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Genetics

If rotten fish smells like roses to you, you have a genetic mutation to blame – Times Now

If rotten fish smells like roses to you, you have a genetic mutation to blame  |  Photo Credit: iStock Images

New Delhi: Whenever we are around a dumpster or somehwere we know it smells awful, we wish we were lucky to be able to switch off our noses, and not smell the awful smell. For some people, it seems, genes have ensured to make it possible.

According to a new study published in Current Biology, it was found that a rare genetic mutation can make some people immune to the nauseating aroma of rotten fish, as reported by the Nature News.

11,000 people participated in the study. They provided DNA samples, and put their noses to test. When presented with a box of six odours, the participants each took a whiff and tried to identify it. For some people, the rotten fish smell was unpleasant and easy to identify, while a small group of people labelled it as neutral.

Researchers further looked into their DNA and found that the small group of people shared a genetic mutation in common. They reportedly had at least one broken version of a gene called the TAAR5.

I can assure you I do not have this mutation, neurologist and co-author of the study Kri Stefnsson, of deCODE Genetics in Reykjavik, tells the New York Times Katherine Wu. I tend to get nauseated when I get close to fish that is not completely fresh.

According to researchers, the gene makes the tools in your cells, that the nose uses to identify a rank chemical called trimethylamine, or TMA, which is also found in faeces, blood and bad breath. TMA is a red flag for iffy food, and peoples disgusted reaction to its sickening smell helps them avoid danger.

TAAR5 is a very conserved gene, so its very similar across species, probably because it has been important to protect us against harmful microorganisms, says deCODE neuroscientist Rosa Gisladottir to New Scientist.

The researchers further asked the participants to smell samples with synthetic odours. These consisted of cinnamon, peppermint, banana, liquorice, lemon, and rotten fish. They found that the success of identifying these smells reduced with age, but even young people could confuse between certain smells. They were also asked to rate how unpleasant the smell was, and rotten fish won, hands down.

However, for people with the broken TAAR5 genes, the rotten fish smelled neutral. While some could not smell it at all, some identified it as potato, caramel, ketchup, or even roses.

This study was conducted in Ireland, where a large number of people have the genetic mutation, as compared to other places in the world.

If they hadnt looked at this population, they might not have found the variant, says Bettina Malnic, who studies olfaction at the University of So Paulo, to theNew York Times. Another sensory science researcher, Paule Joseph, tells theTimesthat a future study with a more diverse study population could show whether different diets affect the prevalence of the mutation.

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If rotten fish smells like roses to you, you have a genetic mutation to blame - Times Now

Genetics

University of Utah researcher among 21 awarded genius grant – Deseret News

SALT LAKE CITY A University of Utah researcher recently received one of the nations most prestigious fellowships.

Nels Elde, an associate professor of human genetics at the University of Utah, studies evolutionary cell biology.

Now he can also be considered an honorary genius, though hes not anxious to add that title.

I mean the word genius is a little ambitious here, at least in my case, Elde said. A lot of scientists kind of shy away from the limelight I think myself included. So putting myself in the category of genius seems a little out there.

Among grants that scientific researchers are eligible to receive, the MacArthur Fellowship, colloquially known as the genius grant, is unique for several reasons.

First, the money comes with no strings attached. Rather than financial backing for a project or an idea, the grant is an investment in a person a creator. As such, the fellows arent just scientists, they hail from every field of human endeavor.

This years winners include a playwright, two fiction writers, a poet and a historian.

The foundation trusts that recipients will do their best work if theyre not confined by pre-set boundaries or limitations. And they attest to that belief with money a lot of money. Thats the second aspect of the fellowship that makes it special: its size.

The stipend is $625,000.

Thats how much Elde and 20 others will each receive in payments over five years now that theyve been named 2020 fellows.

Dr. Elde has achieved a hallmark in the scientific community, Dr. Michael L. Good, senior vice president for Health Sciences and CEO of University of UTah Health, said in a news release. His innate ability to think creatively about unsolved problems inspires all of us to do the same in our quests to advance knowledge. University of Utah Health is extremely proud of him and his accomplishment, which is representative of our facultys desire to improve the world.

The third unique aspect of MacArthur grants is that theyre based on recommendations, not applications, which also shows how highly Eldes colleagues think of him.

An entire roomful of people will be listening to the same scientific talk and he has the insight to ask the one question that no one else is asking but that everyone should be asking, Harmit Malik, a professor at the Fred Hutchinson Cancer Research Center and Eldes postdoctoral mentor, said in the release. Its not fair to call him outside the box because he is so far beyond that.

Elde credits his upbringing and family for his interest in science as well as his creativity.

He grew up in Minnesota and is from a family of artists, scientists and ministers. He remembers being curious about nature from a young age. And not just animals and plants, but microorganisms as well.

Dip into a mud puddle and look under a microscope, he said. There is all this interesting energy, complexity. Theres lifeforms.

This fascination led him to pursue a doctoral degree at the University of Chicago, where he sought to answer questions about how cells work about their biology.

I think those sort of forces somehow came together to just put me on a path to continue thinking about science, thinking about nature, thinking about ideas more philosophical ideas. Where are we from? What explains all of the diversity of life around us? he said.

