StemCell Therapy

VALENCIA, Calif. and MELBOURNE, Australia, Aug. 17, 2022 (GLOBE NEWSWIRE) -- AVITA Medical, Inc. (NASDAQ: RCEL, ASX: AVH), a regenerative medicine company that is developing and commercializing a technology platform that enables point-of-care autologous skin restoration for multiple unmet needs, announced today that a poster presentation on cell characterization and potential clinical benefits of the RECELL Autologous Cell Suspension System (RECELL System) for the treatment of stable vitiligo will be shared at the Controversies and Conversations in Laser & Cosmetic Surgery Annual Meeting. The conference will be held in Santa Barbara, CA, on August 19-21 bringing experts together to discuss controversial issues in cutaneous and aesethetic surgery or challenging therapeutic problems within dermatology.

Given the unique format of this meeting, we look forward to the presentation of RECELL and, more importantly, the conversation amongst dermatology experts as they discuss the unique attributes of this platform, including the potential for in-office point-of-care treatment in about 30 minutes, said Dr. Mike Perry, Chief Executive Officer of AVITA Medical. Following review by the FDA, we believe the RECELL System may well offer a welcome treatment option for patients seeking repigmentation for stable vitiligo lesions.

RECELL System Presentations

In the U.S., the RECELLSystem is indicated for the treatment of acute thermal burn wounds in patients 18 years of age and older or application in combination with meshed autografting for acute full-thickness thermal burn wounds in pediatric and adult patients. Physician-initiated research beyond the FDA approved indicationis not sponsored by AVITA Medicaland contains independentdata.

AVITA Medical is currently completing a pivotal trial for the use of the RECELL System for treatment of stable vitiligo. The vitiligo clinical trial aims to demonstrate safe and effective repigmentation when using the RECELL System in combination with phototherapy. AVITA anticipates FDA approval in 2023.

ABOUT AVITA MEDICAL, INC.

AVITA Medical, Inc. is a regenerative medicine company with a technology platform positioned to address unmet medical needs in burns, chronic wounds, and aesthetics indications. AVITA Medical Inc.s patented, and proprietary collection and application technology provides innovative treatment solutions derived from the regenerative properties of a patients own skin. The Companys lead product is the RECELL System, a device that enables healthcare professionals to Spray-On Skin Cells using a small sample of the patients own skin to create an autologous suspension. The RES Regenerative Epidermal Suspension is then sprayed onto the areas of the patient requiring treatment to regenerate natural healthy epidermis.

AVITA Medicals first U.S. product, the RECELL System, was approved by the U.S. Food and Drug Administration (FDA) in September 2018. The RECELL System is approved for acute partial-thickness thermal burn wounds in patients 18 years of age and older or application in combination with meshed autografting for acute full-thickness thermal burn wounds in pediatric and adult patients. In February 2022, the FDA reviewed and approved the PMA supplement for RECELL Autologous Cell Harvesting Device, an enhanced RECELL System aimed at providing clinicians a more efficient user experience and simplified workflow.

The RECELL System is used to prepare Spray-On Skin Cells using a small amount of a patients own skin, providing a new way to treat severe burns, while significantly reducing the amount of donor skin required. The RECELL System is designed to be used at the point of care alone or in combination with autografts depending on the depth of the burn injury. Compelling data from randomized, controlled clinical trials conducted at major U.S. burn centers and real-world use in more than 15,000 patients globally, reinforce that the RECELL System is a significant advancement over the current standard of care for burn patients and offers benefits in clinical outcomes and cost savings. Healthcare professionals should read the INSTRUCTIONS FOR USE - RECELL Autologous Cell Harvesting Device ( https://recellsystem.com/ ) for a full description of indications for use and important safety information including contraindications, warnings, and precautions.

In international markets, our products are approved under the RECELL System brand to promote skin healing in a wide range of applications including burns, chronic wounds, and aesthetics. The RECELL System is TGA-registered in Australia, received CE-mark approval in Europe, and received Japans Pharmaceuticals and Medical Devices Act (PMDA) approval for burns in Japan.

CAUTIONARY NOTE REGARDING FORWARD-LOOKING STATEMENTS

This press release includes forward-looking statements. These forward-looking statements generally can be identified by the use of words such as anticipate, expect, intend, could, may, will, believe, estimate, look forward, forecast, goal, target, project, continue, outlook, guidance, future, other words of similar meaning and the use of future dates. Forward-looking statements in this press release include, but are not limited to, statements concerning, among other things, our ongoing clinical trials and product development activities, regulatory approval of our products, the potential for future growth in our business, and our ability to achieve our key strategic, operational, and financial goal. Forward-looking statements by their nature address matters that are, to different degrees, uncertain. Each forward-looking statement contained in this press release is subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statement. Applicable risks and uncertainties include, among others, the timing and realization of regulatory approvals of our products; physician acceptance, endorsement, and use of our products; failure to achieve the anticipated benefits from approval of our products; the effect of regulatory actions; product liability claims; risks associated with international operations and expansion; and other business effects, including the effects of industry, economic or political conditions outside of the companys control. Investors should not place considerable reliance on the forward-looking statements contained in this press release. Investors are encouraged to read our publicly available filings for a discussion of these and other risks and uncertainties. The forward-looking statements in this press release speak only as of the date of this release, and we undertake no obligation to update or revise any of these statements.

This press release was authorized by the review committee of AVITA Medical, Inc.

FOR FURTHER INFORMATION:

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RECELL System Data to be Presented at the Controversies and Conversations in Laser & ... - The Bakersfield Californian

PRINCETON, N.J., Aug. 16, 2022 (GLOBE NEWSWIRE) -- Integra LifeSciences Holdings Corporation (NASDAQ:IART), a leading global medical technology company, today announced that Dr. Richard Caruso, founder and former chairman and CEO of Integra LifeSciences passed away over the past weekend.

Dr. Richard Caruso made an impact on not only the medical technology industry, but more importantly, on the countless lives around the world who have benefited from the products and technologies that Integra LifeSciences has today, said Stuart Essig, chairman of the board at Integra LifeSciences. His vision, transformative ideas and entrepreneurial spirit have revolutionized the way surgeons treat their patients in the field of regenerative medicine.

Dr. Caruso founded Integra LifeSciences in 1989 with a vision that the human body could be enabled to regenerate many of its own damaged or diseased tissues, paving the way for a new discipline back then known as regenerative medicine. Through his vision, Integra became the first company to develop and bring to market a tissue regeneration product, Integra Dermal Regeneration Template, which was approved by the FDA in 1996 as a skin replacement system with a claim for regeneration of dermal tissue for the treatment of life-threatening burns and repair of scar contractures. That technology led to the development of DuraGen Dural Graft Matrix, for repair of the dura mater, the protective covering of the brain after cranial and spine surgery, and NeuraGen Nerve Guide, which creates a conduit for axonal growth across a severed nerve.

Dr. Caruso served as Integra's chairman from 1992 until 2011, and served as CEO from 1992 to 1997. In addition, he served on the Board of Susquehanna University and the Baum School of Art. Dr. Caruso received his B.S. degree from Susquehanna University, an M.S.B.A. degree from Bucknell University, and a Ph.D. degree from the London School of Economics, University of London. He was also the founder and director of The Uncommon Individual Foundation, a non-profit foundation that encourages individuals to form and follow their dreams of personal success and become the entrepreneurs of their personal lives.

About Integra LifeSciencesIntegra LifeSciences is a global leader in regenerative tissue technologies and neurosurgical solutions dedicated to limiting uncertainty for clinicians so they can focus on providing the best patient care. Integra offers a comprehensive portfolio of high quality, leadership brands that include AmnioExcel, Aurora, Bactiseal,BioD, CerebroFlo, CereLinkCertasPlus, Codman, CUSA, Cytal, DuraGen, DuraSeal, Gentrix, ICP Express, Integra, Licox, MAYFIELD, MediHoney, MicroFrance, MicroMatrix, NeuraGen, NeuraWrap, PriMatrix, SurgiMend, TCC-EZand VersaTru. For the latest news and information about Integra and its products, please visitwww.integralife.com.

Investor Relations Contact:Chris Ward(609) 772-7736chris.ward@integralife.com

Media Contact:Laurene Isip(609) 208-8121laurene.isip@integralife.com

A photo accompanying this announcement is available at https://www.globenewswire.com/NewsRoom/AttachmentNg/fe4238dd-d2f8-487f-8f14-19e855e9b041.

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Integra LifeSciences Announces the Passing of Dr. Richard Caruso, Founder and Former Chairman and CEO - GlobeNewswire

Under-resourced high school students need to be familiarized with multiple components of research in order to give back to their communities, said Dolores Caffey Fleming, MS, MPH.

Fleming is the director of Project STRIDE (Students Training in Research Involving Disparity Elimination), Project STRIDE II, and Project ExSTRM (Exposing Students To Regenerative Medicine).

The STRIDE programs are funded by the Doris Duke Charitable Foundation while the ExSTRM program is funded by the California Institute of Regenerative Medicine (CIRM). According to Fleming, the goal of all the programs is to allow students to be exposed to research and various healthcare careers in order for them to give back to their communities.

This year, these programs were sort of combined as a lot of the activities that they did were interconnected. These research programs for high schoolers at Charles R. Drew University (CDU) have been consistently supported by Jay Vadgama, Ph.D., the Vice President for Research and Health Affairs (CDU), and have continued to operate for the past several years

Before actually going onto campus, we had to do CITI (Collaborative Institutional Training Initiative) training before we entered any labs or facilities. We took seven courses ranging from Biosafety for Researchers to Good Clinical Practice. After finishing, I had a virtual introduction with my mentor, Dr. Juanita Booker-Vaughns, and we talked about potential project ideas and her experience in research.

For the first week, Elizabeth Delgado, a project coordinator, taught us and administered quizzes from the university about lab safety, chemical hazards, and the Code of Conduct. The next week, I personally got to shadow some professionals in the Cancer Division lab and was able to watch them perform procedures like the Western Blot Test and Polymerase Chain Reactions (PCR). Although this was not related to my project, it was cool to learn and observe an important procedure. Many Tuesdays and Thursdays were also reserved for leadership training and resume-building classes.

A Polymerase Chain Reaction, or PCR. (Photo by Shaun Thomas)

My research project was centered around examining colorectal cancer (CRC) risk factors in a specific area of Los Angeles County known as Service Planning Area (SPA) 6. With my mentors help, we looked at public health data about all these risk factors in SPA 6, as opposed to L.A. County as a whole.

I first conducted literature about colorectal cancer risk factors in general ranging from biological factors like Inflammatory Bowel Disease (IBD) to behavioral health factors like diet. After that, using the data from the Key Indicators of Health Report (2017) by Los Angeles Countys Department of Public Health, I created graphs and analyzed the data. To put everything together, I created a poster showcasing my findings.

I had the chance to interview one student from each of the three cohorts.

I first interviewed Ivan Ixtlilco, a Project STRIDE senior at King Drew Magnet High School, whose project was about how urban ecology affects epigenetics and how this, in turn, increases the risk of cardiovascular disease, he said. He added on about how his mentor introduced him to a whole variety of careers in research that he had no idea about.

Afia Ahmed, a Project STRIDE II rising second-year student at UC Irvine said, Project STRIDE allowed [her] to gain a foundation for building a whole manuscript, skimming through articles for crucial information. She said these skills were beneficial for her public health classes at UCI.

She also pointed out some key differences between the two. Now that she is doing STRIDE II, she mentioned doing a manuscript and going more into depth with her research on the mental health of Asian American females who are infertile in order to build an abstract and submit her abstract to conferences. She noted that there was a significant literature gap between Asian American female infertility and female infertility in general.

Ricardo Rodriguez, an ExSTRM senior at St. John Bosco High School, focused on a project that involved more lab work: ancestry-specific expression of stem-like markers in breast cancer cells. He believes stem cells are the future of research and can even be key to processes like regeneration. However, he also believes that governments will decide the fate of using this research. He had the opportunity to present his poster at the CIRM SPARK conference which took place on August 3 in Oakland, Calif.

Shaun Thomas with Dr. Jay Vadgama at the symposium. (Photo courtesy of Shaun Thomas)

The climax of the program was the Charles Drew Symposium which took place on August 5. At the symposium, some of us were chosen to present our projects in front of guests, university faculty, and all of our mentors. After the presentations, we all presented our posters in a gallery. The two-hour event showcased the culmination of our work over.

