#innate lymphoid cells

[incorrect-immunology-facts]

ILCs are such annoying Mary Sues. Oh sure, you can do all the same things as the elite helper T cells immediately, without any sort of special training? How ridiculous and insulting to the T cells who work their asses off to pass positive and negative selection in the thymus and still have to go through so much just to become activated, and these little shits are just out there making T helper cytokines with their super special innate powers. Ugh, who is responsible for the character development on this show?

[mindblowingscience]

A study led by Professor Sebyung Kang and Professor Sung Ho Park in the Department of Biological Sciences at UNIST has unveiled a remarkable breakthrough in cancer treatment. The research team has successfully developed unprecedented "NK cell-engaging nanodrones" capable of selectively targeting and eliminating cancer cells, offering a potential solution for intractable types of cancers. The innate lymphoid cells known as natural killer (NK) cells play a vital role in the body's immune response against cancer. Numerous efforts have been made to harness the power of NK cells to develop effective cancer therapies. Now, the research team has designed and fabricated exceptional NK cell-engaging nanodrones, referred to as NKeNDs, using AaLS protein cage nanoparticles.

Continue Reading.

[humancelltournament]

Human Cell Tournament Round 1

Propaganda!

ILC2 cells, or type 2 innate lymphoid cells are a type of innate lymphoid cell. Not to be confused with the ILC. They are derived from common lymphoid progenitor and belong to the lymphoid lineage. These cells lack antigen specific B or T cell receptor because of the lack of recombination activating gene. ILC2s produce type 2 cytokines (e.g. IL-4, IL-5, IL-9, IL-13) and are involved in responses to helminths, allergens, some viruses, such as influenza virus and cancer. ILC2s play the crucial role of secreting type 2 cytokines in response to large extracellular parasites. They express characteristic surface markers and receptors for chemokines, which are involved in distribution of lymphoid cells to specific organ sites. ILC2s are activated upon respiratory virus infections in mice and humans. For instance, during Influenza A virus infection, which induces IL-33 production, ILC2s are activated and drive airway hyper-responsiveness. [image credit]

The Y chromosome is one of two sex chromosomes in therian mammals and other organisms. Along with the X chromosome, it is part of the XY sex-determination system, in which the Y is the sex-determining chromosome because the presence of the Y chromosome causes offspring produced in sexual reproduction to be of male sex. In mammals, the Y chromosome contains the SRY gene, which triggers development of male gonads. The Y chromosome is passed only from male parents to male offspring. Most therian mammals have only one pair of sex chromosomes in each cell. Males have one Y chromosome and one X chromosome, while females have two X chromosomes. In mammals, the Y chromosome contains a gene, SRY, which triggers embryonic development as a male. The Y chromosomes of humans and other mammals also contain other genes needed for normal sperm production.

[bpod-bpod]

Great Innate

Two prongs of your immune system tackle invaders with a precision pincer movement to keep infections at bay. The innate immune system is fast-responding and unspecialised, while the adaptive develops tailored defences against specific foes with each infection it encounters. How precisely the innate system works, or even whether some parts might be redundant accompaniments to the adaptive elements, is not fully understood. A new study examined the effect of blocking one component of the innate system, group 2 innate lymphoid cells, in mice. Without these cells, the inflammatory response – key to staving off attacks – could not develop properly, and mucus (yellow in the infected intestine cross-section pictured) production was limited meaning parasites could not be expelled. Allergy responses were also worsened by a lack of these cells, highlighting the innate immune system’s integral importance, and perhaps pointing to new treatment approaches.

Written by Anthony Lewis

Image by Patrycja M. Topczewska from work by Katja J. Jarick and colleagues

Department of Microbiology, Infectious Diseases and Immunology, Charité–Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany

Image copyright held by the original authors

Research published in Nature, November 2022

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[shrutirathi226]

Human Milk Oligosaccharides: Insights from Recent Research and Clinical Trials

Breast milk is a rich source of complex carbohydrates called human milk oligosaccharides (HMOs). After fat and lactose, they are the third most common solid component in human milk, yet they play an important role that goes well beyond simple nourishment. Human Milk Oligosaccharides are important because of their intricate biological roles and complicated structure, which are essential to a baby’s proper growth.

Human Milk Oligosaccharides are only found in human milk, and the makeup of this unique substance changes across people and lactation phases. More than 200 distinct kinds of Human Milk Oligosaccharides exist, and they can have very complicated structures made up of multiple sugar units connected in sophisticated ways. HMOs may perform a variety of tasks that are critical to the health of newborns because of their intricacy.

Serving as prebiotics is one of Human Milk Oligosaccharides main functions. They supply Bifidobacteria and other good gut flora with nourishment, which is essential for the development of a baby’s microbiome. Human Milk Oligosaccharides assist in maintaining a balanced gut flora, which is essential for healthy digestion and immune system performance, by encouraging the growth of these advantageous bacteria.

