Category Archives: Biochemistry

Finding a way to combat long COVID – EurekAlert

A newstudyhas identified potential neurological biomarkers of long COVID-19 in nonhuman primates that may help physicians diagnose, monitor and treat this condition.

Over65 million peopleworldwide have developed long COVID after being infected with SARS-CoV-2, and cases are only becoming more common.Long COVIDsymptoms can last weeks, months or years. Even more perplexing is the fact that symptoms can vary widely between individuals and consist of any combination of fatigue, fever, chest pain, trouble breathing, neurological symptoms such as brain fog, and many more. Long COVID puts a gigantic burden on theU.S. healthcare system, and some doctors doubt the condition exists, leaving some patients unable to find care.

A team of researchers at Tulane University is trying to shed light on this condition and find tools to manage it. They published their work in the journal Molecular & Cellular Proteomics.

Our primary goal was to better understand the inside of the brain after COVID infection, said Jia Fan, an assistant professor of biochemistry and molecular biology who oversaw the study. This understanding could provide a potential target to use in the clinic for long COVID evaluation and monitoring. We also thought this study may give us some clues to find a potential treatment strategy for long COVID in patients.

However, because long COVID can vary drastically between individuals, studying this disorder has been difficult for scientists and clinicians alike.

There's a very limited understanding of the neuropathogenesis of long COVID, Fan said. It is almost impossible to get any brain tissue or samples of any kind from patients that have mild symptoms or no long COVID symptoms because there is no reason for invasive procedures.

Therefore, the group turned to a nonhuman primate model of long COVID.

The team found that certain proteins associated with neurodegenerative disorders, such as Parkinson's disease, were elevated in the brain, cerebrospinal fluid and blood after SARS-CoV-2 infection even in nonhuman primates that showed mild or no symptoms. Maity explained that these elevated proteins indicate that the immune systems of the monkeys remained activated even after infection.

Our findings suggest that the major neurological complications are arising due to the body's natural immune defenses, Maity said. The immune system has a very important and significant impact on the neurological complications of COVID.

The next steps of the project involve validating the biomarkers the team identified in human samples such as blood, said Fan.

It is currently hard to score the severity of (long COVID) patient symptoms because they are based on self-reports, Fan said. If we can find a group of proteins in the blood associated with long COVID, this is a less invasive way to easily evaluate the severity of the long COVID patients. We hope what we started can provide a clue to find a potential treatment to better the long COVID patient experience.

About the American Society for Biochemistry and Molecular Biology (ASBMB): The ASBMB is a nonprofit scientific and educational organization with more than 12,000 members worldwide. Founded in 1906 to advance the science of biochemistry and molecular biology, the society publishes three peer-reviewed journals, advocates for funding of basic research and education, supports science education at all levels, and promotes the diversity of individuals entering the scientific workforce. For more information about the ASBMB, visitwww.asbmb.org.

Molecular & Cellular Proteomics

Experimental study

Animals

Cerebrospinal fluid protein markers indicate neuro-damage in SARS-CoV-2-infected non-human primates

29-Mar-2023

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Finding a way to combat long COVID - EurekAlert

High schoolers awarded for action research | Sioux Center News – nwestiowa.com

SIOUX CENTERA small group of high school students got their chance to pitch their science projects at the 2023 State Science Technology Fair of Iowa in Ames on Thursday and Friday.

Its all part of a new course called action research offered at Sioux Center High School.

Its individualized project-based learning, said science teacher Christine Brasser. The students need to create their own research project to do throughout the year. They start off with what are the things that I like, what are the things Im interested in, do I have any questions about those things? Then they build from there.

They then begin the work of applying the scientific method to those interests and budding questions by coming up with a question, hypothesis and a plan for how to gather the needed data. When a conclusion is eventually reached, they need to present that information.

I want them to be able to ask good questions, analyze data and come to their own conclusions. I think the biggest thing in this class is the ability to look at everyday things with a scientific perspective, Brasser said. Looking at data and knowing what makes for good data, good data sources and how its collected is important. During your life, you might not think of using the scientific method, but you can use it without really thinking about it.

The parameters the students have to work with when coming up with a project topic are simple enough: The question they investigate must be able to be tested and something based in typical life.

One of my students is testing supplements, what are in these supplements that are not regulated. Another one is about protein in corn. Its real-life questions that people might be interested in knowing the answer to, she said.

As part of the research, the students reach out to experts who can help provide data or guide their research. This helps the students learn communication skills as they send out e-mail, make phone calls and ask questions.