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Column: My summer research experience at Charles R. Drew University for Medicine and Science - Los Angeles Times

NEW YORK Tessa Therapeutics said on Wednesday that it has dosed the first lymphoma patient in a Phase Ib trial of its investigational CAR T-cell therapy TT11 plus Bristol Myers Squibb's Opdivo (nivolumab).

The trial, dubbed ACTION, is designed to evaluate the autologous CD30-directed CAR T-cell therapy plus the PD-1 inhibitor as second-line treatment for up to 14 patients with CD30-positive relapsed or refractory classical Hodgkin lymphoma after chemotherapy.

Singapore-based Tessa Therapeutics is calling the treatment regimen evaluated in the trial a "sandwich" design. Patients enrolled in the trial will receive two cycles of Opdivo followed by a lymphodepleting chemotherapy regimen, then a single infusion of the autologous TT11 CAR T-cell therapy, then another two cycles of Opdivo. The primary goal of the trial is to evaluate the treatment's safety and tolerability, and secondary aims include overall response rate, duration of response, and progression-free survival.

Tessa is also evaluating TT11 as a monotherapy for CD30-positive relapsed or refractory classical Hodgkin lymphoma in the Phase II CHARIOT trial. Initial data from that study showed that the cell therapy had a favorable safety profile and promising efficacy, with a 57.1 percent complete response rate and a 71.4 percent overall response rate among 14 patients. Tessa expects to begin the pivotal Phase II portion of that trial later this year.

"We welcome the opportunity to capitalize on this clinical progress by investigating TT11 as a second-line combination therapy, which offers the opportunity to greatly increase the patient population who could potentially benefit from this course of care," John Ng, chief technology officer and acting CEO of Tessa, said in a statement.

The firm believes that combining the CAR T-cell therapy with Opdivo will improve its efficacy and offer classical Hodgkin lymphoma patients a second-line treatment option that is more tolerable than chemotherapy. The US Food and Drug Administration has designated TT11 a regenerative medicine advanced therapy and the European Medicines Agency has designated it a priority medicine.

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Tessa Therapeutics Starts Trial of CAR T-Cell Therapy, BMS's Opdivo in Classical Hodgkin Lymphoma - Precision Oncology News

This includes the analogous nature of articular cartilage, muscle fascia, and intervertebral disc confirmed by way of comparative Scanning Electron Microscope analysis

PENSACOLA, Fla., Aug. 15, 2022 /PRNewswire/ -- Regenative Labs, a leading HCT/P manufacturer, has co-authored a pioneering papertogether with experts from The Institute of Regenative Medicine and the Department of Pharmacology and Chemical Biology, Baylor College of Medicine.

"This paper is a market disruptorand will be our most significant paper released to date. This is the first literature thatwe are aware of to utilize Scanning Electron Microscope (SEM) images of actual tissue samples to objectively demonstrate on a qualitative and quantitative basis that collagen structural tissuematrices in our post-processed Wharton's Jelly allografts and those in articular cartilage, muscle fascia, and intervertebral discs are analogous," said Regenative Labs CEO, Tyler Barrett.

This research highlights our commitment to the Regenerative Medicine community. We believe the combination of our IRB-approved observational studies, peer-reviewed publications, ISO-certified laboratory processes, and our commitment to compliance with FDA and American Association of Tissue Banks (AATB) standards, sets the standard for HCT/P manufacturers. Regenative Labs has pioneered the use of perinatal tissue allografts and is pleased that this paper supports our current homologous use practices, consistent with our 361 status.

Currently, the treatments for the Intervertebral Disc (DDD) range in cost and effectiveness from an $8 bottle of Ibuprofen to $150,000 for spinal fusion (1). Neither of these treatment options target the foundational issue of ECM cartilage breakdown in the intervertebral discs. By age 35, 30% of people show signs of DDD; by age 60, this increases to 90% (2). That we are aware of, this is the first perinatal tissue allograft in the medical marketplace that may be applied in a homologous fashion per FDA 361 guidelines to replace or supplement missing or damaged connective tissue. All other non-surgical paradigms focus on symptom management and do not address the disc's collagen structural degeneration. In collaboration with medical providers across the country, we are actively investigating additional homologous use applications for this technology in tissue defects associated with the load-bearing joints of the knee, hip, shoulder, spine, ankle, and foot.

Billions of dollars are spent annually on the surgical care and treatment of patients suffering from degeneration of load-bearing joints and intravertebral discs. We are honored to offer patients evidence-based and structural tissue defect-specific non-surgical applications on a global scale.

Additional Sources:

About Regenative Labs: Regenative Labs produces regenerative medicine products to address the root cause of a patient's conditions using Wharton's Jelly innovations rather than masking the pain with other treatments. Regenative Labs works closely with scientists, physicians, hospitals, and surgery centers to constantly monitor and improve patient progress and outcomes for new product development. Formed by veteran industry professionals familiar with daily challenges of innovations in healthcare, the company providesnon-addictive, non-invasive options for patients. Regenative Labs's expert product research and development team compliesFDA guidelines of minimal manipulation for homologous use. The company adheres to AATB and FDA guidelines. Learn more at Regenative's website: http://www.regenativelabs.com

SOURCE Regenative Labs

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Regenative Labs announces groundbreaking Wharton's Jelly research demonstrating HCT/P compliance after processing - PR Newswire

Each year, Baylor College of Medicine faculty are recognized for their outstanding published scientific contributions to clinical and basic science research over the past three years through the Michael E. DeBakey M.D. Award for Excellence in Research.

This years 2022 recipients are Dr. Peter Hotez and Dr. Maria Elena Bottazzi (joint awardees), Dr. Joseph Hyser, Dr. Katherine King, Dr. Irina Larina, Dr. Scott A. LeMaire and Dr. Ying Shen (joint awardees) and Dr. Sundeep Keswani.

Each year we celebrate and honor researchers from our Baylor community who have made significant contributions to improving healthcare, said Dr. Paul Klotman, Baylor president, CEO and executive dean. These awards celebrate the legacy of innovation in research and medicine set forth by Dr. DeBakey.

The awards, named in honor of pioneering heart surgeon Dr. Michael E. DeBakey, the first president of Baylor College of Medicine, and sponsored by the DeBakey Medical Foundation, include a commemorative medallion and funds to support further research.

The eight researchers were recognized and presented their work at a small in-person ceremony on Wednesday, Aug. 17.

It is an honor to recognize this group. They represent the continued work here at Baylor to improve health and humanity and each researcher demonstrates the impact to science and the community, said Dr. Mary Dickinson, senior vice president and dean of research at Baylor.

Dr. Maria Elena BottazziAssociate dean of the National School for Tropical Medicine at Baylor College of Medicine and co-director of the Texas Children's Hospital Center for Vaccine Development

Dr. Bottazzi is an internationally recognized tropical and emerging disease vaccinologist, global health advocate and co-creator of a patent-free, open science COVID-19 vaccine technology that led to the development of Corbevax, a COVID-19 vaccine for the world. She pioneers and leads the advancement of a robust infectious and tropical disease vaccine portfolio tackling diseases such as coronavirus, hookworm, schistosomiasis and Chagas that disproportionally affect the worlds poorest populations. She also has established innovative partnerships in Latin America, the Middle East and Southeast Asia, making significant contributions to innovative educational and research programs, catalyzing policies and disseminating science information to reach a diverse set of audiences.

As global thought-leader she has received national and international highly regarded awards, has more than 280 scientific papers and participated in more than 250 conferences worldwide. She is a member of the National Academy of Science of Honduras and an Emerging Leader in Health and Medicine of the National Academy of Medicine in the U.S.

Bottazzi is a fellow of the American Society of Tropical Medicine and Hygiene (ASTMH), the Executive Leadership in Academic Medicine (ELAM) and the Leshner Leadership Institute for Public Engagement and senior fellow of the American Leadership Forum (ALF). Forbes LATAM in 2020 and 2021 selected Bottazzi as one of 100 Most Powerful Women in Central America. Bottazzi has served in several national academies ad-hoc committees and serves as co-chair of the Vaccines and Therapeutics Taskforce of the Lancet Commission on COVID-19. In 2022, alongside Dr. Peter Hotez, she was nominated by Congresswoman Lizzie Fletcher of Texas for the Nobel Peace Prize.

Dr. Peter HotezDean of the National School of Tropical Medicine at Baylor College of Medicine and co-director of the Texas Childrens Hospital Center for Vaccine Development

Dr. Hotez is an internationally recognized physician-scientist in neglected tropical diseases and vaccine development. As co-director of the Texas Childrens Center for Vaccine Development, he leads a team and product development partnership for developing new vaccines for hookworm infection, schistosomiasis, leishmaniasis, Chagas disease and SARS/MERS/SARS-2 coronavirus, diseases affecting hundreds of millions of children and adults worldwide, while championing access to vaccines globally and in the U.S.

In December 2021, Hotez led efforts at the Texas Childrens Center for Vaccine Development to develop a low-cost recombinant protein COVID vaccine for global health, resulting in emergency use authorization in India. In 2022 Hotez and his colleague Dr. Maria Elena Bottazzi were nominated for the Nobel Peace Prize for their work to develop and distribute a low-cost COVID-19 vaccine to people of the world without patent limitation.

In 2014-16, he served in the Obama Administration as U.S. Envoy, focusing on vaccine diplomacy initiatives between the U.S. government and countries in the Middle East and North Africa. In 2018, he was appointed by the U.S. State Department to serve on the Board of Governors for the U.S.-Israel Binational Science Foundation, and he is frequently called on frequently to testify before U.S. Congress. He has served on infectious disease task forces for two consecutive Texas governors. For these efforts in 2017 he was named by FORTUNE Magazine as one of the 34 most influential people in healthcare, while in 2018 he received the Sustained Leadership Award from Research!America.

Most recently as both a vaccine scientist and autism parent, he has led national efforts to defend vaccines and to serve as an ardent champion of vaccines going up against a growing national antivax threat. In 2019, he received the Award for Leadership in Advocacy for Vaccines from the American Society of Tropical Medicine and Hygiene. In 2021 he was recognized by scientific leadership awards from the Association of American Medical Colleges and the American Medical Association, in addition to being recognized by the Anti-Defamation League with its annual Popkin Award for combating antisemitism.

Dr. Joseph HyserAssistant professor of molecular virology and microbiology and member of the Alkek Center for Metagenomics and Microbiome Research

Dr. Joseph Hysers research work is dedicated to improving our understanding of host-pathogen interactions. He has focused on characterizing host signaling pathways that enteric viruses, such as rotavirus, destabilize to cause gastrointestinal disease. His work stands out because it is shifting prevailing paradigms within the field.

In recent work, Hyser used calcium biosensor cell lines and organoids he developed to perform long-term live calcium imaging throughout rotavirus infections. This work is paradigm shifting because it firmly established that rotavirus increase calcium through hundreds of discrete calcium signaling events rather than a general, monophasic increase in cytosolic calcium levels. This study also led to the discovery of multiple distinct types of calcium signals present at different stages of the infection.Another study showed that calcium-conducting viroporins are a broadly conserved strategy used by viruses to exploit host calcium signaling pathways. This finding has opened the door to identify commonly exploited host pathways for which host-targeted antiviral drugs could be developed.

Recently, Hyser published the first direct evidence that viruses can trigger aberrant calcium signaling in uninfected cells by exploiting a host paracrine signaling pathway. Live imaging data show calcium signals coming from rotavirus-infected cells and spreading to surrounding uninfected cellsa type of signal called intercellular calcium waves. He found that eliminating the calcium waves severely reduced rotavirus replication, suggesting that rotavirus has evolved to co-opt this host intercellular signal to increase its replication. Taken together, Hysers work establishes a new mechanism by which viruses commandeer nearby uninfected cells to contribute to pathogenesis through paracrine signaling.

Dr. Katherine KingAssociate professor of pediatrics infectious diseases and member of the Dan L Duncan Comprehensive Cancer Center and Center for Cell and Gene Therapy

Dr. Kings research focuses on the effects of infection and inflammation on primitive hematopoiesis. As a pediatric infectious diseases physician at Texas Childrens Hospital, King recognized the need to understand bone marrow suppressive effects of chronic infection, and she led the field to characterize hematopoietic stem cell responses in the context of animal models of infection. Her review on the topic of inflammatory modulation of hematopoietic stem cells altered the way the field views the interactions between systemic inflammation and stem cells, with continuing repercussions in the fields of malignant and nonmalignant hematology, aging and immunology.

