The Effect of Laughter on Stress and Natural Killer Cell Activity
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Classification of Cell Death
Cell Death and Differentiation (2005) 12, 1463–1467 & 2005 Nature Publishing Group All rights reserved 1350-9047/05 $30.00 www.nature.com/cdd News and Commentary Classification of cell death: recommendations of the Nomenclature Committee on Cell Death G Kroemer*,1, WS El-Deiry2, P Golstein3, ME Peter4, D Vaux5, with or without, caspase activation and that ‘autophagic cell P Vandenabeele6, B Zhivotovsky7, MV Blagosklonny8, death’ represents a type of cell death with (but not necessarily W Malorni9, RA Knight10, M Piacentini11, S Nagata12 and through) autophagic vacuolization. This article details the G Melino10,13 2005 recommendations of NCCD. Over time, molecular definitions are expected to emerge for those forms of cell 1 CNRS-UMR8125, Institut Gustave Roussy, 39 rue Camille-Desmoulins, death that remain descriptive. F-94805 Villejuif, France 2 University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA Preface 3 Centre d’Immunologie INSERM/CNRS/Universite de la Mediterranee de Marseille-Luminy, Case 906, Avenue de Luminy, 13288 Marseille Cedex 9, It is obvious that clear definitions of objects that are only France shadows in Plato’s cage are difficult to be achieved. Cell death 4 The Ben May Institute for Cancer Research, University of Chicago, 924 E 57th and the different subroutines leading to cell death do not Street, Chicago, IL 60637, USA 5 escape this rule. Even worse, the notion of death is strongly Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, influenced by religious and cultural beliefs, which may UK 6 Molecular Signalling and Cell Death Unit, Department for Molecular Biomedical subliminally influence the scientific view of cell death. -
Eosinophils but Not of Neutrophils Stimulates Effector Functions of Human Interaction with Secretory Component
Interaction with Secretory Component Stimulates Effector Functions of Human Eosinophils But Not of Neutrophils This information is current as Youichi Motegi and Hirohito Kita of September 23, 2021. J Immunol 1998; 161:4340-4346; ; http://www.jimmunol.org/content/161/8/4340 Downloaded from References This article cites 49 articles, 20 of which you can access for free at: http://www.jimmunol.org/content/161/8/4340.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 23, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 1998 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Interaction with Secretory Component Stimulates Effector Functions of Human Eosinophils But Not of Neutrophils1 Youichi Motegi and Hirohito Kita2 Eosinophils and their products are important in the pathophysiology of allergic inflammation in mucosal tissues. Secretory component bound to IgA mediates transepithelial transport of IgA and confers increased stability on the resultant secretory IgA; however, the effect of secretory component on the biologic activity of IgA is unknown. -
Detailed Structure and Pathophysiological Roles of the Iga-Albumin Complex in Multiple Myeloma
International Journal of Molecular Sciences Article Detailed Structure and Pathophysiological Roles of the IgA-Albumin Complex in Multiple Myeloma Yuki Kawata 1, Hisashi Hirano 1, Ren Takahashi 1, Yukari Miyano 1, Ayuko Kimura 1, Natsumi Sato 1, Yukio Morita 2, Hirokazu Kimura 1,* and Kiyotaka Fujita 1 1 Department of Health Sciences, Gunma Paz University Graduate School of Health Sciences, 1-7-1, Tonyamachi, Takasaki-shi, Gunma 370-0006, Japan; [email protected] (Y.K.); [email protected] (H.H.); [email protected] (R.T.); [email protected] (Y.M.); [email protected] (A.K.); [email protected] (N.S.); [email protected] (K.F.) 2 Laboratory of Public Health II, Azabu University School of Veterinary Medicine, 1-17-71, Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan; [email protected] * Correspondence: [email protected]; Tel.: +81-27-365-3366; Fax: +81-27-388-0386 Abstract: Immunoglobulin A (IgA)-albumin complexes may be associated with pathophysiology of multiple myeloma, although the etiology is not clear. Detailed structural analyses of these protein– protein complexes may contribute to our understanding of the pathophysiology of this disease. We analyzed the structure of the IgA-albumin complex using various electrophoresis, mass spectrom- etry, and in silico techniques. The data based on the electrophoresis and mass spectrometry showed that IgA in the sera of patients was dimeric, linked via the J chain. Only dimeric IgA can bind to albumin molecules leading to IgA-albumin complexes, although both monomeric and dimeric forms of IgA were present in the sera. -