Those might seem simple for the average adult, but for high school kids, that can be very intimidating, she said. One student was on a Zoom call with a professor from South Dakota State University, and hed never met him in person. Its really good to see these kids grow by having to do these things.

Its also been an exercise in working with deadlines, with time frames for when students should develop their topic idea and hypothesis, conducting their studies and gathering data and so on.

For the end of the class, the students create a professional poster displaying and explaining their project in detail so it can be used in the state science fair competition.

Since this is a new class, its beginning small, with four students, which Brasser said has been a good number to start with.

Its a class Ive always wanted to offer but we didnt have the periods open, she said. With the addition of a fourth science teacher, we were able to offer this class. For next year, I think our enrollment will be closer to 10 or 12.

In the meantime, she has been excited to see her class get ready for the State Science Technology Fair of Iowa. Judges review the submitted projects, which are categorized into 12 different fields of biological or physical sciences. Topic areas include animal and plant science, biochemistry, microbiology, energy and transportation, chemistry and computer science, robotics and intelligent machines.

Im excited for them to compete, Brasser said, and that Sioux Center is able to add this to the list of the many great things we can offer for kids.

For the state science fair, Sioux Center students Everett Fedders and William Hurst won scholarship dollars for their work. Fedders won a $1,000 scholarship award to Loras College and $2,000 scholarship award to Northwestern College in Orange City for microbiology. Hurst won a $2,000 scholarship award to Northwestern for biochemistry.

As part of the concurrently held Iowa FFA AgriScience Fair, Fedders won second place in the food products and processing systems division and Hannah Woudstra won first place in the plant systems division of the concurrent Iowa FFA Agriscience Fair.

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High schoolers awarded for action research | Sioux Center News - nwestiowa.com

Emory researchers discover key pathway for COVID-19 organ … – Emory News Center

Even after three years since the emergence of COVID-19, much remains unknown about how it causes severe disease, including the widespread organ damage beyond just the lungs. Increasingly, scientists are learning that organ dysfunction results from damage to the blood vessels, but why the virus causes this damage is unclear. Now a multidisciplinary team of Emory researchers has discovered what they believe is the key molecular pathway.

Results of their study, published today in Nature Communications, show that COVID-19 damages the cells lining the smallest blood vessels, choking off blood flow. These results could pave the way for new treatments to save lives at a time when hundreds of people are still dying from COVID-19 each day.

Doctors at Emory started this study in the early days of the pandemic to better understand drivers of severe COVID-19 and why adults develop severe disease more often than children. They used a so-called multi-omics approach, studying multiple data sets at once, to examine the biochemistry of blood from COVID-19 patients and compared it to non-COVID-19 patients, looking for clues.

We were surprised by the little overlap between our adult and pediatric patients, says Cheryl Maier, MD, PhD, assistant professor in the Department of Pathology and Laboratory Medicine, Emory University School of Medicine, and the studys senior author. Both groups had abnormalities related to clotting, but one unique pathway that stood out in the adults was related to vessel health and blood flow.

Maier says this finding was particularly interesting given their clinical observations that blood from patients severely ill with COVID-19 was unusually viscous: think maple syrup rather than water.

Maier worked with collaborator and co-senior author Wilbur Lam, professor in the Department of Pediatrics at Emory University and in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Institute of Technology and Emory University, to create cutting-edge models of the smallest blood vessels, expected to be the most sensitive to altered blood flow, which allowed them to visualize how blood from COVID-19 patients versus other patients might be flowing in the human body.

Watching videos from these microfluidic devices is like seeing how COVID-19 might be affecting our blood vessels in real time, Maier says. These lab-made blood vessels are lined with real human vascular cells, called endothelial cells. You can put in plasma and red cells, any of the key components of blood and in different combinations, to watch how it behaves and see how the damage happens.

Since the earliest days of the pandemic, physicians have seen that a blood protein called fibrinogen was extremely elevated in patients with severe COVID-19. This protein is often elevated in other acute illnesses, but the elevations seen in the sickest COVID-19 patients were much higher. The body forms blood clots in part by cutting fibrinogen to form fibrin, a key component of clots, but fibrinogen itself is not thought to form clots and levels are not affected by anticlotting medications. But the Emory researchers found that in COVID-19 patients, the sky-high levels of fibrinogen cause red blood cells to clump together, altering blood flow and directly damaging the endothelial glycocalyx, a gelatinous protective layer lining the microvessels.

Fibrinogen is one of the top three most abundant proteins in plasma, Maier says. Its been hiding in plain sight.