Using a multidisciplinary approach, she has pioneered the concept that hematopoietic stem cells are extremely sensitive to inflammatory signals in the bone marrow environment. Her research has defined a role for inflammatory signaling in bone marrow suppression following chronic infection and in the emergence of clonal hematopoiesis, a recently defined phenomenon that drives cancer risk and cardiovascular disease in advanced age.

Over the past three years, her research efforts have resulted in 9 senior-author research articles in leading journals in her field including Cell Stem Cell, Cell Reports, and eLife. Kings highly innovative and impactful work at the intersection of immunology and hematology has made her an international leader in the field of stem cell biology. She is a skilled clinician, a healthcare advocate, scientist, administrative leader and trusted mentor.

Dr. Irina LarinaAssociate professor of integrative physiology

Dr. Irina Larinas lab is dedicated to the development of new biophotonic technologies to define pathways involved in live embryo progression and, specifically, cardiac development. She also applies her new biophotonic methods to image developmental processes in various mouse models to elucidate pathophysiological mechanisms underlying reproductive disorders. Larina also develops data processing methods that enable her to uncover new information about congenital defects and reproductive disorders that reveal the dynamics of developmental processes, which have not been accessible before.

Most recently she used second harmonic generation microscopy to image collage fibers in embryonic hearts, revealing a link between structural collagen and regional contractility that suggested a regulatory role for cardiomyocyte contractility in establishing mechanical homeostasis in the developing heart. These findings revealed new features of the biochemical alterations found in congenital heart defects and heart failure. In addition, her lab recently established a method to study the interactions between genetic and mechanical factors in both normal and pathogenic cardiogenesis in vivo, such as arrhythmias.

In the area of reproduction, Larinas innovative biophotonics technology provided direct visualization of the movement of oocytes and embryos in the fallopian tube. Identifying abnormalities in this process is critical for defining defects in mammalian fertilization and embryogenesis. Using her new approach, which combines optical coherence tomography with intravital imaging, Larina showed that cilia do not drive directional oocyte/embryo transport. The timing of the oocyte/embryo transport is primarily regulated by smooth muscle dynamics at different locations within the oviduct.

Dr. Scott A. LeMaireJimmy and Roberta Howell Professor of Cardiovascular Surgery, vice chair for research in the Michael E. DeBakey Department of Surgery, director of research in the Division of Cardiothoracic Surgery and professor of molecular physiology and biophysics

Dr. LeMaires primary clinical interest focuses on the management of patients with thoracic aortic disease, with a particular emphasis on treatment of aortic dissection and thoracoabdominal aortic aneurysms. His corresponding research program focuses on organ protection during aortic surgery, genetic aspects of thoracic aortic disease and molecular mechanisms of aortic degeneration.

He has received funding from the National Institutes of Health, the American Heart Association, the Thoracic Surgery Foundation and the Marfan Foundation for his research studying the pathobiology of thoracic aortic aneurysms and aortic dissection. LeMaire is a past-president of the Association for Academic Surgery and is the current editor-in-chief of the Journal of Surgical Research.

LeMaire also serves as a physician associate in the Department of Cardiovascular Surgery at the Texas Heart Institute and Baylor St. Lukes Medical Center.

Dr. Ying ShenProfessor of surgery and director of the Aortic Disease Research Laboratory

Dr. Shens research focuses on understanding the development of vascular diseases. She became the director of the Aortic Disease Research Laboratory in 2008, and has since focused on aortic aneurysms and dissections, highly lethal but poorly understood diseases. She has worked closely with collaborator Dr. Scott LeMaire and together, they have built a translational research program and developed several research directions to investigate the mechanisms of aortic injury, repair and remodeling. The ultimate goal of her research is to develop pharmacological treatments to prevent progressive aortic destruction, maladaptive remodeling and disease deterioration.

Dr. Sundeep KeswaniProfessor of surgery, pediatrics and obstetrics and gynecology, division chief of pediatric surgery and surgical director of basic science research at Texas Childrens Hospital

Dr. Sundeep Keswanis lab, the Laboratory for Regenerative Tissue Repair, is focused on understanding the molecular mechanism that underlies the fetus ability to regeneratively heal cutaneous wounds, as well as the development of novel therapies to achieve scarless wound healing in postnatal tissues, specifically the interaction of inflammation and extracellular matrix to drive fibrotic responses within human skin in response to injury. Most recently he has shown that bacteriophage trigger antiviral immunity and prevent clearance of bacterial infection and that Interleukin-10 producing T lymphocytes (TR1 cells) reduce dermal scarring. In addition to his work in skin, his group also has discovered that hyaluronan attenuates tubulointerstitial scarring in kidney injury.During the last three years, he has published his research outcomes in highly prestigious journals such as Science, Annals of Surgery and JCI Insight.

Keswani also serves as a governor of the American College of Surgeons and continually publishes articles that examine the state of research and surgery, keeping surgeon-scientists highly relevant nationally.

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Baylor College of Medicine recognizes research excellence with DeBakey Awards - Baylor College of Medicine News

GRAND RAPIDS, Mich. (WOOD) The soldiers of our immune system were long thought to be fueled only by the foods we eat. However, researchers at Van Andel Institute believe the findings from their new study reveal T cells have a much wider appetite than originally thought.

Every process in the body is powered by metabolism, which in turn is fueled by the nutrients we consume through our diet, Russell Jones, Ph.D., chair of Van Andel Institutes Department of Metabolism and Nutritional Programming said. We found that immune cells are much more flexible in selecting the nutrient fuels they consume and, importantly, that they prefer some nutrients that were previously dismissed as waste. This understanding is crucial for optimizing T cell responses and developing new strategies for boosting our ability to fight off disease.

Jones, who is the co-author of the study published this week in Cell Metabolism, says the findings could create a path for personalized dietary recommendations that would supercharge immune cells and provide more effective therapies for cancer and other diseases.

Joneses research took a new approach to studyin T cells. In previous studies, the cells were grown in lab dishes with nutrient-contatining media. But Jones believed those nutrients were similar to a diet of eggs and toast. This time, Jones and his colleagues developed a more diverse sample of nutrients for the research and the outcome was much different.

We found that, when we offer them a full buffet, these cells actually prefer a wider array of fuels than previously believed, Jones said. This has major implications for how we tailor dietary recommendations as ways to promote health and combat disease.

Jones explains the research through what they discovered from lactate, a cellular waste that causes muscle aches and pains and a byproduct of cancer cells that allows the disease to attack other tissue and avoid the immune system. When the T cells were given the choice between glucose and lactate, they chose the lactate to power their energy production which enhanced their overall function.

According to VAI, there is research that suggests too much lactate is bad for T cells, but Jones work provides the idea that small amounts may increase their overall function.

Jones and his team plan to take their findings and use them to take a closer look at the unique connection between metabolism and the immune system to learn more about how they work together.

Hear from Dr. Jones below.

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New study could change what we eat to supercharge immune system and fight disease - WOODTV.com

Ecological model

We start with an ecological model of resident host-pathogen dynamics that assumes these populations are, respectively, genetically homogeneous. The ecological model underlies the evolutionary model we develop later. A complete description of the model, and the methods of analysis that follow, can be found in theSupplementary Information.

We consider a population of hosts classified according to their sex and disease status. At time t, there are Si=Si(t) sex-i individuals not infected by the pathogen, but susceptible to future infection (i=f for females, i=m for males). At time t there are also Ii=Ii(t) sex-i individuals who are not only infected with the pathogen but also able to transmit their infection to others. Our specific goal in this section is to develop a mathematical description of how the numbers of hosts in the various classes change over time.

The number of hosts in the population changes as a result of birth events. Following previous work44,45, we model the host mating rate using the harmonic mean of the population sizes of females and males. Assuming a one-to-one birth sex ratio, then newly born hosts of either sex join the population at rate (frac{b({S}_{f}+{I}_{f})({S}_{m}+{I}_{m})}{N}) where b>0, and N=N(t) denotes the total population size at time t. We assume that newborns produced by susceptible mothers are, themselves, susceptible. By contrast, we suppose that newborns produced by infected mothers acquire their mothers infection with probability v, where v is what we have called the vertical transmission rate31. Host number also changes because of death events. Hosts in every class experience natural mortality at per-capita rate N, where is a positive constant. Hosts infected by the pathogen also experience disease-related mortality at per-capita rate i (a measure of pathogen virulence) (Fig.7).

This model incorporates two sexes (females in red and males in blue) and vertical transmission (dashed line). The flow between compartments is represented by arrows and expressions next to each arrow represent the flow rate. Evolving phenotypes and drivers of their evolution are indicated in green and purple, respectively. Source data are provided as a Source Data file.

Numbers of hosts in any particular class changes as their disease-status changes. For example, we allow infected individuals to recover at per-capita rate i (a measure of host immunocompetence). We assume that, upon recovery, hosts move immediately into the appropriate susceptible group. In this way, we ignore the possibility that recovery implies immunity to subsequent infection. The disease status of hosts can also change because of horizontal disease-transmission events. We approach horizontal transmission in a standard way and assume that susceptible sex-i hosts acquire the pathogen horizontally from their infected sex-j counterparts at a total rate of SiijIj. Here, ij is a constant that reflects the transmissibility of the pathogen. We assume that when a host acquires an infection horizontally, it immediately becomes infectious (Fig.7).

The model described above is summarised mathematically using the following system of differential equations:

$$frac{d{S}_{f}}{dt}=frac{b({S}_{f}+(1-v){I}_{f})({S}_{m}+{I}_{m})}{N}+{gamma }_{f}{I}_{f}-{S}_{f}{beta }_{ff}{I}_{f}-{S}_{f}{beta }_{fm}{I}_{m}-mu N{S}_{f}$$

(1a)

$$frac{d{S}_{m}}{dt}=frac{b({S}_{f}+(1-v){I}_{f})({S}_{m}+{I}_{m})}{N}+{gamma }_{m}{I}_{m}-{S}_{m}{beta }_{mf}{I}_{f}-{S}_{m}{beta }_{mm}{I}_{m}-mu N{S}_{m}$$

(1b)

$$frac{d{I}_{f}}{dt}=frac{bv{I}_{f}({S}_{m}+{I}_{m})}{N}+{S}_{f}{beta }_{ff}{I}_{f}+{S}_{f}{beta }_{fm}{I}_{m}-({gamma }_{f}+{alpha }_{f}+mu N){I}_{f}$$

(1c)

$$frac{d{I}_{m}}{dt}=frac{bv{I}_{f}({S}_{m}+{I}_{m})}{N}+{S}_{m}{beta }_{mf}{I}_{f}+{S}_{m}{beta }_{mm}{I}_{m}-({gamma }_{m}+{alpha }_{m}+mu N){I}_{m}.$$

(1d)

Under a reasonable set of conditions, the previous system tends, over time, to an equilibrium state in which infections are endemic.

To study how pathogens disease-induced mortality and the hosts immune system respond to selection, we assume that each faces a life-history trade-off.

First, the pathogens ability to transmit horizontally trades off against the duration of any given infection it establishes. Following the previous authors30,46,47, we capture this trade-off by assuming

$${beta }_{ij}=beta ({alpha }_{j})=frac{{beta }_{max }{alpha }_{j}}{{alpha }_{j}+d}quad ,{{mbox{for}}},,j=f,;m,$$

(2)

where ({beta }_{max },,d , > , 0) are constants. Equation (2) implies that the nature of the trade-off faced by a pathogen is the same in both female and male hosts. Specifically, a pathogen can only increase its rate of horizontal transmission by increasing the disease-induced mortality rate experienced by its host (which, in turn, reduces the duration of infection). Equation (2) also says the horizontal transmission rate saturates at ({beta }_{max }) (independent of host sex), and does so more quickly as the parameter d is reduced (again, independent of host sex). Note also that Equation (2) does not depend on i: the sex of the susceptible host to whom the pathogen is transmitted.

