Podcasts about g igg

Dr. Azra Frkatović-Hodžić from Genos Glycoscience Research Laboratory in Zagreb, Croatia, discusses a #research paper she co-authored that was #published by Aging (Aging-US) in Volume 15, Issue 24, entitled, “Mapping of the gene network that regulates glycan clock of ageing.” DOI - https://doi.org/10.18632/aging.205106 Corresponding authors - Azra Frkatović-Hodžić - afrkatovic@genos.hr, and Gordan Lauc - glauc@genos.hr Video - https://www.youtube.com/watch?v=5ExLCMDhpdE Video transcription - https://aging-us.net/2024/03/13/behind-the-study-mapping-of-gene-network-that-regulates-glycan-clock-of-aging/ Abstract Glycans are an essential structural component of immunoglobulin G (IgG) that modulate its structure and function. However, regulatory mechanisms behind this complex posttranslational modification are not well known. Previous genome-wide association studies (GWAS) identified 29 genomic regions involved in regulation of IgG glycosylation, but only a few were functionally validated. One of the key functional features of IgG glycosylation is the addition of galactose (galactosylation), a trait which was shown to be associated with ageing. We performed GWAS of IgG galactosylation (N=13,705) and identified 16 significantly associated loci, indicating that IgG galactosylation is regulated by a complex network of genes that extends beyond the galactosyltransferase enzyme that adds galactose to IgG glycans. Gene prioritization identified 37 candidate genes. Using a recently developed CRISPR/dCas9 system we manipulated gene expression of candidate genes in the in vitro IgG expression system. Upregulation of three genes, EEF1A1, MANBA and TNFRSF13B, changed the IgG glycome composition, which confirmed that these three genes are involved in IgG galactosylation in this in vitro expression system. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205106 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, genome-wide association study, glycosylation, glycan clock, immunoglobulin G, CRISPR/dCas9 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- January 3, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 24, entitled, “Mapping of the gene network that regulates glycan clock of ageing.” Glycans are an essential structural component of immunoglobulin G (IgG) that modulate its structure and function. However, regulatory mechanisms behind this complex posttranslational modification are not well known. Previous genome-wide association studies (GWAS) identified 29 genomic regions involved in regulation of IgG glycosylation, but only a few were functionally validated. One of the key functional features of IgG glycosylation is the addition of galactose (galactosylation), a trait which was shown to be associated with ageing. In this new study, researchers Azra Frkatović-Hodžić, Anika Mijakovac, Karlo Miškec, Arina Nostaeva, Sodbo Z. Sharapov, Arianna Landini, Toomas Haller, Erik van den Akker, Sapna Sharma, Rafael R. C. Cuadrat, Massimo Mangino, Yong Li, Toma Keser, Najda Rudman, Tamara Štambuk, Maja Pučić-Baković, Irena Trbojević-Akmačić, Ivan Gudelj, Jerko Štambuk, Tea Pribić, Barbara Radovani, Petra Tominac, Krista Fischer, Marian Beekman, Manfred Wuhrer, Christian Gieger, Matthias B. Schulze, Clemens Wittenbecher, Ozren Polasek, Caroline Hayward, James F. Wilson, Tim D. Spector, Anna Köttgen, Frano Vučković, Yurii S. Aulchenko, Aleksandar Vojta, Jasminka Krištić, Lucija Klarić, Vlatka Zoldoš, and Gordan Lauc from Genos Glycoscience Research Laboratory, University of Zagreb, Novosibirsk State University, Lomonosov Moscow State University, University of Edinburgh, University of Tartu, Leiden University Medical Center, Delft University of Technology, Helmholtz Zentrum Muenchen, German Center for Diabetes Research (DZD), King's College London, Guy's and St Thomas' Foundation Trust, University of Freiburg, University of Rijeka, German Institute of Human Nutrition Potsdam-Rehbruecke, University of Potsdam, Harvard T.H. Chan School of Public Health, Chalmers University of Technology, University of Split School of Medicine, Algebra University College, Johns Hopkins Bloomberg School of Public Health, and Institute of Cytology and Genetics SB RAS performed GWAS of IgG galactosylation (N=13,705) and identified 16 significantly associated loci, indicating that IgG galactosylation is regulated by a complex network of genes that extends beyond the galactosyltransferase enzyme that adds galactose to IgG glycans. “Here, we conducted a GWAS of IgG galactosylation phenotypes in a study that almost doubles the sample size (N=13,705) compared to previous GWAS of IgG N-glycome [33] and focused on the genes with in silico evidence for involvement in the IgG galactosylation process.” Gene prioritization identified 37 candidate genes. Using a recently developed CRISPR/dCas9 system, the researchers manipulated gene expression of candidate genes in the in vitro IgG expression system. Upregulation of three genes, EEF1A1, MANBA and TNFRSF13B, changed the IgG glycome composition, which confirmed that these three genes are involved in IgG galactosylation in this in vitro expression system. “Further research is needed to fully elucidate [the] functional mechanism behind their role in ageing and to reveal the complete network of gene interactions regulating the complex process of IgG glycosylation.” DOI - https://doi.org/10.18632/aging.205106 Corresponding authors - Azra Frkatović-Hodžić - afrkatovic@genos.hr, and Gordan Lauc - glauc@genos.hr Visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ MEDIA@IMPACTJOURNALS.COM

