Monthly Archives: January 2020

Neuroscience

These Breakthroughs Made the 2010s the Decade of the Brain – Singularity Hub

I rarely use the words transformative or breakthrough for neuroscience findings. The brain is complex, noisy, chaotic, and often unpredictable. One intriguing result under one condition may soon fail for a majority of others. Whats more, paradigm-shifting research trends often require revolutionary tools. When were lucky, those come once a decade.

But I can unabashedly say that the 2010s saw a boom in neuroscience breakthroughs that transformed the field and will resonate long into the upcoming decade.

In 2010, the idea that wed be able to read minds, help paralyzed people walk again, incept memories, or have multi-layered brain atlases was near incomprehensible. Few predicted that deep learning, an AI model loosely inspired by neural processing in the brain, would gain prominence and feed back into decoding the brain. Around 2011, I asked a now-prominent AI researcher if we could automatically detect dying neurons in a microscope image using deep neural nets; we couldnt get it to work. Today, AI is readily helping read, write, and map the brain.

As we cross into the next decade, it pays to reflect on the paradigm shifts that made the 2010s the decade of the brain. Even as a boo humbug skeptic Im optimistic about the next decade for solving the brains mysteries: from genetics and epigenetics to chemical and electrical communications, networks, and cognition, well only get better at understanding and tactfully controlling the supercomputer inside our heads.

Weve covered brain-computer interfaces (BCIs) so many times even my eyes start glazing over. Yet I still remember my jaw dropping as I watched a paralyzed man kick off the 2014 World Cup in a bulky mind-controlled exosuit straight out of Edge of Tomorrow.

Flash forward a few years, and scientists have already ditched the exosuit for an implanted neural prosthesis that replaces severed nerves to re-establish communication between the brains motor centers and lower limbs.

The rise in BCIs owes much to the BrainGate project, which worked tirelessly to decode movement from electrical signals in the motor cortex, allowing paralyzed patients to use a tablet with their minds or operate robotic limbs. Today, prosthetic limbs coated with sensors can feed back into the brain, giving patients mind-controlled movement, sense of touch, and an awareness of where the limb is in space. Similarly, by decoding electrical signals in the auditory or visual cortex, neural implants can synthesize a persons speech by reconstructing what theyre hearing or re-create images of what theyre seeingor even of what theyre dreaming.

For now, most BCIsespecially those that require surgical implantsare mainly used to give speech or movement back to those with disabilities or decode visual signals. The brain regions that support all these functions are on the surface, making them relatively more accessible and easier to decode.

But theres plenty of interest in using the same technology to target less tangible brain issues, such as depression, OCD, addiction, and other psychiatric disorders that stem from circuits deep within the brain. Several trials using implanted electrodes, for example, have shown dramatic improvement in people suffering from depression that dont respond to pharmaceutical drugs, but the results vary significantly between individuals.

The next decade may see non-invasive ways to manipulate brain activity, such as focused ultrasound, transcranial magnetic or direct current stimulation (TMS/tDCS), and variants of optogenetics. Along with increased understanding of brain networks and dynamics, we may be able to play select neural networks like a piano and realize the dream of treating psychiatric disorders at their root.

Rarely does one biological research field get such tremendous support from multiple governments. Yet the 2010s saw an explosion in government-backed neuroscience initiatives from the US, EU, and Japan, with China, South Korea, Canada, and Australia in the process of finalizing their plans. These multi-year, multi-million-dollar projects focus on developing new tools to suss out the brains inner workings, such as how it learns, how it controls behavior, and how it goes wrong. For some, the final goal is to simulate a working human brain inside a supercomputer, forming an invaluable model for researchers to test out their hypothesesand maybe act as a blueprint for one day reconstructing all of a persons neural connections, called the connectome.

Even as initial announcements were met with skepticismwhat exactly is the project trying to achieve?the projects allowed something previously unthinkable. The infusion of funding provided a safety blanket to develop new microscopy tools to ever-more-rapidly map the brain, resulting in a toolkit of new fluorescent indicators that track neural activation and map neural circuits. Even rudimentary simulations have generated virtual epilepsy patients to help more precisely pinpoint sources of seizures. A visual prosthesis to restore sight, a memory prosthesis to help those with faltering recall, and a push for non-invasive ways to manipulate human brains all stemmed from these megaprojects.

Non-profit institutions such as the Allen Institute for Brain Science have also joined the effort, producing map after map at different resolutions of various animal brains. The upcoming years will see individual brain maps pieced together into comprehensive atlases that cover everything from genetics to cognition, transforming our understanding of brain function from paper-based 2D maps into multi-layered Google Maps.

