Category Archives: Cell Biology

Vast diversity of human brain cell types revealed in trove of new … – Spectrum – Autism Research News

Cell spectrum: Single-cell techniques identify subtypes of interneurons that have distinct shapes and firing patterns.

Allen Institute for Brain Science

New catalogs detail thousands of cell types that populate the human brain and that of our closest primate relatives. The findings appear in 21 papers published today in Science, Science Advances and Science Translational Medicine.

Its a huge, huge enterprise, says Joshua Sanes, professor of molecular and cellular biology at Harvard University, who was not involved in the work. It really is what translational neuroscience and systems neuroscience, as well as molecular neuroscience, will be building on for the next 10, 20 years.

The new work used single-cell molecular approaches to identify more than 3,000 distinct neuronal and non-neuronal cell types within the developing and the adult human brain. Individual studies also compare cell composition across samples from 75 people and eight cortical regions, and across humans and four non-human primate species.

This effort represents a step toward a single-cell atlas of the human brain and begins to provide information about what might make us uniquely human at the cellular level, says Andrea Beckel-Mitchener, deputy director of the U.S. National Institutes of Healths BRAIN Initiative, which funded the project.

The resulting datasets, which are available online, are the product of five years of research by more than 250 researchers who make up the BRAIN Initiative Cell Census Network (BICCN), a project that launched in 2017 to catalog mammalian brain cell types. In 2021, the BICCN team unveiled detailed atlases of the motor cortex in human, macaque and marmoset brains. And earlier this year, BICCN scientists posted preprints that establish the most complete cell atlases of the mouse brain to date.

The datasets provide researchers with benchmarks for typical cell composition across humans, non-human primates and other mammals, says Ed Lein, senior investigator at the Allen Institute for Brain Science in Seattle, Washington, and a researcher on multiple papers in todays collection. And in the future, they could help scientists select the best model organisms for a given study and even identify cells implicated in disease, he says.

The BICCN identified distinct cell types based on a variety of features, including their individual patterns of gene expression (the transcriptome) and patterns of tags on DNA (the epigenome), combined with other measures, such as cell morphology and physiology.

Some scientists have long questioned whether single-cell transcriptomics could distinguish cells in ways that are as useful as morphology or physiology have been for decades, Sanes says its biology; its complicated. But the new work suggests that identifying cells by their molecular components offers a complementary, if not always overlapping, way of categorizing cells throughout the brain, he says.

There is utility in describing the cells gene expression, agrees Jason Shepherd, associate professor of neurobiology at the University of Utah in Salt Lake City, who was not involved in the new work. The subsequent interpretation of what that means is where it starts to get a little muddy.

Even researchers involved in the BICCN were initially uncertain about whether their single-cell techniques, which were originally used in animals, would translate to people, particularly at a large scale. Anything from difficulty in handling the samples of human tissue to unforeseen species differences could have thwarted the work, Lein says.

But the new work confirms that single-cell methods can reveal new insights about the cell composition of our own species, Lein says. Its really quite remarkable. The diversity that we all thought was there, really is there. That diversity is highest in the midbrain and hindbrain, the new work shows areas that have been studied less extensively than the cerebrum.

Throughout the brain, cell composition relates to function, the new work suggests. The same 24 major cell types appear consistently across all eight areas of the cerebral cortex that Lein and his colleagues sampled in one of the new studies, but these cells proportion changes from region to region. One brain region that stands out for its unusual composition is the primary visual cortex, which the new work shows has distinct subtypes of excitatory and inhibitory cells. That likely reflects the fact that the primate brain is wildly specialized for visual inputs, Lein says.

Different people also tend to share all the same brain cell types but vary in how those cells particularly excitatory neurons and glia express genes, according to another study, which examined live tissue samples collected from 75 people as they underwent surgery to treat various brain conditions. Most of that variation is not explained by demographic factors such as age or sex but instead may stem from things such as life experience, says study investigator Trygve Bakken, assistant investigator at the Allen Institute for Brain Science.

Another new study revealed that children with early-life brain inflammation have changes to gene expression in two types of inhibitory neurons within their cerebellum. Many of the affected genes have been linked to autism, pointing to a potential place of convergence for some forms of the condition.

Some of the new papers also document cell-type composition across non-human primates, including macaque monkeys and marmosets. These studies, coupled with the BICCNs mouse atlases, offer a way to assess which cell types are shared across evolution and which are specific to humans findings that can help researchers select the best model organisms for a given study.

This really opens the door to ask, Can we translate findings from model organisms to humans? Bakken says.

Other studies, which document how brain cells change throughout the early stages of development, can help guide researchers who seek to model human development using organoids, Lein says.

The scale of the project is unprecedented in neuroscience, Beckel-Mitchener says. The only comparable biology program is the Human Gene Project, she says.

Moving forward, the network aims to fill out the contours of the prototype atlas. Last year, it transitioned to its next phase, called the BRAIN Initiative Cell Atlas Network. Were ramping up to hundreds of donors across a much broader collection of ages and ancestries, Beckel-Mitchener says.

Ultimately, the goal is that these atlases will provide a good understanding of what the normal brain actually looks like, Lein says. When used as a reference, the atlases can serve as a basis for understanding which cells are affected in disease, and when. That would enable researchers to ask questions that are much more directed and much more data driven when deciding which brain areas to study for a given condition, says Tomasz Nowakowski, associate professor of anatomy, psychiatry and neurological surgery at the University of California, San Francisco, who led one of the studies published today.

Theres a lot of work to do, says Seth Ament, associate professor of psychiatry at the University of Maryland School of Medicine in Baltimore, who worked on the study of inflammation in the cerebellum. But thats the mark of any important project, right?

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Vast diversity of human brain cell types revealed in trove of new ... - Spectrum - Autism Research News

Singamaneni to develop advanced protein imaging method – The … – Washington University in St. Louis

Cell-secreted proteins, such as antibodies, hormones and neurotransmitters, play a crucial role in maintaining overall health and well-being. They are also key components in disease research and in developing diagnostic tools and personalized medicines. However, current methods for studying these proteins are limited to observing large groups of cells together, which makes it difficult to discern individual cell behaviors and differences.

