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Biogen and Eisai launch multiple initiatives to help patients with Alzheimer’s disease access ADUHELM™

By Dr. Matthew Watson

Programs now available to support patients and families with their treatment journey

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Reata Pharmaceuticals Announces Participation in The Goldman Sachs 42nd Annual Global Healthcare Conference

By Dr. Matthew Watson

PLANO, Texas, June 07, 2021 (GLOBE NEWSWIRE) -- Reata Pharmaceuticals, Inc. (Nasdaq: RETA) (“Reata,” the “Company,” or “we”), a clinical-stage biopharmaceutical company, today announced that management will participate in a virtual Fireside chat and hold 1x1 meetings at the Goldman Sachs 42nd Annual Global Healthcare Conference on Tuesday, June 8, 2021.

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Design Therapeutics Expands Board of Directors with Key Appointments

By Dr. Matthew Watson

CARLSBAD, Calif., June 07, 2021 (GLOBE NEWSWIRE) -- Design Therapeutics, Inc. (Nasdaq: DSGN), a biotechnology company developing treatments for degenerative genetic disorders, today announced the appointments of industry veterans, Heather Behanna, Ph.D., principal of SR One, and Deepa Prasad, managing director of WestRiver Group, to its board of directors effective June 15, 2021.

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Design Therapeutics to Participate in Goldman Sachs 42nd Annual Global Healthcare Conference

By Dr. Matthew Watson

CARLSBAD, Calif., June 07, 2021 (GLOBE NEWSWIRE) -- Design Therapeutics, Inc. (Nasdaq: DSGN), a biotechnology company developing treatments for degenerative genetic disorders, today reported that João Siffert, M.D., president and chief executive officer, will participate in a fireside chat during the Goldman Sachs 42nd Annual Global Healthcare Conference on Wednesday, June 9, 2021 at 1:20 p.m. ET.

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Centessa Pharmaceuticals to Present at the Goldman Sachs 42nd Annual Global Healthcare Conference

By Dr. Matthew Watson

CAMBRIDGE, Mass. and LONDON, June 07, 2021 (GLOBE NEWSWIRE) -- Centessa Pharmaceuticals plc (Nasdaq: CNTA) announced today that Saurabh Saha, M.D., Ph.D., Chief Executive Officer, will participate in an analyst-led fireside chat at the Goldman Sachs 42nd Annual Global Healthcare Conference on Tuesday, June 8, 2021, beginning at 5:30 p.m. Eastern Time.

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Arvinas Participates in Groundbreaking Ceremony for New Space Within Downtown Crossing Development in New Haven

By Dr. Matthew Watson

NEW HAVEN, Conn., June 07, 2021 (GLOBE NEWSWIRE) -- Arvinas, Inc. (Nasdaq: ARVN), a clinical-stage biotechnology company creating a new class of drugs based on targeted protein degradation, today joined state and local officials, fellow tenants, and community partners, in a groundbreaking ceremony for 101 College Street, a new 525,000-square-foot-building to be constructed as part of New Haven’s Downtown Crossing revitalization project. Arvinas will lease three of the 10 floors at 101 College and this space will serve as the Company’s headquarters beginning in 2024.

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Zymergen to Present at Goldman Sachs Annual Global Healthcare Conference

By Dr. Matthew Watson

EMERYVILLE, Calif., June 07, 2021 (GLOBE NEWSWIRE) -- Biofacturing leader Zymergen today announced the company will be participating in the upcoming Goldman Sachs Annual Global Healthcare Virtual Conference.

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HOOKIPA Phase 1 HB-200 data show unprecedented T cell response, favorable tolerability, and preliminary efficacy as monotherapy for advanced HPV16+…

By Dr. Matthew Watson

NEW YORK and VIENNA, Austria, June 07, 2021 (GLOBE NEWSWIRE) -- HOOKIPA Pharma Inc. (NASDAQ: HOOK, ‘HOOKIPA’), a company developing a new class of immunotherapeutics based on its proprietary arenavirus platform, today reported positive Phase 1 data from its ongoing Phase 1/2 study (NCT04180215) of HB-200 for the treatment of advanced Human Papillomavirus 16-positive (HPV16+) cancers. Data presented as an oral presentation (abstract #2502) at the 2021 American Society of Clinical Oncology (ASCO) Annual Meeting showed outstanding T cell responses, preliminary efficacy as a monotherapy in heavily pretreated patients who progressed on standard of care, including checkpoint inhibitors, and favorable tolerability. The company also announced translational data suggesting a relationship between T cell response and potential clinical efficacy. The company will host an investor event today at 6:30pm EDT.

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Avicanna Provides Bi-Weekly Update On Status Of Management Cease Trade Order

By Dr. Matthew Watson

/NOT FOR DISTRIBUTION TO UNITED STATES NEWSWIRE SERVICES OR FOR DISSEMINATION IN THE UNITED STATES. ANY FAILURE TO COMPLY WITH THIS RESTRICTION MAY CONSTITUTE A VIOLATION OF UNITED STATES SECURITIES LAWS/

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Orion and the Blood Service launch collaboration to develop new CAR T-cell cancer therapy

By Dr. Matthew Watson

ORION CORPORATION                 PRESS RELEASE                8 JUNE 2021         AT 8.00 a.m. EEST

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Roche obtains CE mark for the SARS-CoV-2 Antigen Self Test Nasal allowing for rapid self testing of COVID-19 at home