Like many scientists, he seems to love talking about his research. In fact, in his interview with the Deseret News, he talked more about his work than the $625,000 he was just awarded.

He discussed his graduate training in Chicago and his current research at the University of Utah.

He talked about how interactions between infectious microbes and other living species have shaped evolutionary biology.

These infections, these collisions or actions between infectious microbes and hosts have really big outcomes, as I think we are all ... grappling with (in) this current pandemic, he said. If we kind of step back and put that in a bigger perspective, then what I think you begin to see is how, depending on how an infection unfolds ... that might influence whether that population lives or has kids.

At the end, he admitted while laughing, thats sort of a long answer.

He explained that what he loves most about science is the creative aspect of it, the exploration and discovery of new things sometimes without even meaning to. In some ways, he is still the kid who simply loves nature and wonders why it is the way it is.

And thats exactly what the fellowship is designed to encourage.

I think it is fun to sidestep, and this is what the MacArthur Foundation does as well. So they consider it an award for creativity. And so I am much more comfortable with that framing of it. In fact, in some ways, I think thats for me what makes it such an incredible and a fun honor is to put the creativity forward. Because thats really what kind of keeps me in this job, or why I got into this job.

Its just such a fun kind of playground to exercise creativity. Science, sometimes, we think about it as dried out, textbook kind of stuff. But I think the kind of research we do, discovery research, it really depends on being kind of creative and curious.

He said the phone call telling him he had been selected was a totally surprising and overwhelming moment to let that sink in. And it is just really a spectacular honor.

He also called it mysterious and said he was originally sent an email by the foundation that told him the calls purpose was so he could weigh in on other candidates.

I was kind of having fun thinking about all of my science mentors and science heroes, people who deserve to get this prize, he said. So I was thinking about how I would describe their work or try to really support their case.

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University of Utah researcher among 21 awarded genius grant - Deseret News

Genetics

Science Paper Examines Genetics of Adaptive Intersexuality in Moles – GenomeWeb

An analysis of the mole genome that reveals the genetic underpinnings of adaptive intersexuality in the animal is published in Science this week. While sex in mammals is determined by genetic elements that direct the differentiation of the bipotential gonad into either testicular or ovarian tissue, in the Iberian mole (Talpa occidentalis) genotypic females develop ovotestes instead of ovaries.

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Science Paper Examines Genetics of Adaptive Intersexuality in Moles - GenomeWeb

Biochemistry

U of T’s Medicine by Design invests $1 million to advance new ideas in regenerative medicine – News@UofT

Patients with cystic fibrosis experience recurrent lung infections that eventually destroy their airways, shortening their average life expectancy to 50 years in Canada. Current drug treatments, which target a malfunctioning pathway in cells that causes the infections, are costly and have varying effectiveness.

Now, with funding from Medicine by Design, a researcher at the Hospital for Sick Children (SickKids) is combining stem cells, gene editing and computational modelling to try to hijack an alternative cell pathway in the hopes of restoring lung function in these patients.

If successful, our study will be the first to provide proof-of-concept that this alternative approach to treating cystic fibrosis is effective, saysAmy Wong, a scientist working in developmental and stem cell biology at SickKids who is also an assistant professor in the department of laboratory medicine and pathobiology in the University of Torontos Temerty Faculty of Medicine.

Wongs project is one of seven across U of T and its affiliated hospitals that have been awarded 2020New Ideas AwardsandSeed Fundawards from Medicine by Design. Through a $1 million investment, Medicine by Design is supporting research aimed at advancing new concepts expected to be important to regenerative medicine in the coming years. The funded projects will have potential impacts in diseases and conditions such as vision loss, amyotrophic lateral sclerosis (ALS), intestinal disease in premature babies and more.

Supporting novel strategies and approaches is crucial to moving regenerative medicine into the future, saysMichael Sefton, executive director of Medicine by Designand a University Professor at U of Ts Institute of Biomedical Engineeringand thedepartment of chemical engineering & applied chemistry in the Faculty of Applied Science & Engineering.

Our 2020 New Ideas project portfolio integrates mathematical modelling, physics and computational biology with stem cell biology and biomedical engineering, and strengthens engagement with clinicians who are key to translating our research into patient impact. We are particularly delighted this year to support so many outstanding early-career researchers, who will ensure Toronto remains a global leader in regenerative medicine for years to come.

Wong is one of three investigators to receive a 2020 New Ideas Award, which is valued at $100,000 per year for up to two years. Four additional projects were selected for Seed Fund Awards of $100,000 each for one year to further develop their potential.

Medicine by Design selected the funded projects from among 36 short-listed proposals, which were evaluated and ranked through an external peer review process. Applications were submitted by clinicians and researchers at U of T and its affiliated hospitals from a wide range of disciplines including biochemistry, biomedical engineering, developmental and stem cell biology, immunology, neuroscience and surgery.

Medicine by Design builds on decades of made-in-Canada excellence in regenerative medicine dating back to the discovery of stem cells in the early 1960s by Toronto researchers James Till and Ernest McCulloch. Regenerative medicine uses stem cells to replace diseased tissues and organs, creating therapies in which cells are the biological product. It can also mean triggering stem cells that are already present in the human body to repair damaged tissues or to modulate immune responses. Increasingly, regenerative medicine researchers are using a stem cell lens to identify critical interactions or defects that prepare the ground for disease, paving the way for new approaches to preventing disease before it starts. Medicine by Design is made possible thanks in part to a $114-million grant from theCanada First Research Excellence Fund.