With a $450,000 grant from the National Science Foundation, Srikanth Singamaneni, the Lilyan & E. Lisle Hughes Professor in the McKelvey School of Engineering at Washington University in St. Louis, will develop a method called Plasmon-Enhanced Expansion FluoroSpot (PEEFS) to address these limitations. PEEFS combines a very bright fluorescent nanoparticle with expansion microscopy to image secreted proteins with high sensitivity and precision and accurately measure differences between cells.

The project represents a potentially transformative advance, particularly in immunology, oncology, stem cell biology and other life-science disciplines. With PEEFS, researchers will be able to image and quantify protein secretion at extremely high resolutions down to the level of a single cell revealing cell-to-cell variability and interactions and the spatial and temporal dynamics of cell-secreted proteins.

This story was originally published on the McKelvey School of Engineering website.

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Singamaneni to develop advanced protein imaging method - The ... - Washington University in St. Louis

Researchers find certain cancers can activate ‘enhancer’ in the … – University of Toronto

Researchers at the University of Toronto have found that cancer cells can enhance tumour growth by hijacking enhancer DNA normally used when tissues and organs are formed.

The mechanism, called enhancer reprogramming, occurs in bladder, uterine, breast and lung cancer and could cause these types of tumors to grow faster in patients.

The research was conducted in the lab of Jennifer Mitchell, a professor in the department of cell and systems biologyin the Faculty of Arts & Science, andpublished recently in the journalNucleic Acids Research. It pinpoints the role that specific proteins play in regulating the enhancer region which may lead to improved treatments for these cancer types.

Living cells, even cancer cells, follow instructions in the genome to turn genes on and off in different contexts, says first authorLuis Abatti, a PhD candidate in Mitchells lab.

The genome is like a recipe book written in DNA that gives instructions on making all the parts of the body, Abatti says.

In each organ, only the recipes relevant to that organ should be followed whether its the instructions for lung, breast or some other tissue. Like flipping pages in a recipe book, the DNA containing the instructions for turning genes on in the lung is open and used in the lung, for example, but closed and ignored in other types of cells.

We know that some cancer cells are opening the wrong pages in the recipe book ones that contain the SOX2 gene, which can cause tumours to grow uncontrollably. We wanted to find out: How does the gene become expressed in cancer cells?

The researchers analyzed genome data to look for enhancer DNA that could activate SOX2 in cancer cells. The enhancer they found is open in many different types of patient tumours, meaning this could be a cancer enhancer active in bladder, uterus, breast and lung tumours. Unlike many cancer-causing changes, the enhancer reprogramming mechanism does not arise out of mutation due to DNA damage it is caused by part of the genome opening when it should be staying closed.

The researchers then determined that the enhancer causes increased cancer cell growth because when they removed the enhancer in lab-grown cells, the cancer cells created fewer new tumour colonies.

To figure out why cells have a DNA region that makes cancer worse, the team examined mice without this DNA region and found they do not form a separate passage for air and food in their throat as they develop. Thus, this potentially dangerous cancer-enhancer region is likely in the human genome to regulate airway formation as the human body forms. However, if a developing cancer cell opens this region, it will form a tumour that grows faster and is more dangerous for the patient.

We also found that two proteins known to have a role in the developing airways FOXA1 and NFIB are now regulating SOX2 in breast cancer, says Mitchell, who is associate chair of research in the department of cell and systems biology and is cross-appointed to thedepartment of laboratory medicine and pathobiologyin the Temerty Faculty of Medicine.

The enhancer is activated by the FOXA1 protein and suppressed by the NFIB protein. This means that drugs suppressing FOXA1 or activating NFIB may lead to improved treatments for bladder, uterine, breast and lung cancer.

Now that we know how the SOX2 gene is activated in certain types of cancers, we can look at why this is happening, Mitchell says.

Why did the cancer cells end up on the wrong page of the genome recipe book?

The research received support from the Canadian Institutes of Health Research, the Canada Foundation for Innovation and the Ontario government.

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Researchers find certain cancers can activate 'enhancer' in the ... - University of Toronto

2023 Hettleman Prizes awarded to five exceptional early-career … – UNC Research

The annual Phillip and Ruth Hettleman Prizes for Artistic and Scholarly Achievement have been awarded to five promising faculty members who exemplify groundbreaking and innovative research along with future career promise.

The late Phillip Hettleman, a member of the Carolina class of 1921, and his wife Ruth established their prestigious named award in 1986 to recognize the achievements of outstanding junior faculty. The recipients of the $8,000 prize will be recognized at the November 3 Faculty Council Meeting. They will also deliver a presentation on their research during University Research Week on October 24 from 3 to 5 p.m. in the School of Social Works Tate-Turner-Kuralt Auditorium.

This years Hettleman Prize awardees are: Yaiza Canzani, associate professor in the Department of Mathematics within the College of Arts and Sciences; Brian Conlon, associate professor in the Department of Microbiology and Immunology within the School of Medicine; Angel Hsu, assistant professor in the Department of Public Policy within the College of Arts and Sciences; Pengda Liu, associate professor in the Department of Biochemistry and Biophysics within the School of Medicine; and Alex Worsnip, associate professor in the Department of Philosophy within the College of Arts and Sciences.

Yaiza Canzanis research focuses on understanding the behavior of Laplace eigenfunctions, which play a crucial role in explaining physical phenomena such as wave propagation, heat conduction, acoustics and quantum evolution.

Canzanis work bridges microlocal analysis, partial differential equations, probability, geometry, and dynamical systems. Her scholarship is internationally recognized she was awarded a Sloan Fellowship, the Sadosky Research Prize in Analysis, and a National Science Foundation CAREER grant.

In his nomination letter for Canzani, Bowman and Gordon Gray Distinguished Term Professor of Mathematics Jason Metcalfe says, Within an extremely active and competitive field of mathematics Canzani is developing transformative tools that will have an immense and long-lasting impact. She is obtaining historic results and is an elite scholar whose promise for discovery cannot be exceeded.

Over the past several years, Canzani developed a research program that aims to describe how Laplace eigenfunctions concentrate near a given point by understanding how they behave when localized to tubes centered along the geodesics that run through the point.