When the researchers combined plasma from COVID-19 patients with red blood cells in lab-made blood vessels, they could visualize the cellular aggregation and quantify the destruction of the endothelial cell glycocalyx. You have these large clusters of red cells that are all stuck together, Maier says. Normally this wouldnt happen. Capillaries are so narrow that red blood cells must pass through single file. But in COVID, these aggregates stick together even under flow. Its easy to imagine how this mechanically damages the microvasculature.

Much of the new technology was developed by study co-first author Elizabeth Iffrig, MD, PHD, a critical care fellow in Emorys Department of Medicine. The foundation of what we did was looking at how red blood cells would form these big globules that would gunk up the microvascular system, Iffrig says. Our methodology let us look at this in a dynamic process, seeing what happens to these aggregates as we mimic a true physiologic state of blood flow instead of just suspending them in a fluid and measuring how big they are. The methodology allowed us to quantify all those things simultaneously.

Taken together, these data suggest to Maier that the fibrinogen-induced red blood cell aggregation and resulting microvascular damage could be the major pathway by which COVID causes organ damage and even death. Theres presently no medications targeting high fibrinogen in the blood. However the team has done exploratory research using therapeutic plasma exchange: removing plasma with high fibrinogen from COVID-19 patients and replacing it with donor plasma that has normal fibrinogen levels. Maier thinks her teams discovery is critical because it provides a target that might help save lives.

Additional key members of the research team include co-first author Sam Druzak, PhD, and co-senior author Eric Ortlund, PhD, professor in the Department of Biochemistry at Emory University.

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Emory researchers discover key pathway for COVID-19 organ ... - Emory News Center

Auburn chemistry graduate student shines as only Southeastern … – Office of Communications and Marketing

Kacey Ortiz, a graduate student in the College of Sciences and Mathematics, or COSAM, was chosen to be part of a highly competitive 2023 class of Future Leaders by the American Chemical Society, or ACS.

Im excited for this award because Ill get to travel to the ACS Headquarters and ACS San Fran, hear about a lot of incredible science and meet a lot of fantastic individuals also doing fantastic research, Ortiz said. The award itself is awesome because Ill be getting to network with other young scientists in the chemistry field who will be working in both academia and industry, and those same people might be the same individuals I get to do collaborative research with one day.

In this years class, hundreds of students from around the globe submitted applications. However, only a total of 35 students and postdoctoral scientists were selected. Of those, only 22 are from the United States, and Ortiz was the only recipient in the entire Southeast region.

I am proud that Kacey was selected as a future leader by the American Chemical Society, said Doug Goodwin, chair of the Department of Chemistry and Biochemistry, or DCB. Kacey has exceled in his research in Dr. Karimovs lab. More than this, Kacey has been an integral part of every aspect of our departments life, mission and programs.

He was selected as a 2022 Outstanding DCB GTA, he is a member of DCBs Inclusion, Equity and Diversity Committee, he is vice president of the local affiliate of the ACS Younger Chemists Committee, he recently presented his research at COSAMs Graduate Student Research Forum and he was a volunteer judge for the Alabama Science and Engineering Fair. He has been a driving force for the department reestablishing its social connections on this side of the pandemic. Kaceys selection by ACS represents a great opportunity for him to develop his skills as a leader that much further.

As a Future Leader, Ortiz will receive leadership training, have access to networking opportunities, learn from industry leaders, receive coaching from professionals, travel to the ACS headquarters and conferences and present his research.

Submitted by: Maria Gebhardt

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Auburn chemistry graduate student shines as only Southeastern ... - Office of Communications and Marketing

Broccoli intake protects the small intestine lining, inhibits development of disease – News-Medical.Net

Broccoli is known to be beneficial to our health. For example, research has shown that increased consumption of the cruciferous vegetable decreases incidences of cancer and type 2 diabetes. In a recent study, researchers at Penn State found that broccoli contains certain molecules that bind to a receptor within mice and help to protect the lining of the small intestine, thereby inhibiting the development of disease. The findings lend support to the idea that broccoli truly is a 'superfood.'

We all know that broccoli is good for us, but why? What happens in the body when we eat broccoli? Our research is helping to uncover the mechanisms for how broccoli and other foods benefit health in mice and likely humans, as well. It provides strong evidence that cruciferous vegetables, such as broccoli, cabbage, and Brussels sprouts should be part of a normal healthy diet."

Gary Perdew, H. Thomas and Dorothy Willits Hallowell Chair in Agricultural Sciences, Penn State

According to Perdew, the wall of the small intestine allows beneficial water and nutrients to pass into the body but prevents food particles and bacteria that could cause harm. Certain cells that line the intestine -; including enterocytes, which absorb water and nutrients; goblet cells, which secrete a protective layer of mucus on the intestinal wall; and Paneth cells, which secrete lysosomes that contain digestive enzymes -; help to modulate this activity and keep a healthy balance.