By Dr. Matthew Watson

Basel, 08 June 2021 - Roche (SIX: RO, ROG; OTCQX: RHHBY) today announced it has received CE mark for its SARS-CoV-2 Antigen Self Test Nasal for at-home testing. The test will be available in countries accepting the CE mark through pharmacies and other locations, in packs of five tests. An early version of the test has already been available as a home-test in a number of European markets under local special approval pathways since February 2021. With the CE Mark, the SARS-CoV-2 Antigen Self Test Nasal for rapid self testing of COVID-19 test has received official approval following the traditional registration pathway and can now also be used in markets that have not established regulatory exemption pathways. By following simple instructions, individuals can perform the test at home using a nasal swab without special training or the supervision of a healthcare worker. The test provides results in as little as 15 minutes and can help people to conveniently check if they are likely to be infectious from the comfort of their home. In the case of children under 18 years of age, the test must be performed by an adult or under close adult supervision.As societies begin to reopen and in line with local health regulations, the convenient test allows individuals planning to attend an event or gathering to use the test as a tool to confirm that they are not likely to be carriers of a substantial amount of the virus thus helping them make informed decisions and reduce the risk of transmission to others. Complementary to the SARS-CoV-2 Antigen Self Test Nasal, Roche is offering NAVIFY® Pass. This digital solution allows individuals and healthcare professionals to remotely store, display, and share their COVID-19 test results and vaccine status through a personalised QR code. Having easy digital access to test results and vaccination status could potentially be used by both individuals and companies to facilitate access to locations with COVID-19 entry protocols, such as restaurants or entertainment venues, as well as to validate safety to travel.“As the world prepares to reopen, high-quality, home-based testing will play an important role in the battle against the pandemic,” said Thomas Schinecker, CEO, Roche Diagnostics. “Regular self-testing at home can reduce pressure on healthcare systems. It can quickly identify people with the highest potential to be infectious so they can take immediate action to seek medical advice, manage their infection and protect others.”This test is part of a partnership with SD Biosensor Inc., with whom Roche has also launched a SARS-CoV-2 Rapid Antibody Test in July 2020 and two SARS-CoV-2 Rapid Antigen Tests for professional use in September 2020 and February 2021. These tests will continue to play an important role in fighting this pandemic and remain available for healthcare professional testing.In addition to diagnostic testing, preventive measures remain key to protecting yourself and others against SARS-CoV-2. It is recommended to continue wearing masks, socially distance and practice good hygiene, especially if you have symptoms or known contact with others who have tested positive for the virus. Roche continues to expand its comprehensive COVID-19 portfolio to support healthcare systems in diagnosing SARS-CoV-2 infection.About the SARS-CoV-2 Antigen Self Test Nasal for at-home patient self-testingThe SARS-CoV-2 Rapid Antigen Self Test Nasal is a rapid chromatographic immunoassay (lateral flow assay) for the detection of the nucleocapsid protein of SARS-CoV-2 in human nasal samples. Each test contains a unique QR code to enable individuals to share their test results and vaccine status using NAVIFY Pass, Roche’s digital solution. For more information on NAVIFY Pass, visit www.navifypass.comThe clinical performance of the test was measured by head to head comparison with Roche’s highly sensitive reverse transcriptase polymerase chain reaction (RT-PCR) test using nasopharyngeal swab samples as a comparator, the gold standard sampling and detection method for SARS-CoV-2 detection.1,2 Combined study results showed that the relative sensitivity of the SARS-CoV-2 Antigen Self Test Nasal was 91.1%.** The overall relative specificity was 99.6 %,3 which represents the ability of the test to correctly identify patients without the virus. In one comparative independent self testing study where patients followed written and illustrated instructions to sample, test and read-out the results themselves, the majority of study participants considered the procedures easy to perform.4 About antigen testingAn antigen test detects proteins which are structural or functional components of a pathogen and are very specific to that pathogen.5 In this case, the test would provide a qualitative “yes/no” answer on the presence of the antigen in the patient sample and can be offered as a rapid strip test that is performed at the point of care. If the target antigen (nucleocapsid protein) is present in sufficient concentrations in the sample, it will bind to specific antibodies and generate a visually detectable signal on the test strip, typically with results ready in 15 minutes. A rapid antigen test can reliably detect individuals with a high viral load allowing healthcare professionals to quickly identify those patients at the greatest risk of spreading the infection.6About Roche’s response to the COVID-19 pandemicThe COVID-19 pandemic continues to evolve globally with varying developments from country to country and we are partnering with healthcare providers, laboratories, authorities and organisations to help make sure that patients receive the tests, treatment and care they need. This new test is an additional step in Roche’s fight against the COVID-19 pandemic, which has already included:

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OXURION Completes Patient Enrollment for Part A of Phase 2 Study Evaluating THR-149 for Treatment of Diabetic Macular Edema (DME)

By Dr. Matthew Watson

THR-149 is a potent plasma kallikrein inhibitor for the treatment of DME in the roughly 40% of the patient population responding suboptimally to anti-VEGF therapy

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OXURION Completes Patient Enrollment for Part A of Phase 2 Study Evaluating THR-149 for Treatment of Diabetic Macular Edema (DME)

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Polyphor Hosting Key Opinion Leader Roundtable on Covid-19: The Need for Novel Therapies for Severe Infections and the Potential Role of…

By Dr. Matthew Watson

Webinar Roundtable Being Held Thursday, June 10th @ 8amET/2pmCET Webinar Roundtable Being Held Thursday, June 10th @ 8amET/2pmCET

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Novo Nordisk partners with Heartseed on heart failure cell therapy – PMLiVE

By daniellenierenberg

Danish pharma company Novo Nordisk has announced a new collaboration and licence agreement with Japans Heartseed to develop the companys investigational cell therapy HS-001 for heart failure.

HS-001, Heartseeds lead asset, is an investigational cell therapy using purified cardiomyocytes derived from induced pluripotent stem cells (iPSC). The therapy is currently being developed as a treatment for heart failure.

Heartseed is already planning to launch a phase 1/2 study of HS-001 in Japan in the second half of 2021, which will evaluate the safety and efficacy of the therapy for the treatment of heart failure caused by ischaemic heart disease.

Under the terms of their agreement, Novo Nordisk will gain exclusive rights to develop, manufacture and commercialise HS-001 globally, excluding Japan where Heartseed will retain the rights to solely develop the therapy.

However, Novo Nordisk has the rights to co-commercialise HS-001 with Heartseed in Japan, with equal profit and cost sharing.

In return, Heartseed is eligible to receive up to a total $598m, with $55m earmarked in upfront and near-term milestone payments.

The Japanese biotech company is also eligible to receive tiered high single-digit to low double-digit royalties of annual net sales on the product outside Japan.

"We are delighted to have a company with the expertise and resources of Novo Nordisk as our partner for development and commercialisation of HS-001, and are also honoured that Novo Nordisk has recognised the innovativeness and high potential of our technology," said Keiichi Fukuda, chief executive officer of Heartseed.

"We believe that the partnership with Novo Nordisk is very valuable as we seek to disseminate our Japan-origin innovation globally as early as possible, he added.

Through this important collaboration with Heartseed, we aim to pioneer novel treatment solutions for people with cardiovascular disease, said Marcus Schindler, chief scientific officer, EVP research and early development at Novo Nordisk.

We [will] gain access to an innovative clinical asset, underlying technology and deep expertise within the field of iPSC biology and cardiac cell transplantation, which can be combined with our knowledge and capabilities in stem cell biology and manufacturing, he added.

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Accumulating Evidence Suggests E-Cigarettes Are Likely As Harmful To The Brain As Regular Smoking – Forbes

By daniellenierenberg

Comparing the effects of e-cigarettes and regular smoking on the brain.

An ever accumulating volume of scientific and preclinical data shows new evidence of ways that e-cigarettes are dangerous. Understandably, most of the focus has been on the effects on the lungs, cardiovascular disease, and addiction. But recently, a growing body of scientific studies are starting to show the serious potential negative effects e-cigarette use may have on the brain.

Electronic-cigerettes (e-cigarettes), and more broadly electric vaporizers, have a history that goes back almost 100 years. The modern commercial version of the e-cigarette is usually attributed to the Chinese pharmacist Hon Lik, although numerous patents and related technologies developed by others were prevalent throughout the 1980s and 90s.

The immediate urgency in attempting to understand the health effects of e-cigarettes stems from their increasing rate of use, most concerning among young people. The challenge though is that they are simply too new, and not enough time has passed to understand and really appreciate their potential long term clinical effects due to sustained or chronic use.

Among high school students, the use of tobacco products had been on the decline until 1998, attributed to aggressive anti-smoking campaigns through the 90s. But this changed that year, with an increase in tobacco use due exclusively to the use of e-cigarettes. By 2014 e-cigarettes overtook all other tobacco products among this population. Even more concerning is the rate at which their use is increasing. According to the Centers for Disease Control and Prevention (CDC) e-cigarette use among high schoolers increased 77.8% in 2018 over 2017, with similar trends observed internationally.