Human Milk Oligosaccharides have also been demonstrated to have anti-infection properties. They function as fictitious receptors, blocking the attachment of dangerous bacteria to the gut lining. Human Milk Oligosaccharides lessen the chance of infections, including those brought on by gastrointestinal pathogens like E. coli, by taking up these binding sites. This defense system enhances the infant’s general health and wellbeing.

Another major area of study for Human Milk Oligosaccharides is their ability to modulate the immune system. Human Milk Oligosaccharides interact with immune cells and signaling pathways to affect how the baby’s immune system develops. They support the growth of the infant’s innate and adaptive immunity as well as the maturation of the gut-associated lymphoid tissue (GALT). In the early months of life, when the infant’s immune system is still growing, this immunological support is especially important.

Human Milk Oligosaccharides may also be important for the development of cognition and for delaying the onset of chronic illnesses later in life, according to recent studies. Although research in these areas is still ongoing, encouraging first results indicate that Human Milk Oligosaccharides offer advantages beyond their direct impact on health.

The genetic makeup of the mother has an impact on the composition of Human Milk Oligosaccharides, which can differ greatly. Because of this variation, each mother’s milk is specific to the demands of her infant and may provide health advantages that are unique to each individual.

To sum up, Human Milk Oligosaccharides are an essential part of breast milk that have a variety of intricate roles that promote the health of the baby. Their relevance in the early stages of life is highlighted by their roles as prebiotics, immunological modulators, and agents that guard against infections. Human Milk Oligosaccharides importance for baby nutrition and health is becoming more and more clear as research reveals the entire range of advantages they offer.illnesses in later life. Although research in these areas is still ongoing, encouraging first results indicate that Human Milk Oligosaccharides offer advantages beyond their direct impact on health.

[jobrxiv]

Staff Associate III (Microbiology and Immunology) Columbia University Irving Medical Center: Vagelos College of Physicians and Surgeons: The Staff Associate III will research the immunological roles of innate lymphoid cells in allergies and infections. See the full job description on jobRxiv: https://jobrxiv.org/job/columbia-university-irving-medical-center-vagelos-college-of-physicians-and-surgeons-27778-staff-associate-iii-microbiology-and-immunology/?feed_id=80237 #ScienceJobs #hiring #research

[gastroenterologyucgconferences]

Track 24: Gastrointestinal Immunology

Introduction:

Gastrointestinal immunology is a specialized field within immunology that focuses on understanding the intricate interplay between the immune system and the gastrointestinal tract. The gastrointestinal tract, or GI tract, is a complex system responsible for digestion, absorption of nutrients, and protection against pathogens and foreign substances. The immune system within the GI tract plays a crucial role in maintaining gut homeostasis, defending against infections, and regulating immune responses to dietary antigens and commensal microorganisms.

Key Components of Gastrointestinal Immunology:

Mucosal Immunity: The gastrointestinal tract is lined with a specialized mucosal layer that serves as a barrier between the external environment and the body's internal tissues. Mucosal immunity involves a network of immune cells, including lymphocytes, macrophages, dendritic cells, and specialized epithelial cells, which work together to detect and respond to potential threats while maintaining tolerance to harmless antigens.

Microbiota Interactions: The gut microbiota, consisting of trillions of microorganisms such as bacteria, viruses, fungi, and archaea, plays a pivotal role in gastrointestinal immunology. The immune system interacts dynamically with the microbiota to establish mutualistic relationships, promote immune tolerance, and protect against pathogenic invaders. Dysregulation of microbiota-immune interactions has been implicated in the pathogenesis of various gastrointestinal disorders, including inflammatory bowel disease and colorectal cancer.

Immune Tolerance and Inflammation: Gastrointestinal immunology involves mechanisms of immune tolerance to dietary antigens and commensal microorganisms to prevent inappropriate immune responses and maintain gut homeostasis. Dysregulation of immune tolerance can lead to aberrant immune activation and chronic inflammation, contributing to the development of autoimmune diseases, food allergies, and inflammatory bowel conditions.

Innate and Adaptive Immunity: The gastrointestinal immune system comprises both innate and adaptive immune components that collaborate to provide protection against pathogens and regulate immune responses. Innate immune cells, such as macrophages, dendritic cells, and innate lymphoid cells, serve as the first line of defense against invading microorganisms. Adaptive immune cells, including T cells, Bcells, and antibody-producing plasma cells, mediate antigen-specific immune responses and immunological memory.

Immunomodulatory Therapies: Understanding the principles of gastrointestinal immunology is critical for the development of novel immunomodulatory therapies for the treatment of gastrointestinal disorders. Targeted interventions aimed at modulating immune responses, restoring immune tolerance, and reshaping the gut microbiota hold promise for managing conditions such as inflammatory bowel disease, celiac disease, and functional gastrointestinal disorders.

Treatment

Treatment approaches in gastrointestinal immunology vary depending on the specific condition being addressed and the underlying immunological mechanisms involved. Here are some common treatment strategies used in the management of immune-mediated gastrointestinal disorders:

Inflammatory Bowel Disease (IBD):

Anti-inflammatory Medications: Corticosteroids, immunomodulators (such as azathioprine, methotrexate), and biologic therapies (such as anti-TNF agents like infliximab, adalimumab) are commonly used to reduce inflammation and manage symptoms.