In their study, which published in the journal Laboratory Investigation, Perdew and his colleagues found that molecules in broccoli, called aryl hydrocarbon receptor ligands, bind to aryl hydrocarbon receptor (AHR), which is a type of protein called a transcription factor. This binding, they found, initiates a variety of activities that affect the functions of intestinal cells.

To conduct their study, the researchers fed an experimental group of mice a diet containing 15% broccoli -; equivalent to about 3.5 cups per day for humans -; and fed a control group of mice a typical lab diet that did not contain broccoli. They then analyzed the animals' tissues to determine the extent to which AHR was activated, as well as the quantities of various cell types and mucus concentrations, among other factors, in the two groups.

The team found that mice that were not fed broccoli lacked AHR activity, which resulted in altered intestinal barrier function, reduced transit time of food in the small intestine, decreased number of goblet cells and protective mucus, decreased Paneth cells and lysosome production, and decreased number of enterocyte cells.

"The gut health of the mice that were not fed broccoli was compromised in a variety of ways that are known to be associated with disease," said Perdew. "Our research suggests that broccoli and likely other foods can be used as natural sources of AHR ligands, and that diets rich in these ligands contribute to resilience of the small intestine."

More broadly, added Andrew Patterson, John T. and Paige S. Smith Professor of Molecular Toxicology and of Biochemistry and Molecular Biology, "these data suggest that dietary cues, relayed through the activity of AHR, can reshape the cellular and metabolic repertoire of the gastrointestinal tract."

Other authors on the paper include Xiaoliang Zhou, Debopriya Chakraborty, Iain A. Murray, Denise Coslo, Zoe Kehs, Anitha Vijay, Carolyn Ton, Dhimant Desai and Shantu G. Amin.

The National Institutes of Health Grants, U.S. Department of Agriculture and Penn State Cancer Institute supported this research.

Source:

Journal reference:

Zhou, X., et al. (2023). Aryl Hydrocarbon Receptor Activation Coordinates Mouse Small Intestinal Epithelial Cell Programming. Laboratory Investigation. doi.org/10.1016/j.labinv.2022.100012.

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Broccoli intake protects the small intestine lining, inhibits development of disease - News-Medical.Net

The Greek who gave $600 million to education – Kathimerini English Edition

My wife and I help students study without being shackled by debt on their chosen career path, says Greek-American Roy Vagelos, 93, a prominent figure in the pharmaceutical industry. He is so committed to helping create the next generation of scientists, he recently donated an additional $175 million to the University of Columbia to support doctors embarking on the first steps of their careers and PhD candidates. It is not, however, the only donation made by Roy and Diana Vagelos to the American institution, which is why they have a school named after them: the Vagelos College of Physicians and Surgeons.

Born in the US to Greek parents, Roy, or Pindaros as he was baptized, grew up admiring his grandfathers degree in physics from the University of Athens. He was very young when he died and his children migrated to the United States, without having been able to study, he reminisces in a recent conversation with Kathimerini.

Ancient names ran in the family. My father was Herodotus and my uncles were named Homer and Thucydides, he says.

The Vagelos brothers were in the catering business and Herodotus later opened a restaurant in New Jersey, where everyone pitched in. It was particularly popular among the executives working at Merck, whose headquarters were located nearby.

As he bused their tables and made small talk about the weather, young Roy could hardly have imagined that one day he would be the executive director of the pharmaceutical giant. These are the people I consulted when I was applying for college, he says.

Vagelos started studying chemistry but medicine and biochemistry soon caught his interest. I didnt have any problems studying because I was a very good student and got a scholarship immediately, he says. But I know that this is not always the case for youngsters with their eye on an academic career.

It is estimated that half of the students in the US have taken out some kind of loan to study. Tuition at the graduate level ranges from $30,000 to $35,000 at state universities and can reach $55,000 at private colleges, while it goes up even more at the postgraduate level.

I didnt have any problems studying because I was a very good student and got a scholarship immediately. But I know that this is not always the case for youngsters with their eye on an academic career

Love and marriage

Vagelos met his wife Diana also of Greek roots while he was at the University of Columbia and she was at Barnard College. We got married in 1955 and would have done so sooner if our finances had allowed it, he says.

Thanks to Dianas first job and a decent salary, the young couple were able to tie the knot.

Roy got a job at Massachusetts General Hospital, then became a researcher at the National Institutes of Health (NIH) and later went on to become the head of the Biochemistry Department at Washington University in St Louis, before climbing to the top of the ranks at Merck.