And while it is possible to find e-cigarette pods and inserts that do not have nicotine, the vast majority do. Whats worse, the trend has been to increase the concentration of nicotine delivered by these products. In the case of the popular Juul brand, the average concentration of nicotine considerably exceeds the concentration in regular cigarettes.

To be fair, one potential positive use of these devices might be in helping long time smokers reduce the use of regular cigarettes. The CDC has stated that that while e-cigarettes are not safe for people that dont use tobacco, they are dohave potential to benefit adult smokers. By triturating the chemical composition and rate of nicotine delivery, it may offer a new tool to assist these individuals. Getting a long time smoker to reduce their dependency on combustible cigarettes is a meaningful thing.

And a National Academies report concluded, ecigarettes are not without risk, but compared to combustible tobacco cigarettes they contain fewer toxicants and are likely to be far less harmful than combustible tobacco cigarettes. The Federal Drug Administration (FDA) has stated that nicotine is what addicts and keeps people using tobacco products, but it is not what makes tobacco use so deadly. Yet, at the same time, even within the FDA and CDC, they state that they continue to investigate the distressing incidents of severe respiratory illness associated with use of vaping products. However, this does not necessarily imply that nicotine is responsible, but rather, that other additives and the delivery technologies themselves may be contributing to such clinical effects.

When it comes to the brain, the potential dangerous effects e-cigarettes may have on the brain and their long term consequences stem from the well established effects nicotine in general has on the brain and brain development, the degree and concentration of nicotine e-cigarettes are capable of delivering, and the chemistry associated with how these devices deliver it. The microvascuature of the brain - the collection of specialized blood vessels that feed the brain and spinal cord and regulate their chemical environment - as well as the cells that make up the brain itself (neurons and other cells), are all vulnerable to damage.

The microvascuature of the brain and spinal cord consists of a vast collection of capillaries that provide brain cells with oxygen and nutrients. It also shuttles away cellular waste products. The brains microvascuature is unique compared to the rest of the body. The endothelial cells that make up these tiny blood vessels form a regulated barrier between the blood on one side (the lumen side of the blood vessels) and the chemical environment the brain and spinal cord float in on the other side. This barrier is called the blood brain barrier.

The normal compliment of molecules and immune cells capable of moving between the blood and the cellular spaces in the other tissues of the body cannot freely do so with the brain and spinal cord - which collectively form the central nervous system. The unique chemical environment of the central nervous system formed by the blood brain barrier is the cerebral spinal fluid.

There is a strong correlation between long term smoking, cognitive decline in the later decades of life, and disruption of the blood brain barrier and microvasculature of the brain. In fact, cognitive decline and microvascular dysfunction are essentially universal consequences of long term smoking for everyone. The exact pathophysiological mechanisms involved are still not completely clear though, warranting continued research. But a recently published paper suggests how the negative physiological effects nicotine has on brain cells when delivered via e-cigarettes mirrors the effects observed with combustible cigarettes.

The endothelial cells that make up the microvasculature are particularly vulnerable. This means that the normal regulatory mechanisms responsible for maintaining the unique chemical environment of the cerebral spinal fluid via the blood brain barrier may slowly break down, contributing to cognitive decline.

And in at least one mouse model study, the authors suggest that e-cigarettes may also have short term disruptive effects on cognitive and memory functions. So there may be more immediate and acute concerns with e-cigarette use, in particular in younger populations where the brain is still developing.

In another study, scientists found that e-cigarettes produce a stress response in neural stem cells, which are populations of cells that eventually become neurons and other important cell types in the brain. Again, potential effects on the still developing brain of adolescents is of immediate concern.

On a positive note, a clinically significant exception to the above effects is the use of nicotine to potentially treat Parkinsons disease. Nicotine and chemically related drugs have been shown to be effective in protecting the parts of the brain that are affected and degenerate in Parkinsons, as well as in treating the symptoms of the disease. Its use has also been indicated in reducing the significant side effects of other Parkinsons drugs.

At the moment there are more questions than answers when it comes to understanding the physiological and cellular effects e-cigarettes - and in particular high concentration nicotine delivery via these devices - has on the brain. The inclusion of additional additives may further exacerbate microvasculature and cellular damage to the brain. These risks should of course be balanced against e-cigarettes ability to help people quit combustible tobacco products, which for that population is judged to be significantly more dangerous than e-cigarettes. The long term epidemiological and public health consequences of e-cigarettes - both good and bad - will not be fully appreciated for years to come. But the data at the moment seems to suggest potential significant pathophysiological effects on brain function.

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How STEM Can Be More Inclusive of Scientists with Disabilities – The Scientist

By daniellenierenberg

Justin Yerbury | University of Wollongong

According to a 2019 National Science Foundation report, only 10 percent of employed scientists and engineers self-identify as having at least one disability, despite that fact that almost 20 percent of all undergraduates self-report the same, with disabled undergraduates enrolling in STEM programs at roughly the same rate as those without. These statistics are likely an underestimate of the true number of scientists living with disabilities, as a culture of stigmatization and ableismdiscrimination that favors people with typical physical and mental abilitiesin academia makes the choice over whether to disclose a disability a difficult one, according to a commentary published May 18 in Trends in Neuroscience.

Justin Yerbury, a molecular biologist at the University of Wollongong in Australia who coauthored the report with his wife, Wollongong psychology researcher Rachael Yerbury, studies motor neuron diseases, including a rare form that he himself was diagnosed with in 2016. Yerbury has amyotrophic lateral sclerosis, otherwise known as Lou Gehrigs disease, which causes nerve cells in the brain and spinal cord to break down, leading to a loss of muscle control. In the piece, the Yerburys write that disabled scientists may feel misunderstood, undervalued, defined by their disability, or worsedismissed as not being able to contribute or compete in academia, leading them to keep their differences a secret, or in some cases, to avoid STEM entirely.

Justin Yerbury answered questions by email about what prompted him to write the piece and how academia can be more inclusive of scientists with disabilities.

Justin Yerbury:I had just been through the process of assisting the National Health and Medical Research Council (Australias primary medical research funding body) with an update to their Relative to Opportunity policy to be more inclusive of people with a permanent disability and I wondered why this lack of disability access hadnt been pointed out before. While this rattled around in my brain for a while I saw something on Twitter that made me wonder if people with a disability were not actually revealing their disability in grant applications, job applications and promotion applications. I posed the question to the disabled in academia community on Twitter and the responses inspired me to explore this further.

JY: While we cant say for certain why people with a disability are under represented in academia, we do know that a proportion of people do not disclose their disability resulting in an underestimation of academics with a disability. In addition, the ablest culture in academia that judge academic success by a high standard of outputs excludes those that dont fit the mold must also contribute to the relative under representation of disability in academia.

JY: There are other groups that are also underrepresented that would also benefit from a more inclusive academic community. I think that if opinions were to change tomorrow we would still need time for opportunities to arise and for people with a disability to find their place. With years or decades of ableism I dont think that there is an immediate fix but what it would do is hopefully set the standard for current students so that they dont have to fight for access.

If anything positive has come from the COVID-19 pandemic, it has shown us that the way things have been done in the past can change and that different ways of doing things are not only possible but are more inclusive. That can only be a good thing.