Immune Modulators: These medications help to modulate the immune response and reduce inflammation in the gastrointestinal tract.

Dietary Modifications: Some patients may benefit from dietary changes, including low-residue diets or specific carbohydrate diets, to help manage symptoms and reduce inflammation.

Surgery: In severe cases or when medical management is ineffective, surgical intervention may be necessary to remove diseased portions of the intestine or create an ostomy.

Celiac Disease:

Gluten-Free Diet: The primary treatment for celiac disease involves strict adherence to a gluten-free diet, which eliminates wheat, barley, and rye from the diet.

Nutritional Supplements: Patients with celiac disease may require vitamin and mineral supplements to address deficiencies caused by malabsorption.

Monitoring and Follow-up: Regular monitoring of celiac disease markers and follow-up with healthcare providers is essential to ensure compliance with the gluten-free diet and monitor for potential complications.

Food Allergies:

Food Elimination Diet: Identifying and eliminating trigger foods from the diet is the primary treatment for food allergies.

Epinephrine (Adrenaline) Autoinjector: Patients with severe food allergies may be prescribed an epinephrine autoinjector for emergency use in case of anaphylaxis.

Allergen Immunotherapy: For certain food allergies, allergen immunotherapy may be considered under the guidance of an allergist.

Autoimmune Hepatitis:

Immunosuppressive Therapy: Corticosteroids and other immunosuppressive medications are used to suppress the immune response and reduce inflammation in autoimmune hepatitis.

Liver Transplant: In severe cases of autoimmune hepatitis that do not respond to medical therapy, liver transplant may be necessary.

Inflammatory Bowel Syndrome (IBS):

Dietary Modifications: Some patients with IBS may benefit from dietary changes, such as a low-FODMAP diet, to help manage symptoms.

Medications: Depending on the predominant symptoms, medications such as antispasmodics, laxatives, or anti-diarrheal medications may be prescribed to alleviate symptoms.

Stress Management: Stress reduction techniques, such as cognitive-behavioral therapy or relaxation techniques, may help manage symptoms in some patients with IBS.

Other Gastrointestinal Disorders:

Treatment for other gastrointestinal disorders, such as eosinophilic esophagitis, microscopic colitis, and autoimmune enteropathy, may involve a combination of medications, dietary modifications, and other targeted therapies aimed at reducing inflammation and managing symptoms.

Important Information:

Conference Name: 14th World Gastroenterology, IBD & Hepatology Conference Short Name: 14GHUCG2024 Dates: December 17-19, 2024 Venue: Dubai, UAE Email:  gastroenterology@ucgcmeconference.com Visit: https://gastroenterology.universeconferences.com/ Call for Papers: https://gastroenterology.universeconferences.com/submit-abstract/ Register here: https://gastroenterology.universeconferences.com/registration/ Exhibitor/Sponsor: https://gastroenterology.universeconferences.com/exhibit-sponsor-opportunities/ Call Us: +12073070027 WhatsApp Us: +442033222718

[testbankprovidersell]

Test Bank For Porth's Pathophysiology: Concepts of Altered Health States, Ninth Edition Sheila Grossman