During his 20 years at the firm, he was instrumental in the development of top cholesterol and drug pressure drugs, antibiotics and vaccines. I left the position of executive director, which Id held for 10 years, because I retired, says Vagelos, who is still active as president of the board at Regeneron.

I chose jobs that I found interesting, not those that would bring me more money. This is a luxury I would like young scientists to have, he says.

A lot of students in America graduate with massive debts of like $100,000 and this really clips their wings, adds Vagelos. These young people will not go into research or do a PhD or become pediatricians as these choices are less well-paid.

If they dont have the burden of debt, however, they may follow their calling and this will be for the good of society as a whole.

Vagelos, who has been supporting educational institutions since the 1980s, keeps in touch with many of the young scientists who have benefited from his donations. They are very talented and I am so proud of them, he says. Overall, the couple has supported the universities of Pennsylvania and Columbia their alma maters with donations worth almost $600 million. Their names, needless to say, are on many department plaques.

Their aim is to give medical students financial independence, support researchers, promote women in the sciences and also to fund research into tackling climate change. This is the second most important thing I am concerned about, says Vangelos, who helped develop the Climate Schools at Columbia and Penn.

Mentors for young scientists

It is important for our young colleagues to learn how to look for work, how to write a paper, but also how to say no, which is especially pertinent for women scientists, who often feel that turning down additional tasks will be perceived as a sign of weakness, says Dr Litsa Kranias, who sought to bolster these skills with her donation to the University of Cincinnati, where she is a professor and head of cardiovascular biology at the Medical School.

I pondered the idea for 10 years and three years ago made my wishes known to the relevant committee, says the Greek academic.

Thanks to the interest from her donation, the future of the annual Kranias Symposium on Early Career Mentorship is secured. There, a guest mentor advises doctoral and post-doctoral students and new professors on their next career moves. This is followed by a round-table discussion with four professors and then one-on-one consultations.

I have always wanted to help younger scientists do well, says Kranias, who is still grateful for the full scholarship that allowed her to move from Greece to the United States. I studied at the University of Chicago, which was one of the top five schools at the time, and it had just started taking graduates from universities outside the US on a trial basis, says Kranias, whose stellar academic performance paved the way for other foreign students.

Other initiatives giving back

Americans are very familiar with the notion of giving back. Young professionals often support their alma maters soon after graduating, even with a small amount like 100 dollars a year, says George Tsetsekos, Francis Professor of Finance and dean emeritus at Drexel Universitys LeBow College of Business.

Second- and third-generation Greeks whose parents had high aspirations for their futures and wanted them to study are no exception.

At first the Greeks gave money to the Church and associated organizations like the Theology School in Boston. Then they started giving to universities with which they had personal ties, says Tsetsekos.

He acknowledges that the cost of an education and the loans that make it possible are a big problem for young Americans. That said, I also believe that they are not getting realistic advice about their career prospects; they are encouraged to follow their dreams without being told that only certain professions can ensure a high standard of living in the US, where costs are admittedly high.

The list of benefactors is interesting and, apart from the sciences, also includes significant donations for Classical studies.

John Calamos, for example, founded a philosophy chair at the University of Illinois, where students learn about the ancient Greek philosophers. Angelo Tsakopoulos founded the Chair of Modern Greek Studies at Stanford and supports many similar programs across the US. Nicholas and Athena Karabots founded the archaeology program at the University of Arizona, which is responsible for the excavations in the Peloponnese at the Temple of Lycian Zeus, while they also cover the salary of one professor of ancient Greek archaeology.

Theres also the Nicholas & Nancy Vidalakis Scholarship for students who want to train in his native Crete, while the Clinical Cancer Center at the University of Iowa exists thanks to John Pappajohn, who has endowed many of the institutions programs. John Rangos is behind, among others, a pediatric hospital in Pittsburgh, and George Behrakis funded the Behrakis Health Science Center at Northeastern. Last but not least, the University of Boston has the Alexis Gavras Scholarship for Greek and Greek-American students.

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The Greek who gave $600 million to education - Kathimerini English Edition

Study uncovers aspect of how muscular dystrophies progress – ASBMB Today

A research study has shed new light on how congenital muscular dystrophies such as WalkerWarburg syndrome progress, bringing hope for better understanding, early diagnosis and treatments of these fatal disorders.