Canzani received her doctorate from McGill University. She was a Benjamin Peirce Fellow at Harvard University and a member of the Institute for Advanced Study.

Brian Conlon is a leader in the field of antibiotic resistance and focuses on alternative strategies to treating infections with existing antibiotics. He aims to make previously ineffective treatments work better by manipulating how the treatment is delivered on a microbial level and reversing resistance by tricking the bacteria into responding to medication.

Conlon also researches how diabetes impacts treatment for antimicrobial resistance, and how to make the battleground inside someones body more hospitable to treatment by pairing an antibiotic with another drug.

His finding that innate immune cells can inhibit antibiotic activity is a major discovery and paves the way for the future development of therapeutics to augment the immune response and make antibiotics work better in patients, says Craig Cameron, professor and chair of the Department of Microbiology and Immunology, in his nomination letter for Conlon.

As a postdoctoral researcher Conlon published nine papers and his work appeared in the journals Nature and Nature Microbiology. Since establishing his lab at Carolina in 2016, Conlon has published 17 papers in journals including PLoS Biology, Cell Chemical Biology, eLife, and Nature Microbiology. His work has also led to two patents that promise to form the basis of novel therapeutic developments.

Conlon earned a doctorate in microbiology from University College Dublin and completed postdoctoral training at the Antimicrobial Discovery Center at Northeastern University.

Angel Hsu applies data-driven approaches to evaluate climate and environmental policy, primarily at the state and local levels. She leads The Data-Driven EnviroLab, frequently calling upon others from different disciplines to collaborate on research.

Collectively, her work has been influential in shaping the research agenda among those studying global climate governance and developing the quantitative approaches used to assess the impact and performance of subnational and non-state actors.

In his nomination letter for Hsu, Daniel P. Gitterman, Duncan MacRae 09 and Rebecca Kyle MacRae Professor of Public Policy, says, Hsu has made important theoretical, substantive, and methodological contributions to climate policy. Her research is highly visible and influential, and her trajectory and future promise are highly positive. Her contributions to research, teaching and service at Carolina are exemplary.

Hsus work has been published in several leading journals, including Nature, Environmental Research Letters, and Climate Policy, contributing novel research in ways that are indicative of her status as a leading scholar in global environmental policy and her engagement in timely policy debates.

Hsu earned an MPhil in environmental policy from the University of Cambridge and a doctorate in environmental policy from the Yale School of Environment. Following her PhD, she served for two years as a postdoctoral associate with the Urbanization and Global Change Group at Yale University.

Pengda Liu studies cancer biology and the molecular mechanisms underlying aberrant cell signaling events in human cancer. He is using this knowledge to develop novel anti-cancer therapies.

He has established a highly productive lab at UNC-Chapel Hill as an independent and collaborative investigator. Both styles of research have led to ground-breaking discoveries and to highly cited articles. Liu has an innovative approach, melding bioengineering expertise with hi-tech biochemistry, cell biology, genetics, and applying this to drug development. His lab focuses on two key cellular signaling pathways that can lead to disease and cancer when mutated.

In her nomination letter for Liu, professor and chair of the Department of Biochemistry and Biophysics Jean Cook says, Liu has made seminal discoveries, and his research has great promise for future clinical advances. We believe that he represents the best in research, mentoring, teaching, and service that the School of Medicine has to offer.

His postdoctoral work was published in high-impact journals, including Nature, Cancer Discovery, Nature Cell Biology, and Molecular Cell. In his seven years at Carolina, Liu has published 24 original research articles, seven review articles and one book chapter.

Liu earned his doctoral degree from East Carolina University and completed postdoctoral studies at Harvard University.

Alex Worsnips research of epistemology the theory of knowledge has made groundbreaking advances in the understanding of the nature of rationality. He proposes that there are two fundamentally distinct kinds of rationality substantive and structural with neither being reducible to the other, which has fascinating motivations and profound payoffs.

Worsnip made these advances in his field through a series of widely acclaimed articles published in top philosophy journals including the Journal of Philosophy, Mind, and Ethics. His work on rationality culminated in a book, Fitting Things Together: Coherence and the Demands of Structural Rationality, which was published by Oxford University Press in 2021. He also won the prestigious Young Epistemologist Prize from Rutgers University in 2019.

Worsnips work has received a great deal of attention from other philosophers, including significant and widespread attention in articles appearing even before Worsnips own paper had appeared in print, says Theda Perdue Distinguished Professor of Philosophy Marc Lange in his nomination letter for Worsnip.

Worsnips most recent and current research concerns the application of epistemology to social and political issues, with particular attention to the epistemic responsibilities of ordinary citizens in a democracy. For example, he has argued that being an epistemically responsible participant in democratic deliberation requires consuming news from sources of different politically partisan affiliations. Since 2022, he has been director of the Applied Epistemology Project at UNC.

Worsnip earned a BPhil in philosophy from the University of Oxford and his doctorate from Yale University. He completed postdoctoral training at New York University.

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Faeth Therapeutics Announces National Academy of Medicine … – BioSpace

AUSTIN, Texas--(BUSINESS WIRE)-- Faeth Therapeutics, a leader in metabolic oncology research and treatment innovation, proudly announces the induction of its co-founder, Dr. Siddhartha Mukherjee, Assistant Professor at Columbia, Pulitzer Prize Winner, and one of Time 100's Most Influential People, into the esteemed National Academy of Medicine (NAM).

Dr. Mukherjee was honored for contributing important research in the immunotherapy of myeloid malignancies, such as Acute Myeloid Leukemia, for establishing international centers for immunotherapy for childhood cancers, and for the discovery of tissue-resident stem cells. His book, The Emperor of All Maladies, won the Pulitzer Prize and was nominated by Time as among the centurys 100 most influential books, introducing millions to modern cancer research. This recognition accentuates the collective dedication and caliber of Faeth's team and the company's commitment to advancing the realm of cancer care.