JY: The University of Wollongong has provided accessible tech for me in terms of computers and software that helps me communicate and continue to work. In addition, access to my office has been improved with automatic sliding doors and parking under my building. In addition, the University has provided administrative support to help with certain aspects of academia.

JY: The medical model explanation of disability implies that there is something wrong with people that have a disability and that they are not a complete person. That is, people with a disability have deficits. The deficit approach presumes that a disability is a disadvantage and a liability, meaning that we can never be viewed as an equal to our peers.

Rather than seeing differences as a liability we must see diversity and the lived experience it brings as an asset.

JY: Put simply, equality means that everyone is given the same opportunities. While equity is the ability to recognise that each individual has a distinct set of circumstances which is then utilized to reasonably adjust opportunities to achieve an equal outcome.

What this looks like in STEM is policies that apply to everyone, for example funding criteria, that in some instances disadvantage those with a disability. For example, the National Health and Medical Research Council of Australia didnt provide an opportunity for me to explain my permanent disability in my grant application meaning my outputs were directly compared to able bodied researchers without taking my disability into account.

JY:If anything positive has come from the COVID-19 pandemic, it has shown us that the way things have been done in the past can change and that different ways of doing things are not only possible but are more inclusive. That can only be a good thing.

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Lymph nodes: Purpose, location, and disease warning signs – Medical News Today

By daniellenierenberg

Lymph nodes are small, bean-shaped glands that play a crucial role in the immune system. They filter lymphatic fluid, which helps rid the body of germs and remove waste products.

The body contains hundreds of lymph nodes. They form clusters around the body and are particularly prominent in areas such as the neck, armpit and groin and behind the ears.

The bodys cells and tissues dispose of waste products in lymphatic fluid, which lymph nodes then filter. During this process, they catch bacteria and viruses that could harm the rest of the body.

Lymph nodes are an essential part of the bodys immune system. Due to their function, they come into contact with toxins, which can cause them to swell. Although swollen lymph nodes are common, they may occasionally indicate lymph node cancer, or lymphoma.

Keep on reading to learn more about lymph nodes and their function within the immune system.

Lymph nodes are part of the lymphatic system, which is a complex network of nodes and vessels.

In certain areas of the body, such as the neck, armpit, and groin, lymph nodes sit close to the skin. This means a person may feel them swell when an infection develops.

Lymph nodes are also present in the stomach and between the lungs. However, there are no lymph nodes in the brain or spinal cord.

The name of a lymph node depends on its location in the body.

Lymph nodes form clusters throughout the body. Their main function is to filter out potentially harmful substances.

All tissues and cells in the body excrete lymphatic fluid, or lymph, in order to eliminate waste products. The lymph then travels through vessels in the lymphatic system and passes through lymph nodes for filtering.

Lymph nodes contain lymphocytes. These are a type of white blood cells that help destroy pathogens, such as bacteria, viruses, and fungi. When lymph nodes detect a pathogen in the lymph, they produce more lymphocytes, which causes them to swell.

Upon encountering bacteria or damaged cells, lymph nodes destroy them and turn them into a waste product.

When the lymph reenters the bloodstream, waste products travel to the kidneys and liver. The body then excretes waste products in the urine and feces.

Learn more about how the lymphatic system works here.

Swollen lymph nodes do not always indicate cancer. Below, we list some of many conditions that can cause lymph node swelling.

Lymphadenitis occurs when bacteria, viruses, or fungi in the lymph infect lymph nodes. When this happens, lymph nodes swell and are painful to the touch.

If multiple clusters of nodes become infected, a person may feel pain and swelling in both their neck and groin.

The most common type of lymphadenitis is localized lymphadenitis. This means the condition only affects a few nodes. If the infection occurs in several node clusters, a doctor will likely diagnose generalized lymphadenitis.

The condition usually results from an infection elsewhere in the body.

Symptoms of lymphadenitis include:

Lymphadenitis treatments include:

The type of treatment necessary will depend on a variety of factors, such as the severity of the disease and a persons underlying conditions and allergies. A doctor will help a person choose the most suitable treatment based on these factors.

Learn more about swollen lymph nodes in the neck here.

Swollen lymph nodes in the neck may be due to a viral or bacterial throat infection, such as strep throat.

Viral throat infections, such as colds, can present with swollen lymph nodes, a runny nose, and pinkeye.

These infections usually resolve on their own. However, a person can take over-the-counter pain relievers to alleviate pain they may experience when swallowing.

Strep throat is a bacterial infection that develops in the throat and tonsils due to group A streptococcus. People may contract strep throat if they come into contact with droplets containing the strep bacteria.

A person with strep throat may experience swollen lymph nodes on the neck, a sore throat, a fever, and red spots on the roof of the mouth.

Doctors treat strep throat with antibiotics.

Impetigo is an infection that develops due to group A streptococcus and may cause lymph nodes in the armpits and groin to swell.

A person can contract impetigo when the bacteria enter the body through a break in the skin. This can happen through sharing a towel, razor, or yoga mat.

Symptoms of impetigo include:

If a person has impetigo, they should seek medical attention to address their symptoms and prevent the condition from spreading to others.

Treatment will usually involve antibiotics.

Ringworm, or jock itch, is a fungal infection that can affect many areas of the body. If the fungus develops in the groin, a person may experience lymph node swelling in that area.

Typically, ringworm starts as a fungal lesion. The fungus often transmits when people share towels or razors.

Ringworm thrives in moist environments, and therefore a person should take care to dry thoroughly after a wash and try not to stay in damp clothes.

Common ringworm symptoms include:

A doctor will prescribe an antifungal treatment to address ringworm.

The best way to prevent ringworm is to wear breathable fabrics, avoid sharing towels and razors, and dry thoroughly after bathing.

Learn more about swollen lymph nodes in the groin here.

Lymphoma is a type of cancer that affects the lymphatic system. The two main types of lymphoma are Hodgkin lymphoma and non-Hodgkin lymphoma.

Hodgkin lymphoma occurs when cancer cells spread from one cluster of lymph nodes to another. By contrast, in non-Hodgkin lymphoma, there is no order in how cancer cells spread throughout the lymphatic system.

Typical symptoms of lymphoma include:

These are also common symptoms of viral infections, which can make lymphoma hard to diagnose. However, in people with lymphoma, symptoms tend to persist for longer periods of time.

It is of note that these symptoms do not clearly indicate cancer. If a person experiences any of these, they should contact a doctor to identify the cause of their symptoms.

Treatment options for lymphoma include:

A person should contact a healthcare professional if they are experiencing persistent swelling of lymph nodes.

Swelling usually indicates an infection, and therefore a person should not immediately worry about lymphoma.

After reaching a diagnosis, a doctor will recommend the appropriate course of treatment.

Lymph nodes are a part of the lymphatic system. They filter lymph, which contains pathogens and damaged cells, and send the dead cells to the kidneys and liver.

Lymph node swelling usually results from an infection. In rare cases, however, it may be due to lymphoma.

If a person is concerned about swelling and other symptoms they have, they should contact a doctor.

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Global Cell Therapy Markets, Technologies, and Competitive Landscape Report 2020-2030: Applications, Cardiovascular Disorders, Cancer, Neurological…

By daniellenierenberg

DUBLIN, May 21, 2021 /PRNewswire/ -- The "Cell Therapy - Technologies, Markets and Companies" report from Jain PharmaBiotech has been added to ResearchAndMarkets.com's offering.