Current cystic fibrosis drug treatments target a genetic mutation that causes epithelial cells, which line the airway and act as a barrier against viruses, to function improperly. The mutation affects the function of an important ion channel in cells, called CFTR, which helps to maintain the right balance of fluid in the airways. Poor function causes mucosal obstructions in the airways and prevents clearance of foreign pathogens, which leads to chronic infections and ultimately destroys airway tissue.

In her project, Wong will explore an alternative ion channel in the epithelial cells to determine if it can be hijacked and used to compensate for the lack of function caused by the mutant CFTR. The research will be conducted using a combination of stem cell-derived lung models, gene editing and computational modelling.

Wongs project builds on decades of cystic fibrosis research at SickKids, where the cystic fibrosis gene was first identified 30 years ago.

To date, more than 2,000 mutations in the cystic fibrosis gene have been identified, says Wong. SickKids scientists and U of T researchers have become the epicentre of incredible cystic fibrosis research to understand how this disease works at the genetic and molecular level.

Wong says that, while the idea of targeting an alternative pathway is not necessarily ground-breaking on its own, its the array of tools now available that makes the idea a potential game changer.

We have access to an incredible resource of primary cells and stem cells from more than 100 individuals with cystic fibrosis harbouring various mutations. Wong says.Our lab has developed human lung models from stem cells that can be used to model lung disease such as cystic fibrosis. And with new advanced tools in single-cell genomics and gene-editing, coupled with key collaborations for computational modelling, we are poised to find new therapeutic targets for cystic fibrosis.

Leo Chou, an assistant professor at the Institute of Biomedical Engineering, andHyun Kate Lee, an assistant professor in the department of biochemistry in the Temerty Faculty of Medicineboth Medicine by Design New Investigators are also leading 2020 New Ideas projects.

Chou, along with co-investigatorsJulie Lefebvre, a scientist at SickKids and U of T assistant professor of molecular genetics, andValerie Wallace, a senior scientist at the Krembil Research Institute, University Health Network and a U of T professor of laboratory medicine and pathobiology and ophthalmology, will focus on cell transplantation in the retina, a process that has demonstrated encouraging pre-clinical results such as partial vision restoration in several animal disease models.

Recent research had demonstrated that this restoration is a result of the transfer of proteins complex molecules required for the structure, function and regulation of the bodys tissues between host tissue and donor cells. But the scope of that transfer process is not well understood. Chous project will develop an imaging approach to detect the transfer of mRNA molecules between host and donor cells. The outcomes from this project will inform the future design of cell transplantation therapies and lead to novel methods to deliver therapeutics. This project could improve therapies for retinal diseases and visual impairments, and inform strategies for other degenerative disorders.

Lee and co-investigatorPenney Gilbert,an associate professor at the Institute of Biomedical Engineering, will look at a common but not well-understood structure called the neuromuscular junction (NMJ), which mediates communication between neurons and muscles throughout the body. Defects in NMJ integrity and function underlie fatal diseases such as ALS. NMJ diseases, which affect more than 500,000 people globally, lack effective treatments. This project will use stem cells derived from reprogrammed skin cells of healthy people to develop NMJs in culture. Through high-resolution imaging, the healthy human NMJs will be studied both on their own and along with NMJs built from ALS patient cells. Through this work, the research team aims to identify genes to target to improve the health of NMJs, which could eventually help prevent or delay NMJ degeneration and even promote regeneration.

Michael Garton, an assistant professor at the Institute of Biomedical Engineering, has received a Seed Fund award to tackle the challenge of translating the genetic tools of synthetic biology an area of research that aims to create or redesign biological components using engineering methods into effective medical therapies against a number of diseases.

But they are difficult to translate into human therapies, Garton says, because the bodys T-cells immune cells that detect and destroy cells containing foreign material will identify these tools as foreign and destroy them.

Instead of switching off the T-cells, Gartons goal is to use computational modelling and high-throughput screening to selectively turn off the bodys foreign antigen display system so the immune system will still respond to foreign invaders when necessary, but allow cells containing synthetic tools to survive. If successful, this approach could enable a new generation of synthetic biology-enhanced cell therapies for a range of diseases.

Medicine by Design funding will help to facilitate the integration of synthetic biology and regenerative medicine and aid the development of cell-based therapies that perform better than nature, says Garton.

Other Seed Fund projects will encompass research in repairing the heart after paediatric cardiac surgery, treating an intestinal emergency in premature babies and creating a database for cell lineage paths.

John Parkinson, a senior scientist at SickKids and a U of T professor of biochemistry and molecular genetics, along with co-investigatorsJason Maynes, Wasser Chair in Anesthesia and Pain Medicine at SickKids and a U of Tassociate professor of anesthesiology and biochemistry, andWilliam Navarre, an associate professor in the department of molecular genetics, will investigate manipulating the microbiome, or community of microorganisms in the gut, to improve cardiac repair in post-operative treatment of a congenital heart disorder. Through a process that will identify prebiotics in breast milk that help enhance the production of molecules that research has shown can aid cardiac repair, the team will organize both observational (how disease alters the microbiome) and interventional (how the microbiome alters the disease) multi-site trials, which will provide the opportunity to immediately translate findings into changes in patient care regimens and improve outcomes.