With Dr. Mukherjee's recent induction into the National Academy of Medicine, he joins fellow Faeth co-founders who have previously received this honor from the National Academy of Science: Karen Vousden, PhD, Chief Scientist of CRUK, Group Leader at the Crick Institute, and Director at Bristol Myers Squibb; Lew Cantley, PhD, Professor of Cell Biology at the Dana Farber Cancer Institute at Harvard University; Greg Hannon, PhD, Director of CRUK Cambridge Institute; and Scott Lowe, PhD, Chair of Cancer Biology & Genetics at Memorial Sloan Kettering, underlining the depth of Faeth Therapeutics' commitment to scientific excellence and innovation.

"Dr. Mukherjee's induction into the National Academy of Medicine reaffirms Faeth Therapeutics' dedication to unparalleled scientific rigor and innovation. We are immensely proud to have such an impressive team of co-founders driving our mission to redefine and elevate standards in oncology care," said Anand Parikh, J.D., Chief Executive Officer of Faeth Therapeutics.

Mukherjee is one of 100 new members announced by the academy. In the National Academy of Medicine, members are elected by their colleagues as a testament to their exceptional accomplishments. Being inducted into the academy represents one of the most prestigious accolades within the realm of medicine.

About Faeth Therapeutics

Faeth Therapeutics is a clinical-stage biotechnology company focused on bringing breakthrough research in metabolic oncology into the clinic. The company leverages its machine-learning platform to identify therapeutic programs that combine traditional therapeutics and a dietary metabolic regimen to enhance outcomes, with the goal of transforming the treatment landscape. Lead asset, FTH-001, combines serabelisib and an insulin-suppressing regimen to slow tumor growth via PI3K pathway inhibition. Faeths scientific founders include industry leaders Drs. Lew Cantley, Sid Mukherjee, Karen Vousden. For additional information, visit http://www.faeththerapeutics.com.

View source version on businesswire.com: https://www.businesswire.com/news/home/20231013531071/en/

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Finding the golden ticket? Cyclin T1 is required for HIV-1 latency … – Fred Hutch News Service

More than 20 years after the discovery of combination antiretroviral therapy (ART), complete eradication of HIV infection has not yet been achieved. While ART controls viral replication, it is not a cure. This is due to HIV latency, in which the virus is hidden in an inactive state in the genomes of long-living host cells (such as memory CD4 T cells). This allows the virus to evade immune surveillance. As ART acts on the viral replication machinery, latent HIV that is not actively replicating can escape ART. Thus, a cure for HIV requires the ability to either eliminate the latent reservoir or to permanently silence the provirus in the reservoir (or a combination of both).

To improve our understanding of what host genes are require forHIV to emerge from latency, ina newstudy published inViruses, researchers from the Emerman lab in the Human Biology and Basic Sciences Divisions reported that the host factor Cyclin T1 is required for promoting HIV reactivation under a large variety of conditions that would otherwise activate it.

Terry Hafer, the lead author of the study and a graduate student in the Emerman lab, performed a latency HIV-CRISPR screen to identify host factors required for HIV to come out of latency in the presence of small molecule latency reactivation agents (LRAs). Cyclin T1 (CCNT1) was the top hit on the screen.It has been shown previously that Cyclin T1 and Cyclin-dependent kinase 9 (CDK9) form a complex with the positive transcription elongation factor b (P-TEFb) to promote HIV transcription elongation. Cyclin T1 and its role in viral transcription elongation is not novel, said Hafer.But what was striking for us was that Cyclin T1 has always been implicated as an essential gene for its role in transcription elongation as part of the P-TEFb complex, he added. Knockouts of Cyclin T1 showed that cyclin T1 loss impacted HIV gene transcription far more than any other host gene, however, Cyclin T1 knockout did not have noticeable effects on host cell function, Hafer explained.

The latency HIV-CRISPR screen was performed on infected Jurkat T cells (J-Lats 10.6 and 5A8) using a HIV dependency factor gene library (HIV-Dep). Here is the catch, the guide RNAs have been modified to be incorporated into the newly produced virions of the infected cells after LRA treatment. The idea behind this was that if a cell lacks a gene that is essential for latency, HIV will not reactivate. Consequently, the specific guide RNA (targetinga gene essential for reactivation) will not be packaged into newly formed virions.By performing deep sequencing, the team was able to identify guide RNA sequences that are underrepresented in the pool of released viruses. One of the top hits on the screen was Cyclin T1 (CCNT1). To validate the screen, the team knocked out CCNT1 in J-Lats cells, followed by treatment with several LRAs. In all treatments, wild-type (WT) CCNT1 cells were able to reactivate HIV, but KO CCNT1 cells failed to reactivate HIV in the presence of LRAs, indicating that Cyclin T1 is essential for HIV reactivation from latency. Moreover, loss of CCNT1 did not affect the expression of CCNT2, a paralog of CCNT1 that also binds to CDK9 as part of complex p-TEFb, suggesting that CCNT1 plays a unique role. Furthermore, CCNT1 KO did not affect cell proliferation in the J-Lat model. The findings were validated in primary CD4 T cells (the primary target of HIV in infected individuals) as well as the loss of CCTN1 did not affect the activation of primary CD4 T cells.

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From Migrant Farm Worker to Duke Scientist, Everardo Macias … – Duke University School of Medicine

Everardo Macias, PhD, assistant professor of pathology at Duke University School of Medicine, explores the complexities of prostate cancer, the second leading cause of cancer death in men.

His quest to find innovative cancer treatments mirrors his own incredible journey from a migrant farm worker to a groundbreaking scientist.

Years ago, the future he envisioned for himself was entirely different. A first-generation high school graduate working in the fields of Minnesota as a migrant farm worker, he never even planned to go to college.

Today, with human cancer genetics and advanced gene testing, hes tackling one of prostate cancers trickiest players: cancer cells that dodge usual treatments. In lab studies, his method of targeting a protein called NUAK2 successfully slowed down the lethal spread of these cells.

Although still in its preliminary stages, with one in eight men facing prostate cancer in their lifetime, every breakthrough counts.

It still baffles me how traveling in the back of a pickup truck one summer in high school got me all the way to Duke, said Macias, a member of the Duke Cancer Institute and an assistant research professor in the Department of Cell Biology.

A harrowing ride across the country, inadvertently set him on a course for higher education and a career in science.