Warm autoimmune hemolytic anemia (wAIHA) is the most common type (60-70%) of autoimmune hemolytic anemia (AIHA). In most cases, wAIHA is due an immunoglobulin G (IgG) autoantibody that binds to red blood cells (RBC), leading to hemolysis. Current recommendations for managing people with wAIHA are largely based on case series and retrospective studies involving off-label medications. Also, while there are currently no medications specifically approved to treat wAIHA, data are emerging on new therapies under investigation which may impact treatment in the future. This 60-minute CME program, hosted by Irina Murakhovskaya, MD, of the Montefiore Medical Center, Albert Einstein College of Medicine, in New York, NY and Bruno Fattizzo, MD, of the University of Milan and Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, in Milan, Italy, describes current best practices to manage patients with wAIHA.Supported by an educational grant from Janssen Biotech. For complete activity information and to obtain CME credit, please, go to www.checkrare.com

Warm autoimmune hemolytic anemia (wAIHA) is the most common type (60-70%) of autoimmune hemolytic anemia (AIHA). In most cases, wAIHA is due an immunoglobulin G (IgG) autoantibody that binds to red blood cells (RBC), leading to hemolysis. Current recommendations for managing people with wAIHA are largely based on case series and retrospective studies involving off-label medications. Also, while there are currently no medications specifically approved to treat wAIHA, data are emerging on new therapies under investigation which may impact treatment in the future. This 60-minute CME program, hosted by Irina Murakhovskaya, MD, of the Montefiore Medical Center, Albert Einstein College of Medicine, in New York, NY and Bruno Fattizzo, MD, of the University of Milan and Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, in Milan, Italy, describes best practices to diagnose patients with wAIHA.Supported by an educational grant from Janssen Biotech. For complete activity information and to obtain CME credit, please, go to www.checkrare.com

Warm autoimmune hemolytic anemia (wAIHA) is the most common type (60-70%) of autoimmune hemolytic anemia (AIHA). In most cases, wAIHA is due an immunoglobulin G (IgG) autoantibody that binds to red blood cells (RBC), leading to hemolysis. Current recommendations for managing people with wAIHA are largely based on case series and retrospective studies involving off-label medications. Also, while there are currently no medications specifically approved to treat wAIHA, data are emerging on new therapies under investigation which may impact treatment in the future. This 60-minute CME program, hosted by Irina Murakhovskaya, MD, of the Montefiore Medical Center, Albert Einstein College of Medicine, in New York, NY and Bruno Fattizzo, MD, of the University of Milan and Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, in Milan, Italy, describes common complications that can impact the management of patients with wAIHA.Supported by an educational grant from Janssen Biotech. For complete activity information and to obtain CME credit, please, go to www.checkrare.com

Warm autoimmune hemolytic anemia (wAIHA) is the most common type (60-70%) of autoimmune hemolytic anemia (AIHA). In most cases, wAIHA is due an immunoglobulin G (IgG) autoantibody that binds to red blood cells (RBC), leading to hemolysis. Current recommendations for managing people with wAIHA are largely based on case series and retrospective studies involving off-label medications. Also, while there are currently no medications specifically approved to treat wAIHA, data are emerging on new therapies under investigation which may impact treatment in the future. This 60-minute CME program, hosted by Irina Murakhovskaya, MD, of the Montefiore Medical Center, Albert Einstein College of Medicine, in New York, NY and Bruno Fattizzo, MD, of the University of Milan and Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, in Milan, Italy, describes current treatment options, and treatments in development, for patients with wAIHA.Supported by an educational grant from Janssen Biotech. For complete activity information and to obtain CME credit, please, go to

