Category Archives: Cell Medicine

Usually contained in the human physique, T cells are assigned the obligation to detect and battle threatening micro organism or viruses. T cells guard and defend our immune system. Most cancers cells are a definite story. Most cancers cells are sneaky. They duplicate and switch throughout the physique in a stealthy technique inflicting points and havoc. Sadly for the immune system, T cells are normally not always able to detect most cancers cells.

Within the earlier, there have been many challenges treating positive types of blood and bone marrow cancers along with leukemia, lymphoma, and quite a few myeloma.

That is the place CAR T-cell treatment can step in and alter the immune system paradigm.

Here is the best way it really works. Step one is to retrieve frequent T cells from the affected individual or a specific donor. The affected individual or donors blood sample goes to a lab. The T cells are then separated from the blood. A singular receptor that binds to positive proteins on most cancers cell surfaces is added to the T cells. This imported receptor is named the chimeric antigen receptor or CAR. These new and improved T cells are administered once more into the physique like a blood transfusion.

As soon as the CAR T cells enter the physique, theyll destroy cancerous cells along with tumors. The excellent news is that these modified CAR T cells will not impact healthful cells. It is a win-win situation.

In 2017, the Moffitt Malignant Hematology & Mobile Remedy program was established in partnership with Memorial Healthcare System. Oncologists now have additional decisions to take care of blood and bone marrow most cancers victims. Medical professionals can also conduct evaluation that will revenue every newly recognized and relapsed blood most cancers victims.

Malignant Hematology & Mobile Remedy at Memorial Healthcare System, located on the campus of Memorial Hospital West, is the one facility in Broward and Palm Seaside counties to provide this array of distinctive corporations and most cancers treatments.

Were at all times trying to present our group probably the most progressive and highest high quality healthcare obtainable anyplace, says Memorial Hospital West CEO Vedner Guerrier, and this development with our companions at Moffitt does that for most cancers sufferers.

CAR T-cell treatment must be considered for a number of kinds of most cancers:

Diffuse large B-cell lymphoma

Mantle cell lymphoma

Acute lymphoblastic leukemia

A number of myeloma

Follicular lymphoma

Remodeled follicular lymphoma

Major mediastinal B cell lymphoma

We see 70-80 new a number of myeloma instances every year and greater than 300 with relapse illness so, whereas not each affected person can be a CAR T candidate, were hoping many extra can be as progress continues, acknowledged Dr. Claudia Paba Prada, an assistant member of Moffitt Malignant Hematology and Mobile Remedy at Memorial Healthcare System. Were utilizing medicine underneath analysis that are not obtainable anyplace else in Florida.

Immunotherapy may be used to supply stem-cell transplants or preserve a higher top quality of life for victims who arent transplant candidates. CAR T-cell treatment can substitute or be used as a complement for chemotherapy. This implies the prospect for a lot much less toxins inside the physique all through most cancers remedy. In the long run new kinds of immunotherapies will help victims win the battle in the direction of most cancers.

For additional data, go to https://www.mhs.web/companies/most cancers/sorts/leukemia-lymphoma.

Content material provided by Memorial Healthcare System

Link:
CAR T-Cell Therapy: The New Way To Fight Cancer - Black Chronicle

video:The video shows the water build-up in the cathode channels during the first 600 s of the fuel cell start-up. The water starts to nucleate on the channel edges and corners. view more

Credit: HZB

"In a fuel cell, hydrogen and oxygen are combined to form water. This produces electrical energy," explains Ralf Ziesche from the imaging group at HZB. "Probably the most important component inside the fuel cell is the membrane." It is only about 20 micrometres thick (half as wide as a human hair) and connected with various functional layers to form a separation area about 600 micrometres wide inside the fuel cell.

"The membrane composite snatches the electrons from the hydrogen atoms. Only the hydrogen nuclei - the protons - can pass through the membrane." The electrons, on the other hand, flow off via an electrical connection and are used as an electric current. Air is let in on the other side of the separating wall. The oxygen it contains reacts with the protons that come through the membrane and the electrons that flow back from the other side of the electric circuit. Pure water is produced.

"Some of the water is discharged. Another part must remain in the fuel cell, because the membrane must not dry out," Ralf Ziesche explains. "But if there is too much water in it, the protons can no longer penetrate the membrane. Dead areas develop at these points, and the reaction can no longer take place there. The efficiency of the entire fuel cell drops." To allow hydrogen, air and water to flow in and out, tiny channels are milled into metal plates on both sides of the membrane. These channels can be used to optimise fuel cells and increase efficiency. Hereby, the channel design is the key for a balanced cell wetting and optimal efficiency.