Unit I: Concepts of Health and Disease Chapter 01: Concepts of Health and Disease Chapter 02: Concepts of Altered Health in Children Chapter 03: Concepts of Altered Health in Older Adults Unit II: Cell Function and Growth Chapter 04: Cell and Tissue Characteristics Chapter 05: Cellular Adaptation, Injury, and Death Chapter 06: Genetic Control of Cell Function and Inheritance Chapter 07: Genetic and Congenital Disorders Chapter 08: Neoplasia Unit III: Disorders of Integrative Function Chapter 09: Stress and Adaptation Chapter 10: Alterations in Temperature Regulation Chapter 11: Activity Tolerance and Fatigue Unit IV: Infection, Inflammation, and Immunity Chapter 12: Mechanisms of Infectious Disease Chapter 13: Innate and Adaptive Immunity Chapter 14: Inflammation, Tissue Repair, and Wound Healing Chapter 15: Disorders of the Immune Response Chapter 16: Acquired Immunodeficiency Syndrome Unit V: Disorders of Neural Function Chapter 17: Organization and Control of Neural Function Chapter 18: Somatosensory Function, Pain, and Headache Chapter 19: Disorders of Motor Function Chapter 20: Disorders of Brain Function Chapter 21: Sleep and Sleep Disorders Chapter 22: Disorders of Thought, Emotion, and Memory Unit VI: Disorders of Special Sensory Function Chapter 23: Disorders of Visual Function Chapter 24: Disorders of Hearing and Vestibular Function Unit VII: Disorders of the Hematopoietic System Chapter 25: Blood Cells and the Hematopoietic System Chapter 26: Disorders of Hemostasis Chapter 27: Disorders of Red Blood Cells Chapter 28: Disorders of White Blood Cells and Lymphoid Tissues Unit VIII: Disorders of Cardiovascular Function Chapter 29: Structure and Function of the Cardiovascular System Chapter 30: Disorders of Blood Flow in the Systemic Circulation Chapter 31: Disorders of Blood Pressure Regulation Chapter 32: Disorders of Cardiac Function Chapter 33: Disorders of Cardiac Conduction and Rhythm Chapter 34: Heart Failure and Circulatory Shock Unit IX: Disorders of Respiratory Function Chapter 35: Structure and Function of the Respiratory System Chapter 36: Respiratory Tract Infections, Neoplasms, and Childhood Disorders Chapter 37: Disorders of Ventilation and Gas Exchange Unit X: Disorders of Renal Function and Fluids and Electrolytes Chapter 38: Structure and Function of the Kidney Chapter 39: Disorders of Fluid and Electrolyte Balance Chapter 40: Disorders of Acid—Base Balance Chapter 41: Disorders of Renal Function Chapter 42: Acute Renal Injury and Chronic Kidney Disease Chapter 43: Disorders of the Bladder and Lower Urinary Tract Unit XI: Disorders of Gastrointestinal Function Chapter 44: Structure and Function of the Gastrointestinal System Chapter 45: Disorders of Gastrointestinal Function Chapter 46: Disorders of Hepatobiliary and Exocrine Pancreas Function Chapter 47: Alterations in Nutritional Status Unit XII: Disorders of Endocrine Function Chapter 48: Mechanisms of Endocrine Control Chapter 49: Disorders of Endocrine Control of Growth and Metabolism Chapter 50: Diabetes Mellitus and the Metabolic Syndrome Unit XIII: Disorders of Genitourinary and Reproductive Function Chapter 51: Structure and Function of the Male Genitourinary System Chapter 52: Disorders of the Male Genitourinary System Chapter 53: Structure and Function of the Female Reproductive System Chapter 54: Disorders of the Female Reproductive System Chapter 55: Sexually Transmitted Infections Unit XIV: Disorders of Musculoskeletal Function Chapter 56: Structure and Function of the Musculoskeletal System Chapter 57: Disorders of Musculoskeletal Function: Trauma, Infection, Neoplasms Chapter 58: Disorders of Musculoskeletal Function: Developmental and Metabolic Disorders Chapter 59: Disorders of Musculoskeletal Function: Rheumatic Disorders Unit XV: Disorders of Integumentary Function Chapter 60: Structure and Function of the Skin Chapter 61: Disorders of Skin Integrity and Function Read the full article

[tumimmtxpapers]

Orchestration of immune response by innate lymphoid cell subtype 2 at various tumor microenvironment, a suitable target for cancer immunotherapy

Innate lymphoid cells are a mixed population of cells and critical regulators of our innate immune system. According to recent scientific literature, tissue resident innate lymphoid cell subtype 2 has been recognized as an important player of type 2 inflammatory responses, involved in different human malignancies like pancreatic, lung, acute myeloid leukemia, gastrointestinal tract cancer, etc. The current reports have revealed that, among the three main ILC sub types, subtype 2 (ILC 2), as the... http://dlvr.it/Sty0BG

[rnomics]

Viruses, Vol. 15, Pages 1566: Alternative Splicing of RIOK3 Engages the Noncanonical NFκB Pathway during Rift Valley Fever Virus Infection

Although the noncanonical NFκB pathway was originally identified as a cellular pathway contributing to lymphoid organogenesis, in the past 20 years, its involvement in innate immunity has become more appreciated. In particular, the noncanonical NFκB pathway has been found to be activated and even exploited by some #RNA viruses during infection. Intriguingly, activation of this pathway has been shown to have a role in disrupting transcription of type 1 interferon (IFN), suggesting a rationale for why this response could be co-opted by some viruses. Rift Valley fever virus (RVFV) is a trisegmented ambisense #RNA virus that poses a considerable threat to domestic livestock and human health. Previously, we showed the atypical kinase RIOK3 is important for mounting an IFN response to RVFV infection of human epithelial cells, and shortly following infection with RVFV (MP12 strain), RIOK3 #mRNA is alternatively spliced to its X2 isoform that encodes a truncated RIOK3 protein. Alternative splicing of RIOK3 #mRNA has an inhibitory effect on the IFN response but also stimulates an NFκB-mediated inflammatory response. Here, we demonstrate alternative splicing of RIOK3 #mRNA is associated with activation of the noncanonical NFκB pathway and suggest this pathway is co-opted by RVFV (MP12) to enhance viral success during infection. https://www.mdpi.com/1999-4915/15/7/1566?utm_source=dlvr.it&utm_medium=tumblr

[thebrokencrescent-blog]

Virus particles often hide in “immunoprivileged sites” around the human body, also sometimes called sanctuary sites, that our immune systems don’t monitor or protect as closely as the rest of our bodies. These include the brain, spinal cord, pregnant uterus, testes, and eyes, for which damage by immune cells would be highly problematic. The testes can harbour Zika and Ebola viruses, for example.