Go online to PeerView.com/VZG860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Generalized myasthenia gravis (gMG) is a rare, chronic autoimmune disorder that is highly variable in clinical presentation and treatment response. Traditionally used treatments for gMG are broadly immunosuppressive, do not target pathogenic immunoglobulin G (IgG) autoantibodies, and provide insufficient symptom relief with significant side effects. Fortunately, advances in the understanding of gMG pathogenesis are leading to the development of new treatment options, including neonatal Fc receptor (FcRn) modulators such as the recently approved efgartigimod, and rozanolixizumab, which recently completed phase 3 trials. As with all new and emerging therapeutics, it is important for clinicians to remain abreast of the latest data. At a recent live event, a multidisciplinary panel of experts compared the safety, efficacy, and tolerability of new treatment options with traditional therapies for gMG. Audience members received expert advice from the perspective of a neurologist, pharmacist, and infusion nurse, with the goal of providing their patients with individualized care through FcRn modulation therapy. Upon completion of this activity, participants should be better able to: Compare safety, efficacy, and tolerability of new treatment options with traditional therapies for generalized myasthenia gravis (gMG); Apply an understanding of the rationale and mechanisms for reducing levels of autoreactive IgG antibodies using FcRn-modulating therapies when making gMG treatment decisions; and Implement a safe administration protocol for the use of FcRn-modulating therapy that includes infusion procedures, premedications, vaccinations, and treatment cycle timing.

Go online to PeerView.com/VZG860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Generalized myasthenia gravis (gMG) is a rare, chronic autoimmune disorder that is highly variable in clinical presentation and treatment response. Traditionally used treatments for gMG are broadly immunosuppressive, do not target pathogenic immunoglobulin G (IgG) autoantibodies, and provide insufficient symptom relief with significant side effects. Fortunately, advances in the understanding of gMG pathogenesis are leading to the development of new treatment options, including neonatal Fc receptor (FcRn) modulators such as the recently approved efgartigimod, and rozanolixizumab, which recently completed phase 3 trials. As with all new and emerging therapeutics, it is important for clinicians to remain abreast of the latest data. At a recent live event, a multidisciplinary panel of experts compared the safety, efficacy, and tolerability of new treatment options with traditional therapies for gMG. Audience members received expert advice from the perspective of a neurologist, pharmacist, and infusion nurse, with the goal of providing their patients with individualized care through FcRn modulation therapy. Upon completion of this activity, participants should be better able to: Compare safety, efficacy, and tolerability of new treatment options with traditional therapies for generalized myasthenia gravis (gMG); Apply an understanding of the rationale and mechanisms for reducing levels of autoreactive IgG antibodies using FcRn-modulating therapies when making gMG treatment decisions; and Implement a safe administration protocol for the use of FcRn-modulating therapy that includes infusion procedures, premedications, vaccinations, and treatment cycle timing.

Go online to PeerView.com/VZG860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Generalized myasthenia gravis (gMG) is a rare, chronic autoimmune disorder that is highly variable in clinical presentation and treatment response. Traditionally used treatments for gMG are broadly immunosuppressive, do not target pathogenic immunoglobulin G (IgG) autoantibodies, and provide insufficient symptom relief with significant side effects. Fortunately, advances in the understanding of gMG pathogenesis are leading to the development of new treatment options, including neonatal Fc receptor (FcRn) modulators such as the recently approved efgartigimod, and rozanolixizumab, which recently completed phase 3 trials. As with all new and emerging therapeutics, it is important for clinicians to remain abreast of the latest data. At a recent live event, a multidisciplinary panel of experts compared the safety, efficacy, and tolerability of new treatment options with traditional therapies for gMG. Audience members received expert advice from the perspective of a neurologist, pharmacist, and infusion nurse, with the goal of providing their patients with individualized care through FcRn modulation therapy. Upon completion of this activity, participants should be better able to: Compare safety, efficacy, and tolerability of new treatment options with traditional therapies for generalized myasthenia gravis (gMG); Apply an understanding of the rationale and mechanisms for reducing levels of autoreactive IgG antibodies using FcRn-modulating therapies when making gMG treatment decisions; and Implement a safe administration protocol for the use of FcRn-modulating therapy that includes infusion procedures, premedications, vaccinations, and treatment cycle timing.

Go online to PeerView.com/VZG860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Generalized myasthenia gravis (gMG) is a rare, chronic autoimmune disorder that is highly variable in clinical presentation and treatment response. Traditionally used treatments for gMG are broadly immunosuppressive, do not target pathogenic immunoglobulin G (IgG) autoantibodies, and provide insufficient symptom relief with significant side effects. Fortunately, advances in the understanding of gMG pathogenesis are leading to the development of new treatment options, including neonatal Fc receptor (FcRn) modulators such as the recently approved efgartigimod, and rozanolixizumab, which recently completed phase 3 trials. As with all new and emerging therapeutics, it is important for clinicians to remain abreast of the latest data. At a recent live event, a multidisciplinary panel of experts compared the safety, efficacy, and tolerability of new treatment options with traditional therapies for gMG. Audience members received expert advice from the perspective of a neurologist, pharmacist, and infusion nurse, with the goal of providing their patients with individualized care through FcRn modulation therapy. Upon completion of this activity, participants should be better able to: Compare safety, efficacy, and tolerability of new treatment options with traditional therapies for generalized myasthenia gravis (gMG); Apply an understanding of the rationale and mechanisms for reducing levels of autoreactive IgG antibodies using FcRn-modulating therapies when making gMG treatment decisions; and Implement a safe administration protocol for the use of FcRn-modulating therapy that includes infusion procedures, premedications, vaccinations, and treatment cycle timing.