To do this, it is advantageous to have as accurate a picture as possible of the water distribution within the channels. This was the goal of a collaboration between the research group from the Electrochemical Innovation Lab (EIL) at University College London (UCL) and HZB. "In principle, we subjected the fuel cell to computed tomography, as it is used in medicine," explains Nikolay Kardjilov from the imaging group at HZB. But while X-rays are used for medical analyses, Nikolay Kardjilov and his team preferred to use neutron radiation. "Because X-rays provide far too low an image contrast between hydrogen and water on one side and the metal structure on the other. Neutrons, on the other hand, are ideal here."

This was quite tricky. Because in order to get a three-dimensional image, the radiation source has to go around the object to be imaged. In medicine, this is quite easy to solve. There, the radiation source and scanner rotate around the patient, who is resting on a table. "But our radiation source was the Berlin Experimental Reactor BER II, where we had set up our imaging station CONRAD. And we can't simply rotate it around our fuel cell sample," says Nikolay Kardjilov. But with an engineering trick, his team managed to move the fuel cell, including the supply lines for hydrogen and air, the discharge line for water and the electric cables, into the neutron beam. "Until now, neutron imaging has only been able to produce two-dimensional images from inside the fuel cell. Now, for the very first time, we have also made the water distribution visible in three dimensions and in real time," the physicist is pleased to report. The BER II is shut down since the end of 2019. But the work will be continued as part of the joint research group "NI-Matters" between HZB, the Institut Laue-Langevin (ILL, France) and the University of Grenoble (France).

Kai Drfeld

Nature Communications

Experimental study

Not applicable

High-speed 4D neutron computed tomography for quantifying water dynamics in polymer electrolyte fuel cells

25-Mar-2022

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Read the rest here:
Water distribution in the fuel cell made visible in 4D - EurekAlert

Scientists at the University of Toronto and Sinai Health say they have identified a new way to control the fate of neural stem cells, bringing researchers one step closer to unlocking the mystery of how to repair the brain after injury or stroke.

The findings, published recently in the journalNature Communications, outline a small set of molecules able to keep two major classes of neural stem cells from losing their ability to differentiate into critical components of a mammals cortex, a part of the brain that controls language and information processing.

This discovery is an exciting extension of platform technologies developed by our lab in recent years, which make cell therapy safe and universal with off-the-shelf products to treat degenerative diseases, saidAndras Nagy, who is principal investigator on the study,a professor ofobstetrics and gynaecologyU of Ts Temerty Faculty of Medicine,and a senior investigator at theLunenfeld-Tanenbaum Research Instituteat Sinai Health.

GABAergic and glutamatergic neurons are two major neuronal subtypes in the mammalian forebrain, or cerebral cortex. Both classes develop from cells known as neuroepithelial progenitors and play an early and important role in brain development, but then quickly lose their ability to form other cortical cell types.

To overcome this limitation, scientists in the Nagy lab identified a set of small molecules capable of keeping the progenitor cells growing without losing their developmental potential.

Furthermore, when researchers withdrew that cocktail of molecules from the stem cells, the cells continued to differentiate into cells of the human forebrainin large numbers.

The ability to obtain an unlimited number of forebrain-forming neural epithelium from stem cells is essential for disease modelling and toxicity testing needed in the development of new drugs, said Nagy, who is also affiliated with U of T'sInstitute of Medical Scienceand holds the Canada Research Chair in Stem Cells and Regeneration. These cells could be used in cell therapies, with the potential to treat strokes and other neurological diseases.

Balazs Varga, first author on the paper who developed cell-based therapeutic approaches over the span of a decade for the project, said that understanding the forces orchestrating brain development will help identify underlying causes of diseases, leading to new treatments.

"Our work identified one way we can control the fate of neural stem cells, said Varga, formerly a post-doctoral researcher in the Nagy lab who is now a research associate at Wellcome Trust Medical Research Council Cambridge Stem Cell Institute. Better understanding the behaviour of the neuroepithelial cells will provide us with ideas about how we could control progenitor cell function and brain regeneration.

The research was supported by the Canadian Institutes of Health Research.

Read the original:
Researchers look to unleash the power of stem cells to repair brain injuries - University of Toronto

image:A breast cancer cell captured in the process of division, with tubulin (a structural protein) in red; mitochondria in green; and chromosomes in blue. view more

Credit: Wei QianNational Cancer Institute

Breast cancer and type 2 diabetes would seem to be distinctly different diseases, with commonality only in their commonality. Breast cancer is the second most diagnosed malignancy after some types of skin cancer; approximately 1 in eight U.S. women will develop invasive breast cancer over the course of their lifetime. More than 10 percent of the U.S. population has diabetes, with an estimated 2 in 5 Americans expected to develop the chronic disease during their lifetime.

