By Sandy Cohen September 20, 2022

If COVID-19 becomes a seasonal virus like three of the four common-cold coronaviruses an annual COVID vaccine alongside our flu shot may offer all the protection we need.

President Joe Biden, in a September statement, even described the new COVID-19 boosters as a once-a-year shot.

But its really too soon to know if COVID-19 will become seasonal, says Otto Yang, MD, a professor in the Departments of Medicine and Microbiology, Immunology and Molecular Genetics at the David Geffen School of Medicine at UCLA.

When a virus comes into the human population, it takes a while before it settles into a pattern, Dr. Yang says. When this hit humans, everybody was susceptible and it was easy for the virus to spread, but once a bunch of people have been infected and/or vaccinated, then its not as easy for the virus to spread and a seasonal pattern will emerge if its seasonal.

Anthony Fauci, MD, the nations top infectious disease official, predicted at a federal health briefing in September that in the absence of a dramatically different variant, we likely are moving towards a path with a vaccination cadence similar to that of the annual influenza vaccine, with annual updated COVID-19 shots matched to the currently circulating strains for most of the population.

Vaccine- and infection-induced protection against COVID-19 wanes after about four months, Dr. Yang says. So if the virus settles into a seasonal pattern, annual vaccination may be enough to reduce infection rates and illness severity during the viral season.

The flu virus, for instance, is seasonal, with most cases arising in the fall and winter. Thus, an annual flu shot that offers protection during the most infectious season prevents influenza from being as deadly as it once was, even though immunity from the flu vaccine lasts much less than a year.

The new bivalent COVID-19 booster shots introduced in September which encode the spike protein of the original strain of the virus and the omicron sub-variants BA.4 and BA.5 currently responsible for most infections were developed according to a similar rationale as the annual flu vaccine. This new booster aims to protect against the circulating strains of COVID-19, just as the flu vaccine is adjusted each year to protect against predicted circulating strains of that virus.

And, like the annual flu vaccine, the new COVID-19 boosters were developed and authorized without clinical trials with human subjects.

The same RNA platform used for the original COVID-19 vaccine was adapted to include RNA from the omicron variant, Dr. Yang says: This is the normal process with the flu vaccine, which changes every year. Moreover, the omicron variants are much more similar to the original virus than flu vaccine strains are to each other year to year, he says.

Its been a while since weve seen a big new variant, says Dr. Yang, noting omicron sub-variant BA.5 has been dominant for several months.

The virus has evolved to be better at spreading between humans, he says, as evidenced by mutations to the binding receptor domain, which the virus uses to attach to a cell to infect. The latest mutations make that attachment process more efficient against human cells, which reflects that it has adapted to humans after jumping species from an animal host.

Mutations happen randomly, Dr. Yang says. And if a mutation is helpful to a virus, that virus will have an advantage and take over, compared to its peers.

Thats what omicron sub-variants BA.4 and BA.5 have done.

Ashish Jha, MD, the Biden administrations COVID-19 coordinator, says that barring those variant curveballs, a once-a-year shot should suffice to protect the majority of Americans from serious illness from COVID-19.

Dr. Yang says hes fully vaccinated but is eager to get the new shot. He continues to avoid crowded indoor spaces, and when he cant, he wears an N-95 equivalent mask when inside in public settings, such as when grocery shopping.

Its not like I completely avoid indoor spaces or socializing with friends, he says. I just try to make sure its risk-balanced, adding that he does see small groups of low-risk friends indoors, for example.

But he opts for socializing outdoors whenever possible, he says.

I still have not been infected, Dr. Yang says. And I would prefer to keep it that way.

Get the latest information on COVID-19 vaccines.

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CAMBRIDGE, Mass.--(BUSINESS WIRE)--Atavistik Bio, a pre-clinical biotechnology company that is leveraging their scalable and systematic platform to identify novel regulatory sites on proteins to restore function in disease, announced the formation of its Scientific Advisory Board (SAB) comprised of distinguished leaders in protein sciences, inborn errors of metabolism, and cancer.

We are proud and honored to have these accomplished scientific leaders join our Scientific Advisory Board, said Marion Dorsch, President and CSO of Atavistik Bio. Together, they bring a wealth of knowledge and experience for Atavistik Bio as we leverage our powerful screening and analytics platforms to unlock the potential of protein-metabolite interactions with the goal to bring transformative therapies to patients. Atavistik Bio looks forward to the input of these outstanding scientists and their contribution to our research and development efforts. Feedback and collaboration with our SAB will be critical to advance our efforts to develop therapies to patients in need. It is a very exciting time for all of us at Atavistik Bio.

The founding members of the Atavistik Bio Scientific Advisory Board are:

Dr. Ralph DeBerardinis is Chief of Pediatric Genetics and Metabolism at UT Southwestern Medical Center (UTSW) and Director of the Genetic and Metabolic Disease Program at Childrens Medical Center Research Institute at UTSW (CRI). His laboratory studies the role of altered metabolic pathways in human diseases, including cancer and pediatric inborn errors of metabolism. Work from the DeBerardinis laboratory has produced new insights into disease mechanisms in numerous metabolic diseases, including by defining unexpected fuel preferences in human cancer and uncovering new metabolic vulnerabilities in cancer cells. Dr. DeBerardinis is a Howard Hughes Medical Institute Investigator and has received numerous awards including the William K. Bowes, Jr. Award in Medical Genetics, the National Cancer Institutes Outstanding Investigator Award, The Academy of Medicine, Engineering & Science of Texass Edith and Peter ODonnell Award in Medicine, and the Paul Marks Prize for Cancer Research from Memorial Sloan Kettering Cancer Center. He has been elected to the National Academy of Medicine and the Association of American Physicians.