In a way, these national programs ushered in the golden age of brain science, bringing talent from other disciplinesengineers, statisticians, physicists, computer scientistsinto neuroscience. Early successes will likely drive even more investment in the next decade, especially as findings begin translating into actual therapies for people who dont respond to traditional mind-targeting drugs. The next decade will likely see innovative new tools that manipulate neural activity more precisely and less-invasively than optogenetics. The rapid rise in the amount of data will also mean that neuroscientists will quickly embrace cloud-storage options for collaborative research and GPUs and more powerful computing cores to process the data.

First, brain to AI. The physical structure and information flow in the cortex inspired deep learning, the most prominent AI model today. Ideas such as hippocampal replaythe brains memory center replays critical events in fast forward during sleep to help consolidate memoryalso benefit AI models.

In addition, the activation patterns of individual neurons merged with materials science to build neuromorphic chips, or processors that function more like the brain, rather than todays silicon-based chips. Although neuromorphic chips remain mainly an academic curiosity, they have the potential to perform complicated, parallel computations at a fraction of the energy used by processors today. As deep neural nets get ever-more power hungry, neuromorphic chips may present a welcome alternative.

In return, AI algorithms that closely model the brain are helping solve long-time mysteries of the brain, such as how the visual cortex processes input. In a way, the complexity and unpredictability of neurobiology is shriveling thanks to these computational advancements.

Although crossovers between biomedical research and digital software have long existedthink programs that help with drug designthe match between neuroscience and AI is far stronger and more intimate. As AI becomes more powerful and neuroscientists collaborate outside their field, computational tools will only unveil more intricacies of neural processing, including more intangible aspects such as memory, decision-making, or emotions.

I talk a bunch about the brains electrical activity, but supporting that activity are genes and proteins. Neurons also arent a uniform bunch; multiple research groups are piecing together a whos who of the brains neural parts and their individual characteristics.

Although invented in the late 2000s, technologies such as optogenetics and single-cell RNA sequencing were widely adopted by the neuroscience community in the 2010s. Optogenetics allows researchers to control neurons with light, even in freely moving animals going about their lives. Add to that a whole list of rainbow-colored proteins to tag active cells, and its possible to implant memories. Single-cell RNA sequencing is the queen bee of deciphering a cells identity, allowing scientists to understand the genetic expression profile of any given neuron. This tech is instrumental in figuring out the neuron populations that make up a brain at any point in timeinfancy, youth, aging.

But perhaps the crown in new tools goes to brain organoids, or mini-brains, that remarkably resemble those of preterm babies, making them excellent models of the developing brain. Organoids may be our best chance of figuring out the neurobiology of autism, schizophrenia, and other developmental brain issues that are difficult to model with mice. This decade is when scientists established a cookbook for organoids of different types; the next will see far more studies that tap into their potential for modeling a growing brain. With hard work and luck, we may finally be able to tease out the root causes of these developmental issues.

Image Credit: NIH

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These Breakthroughs Made the 2010s the Decade of the Brain - Singularity Hub

Neuroscience

Study ties gene active in developing brain to autism – Spectrum

Puzzling injury: Some children who carry variants in a gene called ZNF292 have injured blood vessels in their brains.

Mutations in a gene called ZNF292 lead to a variety of developmental conditions, including autism and intellectual disability, according to a new study1.

ZNF292 encodes a protein that influences the expression of other genes. It is highly expressed in the developing human brain, particularly in the cerebellum, an area that controls voluntary movement and contributes to cognition. However, its function in neurodevelopment is unknown.

Scientists first linked ZNF292 to intellectual disability in a 2012 study. A 2018 analysis of five ZNF292 variants tied the gene to autism, but the work was preliminary2.

In the new study, researchers identified 28 people who have mutations in ZNF292. The participants come from six countries and are between 10 months and 24 years old. The group carries a total of 24 mutations in the gene, 23 of which are spontaneous meaning that they were not inherited from a parent.

The sheer number of families and children that have been identified so far has been quite high, says Ghayda Mirzaa, lead investigator and assistant professor of genetic medicine at Seattle Childrens Hospital in Washington.

All but one of the participants have intellectual disability. In total, 17 of the participants are suspected or confirmed to have autism and 9 are suspected or confirmed to have attention deficit hyperactivity disorder. All but two have speech delays, and four have had language regression or are minimally verbal.

Mirzaas team found an additional 15 people with mutations in the gene from 12 families. However, the data from these people were incomplete, so the researchers had to exclude them from the analysis. The team has connected with at least 10 other mutation carriers in the six weeks since the study was published in Genetics in Medicine.

The researchers have used their data to classify a new condition. However, it may be premature to call it a syndromic form of autism or intellectual disability, says Holly Stessman, assistant professor of pharmacology and neuroscience at Creighton University in Omaha, Nebraska, who was not involved in the work.

