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Shin Junghee Jenny Par-Young Jennefer Unlu Serhan McNamara Andrew Park Hong-Jai Shin Min Sun Gee Renelle J. Doyle Hester Afinogenova Yuliya Zidan Elena Kwah Jason Russo Armand Mamula Mark Hsu Florence Ida Catanzaro Jason Racke Michael Bucala Richard Wilen Craig Kang Insoo 《Journal of clinical immunology》2022,42(6):1137-1150
Journal of Clinical Immunology - Immune responses to coronavirus disease 2019 (COVID-19) mRNA vaccines in primary antibody deficiencies (PADs) are largely unknown. We investigated antibody and CD4+... 相似文献
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Kallen Michael A. Brown Heather E. Hatton Joeffrey R. Doyle William A. Murphy Ryan Elliott Ryan Gutierrez Mark A. Catherwood Emma L. Pitman Heather P. Liu Vincent X. Gershon Richard C. 《Quality of life research》2022,31(7):2201-2212
Quality of Life Research - To develop two item content-matched, precise, score-level targeted inpatient physical function (PF) short form (SF) measures: one clinician-reported, one... 相似文献
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Yu-Tzu Chan Alan C.-Y. Lai Ruey-Jen Lin Ya-Hui Wang Yi-Ting Wang Wen-Wei Chang Hsin-Yi Wu Yu-Ju Lin Wen-Ying Chang Jen-Chine Wu Jyh-Cherng Yu Yu-Ju Chen Alice L. Yu 《International journal of cancer. Journal international du cancer》2020,146(6):1674-1685
G protein-coupled estrogen receptor-1 (GPER), a member of the G protein-coupled receptor (GPCR) superfamily, mediates estrogen-induced proliferation of normal and malignant breast epithelial cells. However, its role in breast cancer stem cells (BCSCs) remains unclear. Here we showed greater expression of GPER in BCSCs than non-BCSCs of three patient-derived xenografts of ER−/PR+ breast cancers. GPER silencing reduced stemness features of BCSCs as reflected by reduced mammosphere forming capacity in vitro, and tumor growth in vivo with decreased BCSC populations. Comparative phosphoproteomics revealed greater GPER-mediated PKA/BAD signaling in BCSCs. Activation of GPER by its ligands, including tamoxifen (TMX), induced phosphorylation of PKA and BAD-Ser118 to sustain BCSC characteristics. Transfection with a dominant-negative mutant BAD (Ser118Ala) led to reduced cell survival. Taken together, GPER and its downstream signaling play a key role in maintaining the stemness of BCSCs, suggesting that GPER is a potential therapeutic target for eradicating BCSCs. 相似文献
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In this article, we examine the social management of fatness via an analysis of 4 years of participant‐observation in military‐style fitness boot camps and interviews with camp participants, trainers and organisers/owners. We begin by focusing on popular imagery of the ‘boot camp’. The boot camp model takes various forms; yet, whether it involves civilian participants, as on reality television shows, or the imagined military ones of films, the boot camp model emphasises the re‐fashioning of the individual via the disciplining of bodies and selves. Such constructions of boot camps were employed by our respondents to lay claim to identities which highlight their hard work, strength of character, fundamental ‘goodness’ and self‐discipline, as those qualities are demonstrated through the body – even though participants’ actual bodies change little at camp. Such meanings stand in direct contradiction to broader social constructions of fatness and participants’ own negative perceptions of fat people. Moreover, even within the camps themselves, such identity claims are contested, both by camp trainers and by slimmer and ‘fitter’ attendees. These counterclaims are grounded in ideas about the characterological implications of the fat body, beliefs about the purpose of boot camp and notions of the body's capacity for change. 相似文献
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Peter B. Soeters Robert R. Wolfe Alan Shenkin 《JPEN. Journal of parenteral and enteral nutrition》2019,43(2):181-193
Hypoalbuminemia is associated with inflammation. Despite being addressed repeatedly in the literature, there is still confusion regarding its pathogenesis and clinical significance. Inflammation increases capillary permeability and escape of serum albumin, leading to expansion of interstitial space and increasing the distribution volume of albumin. The half‐life of albumin has been shown to shorten, decreasing total albumin mass. These 2 factors lead to hypoalbuminemia despite increased fractional synthesis rates in plasma. Hypoalbuminemia, therefore, results from and reflects the inflammatory state, which interferes with adequate responses to events like surgery or chemotherapy, and is associated with poor quality of life and reduced longevity. Increasing or decreasing serum albumin levels are adequate indicators, respectively, of improvement or deterioration of the clinical state. In the interstitium, albumin acts as the main extracellular scavenger, antioxidative agent, and as supplier of amino acids for cell and matrix synthesis. Albumin infusion has not been shown to diminish fluid requirements, infection rates, and mortality in the intensive care unit, which may imply that there is no body deficit or that the quality of albumin “from the shelf” is unsuitable to play scavenging and antioxidative roles. Management of hypoalbuminaemia should be based on correcting the causes of ongoing inflammation rather than infusion of albumin. After the age of 30 years, muscle mass and function slowly decrease, but this loss is accelerated by comorbidity and associated with decreasing serum albumin levels. Nutrition support cannot fully prevent, but slows down, this chain of events, especially when combined with physical exercise. 相似文献
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