Allergen-Specific Igg1 and Igg3 Through Fc Gamma RII Induce Eosinophil Degranulation
Allergen-specific IgG1 and IgG3 through Fc gamma RII induce eosinophil degranulation. M Kaneko, … , G J Gleich, H Kita J Clin Invest. 1995;95(6):2813-2821. https://doi.org/10.1172/JCI117986. Research Article Evidence suggests that eosinophils contribute to inflammation in bronchial asthma by releasing chemical mediators and cytotoxic granule proteins. To investigate the mechanism of eosinophil degranulation in asthma, we established an in vitro model of allergen-induced degranulation. We treated tissue culture plates with short ragweed pollen (SRW) extract and sera from either normal donors or SRW-sensitive patients with asthma. Eosinophils were incubated in the wells and degranulation was assessed by measurement of eosinophil-derived neurotoxin in supernatants. We detected degranulation only when sera from SRW-sensitive patients were reacted with SRW. Anti-IgG and anti-Fc gamma RII mAb, but not anti-IgE or anti-Fc epsilon RII mAb, abolished the degranulation. IgG-depleted serum did not induce degranulation; IgE-depleted serum triggered as much degranulation as untreated serum. Furthermore, serum levels of SRW-specific IgG1 or IgG3 correlated with the amounts of released eosinophil-derived neurotoxin. When eosinophils were cultured in wells coated with purified IgG or IgE, eosinophil degranulation was observed only with IgG. Finally, human IgG1 and IgG3, and less consistently IgG2, but not IgG4, induced degranulation. Thus, sera from patients with SRW-sensitive asthma induce eosinophil degranulation in vitro through antigen-specific IgG1 and IgG3 antibodies. These antibodies may be responsible for degranulation of eosinophils in inflammatory reactions, such as bronchial asthma. Find the latest version: https://jci.me/117986/pdf Allergen-specific IgG1 and IgG3 through FcRIl Induce Eosinophil Degranulation Masayuki Kaneko, Mark C. -
Different Innate and Adaptive Immune Response to SARS-Cov-2 Infection of Asymptomatic, Mild and Severe Cases
medRxiv preprint doi: https://doi.org/10.1101/2020.06.22.20137141; this version posted September 28, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . Title: Different innate and adaptive immune response to SARS-CoV-2 infection of asymptomatic, mild and severe cases Rita Carsetti1,2*, Salvatore Zaffina3,4, Eva Piano Mortari1#, Sara Terreri1#, Francesco Corrente2, Claudia Capponi2, Patrizia Palomba2, Mattia Mirabella2, Simona Cascioli5, Paolo Palange6, Ilaria Cuccaro6, Cinzia Milito7, Alimuddin Zumla8,9, Markus Maeurer10,11, Vincenzo Camisa3,4, Maria Rosaria Vinci3,4, Annapaola Santoro3,4, Eleonora Cimini12, Luisa Marchioni13, Emanuele Nicastri13, Fabrizio Palmieri13, Chiara Agrati12, Giuseppe Ippolito14, Ottavia Porzio15,16, Carlo Concato17, Andrea Onetti Muda18, Massimiliano Raponi4, Concetta Quintarelli19,20, Isabella Quinti7, Franco Locatelli19,21 Affiliations: 1B Cell Pathophysiology Unit, Immunology Research Area, Bambino Gesù Children's Hospital IRCCS, Rome, Italy; 2Diagnostic Immunology Unit, Department of Laboratories, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy 3Occupational Medicine/Health Technology Assessment and Safety Research Unit, Clinical- Technological Innovations Research Area, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy 4Health Directorate, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy 5Research Laboratories, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy 6Department of Public Health and infectious diseases pulmonary division, Policlinico Umberto I Hospital, Rome, Italy. 7Department of Molecular Medicine, Sapienza University of Rome, Rome, Italy NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. -
The Biochemistry of Cell Death Cell Death: Apoptosis and Other Means to an End, Second Edition by Douglas R