This report describes and evaluates cell therapy technologies and methods, which have already started to play an important role in the practice of medicine. Hematopoietic stem cell transplantation is replacing the old fashioned bone marrow transplants. The role of cells in drug discovery is also described. Cell therapy is bound to become a part of medical practice.

The cell-based markets was analyzed for 2020, and projected to 2030. The markets are analyzed according to therapeutic categories, technologies and geographical areas. The largest expansion will be in diseases of the central nervous system, cancer and cardiovascular disorders. Skin and soft tissue repair, as well as diabetes mellitus, will be other major markets.

The number of companies involved in cell therapy has increased remarkably during the past few years. More than 500 companies have been identified to be involved in cell therapy and 316 of these are profiled in part II of the report along with tabulation of 306 alliances. Of these companies, 171 are involved in stem cells.

Profiles of 73 academic institutions in the US involved in cell therapy are also included in part II along with their commercial collaborations. The text is supplemented with 67 Tables and 26 Figures. The bibliography contains 1,200 selected references, which are cited in the text.

Stem cells are discussed in detail in one chapter. Some light is thrown on the current controversy of embryonic sources of stem cells and comparison with adult sources. Other sources of stem cells such as the placenta, cord blood and fat removed by liposuction are also discussed. Stem cells can also be genetically modified prior to transplantation.

Cell therapy technologies overlap with those of gene therapy, cancer vaccines, drug delivery, tissue engineering, and regenerative medicine. Pharmaceutical applications of stem cells including those in drug discovery are also described. Various types of cells used, methods of preparation and culture, encapsulation, and genetic engineering of cells are discussed. Sources of cells, both human and animal (xenotransplantation) are discussed. Methods of delivery of cell therapy range from injections to surgical implantation using special devices.

Cell therapy has applications in a large number of disorders. The most important are diseases of the nervous system and cancer which are the topics for separate chapters. Other applications include cardiac disorders (myocardial infarction and heart failure), diabetes mellitus, diseases of bones and joints, genetic disorders, and wounds of the skin and soft tissues.

Regulatory and ethical issues involving cell therapy are important and are discussed. The current political debate on the use of stem cells from embryonic sources (hESCs) is also presented. Safety is an essential consideration of any new therapy and regulations for cell therapy are those for biological preparations.

Key Topics Covered:

Part One: Technologies, Ethics & Regulations

Executive Summary

1. Introduction to Cell Therapy

2. Cell Therapy Technologies

3. Stem Cells

4. Clinical Applications of Cell Therapy

5. Cell Therapy for Cardiovascular Disorders

6. Cell Therapy for Cancer

7. Cell Therapy for Neurological Disorders

8. Ethical, Legal and Political Aspects of Cell therapy

9. Safety and Regulatory Aspects of Cell Therapy

Part II: Markets, Companies & Academic Institutions

10. Markets and Future Prospects for Cell Therapy

11. Companies Involved in Cell Therapy

12. Academic Institutions

13. References

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

Media Contact:

Research and Markets Laura Wood, Senior Manager [emailprotected]

For E.S.T Office Hours Call +1-917-300-0470 For U.S./CAN Toll Free Call +1-800-526-8630 For GMT Office Hours Call +353-1-416-8900

U.S. Fax: 646-607-1907 Fax (outside U.S.): +353-1-481-1716

SOURCE Research and Markets

http://www.researchandmarkets.com

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Global Cell Therapy Markets, Technologies, and Competitive Landscape Report 2020-2030: Applications, Cardiovascular Disorders, Cancer, Neurological...

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Global Cardiovascular Drug Delivery Markets Report 2021: Cell and Gene Therapies, Including Antisense and RNA Interference are Described in Detail -…

By daniellenierenberg

DUBLIN, May 21, 2021 /PRNewswire/ -- The "Cardiovascular Drug Delivery - Technologies, Markets & Companies" report from Jain PharmaBiotech has been added to ResearchAndMarkets.com's offering.

The cardiovascular drug delivery markets are estimated for the years 2018 to 2028 on the basis of epidemiology and total markets for cardiovascular therapeutics.

The estimates take into consideration the anticipated advances and availability of various technologies, particularly drug delivery devices in the future. Markets for drug-eluting stents are calculated separately. The role of drug delivery in developing cardiovascular markets is defined and unmet needs in cardiovascular drug delivery technologies are identified.

Drug delivery to the cardiovascular system is approached at three levels: (1) routes of drug delivery; (2) formulations; and finally (3) applications to various diseases.

Formulations for drug delivery to the cardiovascular system range from controlled release preparations to delivery of proteins and peptides. Cell and gene therapies, including antisense and RNA interference, are described in full chapters as they are the most innovative methods of delivery of therapeutics. Various methods of improving the systemic administration of drugs for cardiovascular disorders are described including the use of nanotechnology.

Cell-selective targeted drug delivery has emerged as one of the most significant areas of biomedical engineering research, to optimize the therapeutic efficacy of a drug by strictly localizing its pharmacological activity to a pathophysiologically relevant tissue system. These concepts have been applied to targeted drug delivery to the cardiovascular system. Devices for drug delivery to the cardiovascular system are also described.

The role of drug delivery in various cardiovascular disorders such as myocardial ischemia, hypertension, and hypercholesterolemia is discussed. Cardioprotection is also discussed. Some of the preparations and technologies are also applicable to peripheral arterial diseases. Controlled release systems are based on chronopharmacology, which deals with the effects of circadian biological rhythms on drug actions. A full chapter is devoted to drug-eluting stents as treatment for restenosis following stenting of coronary arteries.Fifteen companies are involved in drug-eluting stents.

New cell-based therapeutic strategies are being developed in response to the shortcomings of available treatments for heart disease. Potential repair by cell grafting or mobilizing endogenous cells holds particular attraction in heart disease, where the meager capacity for cardiomyocyte proliferation likely contributes to the irreversibility of heart failure.

Cell therapy approaches include attempts to reinitiate cardiomyocyte proliferation in the adult, conversion of fibroblasts to contractile myocytes, conversion of bone marrow stem cells into cardiomyocytes, and transplantation of myocytes or other cells into injured myocardium.

Advances in the molecular pathophysiology of cardiovascular diseases have brought gene therapy within the realm of possibility as a novel approach to the treatment of these diseases. It is hoped that gene therapy will be less expensive and affordable because the techniques involved are simpler than those involved in cardiac bypass surgery, heart transplantation and stent implantation.

Gene therapy would be a more physiologic approach to deliver vasoprotective molecules to the site of vascular lesions. Gene therapy is not only a sophisticated method of drug delivery; it may at times need drug delivery devices such as catheters for transfer of genes to various parts of the cardiovascular system.

Selected 83 companies that either develop technologies for drug delivery to the cardiovascular system or products using these technologies are profiled and 80 collaborations between companies are tabulated. The bibliography includes 200 selected references from recent literature on this topic.

