All posts by medical

Immunology

With Key Data Nearing, Tonix Looks to Spotlight Robust Pipeline In Immunology And CNS Therapeutics – Yahoo Finance

The following article is sponsored by the clinical communications unit of Redington, Inc. The information contained in this article in no way represents investment advice or opinion on the part of Benzinga or its writers and is intended for informational purposes only.

Tonix Pharmaceuticals Holding Corp. (NASDAQ: TNXP) has been operating under the radar of major institutional investors, but that may soon change.

After a series of near misses in a handful of clinical trial programs, the company is closing in on data from two important programs. Positive readouts from either one promises to spotlight the companys diverse portfolio built on unmet needs in billion-dollar medical categories.

Before yearend, Tonix expects to release data from advanced non-human primate studies of its lead Covid-19 T cell eliciting vaccine candidate utilizing live attenuated virus vectors. Vaccines made with attenuated viruses are known to confer long term immunity with a single dose (think vaccines for smallpox, measles, mumps and rubella) and they are the only ones known to prevent forward transmission or contagion.

Tonixs decision to develop T cell vs. antibody eliciting vaccines puts it in a race alongside Merck & Co. (NYSE: MRK), the only other US company developing Covid-19 vaccines with a similar approach.

Another expected fourth quarter highlight could position Tonix to tap into a nearly $9 billion fibromyalgia drug market, one that was created by Pfizer, Incs (NYSE: PFE) Lyrica and Eli Lilly and Companys (NYSE: LLY) Cymbalta before both products went generic two years ago.

Tonixs fibromyalgia candidate, TNX-102 SL, is more than half-way through a Phase 3 registration trial, with topline results due before yearend.

No new branded fibromyalgia drug has entered the market since Cymbalta and Lyrica went generic a void Tonix hopes to fill with a better, more tolerable product following completion of its Phase 3 programs.

We are nimble, focused and we work on big medical challenges, said Tonix CEO Seth Lederman, MD in a recent interview with Benzinga. Many other companies are focused on a particular proprietary technology, while we are opportunity-focused.

Driven By Opportunity

In describing the driving philosophy underlying Tonix Pharmaceuticals trials of its leading and exploratory drug candidates, Dr. Lederman emphasized the companys focus on discovering impactful approaches to often overlooked clinical diagnoses.

This is particularly reflected in Tonixs pursuit of a non-addictive treatment for fibromyalgia, a generalized pain disorder that is often misdiagnosed or mistreated due to the multifarious manifestations of the condition.

We like the opportunity-focused model better because it fits more directly with our passion for tackling medical problems that others avoid because of past failures or other difficulties, Dr. Lederman elaborated. We believe we can win some victories for desperate patients that medicine has heretofore overlooked because the hill seemed too steep to climb. The solutions we seek have the potential to be tremendously meaningful and rewarding

In this interview, Dr. Lederman spoke to the history and progress of both drug candidates as well as the unique markets they aim to serve. He also touches on his personal history in rheumatology, patient pain-management and immunology and what the future looks like for Tonixs lead drug candidates and for the company.

The companys strategy often involves looking at markets that have been created by blockbuster products, identifying their shortcomings, and then developing novel approaches to deliver a unique product profile.

One of the big triumphs of rheumatology was the recognition some 15 years ago that fibromyalgia was a distinct disorder, not a stigmatized set of complaints offered up by folks who doctors thought were malingerers with fabricated symptoms, Dr. Lederman explained.

That victory has led to other advances, for example, the understanding that fibromyalgia is a chronic pain disorder relating to central pain.

As the formal diagnoses of fibromyalgia were being advanced, Pfizer launched Lyrica and Lilly launched Cymbalta, which had combined peak sales of roughly $9 billion before they went off patent. Now there is only one remaining branded product on the market Savella from AbbVie Inc. (NYSE: ABBV) a Cymbalta-like drug selling at the rate of about $400 million a year.

Story continues

At peak sales, Cymbalta was a $5 billion product and Lyrica wasnt far behind at $3.5 billion, Dr. Ledrman elaborated. Now that both are generic, the dollar value of the market is smaller, but the patients havent disappeared in fact, if anything, theyve grown in number and there is still widespread dissatisfaction within their ranks. Our research indicates that doctors and patients are constantly on the search for other options. We think we can capitalize on that dissatisfaction with a substantially differentiated product.

For Dr. Lederman, the pursuit is more than simply one of opportunity. He has a longstanding interest in the diagnosis of fibromyalgia dating back to his medical training with Columbia Universitys Division of Rheumatology 35 years ago.

It is all about knowing the cause and source of the pain, he said.

Dr. Lederman explained that, as opposed to nociceptive and neuropathic, which denote pain caused by injury to the body or parts of the central nervous system, central pain originates in an individuals brain. This distinction, as well as advances in patient care, helped to foster the recognition of fibromyalgia as a distinct medical condition affecting about seven million adults in the United States, with 95% of those being female over the age of 50 who generally begin experiencing symptoms with the onset of menopause.

With the introduction of FDA-approved Cymbalta and Lyrica and later a drug called Savella doctors moved many patients away from off-label treatments, but dissatisfaction still runs high with a lot of switching and on-off use, often due to side effects becoming intolerable.

As a result, there is still widespread use of addictive opiates. Although they are not approved for this indication, Dr. Lederman asserts that one-third of fibromyalgia patients end up on long-term opiates. These patients often end up in a very bad place and become part of the rising death toll attributed to opiate overdose.

We believe TNX-102 SL will provide a meaningful alternative, a better option.

Seeking Solutions To A Painful Syndrome

The current Phase 3 trial of TNX-102 SL in fibromyalgia was initiated last year following a prior, lower-dose trial that fell short of endpoint results.

TNX-102 SL aims to distinguish itself from existing fibromyalgia treatments by acting on a patients central nervous system to inhibit symptoms of pain by improving sleep quality, which Dr. Lederman sees as a key feature in addressing one of the most consistent aspects of the overall condition.

Fibromyalgia is a syndrome that is defined by a collection of symptoms, he explained. By addressing this sleep disturbance symptom with TNX-102 SL, we've shown in two large studies that there was improvement in fibromyalgia that extends beyond sleep and into improvement across the spectrum of other fibromyalgia symptoms. Because TNX-102 SL provides improvement of many different symptoms, beyond the sleep quality improvement, we believe that TNX-102 SL acts at a syndrome-level and not just at the symptom-level.

Dr. Lederman sees the opportunity in TNX-102 SL as an alternative for patients who might suffer deleterious side effects that impact the quality of the treatment or cause patients to stop taking them altogether.