Dr. DeBerardinis received a BS in Biology from St. Josephs University in Philadelphia before earning MD and PhD degrees from the University of Pennsylvanias School of Medicine. He completed his medical residency and post-doctoral training at The Childrens Hospital of Philadelphia (CHOP) in Pediatrics, Medical Genetics and Clinical Biochemical Genetics.

Dr. Jared Rutter is a Distinguished Professor of Biochemistry and holds the Dee Glen and Ida Smith Endowed Chair for Cancer Research at the University of Utah where he has been on the faculty since 2003. His laboratory has identified the functions of several previously uncharacterized mitochondrial proteins, including the discovery of the long-sought mitochondrial pyruvate carrier. This knowledge has demonstrated that this critical metabolic step is impaired in a variety of human diseases, including cancer and cardiovascular disease. In addition, the Rutter lab is taking multiple approaches to understand how metabolic state influences cell fate and cell behavior decisions. Dr. Rutter has been an Investigator of the Howard Hughes Medical Institute since 2015 and serves as co-Director of the Diabetes and Metabolism Center at the University of Utah and co-Leader of the Nuclear Control of Cell Growth and Differentiation at Huntsman Cancer Institute.

Dr. Rutter performed undergraduate studies at Brigham Young University and received his PhD from the University of Texas Southwestern Medical Center in 2001, working with Dr. Steve McKnight. After receiving his PhD, he spent 18 months as the Sara and Frank McKnight Independent Fellow of Biochemistry before joining the faculty at the University of Utah.

Karen Allen, Ph.D. is Professor and Chair of Chemistry at Boston University. For over 25 years, she has led research teams at Boston University, in the Departments of Physiology and Biophysics at the School of Medicine, and Chemistry. She is also a Professor of Material Science and Engineering and on the faculty of the Bioinformatics program at Boston University. The structure-aided design approach in the Allen lab encompasses the use of macromolecular X-ray crystallography, small-angle X-ray scattering, molecular modeling, and kinetics.

Karen received her B.S. degree in Biology, from Tufts University and her Ph.D. in Biochemistry from Brandeis University in the laboratory of the mechanistic enzymologist, Dr. Robert H. Abeles. Following her desire to see enzymes in action she pursued X-ray crystallography during postdoctoral studies as an American Cancer Society Fellow in the laboratory of Drs. Gregory A. Petsko and Dagmar Ringe.

Kivanc Birsoy, Ph.D. is a Chapman-Perelman Associate Professor at Rockefeller University. His research at Rockefeller focuses on how cancer cells rewire their metabolic pathways to adapt to environmental stresses during tumorigenesis and other pathological states. He is the recipient of numerous awards, including the Leukemia and Lymphoma Society Special Fellow award, Margaret and Herman Sokol Award, NIH Career Transition Award, Irma Hirschl/Monique Weill-Caulier Trusts Award, Sidney Kimmel Cancer Foundation Scholar Award, March of Dimes Basil OConnor Scholar Award, AACR NextGen award for Transformative Cancer Research, Searle Scholar, Pew-Stewart Scholarship for Cancer Research and NIH Directors New Innovator Award.

Kivanc received his undergraduate degree in Molecular Genetics from Bilkent University in Turkey in 2004 and his Ph.D. from the Rockefeller University in 2009, where he studied the molecular genetics of obesity in the laboratory of Jeffrey Friedman. In 2010, he joined the laboratory of David Sabatini at the Whitehead Institute of Massachusetts Institute of Technology (MIT) where he combined forward genetics and metabolomics approaches to understand how different cancer types rewire their metabolism to adapt nutrient deprived environments.

Benjamin Cravatt, Ph.D. is the Gilula Chair of Chemical Biology and Professor in the Department of Chemistry at The Scripps Research Institute. His research group develops and applies chemical proteomic technologies for protein and drug discovery on a global scale and has particular interest in studying biochemical pathways in cancer and the nervous system. His honors include a Searle Scholar Award, the Eli Lilly Award in Biological Chemistry, a Cope Scholar Award, the ASBMB Merck Award, the Wolf Prize in Chemistry, and memberships in the National Academy of Sciences, National Academy of Medicine, and American Academy of Arts and Sciences. Ben is a co-founder of several biotechnology companies, including Activx Biosciences (acquired by Kyorin Pharmaceuticals), Abide Therapeutics (acquired by Lundbeck Pharmaceuticals), Vividion Therapeutics (Acquired by Bayer Pharmaceuticals), Boundless Bio, Kisbee Therapeutics, and Kojin Therapeutics.

Ben obtained his undergraduate education at Stanford University, receiving a B.S. in the Biological Sciences and a B.A. in History. He then received a Ph.D. from The Scripps Research Institute (TSRI) in 1996, and joined the faculty at TSRI in 1997.