Key Markets

Key Topics Covered:

Executive Summary

1. Cardiovascular Diseases

2. Methods for Drug Delivery to the Cardiovascular System

3. Cell Therapy for Cardiovascular Disorders

4. Gene Therapy for Cardiovascular Disorders

5. Drug-Eluting Stents

6. Markets for Cardiovascular Drug Delivery

7. Companies involved in Cardiovascular Drug Delivery

8. References

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

Media Contact:

Research and Markets Laura Wood, Senior Manager [emailprotected]

For E.S.T Office Hours Call +1-917-300-0470 For U.S./CAN Toll Free Call +1-800-526-8630 For GMT Office Hours Call +353-1-416-8900

U.S. Fax: 646-607-1907 Fax (outside U.S.): +353-1-481-1716

SOURCE Research and Markets

http://www.researchandmarkets.com

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Global Cardiovascular Drug Delivery Markets Report 2021: Cell and Gene Therapies, Including Antisense and RNA Interference are Described in Detail -...

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Obesity-Related Inflammation and Endothelial Dysfunction in COVID-19: | JIR – Dove Medical Press

By daniellenierenberg

Obesity, COVID-19 and Inflammation

The coronavirus disease 2019 (COVID-19) pandemic has put into evidence another pandemic obesity, an increasing threat to societies around the world.1 The first studies of COVID-19 did not provide body mass index (BMI) data,2 and the association between disease severity and obesity was not perceived initially. Subsequent data from several countries, however, cast light on this association,3,4 and several studies have documented the association between obesity and COVID-19 severity.47 Currently, obesity may be considered a true independent risk factor for COVID-19 mortality.8

The mechanisms underlying the increased risk of complications and mortality in obese patients with COVID-19 are many, and of diverse nature (Figure 1). Obesity is associated with several disorders, related to defective homeostasis of the dysfunctional adipose tissue, in which local and systemic chronic inflammation, oxidative stress, altered release of cytokines, and impaired immune response play important roles911; all of these have been demonstrated to be associated with higher risk and worse prognosis of infectious diseases in this patient population.1214

Figure 1 The mechanisms underlying the increased risk of complications and mortality in obese patients with COVID-19 based on the association of low-grade inflammation, adipose tissue dysfunction and endothelial dysfunction: In obese patients with COVID-19 or SARS-CoV-2, as well as, the bacterial endotoxins (LPS) of the intestinal bacterial translocation promote the activation of TLR4 in favor of the MyD88-dependent pro-inflammatory pathway. The activation of NF-B is linked to the production of TNF-, IL-1, IL-6, IL-12 and other cytokines, contributing to the activation of NLRP3 inflammasomes and increased expression of ECA2. In the adipose tissue of patients with COVID-19, there is an increase in the expression of ECA2, promoting greater entry of SARS-CoV-2, making this tissue a viral reservoir. Metabolic inflammation in obese patients is characterized by dysfunctional adipose tissue, with mitochondrial dysfunction and decreased fatty acid oxidation, causing an amount of inflammatory cells showing an increase in the influx of M1 macrophages and chemotactic signaling, via MCP-1 and release of IL-8 by adipocytes, associated with an increase in reactive oxygen species. Associated with this process of immune activation, obese patients with COVID-19 have systemic microvascular dysfunction and a predisposition to thrombus formation that is exacerbated by higher levels of circulating inflammatory cytokines, such as TNF-, IL-1 and IL-6, worsening the outcomes in COVID-19.

Inflammation plays a central role in obesity.15 Obesity promotes profound changes in the structure and function of adipose tissue, as adipocytes undergo hypertrophy and hyperplasia, increasing oxygen need, which remains unmet due to the insufficient vascularization relative to the enlarged adipose tissue. This leads to tissue hypoxia and immune cell infiltration that perpetuates local inflammation.1618 Insulin resistance is also a link between obesity-related metabolic disorders and inflammation, as the remodeling of the adipose tissue leads to activation of NLRP3-inflammasome, which ultimately impairs of the insulin-signaling pathway and insulin resistance, a key factor in the development of the metabolic syndrome.19

Additionally, mitochondrial dysfunction in adipocytes may be a cause of adipose tissue inflammation and insulin resistance. The defective mitochondrial function and decreased fatty acid oxidation in adipocytes increase triglyceride accumulation, adipocyte enlargement and consequent adipose tissue hypoxia; this, in its turn, leads to accumulation of hypoxia-inducible factor-1 (HIF-1), which promotes adipose tissue inflammation and fibrosis.20 This continuous inflammatory cycle also contributes to a neuro-immuno-endocrine dysregulation in the context of the metabolic syndrome.21 The inflammatory state affecting obese individuals is called metabolic inflammation or metainflammation, in which there is also an increased influx of M1 macrophages occurring, as well as decreased M2 macrophages and Treg cells in the visceral adipose tissue22 through chemotactic signaling, via MCP-1 and IL-8 released by adipocytes.23

The excessive intake of carbohydrates is an important trigger for these processes.24 In addition, peripheral inflammation and various pro-inflammatory signals in the nucleus accumbens, including reactive gliosis, increased expression of cytokines, antigen-presenting markers and transcriptional activity of NFB25 contribute to the activation of the innate immune response, mainly through activation of Toll-type receptors (TLR), specifically TLR-4, considered an intersection of dysfunctional metabolism and activated immunity in obesity.26 NF-B is a molecular hub for pro-inflammatory gene induction both in innate and adaptive immune responses since it is highly regulated and regulates the expression of a vast array of genes.27 Among many different immune effects, NF-B activation is linked to the production of TNF-, IL-1, IL-6, IL-12 and other cytokines, and is also involved in NLRP3 inflammasome regulation and activation of CD4+ T-helper cells.28 It is noteworthy that there is evidence that the virus can bind and activate TLR4 signaling in favor of the proinflammatory MyD88-dependent and contributing to increased expression of ACE2 and promoting greater viral entry.29

The chronic impairment of systemic vascular endothelial function in patients with cardiovascular and metabolic disorders, including hypertension, obesity, diabetes mellitus, coronary artery disease and heart failure, when intensified by the detrimental effects of the severe acute respiratory syndrome coronavirus (SARS-CoV-2) over the endothelium, may explain their worse outcomes in COVID-19.3033 Regarding obesity, a community-based clinical trial (n=521; mean follow-up of 8.5 years) showed that increases in weight, body mass index, waist circumference and body-fat percentage over time were associated with worsening of microvascular endothelial function, assessed by flow-mediated dilation in the brachial artery.34 Most subjects (84%) were overweight or obese at baseline; those who lost weight over time had improved vascular endothelial function.34

In fact, vascular endothelial dysfunction and increased arterial stiffness are thought to contribute to a unfavorable response of the endothelium to the infection by SARS-CoV-2, whereas alterations in cardiac structure and function and the prothrombotic environment in obesity could provide a link for the augmented cardiovascular events in these patients.35 Moreover, fast increasing evidence from basic science, imaging and clinical observations suggest that COVID-19 could be considered as a vascular disease.36,37

