting and

The coronavirus pandemic represents a significant stress to youth and adults alike. Moreover, the images of police brutality, looting and mass demonstrations can exacerbate feelings stress and uncertainty. We are living through an unprecedented experience and our adaptability to it may vary.

To understand the potential effects of this period of time on children, its helpful to have a closer understanding of early life stress.

Stress is a physiological reaction that prepares an individual to respond to a stressor. The stressor is usually something that threatens the well-being or homeostasis (stable equilibrium) of the individual. The benefits and detriments of stress operate on an inverted U shape curve. On the first part of the curve we encounter the benefits; for example, stress helps develop our immune system, increases our performance and motivates us to take action, but only up to an optimal point. After this critical point, we start seeing a decline in health, performance and well-being.

[READ: Coping With Anxiety and Depression During the Coronavirus Pandemic.]

Stress accumulates. Early life stress refers to a load of stress that starts early in development. Think of a backpack; we can all carry one, but if it gets too heavy for the individual, it will affect his or her balance. It becomes an allostatic load, which means it impacts the physiology and health of the individual.

Support, coping strategies, genetic makeup, temperament, cognitive flexibility and other factors all contribute to the way we carry our stress burden. When stress is present early in life, it may interfere with key physical, emotional, academic and social developmental milestones.

Elements of the current COVID-19 pandemic represent early life stress for children. For example, not being at school, not interacting with friends, having play and exercise limited, feeling concerned about the well-being of their caretakers and themselves, and the threat of illness are all stressors.

Teenagers face specific challenges: Their sense of control over their lives may be limited, they have to strictly adhere to rules and they may experience loss of privacy. Other associated stressors for all include the monitoring of their health by themselves and others, the cancellation or postponement of important activities, and in critical situations, the grief of losing friends or loved ones.

[See: 8 Proven Strategies to Stop Overthinking and Ease Anxiety Now.]

Anxiety, which is not only the physical response, but the negative thoughts associated with an experience, can have a negative impact on all of us, children and adults alike. Although at a time like this its human to be anxious, failing to control the anxiety can influence our judgment or problem-solving ability. This may lead to irrational decisions, such as disobeying health ordinances, or falsely attributing blame at a time when we all need to practice good citizenship and be responsive together.

Parents and caregivers become the meter by which youth measure their safety. They should open communication about this crisis by making themselves available to answer questions, and communicate a message of safety. Kids want to know that their caregivers feel competent and confident in providing safety and security.

Of course, were not always going to have all the answers, and were not always going to feel like talking about the subject. Choose a time that works for you and your child, and if you dont know the answer to their question, tell them youll look into it.

Make sure you use reliable sources, such as the Centers for Disease Control and Prevention or Substance Abuse and Mental Health Services Administration for health issues.

For issues specific to kids, the American Academy of Child and Adolescent Psychiatry has useful resources, including Facts for Families. The Stanford Early Life Stress and Resilience Program has a number of significant resources as well, including online physical and mind exercises and educational tools.

Parents also need to know when to seek professional help.

[Read: Meditation Tips During the Coronavirus Pandemic.]

If your child demonstrates a saddened affect that lasts longer than two days, avoids activities they usually enjoy, has difficulty concentrating, exhibits unhealthy sleeping or eating, engages in use of alcohol, tobacco or other drugs, or demonstrates any new, uncharacteristic behavior that worries you, you should contact your family doctor to discuss. It doesnt necessarily mean that your child requires medical attention, but your doctor can help assess if more specialized help is needed.

Every child and every family is unique. These guidelines are meant to support your efforts, but you need to adapt them to your situation, your family life and family composition. Use this time as an opportunity to teach the value of working as a community for a common benefit.