The SAB will be co-chaired by Dr. DeBerardinis and Dr. Rutter, the scientific founders of Atavistik Bio, and work closely with the company to advance their leading-edge metabolite protein screening platform discovery programs. Im delighted to be appointed Co-Chair of Atavistik Bios Scientific Advisory Board, and to be part of such a distinguished group of experts, said Dr. DeBerardinis. Together we aim to guide Atavistik Bio through the development of its pipeline while maximizing the potential of the companys technology platform, stated Dr. Rutter.

About Atavistik Bio

Atavistik Bio is a pre-clinical biotechnology company that is harnessing the power of protein-metabolite interactions to add a new lens to drug discovery with the aim of transforming the lives of patients. By leveraging its optimized Atavistik Metabolite Protein Screening (AMPS) platform and computational approaches, Atavistik Bio aims to evaluate metabolite-protein interactions by screening proteins with their proprietary metabolite library to determine where binding sites with biological relevance might exist. This will enable Atavistik Bio to build an extensive protein-metabolite database map (the Interactome) to reveal unique insights into the crosstalk between metabolite-protein pathways that were previously thought to be unrelated. Utilizing advanced informatics tools, deep expertise in chemistry and computationally rich structure-based drug design, Atavistik Bio will be able to identify and understand the role of these interactions across important biological and disease-relevant pathways to drive the discovery of novel therapeutics with an initial focus on inborn errors of metabolism and cancer. Atavistik Bio is located in Cambridge, Massachusetts. For more information, visit http://www.atavistikbio.com.

More:
Atavistik Bio Announces Formation of Scientific Advisory Board - Business Wire

Ancient Greeks are credited with saying the truth is often the first casualty in war. I think in political campaigns, truth is also the first casualty, and we have started to see that already in the current election cycle in Nigeria.

In this column, I highlight a few of the unrelenting lies about Labour Partys Peter Obi, Peoples Democracy Partys Atiku Abubakar, and All Progressives Congresss Bola Tinubu that people peddle with misplaced confidence.

Until Peter Obi caused his bachelors degree certificate to be published online a few days ago, his traducers had said hed earned a Third Class degree in Philosophy from the University of Nigeria, Nsukka. Some people even went as far as saying he actually got a Pass degree, which is the twilight zone between failing and merely satisfying the examiners.

The persistence of the claims and their corroboration by people who should know helped solidify them as fact. For example, on July 5, 2022, Ifeoma Ezeonu, a Professor of Medical Microbiology and Molecular Genetics at the University of Nigeria, Nsukka, appeared to confirm that Obi got a Pass degree in Philosophy.

In a tweet that was designed to defend Obi, Professor Ezeonu said Obis subpar degree was the consequence of a misalignment between his actual talents and his course of study.

As a lecturer, when I hear them talk about @PeterObis Pass in Philosophy, I laugh, she wrote. From what we know of PO today, I wonder what he was even doing in a Philosophy Dept. Lol I didnt meet him in UNN, but those who knew him say that even as an undergrad the guy was doing business.

After some Obi supporters attacked her for calling attention to Obis Pass degree (which they, apparently, thought was true,) she sent another tweet to make clear that she didnt intend to disparage Obi or question his intelligence.

Just in case some people didnt get my point, [Obi] made a Pass because he was in the wrong Dept not because hes not intelligent, she wrote. Since then, he has earned other certificates in what he actually loves doing Business and Economics. That Pass is irrelevant to what he can do.

Although Ezeonu is a professor at Obis alma mater, she lied and helped to validate the narrative that Obi graduated with a Pass.

When I saw Professor Ezeonus tweet in July, my curiosity about the class of Obis degree was piqued, so I searched the Internet for more information. Then I came across a March 13, 2021, denial of this claim from Obis spokesperson by the name of Valentine Obienyem.

I do not know the source of that misinformation, Obienyem told the Source Magazine. I have considered it a trifle that does [sic] not worth a response. Since you have gone the extra mile, may I, respectfully, inform you THAT MR. PETER OBI GRADUATED WITH A SECOND CLASS AND NOT THIRD CLASS.

The release of Obis degree certificate has proved that Obienyem was right. Obi graduated with a Lower Second Class degree. Can we now stop talking about Obis Third Class or Pass degree because we now know for a fact that its a lie?

But why did such a large number of Nigerians (including Obis overenthusiastic supporters) unquestioningly believe that Obi received a Third Class or Pass degree? My guess is that Obis uncomfortably poor command of the English language, especially for a graduate of philosophy from one of Nigerias finest universities, inclined people to think he must not have paid attention at school when he studied for his degree and was liable to earn worse-than-expected grades.

Atiku Abubakar, like Peter Obi, is also the victim of misrepresentation about his qualifications and identity. A recent Sahara Reporters story that revealed that Atiku bore Siddiq in his name when he was in high school, which he later changed to Abubakar via a court affidavit, is the immediate trigger for this.

In Muslim culture, every Abubakar is Siddiq and vice versajust like every Umar is Farooq and vice versa. Theres Umar in my secondary school and university certificates which I later removed through a court affidavit in 1999. Does that make me inauthentic?