Obesity is accompanied by functional and structural systemic microvascular dysfunction,38 and endothelial-dependent microvascular vasodilation is severely impaired in obesity.3941 Endothelial-dependent capillary recruitment, induced either by reactive hyperemia or by shear stress, is blunted in obese subjects, compared to non-obese counterparts.42,43 In the clinical setting, endothelial function and reactivity can be assessed using different technologies that evaluate microvascular flow and tissue perfusion coupled to physiological or pharmacological stimuli,44,45 to activate different vasodilator pathways resulting in increased microvascular conductance. The most commonly used provocations are the administration of endothelial-dependent vasodilators by transdermal iontophoresis,4648 thermal hyperemia49,50 and post-occlusive reactive hyperemia.5153 In this context, the cutaneous microcirculation is now considered as an accessible and representative vascular bed for the assessment of systemic microcirculatory reactivity.45,5456 A reduced vasodilation response to these different stimuli is indicative of microvascular endothelial dysfunction and is also considered to be predictive for cardiovascular and metabolic diseases and clinical prognosis.5760

In patients with established cardiovascular disease, the reduction of microvascular endothelial-dependent vasodilation (ie, endothelial dysfunction) is associated with increasing BMI, even after adjustment for treated diabetes mellitus, hypertension, hypercholesterolemia, and smoking.61 In that study, BMI was classified in three different intervals: <25, 25-to 30 and >30 kg/m2.61 Moreover, Csipo et al showed that weight loss (reduction of BMI from 31.8 to 27.5 kg/m2, accompanied by a reduction of serum cholesterol, LDL, triglycerides, and increased HDL) after a low-carbohydrate, low-calorie diet, resulted in improvement of microvascular endothelial function in geriatric obese (class 1) patients,62 assessed by laser speckle contrast imaging in the skin, after post-occlusive reactive hyperemia. Additionally, endothelial function of resistance arterioles of the gluteal subcutaneous tissue is impaired in non-diabetic subjects with moderate levels of obesity (BMI 34.7 4.0 kg/m2), in association with systemic inflammation. In women, BMI was significantly associated with high-sensitivity C-reactive protein.63

Regarding mechanisms of microvascular dysfunction, using a new methodology of microdialysis in the skeletal muscle, La Favor et al showed a significant increase in superoxide anions, as well as in NADPH oxidase subunit expression, associated with microvascular endothelial dysfunction in obese subjects relative to lean and overweight/mildly obese subjects.64 Interestingly, 8 weeks of aerobic exercise training resulted in decreased H2O2 levels and improved microvascular endothelial function in the muscle tissue of obese subjects.64 The study therefore linked NADPH oxidase, as a source of reactive oxygen species, to microvascular endothelial dysfunction in obese individuals, with amelioration induced by aerobic exercise.

Microvascular dysfunction has been considered to be a pathophysiological link between overweight/obesity and cardiometabolic diseases, including arterial hypertension, insulin resistance, and glucose intolerance.43,6569 Acknowledged mechanisms include changes in the secretion of adipokines, leading to increased levels of free fatty acids and inflammatory mediators, and decreased levels of adiponectin, all of which may impair endothelial insulin signaling.7073 It is also of note that there are changes at the level of the microvascular network in obesity, involving a reduction in the number of arterioles or capillaries within vascular beds of various tissues (such as the skeletal muscle and skin), which is defined as vascular (capillary) rarefaction.7477 In fact, obese individuals have both structural and functional alterations in skin microcirculation that are proportional to the increase in the degree of global and central obesity, arterial pressure levels and with the degree of insulin resistance.42 In non-diabetic, untreated hypertensive patients, reduced capillary density has also been related to obesity and other cardiometabolic risk factors.78 In addition, in adults and also in prepubertal children, visceral adiposity measured with magnetic resonance imaging is inversely associated with endothelial-dependent skin capillary recruitment, and is accompanied by increased plasma levels of inflammatory markers.79

Impaired left ventricular diastolic function and higher risk of heart failure in obese individuals has been suggested to be associated with myocardial microvascular dysfunction.80 In obese patients undergoing coronary artery bypass graft surgery, coronary microvascular density is significantly lower, compared to non-obese patients, and accompanied by increased body mass index and percent body fat together with increased left ventricular filling pressures.80 Moreover, in patients with suspected coronary artery disease, increasing body mass index is associated with reduced microvascular endothelial function, even after adjustment for treated diabetes mellitus, hypertension, hypercholesterolemia, and smoking.61 Interestingly, the study evaluated microvascular endothelial function three different technologies, including peripheral arterial tonometry, laser Doppler flowmetry and digital thermal monitoring.61

Reduced skeletal muscle capillary density and microvascular reactivity in obese subjects improved after 4 weeks of either sprint interval training, or moderateintensity continuous training, together with increased endothelial eNOS content.81

It has also been shown that bariatric surgery improves microvascular dysfunction in obese patients who were free of metabolic syndrome after surgery, in association with postoperative increases in HDL-cholesterol levels and decreases in oxidized LDL levels.82

Another clinical study investigated microvascular endothelial function using flow-mediated dilation in arterioles isolated from subcutaneous adipose tissue in young women presenting with obesity (age: 33 2 years, body mass index: 33.0 0.6 kg/m2).83 The results showed that a 6-week low-carbohydrate diet, associated or not with caloric restriction, improve endothelial-dependent microvascular function through increases in nitric oxide bioavailability.83 On the other hand, this nutritional intervention did not affect macrovascular endothelial function, evaluated using brachial artery flow-mediated dilation.83

Regarding putative pathophysiological mechanisms, a study by Dimassi et al84 in young individuals with obesity (BMI >30 kg/m2, n = 69), compared with controls with normal weight, suggested that the expression of circulating microparticles containing endothelial nitric oxide synthase (eNOS) is significantly reduced in obesity individuals with endothelial-dependent microvascular dysfunction characterized using cutaneous laser Doppler flowmetry.84

Low-grade inflammation is the common feature that encompasses all the high-risk patients for developing severe COVID-19. Obesity is associated with a fivefold increased risk of developing SARS in SARS-CoV-2 infected individuals, and the well-documented increased susceptibility of obese patients to develop severe forms of COVID-19 may be linked to the elevated systemic metabolic inflammation in these patients.19 Metabolic alterations seen in obese and in diabetic patients are related to an inflammatory response,85,86 and several studies report elevated levels of circulating inflammatory cytokines such as TNF-, IL-1 and IL-6 in obese patients.87 Furthermore, visceral fat shows significant univariate association with the need for intensive care in COVID-19 patients,15 and deregulated expression of adipokines, such as leptin and resistin, increases the expression of vascular adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) that contribute to increased vascular leukocyte adhesiveness and additional oxidative stress.88 To further complicate the scenario, adipose-derived mesenchymal stem cell (ASCs), a specialized cell population in adipose tissue, are functionally compromised in obesity and changes its regulatory protective activity to a pro-inflammatory profile increasing its ability to secrete TNF-, IL-8, IL-6 and MCP-1.89,90 Therefore, ASCs from obese patients may not be able to modulate the immune response and tissue repair in SARS-CoV-2 infection contributing to more severe tissue injury.10