TNX-102 SL is a medicine taken every night at bedtime, and it has been well-tolerated in all the studies we've done, although some patients experience side effects like transient numbness in the mouth, sleepiness and dry mouth explained Dr. Lederman. Based on the two prior studies and our experience with the 5.6 mg dose in PTSD, we believe TNX-102 SL could have a tolerability edge.

While the peaks sales numbers for Cymbalta and Lyrica may seem lofty, Dr. Lederman is encouraged by the numbers and the need they demonstrate for an array of fibromyalgia treatment options. Tonix is also exploring other potential indications for TNX-102 SL, including for symptoms associated with alcoholism and Alzheimers disease.

This is an exciting time for our portfolio of 10 CNS indications, and especially for TNX-102 SL in fibromyalgia. We look forward to an interim analysis in the Phase 3 study to be reported next month, and we expect top line data from that study in the fourth quarter of this year.

Live Vaccines in An Ongoing Pandemic

In addition to progress on the TNX-102 SL trials, Dr. Lederman also touched on the other leading drug candidates that Tonix is currently putting resources toward investigating, several self-attenuated vaccines for the COVID-19 virus strain. The pursuit is especially dire in Dr. Ledermans estimation, characterizing the ongoing pandemic as the biggest global public health threat since the Spanish Flu in 1918.

We have several vaccine candidates in development, all based on our proprietary live attenuated-virus vector platform, said Dr. Lederman. Live attenuated viruses like horsepox or bovine parainfluenza virus can induce infected lung cells to present antigens to T cells directly. TNX-1800, our lead vaccine in development, is designed to express the spike protein from CoV-2, the virus that causes Covid-19.

The interest in developing a novel and effective vaccine should be self-evident to most given the mounting infection rates. And while many of the potential early vaccine candidates from firms like Moderna, Inc. (NASDAQ: MRNA) or AstraZeneca PLC (NYSE: AZN) have progressed into trial stages, Dr. Lederman highlighted the need for a variety of vaccine platforms. This is in order to both find an ideal vaccine for the virus as well as a greater variety of effective vaccines that can be used in case others are ineffective in certain individuals.

There are currently over 150 potential Covid-19 vaccines in various stages of development but relatively few utilize live attenuated viral platforms. Live attenuated viruses have the potential to confer long-term immunity and prevent forward transmission, Dr. Lederman said. These vaccines are live, attenuated vaccines, like the vaccines that successfully eradicated smallpox, and helped to contain rubella, mumps, measles, and several other lethal viruses.

In a practical sense, Dr. Lederman explained that the ability to prevent forward-transmission the spread of the virus from one host to another is what sets live-attenuated vaccines apart from vaccines derived from inactivated virus strains. The active stimulation of the immune systems Tcells that result from effective live-attenuated vaccines is what evokes a strong, long-lasting and durable immunity to the virus strain.

The challenge of developing such a vaccine lies in working with similar viral strains as a platform and, even then, no one vaccine is 100% effective in all cases. This is another area of opportunistic research on the part of Tonix, which recently announced a sponsorship with Columbia University that Dr. Lederman explained is meant to address these potential variables and to develop precision medicine tools that would allow tailoring of vaccines based on a persons biomarkers.

At the moment, Tonix is still exploring the potential of the horsepox and BPI virus platforms, with the former producing one of the companys more viable vaccine candidates, TNX-1800, which is in pre-IND phase of development.

Should the animal studies prove positive, the company expects to start human trials of TNX-1800 next year.

Said Dr. Lederman, We recently announced a partnership with Fujifilm Diosynth in College Station, Texas, who will be manufacturing the vaccine. We expect it will be manufactured at the level of quality and in a sufficient quantity to conduct clinical trials next year. We are also guiding that we will have the results of both small animal and non-human primate studies in the fourth quarter of this year. Those results will include studies of non-human primates that were challenged with the CoV-2 virus.

Drawing the interview to a close, Dr. Lederman reflected that, between the phase 3 fibromyalgia treatment and the ongoing exploration of a COVID-19 vaccine, Tonix Pharmaceuticals is focused on exactly the specialized and targeted drug development that has guided its mission thus far.

We are well-funded at the moment with $67 million pro forma cash on hand at June 30 and all in all, we think this is a very exciting time for Tonix he said.

See more from Benzinga

2020 Benzinga.com. Benzinga does not provide investment advice. All rights reserved.

Read the original post:
With Key Data Nearing, Tonix Looks to Spotlight Robust Pipeline In Immunology And CNS Therapeutics - Yahoo Finance

Immunology

Global Immunology Market 2020 Research Report with COVID-19 Impact, by Future Trend, Growth rate and Industry Analysis to 2025 – Good Night, Good…

An up-to-date intelligence study by Global Immunology Market 2020 by Company, Regions, Type and Application, Forecast to 2025 provides the present scenario of the market and offers a comparative assessment of the market. The report provides historical data, significance, statistical data, size & share, market price & demand, business overview, market analysis by product and market trends by key players. It detects that the global Immunology market by technological advancements and the presence of a large number of players, who are making the competitive landscape distributed. The report further highlights current growth factors, market threats, attentive opinions, and competitive analysis of major Immunology market players, value chain analysis, and future roadmap.

Competitiveness:

The Immunology market is fragmented and is characterized by the presence of key vendors and other prominent vendors. Key vendors are trying to maintain themselves in the global Immunology market, whereas, regional vendors are focusing on product offerings to establish themselves in the market. Vendors are providing a different range of product lines intensifying the competitive scenario.

NOTE: Our report highlights the major issues and hazards that companies might come across due to the unprecedented outbreak of COVID-19.

DOWNLOAD FREE SAMPLE REPORT: https://www.researchstore.biz/sample-request/11508

Market Potential:

The market vendors have been forecasted to obtain new opportunities as there has been an increased emphasis on spending more on the work of research and development by many of the manufacturing companies. Additionally, many of the market participants are anticipated to make a foray into the emerging economies that are yet to be explored so as to find new opportunities. The global Immunology market has gone through rapid business transformation by good customer relationships, drastic and competitive growth, significant changes within the market, and technological advancement in the worldwide market.