The news report also said Atiku earned a masters degree with a GCE result. Thats incorrect. Atiku has two diplomas: a diploma from the School of Hygiene in Kano and a diploma in law from the Ahmadu Bello University in Zaria.

The UAE campus of the Anglia Ruskin University in the United Kingdom, which awarded him a masters degree in 2021, must have counted his 40-plus years of post-diploma work experience as the equivalent of a university degree.

In US higher education, for example, we have something called experiential credit conversion where adult students can apply to get their life skills converted to college credit.

If youre a news reporter and a photojournalist without a degree, for instance, you wont be required to take courses in news reporting and photojournalism if you decide to get a degree in journalism. Your experience will be converted to college credit.

UK universities have a similar system. I am certain that Anglia Ruskin University counted Atiku Abubakars work as a health inspection and customs officer and later vice president and businessman as experiential learning credits that were equivalent to a bachelors degree.

Finally, it is now almost becoming mainstream to claim that Bola Tinubu has no certificate and that he is close to 100 years old even when he claims to be 70 years old. Whats the truth?

Well, although Tinubu has shown that he does not possess a (or has purposely chosen to hide his) primary or secondary certificate, he does have a bachelors degree in accounting from the Chicago State University. After what seemed like an organized dissemination of falsehood about his degree certificate being fake in late June this year, I reached out to my colleagues at Chicago State University to find out if Tinubu attended their university.

On June 27, I shared official communication from Chicago State Universitys registrar stating that Tinubu indeed received a degree in Business Administration (with a major in accounting) from the school in 1979.

In the social media update where I shared this communication, I was careful to say A Bola Tinubu Graduated From Chicago State University because I hadnt established that the Bola A. Tinubu who graduated from CSU is the Bola A. Tinubu we know.

It has since been shown beyond all shadows of doubt that the Bola A. Tinubu who graduated from CSU in 1979 is the Bola A. Tinubu who is running for president. I know this because the class photo of the 1979 CSU cohort features his headshot even though his last name was unintentionally misspelled.

And although critics say Tinubu is significantly older than the 70 years he officially claims, I have seen his transcripts from Richard Daley College (where he earned his associate degree, which is equivalent to Nigerias National Diploma) and Chicago State University (where he earned above 3.5 GPA on a scale of 4.0, which is equivalent to a First Class in Nigeria), and found that he has claimed to be born in 1952 in his transcripts since he enrolled in the American higher ed system.

He may have lied about being born in 1952, but he has been consistent in this lie (if its indeed a lie) since the early 1970s. Claims that he has changed his age are outright lies.

As I pointed out in a January 29, 2022, column titled Clarity on Tinubus Age and Postsecondary Education, it was only Tinubus Chicago State University transcript that gave his year of birth as 1954, but this was attributed to a clerical error. In any case, 1954 is two years younger than 1952. Had the year been significantly older than 1952, there would have been a valid basis to speculate that it was his real birth year that he accidentally let out.

The lies against Tinubu are difficult to extirpate because of the multiple threads of lies he has spun around himself. He had claimed to have attended primary and secondary schools that he did not attend. He claimed to have attended the University of Chicago when he didnt, and he claims to be the son of Alhaja Abibat Mogaji and a scion of the Tinubu family in Lagos when he isnt.

Everyone deserves freedom from malicious falsehood. It is immaterial whether we like them or not.

Originally posted here:
Farooq Kperogi: Lies and truth about Obi, Atiku, and Tinubu - Peoples Gazette

LIVERMORE An eminent biological scientist with ties to Lawrence Livermore National Laboratory (LLNL) is part of a major effort to develop a national research program that can explore the detailed health effects of low-level radiation exposures.

These are the kinds of exposures that people get from medical tests, long airplane flights and certain jobs in medicine, in the nuclear industry and in mining.

They can come from radiological events like nuclear accidents, but also from living in areas with naturally high levels of radiation from radon gas and from certain soils.

The scientist is Joe Gray, who worked at LLNL in the 1970s and 1980s before moving to UC San Francisco and then to Lawrence Berkeley National Laboratory as associate director.

Gray has had a distinguished career with 93 patents and more than 500 publications, contributing especially to the fields of genetics and cancer. Today he is professor emeritus atOregonHealthSciencesUniversity.

He recently served as chair of a National Academies of Science panel that was assembled at the request of Congress to explore how to revitalize a national research program on the health effects of low-dose radiation.

The panels report, Leveraging Advances in Modern Science to Revitalize Low-Dose Radiation Research in theUnited States, can be downloaded free from the National Academies website.

As the word revitalize suggests, theU.S.once carried out an active low-level exposure research program but no longer does.

For decades,the most common concern about low level radiation exposure has been that it could cause cancer, Gray said in an interview.

Thats a genuine concern, but there are major uncertainties for several reasons, he said.

Much of the knowledge of radiation-induced cancer came from exposures experienced by survivors of the atomic bombings ofHiroshimaandNagasakiin 1945.

Those are difficult to compare with todays low-level exposures, because the doses are different in type, rate and quantity.

In addition, he wrote in a preface to the National Academies report, there is increasing evidence that low level exposures may produce non-cancer health outcomes, such as cardiovascular disease, neurological disorders, immune dysfunction and cataracts.