However, past research has uncovered associations between the two diseases. Women with diabetes, for example, have a 20 to 27 percent increased risk of developing breast cancer. Insulin resistance a key characteristic of diabetes has been associated with breast cancer incidence and poor survival. Population studies suggest diabetes risk begins to increase two years after a breast cancer diagnosis, and by 10 years post-diagnosis, the risk is 20 percent higher in breast cancer survivors than in age-matched women without breast cancer.

But these epidemiological linkages are not clear-cut or definitive, and some studies have found no associations at all. In a new paper, publishing May 30, 2022 in Nature Cell Biology, a research team led by scientists at University of California San Diego School of Medicine describe a possible biological mechanism connecting the two diseases, in which breast cancer suppresses the production of insulin, resulting in diabetes, and the impairment of blood sugar control promotes tumor growth.

No disease is an island because no cell lives alone, said corresponding study author Shizhen Emily Wang, PhD, professor of pathology at UC San Diego School of Medicine. In this study, we describe how breast cancer cells impair the function of pancreatic islets to make them produce less insulin than needed, leading to higher blood glucose levels in breast cancer patients compared to females without cancer.

Wang said the study was inspired by early work and guidance from Jerrold Olefsky, MD, professor of medicine and associate dean for scientific affairs in the Division of Endocrinology and Metabolism at UC San Diego School of Medicine. Olefsky is co-senior author of the study with Wang.

The culprit, according to Wang and Olefsky, are extracellular vesicles (EV) hollow spheres secreted or shed by cells that transport DNA, RNA, proteins, fats and other materials between cells, a sort of cargo communication system.

In this case, the cancer cells were found to be secreting microRNA-122 into the vesicles. Wang said when vesicles reach the pancreas, they can enter the islet cells responsible for insulin production, dispense their miR-122 cargo and damage the islets critical function in maintaining a normal blood glucose level.

Cancer cells have a sweet tooth, Wang said. They use more glucose than healthy cells in order to fuel tumor growth, and this has been the basis for PET scans in cancer detection. By increasing blood glucose that can be easily used by cancer cells, breast tumors make their own favorite food and, meanwhile, deprive this essential nutrient from normal cells.

The research was conducted using mouse models, which found that slow-releasing insulin pellets or a glucose-lowering drug known as an SGLT2 inhibitor restored normal control of glucose in the presence of a breast tumor, which in turn suppressed the tumors growth.

These miR-122 inhibitors, which happen to be the first miRNA-based drugs to enter clinical trials, might have a new use in breast cancer therapy, Wang said.

Co-authors include: Minghui Cao, Roi Isaac, Wei Yan, Xianhui Ruan, Li Jiang, Yuhao Wan, Jessica Wang, Christine Caron, Donald P. Pizzo, Xuxiang Liu, Andrew R. Chin, Miranda Y. Fong, Oluwole Fadare, Richard B. Schwab, Wei Ying and Jack D. Bui, all at UC San Diego; Dorothy D. Sears, Arizona State University; Steven Neben and Denis Drygin, Regulus Therapeutics, Inc., San Diego; Xiwei Wu, Joanne Mortimer, Yuan Yuan and Susan E. Yost, all at City of Hope, Duarte, CA; Ziting Gao, Kaizhu Guo and Wenwan Zhong, all at UC Riverside.

# # #

Nature Cell Biology

30-May-2022

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Read the rest here:
The paired perils of breast cancer and diabetes - EurekAlert

A new study led by Hospital for Special Surgery (HSS) investigators in New York City has found that their computer vision tool effectively distinguishes rheumatoid arthritis (RA) from osteoarthritis (OA) in joint tissue taken from patients who underwent total knee replacement (TKR). The results suggest the machine learning model will help improve research processes in the short term and optimize patient care in the future. The findings were presented today at the European Alliance of Associations for Rheumatology (EULAR) Congress 2022.

TKR is often the only management option for patients with severe knee joint damage. Identifying which disease caused the joint damage is essential for guiding treatment plans, given that RA is a systemic, inflammatory disease that may also affect the eyes or lining around the heart, while OA affects just the joints. We know there are many more immune cells present in the synovium, or joint tissue, of patients with RA compared to those with OA, said Bella Mehta, MBBS, MS, rheumatologist at HSS and lead author of the study. But precisely how many more has not been clear.