Beyond academia, he celebrates his roots with a renowned food truck, Evelyn's Tex Mex BBQ, named after his daughter and operated with wife Lucia Collado and stepson Frank. ("Smoking good food with a little bit Tex, y un poco de Mex.")

As a Hispanic of Mexican American descent with roots in a small Texas town, my journey to becoming an independent investigator has been enriched tremendously by great mentorship and programs geared toward increasing diversity in biomedical research.

His career researching druggable targets for prostate cancer illustrates the power education and mentorship.

As a child, Macias moved back and forth between the United States and Aguascalientes, Mexico. After his parents separated, he and his four siblings settled with their mother in Sabinal, a small town in Southwest Texas.

In the summer prior to his senior year in high school, Macias traveled to northern Minnesota in the back of a pickup truck for three days with another family to work as a migrant farm worker on sugar beet farms.

Although it was far from home and the work was back-breaking, the pay was better than working on local farms in Texas. For decades, a predominantly Mexican workforce has migrated around the United States, harvesting the countrys food.

The jobs can offer government-backed benefits to address job training and seasonal unemployment, but its a way of life thats rife with labor rights violations, poor housing, and financial instability.

When he returned for senior year, his guidance counselor mentioned an opportunity in Austin, Texas, at St. Edwards University: a College Assistance Migrant Program (CAMP) Scholarship that would pay for the first year of college.

At the time, he wanted to be an accountant, but when he started taking general chemistry and science classes, his professors said he had a knack for it.

Although I worked on farms in Mexico and Texas, I only worked one summer as a true migrant farm worker. When I met other students in the CAMP program who were bona-fide migrant farm workers for as long as they could remember, they told stories of what they went through and how much work and suffering it took. I knew I couldnt squander the opportunity, Macias said.

As an undergraduate at St. Edwards, he held summer internships at Monsanto, the St. Louis-based manufacturer of agricultural and biochemical products.

I realized that my life had taken a 180-degree turn, that I was now conducting research on transgenic seed varieties for a company whose products I was working with in fields just three years before, he said. It hit me how powerful higher education is. It was an ah-ha moment for me.

He earned a Bachelor of Science degree in chemistry from St. Edwards, but graduate school wasnt on the radar for Macias until his advisors recommended it.He would eventually earn a PhD in comparative biomedical sciences from North Carolina State University.

After refining his expertise during postdoctoral fellowships at the University of North Carolina at Chapel Hill and the University of Texas-Austin, he made a significant transition, trading his Tar Heel blue for the Blue Devil spirit.

From 2013-2015, he served as a project scientist in the Department of Surgery at Duke. After a stint as an assistant professor at Cedars-Sinai in Los Angeles in 2015, he rejoined Duke in 2018 as a cancer researcher.

Everardo is working at the cutting edge of prostate cancer research, said Jiaoti Huang, MD, PhD, professor and chair of the Duke Department of Pathology and member of the Duke Cancer Institute who collaborates with Macias.

His trajectory demonstrates his personal quality, perseverance, determination, and the opportunities this great country affords people of different backgrounds. His story is an inspiration to us all.

From diagnosis to treatment, the prostate cancer journey is fraught with challenges, chief among them is the task of distinguishing between deadly and less severe cases.

Very rarely, prostate cancer starts in neuroendocrine cells. Some prostate cancers become resistant to treatment and turn into neuroendocrine tumors, which are more aggressive and have a poorer outlook.

In 2022, Macias earned a Department of Defense Prostate Cancer Research Program (PCRP) Idea Development Award to pursue new treatments for neuroendocrine tumors. The DOD recently committed to funding Macias research for three more years.

Hes principal investigator of the DOD grant that includes Huang and co-investigators, Ming Chen, PhD, associate professor in pathology; and Jung Wook Park, PhD, assistant professor of pathology.

Macias lab delves into the genetics behind tumor growth, focusing on targets with tangible clinical implications. Through functional genomic screens, he has identified lesser-known protein kinases that are critical to prostate cancer tumor growth.Kinases are high-value targets because they are potentially susceptible to drug treatments.

In lab experiments, Macias and colleagues discovered that blocking NUAK2, a protein kinase prevalent in prostate cancer cells, curtailed neuroendocrine tumor cell growth.

In human cancer samples, NUAK2 gene levels were found to be highest in the lethal neuroendocrine prostate cancer subtype, Macias said. NUAK2 may be a key factor in taking on these tough tumors.

Using his research as a starting point, he collaborates with medicinal chemists and structural biologists to pinpoint pharmacological molecules in cancer cells to target with medicines, aiming for an approach that could save lives from prostate cancer.

In a career backed by major grants and teamwork with top-notch scientists, he ranks mentoring his first graduate student, Amelia Schirmer, PhD, a skilled cancer researcher, as one of his proudest achievements.

"He took a chance on me as his first student, said Schirmer who credits Macias for a productive graduate experience at Duke. I learned a lot and I will always be grateful for Dr. Macias and his mentorship.

Macias is one of nearly 40 Duke faculty mentors in the Duke Preparing Research Scholars in Biomedical Sciences Post-Baccalaureate Research Education Program (PRIME-PREP).

READ MORE: Duke University PRIME-PREP

Additionally, Macias has mentored two undergraduate Duke University students who graduated with first-author publications. The students, Peter Nam and Megan Zhao, are now applying to medical school.

When I joined the Macias lab, I had little idea of what research entailed, (but) Dr. Macias took me under his wing and showed me all that it could be, Zhao said.

He readily spent hours each week sitting with me, drawing diagrams and explaining figures, she said. Not only did he take the time to explain the purpose of each experiment we were doing, but he also trusted me to explore on my own, whether through designing next steps or troubleshooting new lab protocols.

Under his direction, Zhao went from washing glassware and taking inventory to conducting mouse studies and presenting at conferences.

Beyond the tangibles of posters and papers, Dr. Macias taught me that research comes to life in the form of a compelling story, she said. Along the way, he gave me the courage to tell my story as I work towards my dream of becoming a clinician.