Advances made in recent years by the medical community in fields ranging from molecular biology to epidemiology and experimental design now make it possible to extract direct information on health effects, according to the report.

Carrying out this research is vital because low level exposures are on the rise with increasing numbers of medical tests like X-rays and CAT scans and treatment using radiopharmaceuticals.

These tests may well be worthwhile, he said, but since we are now able to measure their health effects, we should do so.

While these exposures may yield individual or societal benefit, they may also adversely affect human health, he wrote.

Some communities like indigenous groups, atomic veterans and uranium miners have been exposed involuntarily and may not receive or even agree with the presumed societal benefit, he continued.

Such disparities also raise social questions regarding environmental injustice.It is imperative that risks to all exposed populations be known, as well as is scientifically possible and that risk mitigation efforts be guided by that knowledge.

Current funding for low level radiation research at the U.S. Department of Energy is $5 million per year, not enough to get a research program off the ground, let alone fund the research itself, Gray and two co-authors argued early this summer inan article for the medical journal STAT.

The National Academies panel called for a research program that ramps up quickly to annual funding of $100 million and lasts at least 15 years.

The funding would support competitive proposals in epidemiological and biological research and also train and retain a new generation of radiation scientists across a range of disciplines, according to the STAT article.

The program would leverage recent developments in other fields, making use of new epidemiological methods and databases; and powerful new biological, measurement, and computational tools that previous researchers did not have at their disposal.

In addition to Gray, the National Academies panel consisted of 12 experts fromU.S.medical schools and health agencies, and one from theUKs Health Security Agency.

Go here to read the rest:
Scientific Advances Point to Improved Understanding of Radiation Exposure - Livermore Independent

Five world-class teams are set to receive a total of over 19 million from the UK's Biotechnology and Biological Sciences Research Council (BBSRC) to support adventurous research aimed at tackling significant fundamental questions in bioscience.

Each of these teams - involving 39 investigators from 16 research organisations - will look to advance the frontiers of bioscience knowledge by exploring bold and exciting questions at the forefront of contemporary bioscience.

By pursuing world-class ideas and multidisciplinary research, these projects will convene the people, places, and transformative technologies necessary to tackle complex biological problems from a multitude of perspectives.

The funding through BBSRCs strategic Longer and Larger (sLoLa) grants programme aims to catalyse ground-breaking collaborations that advance our understanding of fundamental rules of life, with potentially far reaching implications for agriculture, health, biotechnology, and the green economy.

The five projects aim to:

Professor Melanie Welham, Executive Chair of BBSRC, said: Long-term support for discovery science is key to delivering the fundamental breakthroughs that keep the UK at the leading edge of bioscience research.

These five very different projects will each pursue adventurous avenues of investigation at the frontiers of biology by convening the multidisciplinary teams of people, skills and national facilities over the longer timeframes necessary to realise transformational change.

The projects have huge potential to make underpinning discoveries in the life sciences, which could produce future advances to address global challenges from tackling plastic pollution to treating cancer and discoveries with commercialisation potential for biopharma, biotechnology and other industries.

The projects

Specialised ribosomes

Led by Dr Julie Aspden, University of Leeds

Ribosomes are machines within cells that read the instructions from genes and use those instructions to construct proteins. The pivotal role of ribosomes in translating our genetic instructions means that a better understanding of how ribosomes function could be important to understand many diseases, including cancers.

Recently, it has been shown that ribosomes, once considered to be identical and inflexible decoding machines that translate RNA into proteins, can in fact be structurally and functionally specialised.

This specialisation promotes the selective translation of RNAs. In other words, ribosome specialisation can regulate the expression of genes at the level of translation.

However, there are only a handful of examples of ribosome specialisation known to science. This means we lack an in-depth understanding of how widespread this mode of gene regulation is, how it functions mechanistically, and what kind of ribosome code might exist.

Using a synthesis of evolutionary, functional genomic, and biophysical approaches, this project aims to tackle these big questions in four different groups of organisms (fungi, insects, plants and humans).

The team will use machine learning approaches to integrate data generated by a series of cutting-edge technologies in four major eukaryotic models (fungi, insects, plants and humans):

This will allow them to decipher the ribosome code, which has the potential to re-write our understanding of the fundamental principles of translation regulation.

Cracking the ribosome code could provide insight into how translation goes wrong in ribosomopathies and certain cancers. It could also reveal promising new avenues for manipulating the proteome, thus expanding the toolkit for future engineering biology approaches.

This project is a collaboration between eight investigators based at:

Enzymatic photocatalysis

Led by Professor Nigel Scrutton, The University of Manchester

Enzymes are proteins which catalyse biochemical reactions in all living organisms.

Most of the enzymes found in nature are heat-activated. However, there exists a few rare examples of natural light-activated enzymes or photocatalysts which use a photo-sensitive cofactor called flavin.

As their name suggests, heat-activated enzymes require heat to function. They also work with highly specific and often expensive coenzymes and catalyse reaction types limited to those found in the living cell.

In contrast, photocatalysts require light to function and have fewer chemical restraints. This enables photocatalysts to catalyse reactions that are unavailable to heat-activated enzymes, harnessing a process known as photo-biocatalysis.

There is a pressing need to better understand how photo-biocatalysis works. This would not only provide insight into how biology works with light but could also facilitate the exploitation of this process in industrial biocatalysis.