People with ZNF292 variants have a broad spectrum of physical traits. For instance, 11 of the people in the study have growth abnormalities such as short stature; 10 have low muscle tone; and 3 have stiff or mixed muscle tone. The researchers had access to magnetic resonance imaging scans for 17 of the participants: 9 show brain abnormalities such as atypically shaped regions, and 3 of those 9 appear to have blood-vessel injuries in the brain.

Nearly half of the participants also have unusual facial characteristics, including an undersized jaw or eyes that are unusually far apart. Vision problems, such as involuntary eye movement or crossed eyes, affect nine people in the group. Less common facial differences include prominent incisors and protruding ears.

Autism genes are often linked to a wide range of characteristics, says Santhosh Girirajan, associate professor of biochemistry and molecular biology at Pennsylvania State University, who was not involved in the study. Variability has become the rule now, rather than the exception, he says.

Mirzaa says her group plans to study more individuals with variants in ZNF292, and to investigate the genes function.

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Study ties gene active in developing brain to autism - Spectrum

Neuroscience

Brain Mapping Instruments Market Demand, Growth, Opportunities and Analysis Of Top Key Player Forecast To 2026 – Instanews247

The utilization of brain mapping instruments has expanded because of increasing occurrences of brain ailments in different parts of the world. Increasing health concerns and enhanced healthcare infrastructure are a few of the foremost aspects driving the expansion of the worldwide market for brain mapping instruments. Furthermore, an increasing number of diagnostics centers is likewise driving the expansion of the market. Nonetheless, poor healthcare insurance coverage and high expenses related to the brain mapping procedure are limiting the expansion of the worldwide market for brain mapping instruments. Also, lack of helium for magnetic resonance imaging systems, saturation in mature markets and technological constraints related to independent systems are likewise constraining expansion of the worldwide market.

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High affecting aspects, for example, continuous brain mapping investigation and examination projects, neuroscience-based activities by government bodies as well as technological progressions in algorithms and tools which are applied in neuroscience space are considered to enhance the market expansion. These variables are foreseen to support revenue generation by impelling the product implementation in this market over the years to follow.

The existence of institutes & organizations, for example, NIH, University of Utah, NeuroScience Canada, Ontario Brain Institute, Max Planck Florida Institute, along with the University of Pennsylvania; in the space are anticipated to significantly affect the advancement of neuroscience field. These entities act a significant part in quickening neuroscience-based r&d to enhance patient results in those suffering from neurological ailments.

Various activities are embraced by the healthcare communities to take cerebrum related innovations and studies above and beyond. For example, in 2014, the University of Utah presented the Neuroscience Initiative keeping in mind the end goal to help mitigate the staggering impacts of brain disorders. The launch was made for developing the understanding of the impacts of brain disorders on wellbeing and channelizing the learning into inventive solutions for patient care.

Constant presentation of new products by prominent market players in the market to the battle different neurological issue will probably support the Y-O-Y development of this market. For example, in September 2015, Codman Neuro (functioning unit of DePuy Synthes) presented CODMAN CERTAS plus programmable valve, an MRI-safe programmable valve along with eight dissimilar weight settings.

Moreover, key aspects that have quickened the research studies about in this field is the development of a number of different harmful CNS issues, for example, Alzheimers and Parkinsonism sickness. As geriatric populace is inclined to different central sensory systems related disorders, for example, Alzheimers, schizophrenia and Parkinsonism with the rise in the aging populace, this market is foreseen to see lucrative development.

The requirement for minimally invasive, more precise along with manifold neuron recording system is additionally anticipated that would drive r&d of hardware and software utilized for neuro-scientific analyses. This, thusly, is considered to reinforce the overall product portfolio accessible in the market and enhance revenues all through the years to come.

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Enhancing healthcare infrastructure in developing nations, for example, India and China would generate prospects for the worldwide market for brain mapping instruments. Expanding implementation of refurbished diagnostic imaging systems would represent a challenge for expansion of the mind-brain mapping instruments market globally. A few of the foremost companies functioning in the global market are Philips Healthcare, GE Healthcare, Natus Medical, Inc and Siemens Healthcare. Other market players active in the market are Nihon Kohden Corporation, Covidien, PLC., and Advanced Brain Monitoring, Inc.

Partnerships and collaboration are preferred as a feasible strategy to remain competitory in the market by foremost companies. Companies are engrossed in strategic alliances outside the region and within the region, which helps the expansion of both the parties along with the connected regional market.