Published in March in the Journal of Biological Chemistry, the research was led by scientists in the lab of Vlad Panin, professor in the Department of Biochemistry and Biophysics in the Texas A&M College of Agriculture and Life Sciences. The study is titled Protein tyrosine phosphatase 69D is a substrate of protein O-mannosyltransferases 1-2 that is required for the wiring of sensory axons in Drosophila. The primary author is Pedro MonagasValentin, one of Panins doctoral students.

The study uncovers new ways of how genetic mutations seen in patients with muscular dystrophies may lead to disease and create neurological problems. Namely, the mutations disrupt a newly discovered gene function and prevent neurons from forming connections properly. The research used fruit flies as a model system and has implications for humans.

Courtesy of Pedro MonagasValentin

This fruit fly brain shows the mutation the new study links to muscular dystrophies. The fly has wiring defects in sensory axons, pictured in fluorescent green.

Funders of the research included the National Institutes of Health and the Texas A&M AgriLife Institute for Advancing Health Through Agriculture.

WalkerWarburg and muscle-eye-brain syndromes are rare, severe muscular dystrophies. Typically diagnosed in very young children, these conditions progress rapidly. They affect skeletal, heart and lung muscles as well as the brain, eyes and other organs. No cure exists for these diseases, and patients usually do not survive into adulthood.

Certain genes affected in these disorders are known, Panin said. But much remains unknown about how these genetic defects affect molecular and cellular processes to cause neurological and other problems.

This gap in understanding of pathological mechanisms impedes the development of treatments and efficient diagnostics, he said.

Many of the genetic mutations that occur with muscular dystrophies affect something difficult to study, Panin said, and that is the way our bodies build and use complex sugars.

The sugars, called glycans, are made by all living things. In addition to energy storage and regulation, glycans have countless functions that regulate other molecules in animal cells.

There are four languages of life, if you think about it in general, Panin said. Two are proteins and nucleic acids like DNA and RNA. And there are two more languages: lipids and glycans. The fourth one is arguably the most complex language, and this is what we study as glycobiologists.

Glycans can be complex and branching. Unlike DNA or proteins, they are not created from a genetic template. The mutations in muscular dystrophy patients disturb a complex chain of events needed to build and attach glycans to the right molecules inside our bodies. To understand that chain of events, scientists must study the structures and locations of glycans, and the technology to do that is still being developed.

To track the role of several genetic mutations in muscular dystrophies, the team genetically modified fruit flies, then studied how the mutations affected the flies nervous system structure and glycobiology.

My work involved a lot of crossing different lines of fruit flies to either raise or lower the activity of genes we wanted to learn more about, MonagasValentin said. Then I did a lot of fly brain dissections under the microscope, of multiple genetic combinations, with a lot of practice and a lot of messing up.

MonagasValentin used fluorescence microscopy and other methods to compare how different mutations in flies affected fly bodies and brains. He also sent samples for analysis using methods specifically designed for glycobiology. For that analysis, MonagasValentin and Panin collaborated with researchers at the Complex Carbohydrate Research Center at the University of Georgia in Athens.

Our collaborators have expertise in glycan sample preparation, data analysis, protocol development every step is important, Panin said.

Putting all the data together, the team found that a protein called PTP69D enables the proper wiring of sensory axons in flies. The researchers also revealed that the genes mutated in muscular dystrophy patients are important for PTP69D to function properly. Whats more, PTP69D belongs to a large family of proteins that have very similar structure and function in flies and humans.

This story opens up new directions to understand neurological problems, Panin said.

Although PTP69D and its protein family members are similar in flies and in humans, there are limitations to what the present study says about human biology, Panin said.

The fly nervous system is much simpler, and in humans there may be additional protein and glycan interactions in play, Panin said. We can see the basic mechanisms, but nuances and additional layers cannot be studied in flies.

He said much is still unknown about the proteins and glycans involved in neuron development. The team will now study these molecules and interactions more deeply to see how mutations in muscular dystrophy genes affect individual neurons.

This article first appeared in AgriLife Today, the news hub for Texas A&M AgriLife, which brings together a college and four state agencies focused on agriculture and life sciences within The Texas A&M University System. Read the original.

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Study uncovers aspect of how muscular dystrophies progress - ASBMB Today

Man linked to firebombing of Wisconsin anti-abortion group via leftover burrito – Yahoo News

[Source]

A half-eaten burrito led to the arrest of a man believed to be responsible for firebombing the office of an anti-abortion group in Madison, Wisconsin, authorities announced last week.

Hridindu Sankar Roychowdhury, 29, was charged with one count of attempting to cause damage by means of fire or an explosive for the incident, which took place at Wisconsin Family Actions headquarters last Mothers Day, May 8, 2022.