CliniciansAgostino Pierro, a surgeon at the Division of General and Thoracic Surgery at SickKids and a U of T professor of surgery and physiology, and Philip Sherman, a senior scientist and gastroenterologist at the Division of Gastroenterology, Hepatology and Nutrition at SickKids and U of T professor of dentistry, pediatrics and laboratory medicine and pathobiology, have proposed a novel way of enhancing gut repair for a common intestinal emergency in premature babies, called necrotizing enterocolitis (NEC). A leading cause of death for these infants, NEC causes complications such as blindness, intellectual disability, repeat hospitalizations and gut damage even in those that survive. This project will look at whether intestinal organoids organ-like structures grown in the laboratory from stem cells that mimic some of the functions of native intestines can potentially stimulate repair of the gut and recovery from NEC. The project will define how to best transplant organoids, identify how the organoids protect the intestine from injury and assess if organoid transplantation is a valid new treatment for NEC.

Lincoln Stein, who is head of adaptive oncology at the Ontario Institute for Cancer Research and a professor in the department of molecular genetics at U of T, has received seed funding to build a database called Cytomics Reactome, which will be freely available to Canadian and international researchers. The database will build on recent technologies that open the door to the possibility of deciphering cell lineage paths the series of steps that lead a young, undifferentiated cell into a specialized one at single-cell resolution. To accelerate the path from basic research to clinical application, the database will systematically organize pre-existing knowledge of cell lineage paths into a comprehensive, interactive and easily accessible map that can serve as a framework for interpretation and integration of the latest experimental findings.

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U of T's Medicine by Design invests $1 million to advance new ideas in regenerative medicine - News@UofT

Biochemistry

Faculty and Staff Receive Nearly $9 Million in Grants, Contracts in Q1 – CSUF News

Cal State Fullerton faculty and staff received close to $9 million in funding during the first quarter of the university's 2020-21 fiscal year. Supported projects ranged from developing a robotic aid system for blinded veterans and documenting the experiences of underrepresented women in California agriculture, to funding CSUF's GEAR UP and Upward Bound programs.

Dawn Macy, director of the Center for Internships and Community Engagement: $1,780,840 in total funding

Joshua Bilbrew,director of CSUFs GEAR UP program: $1,116,440 from the U.S. Department of Education in support of Gaining Early Awareness and Readiness for Undergraduate Programs (GEAR UP).

Diana Vasquez, director of CSUF Upward Bound: $728,821 in total from the U.S. Department of Education

David Chenot, professor of social work: $658,279 continuing award from the Health Resources and Service Administration for the Health Careers Opportunity Program.Related: Program Helps Students See the Opportunities inAllied Health Care

Sadeeka Al-Majid, professor of nursing: $650,000 in first-year funding for a $3.25 million grant from the Health Resources and Services Administration for the project "Scholarships for Disadvantaged Students/Enriching Nursing Representation to Impact Community Health."Related: $3.25 Million Grant to Increase Pipeline of Nurses in Underserved Communities

Alyssa Hernandez, director of Educational Talent Search: continuation awards totaling $605,788 from the U.S. Department of Education

Brady Heiner, associate professor of philosophy: $540,218 in total. He received $50,000 from the North Orange County Public Safety Task Force for the "Project Rebound House Initiative, CSUF Year 4" project, and $490,218 from the State of California

Related: Boundless Opportunity: Project Rebound Opens Doors for the Formerly Incarcerated

Stephanie Vaughn, professor of nursing emeritus: $494,061 continuing grant from the Health Resources and Services Administration for the project titled "EMBRACE: Enrichment Markers of Better Relationship, Academics and Cultural Enhancement."Related: EMBRACE Promotes Cultural Sensitivity, Workforce Diversity in Nursing

Nicholas Brubaker, assistant professor of mathematics, and Wylie Ahmed, assistant professor of physics: $364,582 from the National Science Foundation for the project titled "RUI: Active Noise in the Dynamics of Self-Propelled Particles Stochastic Modeling and Experiments."

Gina Passante, associate professor of physics: $347,901 from the National Science Foundation for the project titled "Collaborative Research: Connecting Spins-First Quantum Mechanics Instruction to Quantum Information Science."

Kelvin Billingsley, associate professor of chemistry and biochemistry: $319,500 in continuing funding from the National Institutes of Health for the project titled "Hyperpolarized 13C Probes for Imaging Warburg Metabolism in Cancer."

Joshua Smith, professor of physics: $254,559 in total from the National Science Foundation

Kiran George, professor of computer engineering: $199,211 from the U.S. Department of Veterans Affairs for "Design and Development of a Teach-by-Showing Paradigm-Based Robotic Aid System for Blinded Veterans."

Sara Johnson, professor of anthropology: $150,000 from the U.S. Department of Agriculture for the "U-ACRE Project: Broadening Opportunities for High Impact Service-Learning Experiences in Agroecological Research" project.Related: Lessons From the Lowly Sweet Potato: U-ACRE Researchers Unearth Knowledge and Cultivate Sustainability

Adam Roberts, assistant professor of psychology: $110,985 from the National Institute of Health for the "Mapping Neural Connectivity in Zebrafish Larvae Using a Photoconvertible Protein" project.