04 July 2023

Over the past 20-30 years laboratory measurements have become sensitive enough to pick up on viral RNA outside the known sanctuary locations. “We were surprised to find that this was common in measles—its main site of persistence is lymphoid tissue,” says Diane Griffin, a microbiologist and immunologist at Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland. “Anybody who looks will now find RNA persistent, probably, after acute virus infection.” Such signs have been found in blood, joints, the respiratory tract, gastrointestinal tissues, and kidneys.

How long can viruses hide for?

It varies. Griffin’s team has also found measles RNA months later than it was previously recognised, after the infectious virus has been cleared. A low level of immune activity in sanctuary sites usually keeps the viruses under control without killing the cells. And sometimes—especially outside sanctuary sites—the immune system can clear the virus but leave its genetic material behind to reproduce later, known as a “latent” virus. For example, antibodies in the brain may suppress viral RNA production without harming infected neurons. There are more than a dozen viruses that can become latent, of which Epstein-Barr virus is one of the most common, infecting as much as 90% of the human population. After an initial Epstein-Barr infection, the remaining viral RNA can lead to later disease and asymptomatic viral shedding.

(...)

Transmission can take place months or even years after recovery from acute disease, potentially enabling spread to new geographical regions. As one potential example, in 2021 in Guinea, an Ebola survivor had a recurrence of acute illness one year after their initial infection. This led to community infection and triggered a “new” outbreak. This, says Griffin, is an example of evolving understanding about what persistence means in Ebola and the potential public health and long term consequences. She also points out that some viruses such as Ebola and Zika don’t have a known latent phase, yet “we know people where, six months after recovery, you get transmission of Zika, or Ebola, or reactivation of problems . . . That means that full length RNA is there and can resume production.”

Can different variants hide for longer?

Sometimes. Viruses often evolve so that they avoid inducing innate immune responses, helping them replicate and survive longer inside cells. These are variants that are less likely to burst cells open, or that can limit or prevent the expression of proteins that make them recognisable by antibodies, or both. Griffin notes that such variants may not be so readily transmitted. She highlights the fatal brain infection subacute sclerosing panencephalitis, which occurs seven to 10 years after a measles infection. “That virus is highly mutated by that time,” she says. “There is a good immune response, but the immune response does no good. It’s not capable of getting rid of those cells.”

(...)

[cmlhopeblog]

IL-18 and VEGF-A trigger type 2 innate lymphoid cell accumulation and pro-tumoral function in chronic myeloid leukemia

CMLHope.Com http://dlvr.it/SnRGhK

[humancelltournament]

Propaganda!

Large granular lymphocytes (LGL), also known as natural killer cells or NK cells, are a type of cytotoxic lymphocyte critical to the innate immune system that belong to the rapidly expanding family of known innate lymphoid cells (ILC) and represent 5–20% of all circulating lymphocytes in humans. The role of NK cells is analogous to that of cytotoxic T-cells in the vertebrate adaptive immune response. These cells provide rapid responses to virus-infected cells and other intracellular pathogens, and also respond to tumor formation.

Proto-oncogenes are genes that, under normal circumstances, play a role in stimulating cell division, or in helping cells stay alive. But sometimes a proto-oncogene mutates or creates too many copies of itself; when this happens, it becomes a potentially cancer-causing oncogene.

[prnlive]

Gary Null’s Show Notes 04 25 23

If you listen to Gary’s show, you know that he begins with the latest findings in natural approaches to health and nutrition. Starting this week, we will make some of those findings available each weekday to subscribers to the Gary Null Newsletter.

Exposure to chemicals found in everyday products is linked to significantly reduced fertility, says study

Leafy greens may boost gut immunity: Study

Can positive thinking prolong your life? Science says yes

Exposure to chemicals found in everyday products is linked to significantly reduced fertility, says study

Mount Sinai Hospital, March 20, 2023

Exposure to chemicals commonly found in drinking water and everyday household products may result in reduced fertility in women of as much as 40%, according to a study by Mount Sinai researchers. In a paper published in Science of the Total Environment, the team reported that higher blood concentrations of perfluoroalkyl substances, known as PFAS, were associated with a significant reduction in the likelihood of pregnancy and live birth among a reproductive-age cohort of women in Singapore who were trying to conceive.

"Our study strongly implies that women who are planning pregnancy should be aware of the harmful effects of PFAS and take precautions to avoid exposure to this class of chemicals, especially when they are trying to conceive," says lead author Nathan Cohen, Ph.D., at the Icahn School of Medicine at Mount Sinai. "Our findings are important because they add to the growing body of knowledge implicating PFAS in the development of adverse health conditions, with children being especially vulnerable."