The experience of working in the Macias lab for three years was just as enriching for Nam, who said Dr. Macias went out of his way to make me feel like a valued part of the research group. He ensured that I had meaningful experiences that supported my career path, from experiment design to manuscript preparation.

Macias said he has a deep commitment to mentoring aspiring researchers, especially from rural and underrepresented backgrounds, and hes actively involved in graduate admissions, summer research programs, and lab mentoring.

I believe its as simple as having a mentor of similar heritage, or who may have had a comparable upbringing as you, to make seeking guidance in academia much more approachable, he said.

Jamie Botta is a communications strategist for the Department of Pathology at the Duke University School of Medicine.

Photos by Jim Rogalski and Steve Conlon.

Main Photo: Everardo Machias, PhD, assistant professor in the Department of Pathology, assistant research professor in the Department of Cell Biology, and a member of the Duke Cancer Institute.

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From Migrant Farm Worker to Duke Scientist, Everardo Macias ... - Duke University School of Medicine

Spermidine May Improve Egg Health and Fertility – Lifespan.io News

Reporters publishing in Nature Aging have identified a metabolite that appears to restore the age-related loss of quality of egg cells (oocytes) in mice.

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While it was originally found in semen, the metabolite spermidine has been found in many different tissues, including ovaries [1]. This molecule has been found to be involved in the regulation of multiple fundamental aspects of metabolism and aging, reducing inflammation and influencing oxidative stress, genomic stability, mitochondrial maintenance, and proteostasis [2].

Previous work has found that spermidine administration lengthens the lifespan of model organisms and human cells by inducing autophagy [3]. Other work has found that it improves memory [4] and heart function [5] in mice.

As researchers have previously found that other metabolic molecules, such as NMN, have positive effects on ovarian aging [6], this work sets out to discover whether spermidine may also have an impact.

The experimentation began with a comparison of the metabolome, the collection of metabolic biochemicals, in the the ovaries of younger and older mice. The differences were clear and substantial. Pathways related to steroid hormones were substantially upregulated in older animals, while pyrimidines and purines were downregulated, as was amino acid synthesis. Spermidine was also substantially downregulated.

The researchers then tested the effects of spermidine supplementation and found positive results. As expected, the supplement injection increased spermidine levels in ovaries. In older mice, the ovarian follicles are degenerated, but this appeared to have been partially restored through spermidine injection. The oocytes matured more quickly, and they became more receptive to sperm and more likely to be successfully fertilized.

Autophagy, as expected, was positively affected. In particular, mitophagy, the clearing-out of damaged mitochondria, was critical in the positive effects, which included a decrease in reactive oxygen species. Spermidine also had positive effects on other aspects of the metabolome. While spermidine did not restore the various pathways to the levels seen in young mice, it had substantial metabolic effects, including on the Wnt signaling pathway and the circadian rhythm.

The fertility of the mice was directly tested. Mice give birth to litters, and their litter size is affected by aging. Young mice often give birth to fourteen pups at a time, while older mice normally give birth to only three. However, older mice given spermidine gave birth to an average of six.

Chromosomes were also positively affected. The number of chromosomal aberrations and misalignments were significantly decreased by spermidine. This had downstream consequences: in addition to the increased fertilization rate, embryos from mice given spermidine were more likely to successfully divide and grow into pups.

The effects of spermidine are not unique to mice. Oocytes were taken from pigs and exposed to hydrogen peroxide, which led to an increase in reactive oxygen species. Spermidine was found to alleviate this increase, suggesting a potential improvement in fertility.

However, this does not prove that it increases fertility in pigs or humans. Only clinical trials can prove that, and given the long gestation time of people and the need for a sufficiently large trial, it may be some time before this or another supplement can be said to be clinically proven to improve fertility. However, if it does, it may give hope to aging women who want to birth more children.

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[1] Lefvre, P. L., Palin, M. F., & Murphy, B. D. (2011). Polyamines on the reproductive landscape. Endocrine reviews, 32(5), 694-712.

[2] Partridge, L., Fuentealba, M., & Kennedy, B. K. (2020). The quest to slow ageing through drug discovery. Nature Reviews Drug Discovery, 19(8), 513-532.

[3] Eisenberg, T., Knauer, H., Schauer, A., Bttner, S., Ruckenstuhl, C., Carmona-Gutierrez, D., & Madeo, F. (2009). Induction of autophagy by spermidine promotes longevity. Nature cell biology, 11(11), 1305-1314.

[4] Wang, I. F., Guo, B. S., Liu, Y. C., Wu, C. C., Yang, C. H., Tsai, K. J., & Shen, C. K. J. (2012). Autophagy activators rescue and alleviate pathogenesis of a mouse model with proteinopathies of the TAR DNA-binding protein 43. Proceedings of the National Academy of Sciences, 109(37), 15024-15029.

[5] Eisenberg, T., Abdellatif, M., Schroeder, S., Primessnig, U., Stekovic, S., Pendl, T., & Madeo, F. (2016). Cardioprotection and lifespan extension by the natural polyamine spermidine. Nature medicine, 22(12), 1428-1438.

[6] Miao, Y., Chen, J., Gao, Q., & Xiong, B. (2021). Generation and assessment of high-quality mouse oocytes and embryos following nicotinamide mononucleotide administration. STAR protocols, 2(1), 100298.

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Spermidine May Improve Egg Health and Fertility - Lifespan.io News

Molecule discovered that grows bigger and stronger muscles – Earth.com

Over the years, scientists have embarked on anti-aging research to provide drugs and treatments that can slow or reverse aging and treat age-related diseases.Now, scientists at Stanford University have discovered an aging-related protein that can stimulate growth of stronger and larger muscles.

The 15-PGDH protein is the latest discovery by the Stanford scientists, who are working on possible treatments for diminished strength and paralysis due to trauma, heritable neuromuscular diseases, or aging.

Using a mouse model, the researchers injected a 15-PGDH-blocking molecule in older mice. They followed the simulated injuries to the sciatic nerves of the injected mice with treatments.

This led to more prostaglandin E2 (PGE2) production, followed by the growth of stronger and larger muscle fibers in the mice.

By inhibiting the 15-PGDH, also known as gerozyme, the researchers significantly improved the endurance and strength of the muscles grown in the lab.