Combining state-of-the-art biophysical, computational and protein engineering methodologies, this project will apply a cyclical design-build-evaluate-learn approach to discovering the generalisable principles of photo-biocatalysis.

The team will use cutting-edge biophysical techniques to study photocatalyst functionality:

This will allow them to simultaneously contribute new fundamental knowledge on the function of existing photo-enzymes whilst illuminating a path towards the engineering of entirely new-to-nature flavin-containing photocatalysts.

In the longer-term, these engineered photocatalysts could be used to synthesise novel products that heat-activated enzymes are unable to synthesise, such as fuels and other high-value chemicals.

This project is a collaboration between six investigators based at:

Multi-layered bacterial genome defences

Led by Professor Edze Westra, University of Exeter

Bacteria are able to protect themselves from infection by viruses and other mobile genetic elements (MGEs) using highly sophisticated genome defence systems.

Aside from protecting bacterial populations against infection, these systems also influence the spread of antimicrobial resistance (AMR) which relies on the transfer of mobile antibiotic resistance genes between bacteria.

In addition to the CRISPR-Cas system, which has already been co-opted by scientists to revolutionise the field of DNA editing, new bacterial defence systems continue to be discovered.

In nature, these systems do not work in isolation. However, very little is known about how they integrate and what the consequences of this integration are on bacteria-MGE interactions.

This project aims to develop a broader understanding of multi-layered bacterial genome defence systems, at scales ranging from molecules to populations.

The team will use bioinformatic, biophysical and molecular biology approaches to understand how the interactions between genome defence systems protect bacteria against infection.

They will then combine experimental evolution and mathematical modelling to determine how multi-layered defence systems shape bacterial genome and MGE evolution.

Knowledge generated through this project has the potential to uncover how combinations of natural genome defence systems could be exploited in the fight against AMR. In addition, these combinations could be further refined in the laboratory to produce a new generation of genome editing tools for a wide range of engineering biology applications.

This project is a collaboration between 12 investigators based at:

Novel plastizymes

Led by Professor Florian Hollfelder, University of Cambridge

The number of new and untested proteins available in metagenomic databases is in the billions and is currently doubling each year.

This represents a treasure trove for the discovery of novel enzymes with exciting properties. However, there is a need for better tools to be able to effectively mine these databases and find enzymes of interest.

One group of enzymes which are drawing attention are plastic-degrading enzymes or plastizymes.

Plastizymes could be used to remove the pollution caused by plastic products. This pollution is a fundamental environmental challenge, an enormous waste of resources, and has the potential to become a major world health issue through the ingestion of micro-plastics.

However, there are currently very few known natural plastizymes and these are relatively inefficient and do not degrade all types of plastic pollutants.

This project aims to address these limitations by employing a combination of computational and protein engineering approaches to discovering new plastizymes and improving their catalytic ability.

The team will employ a number of cutting-edge technologies:

This will allow them to simultaneously derive generic pipelines for the discovery and directed evolution of novel enzymes, whilst exploiting these pipelines to produce improved plastizymes.

Longer-term, these novel plastizymes could contribute towards the UKs net-zero ambition by increasing our capacity to recycle plastic waste.

This project is a collaboration between four investigators based at:

Understanding an ancient universal membrane effector

Led by Professor Gavin Thomas, University of York

Cell membranes are generally impermeable to most chemicals, which enables proteins within the membrane to establish chemical gradients between the inside and the outside of cells.

These gradients are used as the driving forces behind some of lifes most essential chemical reactions, including photosynthesis, respiration, and active transport. Therefore, it is vital that any damage to the membrane is rapidly repaired to ensure the continuation of these crucial processes.

In recent studies, a protein belonging to the IM30 protein family has been shown to repair membrane damage in a number of bacterial pathogens and bacteria used in biotechnology to produce toxin chemicals. Interestingly, IM30 proteins are present in a range of diverse bacteria and even in bacterially-derived chloroplasts, demonstrating their ancientness and suggesting that they provided an ancestral mechanism of membrane repair.

However, while some information is known about their structure and localisation in cells, the mechanisms by which they work are still a mystery.

This project aims to functionally characterise the IM30 system in a number of clinically and industrially-relevant microbes, using bioinformatics, microbial genetics, and advanced biophysical approaches.

The team will optimise new transformative technologies to accurately measure membrane potential in live microbial cells:

These will be used to help determine how IM30 proteins protect against membrane damage in evolutionarily-divergent organisms. This will uncover new fundamental knowledge about an early step in the evolution of robust cellular life.

Mechanistic understanding of this cellular process could also reveal new pathways to target in the fight against anti-microbial resistance (AMR), since some bacteria use IM30 proteins to resist membrane-targeting antibiotics.

This project is a collaboration between nine investigators based at:

About sLoLa funding

Advancing our understanding of the rules of life is a key part of BBSRCs Delivery Plan.

The large-scale support offered through the sLoLa awards scheme enables world-class teams to pursue innovative avenues of multidisciplinary investigation over the longer timeframes necessary to realise transformational change.

By encouraging researchers to pursue bold and creative questions, BBSRC aims to catalyse exciting fundamental bioscience discoveries that may have far reaching implications for agriculture, health, biotechnology, and the green economy.