Men and women universally experience a decrease in sex hormones with age. Given this knowledge, researchers previously conducted a study to assess the correlation between aging, estrogen levels and the release of glycans (carbohydrate-based polymers) among all proteins in the body. Glycans are also important components of immunoglobulin G (IgG). IgGs are serum antibodies which provide immune protection against bodily infections and mediate systemic inflammation. Each IgG molecule usually includes about 3% glycans. However, changes in the composition of glycans attached to IgGs can significantly influence antibody activity. A decrease in galactosylation has been correlated with the onset of disease and aging. “The decrease in IgG galactosylation was first reported over 35 years ago in patients with rheumatoid arthritis and osteoarthritis [4].” The researchers found that estrogen regulates glycosylation. However, the data they analyzed did not differentiate IgG glycosylation from the other proteins. The Glycan Age Index (a combination of three IgG glycans that appear to be both biomarkers and effectors of aging) can be used to calculate glycan age. Glycan age is associated with lifestyle and disease-risk biomarkers, and could potentially be used to monitor healthy or unhealthy aging. “Here arises probably the most exciting aspect of the relationship between aging and IgG glycosylation: the potential of IgG glycans to distinguish between healthy and unhealthy aging, and to monitor the effect of introduced life-style changes on biological age.” To identify changes in IgG glycans, researchers—from Genos Glycoscience Research Laboratory, University of Colorado Anschutz Medical Campus, Eastern Colorado VA Geriatric Research, University of Zagreb, Brigham and Women's Hospital, and Boston Children's Hospital—reanalyzed samples from the previous intervention study using state-of-the-art glycoprofiling technology. The focus of this study was to evaluate the effects of estrogen suppression, followed by estradiol supplementation, on biological age measured by the glycan age. Their paper was published in Aging (Aging-US) Volume 12, Issue 19, in 2020, and entitled, “Effects of estradiol on biological age measured using the glycan age index”. Full blog - https://www.impactjournals.com/journals/blog/aging/can-hormone-therapy-improve-aging/ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.104060 DOI - https://doi.org/10.18632/aging.104060 Full text - https://www.aging-us.com/article/104060/text Correspondence to: Gordan Lauc email: glauc@pharma.hr Keywords: biological age, glycan age, estrogen, aging biomarkers, glycosylation About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at http://www.Aging-US.com​​ or connect with us on: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Spore-based probiotics are becoming more popular, and for good reason. Research has shown promising results using spore-based probiotics to help promote a healthy gut, especially in conditions like SIBO and leaky gut syndrome. Although they are becoming more popular, many people don't know what the difference is between spore-based probiotics, regular probiotics, and probiotic yeasts. For this week's episode, "Bloating, Belching, Gassy...the Fix", we have a special guest that will explain to us the differences between different types of probiotics, and how they may be beneficial in the management of different health conditions. Products Mentioned in Today's Show SBI Spore - Probiotics have been extensively studied and are characterized as having broad GI and immune benefits. Bacillus spores remain dormant in harsh environments until they reach more favorable environments like the human gastrointestinal tract. The combination of specific strains, particularly Bacillus coagulans, Bacillus clausii, and Bacillus subtilis, may help relieve symptoms for common GI complaints and reinforce healthy gut function. Saccharomyces Boulardii - Saccharomyces boulardii is a nonpathogenic, transient yeast long used to support normal bowel transit time.† It is a hardy, acid-resistant, temperature tolerant microorganism that is not affected by antibacterial agents. S. boulardii is genetically and functionally distinct from brewer’s yeast (S. cerevisiae) and different from pathogenic Candida species. SBI Support - SBI Support is a purified, dairy-free source of immunoglobulin G (IgG). Pure IgG helps to maintain a healthy intestinal immune system by binding a broad range of microbes and toxins within the gut lumen. You can also listen to Bloating, Belching, Gassy...the Fix on our YouTube channel here.