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Brain Mapping Instruments Market Demand, Growth, Opportunities and Analysis Of Top Key Player Forecast To 2026 - Instanews247

Immunology

Trabectedin Targets Leukemic Cells and Restores Immune Cell Function in Models of Chronic Lymphocytic Leukemia – Cancer Therapy Advisor

The marine-derived compound trabectedin depletes both human primary leukemic cells and myeloid-derived suppressor cells, according to a new study published in Cancer Immunology Research.1 The researchers think their findings could lead to a new therapy that targets both leukemic cells and the protumor microenvironment, repairing the immune dysfunction that is characteristic of chronic lymphocytic leukemia (CLL).

CLLis characterized by lymphocyte accumulation in the blood, bone marrow, andlymphoid tissues.2 Recent advances in CLL therapy have come fromfinding and targeting the appropriate molecular pathways of the disease,explained Kanti R. Rai, MD, a professor of medicine and molecular medicine atthe Donald and Barbara Zucker School of Medicine at Hofstra/Northwell whowasnt involved in the study. Dr Rai said that, for instance, the Brutontyrosine kinase inhibitor ibrutinib binds to the receptor and affects B-cellreceptorsignaling. Another drug, venetoclax, an antagonist to BCL2, can effectivelyinduce apoptosis in CLL cells. However, treatment of this disease remainschallenging due to its immunosuppressive nature. If we [are] to attain a cure,newer compounds have to be identified which have a different mechanism ofcontrolling CLL, he said.

Patientswith CLL have dysfunctional T cells, noted Maria Teresa Bertilaccio, PhD, whois an assistant professor in the department of experimental therapeutics at TheUniversity of Texas MD Anderson Cancer Center in Houston, and the correspondingauthor of the study. Patients [with CLL] have immunosuppression features, sothey might develop an infection because their immune system is not working,she told Cancer Therapy Advisor. Our approach is not only to eradicateleukemia, but also to rearm the immune system to give patients a better qualityof life.

Trabectedintargets tumor-associated macrophages (TAMs); TAMs are thought to support CLLgrowth. A previous study by the Bertilaccio group showed that depleting TAMs byblocking CSF1R signaling reprograms the tumor microenvironment toward anantitumor phenotype.3 This led them to hypothesize that trabectedincould simultaneously target both leukemic cells and nonmalignant cells in thetumor microenvironment.

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Trabectedin Targets Leukemic Cells and Restores Immune Cell Function in Models of Chronic Lymphocytic Leukemia - Cancer Therapy Advisor

Immunology

Johnson & Johnson: The Pharma Giant That Continues To Grow – Seeking Alpha

I do not paint a portrait to look like the subject, rather does the person grow to look like his portrait. - Salvador Dali

Johnson & Johnson (NYSE:JNJ), the worlds biggest pharmaceutical company by market cap, has enjoyed a great end to the year after its stock hit a fresh 2019 high of $147.84 in the previous week. Despite the recent litigation, the company is well positioned to continue growing thanks to its impressive pharmaceutical portfolio.

Most recently, the company has faced legal headwinds in the context of its alleged involvement in the opioid crisis. However, the latest test results released by the company show that J&Js baby powder did not contain asbestos. Previously, the U.S. Food and Drug Administration studies showed that the product contained the material.

The tests that were conducted are part of a large-scale effort by J&J to prove the safety of its widely used consumer product after the test by the FDA prompted J&J to undertake a nationwide recall of one lot of Johnsons Baby Powder in October.

A crisis involving baby powder didnt stop the banking titan Barclays to upgrade the JNJ stock from Equal Weight to Overweight.

In our view, litigation concerns are more than priced in and the risk/reward is attractive. We think J&J checks a lot of boxes heading into 2020, leaving risk/reward skewed to the upside. said Kristen Stewart, an analyst at Barclays.

Furthermore, the bank raised the price target to $173. The stock closed yesterday's trading session at $145.30.

This is the second time J&Js stock was upgraded in one week. Previously, Morgan Stanley analyst David Lewis made the same upgrade - from Equal Weight to Overweight, describing the companys stock as an attractive buying opportunity.

Out of 19 analysts covering Johnson & Johnson, 13 have upgraded the stock to either Buy or Overweight.

The upgrades didnt surprise many as the after the company reported in October that Q3 earnings and revenue beat estimates, thanks to growing sales of cancer and other prescription drugs, regardless of multi-million-dollar legal issues the company.

The pharmaceutical giant reported adjusted earnings of $2.12 per share, beating the expected $2.01 per share. The reported revenue was $20.73, again higher than the expected $20.07 billion. Overall, the companys three main components reported better-than-expected results.

Technically, the price is trading just below the all-time high of $148.99, printed in December 2018. The stock has been rallying since the Q3 earnings report was released on October 23, a day after the stock printed a 9-month low of $126.10. In around two months time, JNJ has managed to increase its market cap by around 15%.