This is the fourth round of sLoLa funding since the scheme relaunched in 2018 and brings its total investment to 64 million. BBSRC plans to invest up to a further 16 million in a fifth round which is ongoing.

Go here to see the original:
19 million to investigate bold ideas in bioscience research - EurekAlert

The full list of National Awardees for 2022 are as follows:

The Order of the Republic of Trinidad and Tobago

Dr Roshan Parasram, Chief Medical Officer, In the Sphere of Public Health

Professor Sterling Frost, Banker, In the Spheres of Banking, Education and Community Service

The Chaconia Medal, GOLD

Mr Balliram Maharaj, Businessman, In the Spheres of Business and Community Service

Professor Betty McDonald, Head, Professional Development Unit: Teaching, Learning and Instructional Support, University of Trinidad and Tobago, Tamana Campus, In the Sphere of Education

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Dr Avery Hinds, Technical Director, Epidemiology Division, Ministry of Health, In the Sphere of Leadership in Public Health Service

Dr Michelle Trotman, National Covid-19 Coordinator and Lecturer, University of Trinidad and Tobago, In the Sphere of Leadership in Public Health Service

Dr Maryam Abdool-Richards, Principal Medical Officer, Ministry of Health, In the Sphere of Leadership in Public Health Service

Professor Christine Carrington, Professor of Molecular Genetics and Virology, In the Spheres of Leadership in Molecular Genetics and Virology

Dr Maryam Abdool-Richards, left, Dr Avery Hinds Dr Roshan Parasram

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The Chaconia Medal, SILVER

Professor Emeritus Gordon Rohlehr, Professor, In the Spheres of Literature, Culture, History and Education

Mr Jarrette Narine, Retired Politician, In the Sphere of Public Service

Mrs Joycelyn Hackshaw, Retired Registered Nurse, In the Spheres of Nursing, Healthcare and Public Service

Mr Victor Edwards, Artistic Director And Playwright, In the Spheres of Theatre, Culture and Education

Ms Hazel Franco, Dance Coordinator, University of West Indies (Retired), In the Sphere of Performing Arts

Mrs Rudylynn DeFour-Roberts, Restoration Architect, In the Sphere of Built Heritage Conservation and Preservation

Ms Claire Gittens, Social Worker, In the Sphere of Social Work

The Chaconia Medal, BRONZE

Professor Emeritus Edgar Julian Duncan, Professor, In the Spheres of Education and Research

The Humming Bird Medal, GOLD

Dr Alfredo Walker, Forensic Pathologist, In the Sphere of Medicine

Professor Kit Fai Pun, Professor of Industrial Engineering, In the Spheres of Engineering Education and Research

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T&Ts 4x400 metres relay team of Machel Cedenio, Jereem Richards, Asa Guevara and Dwight St Hillaire pose after being presented with their gold medals as reigning Commonwealth games champions in Birmingham, England.

Courtesy TTOC

Mr Machel Cedenio, Athlete, In the Sphere of Sport (Track)

Mr Asa Guevara, Athlete, In the Sphere of Sport (Track)

Mr Dwight St. Hillaire, Athlete, In the Sphere of Sport (Track)

Mr Kashief King, Athlete, In the Sphere of Sport (Track)

Mr Che Lara, Athlete, In the Sphere of Sport (Track)

The Humming Bird Medal, SILVER

Mrs Marilyn Gordon, Retired, In the Spheres of Sport, Education and Politics

Dr Marina Salandy-Brown, President of Bocas Lit Fest, In the Spheres of Arts and Literacy Advocacy

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Mr Kyle Greaux, Athlete, In the Sphere of Sport (Track)

The Humming Bird Medal, BRONZE

Mr Evans Hinds, Security Officer, In the Sphere of Gallantry

Master Gregg Mannette, Secondary School Student, In the Sphere of Gallantry

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The Public Service Medal of Merit, GOLD

Mr Rudolph Gordon, Teacher/Principal (Retired), In the Spheres of Education and Community Work

Miss Esme Raphael, Director, In the Sphere of Cooperative and Credit Union Development

Former Chief of Defence Staff Kenrick Maharaj.

Micheal Bruce

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The Medal for the Development of Women, GOLD

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Summary: A mutation in the newly discovered SHMOOSE small protein is associated with an increased risk of developing Alzheimers disease.

Source: USC

A mutation in a newly discovered small protein is connected to a significant increase in the risk for Alzheimers disease, expanding the known gene targets for the disease and presenting a new potential avenue for treatment, according to a new USC study.

The protein, called SHMOOSE, is a tiny microprotein encoded by a newly discovered gene within the cells energy-producing mitochondria. A mutation within this gene partially inactivates the SHMOOSE microprotein and is associated with a 20-50 % higher risk for Alzheimers disease across four different cohorts. Nearly a quarter of people of European ancestry have the mutated version of the protein, according to the researchers.

The research appears Wednesday, September 21 in the journalMolecular Psychiatry.

The researchers say that both the substantial risk and high prevalence of this previously unidentified mutation differentiate it from other proteins involved in Alzheimers disease.

Apart from APOE4 the most potent known genetic risk factor for the disease only a limited number of other gene mutations have been identified and these only mildly increased risk by less than 10%.