For their part, hosts face a trade-off between investing resources in their immune system and their reproductive success. Increased immune investment is reflected in an increased recovery rate. To capture the hosts trade-off, then, we treat birth rate b as a decreasing function of the recovery rate. Moreover, we assume that the decrease in b is experienced by the host regardless of its disease status. In other words, we assume that cost associated with the immune system is an ongoing one, incurred mainly because of maintenance27 (this assumption model innate immunocompetence best) rather than being due to the activation that follows an infection48 (this assumption would model adaptive immunocompetence best). As noted in the Discussion, we relax this assumption in theSupplemental Material and compare the results for maintenance and activation costs. As an example, here, we point to evidence that shows female sex hormones enhance the immune system but simultaneously reduce the likelihood of conception and increase the chances of spontaneous abortion49,50,51. In mathematical terms, we capture the hosts trade-off using

$$b=b({gamma }_{f},{gamma }_{m})={b}_{max },{e}^{-{c}_{f}{gamma }_{f}^{2}},{e}^{-{c}_{m}{gamma }_{m}^{2}}$$

(3)

where ci reflects the rate at which fertility is reduced as sex-i immune function is increased (cost of recovery above). Equation (3) generalises the birth rate functions used previously27,48 to our sex-specific setting. The fact that b in this equation depends on both f and m reflects the fact that the reduced fertility of one mate affects the fertility of its partner16.

Our approach to modelling the co-evolution of host and pathogen is rooted in the adaptive-dynamics methodology52,53,54. For the pathogen population, we build a fitness expression that measures the success of a rare mutant strain in a population close to the endemic equilibrium established by the system (1) (indicated as ({bar{S}}_{i}), ({bar{I}}_{i}), and (bar{N})). Assuming that the mutant strain of pathogen is associated with a disease-induced mortality rate equal to ({tilde{alpha }}_{i}) in sex-i hosts, the number of mutant infections, ({tilde{I}}_{i}={tilde{I}}_{i}(t)) changes according to

$$frac{d{tilde{I}}_{f}}{dt}=frac{bv{tilde{I}}_{f}({bar{S}}_{m}+{bar{I}}_{m})}{bar{N}}+{bar{S}}_{f}beta ({tilde{alpha }}_{f}){tilde{I}}_{f}+{bar{S}}_{f}beta ({tilde{alpha }}_{m}){tilde{I}}_{m}-({gamma }_{f}+{tilde{alpha }}_{f}+mu bar{N}){tilde{I}}_{f}$$

(4a)

$$frac{d{tilde{I}}_{m}}{dt}=frac{bv{tilde{I}}_{f}({bar{S}}_{m}+{bar{I}}_{m})}{bar{N}}+{bar{S}}_{m}beta ({tilde{alpha }}_{f}){tilde{I}}_{f}+{bar{S}}_{m}beta ({tilde{alpha }}_{m}){tilde{I}}_{m}-({gamma }_{m}+{tilde{alpha }}_{m}+mu bar{N}){tilde{I}}_{m}.$$

(4b)

The system in (4) is linear and its long-term behaviour is determined by a dominant Lyapunov exponent of the mapping. We capture the information provided by the dominant Lyapunov exponent with the pathogen-fitness function, ({W}_{alpha }({tilde{alpha }}_{f},{tilde{alpha }}_{m},{alpha }_{f},{alpha }_{m})) using techniques laid out by the ref. 55 (see alsoSupplemental Information). When this function is greater than 1 the mutant invades and eventually displaces56 the resident strain associated with the i phenotype. When the function ({W}_{alpha }({tilde{alpha }}_{f},{tilde{alpha }}_{m},{alpha }_{f},{alpha }_{m})) is less than 1 the mutant does not invade and is eliminated from the population. With these facts in mind, we say that selection acts to move i in the direction given by the sign of (frac{partial {W}_{alpha }}{partial {tilde{alpha }}_{i}}{left|right.}_{tilde{alpha }=alpha }) where (tilde{alpha }=alpha) is shorthand for ({tilde{alpha }}_{i}={alpha }_{i}) for all i. Specifically, when this partial derivative is positive i is increasing, and when it is negative i is decreasing.

We follow a similar procedure for the host population by introducing, into the equilibrium population, a rare mutant-type host genotype that results in a recovery rate of ({hat{gamma }}_{i}) when expressed by sex-i hosts. We denote the numbers of susceptible and infected sex-i mutant-type hosts as ({hat{S}}_{i}) and ({hat{I}}_{i}), respectively. We assume that hosts are diploid, and so, strictly speaking, the hosts who contribute to ({hat{S}}_{i}) and ({hat{I}}_{i}) categories are heterozygotes (the numbers of homozygote mutants are negligible). While it remains rare, the dynamics of the mutant-host lineage can be described using

$$frac{d{hat{S}}_{f}}{dt}= frac{frac{b({hat{gamma }}_{f},{gamma }_{m})}{2}({hat{S}}_{f}+(1-v){hat{I}}_{f})({bar{S}}_{m}+{bar{I}}_{m})+frac{b({gamma }_{f},{hat{gamma }}_{m})}{2}({bar{S}}_{f}+(1-v){bar{I}}_{f})({hat{S}}_{m}+{hat{I}}_{m})}{bar{N}}\ +{hat{gamma }}_{f}{hat{I}}_{f}-{hat{S}}_{f}{beta }_{ff}{bar{I}}_{f}-{hat{S}}_{f}{beta }_{fm}{bar{I}}_{m}-mu bar{N}{hat{S}}_{f}$$

(5a)

$$frac{d{hat{I}}_{f}}{dt}= frac{frac{b({hat{gamma }}_{f},{gamma }_{m})}{2}v{hat{I}}_{f}({bar{S}}_{m}+{bar{I}}_{m})+frac{b({gamma }_{f},{hat{gamma }}_{m})}{2}v{bar{I}}_{f}({hat{S}}_{m}+{hat{I}}_{m})}{bar{N}}\ +{hat{S}}_{f}{beta }_{ff}{bar{I}}_{f}+{hat{S}}_{f}{beta }_{fm}{bar{I}}_{m}-({hat{gamma }}_{f}+{alpha }_{f}+mu bar{N}){hat{I}}_{f}$$

(5b)

$$frac{d{hat{S}}_{m}}{dt}= frac{frac{b({hat{gamma }}_{f},{gamma }_{m})}{2}({hat{S}}_{f}+(1-v){hat{I}}_{f})({bar{S}}_{m}+{bar{I}}_{m})+frac{b({gamma }_{f},{hat{gamma }}_{m})}{2}({bar{S}}_{f}+(1-v){bar{I}}_{f})({hat{S}}_{m}+{hat{I}}_{m})}{bar{N}}\ +{hat{gamma }}_{m}{hat{I}}_{m}-{hat{S}}_{m}{beta }_{mf}{bar{I}}_{f}-{hat{S}}_{m}{beta }_{mm}{bar{I}}_{m}-mu bar{N}{hat{S}}_{m}$$

(5c)

$$frac{d{hat{I}}_{m}}{dt}= frac{frac{b({hat{gamma }}_{f},{gamma }_{m})}{2}v{hat{I}}_{f}({bar{S}}_{m}+{bar{I}}_{m})+frac{b({gamma }_{f},{hat{gamma }}_{m})}{2}v{bar{I}}_{f}({hat{S}}_{m}+{hat{I}}_{m})}{bar{N}}\ +{hat{S}}_{m}{beta }_{mf}{bar{I}}_{f}+{hat{S}}_{m}{beta }_{mm}{bar{I}}_{m}-({hat{gamma }}_{m}+{alpha }_{m}+mu bar{N}){hat{I}}_{m}.$$

(5d)

The birth terms in the preceding system of equations reflect (a) the fact that the mutant host, while it is rare, mates only homozygous resident hosts and (b) only half of the matings between heterozygous mutants and homozygous residents result in mutant offspring. Since the dynamics described by (5) are linear, we can again measure fitness (this time for the host) using the dominant Lyapunov exponent. We summarise the relevant information contained in this exponent with the host fitness function ({W}_{gamma }({hat{gamma }}_{f},{hat{gamma }}_{m},{gamma }_{f},{gamma }_{m})), again using techniques outlined by ref. 55. In keeping with the description of pathogen evolution, we assert that the hosts i is increasing when (frac{partial {W}_{gamma }}{partial {gamma }_{i}}{left|right.}_{hat{gamma=gamma }}) is positive, and decreasing when this partial derivative is negative, where (hat{gamma }=gamma) is shorthand for ({hat{gamma }}_{i}={gamma }_{i}) for all i.

We want to identify where the action of selection takes the resident pathogen and host traits (i and i, respectively) in the long term. As mentioned above, the model is too complicated to support exact mathematical predictions. Consequently, our methods rely on numerical simulation implemented in Matlab57. All Matlab code is publicly available (see Code Availability).

The numerical simulation takes as its input a set of parameters and an initial estimate of the long-term result of selection on co-evolution of pathogen and host ({alpha }_{i}^{*}), and ({gamma }_{i}^{*}) for i=f, m. The estimate is updated by (i) finding the corresponding equilibrium solution to Equation (1) in a manner that verifies its asymptotic stability, (ii) using that equilibrium solution to estimate partial derivatives (frac{partial {W}_{alpha }}{partial {tilde{alpha }}_{i}}{left|right.}_{tilde{alpha=alpha }}) and (frac{partial {W}_{gamma }}{partial {hat{gamma }}_{i}}{left|right.}_{hat{gamma=gamma }}) for i=f, m, and finally (iii) incrementing or decrementing elements of the estimate following the sign of the appropriate partial derivative. Steps (i)(iii) are repeated until the absolute value of all partial derivatives is within a tolerance of zero. The result of the simulation is an estimate of the convergence stable58,59 co-evolutionary outcome, assuming f and m, and f and m can be adjusted independently. Importantly, this predicted co-evolutionary outcome also corresponds to a system in which the pathogen is established in a stable equilibrium population of hosts.

Finally, we verified numerically that the convergence-stable estimate corresponded to a two-dimensional evolutionarily stable result60 for pathogen and host, respectively. For this reason, we can also refer to predictions generated by our numerical simulation as a continuously stable state, in analogy to the definition established by ref. 61.

Further information on research design is available in theNature Research Reporting Summary linked to this article.

Continued here:
On maternity and the stronger immune response in women - Nature.com

Matt Kaeberlein is what you might call a dog person. He has grown up with dogs and describes his German shepherd, Dobby, as really special. But Dobby is 14 years oldaround 98 in dog years. Im very much seeing the aging process in him, says Kaeberlein, who studies aging at the University of Washington in Seattle.

Kaeberlein is co-director of the Dog Aging Project, an ambitious research effort to track the aging process of tens of thousands of companion dogs across the US. He is one of a handful of scientists on a mission to improve, delay, and possibly reverse that process to help them live longer, healthier lives.

But dogs are just the beginning. Because theyre a great model for humans, anti-aging or lifespan-extending drugs that work for dogs could eventually benefit people, too. In the meantime, attempts to prolong the life of pet dogs can help people get onboard with the idea of life extension in humans. Read the full story.

Jessica Hamzelou

The quest to show that biological sex matters in the immune system

For years, microbiologist Sabra Klein has painstakingly made the case that sexdefined by biological attributes such as our sex chromosomes, sex hormones, and reproductive tissuescan influence immune responses.

Through research in animal models and humans, Klein and others have shown how and why male and female immune systems respond differently to the flu virus, HIV, and certain cancer therapies, and why most women receive greater protection from vaccines but are also more likely to get severe asthma and autoimmune disorders (something that had been known but not attributed specifically to immune differences.)

In the 1990s, scientists often attributed such differences to gender rather than sexto norms, roles, relationships, behaviors, and other sociocultural factors as opposed to biological differences in the immune system. Klein has helped spearhead a shift in immunology, a field that long thought sex differences didnt matterand shes set her sights on pushing the field of sex differences even futher. Read the full story.

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Extending dogs' lives, and sex and the immune system - MIT Technology Review

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Your Immune System Will Thrive With This Elderberry Hill Liquid Morning Multivitamin - Men's Journal

Prioritizing your health has never been more important. As COVID cases continue to spike and the monkeypox outbreak has now become a public health emergency, having a strong immune system is essential. Daily habits can impact our immune health and lifestyle choices such as smoking, poor diet, and too much alcohol consumption can weaken your immunity. But there are ways to help strengthen our body and knowing the signs of a troubled immune system is a start. Eat This, Not That! Health spoke with Dr. Tom Yadegar, Pulmonologist and Medical Director of the Intensive Care Unit at Providence Cedars-Sinai Tarzana Medical Center who shares what to know about your immune system and warning signals it's not as healthy as it should be. Read onand to ensure your health and the health of others, don't miss these Sure Signs You've Already Had COVID.