The price action is supported by the horizontal support near the $145 mark, the previous 2019 high, and $141.50 where the broken descending trend line that connects two previous lower highs sits.

If the bulls continue to move the price higher, the initial target is the zone around the $150 mark where the 127.2% Fibonacci extensions of the June 19-October 19 correction lower lie. Overall, any move above $149 will mark a new all-time high for shares of JNJ.

As I mentioned in the Lead-Lag Report, the US stock market is well-positioned to continue rising in 2020, hence a future upside is a strong possibility for a healthy businesses such as Johnson & Johnson.

Arguably the biggest strength of the company is portfolio diversification. JNJ continues to impress with its performance in the areas of oncology and immunology, where its products such as Imbruvica, Stelara and Tremfya continue to yield profits. For instance, Tremfyas portfolio increased as much as 69% in the third quarter.

I wouldnt be surprised if the company goes aggressive on the expansion front. It is expected that the growth in the pharmaceutical sector should further pick up in 2020, which should benefit the company given the historical correlation between J&J's stock and pharma growth.

Johnson & Johnson finds itself in a great financial shape as its operations in the healthcare industry are unrivaled. Thanks to the diversified portfolio, especially within the oncology and immunology fields, shares of Johnson & Johnson appear to be a solid investment option as the bulls look determined to push the price north of $150.

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Johnson & Johnson: The Pharma Giant That Continues To Grow - Seeking Alpha

Immunology

New Way to Deliver Old Tuberculosis Vaccine Provides ‘Incredible Protection’ in Monkeys – ScienceAlert

What if you could make the tuberculosis vaccine much more powerful, not by altering the ingredients, but just by changing the way it is given to people? It would help prevent the infection that kills more people every year than any other microbe.

Tuberculosis is caused by a bacterium, called Mycobacterium tuberculosis, which causes a lung infection that progresses slowly but can destroy the lungs if not treated. Although we might not think of it too often here in the United States, it remains a major killer worldwide.

In 2018 alone, there were 10 million new cases of active TB and almost 1.5 million deaths from TB infections. What makes the disease particularly insidious is that because symptoms are slow to manifest and can resemble other diseases, it takes a long time before people with TB are diagnosed and given treatment.

But until a person with TB gets treated with drugs, they can pass it on to other people - and this bacterium spreads fast through coughing, sneezing, and even singing.

You might be surprised to learn that most of the people who die from TB were actually vaccinated as a baby, using a vaccine called bacille Calmette-Guerin (BCG). BCG has been used for almost 100 years and is a live but crippled version of a similar bacterium to the one that causes TB.

This vaccine is pretty good at preventing certain types of TB in children, but not adolescents or adults. My team here in Pittsburgh together with collaborators at the National Institutes of Health have figured out a better way to administer this vaccine to prevent this devastating disease which often affects the poorest people in the world.

(Timonina/Shutterstock.com)

I was originally trained as a microbiologist, studying bacteria that cause disease, and later developed an interest in how the body's immune system fights off infections. Combining my passions for microbiology and immunology, I began investigating tuberculosis almost 30 years ago.

I started my own lab at the University of Pittsburgh School of Medicine with the goal of understanding TB disease and how we might prevent it.

I started by using mice to study TB. But then, 20 years ago, I began using monkeys and discovered that monkeys develop the same type of TB disease that humans do. Studying TB in monkeys was a breakthrough that enabled me to begin the search for new vaccines against this deadly disease.

TB is such a fascinating disease and has been causing illness in humans for thousands of years. Anthropologists have discovered, for example, tuberculosis in Egyptian mummies. It infects nearly all mammals.

Yet, even though the cause of TB has been known since the late 1800s, it is still not clear why some humans can suppress the infection and not become sick while others are more vulnerable and develop disease.

I wanted to use my understanding of this complicated bacterium to find more effective ways to prevent the disease.

My colleague Robert Seder, a vaccine expert at the National Institutes of Health, had discovered that delivering a malaria vaccine directly into the bloodstream, through a vein, was much more effective than any other route of delivery such as the skin or muscle, and was a much better way to prevent the disease.

Together, we decided to try a similar approach with TB using the current BCG vaccine. We vaccinated monkeys with BCG by injecting the vaccine under the skin (the usual route for babies), by aerosolizing the vaccine and spraying it directly into the lungs, or injecting it directly into the the blood using an IV.

After two months we found that when the vaccine was delivered via IV, the numbers of specialized immune cells, called T cells, which can recognize and kill the bacteria, increased by 100-fold in the lungs. Then, months later, we exposed the monkeys to M. tuberculosis.

Unvaccinated monkeys developed severe TB disease within a few months. BCG administered through the skin or into the lungs gave a little bit of protection, but the monkeys still had signs of TB.