Yinfei Kong, associate professor of information systems and decision sciences: $98,632 continuing award as part of a four-year National Institutes of Health grant for the project "Gender Disparities in Access and Engagement In Medication-Assisted Treatment for Opioid Use Disorder" in collaboration with the University of Chicago.Related: Titan Data Scientist to Study Gender Differences inOpioid Treatment

Geoffrey Lovelace, associate professor of physics: $84,668 continuing award from the National Science Foundation for the CAREER project titled "Computational Gravitational-Wave Science and Education."

Zair Ibragimov, professor of mathematics: two awards from University Enterprises, Inc., totaling $82,500 for "CSU-LSAMP 2018-2023." The Louis Stokes Alliance for Minority Participation is a program to increase disadvantaged students' preparedness, persistence and retention in STEM programs.

Adriana Badillo, program director of the Center for Educational Partnerships: $76,621 continuation award from the City of Anaheim for the College Internship Program.

Jocelyn Read, assistant professor of physics: $67,213 from the National Science Foundation for "RUI: Dense Matter and Gravitational Waves: The Coalescence of Neutron Star Binaries."

Michael Boytim, assistant director of the nurse anesthesia program: $44,630 from the Health Resources and Services Administration for the Nurse Anesthetist Traineeships project.Related: Titans Test Use of Anesthesia Machinesas Ventilators for COVID-19 Patients

Danielle Zacherl, professor of biological sciences: $33,304 from Orange County Coastkeepers for the project titled "Newport Bay Living Shorelines Project."

Marcelo Tolmasky, professor of biological science: $24,659 from the San Diego State University Research Foundation for the San Diego-MHRT project.

Natalie Fousekis, professor of history: $24,580 from the U.S. Department of Interior, National Park Service for "Documenting the Experiences of Mexican, Filipina and Chicana Women in California Agriculture."

Jessica Jaynes, assistant professor of mathematics and Valerie Poynor, assistant professor of mathematics: $19,812 from Los Angeles City College for the "STEM Pathways Program Summer Research 2020" project.

Robert Lockie, associate professor of kinesiology: $19,071 from the National Strength and Conditioning Association Foundation for the project titled "The Effects of Structured Strength and Conditioning Programs on Motor Skills, Movement Competency and Physical Fitness of High School Athletes."

Jennifer Burnaford, professor of biological science: $16,238 continuing award from UC Santa Cruz for "Assessment of Rocky Intertidal habitats for the California Marine Protected Area Monitoring Program."

Michael Groves, assistant professor of chemistry and biochemistry: $16,005 in first-year funding of a three-year award from the American Chemical Society for the project titled "Calculating Reaction Barriers for Benzene Hydroxylation to Phenol Using Graphene Based Catalysts."

Dorothy Woolum, professor emeritus of physics: $10,000 from the California Institute of Technology for the project titled "Genesis Samples."

Do Kyeong Lee, assistant professor of kinesiology: $8,820 continuation award from New York University for the "Play and Learning Across a Year" project.

Bo Y. Park, assistant professor of public health: $8,000 from the University of Southern California for "Planning and Engaging in Advance Care for Health (PEACH)."

Contact: Karen Lindell, klindell@fullerton.edu

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Faculty and Staff Receive Nearly $9 Million in Grants, Contracts in Q1 - CSUF News

Biochemistry

UCI researcher receives NIH Transformative Research Award – UCI News

Irvine, Calif., Oct. 6, 2020 University of California, Irvine biomedical engineer Chang Liu is the recipient of one of nine Directors Transformative Research Awards this year from the National Institutes of Health under its High-Risk, High-Reward Research Program, the agency announced today.

Lius five-year, $8.4 million grant will support a project to develop a system for making antibody generation a routine and widely accessible process.

It is hard to overstate the importance of monoclonal antibodies in the life sciences, said Liu, UCI associate professor of biomedical engineering who also holds appointments in the Department of Chemistry and Department of Molecular Biology & Biochemistry. Antibodies are critical tools in biomedical research and diagnostics, and they are a growing class of therapeutics to combat cancer and pathogens up to and including the virus responsible for COVID-19.

Liu said current methods for making custom antibodies are slow, costly, inaccessible to most researchers and often unsuccessful. His NIH proposal centers on simplifying the process through continuous and rapid evolution of high-quality antibodies requiring only the simple culturing of yeast cells.

He said his autonomously evolving yeast-displayed antibodies technology could have a transformative impact across the biomedicine field by turning monoclonal antibody generation into a rapid, scalable and accessible process where any lab with standard molecular biology capabilities can generate custom antibodies on demand.

We believe this can be achieved by combining our new technology for continuous protein evolution, a yeast antigen-presenting cell that we will engineer, and cutting-edge generative machine learning algorithms for antibody library design, he said.

Liu said that in addition to the continuous directed-evolution techniques that he has invented in his UCI laboratory, the project will rely on antibody design and artificial intelligence expertise provided by his collaborators and co-PIs of the project, Andrew Kruse and Debora Marks at Harvard Medical School.