Dr. Yadegar states, "The immune system is the defender of the body. Composed of two arms, innate and adaptive, the innate system is a nonspecific response that fights any type of foreign invader that comes into contact with the body. This arm is generally the same in most people and is composed of white cells. The second arm, known as the adaptive immune system, is specific to the foreign invader and targets it using antibodies from previous infections or vaccines."

"When exposed to a foreign invader, the immune system creates antibodies in response to prevent severe symptoms in case of repeated exposure," says Dr. Yadegar. "When this process turns against healthy tissue instead of foreign pathogens, the immune system attacks the body, leading to an autoimmune state."

Dr. Yadegar shares, "Getting proper sleep, nutrition and regular exercise is a hallmark to keeping the immune system functional. Adequate vitamin intake, including vitamin C and vitamin D, is also important in ensuring a strong immune system. Patients who may have immunodeficiency, such as IgG deficiency, can also receive infusions to help keep their immune system healthy."

Dr. Yadegar tells us, "Fighting infections requires a lot of energy. When the body is depleted of its normal energy level, the immune system is weakened and can become susceptible to opportunistic infections. People generally feel this when they are tired. Ensuring a schedule of restful sleep, eating a balanced diet with fruits and vegetables and drinking enough water helps ensure your immune system is ready to answer the call of an infection."6254a4d1642c605c54bf1cab17d50f1e

According to Dr. Yadegar, "Infections that require multiple courses of antibiotics within a year may be a sign of a weakened immune system that is not able to fight off pathogens. Patients should be evaluated by their healthcare provider in order to further investigate the underlying cause."

"Normal wounds require the immune system to bring nutrients to repair damaged tissue," says Dr. Yadegar. "When this process is compromised, wounds are unable to heal properly, which signals a slow immune system. Delayed wound healing is indicative of a poorly-functional immune system, and should be evaluated by a healthcare provider."

Dr. Yadegar explains, "Long-term stress compromises the body's natural immunity, which can lead to higher risk of infections. While stress is inevitable in our fast-paced lives, taking steps to mediate stress can help. Whether meditation, exercise, or deep-breathing, it's important to tailor stress-relief to the individual in order to best improve their stress levels."

Heather Newgen

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Sure Signs Your Immune System Isn't as Strong as it Should Be Eat This Not That - Eat This, Not That

A health-care worker prepares to administer a free monkeypox vaccine in Wilton Manors, Florida. The question: Can vaccination slow the outbreak? Joe Raedle/Getty Images hide caption

A health-care worker prepares to administer a free monkeypox vaccine in Wilton Manors, Florida. The question: Can vaccination slow the outbreak?

Finally, we have a glimmer of good news about monkeypox: The outbreaks in some countries, including the U.K., Germany and parts of Canada, are starting to slow down.

On top of that, the outbreak in New York City may also be peaking and on the decline, according to new data from the city's health department.

All these outbreaks are "far from extinguished," says infectious disease specialist Dr. Donald Vinh at McGill University in Montreal. But there are signs that, in some places, "they're a bit more under control than they had been."

For example, in the U.K., the number of new cases reported each day has steadily declined since late July, dropping from 50 daily cases to only about 25. (By contrast, here in the U.S., daily cases are still increasing. Since late July, the U.S. daily count has risen from 350 new cases to 450 cases.)

Some health officials credit the monkeypox vaccine and its quick rollout as the key factor that's slowing the spread of the virus in the U.K..

"Over 25,000 have been vaccinated with the smallpox vaccine, as part of the strategy to contain the monkeypox outbreak in the UK.," the U.K. Health Security Agency wrote on Twitter on Tuesday. "These 1000s of vaccines, given by the NHS to those at highest risk of exposure, should have a significant impact on the transmission of the virus."

Indeed, the U.K. and parts of Canada rolled out the vaccine in late May, weeks before doses became available in most U.S. cities.

But does the monkeypox vaccine have the ability to stop or curb the spread of the virus? To answer that question, we need to first understand a few basics about this vaccine.

What actually is the monkeypox vaccine? How does it work?

So the monkeypox vaccine is actually the smallpox vaccine. Maybe that sounds a bit strange, but in fact the two pox viruses are related. They're a bit like cousins.

Health-care workers used an earlier version of this vaccine to eradicate smallpox in the 1970s. So versions of this vaccine have been given to hundreds of millions of people over the past century. It has a long track record.

Back in the late 1980s, researchers started to notice something remarkable about this vaccine. During a monkeypox outbreak in the Democratic Republic of the Congo (then called Zaire), people who were immunized against smallpox were less likely to get monkeypox. They were protected. And not by just a little but by quite a bit. In a small study, published in 1988, researchers estimated the smallpox vaccine offered about 85% protection against monkeypox.

Now, the virus in this study was a different variant of monkeypox than the one circulating in the current international outbreak and that variant wasn't spreading primarily through sexual contact, as monkeypox is doing today. So we don't know how well these findings will translate to protection during the current outbreak. Which brings us to the next question.

How well does the vaccine protect against a monkeypox infection?

The short answer is: "We don't know," says infectious disease specialist Dr. Boghuma Titanji at Emory University.

There's no doubt the vaccine will offer some protection, Titanji says. "But right now, we still need studies in people to understand what level that protection actually is."

In North America and Europe, countries are primarily rolling out a vaccine called JYNNEOS, which was developed in the early 21st century. The goal with this vaccine is to increase its safety compared to the older vaccine, whose life-threatening complications, including encephalitis and skin necrosis, occurred in about 4 out of every million people vaccinated. That vaccine also could cause damaging skin lesions in people with eczema or weakened immune systems. (Note: There is a shortage of the JYNNEOS vaccine, and no doses have been shared with or sold to countries in Africa, which have experienced monkeypox outbreaks since the 1970s.)

Although older versions of the vaccine have been tested thoroughly in people, there has never been a large, clinical study to measure JYNNEOS's ability to protect against a monkeypox infection in people or to stop transmission of the virus.

What is known about the vaccine, in terms of its efficacy against monkeypox, comes from studies in macaques, and immunological studies in people, which demonstrated the vaccine triggers the production of monkeypox antibodies in people's blood.

"So we know that the vaccine does stimulate the immune system and people produce antibodies when they receive the vaccine," Titanji says, "but we don't have a clinical data in humans to actually tell us, 'Okay, that immune response translates to this level of protection against getting infected with monkeypox or reducing the severity of monkeypox disease if you do get infected.' "

And it's not a guarantee of protection. In this current outbreak, scientists have already begun to document breakthrough infection with this vaccine, the World Health Organization reported Thursday. "[This] is also really important information because it tells us that the vaccine is not 100% effective in any given circumstance," said Dr. Rosamund Lewis of WHO. "We cannot expect 100% effectiveness at the moment based on this emerging information."

And so when Titanji gives a person the JYNNEOS vaccine at her clinic, she is very clear about what the vaccine can and can't do. "I tell them, 'We do know that you're going to get some protection from this vaccine. Some protection is better than no protection. We also do know that the vaccine can reduce the severity of the disease if you do get infected. But we don't know for a fact that you would be completely protected from getting monkeypox.' "

Can this vaccine if given to the people who need it the most slow down the outbreak?

So the new data from the U.K. and Germany suggest that indeed this vaccine can curb the spread of monkeypox.

But Dr. Vinh at McGill University says it's way too soon to say the vaccine, alone, is the only factor contributing to the slow down in these countries. "No single measure is going to really be the solution here," says Vinh.

In addition to vaccination, people at high risk need to learn how they can protect themselves. And doctors have to learn how to spot monkeypox cases, he says.

Right now the percentage of monkeypox tests coming back positive is still incredibly high, Titanji says. "The positivity rate is close to 40%." And that means doctors are missing many cases. Specifically, they are still mistaking monkeypox for other sexually transmitted diseases such as syphyllis.

"I can tell you, from the lens of a clinician, that monkeypox is very, very easy to mistake for another infectious disease," she says.

Some people have had to visit clinics two or three times and even have been treated for another STD before the clinician suspects monkeypox.

"You really have to maintain a very high index of suspicion because some of the lesions are so subtle and the clinical presentation is so variable," she says. "At this phase of the outbreak, we should be over testing rather than under testing. If a doctor even remotely suspects monkeypox, they should be sending a test for it."

Otherwise people can't receive treatment for monkeypox and they can unknowingly spread it to others. And the outbreak will continue to grow while people wait to receive a vaccine and for that vaccine to begin working.

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Can the monkeypox vaccine stop the current outbreak? : Goats and Soda - NPR

Taiwan researchers sort through eggs used for the cultivation of swine flu vaccine, in a plant in ... [+] Taichung, on June 18, 2009. Taiwan is set to mass produce swine flu vaccine in October, as the island's confirmed cases rose to 58 as of June 17. AFP PHOTO/PATRICK LIN (Photo credit should read PATRICK LIN/AFP via Getty Images)

This is a short series about a recent breakthrough on the road to developing a much sought-after broadly neutralizing vaccine against all influenza A viruses. If successful, it may act as a precursor to a truly universal flu vaccine, one that protects against all types, subtypes, and lineages of the virus. The breakthrough may also provide a blueprint for developing a Covid-19 vaccine that retains its efficacy in the face of new variants.

In the first part of this series, I gave a brief overview of the history and nature of influenza viruses, including why it has been so difficult to develop successful vaccines. The next few articles discuss some of the attempts that have been made to overcome these challenges, including their shortcomings. And in the last installments, I will offer a detailed analysis of the latest and most promising advances in the field.

The Seasonal Approach

Picking up where we left off in the previous article, any successful influenza vaccine has to account for the ability of influenza viruses to mutate. Genetic mutations to vital proteins can lead to antigenic variation changes to parts of the virus that our immune system relies on to stimulate its memory. Although various different parts of the virus serve as antigens, the surface proteins that help it enter and exit host cells are some of the most important. Changes to these proteins can prevent our antibodies from recognizing the virus, rendering them unable to block its spread. Antigenic variation is responsible for influenza reinfections, leading to seasonal flu outbreaks.

In an attempt to circumvent the issue of antigenic variation, vaccine manufacturers update the flu shot each year based on the latest circulating influenza strains. The idea is to expose our immune system to the antigens it is most likely to encounter during flu season, helping it to build up its antigen-specific defenses in advance once our immune system has built up its memory, it can jump into action straight away should we become infected.

Which influenza strains ultimately get used to make the yearly flu shot is decided on the basis of data collected throughout the year by the World Health Organizations (WHO) Global Influenza Surveillance and Response System (GISRS). This surveillance and response system is made up of roughly 150 different laboratories spread across the globe, each of which gathers thousands of influenza samples from sick patients. The most prevalent viral strains are then shared with five WHO Collaborating Centers for Influenza, which perform further analysis. Two times a year once in preparation for flu season in the Northern Hemisphere, and another in preparation for flu season in the Southern Hemisphere Directors of the WHO Collaborating Centers, Essential Regulatory Laboratories, and representatives of a few of the smaller national laboratories come together to: review the results of surveillance, laboratory, and clinical studies, and the availability of flu vaccine viruses and make recommendations on the composition of flu vaccines. Once the WHO vaccine composition committee has made its recommendations, each country makes a final decision on which viruses they will choose to use in their flu vaccines.

In the United States, all influenza vaccines are quadrivalent, meaning they contain four different influenza viruses. This is done to broaden protection against the various influenza subtypes and lineages known to drive seasonal outbreaks: influenza A (H1N1), influenza A (H3N2), influenza B/Victoria, and influenza B/Yamagata. Quadrivalent vaccines will also protect against any other influenza viruses that are antigenically similar.

Although this may seem like a relatively reliable process, there is one glaring drawback to the seasonal vaccination approach: vaccines produced in this way are nowhere near as effective as we might hope. At best, they protect 60% of people from illness, but this number can, and often does, drop much lower. For the influenza A (H3N2) subtype, vaccine effectiveness hovers around 33%. Of course, any protection is better than no protection, but it is still suboptimal remember, these numbers represent best case scenarios, years where the viruses selected for use in vaccines are well matched to those that actually end up circulating during the flu season. So, where are things going wrong?

Missing the Target: Egg-based Vaccines

Selection of candidate vaccine viruses (CVVs) is only one part of the equation, growing them is another. This is no simple feat considering they need to be available in bulk, enough to make millions of vaccines. For the past 70 years, the majority of manufacturers have turned to chicken eggs in order to achieve the necessary growth (Figure 1). The candidate vaccine viruses are injected into fertilized hens eggs and left to incubate for a few days. During this period, the viruses are able to replicate. The fluid in the eggs is then extracted and the viruses are killed (inactivated). Finally, the antigen of choice usually the hemagglutinin surface protein is isolated from the killed viruses and purified, making it ready for use in vaccines. Even now, most flu vaccines continue to be egg-based.