More from U.S. News

How to Handle Workplace Stress

8 Unexpected Signs Youre Stressed

8 Ways to Relax Now

What Is Early Life Stress? originally appeared on usnews.com

Read the original here:
What Is Early Life Stress? - WTOP

Physiology

Sedated Sheep Show How Ketamine Reboots the Brain – Technology Networks

Researchers have identified two brain phenomena that may explain some of the side-effects of ketamine. Their measurements of the brain waves of sheep sedated by the drug may explain the out-of-body experience and state of complete oblivion it can cause.In a study aimed at understanding the effect of therapeutic drugs on the brains of people living with Huntingtons disease, researchers used electroencephalography (EEG) to measure immediate changes in the animals brain waves once ketamine an anesthetic and pain relief drug was administered. Low frequency activity dominated while the sheep were asleep. When the drug wore off and the sheep regained consciousness, the researchers were surprised to see the brain activity start switching between high and low frequency oscillations. The bursts of different frequency were irregular at first, but became regular within a few minutes.

As the sheep came round from the ketamine, their brain activity was really unusual, said Professor Jenny Morton at the University of Cambridges Department of Physiology, Development and Neuroscience, who led the research. The timing of the unusual patterns of sheep brain activity corresponded to the time when human users report feeling their brain has disconnected from their body.

She added: Its likely that the brain oscillations caused by the drug may prevent information from the outside world being processed normally,

The findings arose as part of a larger research project into Huntingtons disease, a condition that stops the brain working properly. The team want to understand why human patients respond differently to various drugs if they carry the gene for this disease. Sheep were used because they are recognized as a suitable pre-clinical model of disorders of the human nervous system, including Huntingtons disease.

Six of the sheep were given a single higher dose of ketamine, 24mg/kg. This is at the high end of the anesthetic range. Initially, the same response was seen as with a lower dose. But within two minutes of administering the drug, the brain activity of five of these six sheep stopped completely, one of them for several minutes a phenomenon that has never been seen before.

This wasnt just reduced brain activity. After the high dose of ketamine the brains of these sheep completely stopped. Weve never seen that before, said Morton. Although the anesthetized sheep looked as though they were asleep, their brains had switched off. A few minutes later their brains were functioning normally again it was as though they had just been switched off and on.

The researchers think that this pause in brain activity may correspond to what ketamine abusers describe as the K-hole a state of oblivion likened to a near-death experience, which is followed by a feeling of great serenity. The study is published in the journal Scientific Reports.

Ketamine abusers are known to take doses many times higher than those given to the sheep in this research. It is also likely that progressively higher doses have to be taken to get the same effect. The researchers say that such high doses can cause liver damage, may stop the heart, and be fatal.

To conduct the experiment sheep were put into veterinary slings, which are commonly used to keep animals safe during veterinary procedures. Different doses of ketamine were given to 12 sheep and their brain activity recorded with EEG.

Ketamine was chosen for the study because it is widely used as a safe anesthetic and pain-relief drug for treating large animals including dogs, horses and sheep. It is also used medically, and is known as a dissociative anesthetic because patients can appear awake and move around, but they dont feel pain or process information normally many report feeling as though their mind has separated from their body.

At lower doses ketamine has a pain-relieving effect, and its use in adult humans is mainly restricted to field situations such as frontline pain-relief for injured soldiers or victims of road traffic accidents.

Our purpose wasn't really to look at the effects of ketamine, but to use it as a tool to probe the brain activity in sheep with and without the Huntingtons disease gene, said Morton. But our surprising findings could help explain how ketamine works. If it disrupts the networks between different regions of the brain, this could make it a useful tool to study how brain networks function - both in the healthy brain and in neurological diseases like Huntingtons disease and schizophrenia.

Ketamine has recently been proposed as a new treatment for depression and post-traumatic stress disorder. Beyond its anesthetic actions, however, very little is known about its effects on brain function.

We think of anaesthetic drugs as just slowing everything down. That's what it looks like from the outside: the animals basically go to sleep and are unresponsive, and then they wake up very quickly. But when we looked at the brain activity, it seems to be a much more dynamic process, said Morton.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

The rest is here:
Sedated Sheep Show How Ketamine Reboots the Brain - Technology Networks