The project could potentially result in an explosion of crowdsourced antibody sequence data that will train our machine-learning algorithms to design better antibody libraries for our autonomous evolution system, starting a virtuous cycle, he said.

In addition to contributing to cancer and anti-viral therapies, Liu said he and his fellow researchers will attempt to generate nanobodies against biogenic receptors that respond to acetylcholine, adrenaline, dopamine and other neurotransmitters. The goal of this work will be to develop a better understanding of psychopharmaceuticals in neurobiology and addiction.

In the past, the Transformative Research Award has allowed some of the most ambitious and impactful ideas in biomedicine to blossom, and several previous winners are scientific heroes of mine, said Liu. We have big shoes to fill, but we are up to the challenge.

About the University of California, Irvine: Founded in 1965, UCI is the youngest member of the prestigious Association of American Universities. The campus has produced three Nobel laureates and is known for its academic achievement, premier research, innovation and anteater mascot. Led by Chancellor Howard Gillman, UCI has more than 36,000 students and offers 222 degree programs. Its located in one of the worlds safest and most economically vibrant communities and is Orange Countys second-largest employer, contributing $5 billion annually to the local economy. For more on UCI, visit http://www.uci.edu.

Media access: Radio programs/stations may, for a fee, use an on-campus ISDN line to interview UCI faculty and experts, subject to availability and university approval. For more UCI news, visit news.uci.edu. Additional resources for journalists may be found at communications.uci.edu/for-journalists.

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UCI researcher receives NIH Transformative Research Award - UCI News

Biochemistry

Growth of Electrolyte and Biochemistry Analyzers in Global IndustryOverview, Size and Share 2020-2025 – PRnews Leader

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15. Methodology and Data Source

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Growth of Electrolyte and Biochemistry Analyzers in Global IndustryOverview, Size and Share 2020-2025 - PRnews Leader

Embryology

Alumni Spotlight- Procopio brothers and the biology of college life – Knight Crier

Submitted Photo

Kyle and Dylan Propcopio, Class of 2020 NPHS grads

The electric buzz backstage before a performance is a feeling known very well to both Dylan and Kyle Procopio.

The dynamic duo reminisce on their time at North Penn with smiles. While at the high school, they were assistants to the Stage Manager in all NPHS theatre productions, cabinet participants in Thespian Troupe, and members of SGS (Stimulation Gaming Society) and National Honors Society. Additionally, they were tremendously involved in Boyscout Troop 51.

Currently studying at Millersville University, the Procopios are both majoring in biology. Kyle, with a concentration in molecular genetics, and Dylan with a double major in secondary education.

Did you have a favorite class you attended while at NP?

Kyle- Definitely Genetics and Embryology with Mr. Christopher! Both Dylan and I enjoyed the curriculum and his teaching style.

Do you plan on being involved in theatre in some aspect during college?

Dylan- Yes! I had a wonderful experience during my involvement with NPHS theatre. I plan on participating in stage crew here at Millersville in any capacity. But, everything is on hold until the pandemic settles down.

What was the transition like from NPHS to Millersville?

Kyle- I was a little nervous about going to Millersville since the coronavirus is still happening. But even with some serious precautions, the transition was pretty smooth. We both found a strong group of friends. And even though the school is a little bigger, it definitely feels like home.

What inspired you to go into biology education?

Dylan- I always loved biology! During boy scouts, I was in charge of instructing some of the newer guys in our troop. I taught them certain nature skills and survival tactics, and I really found it rewarding.

What words of wisdom would you like to give current students at North Penn?

Kyle- Make the most of your time at North Penn! Of course, remember time management is important, but dont forget to make time with friends and activities youre interested in. Those are the memories that will last you a lifetime.

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Alumni Spotlight- Procopio brothers and the biology of college life - Knight Crier

Immunology

What we know about COVID-19 and immunity – PolitiFact

Since his return from Walter Reed National Military Medical Center, President Donald Trump has repeated that he may now be "immune" to the coronavirus. In a video released shortly after he arrived back at the White House, he said, "Now Im better, and maybe Im immune, I dont know."

In a 55-minute interview on Fox Business, he made several claims about his health and COVID-19 immunity, saying, "When you catch it you get better, and then youre immune," and jokingly referred to himself as a "perfect physical specimen."

But medical experts say there are still a lot of unknowns about COVID-19 immunity.

Do all recovered COVID-19 patients become immune, regardless of the severity? For how long? Will the virus behave like the flu, requiring a vaccine each year? How do we achieve herd immunity?

We spoke with immunology and infectious disease experts about what they have learned and still dont know about COVID-19 and immunity.

Heres what we found out.

How does COVID-19 immunity work?

A person achieves immunity to a disease when the bodys immune system has fought off the virus once and is now strengthened to resist further attack. The immune system has a kind of memory for previous pathogens, allowing the body to have a quicker, stronger response the next time it encounters a past invader.

This can happen naturally or via vaccine.

Medical experts say its hard to know for certain the strength and length of immunity for recovering COVID-19 patients, because its a new virus and not enough studies have been done. However, there are indicators that suggest there is some natural protection against the disease post-recovery.

The biggest clue is that recovered patients rarely get reinfected with COVID-19, experts said, especially when considering the huge number of people who have been infected with the virus around the world.