Zampieri et al. Cell Death and Disease (2020) 11:259 https://doi.org/10.1038/s41419-020-2465-5 Cell Death & Disease BOOK REVIEW Open Access The biochemistry of cell death Cell Death: Apoptosis and Other Means to an End, Second Edition by Douglas R. Green, St. Jude Children’s Research Hospital, Cold Spring Harbor Laboratory Press, New York, 2018 Carlotta Zampieri 1, Carlo Ganini 1 and Gerry Melino 1 Can we impress you with a mind-blowing revelation? Douglas Green is one of the worldwide leading experts “Cells are not eternal in our bodies, but rather they on apoptosis and cell death. He has dealt with the role of encounter death!”1. cell death in the regulation of cancer and immune If someone pronounces this sentence at a biology class, response, studying the molecular events that drive the students will laugh. Why? Because cell death has been process, focusing on the induction-activation of apoptosis studied since the 60s of the last century. When we speak in T cells and the role of Myc, death receptors and Bcl-2 about apoptosis nowadays, we regard it as a well-known in this context. His deep understanding of the field truth. Anyway, this truth did not catch the attention of allowed him to write the first edition of this book in a scientists until the 1980s, where the interest in the field clear and straightforward manner, enriched by extremely exploded, leading to a dramatic increase of publications. informative figures. His talent as a biologist, as well as a Cell death passed “from neglect to hysteria” in only a few communicator, has been condensed in this second edi- years, citing Martin Raff2, one of the founders of the field. -
Dual Effects of Thyroid Hormone on Neurons and Neurogenesis
Lin et al. Cell Death and Disease (2020) 11:671 https://doi.org/10.1038/s41419-020-02836-9 Cell Death & Disease ARTICLE Open Access Dual effects of thyroid hormone on neurons and neurogenesis in traumatic brain injury Chao Lin1,2, Nan Li3, Hanxiao Chang1,2,Yuqishen1,2,ZhengLi1,2,Wuwei1,2,HuaChen1,2,HuaLu1,2,JingJi 1,2 and Ning Liu1,2 Abstract Thyroid hormone (TH) plays a crucial role in neurodevelopment, but its function and specific mechanisms remain unclear after traumatic brain injury (TBI). Here we found that treatment with triiodothyronine (T3) ameliorated the progression of neurological deficits in mice subjected to TBI. The data showed that T3 reduced neural death and promoted the elimination of damaged mitochondria via mitophagy. However, T3 did not prevent TBI-induced cell death in phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (Pink1) knockout mice suggesting the involvement of mitophagy. Moreover, we also found that T3 promoted neurogenesis via crosstalk between mature neurons and neural stem cells (NSCs) after TBI. In neuron cultures undergoing oxygen and glucose deprivation (OGD), conditioned neuron culture medium collected after T3 treatment enhanced the in vitro differentiation of NSCs into mature neurons, a process in which mitophagy was required. Taken together, these data suggested that T3 treatment could provide a therapeutic approach for TBI by preventing neuronal death via mitophagy and promoting neurogenesis via neuron–NSC crosstalk. 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; Introduction treatments focus only on preventing complications or Traumatic brain injury (TBI) is considered to be a providing support in nature. leading cause of substantial mortality and long-term dis- Thyroid hormone (TH) is crucial for neural stem cell ability among young adults worldwide1. -
The Effect of Mirthful Laughter on Stress and Natural Killer Cell Activity
Western Kentucky University TopSCHOLAR® Nursing Faculty Publications School of Nursing 2003 The ffecE t of Mirthful Laughter on Stress and Natural Killer Cell Activity Mary P. Bennett Western Kentucky University, [email protected] Janice M. Zeller Lisa Rosenberg Judith McCann Follow this and additional works at: http://digitalcommons.wku.edu/nurs_fac_pub Part of the Alternative and Complementary Medicine Commons, Nursing Commons, and the Oncology Commons Recommended Repository Citation Bennett, Mary P.; Zeller, Janice M.; Rosenberg, Lisa; and McCann, Judith. (2003). The Effect of Mirthful Laughter on Stress and Natural Killer Cell Activity. Alternative Therapies in Health and Medicine, 9 (2), 38-45. Available at: http://digitalcommons.wku.edu/nurs_fac_pub/9 