Police responded at around 6 a.m. to a fire that broke out at the Madison-based building. Inside, they found suspicious items, including a disposable lighter and two mason jars one broken and another containing a clear fluid that smelled like an accelerant.

Meanwhile, the outside of the building was spray-painted with If abortions arent safe then you arent either. Another wall was painted with a large encircled A and 1312.

More from NextShark: Cathay Bank Foundation donates $1 MILLION to help fight anti-Asian hate

Last month, police identified Roychowdhury as a possible suspect and matched his DNA from a leftover burrito he had thrown in a public trash can to the crime scene.

Roychowdhury, who lives in Madison, was arrested in Boston last Tuesday. If convicted, he faces between five to 20 years in prison.

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Violence is never an acceptable way for anyone to express their views or their disagreement, Robert R. Wells, assistant director of the FBIs Counterterrorism Division, said in a statement. Todays arrest demonstrates the FBIs commitment to vigorously pursue those responsible for this dangerous attack and others across the country, and to hold them accountable for their criminal actions.

Wisconsin Family Action, who blamed the attack on a leftist anarchist group, is a nonprofit that defends Gods plan for marriage, family, life and religious freedom.

No one was in the office at the time of the attack.

Story continues

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The incident came about a week after a draft opinion suggesting that the Supreme Court would overturn Roe v. Wade had leaked. The court officially made that call in June, bringing back Wisconsins abortion ban.

Twitter account Antifa Watch has shared social media posts allegedly made by Roychowdhury. In them, he identified himself as a graduate research assistant at the University of Wisconsin-Madison (UW-Madison) and made statements such as Im an anarchist now and I hope to see this country burn.

UW-Madisons May 2022 commencement announcement reportedly listed Roychowdhurdy as a doctoral candidate. A UW-Madison spokesperson confirmed that he received a doctorate in biochemistry but that he is no longer attached to the institution.

The individual that you reference received a PhD in biochemistry from UW-Madison in May 2022. He is no longer affiliated with the university, the spokesperson told Fox News.

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Man linked to firebombing of Wisconsin anti-abortion group via leftover burrito - Yahoo News

Important enzyme for the composition of the gut microbiome discovered – Phys.org

This article has been reviewed according to ScienceX's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility:

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The intestinal microbiome, i.e., the community of bacteria and other microorganisms that live in the human gut, has been shown to affect the metabolism and the immune system. We still do not fully understand how the symbiosis between a healthy microbiome and the host is regulated and how bacterial overgrowth with pathogenic germs can be prevented.

A research team led by Professor Christoph Becker-Pauly from the Institute of Biochemistry at Kiel University (CAU) in collaboration with other working groups has now discovered an important mechanism influencing the intestinal microbiome in mouse models. The results were recently published in the journal Science Advances.

"For the first time, we were able to show that a complex of the enzymes meprin and meprin located on intestinal cells influences the microbiome composition by processing the substrate galectin-3," explained first author Cynthia Blck, Ph.D. student at the CAU's Institute of Biochemistry.

"The activity of this enzyme complex is in turn directly influenced by the microbiome," added Professor Christoph Becker-Pauly, member of the Cluster of Excellence "Precision Medicine in Chronic Inflammation" (PMI) and head of the Unit for Degradomics of the Protease Web. "This means that the microbiome influences host proteins, which in turn influence the microbiome."

The researchers studied this interplay of regulation of the enzyme complex in mouse models with different bacterial colonizations.

The research focused on the protein-cleaving enzymes meprin and meprin , which are strongly expressed in healthy intestine and are significantly downregulated in chronic inflammatory bowel disease (IBD). "On the one hand, we wanted to elucidate the function of meprins in the small and large intestine, and on the other hand, we wanted to understand how the composition of bacteria in the intestine is fundamentally regulated," said Blck.

Meprin proteases are found throughout the entire intestine, but they are not typical digestive enzymes. "In previous studies, we were already able to show that these enzymes are responsible for constant detachment and renewing of the mucus layer that protects the small intestinal epithelium," said Becker-Pauly.

In order to clarify the further functions of meprins, which exist as the meprin / complex in the large intestine, the researchers first employed a mass spectrometry-based method to search for substrates that are processed by this enzyme complex. "We identified galectin-3 as an important substrate in the large intestine," stated Becker-Pauly.

Galectin-3 is permanently produced in the intestinal villi. It is found both within the cells but also outside the cell in the mucus layer and can interact with bacteria, for example by agglutination. Proteolytic cleavage of galectin-3 by meprin / resulted in altered bacterial binding properties. At the same time, depending on the bacterial composition, enzymatic processing of galectin-3 changes. "This means that depending on how many and which bacteria are present, it also has an influence on how much galectin-3 is enzymatically processed," explained Blck. "The host responds to the microbiome via the cleavage of galectin-3, which is then modulated differently."