Pathologists typically assess images of synovium to determine the extent of inflammation using a combination of approaches, including assigning the level of immune cell infiltration on a scale from 0 to 4, said Dana Orange, MD, MS, rheumatologist at HSS, assistant professor at Rockefeller University and senior author of the study. However, these methods are imperfect. For example, a recent study by HSS investigators found that assessments from two highly experienced pathologists evaluating the infiltration of one type of immune cells known as lymphocytes on the same slides agreed only 67 percent of the time.1

Drs. Orange, Mehta and colleagues at HSS and collaborating institutions developed and validated a computer vision tool that rapidly counts tens of thousands of cell nuclei in whole-slide images of synovium.2 For their present study, they measured 14 different pathologist-scored features in synovium from 60 patients with RA and 147 patients with OA who underwent TKR, and used the computer vision tool to determine cell density.

The investigators identified significant differences between RA and OA features in synovium. The RA samples showed increased cell density; low numbers of mast cells, a type of white blood cell; and lower evidence of fibrosis or scarring compared to the OA samples. The probability of correctly distinguishing between RA and OA in synovium was 85 percent when using the 14 pathologist-scored features alone, 88 percent when using the computers score for cell density alone and 91 percent when the researchers combined the pathologists scores and the computers cell density calculation. The researchers determined a cutoff point for distinguishing RA from OA, determining that synovium containing more than 3,400 cells per mm2 should be classified as RA.

While our innovation is not ready for clinical use yet, it holds promise for assisting pathologists in the future, Dr. Orange said. Right now, we see it as a valuable tool for research purposes because it provides an accurate and 100% reproducible score of inflammation and look forward to developing it further.

Dr. Orange added that in the future computer vision could be trained to glean other types of information from tissue samples, including which types of cells are present and whether they are close enough together that they are likely to be communicating with each other. This more granular assessment might enable clinicians to know more precisely which cells are causing tissue damage and tailor treatments accordingly.

Authors: Bella Mehta, MBBS, MS, Susan M. Goodman, MD, Edward F. DiCarlo, MD, Deanna Jannat-Khah, J. Alex Gibbons, Miguel Otero, PhD, Laura Donlin, PhD (HSS), Tania Pannellini, MD, PhD (Weill Cornell Medicine), William Robinson, MD, PhD (Stanford University), Peter K. Sculco, MD, Mark P. Figgie, MD, Jose A. Rodriguez, MD (HSS), Jessica Kirschmann (Stanford University), James Thompson, David Slater, Damon Frezza (The MITRE Corporation), Zhenxing Xu, Fei Wang, PhD (Weill Cornell Medicine), Dana Orange, MD, MS (HSS and Rockefeller University).

References

1. Orange DE, Agius P, DiCarlo EF, et al. Identification of Three Rheumatoid Arthritis Disease Subtypes by Machine Learning Integration of Synovial Histologic Features and RNA Sequencing Data.Arthritis Rheumatol. 2018;70(5):690-701. doi:10.1002/art.40428

2. Guan S, Mehta B, Slater D, et al. Rheumatoid Arthritis Synovial Inflammation Quantification Using Computer Vision.ACR Open Rheumatol. 2022;4(4):322-331. doi:10.1002/acr2.11381

About HSS

HSS is the worlds leading academic medical center focused on musculoskeletal health. At its core is Hospital for Special Surgery, nationally ranked No. 1 in orthopedics (for the 12th consecutive year), No. 4in rheumatology by U.S. News & World Report (2021-2022), and the best pediatric orthopedic hospital in NY, NJ and CT by U.S. News & World Report Best Childrens Hospitals list (2021-2022).In a survey of medical professionals in more than 20 countries by Newsweek, HSS is ranked world #1 in orthopedics for a second consecutive year (2022). Founded in 1863, the Hospital has the lowest complication and readmission rates in the nation for orthopedics, and among the lowest infection rates. HSS was the first in New York State to receive Magnet Recognition for Excellence in Nursing Service from the American Nurses Credentialing Center five consecutive times. An affiliate of Weill Cornell Medical College, HSS has a main campus in New York City and facilities in New Jersey, Connecticut and in the Long Island and Westchester County regions of New York State, as well as in Florida. In addition to patient care, HSS leads the field in research, innovation and education. The HSS Research Institute comprises 20 laboratories and 300 staff members focused on leading the advancement of musculoskeletal health through prevention of degeneration, tissue repair and tissue regeneration. The HSS Innovation Institute works to realize the potential of new drugs, therapeutics and devices. The HSS Education Institute is a trusted leader in advancing musculoskeletal knowledge and research for physicians, nurses, allied health professionals, academic trainees, and consumers in more than 145 countries. The institution is collaborating with medical centers and other organizations to advance the quality and value of musculoskeletal care and to make world-class HSS care more widely accessible nationally and internationally.www.hss.edu.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Read more:
Computer vision tool improves the ability to distinguish rheumatoid arthritis from osteoarthritis in damaged joint tissue - EurekAlert

Immunotherapy unleashes the power of the immune system to fight cancer. However, for some patients, immunotherapy doesnt work, and new research may help explain why. When immune cells called T lymphocytes infiltrate malignant tumors, the genetic program of those T cells and the developmental path they then follow, may affect their response to immunotherapy and predict overall patient survival, according to a new study by Weill Cornell Medicine investigators. The results overturn the prevailing model of immune responses in melanoma and present different therapeutic approaches.