The researchers found that 15-prostaglandin dehydrogenase (15-PGDH), which accumulates with age and promotes muscle atrophy, markedly increased in denervated mouse myofibers and aggregated in target fibers, hallmarks of chronic nerve damage in human myogenic neuropathies, noted Melissa L. Norton, the editor of the published study.

Treating older mice with chronic muscle denervation with the 15-PGDH inhibitor enhanced the motor neurons and rejuvenated the neuromuscular junctions and function.

This could potentially help older adults who experience increasingly weaker muscles with age and people dealing with muscle-wasting diseases like amyotrophic lateral sclerosis (ALS).

Our data suggests that inhibition of 15-PGDH may constitute a therapeutic strategy to physiologically boost prostaglandin E2, restore neuromuscular connectivity, and promote recovery of strength after acute or chronic denervation due to injury, disease or aging, the researchers noted in their report.

Although this latest study expands on existing evidence of protein regulating muscle function during aging in mice, the researchers have described it as unique.

Study co-author Dr. Helen Blau is the director of the Baxter Laboratory for Stem Cell Biology at Stanford.

This is the first time a drug treatment has been shown to affect both muscle fibers and the motor neurons that stimulate them to contract, speeding up healing and restoring strength and muscle mass, said Dr. Blau.

The Stanford scientists want to build on their findings to see if this mechanism can be transitioned into real-life treatments and therapy.

Our next steps will be to examine whether blocking 15-PGDH function in people with conditions like spinal muscular atrophy, in combination with gene therapy or other treatments, can increase lost muscle strength, said Dr. Blau.

We are also looking at ALS to see if something like this might help these patients. Its really exciting that we are able to affect both muscle function and motor neuron growth.

Weak muscle strength is a huge problem among elders. According to a study by the Centers for Disease Control and Prevention (CDC), five percent of adults aged 60 and over have weak muscle strength, while 13 percent have intermediate muscle strength.

But muscle weakness isnt just a concern for older people. It starts creeping in as early as your 50s and comes with a great economic cost. Weaker muscles reduce the ability to move around, work, and care for oneself. This condition also increases the risk of injuries.

The good news is that science is making promising strides toward addressing this widespread problem. With continued research and advancement, a lasting solution for muscle weakness may be on the horizon.

The study can be found in the journal Science Translational Medicine.

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SGIOY: 3 Biotech Stocks With Potential Future Gains – StockNews.com

The pharmaceutical industry has grown substantially in recent years, and the rising demand and tech integration make its outlook promising. Moreover, the industrys ability to maintain stability despite economic uncertainties makes it an attractive investment destination.

Given the favorable industry backdrop, investors could consider buying quality pharma stocks Shionogi & Co., Ltd. (SGIOY), Exelixis, Inc. (EXEL), and Jazz Pharmaceuticals plc (JAZZ) to beat the market.

The pharmaceutical market is experiencing robust growth driven by innovative drugs and increased healthcare demand, especially in emerging markets. Original prescription drugs dominate the market, with a few blockbuster drugs generating over $1 billion in revenue annually.

The industrys growth is also propelled by innovations like cell and gene therapy, mRNA vaccine technology, improving supply chains, and evolving product offerings. As per Statista, the global pharmaceutical market revenue is projected to reach $1.16 trillion this year.

Additionally, progress in the field of cancer biology and the increasing prevalence of severe diseases make precision medicine indispensable. Moreover, ongoing technological advancements and breakthroughs in cell biology continue to drive the market forward.

The Precision Medicine market is expected to grow from $77.02 billion this year to $99.24 billion by 2028, registering a CAGR of 5.2%.

Furthermore, the pharmaceutical industry increasingly embraces artificial intelligence (AI). Strategic investments in AI partnerships are growing, underlining the importance of AI in pharmaceutical advancements. The pharmaceutical industry is also experiencing growth in generative AI for drug discovery, driven by the availability of extensive datasets and collaborative efforts.

The global generative AI in drug discovery market size is projected to surpass around $1.13 billion by 2032, expanding at a CAGR of 27.1%.

Considering these conducive trends, lets analyze the fundamentals of three Biotech picks, beginning with the third choice.

Stock #3: Shionogi & Co., Ltd. (SGIOY)

Headquartered in Osaka, Japan, SGIOY engages in the research, development, manufacture, and distribution of pharmaceuticals, diagnostic reagents, and medical devices. The companys offerings include Fetroja, a multidrug-resistant bacterial infection treatment; Xofluza, an influenza virus drug; and Tivicay, an anti-HIV drug.

On October 12, 2023, SGIOY presented real-world evidence (RWE) at IDWeek2023, suggesting that the use of Fetroja (cefiderocol) effectively treats Gram-negative infections, particularly in patients who received it earlier (within 6-20 days of diagnosis), resulting in lower in-hospital all-cause mortality (IHACM).

The study highlights the clinical utility of Fetroja in the treatment of challenging Gram-negative infections, addressing a significant health concern related to antimicrobial resistance.

On October 6, SGIOY acquired 1,129,800 shares of its common stock, valued at 7.42 billion ($49.56 million) between September 1, 2023, and September 30, 2023. This acquisition aligns with the boards resolution on July 31, 2023, to acquire up to 12,500,000 shares with a maximum cost of 75 billion ($501.29 million) from August 1, 2023, to March 31, 2024. As of September 30, 2023, SGIOY had acquired 3,052,200 shares valued at 19.43 billion ($129.88 million).

SGIOYs revenue grew 52.2% year-over-year to 109.31 billion ($730.62 million) in the fiscal first quarter that ended June 30, 2023. The companys operating profit rose 274.9% year-over-year to 46.59 billion ($311.40 million).

In addition, profit attributable to owners of the parent rose 22.6% from the prior years quarter to 42.56 billion ($286.61 million), and EPS amounted to 144.57 billion, up 25.6% year-over-year.

SGIOYs revenue for the current fiscal year ending March 2024 is likely to rise 5.3% year-over-year to $2.90 billion. Its EPS is expected to be $0.94 in the same year. Also, it has surpassed the consensus revenue estimates in each of the trailing four quarters, which is remarkable.