In today's episode we discuss: —Understanding the Pathology: Physicians from Pisa University Hospital (Italy) remark on Zhao et al's (2020) findings on ABO Blood Group Correlations With COVID-19, stating that their observed association between blood group A and increased risk of COVID-19 may be due to their choice in cohort. In the authors' own study of a group of 7,713 healthy blood donors, there was no significant difference in rate of anti-SARS-CoV-2 nucleocapsid IgG based on blood type and there are other studies with similar findings. While this study does not eliminate the need to examine differential rates of infection and outcomes for COVID-19 patients based on blood type, it does indicate that previous study results may be biased by group selection. —Transmission & Prevention: Vaccines that present the α-gal epitope produced by glycoengineered bacteria or yeast had increased uptake by antigen presenting cells (APCs) by 10 to 200 fold when given to mice. Since anti-Gal is a natural immunoglobulin G (IgG) in the human serum, authors state that vaccines with the α-gal epitope may increase anti-viral immune response of T cells against the SARS-CoV-2 virus. Authors suggest the development of vaccines with α-gal epitopes have been shown to be safe for use in humans through clinical trials and could offer improved efficacy via maximized immune response to SARS-CoV-2. —Resources: A data-driven, ontology-based, and natural language processing approach for analyzing COVID-19 clinical trials was developed by a high school student from The Harker School in San Jose, California who data mined ClinicalTrials.gov using Application Programming Interfaces (APIs) to compile relevant data from COVID-19 clinical trials including drug treatments and interventions, outcomes, Medical Subject Heading (MeSH), and Human Phenotype Ontologies (HPO). The results (available at http://covidresearchtrials.com) provide a public compilation of unique reports in each category analyzed, which could offer guidance to the global research community to support the development of future clinical trials, treatments and interventions, and meta-analyses, as well as general insight into the response to COVID-19. --- Support this podcast: https://anchor.fm/covid19lst/support

In this episode I have guest appearance Deanna McAllister MSN, RN with me to discuss COVID. In this episode we discuss what the virus does to the body. Presenting symptoms and manifestations. We get into detail about supplements to boost your immune system, these include oral, IV and IM nutraceuticals. In Functional Medicine we focus on a "systems" approach, and guess what all the systems are related. The root of these start in the gut! ⠀⠀ ◾GUT HEALTH: (if you have IBS, constipation, diarrhea, GERD, leaky gut, or Auto-Immunity) you should be taking these ▫️PROBIOTICS- helps maintain gut microbiome balance ▫️L-GLUTAMINE-keeps unwanted toxins out of the body ▫️COLOSTRUM-contains immunoglobulins G (IgG), A (IgA), E (IgE), D (IgD), and M (IgM). Each has a specific role in immune health. Yes this is what is found in breast milk! ⠀⠀ ◾Imu-max (this is great for kids and adults) contains: echinacea, and propolis which support immunity and reduce inflammation. ▫️Offers microbial balance in the respiratory tract and help maintain normal inflammatory balance. ⠀⠀ ◾Vitamin D- supports health immune function Shot $25, Liquid $28, capsule $18 ◾Glutatione- protects from free radical damage and powerful anti-oxidant Price: IV $115, Capsule $42 ◾Vitamin C ◾Zinc ◾Selenium (Thyrotain *excellent choice) ◾Berberine: berberine positively influences immune biomarkers related Th1 ◾Curcumin (Trameric *product choice) We close with how we as small business owners keep our clients and patients safe. For questions: Email: Yoodirecthealth@gmail.com Call (317) 523-9160 www.Yoodirecthealth.com Deanna Mcallister MSN, RN (812) 320-2284 https://vanishedaesthetics.com/contact