The IV vaccine provided incredible protection. In most of the animals, there were no M. tuberculosis bacteria in the entire monkey. We also used specialized imaging, called PET-CT, and showed that the lungs of most of these monkeys were free of any disease. This means that BCG vaccine prevented TB infection and disease when given intravenously.

This is an exciting breakthrough in the field of TB, since most vaccines tested in any models provide relatively limited protection. If we can figure out how BCG IV prevents M. tuberculosis infection, we may be on the path to developing a new vaccine for humans.

Although we have a long way to go before it is ready for humans, the lessons we learn from the BCG IV studies will be critical in developing new TB vaccines and, we hope, saving millions of lives.

JoAnne L. Flynn, Professor of Microbiology and Molecular Genetics, University of Pittsburgh.

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

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New Way to Deliver Old Tuberculosis Vaccine Provides 'Incredible Protection' in Monkeys - ScienceAlert

Immunology

Changed route of immunization dramatically improves efficacy of TB vaccine – National Institutes of Health

Media Advisory

Thursday, January 2, 2020

NIH scientists report results from animal study.

Tuberculosis (TB), an ancient disease, is the leading infectious cause of death globally, yet the worlds only licensed TB vaccine, Bacille Calmette-Guerin (BCG), was developed a century ago. Given to infants via a needle placed just under the skin, BCG protects babies from a form of the disease called disseminated TB but is far less effective at preventing pulmonary TB, the major cause of illness and deaths, in teens or adults.

Now, researchers from the National Institutes of Healths National Institute of Allergy and Infectious Diseases (NIAID) and their colleagues have shown that simply changing the dose and route of administration from intradermal (ID) to intravenous (IV) greatly increases the vaccines ability to protect rhesus macaques from infection following exposure to Mycobacterium tuberculosis (Mtb), the bacterium that causes TB. The findings provide a new understanding of the mechanisms of BCG-elicited protection against tuberculosis infection and disease. In addition, the findings support investigation of IV BCG administration in clinical trials to determine whether this route improves its effectiveness in teens and adults.

Study investigators at the NIAID Vaccine Research Center were led by Robert A. Seder, M.D., and Mario Roederer, Ph.D. Their collaborators included JoAnne L. Flynn, Ph.D., of University of Pittsburgh School of Medicine.

To control Mtb infection and prevent clinical disease, a TB vaccine must elicit strong, sustained responses from the immune systems T cells, specifically those in the lungs. However, the standard, ID, route of BCG administration may not generate enough of these critical cells in the lungs. The NIAID researchers and their colleagues hypothesized that administration of BCG by IV or aerosol (AE) routes would overcome this hurdle and thus confer substantially better protection from infection and/or disease in rhesus macaques following challenge with virulent Mtb.

In their study, groups of animals received the BGC vaccine by ID, AE or IV routes. The scientists assessed immune responses in blood and in fluid drawn from the lungs for a 24-week period following vaccination. IV BCG vaccination resulted in the highest durable levels of T cells in the blood and lungs.

Six months after vaccination, the researchers exposed groups of vaccinated rhesus macaques (immunized via ID, AE or IV routes) and a group of unvaccinated macaques to a virulent strain of Mtb by introducing the bacteria directly into the animals lungs. They then tracked the infection and disease development over three months. Nine out of 10 animals vaccinated with IV BCG were highly protected; six showed no detectable infection in any tissue tested and three had only very low counts of Mtb bacteria in lung tissue. All unvaccinated animals and those immunized via ID or AE routes showed signs of significantly greater infection.

The investigators concluded that IV BCG conferred an unprecedented degree of protection in an animal model of severe TB and represents a major step forward in the field of TB vaccine research.

PA Darrah et al. Prevention of tuberculosis in macaques after intravenous BCG immunization. Nature DOI: 10.1038/s41586-019-1817-8 (2020).

NIAID Director Anthony S. Fauci, M.D., is available to comment. Dr. Seder, chief, Cellular Immunology Section, Vaccine Research Center, NIAID, is also available.

This research was funded, in part, by the NIAID Intramural Research Program and through NIH grants 5U24AI118672 and 2RM1HG006193.

NIAID conducts and supports research at NIH, throughout the United States, and worldwide to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

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Changed route of immunization dramatically improves efficacy of TB vaccine - National Institutes of Health

Immunology

Author Angie Fox and Artist Craig Skaggs at The Toyman Toy Show in St. Louis Sunday January 12th – We Are Movie Geeks

TheToyman Toy Showin St. Louis has been going strong for 30 years now and just keeps getting bigger and better! The fun now takes place nine times a year at The Machinists Hall 12365 St Charles Rock Road in Bridgeton, MO 63044. There areover 120 vendors at the Toyman Toy Show spread out over220 tables. all selling vintage toys, comics, dolls, diecast cars, movie memorabilia, and more as well as cosplayers and artists. Its an unbelievable amount of fun for only $5! A Facebook invite for the event can be found HERE

The next Toyman Show is Sunday, January 12th from 9:00a to 3:00p and Author Angie Fox and Artist Craig Skaggs will be special guests.