"The very high-level picture is pretty stable," said Dr. Sarah Fortune, chair of the Immunology and Infectious Diseases department at Harvard T.H. Chan School of Public Health.

"Both the clinical data and the animal studies suggest that there is meaningful protection against disease," Fortune said. "Its not as if youre seeing rampant recurrent infections with recurrent severe symptoms. Its not as if there are no cases, but by and large you're seeing substantial protection against disease."

Experts also said previous studies that looked at common cold coronaviruses showed that people develop immunity for extended periods of time (at least a year), though it varied slightly from case to case.

There may be some differences in the level of immunity for those who had a serious infection, versus those who only experienced mild symptoms, researchers say. Generally, patients who dealt with a severe infection are likely going to have a higher antibody count.

"But that doesnt mean that your mild infection isn't providing you enough immunity to protect you against the disease," Fortune said. "Even if its lower, it appears to be completely proficient in protecting you against the disease. And, in most of the people who are infected, they develop a mild case and we arent seeing many reinfections."

How long does immunity to COVID-19 last?

Theres no standard time frame for immunity after someone recovers from COVID-19. Different public health groups have different estimates, with the most conservative being about four months

Researchers say its likely that people are immune for longer, but note that with a rapidly spreading disease that has no cure, people should keep their guard up rather than return to life as normal and put themselves and others at risk.

One common misconception immunologists raised is the public perception of immunity in general, with many people thinking youre either immune or youre not. Thats not how it works.

"Protection is not like a light switch, its like a dimmer switch," Fortune said. "You will be more protected in the beginning, and over time that protection might wane, but its not going to just go away.

For example, as a persons immunity wanes, they may eventually get infected from the virus again, but not actually get sick. Or even further out, they may get infected and then have mild symptoms but nothing severe.

The takeaway: The loss of immunity is gradual, not drastic.

Will we have to get multiple vaccines for COVID-19, like the flu?

The flu is a respiratory virus like the coronavirus, but its also quite different. The flu rapidly shifts and mutates, making it more resistant to long-term immunity. Thats why there is a new vaccine each year.

If the virus that causes COVID-19 continues to behave like other coronaviruses, people will likely have more stable immunity from a limited vaccination schedule.

"There's no evidence, so far, that people will need to be vaccinated each year because of the virus mutating," said Dr. Stanley Perlman, a professor of microbiology and immunology at the University of Iowa. "That may be because of their immunity waning, but not because the virus is changing."

Fortune agreed. "Theres no evidence that Sars-Cov-2 (the virus that causes COVID-19) is going to, or has undergone, a really dramatic re-shuffling that makes it escape either a natural immunity or even a vaccine-induced immunity," she said. "That's not to say that its not possible there wont be a new one in the future, but just that the virus doesn't share the same characteristics of the seasonal, whole-scale remaking of itself that the flu does."

Does a positive antibody test mean a person is immune?

Positive test results dont guarantee immunity. The presence of antibodies only means that the person has been exposed to the virus in the past.

How sensitive, or how "good," the antibody test is, and the amount of antibodies a person has, weighs heavily on whether or not they would be considered immune from the virus.

The same thing is true with a PCR diagnostic COVID-19 test.

"Some people have very positive PCR tests and thats more of a worry than someone with fluctuating PCR tests negative one day, positive the next because they have less of a viral load," Perlman said. "Its the same thing with antibodies. You can test positive for antibodies but have so little that it doesnt really protect you, or you can have a high number of antibodies, which means youre better protected. The amount matters."

What about herd immunity?

Herd immunity is the idea that when enough people in a population are immune, either by having the infection or receiving a vaccine, the virus will have trouble spreading. Thats because an infected person is less likely to encounter a non-immune person to pass it on to, making them a dead-end in the chain of transmission.

When that happens enough times on a large scale, it drives its rate down and eventually gets the disease under control, but it doesnt necessarily eradicate it.

RELATED: Corralling the facts on herd immunity

The U.S. is still considered far from adequate COVID-19 herd immunity, and experts say there would have to be many more cases and deaths before we get there if a vaccine doesnt arrive first. Fewer than 1 in 10 Americans show signs of past infection as of late July, according to a Sept. 25 study published in The Lancet journal.

So, experts agree that the ideal way to achieve herd immunity is with a vaccine. While some immunity within a population is better than none, with a virus that spreads through the air, the higher the number of people who are immune, the better.

Different numbers have been tossed around by scientists on just how much of the population needs to be immune in order for herd immunity to work well. The mathematical model for Sars-Cov-2 which is derived based on the virus transmission characteristics and on how the population behaves puts it around 60-70 people out of every 100.

For the most highly contagious diseases, like measles, scientists say about 94% of the population needs to be immunized to achieve that level of protection.

"That doesn't mean that it goes away when we reach herd immunity, it just means that you're not propagating the epidemic," Fortune said. "People should have that in mind with herd immunity, and with the future, it's not like one day, we achieved herd immunity and its gone."

See the rest here:
What we know about COVID-19 and immunity - PolitiFact

Immunology

An Autoimmune-Like Antibody Response Has Been Linked With Severe COVID-19 – ScienceAlert

In the earliest days of the pandemic, many immunologists, including me, assumed that patients who produced high quantities of antibodies early in infection would be free from disease. We were wrong.