牛初乳是母牛生下小牛后分泌的最初一批牛奶，量很少，所以卖得比普通牛奶要贵得多。它的成分跟普通牛奶有所不同，含有比较多的免疫球蛋白、生长因子等活性物质，对小牛的生长甚至生存至关重要。例如，小牛刚生下来，免疫系统还不健全，遇到病原体没法产生抗体抵抗，就会死亡。怎么办呢？就要由母牛提供它制造好的抗体，就是通过牛初乳来提供的。抗体属于免疫球蛋白G，简称IgG。牛初乳里含量最多的蛋白质就是IgG。有人想，牛初乳对小牛的健康这么重要，那么人吃了牛初乳也会起到提高免疫力的作用。所以牛初乳就被当成了保健品卖高价。还有的人干脆卖起了免疫球蛋白，认为吃了它就能起到提高免疫力的作用。但是对小牛有好处的东西，未必对人就能够起到同样的好处。人类的母亲也会分泌初乳，但是人初乳和牛初乳的成分存在很大的差别，例如人初乳里头IgG的量很少。是人类初生儿不需要母亲给他预备好抗体吗？不是的，同样需要。但是人和牛不同，在婴儿出生前，母亲的抗体已经通过胎盘把抗体传给他了，所以出生后他就不需要通过母乳来吸收抗体，即使母乳里含有抗体，他也吸收不了，这是因为初生儿一出生消化道的屏障就很完善了，没法直接吸收蛋白质，而抗体是一种蛋白质。牛和人不同，小牛在刚出生的几个小时内，它的消化道还可以把蛋白质吸收进血液中，所以牛初乳中的抗体能够被小牛吸收、利用。但是牛初乳里中的抗体是没法被人吸收、利用的。如果人能够吸收牛初乳里的抗体，反而麻烦了，因为牛的IgG和人的IgG是不同的，它们不是人体产生的蛋白质，而是外源蛋白质，如果进入了血液里，会导致过敏反应。所以幸好牛初乳里的抗体没法被人体吸收。它们经过消化道的时候，会和其他蛋白质一样被消化成氨基酸，再被人体吸收。有人做过实验，健康人在吃了牛初乳后，排出的粪便里几乎找不到IgG了，都被消化掉了。用IgG做实验，结果也是一样。所以吃抗体的结果和吃其他蛋白质没有什么不同，都被消化成了氨基酸，起不到特别的作用。吃牛初乳，不过是在昂贵地补充蛋白质。人类的初生儿消化功能还不健全，蛋白质比较不容易被消化，可能有些抗体没被消化掉，那么它们在经过消化道的时候，能不能起到消灭消化道里的病菌、病毒的作用呢？这也是值得怀疑的，这是因为抗体具有特异性，一种抗体只能针对一种抗原起作用。母牛要在牛初乳里产生针对某种病原体的抗体，它首先要接触到这种病原体。母牛和小牛的生长环境相同，接触的病原体相似，所以母牛产生的抗体也能对小牛起保护作用，但对初生儿就没有用了。如果是对母牛进行免疫，专门用某种人的病原体来刺激母牛产生针对它的抗体，那么才有可能对人有用。这种经过专门免疫接种、针对特定病原体的牛初乳叫超免疫牛初乳，有些试验表明吃超免疫牛初乳可能能起到抵抗相应的消化道传染病的作用。但这种作用也不明显。例如，用人轮状病毒接种母牛，产生了特殊的牛初乳。孟加拉在1995年有一项研究称，让得了轮状病毒腹泻的婴儿吃这种牛初乳，连续吃三天，能把病程从平均72小时缩短为56小时，如此而已。除了抗体，牛初乳里头还含有生长因子等活性物质。有人认为它们也能对人有保健作用。但是生长因子也是蛋白质或多肽，同样没法被人体直接吸收，而是会像其他蛋白质一样被消化掉。然而，因为牛初乳市场不小，涉及到很大的利益，还是不断地有人做实验想要证明它有种种保健作用。例如，国外的运动员流行吃牛初乳，认为它里面的胰岛素样生长因子能增强肌肉、提高体育成绩。所以就有人做试验想要证明这一点。但这些试验都很初步，试验对象人数少，试验设计不合理，结果也不一致，有的发现没有效果，有的发现有效果，但是即使有效果的，也不明显。2002年澳大利亚研究人员做过一个试验，找了26人分成两组，一组每天吃60克牛初乳，一组吃乳清蛋白作为对照，持续8周，然后对比他们体内生长因子的量和跑步的成绩，发现两组并没有区别，也就是说吃牛初乳并不能增加体内生长因子含量，也不能提高体育成绩。但是休息20分钟后再测，发现吃牛初乳的一组成绩要好一些，于是他们认为这可能是因为牛初乳能帮助体力的恢复。其实所谓成绩好一些，不过是跑步高峰速度提高了5%，没有什么意义。总之，吃牛初乳和喝牛奶的结果基本上是一样的，所谓的特殊保健作用并没有得到证实，即使特殊制造的超免疫牛初乳对某些人有些好处的话，作用也是很有限的，不值。至于由牛初乳衍生出来的免疫球蛋白保健品，则连有限的作用也没有，完全是骗人的。