Topmost list manufacturers/ key player/ economy by business leaders leading players of the market are: AbbVie, eFFECTOR Therapeutics, Johnson& Johnson, Amgen, Cellectar Biosciences, F. Hoffmann-La Roche, Celgene, Bionor Pharma

Geographically, this report studies market share and growth opportunity in the following key regions: North America (United States, Canada and Mexico), Europe (Germany, France, UK, Russia and Italy), Asia-Pacific (China, Japan, Korea, India, Southeast Asia and Australia), South America (Brazil, Argentina, Colombia), Middle East and Africa (Saudi Arabia, UAE, Egypt, Nigeria and South Africa)

On the basis of product segment, this report covers: Immuno Boosters, Immunosuppressants,

On the basis of Application segment, this report covers: Autoimmune Diseases, Oncology, Organ Transplantation, Others,

ACCESS FULL REPORT: https://www.researchstore.biz/report/global-immunology-market-11508

Important Take-Away:

Moreover, the report has covered the PEST analysis by region and key economies across the globe, PORTERs analysis, and detailed SWOT analysis of key players to analyze their strategies. It guides companies to make effective business strategy decisions by knowing the global Immunology market conditions and sentiment within the market. The report serves to adjust investment allocation by outlining key focus areas of the industry.

Customization of the Report:This report can be customized to meet the clients requirements. Please connect with our sales team (sales@researchstore.biz), who will ensure that you get a report that suits your needs. You can also get in touch with our executives on +1-201-465-4211 to share your research requirements.

About Us

Researchstore.biz is a fully dedicated global market research agency providing thorough quantitative and qualitative analysis of extensive market research.Our corporate is identified by recognition and enthusiasm for what it offers, which unites its staff across the world.We are desired market researchers proving a reliable source of extensive market analysis on which readers can rely on. Our research team consist of some of the best market researchers, sector and analysis executives in the nation, because of which Researchstore.biz is considered as one of the most vigorous market research enterprises. Researchstore.biz finds perfect solutions according to the requirements of research with considerations of content and methods. Unique and out of the box technologies, techniques and solutions are implemented all through the research reports.

Contact UsMark StoneHead of Business DevelopmentPhone: +1-201-465-4211Email: sales@researchstore.bizWeb: http://www.researchstore.biz

Go here to see the original:
Global Immunology Market 2020 Research Report with COVID-19 Impact, by Future Trend, Growth rate and Industry Analysis to 2025 - Good Night, Good...

Immunology

The American Academy of Allergy, Asthma & Immunology and National Association of School Nurses Release Guidance on School Attendance, Asthma and…

New document summarizes the current overall recommendations for treating students with asthma at school during the ongoing pandemic.

MILWAUKEE, Wis. (PRWEB) August 27, 2020

The American Academy of Allergy, Asthma & Immunology (AAAAI) and National Association of School Nurses (NASN) have released School Attendance, Asthma and COVID-19, a document that contains considerations for school nurses as schools begin to re-open amid the COVID-19 pandemic.

While certain evaluation procedures and treatment recommendations for students with asthma are no longer consistent due to the COVID-19 pandemic and a lack of objective data to guide recommendations, this new document aims to summarize overall recommendations that may be updated as more data surrounding COVID-19 becomes available.

The document addresses considerations when it comes to personal protective equipment (PPE), daily controller medications, and treatment for asthma prior to physical activity. It also touches on asthma action plans and guidance regarding distinguishing symptoms of COVID-19 from asthma. A case scenario is also included to provide school nurses with a concrete example of what procedures should be followed if an asthmatic student reports to them with symptoms of cough or shortness of breath.

Robert F. Lemanske Jr., MD, FAAAAI, a past AAAAI President and Chair of the AAAAI Office of School-based Management of Asthma who helped create the document, expressed why he felt this resource was so important for the AAAAI and NASN to put together. "School nurses are facing a challenging year, particularly for managing conditions such as asthma that may present similar symptoms to COVID-19. While there are no national recommendations, the AAAAI and NASN hope this document can act as a resource to protect school nurses, staff and of course, students while still providing optimal asthma care."

Donna Mazyck, NASN Executive Director, shared the importance for school nurses to have evidence-based considerations for managing asthma in students with asthma while in school buildings during COVID-19. "Asthma is a common chronic illness in students. A science-based approach to guide school nurse practice improves the health and wellbeing of students with asthma."

The AAAAI and NASN previously worked together on the AAAAI's School-based Asthma Management Program (SAMPRO), which details the elements necessary for the education of children, families, clinicians, and school-based personnel based on a "circle of support" that enhances multidirectional communication and promotes better care for children with asthma within the school setting. Further information on SAMPRO, which is endorsed by the NASN and others, can be found here.

You can also learn more about asthma and COVID-19 on the American Academy of Allergy, Asthma & Immunology website, aaaai.org.

About AAAAI

The American Academy of Allergy, Asthma & Immunology (AAAAI) represents allergists, asthma specialists, clinical immunologists, allied health professionals and others with a special interest in the research and treatment of allergic and immunologic diseases. Established in 1943, the AAAAI has more than 7,100 members in the United States, Canada and 72 other countries. The AAAAI's Find an Allergist/Immunologist service is a trusted resource to help you find a specialist close to home.

About NASN

The National Association of School Nurses is a non-profit specialty nursing organization, first organized in 1968 and incorporated in 1977, representing school nurses exclusively. NASN has more than 17,000 members and 50 affiliates, including the District of Columbia and overseas school nurses. The mission of NASN is to optimize student health and learning by advancing the practice of school nursing. Please visit us at http://www.nasn.org.

###

For the original version on PRWeb visit: https://www.prweb.com/releases/the_american_academy_of_allergy_asthma_immunology_and_national_association_of_school_nurses_release_guidance_on_school_attendance_asthma_and_covid_19/prweb17356253.htm

See the original post here:
The American Academy of Allergy, Asthma & Immunology and National Association of School Nurses Release Guidance on School Attendance, Asthma and...

Immunology

Scientists Think They’ve Figured Out a Main Culprit of Inflammatory Bowel Disease – ScienceAlert

Between 6 and 8 million people worldwide suffer from inflammatory bowel disease, a group of chronic intestinal disorders that can cause belly pain, urgent and frequent bowel movements, bloody stools and weight loss.

New research suggests that a malfunctioning member of the patient's own immune system called a killer T cell may be one of the culprits. This discovery may provide a new target for IBD medicines.

The two main types of IBD are ulcerative colitis, which mainly affects the colon, and Crohn's disease, which can affect the entire digestive tract. Researchers currently believe that IBD is triggered when an overactive immune system attacks harmless bacteria in the intestines.

Although there are many treatments for IBD, for as many as 75 percent of individuals with IBD there are no effective long-term treatments. This leaves many patients without good options.

I am a physician-scientist conducting research in immunology and IBD and in a new study, my team and our colleagues specializing in immunology, gastroenterology and genomics examined immune cells from the blood and intestines of healthy individuals and compared them with those collected from patients with ulcerative colitis to gain a better understanding of how the immune system malfunctions in IBD.