Several months into studying COVID-19, like other scientists, I've come to realize the picture is far more complicated. A recent research study published by my colleagues and me adds more evidence to the idea that in some patients, preventing dysregulated immune system responses may be as important as treating the virus itself.

I am an immunologist at Emory University working under the direction of Dr. Ignacio Sanz, Emory's chief of rheumatology. Immune dysregulation is our specialty.

A harrowing turn in the COVID-19 pandemic occurred with the realization that the immune system's power in fighting infection was sometimes pyrrhic.

In patients with severe COVID-19 infections, evidence emerged that the inflammatory process used to fight the SARS-CoV-2 virus were, in addition to fighting the virus, potentially responsible for harming the patient.

Clinical studies described so-called cytokine storms in which the immune system produced an overwhelming quantity of inflammatory molecules, antibodies triggering dangerous blood clots and inflammation of multiple organ systems, including blood vessels, in COVID-recovered children. All these were warning signs that in some patients, immune responses to the SARS-CoV-2 virus, which causes COVID-19, may have tipped from healing to destructive.

Quick thinking and courageous decisions made by physicians on the front lines led to the use of steroids, medicines that dampen the immune response, early on in the course of infection of hospitalized patients. This approach has saved lives.

But it's not yet clear what parts of the immune system physicians are dampening that is having the effect. Understanding the nature of immune dysregulation in COVID-19 could help identify patients in whom these treatments are most effective. It may even justify more targeted and powerful approaches for modulating the immune system currently reserved for autoimmune diseases.

Antibodies are powerful weapons. Produced by white blood cells called B cells, they latch onto infectious agents like viruses and bacteria and prevent them from infecting your healthy cells. These antibody-virus aggregates unleash powerful inflammatory reactions and serve as homing beacons that allow the rest of your immune system to target the pathogens efficiently. In some circumstances, they can even kill.

Antibodies are so powerful that cases of mistaken identity when a B cell produces antibodies that attack a person's own cells can lead to widespread organ damage and establish a perpetual cycle of immune self-targeting. We refer to this state of self-destruction as an autoimmune disease.

To avoid autoimmune disaster, and to ensure effective response against the invading pathogen, B cells undergo a training process. Those that respond to the virus refine their antibodies and mature, ensuring potent antibodies capable of disabling the invader. B cells that target your own tissue are destroyed.

But that maturation process takes time. Two weeks of B cell "training" during a severe infection can mean the difference between life and death. Faster antibody responses are needed.

To bridge that gap, the immune system has an alternative form of B cell activation called extrafollicular activation that generates fast-acting antibodies that seem to bypass many of the known safety checks that accompany a more precise response.

Extrafollicular responses develop quickly, are short-lived by design and die back when the more targeted responses emerge onto the scene.

Except when they don't.

Between 2015 and 2018, our lab found that these extrafollicular immune system responses were a common characteristic of people who suffered from autoimmune diseases, such as lupus.

Patients suffering from this disease show chronically active extrafollicular responses that led to high levels of self-targeted antibodies and destruction of organs such as the lungs, heart and kidneys.

The presence of specific kinds of B cells generated by extrafollicular responses in the blood can be an important indicator of disease severity in lupus, and now also COVID-19.

In a recently published paper, my colleagues and I have identified extrafollicular B cell signatures in cases of severe COVID-19 similar to those we saw in active lupus. We showed that early on in the response to infection, patients with severe disease undergo a rapid activation of this fast-track pathway for antibody production.

These patients produce high levels of viral-specific antibodies, some which are capable of neutralizing the virus. However, in addition to those protective antibodies, some that we saw look suspiciously like the ones found in autoimmune disorders such lupus.

In the end, patients with these autoimmune-like B cell responses fare poorly, with high incidences of systemic organ failure and death.

Let me be clear here: COVID-19 is not an autoimmune disorder. The autoimmune-like inflammatory responses my team discovered could simply reflect a "normal" response to a viral infection already out of hand.

However, even if this kind of response is 'normal', it doesn't mean that it's not dangerous. These prolonged extrafollicular responses have been shown to contribute to autoimmune disease severity both through the production of self-targeted antibodies and through inflammation that can damage tissue like the lung and kidney.

This suggests that these early immune responses to a viral infection like COVID-19 are in tension with the later-targeted antibody response; in other words, the body's rapid antibody production to nab the virus runs the risk of targeting not the virus, but the patient's own organs and tissues.

Immunologists like me need to learn more. Why are only some patients turning on such strong extrafollicular B cell responses? Are the antibodies that result from this response particularly prone to attacking and destroying the host's organs? Would an ongoing autoreactive response help explain instances of "lingering" COVID-19 even after the viral infection has cleared?

Despite these uncertainties, the medical community needs to recognize that, in the appropriate patients, dampening immune responses through steroid treatment (or perhaps even more powerful autoimmune-focused therapies) is a critical weapon in combating COVID-19.

Physicians and scientists must continue to build our arsenal of therapeutics around the idea that in some cases of COVID-19, controlling your response to the virus might be as important as controlling the virus itself.

Matthew Woodruff, Instructor, Lowance Center for Human Immunology, Emory University.

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

Read the rest here:
An Autoimmune-Like Antibody Response Has Been Linked With Severe COVID-19 - ScienceAlert