The stock has gained 7% over the past three months to close the last trading session at $11.23.

SGIOYs POWR Ratings reflect this promising outlook. The stock has an overall rating of B, equating to a Buy in our proprietary rating system. The POWR Ratings are calculated by considering 118 different factors, with each factor weighted to an optimal degree.

SGIOY has a B for Growth, Value, and Quality. It is ranked #15 in the 359-stock Biotech industry.

In addition to the highlighted POWR Ratings, one can see SGIOYs ratings for Stability, Momentum, and Sentiment here.

Stock #2: Exelixis, Inc. (EXEL)

EXEL explores, develops, and markets novel cancer treatments. The company provides CABOMETYX tablets for advanced renal cell carcinoma patients with previous anti-angiogenic therapy and COMETRIQ capsules for progressive and metastatic medullary thyroid cancer treatment.

On September 12, EXEL and Insilico Medicine, a global clinical-stage biotechnology company powered by generative AI, unveiled an exclusive license agreement, granting EXEL global rights to develop and commercialize ISM3091, a potentially best-in-class small molecule inhibitor of USP1, which has emerged as a synthetic lethal target in the context of BRCA-mutated tumors.

The partnership leverages EXELs clinical development expertise and highlights ISM3091s potential in addressing various BRCA-mutant tumors, including those found in ovarian, prostate, and breast cancer.

On August 24, the Alliance for Clinical Trials in Oncologys independent Data and Safety Monitoring Board (DSMB) unanimously recommended prematurely concluding the phase 3 CABINET pivotal trial due to an exceptional surge in efficacy observed at an interim analysis.

This outcome positions EXEL as an oncology innovator, particularly in addressing advanced pancreatic or extra-pancreatic neuroendocrine tumors where no established standard of care exists post-therapy.

In the second quarter that ended June 30, 2023, EXELs total revenues increased 12% year-over-year to $469.85 million. Its income before income taxes rose 13.4% from the year-ago quarter to $100.39 million. The companys non-GAAP net income and non-GAAP net income per share stood at $100.30 million and $0.31, up 11.8% and 10.7% year-over-year, respectively.

EXEL reaffirms its fiscal year 2023 financial guidance, with expectations of total revenues between $1.78 billion and $1.88 billion. Net product revenues are estimated to fall within the range of $1.58 billion to $1.68 billion, while the cost of goods sold is projected to be 4.0% to 5.0% of net product revenues.

Analysts expect EXELs revenue to increase 14.7% year-over-year to $472.33 million in the fiscal third quarter that ended September 2023. The companys EPS for the to-be-announced quarter is expected to be $0.18. Moreover, EXEL exceeded the consensus revenue and EPS estimates in three of the four trailing quarters.

The stock has gained 36.4% over the past year and 10.4% over the past three months, closing the last trading session at $21.36.

EXELs robust prospects are reflected in its POWR Ratings. The stock has an overall rating of B, which translates to a Buy in our proprietary rating system.

EXEL has an A grade for Value and Quality and a B for Sentiment. It is ranked #11 in the same industry. Click here to access EXELs additional ratings for Growth, Momentum, and Stability.

Stock #1: Jazz Pharmaceuticals plc (JAZZ)

JAZZ identifies, develops, and commercializes pharmaceutical products for unmet medical needs in the United States, Europe, and internationally. The company has a portfolio of products and product candidates focusing on neuroscience, including sleep medicine and movement disorders, and oncology, such as hematologic and solid tumors.

On September 21, JAZZ announced that the European Commission had granted marketing authorization for Enrylaze (JZP458), a recombinant Erwinia asparaginase, for the treatment of acute lymphoblastic leukemia (ALL) and lymphoblastic lymphoma (LBL) in patients who are hypersensitive or have silent inactivation to E. coli-derived asparaginase.

Enrylaze, known as Rylaze in the United States and Canada, is a new Erwinia-derived asparaginase with a safe profile. This approval is significant in ensuring patients can complete their asparaginase treatment regimen for improved outcomes in ALL and LBL.

On August 2, JAZZ announced that it had entered into a Letter of Intent (LOI) with the Pan-Canadian Pharmaceutical Alliance (pCPA) for Rylaze in Canada.

During the fiscal second quarter that ended June 30, 2023, JAZZs total revenues increased 2.6% year-over-year to $957.32 million. Its income from operations rose 84.3% year-over-year to $157.64 million, and non-GAAP net income rose 6.4% year-over-year to $325.13 million.

Moreover, its adjusted earnings per share increased 4.9% from the year-ago quarter to $4.51.

JAZZ anticipates strong performance across key metrics in its non-GAAP financial guidance for 2023. The company expects a gross margin of 93% and SG&A expenses in the range of $1.05 billion to $1.11 billion, representing 27% to 30% of total revenues. Research and development (R&D) expenses are projected to be between $675 million and $725 million, comprising 17% to 19% of total revenues.

Additionally, the company had projected a net income of $1.29 billion to $1.34 billion, resulting in a net income per diluted share between $18.15 and $19.00.

Street expects JAZZs revenue for the quarter that ended September 2023 to increase 3.1% year-over-year to $970.04 million. Its EPS for the same quarter is likely to amount to $4.90.

Shares of JAZZ rose marginally intraday to close the last trading session at $129.12.

Unsurprisingly, JAZZ has an overall rating of A, which translates to a Strong Buy in our proprietary rating system.

It has an A grade for Value and a B for Growth and Quality. It is ranked #3 in the same industry. Click here to access JAZZs Momentum, Stability, and Sentiment ratings.

What To Do Next?

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SGIOY shares were trading at $11.40 per share on Monday morning, up $0.17 (+1.51%). Year-to-date, SGIOY has declined -7.92%, versus a 14.99% rise in the benchmark S&P 500 index during the same period.

Her interest in risky instruments and passion for writing made Kritika an analyst and financial journalist. She earned her bachelor's degree in commerce and is currently pursuing the CFA program. With her fundamental approach, she aims to help investors identify untapped investment opportunities. More...

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SGIOY: 3 Biotech Stocks With Potential Future Gains - StockNews.com