FIGURE 1. An overview of the steps involved in producing egg-based vaccines.

But there are two issues with this approach. First, growing the viruses in eggs is a fairly slow process. This means the selection of candidate vaccine viruses has to happen far in advance of flu season, to make sure manufacturers have enough time to produce the amounts needed. In the six to nine months it takes to grow and purify enough virus, the wild type influenza strains continue to mutate and change. If these changes impact the antigen, the wild type viruses may escape the immunity that the vaccines provide us, reducing their effectiveness. When this happens, the viruses are referred to as escape mutants.

A growing body of research suggests that a second factor may be even more important: egg-adapted changes. Because the candidate vaccine viruses are human influenza viruses, growing them in chicken eggs carries the risk that they adapt to the new immune niche while replicating. The immune niche of chickens is different to that of humans, so adaptations that improve viral fitness in chickens may result in genetic and antigenic changes to the viruses. As before, these changes can lead to a drop in vaccine effectiveness, since the vaccine strains no longer resemble the circulating wild type strains; the egg-adapted vaccines end up training our immune system to recognize the wrong viruses, thus hampering its ability to respond efficiently come flu season.

Egg Substitutes: New Ways of Growing Candidate Viruses

In response to these issues, manufacturers have tried to develop new production methods that avoid using chicken eggs to culture candidate viruses. This search has led to a cell-based approach and a recombinant approach (Figure 2).

FIGURE 2. Timeline of current influenza vaccine production methods. Schematic overview of egg-based, ... [+] cell-based and protein-based (recombinant) influenza vaccine production.

Cell-based vaccines are produced using candidate viruses grown in mammalian cells rather than chicken eggs. Aside from this, the manufacturing process between the two is virtually identical: candidate vaccine viruses are grown in mammalian cell cultures by the CDC, these are then handed over to private manufacturers who inoculate the viruses into mammalian cells, the viruses are left to replicate for a few days before being harvested, and finally, purified. Although approved in 2012, it wasnt until this past 2021-2022 flu season that fully egg-free, cell-based vaccines were produced previously, the initial production of candidate vaccine viruses by the CDC was still done using fertilized hens eggs, and only after being handed over to the private sector were the viruses mass-produced in mammalian cells.

Using the cell-based approach eliminates egg-adapted changes in candidate viruses, keeping the viruses as close as possible to the wild type influenza strains predicted to circulate during flu season. An added benefit of cell-based vaccines is that the production process can be scaled up more quickly; mammalian cells can be frozen in advance to ensure steady supply, which could prove especially useful during pandemic outbreaks.

In theory, the lack of egg-adapted changes should improve vaccine effectiveness. But what about in practice? Although there still hasnt been enough research for a clear consensus to develop, initial findings suggest the difference in effectiveness is modest at best, and statistically insignificant at worst. This hints that egg-adapted changes might not play as important of a role as initially suspected; low vaccine efficacy can occur even when eggs are not used in the manufacturing process. That said, the 2021-2022 flu season marks the first time truly egg-free cell-based vaccines in which all four viruses are derived entirely through cell-based methods were used, so perhaps future research will yield different results. For now, things dont look too promising.

Recombinant vaccines provide a third option, and manage to overcome a crucial issue faced by the other two options: the lengthy, tedious virus production process. Whereas egg- and cell-based vaccines depend on candidate virus samples, recombinant manufacturing skips this step. Instead, recombinant vaccines are made by isolating the gene that makes the hemagglutinin surface protein from a wild type influenza virus. Once isolated, this gene is combined with a different kind of virus, called baculovirus. The new virus is known as a recombinant baculovirus and it is used to ferry the gene that makes the hemagglutinin antigen into a host cell line. As soon as the gene enters the cells, they begin to mass produce the hemagglutinin antigen. The antigen can then be extracted and purified before being assembled into a vaccine.

Given that they are entirely egg-free and dont require candidate virus samples, recombinant vaccines bypass the issue of egg-dependent changes. Due to the speed of production, there is also a decreased risk of escape mutants developing. As before, there is a paucity of comparative research, making it difficult to draw any firm conclusions, but early findings suggest recombinant vaccines may be more effective than traditional egg-based and cell-based vaccines, including improved antibody production.

Takeaway

Developing consistently protective influenza vaccines has proven difficult, with effectiveness frequently hovering somewhere between 40 and 60%. Too low, considering the threat posed by influenza.

A big part of the challenge is the mutability of the virus; it is constantly changing, making it hard for our immune system to keep up and retain useful memories of previous encounters. In response, public health agencies and scientists around the world develop new vaccines every year that prime our immune systems for the latest circulating strains. Sometimes scientists miss the mark with their predictions, in which case the circulating influenza strains do not match up with those in the vaccine, undermining vaccine effectiveness. At other times predictions are right on the money, but the vaccine production process impairs effectiveness either by being too slow and giving the wild type viruses time to mutate again, or because of mutations to the candidate vaccine strains during mass-production in chicken eggs.

Cell-based and recombinant vaccines aim to resolve the issues on the production side of things. The former by skipping the need for eggs, and by extension, the threat of egg-adapted changes. The latter by skipping the need for eggs as well as cutting down the time it takes to produce the vaccines, reducing the risk of escape mutants. Despite these advances, vaccine effectiveness has not yet seen the boost it needs.

The below table gives a summary of the advantages and disadvantages associated with these three production processes.

FIGURE 3. Advantages and disadvantages of strategies for influenza virus vaccine production.

The next article in this series will look at two additional technologies: intranasal vaccines and mRNA vaccines. Might they succeed where the more traditional strategies have wavered?

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Getting A Grip On Influenza: The Pursuit Of A Universal Vaccine (Part 2) - Forbes

Your immune system is on a mission, constantly assessing threats, identifying invaders, and neutralizing or killing them off. It is a finely tuned network of organs, cells, proteins, and chemicals engaged in an existential battle. It asks the question: is this me or is this not me? And if its not me, what is it? Friend or foe?

Without the immune system, which has been honed and refined throughout the millennia of our existence as a species, we could not survive.

Samir N. Khleif, M.D., is also on a mission: to outsmart and disable cancer by overcoming its ability to evade or tolerate immunotherapeutic approaches.

Dr. Khleif, a practicing medical oncologist, a Biomedical Scholar, and professor, is the director of the Center for Immunology and Immunotherapy and the Loop Immuno-Oncology Research Laboratory at the Lombardi Comprehensive Cancer Center at Medstar Georgetown University Hospital. He and his team of assistant professors, post docs, research assistants, graduate students, and trainees focus on understanding how the immune system works, delineating the mechanisms of immune response and resistance to immunotherapy and re-engineering the immune cells with the goal of developing novel immune therapeutics.

Khleif is a long-time pioneer in cancer immunotherapy. Before joining Georgetown, he served as Director of Georgia Cancer Center, Augusta University, where he oversaw the development of a large integrated program focused on immunology, inflammation, tolerance basic science, and immune therapy. He also led the Cancer Vaccine Section, a nationally active Immune Therapy Program at the National Institutes of Health-National Cancer Institute, where he was one of the early pioneers of cancer vaccines and led some of the clinical trials. (Fun fact: Moderna and BioNTech, the names behind the mRNA technology now used to protect us against COVID, started out as cancer vaccine companies.)

He currently holds numerous patents and has published several important studies unraveling the understanding of the interaction of immune cells and cancer and on the mechanisms of tumor-induced suppression and the strategies used to overcome them. His research team has also developed models to understand how different kinds of immune therapies can be combined to work synergistically and he translated these findings into clinical trials with the intention of more widespread use.

We recently met with him in his lab to learn more about immunology a subject weve all come to know since the pandemic and to discuss his research. For all his stellar achievements and fierce intellect, he was a gracious host and a passionate teacher. He is also, we later learned, a painter and a musician who plays keyboard, saxophone, piano, and the violin, amateurly, he insists. His top scientist of all time is Albert Einstein and his favorite D.C. restaurant is Komi.

Commenting on the upcoming BellRinger Ride benefit for Lombardi, Khleif sees similarities between his life mission and bicycling: both activities have an anticipation to reach the end goal along with hard work and a sense of exploration or adventure. To find out what BellRingers all about, see our sidebar in our print edition here.

Born in Syria to Palestinian refugee parents, Khleif attended college and medical school in Jordan after spending seven weeks in Vermont to learn English. Although he originally wanted to be a physicist, his father swayed him into medicine where a love of research led him to the study of virology, molecular biology, vaccines and, now, his work in harnessing the power of immune system to disable cancer cell growth and proliferation.

For Khleif, the joy of discovery is the catalyst for his work. The more discoveries you find, he says, the more addicted you get. I tell my team: when you discover something, ask yourself, why did nature create like this? Why does it exist? Can we recreate it when its missing? How can we use this as a tool for therapy?

Khleif and his team concentrate on four main areas of research: tumor immunology and immunotherapeutics (unraveling the mechanism through which the immune system and cancer cells interact ); T-cell plasticity (how T-cells, a type of immune cell, can be re-reengineered to amp up their immune response); immunotherapeutic resistance (how and why tumors learn to override the patients natural defenses and therefore become unresponsive to immuno- and other therapies); and combination immunotherapy design (identifying the best combination of immunotherapeutics to enhance the best clinical response).

Interestingly, the lab is also studying how some natural products, such as vitamin C and selenium, can be used to boost immunity, reprogram and repair immune cells, and reverse the damage that cancer causes on the immune system. So, stock up on your fruits, vegetables and seafood.

In his other life as an advocate for global health and impact-driven healthcare, he led the development and served as the founding CEO of the King Hussein Cancer Center in Amman, Jordan, the regional cancer center in the Middle East. He also led the planning and development of cancer care projects in low-income countries dedicated to bringing cancer education, research, and treatment to underserved areas around the world.

Every day, as your immune system conducts its intricate surveillance, it is working to dispatch dangers before they become serious health risks. Dangers like an errant cell that may grow into cancer. With immunotherapy in their arsenal, Khleif and his team are unlocking new strategies to dethrone the emperor of all maladies and save, he estimates, millions of lives.

To learn more about Dr. Khleif, his research, patents, and publications go to: https://gufaculty360.georgetown.edu/s/contact/00336000019h06bAAA/samir-khleif. You can also view his patient-oriented video on immunotherapy here: https://youtu.be/afdq8Op-jQM

For a highly accessible and entertaining resource on the immune system, check out Philipp Dettmers Immune, https://youtu.be/afdq8Op-jQM. If you or a family member have been diagnosed with cancer and would like to better understand immunotherapy, visit the Cancer Support Community here: https://www.cancersupportcommunity.org/immunotherapy-cancer-it-right-you .

And to support innovative cancer research at the Georgetown Lombardi Comprehensive Cancer Center, join the inaugural BellRinger Bike Ride on Oct. 22. Donate or learn more at bellringer.org.

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Bells Are Ringing! How Immunotherapy is Unlocking Doors to a Cancer Cure - Georgetowner

Berkeley Immune Support Formula provides supplements to the diet that can help in the boosting of the immune system and thus be and remain physically stronger.

Los Angeles, CA (August 13, 2022) The immune system is an essential part of the human body as it works as the shield that protects it from different kinds of diseases. Berkeley Immune Support Formula highly recommends one to be immunoreactive and suggests some of the daily care that one can take as a measure to keep a check on it, such as checking the vitamin D, keeping control of weight, and having an immune support booster, and others.

The product of the organization is mainly derived from many vegetables such as broccoli and cabbage due to which the organization also recommends that one can intake those in other forms as well. As their product is composed of more such elements rich in the DIM, it promises to give a better immune system result and prove itself the best immune support booster.

The product has been designed to aid the cause of raising funds for nature-based biomedical research. The product is said to be rich in Selenium, Zinc, Sulforaphane, Lycopene, Zeaxanthin, Lutein, Citrus Bioflavonoids, and Vitamin D3. The manufacturers of the product have many experiences with the DIM substance. The sulforaphane that is delivered by the immune support booster product is said to be specially manufactured by the scientists for the product.