There are many reasons why current treatments aren't permanent, but one reason is that scientists don't fully understand how the immune system is involved in IBD. It is our hope that closing the current knowledge gap about how the immune system is involved in this disorder will eventually lead to new durable treatments for IBD that target the right immune cells.

The immune system can be divided into innate and adaptive branches. The innate branch is our first line of defense and acts quickly within minutes to hours. But this system senses changes caused by microbes generally. It does not mount a targeted response against a specific pathogen, which means that some invaders can be overlooked.

The adaptive branch is designed to detect specific threats, but is slower and takes a couple of days to get going. T cells are a part of the adaptive immune system and can be further subdivided into CD4 and CD8 T cells.

CD4 T cells are helpers that aid other immune cells by releasing soluble molecules called cytokines that can induce inflammation.

CD8 T cells can also release cytokines, but their main function is to kill cells infected by microbial invaders. This is why CD8 T cells are often referred to as serial killers.

After the infection is cleared and the pathogen has been destroyed, cells called memory T cells remain. These memory T cells "remember" the pathogen they've just encountered and if they see it again, they mount a stronger and faster response than the first time. They and their descendants can also live for a long time, even decades in the case of certain infections like measles.

The goal of a vaccine is to provide a preview of the microbe so that the immune system can build an army of memory cells against an infectious agent, such as SARS-CoV-2, the virus that causes COVID-19. That way, if the virus attacks, the memory T cells will spring into action and activate an immune response including the production of antibodies from B cells.

Immunologists further subdivide memory T cells into different classes depending on if and where they travel in the body. Circulating memory T cells are scouts that look for signs of infection by patrolling the blood, lymph nodes and spleen.

Tissue-resident memory cells, abbreviated TRM, are sentries stationed at key ports of entry into the human body including the skin, lungs, and intestines and act rapidly to counter an infectious threat. Intestinal TRM also function as peacekeepers and do not tend to overreact against the many harmless microbes living in the intestines.

In the new study, our team analyzed blood and intestinal samples to discover that intestinal CD8 TRM come in at least four different varieties, each with unique features and functions.

We noticed that individuals with ulcerative colitis had higher numbers and proportions of cells belonging to one of these four varieties. This particular variety, which we'll call inflammatory TRM here, carried instructions to make very large amounts of cytokines and other protein factors that allow them to kill other cells. High levels of certain cytokines can cause inflammation and tissue damage in the body.

It seems that in individuals with ulcerative colitis, the balance of memory cells is shifted in favor of this rogue population of inflammatory TRM that may become part of the problem by causing persistent inflammation and tissue damage.

We also found evidence consistent with the possibility that these inflammatory TRM might be exiting the intestinal tissue and entering the blood. Other studies in mice and people have shown that TRM, despite being called "tissue-resident," can leave tissues in certain circumstances.

By leaving the tissue and entering the blood, inflammatory TRM may be able to travel to other parts of the body and cause damage. This possibility may explain why autoimmune diseases that start in one organ, like IBD in the digestive tract or psoriasis in the skin, often affect other parts of the body.

The very features that make memory T cells so desirable for vaccines their capacity to live for such a long time and mount a stronger response when they encounter a microbial invader for the second time may explain why autoimmune diseases are chronic and lifelong.

It is important to point out that none of the current drug treatments for IBD specifically target long-lived memory cells, which might be a reason why these therapies don't work long-term in many individuals. One therapeutic approach might be to target inflammatory TRM for destruction, but this could result in side effects like suppression of the immune system and increased infections.

Our findings build on previous studies showing that different TRM varieties, like the CD4 subtype, may also be involved in IBD, while other studies show that TRM play a role in autoimmune diseases affecting other organs like the skin and kidneys.

The possibility that T cell memory is co-opted in IBD is exciting, but there is much that we still don't understand about TRM.

Can we selectively target inflammatory TRM for destruction? Would this be an effective treatment for IBD? Can we do so without causing major side effects? Further research will be needed to answer these important questions and to strengthen the link between TRM and IBD.

John Chang, Professor of Medicine, University of California San Diego.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Go here to see the original:
Scientists Think They've Figured Out a Main Culprit of Inflammatory Bowel Disease - ScienceAlert

Immunology

Video: COVID-19 Why it Matters Video Series Introduction with Brian Merkel – UWGB

This video series features UW-Green Bays Immunologist Brian Merkel on COVID-19 and Why it Matters. This series empowers viewers with knowledge to help them navigate through the pandemic. Merkel has a Ph.D. in Microbiology & Immunology from the Medical College of Virginia. He is an associate professor in UW-Green Bays Human Biology & Biology programs and has an appointment at the Medical College of Wisconsin Department of Microbiology and Immunology. He will be responding to a number of questions related to COVID19 and try to get behind the why its important to be educated in your decision-making as we navigate the pandemic together.

Video Transcript Series Introduction with Brian Merkel:

Brian Merkel, Microbiology and Immunology, I have a Ph.D. from the Department of Microbiology and Immunology from the Medical College of Virginia. I currently have an appointment in the Microbiology Department and Immunology Department for the Medical College of Wisconsin, and I am the incoming chair of Human Biology at the University of Wisconsin Green Bay. And so today we are going to talk about why COVID-19 matters to you. So, the goal of these discussions is to empower you and to help you understand why this disease affects everyone and what you can do about it. So, over the series of several videos that will be our goal to do just that.

See the original post here:
Video: COVID-19 Why it Matters Video Series Introduction with Brian Merkel - UWGB

Immunology

First US novel coronavirus reinfection case identified in … – Thomson Reuters Foundation

(Adds immunology expert's comment)

By Deena Beasley

Aug 28 (Reuters) - Researchers for the first time have identified someone in the United States who was reinfected with the novel coronavirus, according to a study that has not yet been reviewed by outside experts.

The report, published online, describes a 25-year-old man living in Reno, Nevada, who tested positive for the virus in April after showing mild illness. He got sick again in late May and developed more severe COVID-19, the disease caused by the virus.

"This study likely represents a clear example of reinfection ... reinfections are possible - which we already knew, because immunity is never 100%," Kristian Anderson, professor of immunology and microbiology at Scripps Research in La Jolla, California, said in an emailed comment.

Cases of presumed reinfection have cropped up in other parts of the world, but questions have arisen about testing accuracy. Earlier this week, University of Hong Kong researchers reported details of a 33-year-old man who had recovered in April from a severe case of COVID-19 and was diagnosed four months later with a different strain of the virus.