This Other is brought to you for free and open access by TopSCHOLAR®. It has been accepted for inclusion in Nursing Faculty Publications by an authorized administrator of TopSCHOLAR®. For more information, please contact [email protected]. original research THE EFFECT OF MIRTHFUL LAUGHTER ON STRESS AND NATURAL KILLER CELL ACTIVITY Mary P. Bennett, DNSc, RN, Janice M. Zeller, PhD, RN, FAAN, Lisa Rosenberg, PhD, RN, Judith McCann, DNSc, RN Mary P. Bennett is associate professor and assistant dean, function postintervention (t16 =2.52 P=.037) and compared with the Indiana State University School of Nursing in Terre Haute, Ind. remaining participants (t32=32.1; P=.04). Humor response scale scores Janice M. Zeller is professor, Department of Adult Health correlated with changes in NK cell activity (r16=.744;P =.001). Nursing and associate professor, Department of Conclusion • Laughter may reduce stress and improve NK cell activity. As Immunology/Microbiology; and Lisa Rosenberg is assistant pro- low NK cell activity is linked to decreased disease resistance and increased fessor, Department of Community and Mental Health Nursing morbidity in persons with cancer and HIV disease, laughter may be a useful and associate dean, Student Affairs, College of Nursing, at Rush cognitive-behavioral intervention. -
Estimation of Postmortem Interval Based on Cell Death Progression in Biological Fluids
Estimation of Postmortem Interval Based on Cell Death Progression in Biological Fluids Author: Mónica Cristina Francisco Tomé Dissertation submitted to the Faculty of Medicine of University of Porto for the Master degree in Forensic Sciences Supervisor: Prof. Doutor Agostinho Almiro de Almeida (Faculty of Pharmacy, University of Porto) Co-supervisors: Prof. Doutor Agostinho José Carvalho dos Santos (Faculty of Medicine, University of Porto) Doutora Daniela Sofia Almeida Ribeiro (Faculty of Pharmacy, University of Porto) Porto, September 2017 Acknowledgments My special acknowledgments to: My supervisor Professor Agostinho Almeida that accepted to work with me and provided me the indispensable help to finish my master degree. My co-supervisor Professor Agostinho Santos, without him I would not be doing my dissertation, he opened my eyes and I am glad that he did. My co-supervisor Doctor Daniela Ribeiro that welcomed me with open arms and was always with me. Doctor Rui Almeida who is a very professional person and who was always ready to help me in whatever it takes! To Professor Eduarda Fernandes who was always present during the development of this study and was always trying to find solutions to the problems. To all of my friends, especially to Cátia Pereira, Margarida Pereira, Miguel Pinto and Sofia Salsinha, that provided me the emotional strength to continue to fight and get my motivation. To my parents and brother, that always listened to me and gave me the emotional support while I was far away from home. I have to thank also to all of those who were present during this period of my life and never let me give up. -
IG Living Magazine April-May 2018
April-May 2018 IGLiving.com Staying Active How to Keep Moving with Chronic Illness Planning Travel? Follow These Simple Steps Exercises for Better Balance What Is Now Known Assistive Devices About SAD? for Staying Mobile On IGLiving.com Feaatures an easy- to-nnavigate design Indepth content onn IG-treated diseases annd treatment Cononnnnectnne withh oouurur Pattiiieeent Advocateee,, AAbbbbie Cornett RReeaead weeklyklylyy bblogs about isssues relal tted d to living with cchchrhroononionic illnessnessessessss Valuablee Resourcees and more On Facebook Findd timely and relevant informao tion posted dailyy, providing a venue foro connnecting with others in the IG community. On the Go CONTENTS | April-May 2018 Features Up Front 16 Travel Tips for Those 5 Editorial with Chronic Illness Staying Active with By Abbie Cornett and Chronic Illness Ronale Tucker Rhodes, MS By Ronale Tucker Rhodes, MS 6 Abbie’s Corner 20 Exercises to Preventing Isolation Improve Balance By Abbie Cornett By Matthew D. Hansen, DPT, MPT, BSPTS 7 Faces of IG From our Facebook page 24 Specific Antibody Deficiency and/or Impaired Polysaccharide Responsiveness Departments By E. Richard Stiehm, MD 8 Ask the Experts 32 Understanding Healthcare professionals’ NK Cell Deficiency responses to patient questions By Jordan S. Orange, MD, PhD 9 Immunology 101 DiGeorge Syndrome: Thymus Development and the Initiation of T Lymphocyte Development Sources By Terry O. Harville, MD, PhD 42 Product Guide 10 Clinical Brief Mobility Management What Are Immunoglobulins? By Trudie Mitschang By Michelle Greer, RN 44 Book Corner 12 In the News New and useful reading Research, science, product and insurance updates 46 Resource Center Community foundations, associations, forums and other resources Columns 36 Let’s Talk!