Angie Fox is the New York Times bestselling author of the Accidental Demon Slayer series. She claims that researching her books can be just as much fun as writing them. In the name of fact-finding, Angie has ridden with Harley biker gangs, explored the tunnels underneath Hoover Dam and found an interesting recipe for Mamma Coalpots Southern Skunk Surprise (shes still trying to get her courage up to try it).Angie earned a Journalism degree from the University of Missouri. She worked in television news and then in advertising before beginning her career as an author.She also enjoys making up fun quizzes and thinks you should take one right now.

Craig Skaggs started his career as an artist in 1983 illustrating childrens books for a small publishing company when he was a junior in high school. In the early nineties he became a full-time freelancer working for multiple advertising agencies, and publishers of teaching material. he was then picked by Skywalker Ranch to illustrate licensed Star Wars art when they were re-releasing episodes 4, 5 and 6 with new special effects. he also began designing all kinds of toys and products for over thirty companies, doing illustrations for several magazine, game, comic, childrens book and journal publishers, and he was a cover artist for Random House Pub. and Wings Press for several years. Seven years ago he became a lead medical illustrator for the American College of Cardiology, and the Journal of Allergy and Immunology. About three years ago he started doing conventions, and fine art gallery shows. Just recently hes started doing illustrations for Altered Creatures Pub., and toy design work for SG labs.

Over 125+ Vendors on 225+ tables of Toys, Comics, Games, Movie posters, Barbie, Hot Wheels, Die-Cast, Models, Pop Culture and a TOTALLY OPEN BALCONY.

Adult Admission at the Toyman Show: $5.00 Children 16 & under free. Sunday: 9:00am 3:00pm. Early Bird @ 8:00a $12.00 * FREE PARKING *

The Toyman Toy Show site can be foundHERE

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Author Angie Fox and Artist Craig Skaggs at The Toyman Toy Show in St. Louis Sunday January 12th - We Are Movie Geeks

Immunology

Something’s in the Air: San Antonio Enters Peak Cedar Fever Season – Rivard Report

Eyelids feel like sandpaper? Sneezing nonstop? Welcome to cedar fever, an annual malady thatplagues San Antonio and Central Texas every winter.

Ashe juniper trees, commonly known as mountain cedars, cause the seasonal affliction. As part of their reproductive cycle, male trees produce smallpollen cones, while the female trees produce small seed cones that look like blueberries, explained Estelle Levetin, PhD and a professor of biological science at the University of Tulsa who has studied Ashe juniper for decades. Upon maturity, the male trees release billions of pollen granules into the wind usually on a cold, breezy day.That yellow pollen dust, filled with myriad allergenic compounds, can travel up to 200 miles.

The bushy evergreens are native from southern Missouri to northern Mexico, but are especially dense in Central Texas and the Hill Country.

Cedar fever season typically starts after Thanksgiving and continues through February. But climate change may cause those who suffer its effects to adjust to a longer, more intense season. Warming temperatures appear to be extending the trees reproductive cycle and boosting pollen counts, according to the Fourth Annual Climate Change Assessment.

We are early into the season, said Dr. Eliseo Villalobos, an internist and Fellow of the American Academy of Allergy Asthma and Immunology (AAAAI) at the Allergy Institute of San Antonio. Villalobos said that conditions this season seem pretty typical, but that the highest allergy counts are coming earlier in the season.

Usually it peaks mid-January, but the counts last year peaked around late December which it seems to be doing again this year, he said.

The AAAAI pollen counter haslisted San Antonio in the red zone with pollen counts rated very high every day since Dec. 23.

Monika Maeckle for the Rivard Report

Female Ashe juniper trees produce blueberry-like berries.

Allergists point out that cedar pollen is especially bothersome to human beings.

A single tree can produce up to 500 billion pollen grains, said Daniel Katz, a postdoctoral research fellow at the Dell Medical School at the University of Texas at Austin. He added that the pollen itself contains many allergenic compounds and is especially susceptible to bursting, which releases the allergens into the air.

Texas State Botanist Chris Best speculated that the super-abundance of Ashe Juniper trees in Central Texas is a major factor in the severity of local cedar fever.

Just look at the pollen counts during a bad season many thousands, even tens of thousands of particles per cubic meter, he said. Compare that to other pollen or mold spores that reach peaks of hundreds to low thousands per cubic meter.