In the study, published May 9 in Cancer Cell, the investigators analyzed thousands of human tumor samples, plus individual human T cells across many data sets and tumor types, and compared these to many models of T cell behavior in response to infections, cancer and vaccines, including human vaccines. They found that T cells either become stuck in an early activation state or develop into memory cells that are expanded by current immunotherapy approaches.

The T cells dont behave in a singular manner, but we can understand their behavior and model it in a way that can predict patient outcomes and overall survival, said senior author Dr. Niroshana Anandasabapathy, associate professor of dermatology and of dermatology in microbiology and immunology at Weill Cornell Medicine, and a practicing dermatologist for melanoma patients at NewYork-Presbyterian/Weill Cornell Medical Center.

Scientists have long known that the immune system can detect and eliminate tumor cells on its own, but this process sometimes breaks down, leading to the development of cancer. Previous data seemed to support a theory in which, once a tumor is established, T lymphocytes entering the tumor keep seeing and responding to tumor proteins until they become exhausted and unable to attack the cancerous cells. That theory was used to explain the success of a type of therapy called immune checkpoint blockade, which uses cellular signals to improve T cell responses, reawakening the T cells ability to attack and eliminate the tumor.

Some patients tumors dont respond to immune checkpoint blockade, though. To figure out why, the team began looking at larger data sets and analyzing them more broadly than previous studies.

We wanted to take an entirely agnostic approach to trying to understand what happens to a T cell when it enters the tumor microenvironmenta really naive, unbiased approach, said Dr. Anandasabapathy, who is also a member of the Sandra and Edward Meyer Cancer Center and the Englander Institute for Precision Medicine.

By using large programs of many genetic markers and multiple, simultaneous genomic strategies to categorize cell fates, Dr. Anandasabapathy and her collaborators were able to re-classify T cells in tumors, and better model how they develop. The results show that infiltrating T cells dont all meet the same fate in every tumor. In contrast to the standard view, a failure to launch beyond early activation and convert to memory, and not exhaustion appeared to be the problem. The enrichment of long-lived memory programs correlates strongly with overall survival and a successful response to immune checkpoint blockade therapy in melanoma.

In addition to predicting outcomes, the investigators hope to find ways to change them. Getting T cells past their failure to launch and inducing the formation of tumor-infiltrating memory T cells in patients who lack them, for example, could make non-responsive tumors sensitive to immune checkpoint blockade.

While the current work focused on malignant melanoma, the scientists also identified that similar phenomena likely underlie differences in patient T cell responses to other types of cancer, including kidney, bladder, prostate and liver cancer.

The power of the study is really in opening new avenues of discovery and suggesting more rational therapeutics, said first author Abhinav Jaiswal, a doctoral candidate at Weill Cornell Graduate School of Medical Sciences in Dr. Anandasabapathys laboratory.

Many Weill Cornell Medicine physicians and scientists maintain relationships and collaborate with external organizations to foster scientific innovation and provide expert guidance. The institution makes these disclosurespublic to ensure transparency. For this information, see profile for Dr. Niroshana Anandasabapathy.

Read the original post:
T Cell Behavior Determines Which Tumors Respond to Treatment - Weill Cornell Medicine Newsroom

Astrocytes make up almost half of the mammalian brain cells. They are called glial cells because scientists originally thought that these starlight-shaped structures serve as nerve glue.

Research suggests that these cells control the growth of axons, or the neuronal projections that carry electrical impulses.

However, scientists still considered astrocytes to be supporting actors behind neurons, which are the primary cells of the brain and nervous system.

Now, scientists at Tufts University in Massachusetts and other institutions realize that astrocytes may execute a significantly greater performance in brain activity.

Dr. Moritz Armbruster, a research assistant professor of neuroscience at Tufts, led a team of researchers in harnessing novel technology to study astrocyte-neuron exchanges.

To their surprise, the scientists observed electrical activity in astrocyte processes within mouse brain tissue. They reported: This represents a novel class of subcellular astrocyte membrane dynamics and a new form of astrocyteneuron interaction.

Dr. Armbruster and his fellow authors published their findings in Nature Neuroscience.

Using innovative tools, the Tufts team developed a technique to detect and observe electrical activity in brain cell interactions. These properties could not be seen before now.