—SamMichael Long Advertising in IG Living By Trudie Mitschang IG Living Magazine is read by 30,000 subscribers who are patients that depend upon immune globulin products and their healthcare providers. -
Major Histocompatibility Complex Class III Genes and Susceptibility to Immunoglobulin a Deficiency and Common Variable Immunodeficiency
Major histocompatibility complex class III genes and susceptibility to immunoglobulin A deficiency and common variable immunodeficiency. J E Volanakis, … , H W Schroeder Jr, M D Cooper J Clin Invest. 1992;89(6):1914-1922. https://doi.org/10.1172/JCI115797. Research Article We have proposed that significant subsets of individuals with IgA deficiency (IgA-D) and common variable immunodeficiency (CVID) may represent polar ends of a clinical spectrum reflecting a single underlying genetic defect. This proposal was supported by our finding that individuals with these immunodeficiencies have in common a high incidence of C4A gene deletions and C2 rare gene alleles. Here we present our analysis of the MHC haplotypes of 12 IgA-D and 19 CVID individuals from 21 families and of 79 of their immediate relatives. MHC haplotypes were defined by analyzing polymorphic markers for 11 genes or their products between the HLA-DQB1 and the HLA-A genes. Five of the families investigated contained more than one immunodeficient individual and all of these included both IgA-D and CVID members. Analysis of the data indicated that a small number of MHC haplotypes were shared by the majority of immunodeficient individuals. At least one of two of these haplotypes was present in 24 of the 31 (77%) immunodeficient individuals. No differences in the distribution of these haplotypes were observed between IgA-D and CVID individuals. Detailed analysis of these haplotypes suggests that a susceptibility gene or genes for both immunodeficiencies are located within the class III region of the MHC, possibly between the C4B and C2 genes. Find the latest version: https://jci.me/115797/pdf Major Histocompatibility Complex Class Ill Genes and Susceptibility to Immunoglobulin A Deficiency and Common Variable Immunodeficiency John E. -
The Dynamic Tumor Ecosystem: How Cell Turnover and Trade-Offs Affect Cancer Evolution
bioRxiv preprint doi: https://doi.org/10.1101/270900; this version posted February 26, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. The dynamic tumor ecosystem: how cell turnover and trade-offs affect cancer evolution Jill A. Gallaher1, Joel Brown1*, and Alexander R. A. Anderson1* 1 Department of Integrated Mathematical Oncology, H. Lee Moffitt Cancer Center, Tampa, FL USA *These authors contributed equally. ABSTRACT Tumors are not static masses of cells but rather dynamic ecosystems where cancer cells experience constant turnover and evolve fitness-enhancing phenotypes. Selection for different phenotypes may vary with 1) the tumor niche (edge or core), 2) cell turnover rates, 3) the nature of the tradeoff between traits (proliferation vs migration), and 4) whether deaths occur in response to demographic or environmental stochasticity. In an agent based, spatially-explicit model, we observe how two traits (proliferation rate and migration speed) evolve under different trade-off conditions with different turnover rates. Migration rate is favored over proliferation at the tumor’s edge and vice-versa for the interior. Increasing cell turnover rates only slightly slows the growth of the tumor, but accelerates the rate of evolution for both proliferation and migration. The absence of a tradeoff favors ever higher values for proliferation and migration. A convex tradeoff tends to favor proliferation over migration while often promoting the coexistence of a generalist and specialist phenotype.