Cedar fever is so bothersome and pervasive that Katz and other scientists at the University of Texas at Austin recently launched Pollen Trackers,a citizen scienceproject that will gather data on allergens in the atmosphere. Tracking mountain cedar pollen will be the focus of Pollen Trackers first campaign.

The program asksvolunteers to monitor and report data on local cedar trees to alert the community when they release their pollen into the atmosphere.

We dont know yet how much pollen people are exposed to in their daily lives, said Katz. If we can predict airborne pollen concentrations, we can warn people about pollen hotspots in advance and help them maximize the benefits from their allergy medication.

Katz described Ashe junipers phenomenal amount of pollen production, combined with its massive tree population and its particular pollen structure as the perfect storm of allergies. Thats why why cedar fever is one of the worst allergies in the U.S., he said.

So does he recommend getting out the chainsaws and clearing all the cedar, as some Hill Country landowners attempt to do?

I wouldnt go that far, he said, noting that pollen-producing male trees would be better candidates for cutting down than clearing cedar indiscriminately.

The tree species is an important part of the regional ecosystem. Ashe juniper provides food, shelter, and nesting materials for wildlife, specifically the endangered golden-cheeked warbler. Ashe juniper trees also provides a unique, rich bed for particular native plants that thrive in its mulch.

Trees do a lot of benefit for us. Allergenic pollen is just one of the things we need to weigh, he said.

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Something's in the Air: San Antonio Enters Peak Cedar Fever Season - Rivard Report

Genetics

Epilepsy and Genes – Epilepsy Foundation

Is epilepsy genetic?

Advances in science and medicine over the last decade have led to a better understanding of the ways genetic factors contribute to epilepsy.

Not all epilepsies that are due to genetic causes are inherited.

The genetics of epilepsy is a new and emerging field. For some individuals, it is not yet possible to determine whether their seizures are due to genetic factors.

In general, if a person has a first-degree relative (mother, father, sibling) with epilepsy, the risk of developing epilepsy by the age of 40 is less than 1 in 20 (Peljto et al. 2014). The risk differs somewhat between focal and generalized epilepsy. There is an increased risk of developing epilepsy if the first-degree relative has a generalized epilepsy rather than focal epilepsy (Peljto et al. 2014; Helbig et al. 2016). These estimates come from population-based studies, meaning they are based on the average across a large group and may not apply for all individuals.

The likelihood of inheriting epilepsy may differ significantly if a person has a relative with a known genetic epilepsy diagnosis. In this case, the chance of developing epilepsy depends on the specific gene and inheritance pattern involved.

To fully appreciate this, we first need to review a few basic genetic terms.

Genes are sequences of DNA (deoxyribonucleic acid) that determine different proteins made in the body. These proteins have a variety of functions and ultimately determine how we develop, grow and function. There are about 20,000 genes in the human genome. With a few exceptions, humans have two copies of every gene: one inherited from each parent.

A genetic variant is a change in the DNA sequence, which can cause the gene not to work properly and ultimately can affect how the gene (protein) functions.

A de novo genetic variant arises for the first time in one individual. Usually, this is caused by a random change in the DNA of the egg or the sperm cell of the parent but is not otherwise present in either parent.

For some genetic conditions, not everyone with a disease-causing variant will develop the symptoms of the disease. This phenomenon is called incomplete penetrance.

Certain types of epilepsy are associated with specific genetic changes, including changes in an individual gene or changes in a chromosome.

Research is currently ongoing in many medical centers and laboratories around the world to help understand the role of genetics in the development of epilepsy. One long term goal of this research is precision medicine. This means individuals with genetic epilepsies would be treated with approaches specifically targeted to their genetic diagnosis.

Although there are many types of research studies, three main types relate to the field of epilepsy genetics:

Learn More

There are currently a limited number of clinical trials available to individuals and families with some forms of genetic epilepsies, but we anticipate the number of trials will continue to increase. The following links are a good place to start for information about currently available trials for genetic epilepsies:

Helbig I, Heinzen EL, Mefford HC, and Ilae Genetics Commission. Primer Part 1-The building blocks of epilepsy genetics. Epilepsia, 57 (2016): 861-8.

Peljto AL, Barker-Cummings, Vasoli VM, Leibson CL, Hauser WA, Buchhalter JR, and Ottman R. Familial risk of epilepsy: a population-based study. Brain, 137 (2014): 795-805.

National Library of Medicine (US). Adapted from Genetics Home Reference [Internet]: ghr.nlm.nih.gov. Bethesda (MD): The Library; 2013 Sep 16.

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Epilepsy and Genes - Epilepsy Foundation