Through the Berkeley Formula product, the organization makes a promise to the customers to provide the nutrients, which will be equal to a bowl of salad. The product is said to be the first of its kind that is composed of a mixture of bioflavonoids and phytonutrients. The product supplied by the organization is said to be manufactured for the most bioavailability, and it is also said to be giving bioactive quantities of the DIM to the consumers.

The Berkeley Formula product is regarded as a very effective bioavailable supplement of the DIM and immune system booster by many doctors and scientists. In fact, they have been found to do more research on the products along with the addition of other nutrients. The product is also said to be very effective for sportspeople, relieving stress from work or school, pollution of the environment, the process of aging, and sleep deprivation as an immune system booster.

About Berkeley Immune Support Formula

The organization was founded by Dr. Leonard Bjeldanes, Dr. Gary Firestone, Dr. Christopher Benz, Dr. Giuseppe Del Priore, and Dr. Bob Eghbalieh. These doctors have a specialty in the product supplied by the organization which is the DIM supplements, and in clinical research. The main purpose of this research is to contribute to the medical field with the help of their products. The main goal of the organization is to help people lead a healthy life, via the development of top-class nutrition goods. The two divisions of the organization function, that are the nutritional sciences and the biopharmaceuticals functions in the marketing of their product and in the development of the different types of cures for deadly diseases by boosting the immune system of the body.

For more information about the services of the company and knowing the offers, please visit https://www.berkeleyformula.com/

Media Contact:

Berkeley Immune Support Formula

1434 Westwood Blvd. Suite #5, LA, CA 90024

Phone: 877-777-0719

Email: [emailprotected]

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The1918 influenza pandemicresulted in the loss of over 3% of the worlds population at least 50 million people. But it wasnt the flu virus that caused the majority of these deaths.

Ananalysis of lung samplescollected during that flu pandemic indicated that most of the deaths were likely due to bacterial pneumonia, which ran rampant in the absence of antibiotics. Even in more recent history, like the1957 H2N2and2009 H1N1flu pandemics, nearly 18% of patients with viral pneumonia had additional bacterial infections that increased their risk of death. And theCOVID-19 pandemicis no different.

With yet another flu season fast approaching in the midst of the ongoing COVID-19 pandemic, lessening the harm caused by these viruses is important to prevent deaths and reduce infections. However, many deaths associated with the flu and COVID-19 dont occur at the hand of the virus alone. Instead, its asecondary bacterial infectionthat is often at the root of the devastating consequences attributed to an initial viral infection.

I am animmunologistwho studies why and how cells die during bacterial and viral infections. Understanding the synergy between these microbes is critical not only for effective diagnosis and treatment, but also for managing current pandemics and preventing future ones. My colleagues and Ipublished a studyshowing how an immune system protein crucial to fighting against viruses also plays an indispensable role in fighting bacteria.

Multiple pathogens can cause multiple infections in different ways. Scientists distinguish each typebased on the timingof when each infection occurs.Coinfectionrefers to two or more different pathogens causing infections at the same time.Secondary or superinfections, on the other hand, refer to sequential infections that occur after an initial infection. Theyre often caused by pathogens resistant to antibiotics used to treat the primary infection.

How viral and bacterial infections interact with each other increases the potential harm they can cause. Viral respiratory infections can increase the likelihood of bacterial infections and lead to worse disease. The reason why this happens is often multifaceted.

Within your respiratory tract, the epithelial cells lining your airways and lungs serve as the first line of defense against inhaled pathogens and debris. However,viruses can kill these cellsand disrupt this protective barrier, allowing inhaled bacteria to invade. They can alsochange the surface of epithelial cellsto make them easier for bacteria to attach to.

Viruses can also alter the surface ofepithelial and immune cellsbyreducing the number of receptorsthat help these cells recognize and mount a response against pathogens. This reduction means fewer immune cells report to the viral infection site, giving bacteria an opening to launch another infection.

Patients who have a bacterial infection at the same time theyre battling the seasonal flu are more likely to wind up in a hospital.Nearly a quarterof patients admitted to the ICU with severe influenza also have a bacterial infection. One study on the 2010 to 2018 flu seasons found thatnearly 20% of patientsadmitted to the hospital with flu-associated pneumonia had acquired bacterial infections.

Another studyof patients hospitalized with viral or bacterial infections found that nearly half had a coinfection with another pathogen. These patients also had nearly double the risk of dying within 30 days compared to those with only a single infection.

Interestingly, thetwo bacteria speciesmost commonly involved in coinfections with the influenza virus areStreptococcus pneumoniaeandStaphylococcus aureus, which normally exist in the respiratory tract without causing disease. However, the influenza virus can damage the cell barrier of the lungs and disrupt immune function enough to make patients susceptible to infection by these otherwise benign bacteria.

Secondary bacterial infections are also exacerbating the COVID-19 pandemic. A 2021 review estimated that16% to 28% of adultshospitalized for COVID-19 also had a bacterial infection. These patients stayed in the hospital for twice as long, were four times more likely to need mechanical ventilation and had three times greater odds of dying compared to patients with only COVID-19.

The immune systemresponds differentlyto viruses and bacteria.Antiviralsdont work on bacteria, and antibiotics dont work on viruses. A better understanding of what pathways the body uses to regulate both antiviral and antibacterial infections is critical to addressing secondary and coinfections.

Recent workby my colleagues and me may provide a clue. Wesequenced the RNAof one type of immune cell, macrophages, in mice to identify what molecules were present in cells that were either protected from or died due to bacterial infection.

We identifiedZ-DNA binding protein (ZBP1), a molecule already known to play a regulatory role in how the immune system responds to influenza. Specifically, ZBP1detects influenza viruseswithin the lungs and signals infected epithelial and immune cells to self-destruct. This induced cell death eliminates the virus and promotes recruitment of additional immune cells to the infection site.

Building off this finding that ZBP1 is important for fighting viral infection, we found that macrophages infected withYersinia pseudotuberculosis, a type of bacteria that causes foodborne illness, also use this protein to initiatecell death. This limits bacterial replication while also sendinginflammatory signalsthat help clear bacteria.

These findings raise the possibility that ZBP1 may play a dual role in how the body responds to viral and bacterial infections. Its possible that treatments that increase ZBP1 in certain types of cells may be useful in managing bacterial and viral coinfections.

Hayley Muendleinis an assistant research professor of immunology in the Tufts University Graduate School of Biomedical Sciences.

This article was originally published onThe Conversation. Read theoriginal story.

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COVID-19 and Flu Viruses Often Have a Deadly Accomplice: Bacterial Infections - Tufts Now

Eating grapes is potentially the cheapest, easiest way to improve your immune system, your metabolism, and your brain health. Foraround $2.09 per pound, grapes contain a bounty of essential nutrients including Vitamin C, antioxidants, calcium, and more. Now, three new studies suggest that just adding two cups of grapes to a high-fat diet can provideremarkable health benefits, surpassingour understanding of the benefits of grapes.

Dr. John Pezzuto examined the health benefits of grapes with a team of researchers from Western New England University. The three studies focus on lifespan, metabolism, fatty liver disease, and brain health, revealing that grape consumption yielded reductions in fatty liver and extended lifespans. To conduct the studies, the researchers analyzed how grape consumption altered gene expression in mice. Despite not conducting human tests, the researchers emphasize that these resultscan reliablytranslate to human health issues.

We have all heard the saying you are what you eat,' which is obviously true since we all start out as a fetus and end up being an adult by eating food, Western New England University Researcher and senior author of three new studies Dr. John Pezzuto said. But these studies add an entirely new dimension to that old saying. Not only is food converted to our body parts, but as shown by our work with dietary grapes, it actually changes our genetic expression. That is truly remarkable.

Pezzutos first study concluded that grape consumption triggered unique gene expressions in the mice. This study found that grape consumption led to a reduced risk of fatty liver disease and expanded the overall lifespan of the animal consuming the grapes. To properly conduct the study, the animals followed a high-fat western style diet. Published in Foods, this study claims that grape consumption can modulate the adverse effects of a traditional Western diet, preventing oxidative damage.

What is the effect of this alteration of gene expression? Fatty liver, which affects around 25% of the worlds population and can eventually lead to untoward effects, including liver cancer, is prevented or delayed, the researchers stated. The genes responsible for the development of fatty liver were altered in a beneficial way by feeding grapes.

The second study, published in Food & Function, found that the consumption of grapes changes metabolism. When Pezzuto and his research team introduced grapes to mice following high-fat diets,researchers found increased levels of antioxidant genes in the mice. The study concluded that grapes help reprogram the metabolism of the gut microbiota, increasing the efficiency of the liver and energy production.

Many people think about taking dietary supplements that boast high antioxidant activity, Pezzuto said. In actual fact, though, you cannot consume enough of an antioxidant to make a big difference. But if you change the level of antioxidant gene expression, as we observed with grapes added to the diet, the result is a catalytic response that can make a real difference.

Published in the journal Antioxidants, the final study observed how grape consumptionbenefits brain function. Theresearch highlights that a high-fat diet presents negative behavioral and cognitive pressures on the brain. In contrast, grape consumptionhelps alleviate these pressures, havinga positive effect on the brain and brain metabolism. The researchers noted that this initial conclusion will require more research to determine the extent of the positive impacts.

Although it is not an exact science to translate years of lifespan from a mouse to a human, our best estimate is the change observed in the study would correspond to an additional 4-5 years in the life of a human, Pezzuto said. Precisely how all of this relates to humans remains to be seen, but it is clear that the addition of grapes to the diet changes gene expression in more than the liver.

This February, a study found that a mostly plant-based diet can prolong life expectancy by over 10 years. The team of Norweigan researchers found that introducing more plant-based foods earlier in life helps cut down the risk of life-threatening disease and improves your overall health. Following an "optimal" diet defined as primarily plant-based a little fish showed long-term health benefits, whereas diets high in red or processed meat showed an inverse relationship.

Another study from last March found that eating more plant-based is key tomaintaining a healthy gut. This study concluded that by improving gut health, you can improve longevity and prolong your lifespan. The researchers claim that building a healthy microbiome at an earlier age is essential to better health in old age.

For more plant-based happenings, visit The Beet's News articles.

Here are the best foods to eat on repeat, to boost immunity and fight inflammation. And stay off the red meat.

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Eat This Fruit Daily to Stay Sharp and Live Longer, Research Find - The Beet

With the countrys third COVID fall approaching, the United States is expected to soon start ramping up its autumn COVID-19 booster campaign.

This years rollout will include something new. Moderna and Pfizer-BioNtech are working on bivalent boosters that include both the original vaccine formula and a component that targets the Omicron BA.4 and BA.5 subvariants of the coronavirus.

While the Biden administration has yet to reveal details of the rollout plan (expect more on that later), heres what we know so far.

The Omicron variant has overcome much of the protection against infection offered by two doses of the mRNA vaccines (such as Moderna and Pfizer-BioNTech).

A first booster restores some of that protection, but this wanes considerably within about three months after vaccination.

In spite of that, Dr. David Cutler, a family medicine physician at Providence Saint Johns Health Center in Santa Monica, Calif., told Healthline that the current vaccines continue to offer strong protection against severe illness and death.

This is especially true of the boosters.

In May 2022, unvaccinated people were six times more likely to die of COVID-19, compared to people vaccinated with at least a primary series (for most, two doses of the mRNA vaccines), according to the Centers for Disease Control and Prevention (CDC).

Among people 50 years and older, unvaccinated people were 29 times more likely to die of COVID-19 than those who had received the primary series and at least two booster doses, agency data showed.

The current COVID-19 vaccines and boosters are based on the original strain of the virus. As CDC data shows, these still offer strong protection against severe disease caused by Omicron.

However, in order to better target the variants likely to be circulating in the fall, the Food and Drug Administration (FDA) asked vaccine makers in June 2022 to update their boosters to include a component that targets the currently circulating Omicron BA.4 and BA.5 subvariants.

We think the Omicron-specific boosters will improve immunity against the existing Omicron variants. This may be particularly helpful during the anticipated winter surge, Dr. Jimmy Johannes, a pulmonologist and critical care medicine specialist at MemorialCare Long Beach Medical Center in California, told Healthline.

However, not all scientists agree that Omicron-specific boosters will provide greater protection than the current ones.

Cutler thinks the strongest benefit of Omicron-specific boosters will be for people who are unvaccinated or have not received the full primary series and any booster(s) for which they are eligible.

One problem with choosing which booster to use in the fall is its impossible to know for certain which variants will be circulating by then, although some experts expect it to be a descendant of one of the currently circulating Omicron variants.