Also, because the microprotein is approximately the size of the insulin peptide, it can be easily administered, which increases its therapeutic potential.

This discovery opens exciting new directions for developing precision medicine-based therapies for Alzheimers disease, focusing on SHMOOSE as a target area, saidPinchas Cohen, professor of gerontology, medicine and biological sciences and senior author of the study.

Administration of SHMOOSE analogs in individuals who carry the mutation and produce the mutant protein may prove to have benefit in neurodegenerative and other diseases of aging.

Brendan Miller, 22 PhD in neuroscience graduate and first author of the study, used big data techniques to identify genetic variations in mitochondrial DNA associated with disease risk. After analyses revealed a gene mutation increased Alzheimers disease risk, brain atrophy, and energy metabolism, Miller and his colleagues discovered that the mutated gene coded for the SHMOOSE microprotein and began studying its mutated and default forms.

The researchers stated SHMOOSE is the first mitochondrial-DNA-encoded microprotein to have been detected using both antibodies and mass spectrometry.

The microprotein appears to modify energy signaling and metabolism in the central nervous system. It was found in mitochondria of neurons and its levels in cerebrospinal fluid correlated with biomarkers of Alzheimers disease.

A variety of cell culture and animal experiments showed that SHMOOSE alters energy metabolism in the brain in part by inhabiting a crucial part of the mitochondria, the inner mitochondrial membrane.

An emerging field of study

Miller said the findings highlights the importance of the relatively new field of microproteins. For decades, scientists have studied biology mostly by considering a set of 20,000 large protein-coding genes. However, new technology has highlighted hundreds of thousands of potential genes that encode smaller microproteins.

The field of microproteins is still so new, Miller said. We dont yet know how many microprotein genes are even functional, and the cost to study a potential microprotein one-by-one from a list of thousands is just too expensive and inefficient. The approach my colleagues and I used to detect SHMOOSE shows the power of integrating big genetics data with molecular and biochemical techniques to discover functional microproteins.

USC Leonard Davis researchers are leaders in the study of microproteins, especially those coded within the mitochondrial genome. In 2003, Cohen and his colleagues were one of the three research teams to independently discover theprotein humanin, which appears to have protective health effects in Alzheimers, atherosclerosis and diabetes.

In the past few years, the Cohen Laboratory discovered several other mitochondrial microproteins, including, small humanin-like peptides, orSHLPs, and a microprotein calledMOTS-c,an exercise-mimetic peptide that has entered clinical trials for obesity and fatty liver.

Additional coauthors include Su-Jeong Kim, Hemal H. Mehta, Kevin Cao, Hiroshi Kumagai, Neehar Thumaty, Naphada Leelaprachakul, Henry Jiao, Thalida E. Arpawong, Eileen Crimmins, Meral A. Tubi, Evan T. Hare, Meredith N. Braskie, La Dcarie-Spain, Scott E. Kanoski, Lu Zhao, Arthur W. Toga, Junxiang Wan, and Kelvin Yen of USC; as well as Joan Vaughan, Jolene Diedrich, and Alan Saghatelian of the Salk Institute for Biological Studies; Nilfer Ertekin-Taner of the Mayo Clinic; and Francine Grodstein and David A. Bennett of the Rush University Medical Center.

Funding: The study was supported by NIH grants P30AG10161, P30AG072975, R01AG15819, R01AG17917, U01AG61356, R01AG069698, RF1AG061834, R01AG068405, P30AG068345, P01AG055369, DK118402, F31 AG059356, and T32 AG00037; as well as The Quebec Research Funds Postdoctoral Fellowship. Intellectual property related to SHMOOSE has been filed by the University of Southern California.

Author: Leigh HopperSource: USCContact: Leigh Hopper USCImage: The image is in the public domain

Original Research: Open access.Mitochondrial DNA variation in Alzheimers disease reveals a unique microprotein called SHMOOSE by Pinchas Cohen et al. Molecular Psychiatry

Abstract

Mitochondrial DNA variation in Alzheimers disease reveals a unique microprotein called SHMOOSE

Mitochondrial DNA variants have previously associated with disease, but the underlying mechanisms have been largely elusive. Here, we report that mitochondrial SNP rs2853499 associated with Alzheimers disease (AD), neuroimaging, and transcriptomic.

We mapped rs2853499 to a novel mitochondrial small open reading frame called SHMOOSE with microprotein encoding potential. Indeed, we detected two unique SHMOOSE-derived peptide fragments in mitochondria by using mass spectrometrythe first unique mass spectrometry-based detection of a mitochondrial-encoded microprotein to date.

Furthermore, cerebrospinal fluid (CSF) SHMOOSE levels in humans correlated with age, CSF tau, and brain white matter volume. We followed up on these genetic and biochemical findings by carrying out a series of functional experiments.

SHMOOSE acted on the brain following intracerebroventricular administration, differentiated mitochondrial gene expression in multiple models, localized to mitochondria, bound the inner mitochondrial membrane protein mitofilin, and boosted mitochondrial oxygen consumption.

Altogether, SHMOOSE has vast implications for the fields of neurobiology, Alzheimers disease, and microproteins.

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Newly Discovered Protein Connected to Alzheimers Disease Risk - Neuroscience News