SARS-CoV-2 uses its viral spike (S) protein to invade target cells, such as epithelial cells, through binding to angiotensin-converting enzyme 2 (ACE2) after proteolytic activation by transmembrane protease serine 2 (TMPSS2).91 Others enzymes like furin, trypsin and elastase may also activate the S protein and facilitate cellular entry by the virus.9294 Interestingly, adipose tissue highly expresses ACE2 and the expression is even higher in visceral adipose tissue.95 Of relevance, ACE2 expression is upregulated in obesity.96 Also, another suggested receptor for SARS-CoV-2, dipeptidyl peptidase 4 (DPP4), is expressed in adipose tissue and is upregulated in obesity.97,98 Finally, CD147, the alternative receptor for SARS-CoV-2, is positively correlated with an increase in body mass index.99 Taken together, the evidence of high expression of different SARS-CoV-2 receptors in adipose tissue may be the basis for increased severity of COVID-19 in obese patients involving at least two different possibilities: First, infection of adipocytes with SARS-CoV-2 may exacerbate the innate immune response through pathogen recognition receptors in an already inflammation-primed tissue, increasing the magnitude of the response. Second, adipocytes may function as a reservoir for the SARS-CoV-2 and therefore may fuel the inflammatory response in adipose tissue and elsewhere in the organism by releasing viral NA and antigens that, by reaching the circulation generate ripple inflammatory effects across the organism. Importantly, these two possibilities are not mutually exclusive and may well combine their pathophysiological potential towards a deregulate systemic inflammatory response with widespread tissue injury and consequent organ dysfunction. It is important to add that as the pandemic evolves, new mechanistic interactions may unravel. For instance, new virus variants with mutations at the receptor-binding domain of the S protein may change the infectivity of the virus by changing its interactions with cellular receptors. In Brazil, a variant designated as P1, with multiple mutations in the S protein, was recently identified and is seemingly more infective than previous lineages of the virus.100 How this variant may interact with adipocytes increasing infectivity to these cells or potentiating the formation of an adipocyte reservoir of the virus causing a more severe disease in obese individuals is yet unknown. What is known is that a second wave caused by this new P1 variant is promoting devastating effects in Brazil with apparently higher mortality and a faster progression of the disease.

Severe COVID-19 is characterized by a massive production of pro-inflammatory mediators, in special cytokines. Frequently, the term cytokine storm is called up to describe the massive production of cytokines that occurs in viral infections (including SARS-CoV and MERS-CoV), in sepsis and more recently, in severe COVID-19.101 Increased levels of IL-6, TNF-, IP10 are commonly found in patients with severe COVID-19.102 It is reasonable to propose that obese patients who already have an underlying chronic inflammation when infected with SARS-CoV-2 are prone to develop a more intense and deregulated response, and in doing so, developing a severe presentation of the disease. In addition, dysfunctional metabolism, endothelium, and overall immune response would further contribute to an unfavorable evolution of the disease in the obese patients. The questions about the molecular mechanisms behind this disproportional response remain unanswered, but our knowledge about this disease is growing in an unprecedented velocity and we may soon have the answer. However, a few possibilities may be put forward (Figure 1).

As stated above, obesity is characterized by the induction of a low-grade chronic proinflammatory state and NF-B is described as a key factor in the low-grade inflammation state in atherosclerosis and hypertension.103,104 Also, the NF-B pathway is involved in insulin resistance, a condition frequently seen in obese patients, and in -cell dysfunction.105 In addition, free fatty acids can also promote inflammation and activate the NF-B and JNK1 pathways.106 All those pieces put together may point to NF-B being a key player in obese patients with COVID-19. Importantly, cell culture experiments combined with system biology approach showed that overexpression of Nsp1 during infection with SARS-CoV-2 strongly increases signaling through the nuclear factor of activated T cells (NFAT) and increases cytokine production and immune-dependent pathogenesis. Both NF-B and NFAT pathways share common regulation signals, such as Foxp3 and Foxd1, and a similar mechanism of activation against infection.107

We must also consider that binding of SARS-CoV-2 to ACE2 leads to receptor internalization and high cytosolic levels of angiotensin II, which is a recognized activator of NLP3 inflammasome in the lung108 and other tissues. The NLRP3 inflammasome regulates pyroptosis through gasdermin D, along with the release of cytosolic contents into the extracellular spaces. The release of alarmins, ATP, ROS, cytokines, chemokines, LDH and viral particles elicits an immediate reaction from surrounding immune cells, inducing a pyroptotic triggered reaction further fueling inflammation. Interestingly, different studies have reported elevated levels of LDH, a cytosolic enzyme that is measured for monitoring pyroptosis in patients with the severe form of COVID-19.109 On the other hand, diet-induced alterations in the gut leading to increased gut permeability to bacterial endotoxins are known to promote activation of NLRP3 inflammasomes via Toll-like receptors (TLRs). This event is followed by the accumulation of IL-1 family cytokines, which modulate insulin production by pancreatic beta cells.110 Importantly and at the same time, a decrease in endogenous protective mechanisms occurs.111 NLRP3 inflammasome activation is involved in endothelial lysosome membrane permeabilization, cathepsin B release, and impaired glycocalyx thickness,112 thus further contributing to the endothelial cell dysfunction, enhanced susceptibility to cardiovascular injury and thrombotic events, a common complication in severe COVID-19 patients.

In fact, thrombotic events are now recognized as a common feature in COVID-19 patients, and COVID-19 has recently been suggested to be a thrombotic viral fever.113 Obese patients are prone to thrombotic events for many different reasons,113 and COVID-19 may contribute even further to this complication. The imbalance of the ACE/ACE2 system caused by internalization of ACE2 after binding to virus S protein causes a switch towards pro-thrombotic activity by decreasing Ang-(1-7)-Mas axis (antithrombotic) and increasing angiotensin II (prothrombotic). This mechanism may be of central pathogenic relevance explaining the poor outcome of obese patients with COVID-19.113

In summary, there are many different ways by which low-grade inflammation caused by metabolic changes in obesity may contribute to the worse prognosis of obese patients infected by SARS-CoV-2, in a combination of factors and mechanisms leading to a subversion of the defensive responses of the organism against the virus.

The authors report no conflicts of interest in this work.

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3. Docherty AB, Harrison EM, Green CA, et al. Features of 20 133 UK patients in hospital with covid-19 using the ISARIC WHO clinical characterisation protocol: prospective observational cohort study. BMJ. 2020;369. doi:10.1136/bmj.m1985

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5. Hernndez-Garduo E. Obesity is the comorbidity more strongly associated for Covid-19 in Mexico. A case-control study. Obes Res Clin Pract. 2020;14(4):375379. doi:10.1016/j.orcp.2020.06.001

6. Hajifathalian K, Kumar S, Newberry C, et al. Obesity is associated with worse outcomes in COVID-19: analysis of early data from New York city. Obesity. 2020;28(9):16061612. doi:10.1002/oby.22923

7. Busetto L, Bettini S, Fabris R, et al. Obesity and COVID-19: an Italian snapshot. Obesity. 2020;28(9):16001605. doi:10.1002/oby.22918

8. Hussain A, Mahawar K, Xia Z, Yang W, EL-Hasani S. Obesity and mortality of COVID-19. Meta-analysis. Obes Res Clin Pract. 2020;14(4):295300. doi:10.1016/j.orcp.2020.07.002

9. Klting N, Blher M. Adipocyte dysfunction, inflammation and metabolic syndrome. Rev Endocr Metab Disord. 2014;15(4):277287. doi:10.1007/s11154-014-9301-0

10. Louwen F, Ritter A, Kreis NN, Yuan J. Insight into the development of obesity: functional alterations of adipose-derived mesenchymal stem cells. Obes Rev. 2018;19(7):888904. doi:10.1111/obr.12679

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