PFAS are water- and grease-resistant chemicals found in drinking water as well as in a wide range of consumer products such as nonstick cookware, waterproof clothing, food packaging, stain-resistant coatings on carpets and upholstery, paints, and personal care products. Numerous studies have found that virtually every American has PFAS in their blood. While other studies have demonstrated that PFAS impair reproductive functioning in female mice, the Mount Sinai investigation is one of the first to show its impact in humans.

The team found 30% to 40% lower odds of attaining a clinical pregnancy within one year of follow-up and delivering a live birth when the combined effects of seven PFAS as a mixture were considered. The biggest contributor to the PFAS mixture was perfluorodecanoic acid, which was individually linked to reduced fertility. Associations with infertility outcomes were also observed for perfluorooctanesulfonic acid, perfluorooctanoic acid, and perfluoroheptanoic acid.

"PFAS can disrupt our reproductive hormones and have been linked with delayed puberty onset and increased risks for endometriosis and polycystic ovary syndromein few previous studies. What our study adds is that PFAS may also decrease fertility in women who are generally healthy and are naturally trying to conceive," notes senior author Damaskini Valvi,

"We also know that PFAS exposure begins in utero and transfers from the mother to the fetus, as many PFAS have been detected in cord blood, the placenta, and breast milk. Preventing exposure to PFAS is therefore essential to protect women's health as well as the health of their children.

Leafy greens may boost gut immunity: Study

Walter and Eliza Hall Institute, Australia, March 15, 2023

The new study finds that dietary factors, and in particular consumption of cruciferous leafy greens, control the activity of vital immune cells through the activation of a particular gene known as T-bet.

These immune cells, known as innate lymphoid cells (ILCs), play a vital role in protecting the body from infection by 'bad' pathogenic bacteria in our gut - and have also been suggested to play an important role in controlling food allergies, inflammatory diseases, obesity, and even bowel cancers, say the researchers writing Nature Immunology.

"In this study, we discovered that T-bet is the key gene that instructs precursor cells to develop into ILCs, which it does in response to signals in the food we eat and to bacteria in the gut," Dr Gabrielle Belz from the Walter and Eliza Hall Institute, Australia.  ILCs are essential for immune surveillance of the digestive system and this is the first time that we have identified a gene responsible for the production of ILCs."

Belz said that the proteins in cruciferous vegetables are known to interact with a cell surface receptor that switches on T-bet – and might therefore play a role in producing these critical immune cells.

"Proteins in these leafy greens could be part of the same signalling pathway that is used by T-bet to produce ILCs," she said.

Belz and her team noted that ILCs are essential for maintaining the delicate balance between tolerance, immunity and inflammation – by producing a hormone called interleukin-22 (IL-22), which can protect the body from invading bacteria.

"Our research shows that, without the gene T-bet, the body is more susceptible to bacterial infections that enter through the digestive system,” Belz added. “This suggests that boosting ILCs in the gut may aid in the treatment of these bacterial infections.”

Can positive thinking prolong your life? Science says yes

Studies show that staying optimistic about aging can be as beneficial to your health as exercising or eating well.

National Geographic, March 14, 2023

After my father died, my mother joined a community center with a pool and started swimming laps several times a week. Dorothy was nearly 80. She met people, learned about local programs and services for older folks, and discovered a senior center that remains her hangout 18 years later. It serves hot lunch for a dollar. A dee jay comes in and she dances. She has made friends, including a group of women who meet for lunch every Saturday in a restaurant that serves huge portions and free coffee refills. I often say, only half-jokingly, she has a better social life than I do.

Scientists have known for quite a while that people with strong ties to friends and family tend to live long. A team from Brigham Young University looked at results from 148 studies dating back to 1900 that investigated whether solid relationships are a lifesaver. All told, the studies included 308,849 participants and followed subjects for an average 7.5 years. At the end of that time, people with strong social connections were 50 percent more likely to be alive than those who were isolated and lonely.

According to the analysis, a satisfying social life was as beneficial for long-term survival as quitting smoking (something my mother did after a four-decade habit) and may be even more crucial than exercise and overcoming obesity.

Social connections may influence health through what the researchers call “stress buffering.” Support from others helps us adapt emotionally to illness, the death of a loved one, or other challenges that often pile up as we get older. Better coping, in turn, eases the flow of stress-induced hormones that weaken our immune system and increase susceptibility to deadly infections, heart disease, and stroke. Strong relationships also encourage us to take better care of ourselves, and can provide a sense of purpose—another factor associated with longer life.

In research like this, of course, it’s difficult to tease out cause and effect. Does social engagement keep older people healthy—or does robust health give them the zest and desire to spend time with friends? Either way, an editors’ note accompanying the Brigham Young analysis said doctors and other health professionals “should take social relationships as seriously as other risk factors that affect mortality.”

The power of beliefs

Becca Levy, a professor of epidemiology and psychology at Yale University, points to another influence on healthy longevity: our beliefs about aging. She has published scores of studies demonstrating that whether we think of old age as a time to enjoy or something to dread has a powerful influence on how well, or how badly, we do as we inch closer to that stage.