Researchers at the University of Nevada, Reno School of Medicine and the Nevada State Public Health Laboratory said they were able to show through sophisticated testing that the virus associated with each instance of the Reno man's infection represented genetically different strains.

They emphasized that reinfection with the virus is probably rare, but said the findings imply that initial exposure to the virus may not result in full immunity for everyone.

"We don't know at what frequency reinfections occur and how that might change over time," Anderson said. "Before we have broader studies illuminating these questions, we can't conclude what a single case of reinfection means for longevity and robustness of COVID-19 immunity and relevance for a future vaccine." (Reporting by Deena Beasley; Editing by Dan Grebler and Grant McCool)

Our Standards: The Thomson Reuters Trust Principles.

Read more:
First US novel coronavirus reinfection case identified in ... - Thomson Reuters Foundation

Immunology

Scientists Explore Why Some People Are Able To Live With An Infection Unscathed – KPCW

One of the reasons Covid-19 has spread so swiftly around the globe is that for the first days after infection, people feel healthy. Instead of staying home in bed, they may be out and about, unknowingly passing the virus along. But in addition to these pre-symptomatic patients, the relentless silent spread of this pandemic is also facilitated by a more mysterious group of people: the so-called asymptomatics.

According to various estimates, between 20 and 45 percent of the people who get COVID-19 and possibly more, according to a recent study from the Centers for Disease Control and Prevention sail through a coronavirus infection without realizing they ever had it. No fever or chills. No loss of smell or taste. No breathing difficulties. They don't feel a thing.

Asymptomatic cases are not unique to COVID-19. They occur with the regular flu, and probably also featured in the 1918 pandemic, according to epidemiologist Neil Ferguson of Imperial College London. But scientists aren't sure why certain people weather COVID-19 unscathed. "That is a tremendous mystery at this point," says Donald Thea, an infectious disease expert at Boston University's School of Public Health.

The prevailing theory is that their immune systems fight off the virus so efficiently that they never get sick. But some scientists are confident that the immune system's aggressive response, the churning out of antibodies and other molecules to eliminate an infection, is only part of the story.

These experts are learning that the human body may not always wage an all-out war on viruses and other pathogens. It may also be capable of accommodating an infection, sometimes so seamlessly that no symptoms emerge. This phenomenon, known as disease tolerance, is well-known in plants but has only been documented in animals within the last 15 years.

Hints that 'disease tolerance' is at work

Disease tolerance is the ability of an individual, due to a genetic predisposition or some aspect of behavior or lifestyle, to thrive despite being infected with an amount of pathogen that sickens others. Tolerance takes different forms, depending on the infection. For example, when infected with cholera, which causes watery diarrhea that can quickly kill through dehydration, the body might mobilize mechanisms that maintain fluid and electrolyte balance. During other infections, the body might tweak metabolism or activate gut microbes whatever internal adjustment is needed to prevent or repair tissue damage or to make a germ less vicious.

"Why, if they have these abnormalities, are they healthy? Potentially because they have disease tolerance mechanisms engaged. These are the people we need to study." - Janelle Ayres, physiologist, Salk Institute for Biological Studies

Researchers who study these processes rely on invasive experiments that cannot be done in people. Nevertheless, they view asymptomatic infections as evidence that disease tolerance occurs in humans. At least 90 percent of those infected with the tuberculosis bacterium don't get sick. The same is true for many of the 1.5 billion of people globally who live with parasitic worms called helminths in their intestines. "Despite the fact that these worms are very large organisms and they basically migrate through your tissues and cause damage, many people are asymptomatic. They don't even know they're infected," says Irah King, a professor of immunology at McGill University. "And so then the question becomes, what does the body do to tolerate these types of invasive infections?"

While scientists have observed the physiological processes that minimize tissue damage during infections in animals for decades, it's only more recently that they've begun to think about them in terms of disease tolerance. For example, King and colleagues have identified specific immune cells in mice that increase the resilience of blood vessels during a helminth infection, leading to less intestinal bleeding, even when the same number of worms are present.

"This has been demonstrated in plants, bacteria, other mammalian species," King says.

"Why would we think that humans would not have developed these types of mechanisms to promote and maintain our health in the face of infection?" he adds.

Maybe germs aren't the enemy: A more nuanced view

In a recent Frontiers in Immunology editorial, King and his McGill colleague Maziar Divangahi describe their long-term hopes for the field: A deeper understanding of disease tolerance, they write, could lead to "a new golden age of infectious disease research and discovery."

Scientists have traditionally viewed germs as the enemy, an approach that has generated invaluable antibiotics and vaccines. But more recently, researchers have come to understand that the human body is colonized by trillions of microbes that are essential to optimal health, and that the relationship between humans and germs is more nuanced.

Meddlesome viruses and bacteria have been around since life began, so it makes sense that animals evolved ways to manage as well as fight them. Attacking a pathogen can be effective, but it can also backfire. For one thing, infectious agents find ways to evade the immune system. Moreover, the immune response itself, if unchecked, can turn lethal, applying its destructive force to the body's own organs.

"With things like COVID, I think it's going to be very parallel to TB, where you have this Goldilocks situation," says Andrew Olive, an immunologist at Michigan State University, "where you need that perfect amount of inflammation to control the virus and not damage the lungs."

Some of the key disease tolerance mechanisms scientists have identified aim to keep inflammation within that narrow window. For example, immune cells called alveolar macrophages in the lung suppress inflammation once the threat posed by the pathogen diminishes.

Much is still unknown about why there is such a wide range of responses to COVID-19, from asymptomatic to mildly sick to out of commission for weeks at home to full-on organ failure. "It's very, very early days here," says Andrew Read, an infectious disease expert at Pennsylvania State University who helped identify disease tolerance in animals. Read believes disease tolerance may at least partially explain why some infected people have mild symptoms or none at all. This may be because they're better at scavenging toxic byproducts, he says, "or replenishing their lung tissues at faster rates, those sorts of things."

Asymptomatic COVID-19 infections

The mainstream scientific view of asymptomatics is that their immune systems are especially well-tuned. This could explain why children and young adults make up the majority of people without symptoms because the immune system naturally deteriorates with age. It's also possible that the immune systems of asymptomatics have been primed by a previous infection with a milder coronavirus, like those that cause the common cold.

Asymptomatic cases don't get much attention from medical researchers, in part because these people don't go to the doctor and thus are tough to track down. But Janelle Ayres, a physiologist and infectious disease expert at the Salk Institute For Biological Studies who has been a leader in disease tolerance research, studies precisely the mice that don't get sick.