Dr. Chris Dulla, corresponding author of the study, is an associate professor of neuroscience at the Tufts University School of Medicine and Graduate School of Biomedical Sciences. He explained that he and his colleagues []use viruses to express fluorescent proteins in the mouse brain, and thats what lets us measure this activity.

In an interview with Medical News Today, he elaborated:

[W]e had other experiments that made us think that this new type of activity must be happening in astrocytes. We just didnt have a way to show it[] So, we developed these new techniques to image the activity of the astrocytes and, using them, we showed that this thing that we thought must be happening actually was happening.

Neurotransmitters are chemical messengers that facilitate the transfer of electrical signals between neurons and support the blood-brain barrier. Scientists have long understood that astrocytes control these substances to support neuronal health.

This study breaks ground in showing that neurons release potassium ions, which change the astrocytes electrical activity. This modulation affects how the astrocytes control neurotransmitters.

Until now, scientists could not image potassium activity in the brain.

Neurons and astrocytes talk with each other in a way that has not been known about before, Dr. Dulla said.

Dr. Dulla maintains that human brain cells work the same way as mouse tissue. He said that mouse and human brain cells use the same proteins and molecules involved in brain activity.

Besides, using human tissue samples presents ethical challenges, Dr. Dulla noted: [We] have to be really careful and judicious [] with the experiments we design, and [we] dont get a chance to see [human tissue] samples like [we] can do with mice.

However, the professor shared that extensive databases give [scientists] a chance to just access human brain tissue without doing an experiment [themselves], but just getting the data that someone else has already done.

This wealth of information further demonstrates similarities between human and mouse cells and lets researchers deduce that the same processes are happening in each. The main difference is that human cells are larger and more abundant.

He also pointed out that the study highlights a bidirectional relationship between these brain cells, as astrocytes influence the neurons as well.

These findings about astrocyte-neuron interactions open a new world of questions regarding brain pathology, memory, and learning.

MNT also discussed this study with Dr. Santosh Kesari, who was not involved in this research. He is a neurologist at Providence Saint Johns Health Center in Santa Monica, CA, and regional medical director for the Research Clinical Institute of Providence Southern California.

Dr. Kesari said that this study confirms earlier research.

[T]his is one of many studies thats showing increasingly, how astrocytes and neurons interact, how they affect each other and then connecting the dots to how that affects brain function behavior, memory, seizures, dementia, and even in the context of brain tumors, all these cells interact. Dr. Santosh Kesari

Most medication development for brain disorders currently targets neurons. Dr. Kesari agreed that this study might shine light on a new path.

Maybe we should really be understanding the astrocyte side of things to develop drugs that may impact brain health by looking at that astrocytic role in brain disorders, he said.

The ability to image cell processes, as in this study, makes it possible to explore other activities within the brain as well.

The researchers are also screening existing drugs in hopes of manipulating astrocyte-neuron processes. Scientists could come close to repairing brain injuries or helping people increase their learning capacity if this proves successful.

They are also making their tools available to other labs to explore more areas of interest, such as breathing, headache, and many other neurological disorders.

Visit link:
Researchers find new function performed by almost half of brain cells - Medical News Today

DUBLIN--(BUSINESS WIRE)--The "Regenerative Medicine Market by Product Type, Material, Application and End user (Hospitals, Ambulatory Surgical Centers, and Others: Global Opportunity Analysis and Industry Forecast, 2021-2030" report has been added to ResearchAndMarkets.com's offering.

The regenerative medicine market size was valued at $10,107.32 million in 2020, and is estimated to reach $83,196.72 million by 2030, growing at a CAGR of 23.4% from 2021 to 2030.

Regenerative medicine is a process of replacing human cells, tissues or organs to restore or establish normal function. It is field that brings together experts in biology, chemistry, genetics and medicine. This is a promising field which working to restore structure and function of damaged tissues and organs.

It includes cell therapy involves the use of cellular materials such as stem cells, autologous cells, xenogeneic cells, and others, for the therapeutic treatment of patients. Cell therapy is used to replace damaged cells, deliver therapies to target tissues/organs, stimulate self-healing, and various other applications in regenerative medicine.

The major factors boosting the regenerative medicine market growth include technological advancements in tissue and organ regeneration, increase in prevalence of chronic diseases and trauma emergencies, prominent potential of nanotechnology, and emergence of stem cell technology.

In addition, increase in incidence of degenerative diseases and shortage of organs for transplantation are expected to boost the growth of the market. The prominent potential of regenerative medicine to replace, repair, and regenerate damaged tissues and organs has fueled the market growth. In addition, technological advancements in regenerative medicine production and advancement in the stem cell therapy procedures propel the growth of the market.