Levy became curious about the health effects of aging beliefs—and how cultural stereotypes and values about the elderly shape our personal attitudes—as a graduate student visiting Japan. That country has one of the world’s highest life expectancies. For a long time, scientists chalked it up to genes and diet, but Levy wondered if something less obvious was at play.

Her ideas about aging beliefs jelled when a national holiday, Keiro No Hi, which translates as Respect for the Aged Day, rolled around in September. Seniors packed parks and dined at restaurants for free. Schoolchildren delivered meals to shut-ins. In Japan, she observed, older people commanded respect, even reverence. They were not shunted aside or ridiculed as “geezers” or “over the hill.”

“What I actually noticed was how differently the culture seemed to treat the oldest members of the Japanese society, as opposed to some more of the ageism that I was used to seeing in the United States,” Levy recalls.

Levy has found that adults in their 30s and 40s who had positive notions about old age—they equated it with wisdom, for example, instead of decrepitude—were more likely to be in good health decades later. In another study, she showed that people 50 and older who had optimistic views of aging were much better able to perform everyday tasks over their next 18 years—activities like shoveling snow and walking a half-mile—than peers who regarded old age bleakly. Older people who had positive age beliefs at the start of one of Levy’s studies were also much more likely to fully regain function after a new disabling injury.

Levy’s research also suggests that rose-colored perceptions of aging offer protection against cognitive decline, even in adults who are genetically susceptible. Levy and her colleagues studied people who carried the APOE ε4 gene, which increases the risk of Alzheimer’s. At the start of the project, all her subjects were dementia-free. Those who had upbeat views of old age were 47 percent less likely to develop dementia than the APOE ε4 carriers who had grim notions of aging.

In another study, Levy found that relatively young, healthy, cognitively fit people who saw nothing promising about growing old were much more likely to eventually develop plaques and tangles in the brain, the pathological hallmarks of Alzheimer’s. And their hippocampi, the curved brain structures essential for memory, shrank three times as fast.

Perhaps most striking, Levy discovered that people with the brightest view of aging lived an average seven and a half years longer than those with the gloomiest.

Positive mindsets support bodies

How do beliefs exert such power? For one thing, Levy says, people with a positive mindset about aging tend to have better self-efficacy and self-mastery, the ability to take control of their lives and regulate their impulses. They also tend to eat well, exercise, and take prescribed medications. And they have lower levels of the hormone cortisol and other biomarkers of stress.

“What’s important about age beliefs is they’re malleable,” she says.

Writing is one way to shift how we think about aging. In a study, Levy asked groups of adults to imagine a day in the life of a hypothetical older person who is physically and mentally healthy, and briefly write about it once a week. After just four weeks, negative perceptions of aging declined significantly.

She also has had study subjects keep a journal of portrayals of elders on TV. It opened people’s eyes to the condescending and ugly stereotypes that bombard us and twist our perceptions and assumptions about aging. “The idea is to make people more aware of both their own age beliefs, and the age-belief messaging they encounter in everyday life,” Levy says.

I asked Levy if our collective view of aging has improved as the elder population has ballooned and more of us hit and surpass 65. In fact, she told me, ageist biases have gotten worse.

She and her colleagues developed a computerized linguistic program and analyzed a database of more than 400 million words from books, newspapers, magazines, and academic journals going back 200 years. The team looked at adjectives that appeared most frequently with “elderly” and similar words, and at synonyms for “old people.” The language was generally positive until the late 1800s, when life expectancy for white people in America was 41 years. (Researchers at that time did not track life expectancy for other populations.) Since then, old-age-related verbiage has steadily become meaner and more dismissive. For example, the word geezer, which first appeared in 1900, became 11 times more frequent through the twentieth century.

Old people may be the last group our society feels free to mock, Levy says. She points to news reports about cruel jokes early in the COVID pandemic, when people over age 65 were dying at exceptionally high rates and the term “boomer remover” became a widely shared meme on Twitter.

Reading research by scientists trying to unravel the mysteries of aging can make it hard to feel good about growing older. The idea of “curing” aging casts it as pathology. Published studies start, relentlessly, with bad news. “Aging is a degenerative process that leads to tissue dysfunction and death,” begins a typical paper.

“I think by labeling aging as a disease, it ignores the many strengths of aging and the many ways that there can be growth in later life,” Levy says.The future of medicine

The more I learned about the science of longevity, the more excited I felt about the prospects for discoveries that will benefit all of us as we grow older. But as I approached 68, I couldn’t shake off nagging images of the tissue dysfunction and cell death occurring inside me.

Steve Horvath, developer of epigenetic clocks to measure biological age, offered to run one on me—a test with the anxiety-producing name of GrimAge. I sent him two tiny vials of my blood. A few months later I received the results: My biological age was 3.3 years lower than my chronological age.

The report offered a cheerful “congrats” and said, “You are already beating the clock!” Still, I felt let down. I certainly wasn’t in league with some of the longevity scientists I met, like David Sinclair, who exercise religiously, fast, take supplements or off-label drugs, and seem to buck the tempest of time.