The staple of this research is something called the "lethal dose 50" test, which consists of giving a group of mice enough pathogen to kill half. By comparing the mice that live with those that die, she pinpoints the specific aspects of their physiology that enable them to survive the infection. She has performed this experiment scores of times using a variety of pathogens. The goal is to figure out how to activate health-sustaining responses in all animals.

A hallmark of these experiments and something that surprised her at first is that the half that survive the lethal dose are perky. They are completely unruffled by the same quantity of pathogen that kills their counterparts. "I thought going into this ... that all would get sick, that half would live and half would die, but that isn't what I found," Ayres says. "I found that half got sick and died, and the other half never got sick and lived."

Ayres sees something similar happening in the COVID-19 pandemic. Like her mice, asymptomatic people infected with the novel coronavirus seem to have similar amounts of the virus in their bodies as the people who fall ill, yet for some reason they stay healthy. Studies show that their lungs often display damage on CT scans, yet they are not struggling for breath (though it remains to be seen whether they will fully escape long-term impacts). Moreover, a small recent study suggests that people who are asymptomatic mount a weaker immune response than those who get sick suggesting that mechanisms are at work that have nothing to do with fighting infection.

"Why, if they have these abnormalities, are they healthy?" asks Ayres. "Potentially because they have disease tolerance mechanisms engaged. These are the people we need to study."

The goal of disease tolerance research is to decipher the mechanisms that keep infected people healthy and turn them into therapies that benefit everyone. "You want to have a drought-tolerant plant, for obvious reasons, so why wouldn't we want to have a virus-tolerant person?" Read asks.

A 2018 experiment in Ayres' lab offered proof of concept for that goal. The team gave a diarrhea-causing infection to mice in a lethal dose 50 trial, then compared tissue from the mice that died with those that survived, looking for differences. They discovered that the asymptomatic mice had utilized their iron stores to route extra glucose to the hungry bacteria, and that the pacified germs no longer posed a threat. The team subsequently turned this observation into a treatment. In further experiments, they administered iron supplements to the mice and all the animals survived, even when the pathogen dose was upped a thousandfold.

When the pandemic hit, Ayres was already studying mice with pneumonia and the signature malady of COVID-19, acute respiratory distress syndrome, which can be triggered by various infections. Her lab has identified markers that may inform candidate pathways to target for treatment. The next step is to compare people who progressed to severe stages of COVID-19 with those who are asymptomatic to see whether markers emerge that resemble the ones she's found in mice.

If a medicine is developed, it would work differently from anything that's currently on the market because it would be lung-specific, not disease-specific, and would ease respiratory distress regardless of which pathogen is responsible.

But intriguing as this prospect is, most experts caution that disease tolerance is a new field and tangible benefits are likely many years off. The work involves measuring not only symptoms but the levels of a pathogen in the body, which means killing an animal and searching all of its tissues. "You can't really do controlled biological experiments in humans," Olive says.

In addition, there are countless disease tolerance pathways. "Every time we figure one out, we find we have 10 more things we don't understand," King says. Things will differ with each disease, he adds, "so that becomes a bit overwhelming."

Nevertheless, a growing number of experts agree that disease tolerance research could have profound implications for treating infectious disease in the future. Microbiology and infectious disease research has "all been focused on the pathogen as an invader that has to be eliminated some way," says virologist Jeremy Luban of the University of Massachusetts Medical School. And as Ayres makes clear, he says, "what we really should be thinking about is how do we keep the person from getting sick."

Emily Laber-Warren directs the health and science reporting program at the Craig Newmark Graduate School of Journalism at CUNY.

This story was produced by Undark, a nonprofit, editorially independent digital magazine exploring the intersection of science and society.

Read the original:
Scientists Explore Why Some People Are Able To Live With An Infection Unscathed - KPCW

Immunology

Blocking nerve signals to the pancreas halts type 1 diabetes onset in mice – Newswise

Newswise LA JOLLAYour pancreas is a little sweet potato-shaped organ that sits snug behind your stomach. The pancreas is studded with islets, the cell clusters that house insulin-producing beta cells. In people with type 1 diabetes, the body's own immune cells head for the islets and start attacking the beta cells. No one knows exactly what triggers this attack.

One clue may lie in the pattern of beta cell death. Many beta cells are killed off in big patches while other beta cells are mysteriously untouched. Something seems to be drawing immune cells to attack specific groups of beta cells while ignoring others.

In a new Science Advances study, researchers at La Jolla Institute for Immunology (LJI) report that the nervous system may be driving this patchy cell die-off. Their new findings in a mouse model suggest that blocking nerve signals to the pancreas could stop patients from ever developing type 1 diabetes.

"It's astonishing that this process may be stoppable through neuronal influence," says LJI Professor Matthias von Herrath, M.D., who served as the studys senior author.

The von Herrath Lab has been working to uncover the cause of type 1 diabetes. Although there are environmental and genetic risk factors for the disease, type 1 diabetes often seemingly strikes at random. Over the years, researchers have sought an explanation for the observed patchy pattern of cell death. One theory has been that these patches have differences in blood flow or they have been damaged by a virus that might be sparking an immune attack.

But recently, researchers have been exploring a new field called neuroimmunology, which is the idea that nerve signals can affect immune cells. Could nerve signals drive immune cells to attack certain areas of the pancreas?

"We thought that could explain a lot," says study first author Gustaf Christoffersson, Ph.D., a former LJI postdoctoral researcher now at the University Uppsala, Sweden.

To test this theory, the researchers used a mouse model that can be experimentally induced to have beta cell death. They "denervated" the mice, either surgically or through use of a neurotoxin or a pharmacological agent, to block most of the sympathetic nerve signals to the pancreas. The researchers then used LJI's world-class imaging facility to track the pattern of beta cell death in living mice.

The team found that blocking the nerve signals protected mice from beta cell death, compared with no effect in mice given no treatment and mice given only beta blockers. Without innervation, it was like the pancreas had gone dark and immune cells were unable to find their target.

"We were pretty surprised to see that these nerve blockers led to pretty significant differences in the onset of diabetes," says Christoffersson.

More work needs to be done before this method can be tested in people. Von Herrath explains that doctors would first need a reliable way to identify patients at risk of type 1 diabetes onset. Once these patients are identified, von Herrath believes they could be treated either through electrostimulation or drugs to block nerve signals. There are also non-surgical, intravascular methods for blocking nerve signals.

The new discovery might explain much more than the patchiness seen in type 1 diabetes. Several autoimmune diseases share this same patchinessbut in a symmetrical pattern. For example, the skin condition vitiligo causes skin to lose its pigment, often in symmetrical areas across the faces and hands. Arthritis also tends to strike symmetrically, with inflammation in both knee, elbow or wrist joints.