Rise in prevalence of musculoskeletal diseases and increase in dermatological treatments propel the growth of the market. Moreover, utilization of nanomaterial's in wound care, drug delivery, and immunomodulation has opened growth avenues for the regenerative medicine market.

However, stringent regulations, operational inefficiency, and high cost of regenerative medicine treatment are key factors that hinder the market growth. Furthermore, advancements in stem cell technology and increase in R&D activities in the emerging economies are expected to fuel the market growth during the forecast period. Developed nations have adopted technological advancements in tissue engineering and regenerative medicine sectors, which help in the expansion of the global market.

Moreover, rise in development of pharmaceutical and medical device industries and improvement in healthcare spending are anticipated to drive the growth of the regenerative medicine market. In addition, increase in demand for regenerative medicine led to development of innovative technologies in the healthcare sector, thereby propelling growth of the market.

Moreover, initiatives taken by governments for development of advanced stem cell therapies and development of the healthcare sector for manufacturing of regenerative medicine are the key factors that boost growth of the market. Furthermore, surge in geriatric population, who are more vulnerable to chronic disease, propels the market growth.

KEY MARKET PLAYERS

KEY MARKET SEGMENTS

By Product Type

By Material

By Application

By End User

By Region

For more information about this report visit https://www.researchandmarkets.com/r/qek5u

See the rest here:
$83 Bn Regenerative Medicine Markets - Global Opportunity Analysis and Industry Forecast, 2021-2022 & 2030 - ResearchAndMarkets.com - Business...

A second line of defense the immune systems T cells may offer protection from COVID-19 even when vaccine-induced antibodies no longer can, according to new research out of the University of Wisconsin School of Veterinary Medicine.

The researchers discovered that a new, protein-based vaccine against the original version of the COVID-19 virus was able to teach mouse T cells how to recognize and kill cells infected with new, mutated versions of the virus. This T cell protection worked even when antibodies lost their ability to recognize and neutralize mutated SARS-CoV-2, the virus that causes COVID-19.

Marulasiddappa Suresh

Antibodies prevent COVID-19 infection, but if new variants escape these antibodies, T cells are there to provide a second line of protection, explains lead scientist Marulasiddappa Suresh, a professor of immunology and associate dean for research at the School of Veterinary Medicine.

The study, published in the Proceedings of the National Academy of Sciences on May 13, investigates the role of T cells, a specialized type of white blood cell, in defending against COVID-19 when antibodies fail.

When you receive a COVID-19 vaccine, your body learns to produce antibodies, proteins in the immune system that bind to and neutralize SARS-CoV-2. These antibodies circulate in the blood stream and protect you from illness by patrolling the nostrils, airways and lungs and wiping out the virus before it can cause infection or disease.

However, as SARS-CoV-2 mutates, these highly specific antibodies are less able to recognize new viral variants especially if the changes occur on the viruss spike protein, where the vaccines antibodies bind. This was especially apparent during the recent wave of the SARS-CoV-2 omicron variant, which has a staggering 37 mutations on its spike protein, making it more able to evade antibodies targeting the original viruss spike protein.

The biggest problem right now is that none of our current COVID-19 vaccines give complete protection against infection from emerging variants, especially the omicron sublineages BA.1 and BA.2, Suresh says.

Thats where T cells can help. Killer T cells aid the immune system by hunting and eliminating virus factories infected cells, says Suresh. So, when antibodies cannot neutralize the virus prior to infection, T cells can clear it quickly, causing mild or no noticeable symptoms.

With this information in hand, the UWMadison research team, co-led by Suresh and professor of pathobiological sciences Jorge Osorio and assisted by scientist Brock Kingstad-Bakke and doctoral student Woojong Lee, explored how T cells and antibodies can work to prevent COVID-19 infection altogether.

Brock Kingstad-Bakke, a scientist in the UW School of Veterinary Medicine. Photo courtesy of the School of Veterinary Medicine

The researchers developed an experimental protein-based vaccine containing the unmutated version of the spike protein from the original SARS-CoV-2 virus. This vaccine was also designed to elicit a strong T cell response to the viral spike protein, allowing the lab to test the extent to which T cells can protect against COVID-19 infection in the presence and absence of virus neutralizing antibodies.

After injecting mice models with their vaccine, researchers then exposed them to two SARS-CoV-2 variants and tested their susceptibility to infection under different conditions.

While vaccine-stimulated antibodies were unable to neutralize the mutated SARS-CoV-2 variants, mice were still immune to COVID-19 caused by the mutated viruses, due to action by T cells that were induced by the vaccine.

Unlike antibodies, T cells are able to detect unfamiliar strains of virus because the viral fragment that they recognize does not change considerably from one variant to the next.