Introduction: The chemokine CXCL10 is produced during infection and inflammation to activate the chemokine receptor CXCR3, an important regulator of lymphocyte trafficking and activation. The goal of this study was to assess the contributions of CXCL10 to the pathogenesis of experimental septic shock in mice. Methods: Septic shock was induced by cecal ligation and puncture (CLP) in mice resuscitated with lactated Ringer's solution and, in some cases, the broad spectrum antibiotic Primaxin. Studies were performed in CXCL10 knockout mice and mice treated with anti-CXCL10 immunoglobulin G (IgG). Endpoints included leukocyte trafficking and activation, core body temperature, plasma cytokine concentrations, bacterial clearance and survival. Results: CXCL10 was present at high concentrations in plasma and peritoneal cavity during CLP-induced septic shock. Survival was significantly improved in CXCL10 knockout (CXCL10KO) mice and mice treated with anti-CXCL10 IgG compared to controls. CXCL10KO mice and mice treated with anti-CXCL10 IgG showed attenuated hypothermia, lower concentrations of interleukin-6 (IL-6) and macrophage inhibitory protein-2 (MIP-2) in plasma and lessened natural killer (NK) cell activation compared to control mice. Compared to control mice, bacterial burden in blood and lungs was lower in CXCL10-deficient mice but not in mice treated with anti-CXCL10 IgG. Treatment of mice with anti-CXCL10 IgG plus fluids and Primaxin at 2 or 6 hours after CLP significantly improved survival compared to mice treated with non-specific IgG under the same conditions. Conclusions: CXCL10 plays a role in the pathogenesis of CLP-induced septic shock and could serve as a therapeutic target during the acute phase of septic shock.

Background: The relevance of Trichosporon species for cystic fibrosis (CF) patients has not yet been extensively investigated. Methods: The clinical course of CF patients with Trichosporon spp. in their respiratory secretions was analysed between 2003 and 2010 in the Munich CF center. All respiratory samples of 360 CF patients (0 - 52.4 years; mean FEV1 2010 81.4% pred) were investigated. Results: In 8 patients (2.2%, 3 male, mean age 21.8 years) Trichosporon was detected at least once. One patient carried T. asahii. One patient carried T. mycotoxinivorans and one patient T. inkin as determined by DNA sequencing. As potential risk factors for Trichosporon colonization steroid treatment, allergic bronchopulmonary aspergillosis (ABPA) and CF associated diabetes were identified in 6, 5, and 2 patients respectively. For one patient, the observation period was not long enough to determine the clinical course. One patient had only a single positive specimen and exhibited a stable clinical course determined by change in forced expiratory volume in one second (FEV1), body-mass-index (BMI), C-reactive protein (CRP) and immunoglobulin G (IgG). Of 6 patients with repeatedly positive specimen (mean detection period 4.5 years), 4 patients had a greater decline in FEV1 than expected, 2 of these a decline in BMI and 1 an increase in IgG above the reference range. 2 patients received antimycotic treatment: one patient with a tormenting dry cough subjectively improved under Amphotericin B inhalation; one patient with a severe exacerbation due to T. inkin was treated with i.v. Amphotericin B, oral Voriconazole and Posaconazole which stabilized the clinical condition. Conclusions: This study demonstrates the potential association of Trichosporon spp. with severe exacerbations in CF patients.

The electrical activity of the brain is the result of a complex interaction between excitation and inhibition mediated by several types of neurotransmitters. As the majority of neurons in the brain utilize either the inhibitory neurotransmitter γ-aminobutyric acid (GABA) or the excitatory neurotransmitter glutamate, the interplay of these two neurotransmitters principally controls brain excitability and, hence, imbalance between these two neurotransmitters may cause severe pathological conditions. Inhibition of glutamic acid decarboxylase (GAD), the rate-limiting enzyme of GABA synthesis, is believed to change neuronal network activity caused by impaired GABAergic inhibition. Recordings of intrinsic optical signals (IOSs) and whole-cell patch-clamp measurements of GABAA receptor-mediated miniature postsynaptic currents (GABAA Minis) and spontaneous excitatory postsynaptic currents (sEPSCs) were performed in the motor cortex in acute brain slices to unveil the effects of GAD inhibitors at the network level. The first project of this PhD thesis was to prove the IOS technique for its capability of monitoring neuronal network activity over several hours. Concurrently, new software for the analysis of IOS data was developed, which facilitates and significantly accelerates data analysis. Afterwards, changes in neuronal network activity after impairing GAD activity with the well-known GAD inhibitor semicarbazide (SMC) were observed with the IOS technique. If compared to the values of sham-drug application, a stable and reversible increase in both signal intensity and signal area was observed after 2 h of 2 mM SMC application. Consistent with these findings of IOS recordings, patch-clamp measurements of GABAA Minis revealed an SMC-induced reduction in the strength of GABAergic inhibition. The results are in line with the assumption that SMC impairs GABA synthesis by blocking GAD activity. SMC application, however, did not alter spontaneous excitatory neuronal network activity. The final aim of this study was to investigate potential effects of Anti-GAD autoantibodies-containing immunoglobulin G (IgG) derived from patients with stiff-person syndrome (SPS-IgG) on motor cortical neuronal network activity. IOS recordings do not reveal differences in neuronal network activity during SPS-IgG application and control IgG application. However, run-down of IOSs was significantly decelerated during IgG application, which possibly indicates a diminished neuronal cell death caused by an unspecific IgG effect. Compared to brain slices preincubated with IgG-free artificial cerebrospinal fluid, control IgG did not affect GABAA Mini amplitude and frequency as well as sEPSC amplitude. The sEPSC frequency, however, was significantly reduced under these conditions. This decreased excitatory transmitter release might explain the beneficial effect of immunoglobulin treatment in some forms of epilepsy. Similar to SMC, patch-clamp measurements of GABAA Minis revealed a reduction in the strength of GABAergic inhibition after preincubation with SPS-IgG. Consistent with this finding, application of SPS-IgG enhanced sEPSC frequency. This shows that IgG of SPS patients is indeed capable of altering GABAergic synaptic transmission, thus further supporting the hypothesis of an autoimmune origin of the stiff-person syndrome.