The new study suggests that these areas may be innervated by nerves that branch out symmetrically through the body.

"This symmetry is very striking, and it's been almost impossible to explain," says von Herrath.

Von Herrath thinks breakthroughs in neuroimmunology could have broad implications for explaining why the body turns against its own organs in many autoimmune diseases. Going forward, he and Christoffersson hope to investigate the cellular mechanisms that connect the nervous system and type 1 diabetes.

The study, "Interference with pancreatic sympathetic signaling halts the onset of diabetes in mice," was supported by the National Institutes of Health (R01 AI092453), the Swedish Research Council (2014-06840 and 2018-02314), the Swedish Society for Medical Research, the Gran Gustafsson Foundation, and the Science for Life Laboratory.

The study was co-authored by Sowbarnika S. Ratliff of LJI.

###

About La Jolla Institute for Immunology

The La Jolla Institute for Immunology is dedicated to understanding the intricacies and power of the immune system so that we may apply that knowledge to promote human health and prevent a wide range of diseases. Since its founding in 1988 as an independent, nonprofit research organization, the Institute has made numerous advances leading toward its goal: life without disease.

See the article here:
Blocking nerve signals to the pancreas halts type 1 diabetes onset in mice - Newswise

Neuroscience

Author David Eagleman wants you to think much more about the brain – Houston Chronicle

Renowned Baylor College of Medicine neuroscientist and best-selling author, Dr. David Eagleman, will present two lectures at San Jacinto College South on March 28.

Before David Eagleman presents a single sentence of his own construction in Livewired, he lets it be known that the book, subtitled, The Inside Story of the Ever-Changing Brain, offers more than science. He does so with his choice of epigraph: Every man is born as many men and dies as a single one, written by philosopher Martin Heidegger.

Hopefully this book will open eyes to what it means to be a human, Eagleman says. We tend to think of ourselves as static. But in fact were changing all the time.

Eagleman has worked on Livewired over 10 years. The result is a text that is both probing, philosophical and playful, in which wounded British naval officer Horatio Nelson and tragic Spider-Man villain Dr. Otto Octavius appear in close proximity; where philosopher Ren Descartes and soulful country singer Ronnie Milsap are separated by just a few pages. With Livewired Eagleman hopes to educate about plasticity of the brain, a field of study he sees as equal to the deep study of DNA.

Heidegger out of the way, Eaglemans is a book that opens with hemispherectomy, a story about a child suffering from worsening seizures, whose family makes the fraught decision to have half of his brain removed.

by David Eagleman

Pantheon

320 pages, $28.95

I first started studying hemispherectomies 20 years ago and Im still stunned by the fact that we dont talk about this every day, Eagleman, 49, says. You watch the news every day Trump, weather patterns, things that are remarkable. But nothing like this. We dont know how to built technology like this. You cant tear circuitry out of a laptop and have it still function. You can do that with brains.

The books title is Eaglemans effort to put a recognizable name to further investigation into and discussion of the brain.

The brain is not, as we once thought, hardwired, he says. Its not hardware, its liveware.

We talk a lot about the heart. What the heart tells you, what your gut tells you. But its all brain. If you get a heart transplant, an artificial heart from the Texas Medical Center, youre still the same person. Change even a little bit of the brain and that can change a person entirely.

Long before he became a renowned neuroscientist, Eagleman was a literature student at Rice University, where he studied literature and its mechanisms for storytelling that hed later apply to his work. He studied at the Baylor College of Medicine and earned a PhD in neuroscience in 1998.

Immersed in research, Eagleman also found time for fiction. He wrote Sum: Forty Tales From the Afterlives in 2009. The book well-reviewed and a strong seller was a deeply philosophical piece of speculative fiction. Two years later, he landed on various best-seller lists with a book of science that proved inviting rather than daunting: Incognito: The Secret Lives of the Brain.

Like other storytellers in his line of work, Eagleman cites Carl Sagans Cosmos as an early influence. I was so caught up in it, he says. Here was a guy, a real scientist who cares about communicating the beauty and magic of this to me, some random kid sitting in front of the TV in New Mexico. I always wanted to be able to do that.

In addition to his lit workload, Eagleman took several philosophy courses while a student at Rice. For the most part he found them frustrating.

It felt to me like wed argue a question until it ended up in a quagmire and then everyone would stop there, he says.

He found a doorway past those stalled debates in neuroscience.

With neuroscience, you could ask fundamental questions about ourselves, he says. You could do experiments and achieve answers.

The brain has informed Eaglemans work since. Hes published several books and developed and hosted a TV series about the brain. He spent 10 years as director of a neuroscience research lab at the Baylor School of Medicine for a decade. And hes earned enough honors and accolades to keep his shelves and walls cluttered with totems of recognition.

He left Houston in 2016 for Silicon Valley. There he works as an adjunct professor at Stanford University, while also working entrepreneurial territory with the companies BrainCheck and NeoSensory. The latter sounds like something out of a Christopher Nolan film, claiming on its site that the companys research began with the idea that our experience of reality can go beyond our sensory limitations.

Eagleman sees biology as drafting off engineering for centuries now, with remarkable devices engineers build.

He envisions a future in which that engineering is reversed so we build livewired devices. That we do this thing we know is possible because each of us carries three pounds of incredible computational material in our heads.

Eagleman says Livewired is both the beginning and the end of something. He says it represents everything Ive done in my science career over the past 20 years.

While that phrase suggests a culmination of research, he insists its really the doorway to what comes next, which is why he finds himself in Silicon Valley. Livewired is a Cosmos-esque take on his lifes work.

While plenty of papers have been written about brain plasticity, he thinks his is the first comprehensive text that offers an overarching account of a field of study he believes warrants the same attention that greeted the Human Genome Project.

This really is lifes other secret, the other half we need to understand, he says. I think this topic, this area is as important as when Darwin published his theory of evolution. Its a major stepping stone. We get how we end up here genetically. To my mind, brain plasticity is the next step of that. Genetics gets put into the world. Then the organism is shaped by what happens to it. Humans are this incredible plastic species, more so than our neighbors in the animal kingdom. And its like Mother Natures great trick, and also a bit of a gamble on her part: dropping the brain into the world half baked. Let it figure out what to do there.

Eagleman encircles that notion the brain figuring it out throughout Livewired. He shows a grasp for narrative and pacing that mirrors his immersion into neuroscience. So the science is presented with anecdotal stories that are at times remarkable, like that of Matt Stutzmann, who was born with no arms. As he grew older, Stultzmann determined the absence of arms to be an obstacle but not a prohibitive condition to becoming a masterful archer.