Then I thought about my mother, still enjoying life in her late 90s. Becca Levy’s research convinced me that my mom’s outlook at least partly explains her vitality. I’ve never heard her grumble about her birthday or say she can’t do something because she’s too old, a complaint I’m starting to hear from friends my age.

“No,” she says, when I point this out. “I’m not too old. I might do it slower, and I might do less of it. But I’m not too old to dance or walk or do anything I like to do.”

She pauses. “Well, I wouldn’t swim anymore.”

“Because you haven’t done it in a long time?”

“Because I don’t like the way I look in a bathing suit.

About Gary Null

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Test Bank For Porth's Pathophysiology: Concepts of Altered Health States, Ninth Edition Sheila Grossman

Unit I: Concepts of Health and Disease Chapter 01: Concepts of Health and Disease Chapter 02: Concepts of Altered Health in Children Chapter 03: Concepts of Altered Health in Older Adults Unit II: Cell Function and Growth Chapter 04: Cell and Tissue Characteristics Chapter 05: Cellular Adaptation, Injury, and Death Chapter 06: Genetic Control of Cell Function and Inheritance Chapter 07: Genetic and Congenital Disorders Chapter 08: Neoplasia Unit III: Disorders of Integrative Function Chapter 09: Stress and Adaptation Chapter 10: Alterations in Temperature Regulation Chapter 11: Activity Tolerance and Fatigue Unit IV: Infection, Inflammation, and Immunity Chapter 12: Mechanisms of Infectious Disease Chapter 13: Innate and Adaptive Immunity Chapter 14: Inflammation, Tissue Repair, and Wound Healing Chapter 15: Disorders of the Immune Response Chapter 16: Acquired Immunodeficiency Syndrome Unit V: Disorders of Neural Function Chapter 17: Organization and Control of Neural Function Chapter 18: Somatosensory Function, Pain, and Headache Chapter 19: Disorders of Motor Function Chapter 20: Disorders of Brain Function Chapter 21: Sleep and Sleep Disorders Chapter 22: Disorders of Thought, Emotion, and Memory Unit VI: Disorders of Special Sensory Function Chapter 23: Disorders of Visual Function Chapter 24: Disorders of Hearing and Vestibular Function Unit VII: Disorders of the Hematopoietic System Chapter 25: Blood Cells and the Hematopoietic System Chapter 26: Disorders of Hemostasis Chapter 27: Disorders of Red Blood Cells Chapter 28: Disorders of White Blood Cells and Lymphoid Tissues Unit VIII: Disorders of Cardiovascular Function Chapter 29: Structure and Function of the Cardiovascular System Chapter 30: Disorders of Blood Flow in the Systemic Circulation Chapter 31: Disorders of Blood Pressure Regulation Chapter 32: Disorders of Cardiac Function Chapter 33: Disorders of Cardiac Conduction and Rhythm Chapter 34: Heart Failure and Circulatory Shock Unit IX: Disorders of Respiratory Function Chapter 35: Structure and Function of the Respiratory System Chapter 36: Respiratory Tract Infections, Neoplasms, and Childhood Disorders Chapter 37: Disorders of Ventilation and Gas Exchange Unit X: Disorders of Renal Function and Fluids and Electrolytes Chapter 38: Structure and Function of the Kidney Chapter 39: Disorders of Fluid and Electrolyte Balance Chapter 40: Disorders of Acid—Base Balance Chapter 41: Disorders of Renal Function Chapter 42: Acute Renal Injury and Chronic Kidney Disease Chapter 43: Disorders of the Bladder and Lower Urinary Tract Unit XI: Disorders of Gastrointestinal Function Chapter 44: Structure and Function of the Gastrointestinal System Chapter 45: Disorders of Gastrointestinal Function Chapter 46: Disorders of Hepatobiliary and Exocrine Pancreas Function Chapter 47: Alterations in Nutritional Status Unit XII: Disorders of Endocrine Function Chapter 48: Mechanisms of Endocrine Control Chapter 49: Disorders of Endocrine Control of Growth and Metabolism Chapter 50: Diabetes Mellitus and the Metabolic Syndrome Unit XIII: Disorders of Genitourinary and Reproductive Function Chapter 51: Structure and Function of the Male Genitourinary System Chapter 52: Disorders of the Male Genitourinary System Chapter 53: Structure and Function of the Female Reproductive System Chapter 54: Disorders of the Female Reproductive System Chapter 55: Sexually Transmitted Infections Unit XIV: Disorders of Musculoskeletal Function Chapter 56: Structure and Function of the Musculoskeletal System Chapter 57: Disorders of Musculoskeletal Function: Trauma, Infection, Neoplasms Chapter 58: Disorders of Musculoskeletal Function: Developmental and Metabolic Disorders Chapter 59: Disorders of Musculoskeletal Function: Rheumatic Disorders Unit XV: Disorders of Integumentary Function Chapter 60: Structure and Function of the Skin Chapter 61: Disorders of Skin Integrity and Function Read the full article