Investigation of anti-coronavirus-antibodies in the cerebrospinal fluid for the diagnosis of CNS manifestation of feline infectious peritonitis The purpose of the present study was to evaluate the occurence of anti-coronavirus antibodies in the cerebrospinal fluid (CSF) of cats and to assess their diagnostic utility concerning the central nervous system (CNS) manifestation of feline infectious peritonitis (FIP). Anti-coronavirus immunoglobulin G (IgG) was measured in CSF and serum of 67 cats by indirect immunofluorescence assay. Additionally, cell counts, Pandy’s test and total protein were performed in the CSF. Diagnosis of all cats was confirmed by gross and histological examination including the brain. Four different groups were examined: FIP with CNS manifestation (n = 10), FIP without CNS manifestation (n = 13), other CNS disorders than FIP (n = 29) and diseases not associated with FIP and not involving the CNS (n = 15). Anti-coronavirus IgG was detected in the CSF of 18% of all cats (12/67): 6 cats with FIP involving the CNS, 4 cats with FIP not involving the CNS and 2 cats with brain tumours. CSF antibodies were only found in seropositive cats. In addition, only cats with serum titers equal or higher than 1:4096 showed CSF titers. The correlation between serum antibodies and CSF antibodies was statistically highly significant (r=0,652; p=0,000). No statistically significant correlation was found between the erythrocyte count and CSF titers. However, a certain tendency for high CSF titers with increasing numbers of erythrocytes was observed. For all cats of the study (n = 67), testing for anti-coronavirus IgG in the CSF showed a sensitivity of 60% and a specificity of 90%. CSF antibodies had a positive predictive value of 50% for the CNS manifestation of FIP. The negative predictive value was 93%. Calculating only the values of cats with CNS alterations (n = 39), testing for anti-coronavirus IgG in the CSF had a sensitivity of 60% and a specificity of 93%. The positive and negative predictive value was 75% and 87%, respectively. The present study revealed that the determination of anti-coronavirus-titers in the CSF alone does not confirm CNS manifestation of FIP. The statistically highly significant correlation between CSF and serum antibodies indicates a disrupted blood brain barrier or blood contamination. Future studies on CSF anti-coronavirus-antibodies should address the evaluation of the status of the blood brain barrier and the measurement of the intrathecally produced antibody portion.

Several herpesviruses, including cytomegalovirus, induce receptors for the Fc domain of murine immunoglobulin G (IgG) molecules. Viral genes coding for these receptors have been characterized only for alphaherpesviruses. In this report, we describe a new approach that led to the identification of an Fc receptor (FcR) of murine cytomegalovirus (MCMV). The Fc fragment of IgG precipitated glycoproteins (gp) of 86 to 88 and 105 kDa from MCMV-infected cells. Deglycosylation by endoglycosidase F resulted in a protein with a molecular mass of 64 kDa. Injection of complete MCMV DNA or of DNA fragments, and the subsequent testing of cytoplasmic binding of IgG by immunofluorescence microscopy, was used to search for the coding region in the MCMV genome. The gene was located in the HindIII J fragment, map units 0.838 to 0.846, where an open reading frame of 1,707 nucleotides predicts a gp of 569 amino acids with a calculated molecular mass of 65 kDa. The sequence of this gp is related to those of the gE proteins of herpes simplex virus type 1 and varicella-zoster virus. The defined length of the mRNA, 1,838 nucleotides, was in agreement with that of a 1.9-kb RNA expressed throughout the replication cycle, starting at the early stages of infection. Expression of the gene fcr1 by recombinant vaccinia virus resulted in the synthesis of gp86/88 and gp105, each with FcR properties, and the correct identification of the gene encoding the FcR was confirmed by the DNA injection method.