This work has important implications for future T cell-based vaccines that could provide broad protection against emerging SARS-CoV-2 variants. The experimental vaccine is protein-based and designed to evoke a strong T cell response, differentiating it from currently available mRNA vaccines.

Now, the Suresh lab is studying how exactly T cells defend against SARS-CoV-2 and whether commercially available COVID-19 vaccines may induce these same mechanisms of T cell immunity to protect against emerging variants when the virus dodges established antibodies.

I see the next generation of vaccines being able to provide immunity to current and future COVID-19 variants by stimulating both broadly-neutralizing antibodies and T cell immunity, Suresh says.

This work was supported in part by the National Institutes of Health (grants U01 AI124299, R21 AI149793-01A1).

Go here to see the original:
Experimental COVID-19 vaccine provides mutation-resistant T cell protection in mice - University of Wisconsin-Madison

Dr. Melody Zeng, an assistant professor of immunology in pediatrics and a member of the Gale and Ira Drukier Institute for Childrens Research at Weill Cornell Medicine, has received a 2021 Hartwell Individual Biomedical Research Award from The Hartwell Foundation. The award provides support for three years at $100,000 direct cost per year and designation as a Hartwell Investigator.

Dr. Zengs award will support her research into the connection between gut bacteria in infants and an increased risk of developing autism spectrum disorder (ASD) after exposure to maternal antidepressants. The incidence of ASD continues to rise, with the latest estimates showing about 1 in 44 children have been identified with ASD by the age of eight years, according to the Centers for Disease Control and Prevention. ASD causes differences in the brain and typically begins before the age of 3. Patients experience a wide variety and severity of symptoms, which may include problems with social interaction and communication, repetitive behaviors, different ways of moving or paying attention and intellectual disability.

I am excited and honored to receive a Hartwell Award, as it will be instrumental in advancing my early-stage research, Dr. Zeng said. Ultimately, I hope new understandings of the link between gut bacteria and an increased risk of ASD in infants exposed to maternal antidepressants may help us identify potential treatment targets for reversing the adverse effects and lowering the risk for children.

Scientists believe multiple factors contribute to the development of ASD. Recent studies have found a link between gut bacteria and ASD onset, but the underlying mechanisms are not well understood. Evidence has shown that more than 25 percent of children identified with ASD have high blood levels of serotonin, a chemical transmitter produced by gut bacteria in the intestine that plays a role insignal transmission between nerve cells throughout the brain and body. Previously, serotonin production processes were assumed to be the same in adults and babies. Dr. Zeng is among the first researchers to show that babies have much higher serotonin levels in their stool during early developmental stages than adults.

Antidepressants aim to alleviate depression and anxiety by raising serotonin levels in the brain. Their use has greatly increased during pregnancy over the last few decades, and there appears to be a link to ASD. Reports show that infants of mothers who took antidepressants during pregnancy or while breastfeeding had a 60 percent greater risk of developing ASD than infants whose mothers did not take the medications.

Based on our preliminary findings, we think that maternal antidepressant use during pregnancy and breastfeeding may alter the levels of serotonin in infants, potentially leading to brain inflammation and an increased risk of ASD onset, said Dr. Zeng. She and her team will investigate how gut bacteria control serotonin production processes using human infant stool samples and mouse models of maternal antidepressant use. Dr. Zeng has been building a biobank of human neonatal stool samples from infants admitted to the Neonatal Intensive Care Unit or the Well-Baby Nursery at NewYork-Presbyterian/Weill Cornell Medical Center in collaboration with Dr. Jeffrey Perlman, professor of pediatrics at Weill Cornell Medicine. Dr. Zeng is also collaborating with Dr. Virginia Pascual, the Drukier Director of the Drukier Institute for Childrens Health at Weill Cornell Medicine, on using single-cell RNA sequencing to analyze immune cells in the brains of mice transplanted with stool bacteria from infants that have and have not been exposed to maternal antidepressants.

The Hartwell Foundation has funded early-stage biomedical research with the potential to benefit children in the United States since 2006. Hartwell Individual Biomedical Research Awards are awarded annually to a limited number of researchers conducting early-stage, cutting-edge research with the potential to benefit the health of American children and have not yet been funded by other sources. Dr. Zeng is one of 10 awardees selected from eight institutions by the Hartwell Foundation in 2021.

Dr. Zengs Individual Biomedical Research Award qualifies Weill Cornell Medicine to designate a Hartwell Fellowship to fund one postdoctoral candidate in an early stage of their career. The fellowship funded by The Hartwell Foundation provides $50,000 direct cost per year for two years in support of specialized training in biomedical research.

Continue reading here:
Dr. Melody Zeng Receives a Hartwell Foundation Individual Biomedical Research Award - Weill Cornell Medicine Newsroom