The work also showed that the enzymatic cleavage of galectin-3 leads to strong agglutination (clumping) and elimination of the pathogen Pseudomonas aeruginosa, a germ that is responsible for about 10% of all hospital infections in Germany.

"Understanding the physiological role of this enzyme complex in the intestine could provide new insights into the development of diseases as well as new ways to prevent and treat intestinal diseases," emphasized Becker-Pauly. In chronic inflammatory bowel diseases, not only the enzyme complex is reduced, but also the substrate galectin-3 is also downregulated. "This may lead to an imbalance of the the intestinal microbiome so that pathogens can spread more easily," suspects the Kiel biochemist. This constellation is certainly not decisive for the development of chronic inflammatory bowel diseases, as many factors play a role in this regard, but it should be considered.

Further research will now focus on elucidating the mechanisms in more detail that lead to the agglutination of certain types of bacteria. In addition, further immunomodulatory substrates of the meprin / complex have been identified and their function will now be analyzed.

More information: Cynthia Blck et al, Proteolytic processing of galectin-3 by meprin metalloproteases is crucial for host-microbiome homeostasis, Science Advances (2023). DOI: 10.1126/sciadv.adf4055

Journal information: Science Advances

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Important enzyme for the composition of the gut microbiome discovered - Phys.org

Unraveling the protein map of cell’s powerhouse – ASBMB Today

Mitochondria, the so-called powerhouse of the cells, are responsible for the energy supply of the organism and fulfill functions in metabolic and signaling processes. Researchers at the University Hospital Bonnand the University of Freiburg have gained systematic insight into the organization of proteins in mitochondria. The protein map of mitochondria represents an important basis for further functional characterization of the powerhouse of cell and thus provide implications for diseases. The study has now been published in the renowned scientific journal Nature.

Mitochondria are among the most important cell compartments. They are delimited organelles surrounded by a double membrane. Mitochondria are considered the powerhouse of the cell, as they produce the majority of the energy required for all cellular processes. In addition, they take over many other functions in metabolism and provide a signaling surface for inflammatory processes and programmed cell death. Defects in mitochondria lead to numerous diseases, especially of the nervous system.

Model of the quality control mechanism for removing arrested proteins from the mitochondrial entry gate.

Therefore, the molecular understanding of mitochondrial processes is of highest relevance for basic medical research. The molecular workers in the cell are usually proteins. Mitochondria can contain around 1,000 or more different proteins. To execute functions, several of these molecules often work together and form a protein machine, also called a protein complex. Proteins also interact in the execution and regulation of molecular processes. Yet little is known about the organization of mitochondrial proteins in such complexes.

The research groups of Thomas Becker and Fabian den Brave at the UKB, together with the research groups of Bernd Fakler, Uwe Schulte and Nikolaus Pfanner at the University of Freiburg, have created a high-resolution image of the organization of proteins in protein complexes, known as MitCOM. This involved a specific method known as complexome profiling to record the fingerprints of individual proteins at an unprecedented resolution. MitCOM reveals the organization into protein complexes of more than 90% of the mitochondrial proteins from bakers yeast. This allows to identify new proteinprotein interactions and protein complexes an important information for further studies.

Researchers at UKB in cooperation with Collaborative Research Center 1218 (Regulation of cellular function by mitochondria)have shown how this dataset can be used to elucidate new processes. Mitochondria import 99% of their proteins from the liquid portion of the cell, known as cytosol. In this process, a protein machinery called the TOM complex enables the uptake of these proteins through the membrane into the mitochondria. However, it is largely unclear how proteins are removed from the TOM complex when they get stuck during the transport process. To elucidate this, the team led by Becker and den Brave used information from the MitCOM dataset. It was shown that non-imported proteins are specifically tagged for cellular degradation. Research by the Ph.D. student Arushi Gupta further revealed a pathway by which these tagged proteins are subsequently targeted for degradation. Understanding these processes is important because defects in protein import can lead to cellular damage and neurological diseases.

The example from our study demonstrates the great potential of the MitCOM dataset to elucidate new mechanisms and pathways. Thus, this map of proteins represents an important source of information for further studies that will help us to understand the functions and origin of the cells powerhouse, saidBecker, director of the Institute of Biochemistry and Molecular Biology at UKB.

This article was first published by University Hospital Bonn. Read the original.

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Unraveling the protein map of cell's powerhouse - ASBMB Today