Data presented at an FDA vaccine advisory committee meeting in June 2022, though, suggests that vaccination with a variant-specific booster such as one targeting Omicron might lead to a broadened antibody response against the coronavirus.

Data from Moderna shows the potential for this kind of broader immune response. The companys bivalent Omicron BA.1 booster also produced a higher level of neutralizing antibodies against BA.4 and BA.5 than the original booster, according to preliminary data.

On August 15, the United Kingdoms Medicines and Healthcare Products Regulatory Agency approved Modernas bivalent Omicron BA.1 booster for use in adults.

The Moderna and Pfizer-BioNTech boosters based on the original strain of the coronavirus are currently available for anyone who is eligible for a first or second booster.

The bivalent boosters from those companies are expected to be available in early to mid-September, Dr. Ashish Jha, White House COVID-19 response team coordinator, said in a virtual discussion with the U.S. Chamber of Commerce Foundation on August 16.

Before these boosters can be rolled out, though, the FDA will need to authorize them and the CDC will need to sign off on their use.

The fourth vaccine in the country, Novavaxs protein-based vaccine, was authorized by the FDA on July 13, 2022 for use as a two-dose primary series. This vaccine is based on the original strain of the coronavirus.

The company announced the next month that it had applied for FDA authorization of this vaccine as a booster. It is also testing an Omicron-specific vaccine and a bivalent vaccine that targets Omicron and the original strain, the company said in a release.

Everyone currently eligible for a COVID-19 booster will still be eligible in the fall, including:

Johannes said anyone at risk of severe COVID-19, or complications of a coronavirus infection, should consider getting boosted when the bivalent vaccine is available.

This includes older adults, as well as those with chronic medical conditions such as heart disease, liver or kidney disease, a chronic respiratory condition, cancer, an immune compromising condition, high blood pressure or diabetes.

The Biden administration is also expected to open up second boosters this fall to adults under age 50 when the bivalent vaccines are available. This expansion of eligibility was put on hold when vaccine makers said they could deliver the bivalent vaccines in early fall.

When the bivalent boosters are available in the fall, these will be used for all booster shots in the United States, including first and second boosters.

Pregnant women are also eligible for boosters.

The [COVID-19 mRNA] vaccines have now been given to tens of millions of pregnant women. They are extremely safe, said Jha during the online Chamber of Commerce call. We have seen little to no side effects [in pregnant women], the same side effects that most of us get the sore arm, sometimes 24 hours of feeling fatigued or a little bit run down.

Bolstering the safety profile of these vaccines, a large study from Canada published August 17, 2022, in The BMJ found that women who received a COVID-19 vaccine during pregnancy did not have a higher risk of having a preterm birth, a baby who was small for their gestational age at birth, or a stillbirth.

No details are available yet on the fall booster rollout, but it will likely be similar to the initial booster release last year, with vaccines mainly available at doctors offices and pharmacies. Some mass vaccinations may also happen in certain locations.

To find a vaccination site near you, check out the federal Vaccines.gov or your states COVID-19 vaccine website.

Its difficult to know what the coronavirus will do in the fall will there be a large spike early in September or will a new variant emerge? In addition, theres no guarantee that the bivalent vaccines will definitely be available in September.

As a result, the CDC recommends getting boosted as soon as you are eligible, with whichever booster is available. This is especially important for adults 50 years and older or those with compromised immune systems.

It can take one to two weeks after receiving a booster for your immune system to be fully primed. So if you are eligible now and get boosted, you will be better protected should cases surge as we head into the fall and winter.

You can always get the bivalent vaccine when it is available. Jha said you will want to space out those two boosters at least a little bit, probably 4 to 8 weeks.

The CDC may also weigh in on the timing between boosters when it reviews the data on the Omicron-specific boosters.

Jha said if you are planning on getting the seasonal flu shot this fall, you can definitely get this alongside a COVID-19 booster.

The CDC recommends that people get vaccinated against the flu by the end of October to ensure they have strong immune protection at the peak of the flu season, which generally happens in February.

Scientists dont know yet if the coronavirus that causes COVID-19 will follow a similar seasonal pattern, but cases have tended to increase in colder parts of the country as people head indoors for the fall and winter.

Although the FDA asked vaccine makers to update their boosters to include an Omicron-specific component, it did not advise them yet to update the vaccine for the primary series.

This suggests that unvaccinated people will receive the original vaccine, which the agency said provides a base of protection against serious outcomes of COVID-19.

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The Next COVID-19 Booster Shots Will Target Omicron: What to Know - Healthline

Eating a nutrient-dense diet can help someone recover from COVID-19 by supporting their immune system and managing inflammation. This may be particularly important if they lose their sense of taste or smell and have the temptation to eat stronger tasting, less nutritious foods.

People can support their bodies in recovery at home by eating a nutritious diet. This article looks at what experts advise to eat when individuals have COVID-19.

This article also details the symptoms of COVID-19, how the loss of taste and smell affects diet, what to do if vomiting occurs, and some frequently asked questions.

Eating a nutritious diet is an essential consideration in recovering from COVID-19. Research suggests that insufficient nutrition is a risk factor for severe COVID-19, and key nutrients can help support the immune system and manage inflammation.

The following foods and nutrients may help a person recover from the disease.

According to a 2022 review, experts associate a diet involving healthy, plant-based foods with a lower risk and severity of COVID-19. In addition, the study found that a healthy, plant-based diet may particularly benefit people with higher socioeconomic deprivation.

A diet high in saturated fat increases angiotensin-converting enzyme, the main entry point for coronavirus into cells. Research suggests that diets, such as the Mediterranean diet, which are low in saturated fat and high in nutrients from plant foods, can provide more antioxidants for the body. Antioxidants may help fight viruses and support the immune system.

Therefore, eating the following foods can provide fiber, essential vitamins and minerals, and phytochemicals, which are helpful compounds that plants produce.

Learn more about the Mediterranean diet.

According to a 2020 review, high quality proteins, such as fish, eggs, and lean meat, are an essential part of an anti-inflammatory diet that helps produce antibodies and fight off infection.

Learn more about tips and tricks to eat more protein.

The review also notes that dietary fiber consumption correlates with lower mortality from infectious and respiratory diseases. Consuming fiber can also lead to more favorable gut bacteria, which lowers inflammation. People can consume beneficial fiber in:

Learn more about high fiber foods.

Omega-3 fatty acids, especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may have beneficial effects on COVID-19. These include:

Oily fish is a high source of omega-3 fatty acids. Additionally, plant-based foods, such as flaxseed, walnuts, and hemp, contain alpha-linolenic acid, which the body can convert to EPA and DHA. People can also take an omega-3 supplement from fish or algae.

Learn more about omega-3-rich foods.

Some studies have found that vitamin C can shorten the duration of colds and may improve respiratory symptoms. Vitamin C acts as an antioxidant and regulates the immune system and gene expression.

Other research suggests that vitamin C may help improve inflammation markers in people with coronavirus, but people should not consider it as a treatment in supplement form.

However, people can include vitamin C-rich foods in their diet when they have COVID-19 to help support their immune system. These include:

Learn more about foods high in vitamin C.

Vitamin D plays an important role in the bodys immune system. Scientists previously suggested that dietary sources of vitamin D were particularly important during the pandemic because many people had less exposure to the sun during the lockdown.

People get vitamin D from exposure to the sun and foods such as beef liver, egg yolks, cheese, and fortified breakfast cereals.

Learn more about foods high in vitamin D and other sources.

Some research suggests zinc may reduce viral replication and gastrointestinal and respiratory symptoms of COVID-19. However, most research has focused on zinc supplements, so it is difficult to say whether eating zinc foods can help.

However, zinc is an essential mineral for immune function, and eating foods that contain the substance may support recovery from illness.

Foods containing zinc include:

Learn more about foods high in zinc.

A 2020 meta-analysis of research estimates that 48% of patients with COVID-19 globally experienced a loss of smell and around 41% experienced a loss of taste. In some people, these symptoms may persist as part of long COVID.

Learn more about how COVID causes loss of taste and smell.

People who experience a loss of smell or taste may go off foods they usually eat or prefer foods with more salt, sugar, or fat, as they may be able to taste these more. However, individuals need to ensure they eat plenty of fruit and vegetables for their vitamin and antioxidant benefits. Avoiding too many high sugar or high fat foods is also advisable, as these can be inflammatory.

Taste disorder experts advise eating fruits and vegetables individually rather than as combination dishes such as casseroles and one-pots. This is because combination dishes hide individual flavors and dilute the taste.

Additionally, people can try adding more robust flavors such as citrus, herbs, and spices.

Some people experience nausea or vomiting as symptoms of COVID-19. They may not feel like eating but should ensure they hydrate with fluids.

Individuals should consult a doctor if they have excessive vomiting or go off food for longer than expected.

Learn more about food poisoning versus COVID-19.

Here are some frequently asked questions about COVID-19 and food.

According to the CDC, most people with mild to moderate COVID-19 can spread SARS-CoV-2, the virus that causes the disease, no more than 10 days after symptom onset.

However, most individuals with more severe to critical illnesses are likely to be able to spread the virus no more than 20 days after their symptoms began.

The Food and Drug Administration (FDA) advises that there is no evidence of food packaging having associations with the transmission of SARS-CoV-2.

However, people can wipe down food packaging with an antibacterial wipe as an extra precaution.

Research suggests optimal nutrition and dietary nutrient intake can affect the immune system. So eating a nutritious, balanced diet can help people fight the virus.

When someone has COVID-19, they should aim to eat a nutritious, balanced diet that supports their immune system.

Nutrients, such as vitamin C, zinc, and omega-3 fatty acids, can help the process of recovery. Similarly, a person should ensure adequate fiber and protein from nutritious sources.

If someone has lost their sense of taste or smell, they should avoid eating too many inflammatory foods such as sugar and fat. Instead, they may want to try eating individual fruits and vegetables rather than one-pot meals that disguise their flavor.

Read more here:
What to eat when you have COVID - Medical News Today

These days, the word inflammation is enough to make anyone nervous. A growing body of research associates it with diabetes, heart disease, rheumatoid arthritis, asthma, and more leading us to buy anti-inflammatory supplements and eat antioxidant-rich foods. Many of these supplements and eating habits are healthy, but theres an important point that were missing: Good inflammation also exists, and its very important for our bodies. Heres why.

As explained in a 2018 Oncotarget research paper, inflammation is a biological response of the immune system. And it gets useful when an infection enters the body.

Certain signaling molecules in the immune system will recognize foreign molecules in the body as pathogens. When this happens, the molecules issue an alarm to innate immune cells (which recognize certain molecules on many different pathogens think of them as general fighters), which begin attacking the infection. This response results in inflammation, which takes the form of fever, chills and sweats, sinus congestion, and other symptoms.

While innate immune cells do a good job of attacking infections, they arent the best equipped for targeting specific pathogens. Thats where T and B cells come in. (Think of these as specialized fighters). T cells either target specific pathogens and infected cells or help control the immune response. B cells create customized antibodies (proteins) that attach to pathogens in order to help destroy them. T and B cells take longer to respond to an infection, but are crucial to clearing it out of the body.

In addition, the immune system can recognize toxic compounds that enter the body or sit on top of the skin. This recognition process causes an inflammatory response (such as swelling or redness). With time, specific cells help clear the toxic molecules to prevent them from causing further damage to the body.

If youve ever scratched your leg or twisted your ankle, youre familiar with the inflammation that follows. The body sends blood, fluid, and white blood cells to the injured area to start mitigating the damage and begin repairs.

While pain, redness, and swelling arent pleasant, theyre an important step in the healing process. Without an inflammatory response, our cuts and bruises would never heal.

The key difference between good and bad inflammation appears when an inflammatory response becomes chronic. Acute inflammation is generally good, because its a useful response to immediate injuries or infections. Chronic inflammation, however, occurs when the inflammatory response goes on for too long, or the response is too great.

Examples of this include allergic reactions, rheumatoid arthritis, and heart disease. During an allergic reaction, the immune system inaccurately detects an allergen (like peanut butter) as a foreign invader and mounts a response so huge that it harms the body. In heart disease, sustained, low levels of inflammation can irritate blood vessels and promote the formation of plaque. And in rheumatoid arthritis, the immune system attacks the lining of the joints.

The takeaway? Finding ways to reduce chronic inflammation is a good thing. Just remember that good inflammation happens for a reason.

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3 Ways Good Inflammation Helps Your Body - First For Women