Livewired is populated by people and stories that speak to Eaglemans assertion that old beliefs about a compartmental brain with different regions solely responsible for different tasks is outdated. That the brain is instead a dynamic system, capable of remarkable change and adaptation. He outlines his concept of livewiring into seven principles, all of which speak to adaptation by the brain to the world around it.

Through this study, Eagleman has gotten closer to answers he couldnt find in his philosophy classes in the early 90s. Which explains why Heidegger, rather than a scientist, gets the first word in a book that seeks to explain who we are.

As Eagleman writes, There is no you without the external. Your beliefs and dogmas and aspirations are shaped by it, inside and out, like a sculpture from a block of marble. Thanks to livewiring, each of us is the world.

andrew.dansby@chron.com

Andrew Dansby covers music and other entertainment, both local and national, for the Houston Chronicle, 29-95.com and chron.com. He previously assisted the editor for George R.R. Martin, author of "Game of Thrones" and later worked on three "major" motion pictures you've never seen. That short spell in the film business nudged him into writing, first as a freelancer and later with Rolling Stone. He came to the Chronicle in 2004 as an entertainment editor and has since moved to writing full time.

Andrew dislikes monkeys, dolphins and the outdoors. He has no pets.

Read more from the original source:
Author David Eagleman wants you to think much more about the brain - Houston Chronicle

Human Behavior

Why Some People Over-Apologize, And Others Never Do – The Swaddle

As the #MeToo movement demonstrated, some people are so bad at apologies, that you find yourself resisting the urge to tell them to go back in time, and learn how to apologize. On the other hand, some of us are so over-apologetic, that we dont just apologize to inanimate objects we may have accidentally bumped into, but also feel the need to apologize for the actions of others that are beyond our control.

But, why do we apologize at all?Because human behavior is interdependent, people apologize when they have breached someones trust, or wronged them in any manner, with the objective of restoring their relationship. When one breaks a rule of social conduct, a subsequent apology re-establishes the rule by acknowledging that it was broken, and rebuilds trust in the individual wronged that the apologizer wont repeat their mistake again. Moreover, by validating the feelings of the person one wronged, an apology also shows care.

Over-apologizing, on the other hand, can stem from a myriad of formative childhood experiences. For some, over-apologizing is a way to avoid conflict, especially if they grew up in a household where conflict sparked screaming matches, or led to violence. It can also stem from a fear of abandonment. In terms of understanding the history behind one struggling to avoid conflict at all costs, Panthea Saidipour, a psychotherapist, noted that if one has witnessed conflicts being meted out with being iced out and given the cold shoulder, which for a kid can feel tantamount to being abandoned, one steers clear of situations that could spiral the same way by over-apologizing. [Apologizing] for having any needs at all, can stem from being raised by a parent, who had a low tolerance or even contempt for your needs, Saidipour added. This can also result in endeavors to constantly please people, and be perceived as a good person, since apologies minimize the negative repercussions of the incident and repair the actors damaged identity. As such, over-apologizing becomes an internalized coping mechanism.

Related on The Swaddle:

Indias #MeToo Apologies Are Rolling In. Do Any Warrant Forgiveness?

But, in addition to being a coping mechanism, apologizing repeatedly can also serve as a safety manoeuvre to keep oneself safe in abusive relationships. Also, experiencing a severely traumatic childhood, can sometimes, lead people to believe that they are the root cause ofall the terrible things happening around them, even after they grow up, causing them to over-apologize. Those who over-apologize often feel like a burden to others, as if their wants and needs are not important, Kelly Hendricks, a couple and family therapist in San Diego, told Psych Central, explaining how the behavior might also be a result of feeling unworthy.

Further, experts believe that anxiety can also lead to over-apologizing, as a means to manage emotions of fear, nervousness, and worry. It could also be a result of the spotlight effect, which generates extreme self-consciousness by making one believe that others are keeping close note of the minutest details of their failures. Over-apologizing can stem from being too hard on ourselves or beating ourselves up for things, Dr. Juliana Breines, an assistant professor of psychology at the University of Rhode Island, explained. In addition to anxiety, another mental health disorder that can lead people to over-apologize is OCD. Dr. Michael Alcee, clinical psychologist, explained that people with OCD are often very sensitive about harming others and about exhibiting overly-assertive or aggressive thought or action, and by apologizing excessively, they believe theyre undoing any harm they believe they may have caused.

And, while some people cannot stop apologizing, some simply dont apologize. Experts believe those who refrain from apologizing as much as possible, are prone to believe that apologies will open the floodgates to further accusations and conflict, and at the same time, relieve the other party of any culpability, Dr. Guy Winch, a clinical psychologist, noted. In order to offer a heartfelt apology, a person needs to have a solid platform of self-worth to stand on, Harriet Lerner, psychologist and author of Why Wont You Apologize?, told The Cut, adding that people whove done more harm, or are less self-aware, are constantly perched upon a small, rickety platform of self-worth, which makes apologizing difficult for them. Apologizing becomes a challenge for people when they have trouble separating their actions from their character, which makes accepting responsibility, or apologizing, threatening to their basic sense of self-esteem, and their identity.

Related on The Swaddle:

Could an Apology Cause Its Recipients More Harm Than Good? Perhaps.

Also, as studies have established over the years, women apologize more than men. In all cultures studied, men apologize less frequently than women. I think one of the greatest risks of being an under-apologizer is to be raised male, and the greatest risk of being an over-apologizer is being raised female, Lerner notes. Among other factors, researchers believe it is also a result of: first, menhaving a higher threshold for what constitutes offensive behavior, and therefore, requires an apology; and second, women caring more about how their actions emotionally affect people around them, which leads them to have a lower threshold for what requires an apology. And, that develops because, girls are more often rewarded for focusing on others feelings while boys are more often rewarded for asserting themselves, Dr. Stephen P. Hinshaw, psychologist, said.

Irrespective of whether one is a an over-apologizer, an under-apologizer, or simply, an individual who apologizes a regular amount, its important to remember that apologies are not only powerful, but also key to preserving our relationships with people we love. Apologies generate empathy. Apology has the ability to disarm others of their anger and to prevent further misunderstandings. While an apology cannot undo harmful past actions, if done sincerely and effectively, it can undo the negative effects of those actions, Beverly Engel, a psychotherapist and author ofThe Power of Apology,wrote in Psychology Today.

Continue reading here:
Why Some People Over-Apologize, And Others Never Do - The Swaddle