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Our findings point to an important role of peripheral Sig-1R in sensory neuron-macrophage/monocyte communication in the DRG after peripheral nerve injury; thus, these receptors may contribute to the neuropathic pain phenotype. © 2020 Federation of American Societies for Experimental Biology.Mild traumatic brain injury (mTBI) has been linked to mental health disorders (MHDs) and pituitary function alterations. Due to the complex relationship of mTBI, the neuroendocrine system, and MHDs, we propose that neuroendocrine dysfunction (NED) may play a role in negative long-term health outcomes. The goal of this study was to determine if blast-concussed service members (SMs) have a stronger likelihood of developing NED. We hypothesized that NED either pre- or post-injury is associated with poor mental and physical health outcomes. Serum samples from the Armed Forces Health Surveillance Branch were obtained from concussed (n&nbsp;=&nbsp;59) and non-concussed (n&nbsp;=&nbsp;72) SMs treated at the Concussion Restoration Care Center (CRCC) in Afghanistan. Serum was collected within 2&nbsp;years prior to deployment and one or two times within 3&nbsp;years following their CRCC visit. Samples were analyzed for luteinizing hormone (LH), testosterone, human growth hormone, cortisol, and prolactin to assess post-injury neuroendocrine function. Results indicate that SMs who incurred an mTBI exhibited long-term LH and testosterone deficiencies 3&nbsp;years following injury compared to controls. Specifically, 47.6% of head-injured SMs displayed hypofunction in at least one of five hormones at 3&nbsp;years post-injury. Anxiety disorders were the most common MHD observed in concussed SMs with hypopituitarism, while there was also a trend for SMs with chronic pituitary dysfunction to have MHD diagnoses. Findings indicate blast-related mTBI may be associated with long-term health outcomes following a period of incubation. Neuroendocrine screenings may increase treatment opportunities, inform rehabilitation strategies, and improve overall quality of life for patients. Published 2020. This article is a U.S. Government work and is in the public domain in the USA.Endothelin-1 (ET-1) is a member of the endothelin family of peptide hormones first discovered as endothelium-derived mediators regulating vascular tone. ET-1 also regulates the proliferation and differentiation of bone cells that synthesize fibroblast growth factor 23 (FGF23). FGF23 is a hormone controlling renal phosphate and vitamin D metabolism. Here, we studied the role of ET-1 and endothelin receptor B (ETB) for FGF23 production. Fgf23 gene expression was studied in IDG-SW3 bone cells by quantitative RT-PCR. ETB-expressing (etb+/+ ) and rescued ETB-deficient mice (etb-/- ) were studied in metabolic cages. Their serum FGF23, PTH, and 1,25(OH)2 D3 concentrations were determined by ELISA, serum and urinary phosphate and Ca2+ by photometric methods. [https://www.selleckchem.com/products/talabostat.html Val-boroPro molecular weight] ET-1 and ETB agonist sarafotoxin 6c suppressed Fgf23 mRNA in IDG-SW3 cells. Serum C-terminal and intact FGF23 as well as bone Fgf23 mRNA levels were significantly higher in etb-/- mice than in etb+/+ mice. Renal phosphate excretion was significantly higher in etb-/- mice despite lower phosphate levels. In addition, etb-/- animals exhibited calciuria and a significantly higher serum 1,25(OH)2 D3 concentration compared to etb+/+ mice. In conclusion, ETB-dependent ET-1 signaling is a potent suppressor of FGF23 formation. This effect is likely to be of clinical relevance given the use of endothelin receptor antagonists in various diseases. © 2020 Federation of American Societies for Experimental Biology.BACKGROUND Selective immunoglobulin M deficiency (SIgMD) is a rare primary immunodeficiency that is frequently reported in Western countries. However, large epidemiological and clinical studies of SIgMD in China are still lacking. Herein, we describe a cohort of SIgMD subjects in a large tertiary university hospital in China. METHODS A cross-sectional study included 139&nbsp;668 participants at First Affiliated Hospital of Wenzhou Medical University from January 2014 to October 2018 was conducted. Individuals with a serum IgM level less than 0.3&nbsp;g/L with normal levels of serum IgA and IgG were defined as having SIgMD. RESULT A total of 63 subjects met the criteria for SIgMD(63/139668, 0.045%), with a male-to-female ratio of 0.85, aged from 19 to 99&nbsp;years. The most common clinical manifestation was autoimmune disorders (38/63, 60.32%), while the second most common manifestation was infections (21/63, 33.33%). Neither allergies nor tumors were found among these 63 SIgMD subjects. Most importantly, there were 30 patients with systemic lupus erythematosus among these 63 SIgMD subjects, accounting for 47.62% of all SIgMD subjects. CONCLUSION To our knowledge, we describe here the first large single-center cohort of adult patients affected by SIgMD in China. The most common clinical manifestation was autoimmune disorders, specifically systemic lupus erythematosus. © 2020 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals, Inc.Lanthanide ion (Ln III ) complexes, [Ln(3Tcbx) 2 ] 3+ (Ln III = Yb III , Nd III , Er III ), were isolated with a new pyridine-bis(carboxamide)-based ligand with a 2,2'5',2''-terthiophene pendant and their resulting photophysical properties were explored. Upon exciting the complexes at 490 nm, only Ln III emission is observed with efficiencies of 0.29% at 976 nm for Ln III = Yb III and 0.16% at 1053 nm for Ln III = Nd III . Er III emission is observed but weak. When exciting at 400 nm, concurrent 1 O 2 formation is seen, with efficiencies of 11% for the Yb III and Nd III complexes and 13% for the Er III complex. Due to the concurrent generation of 1 O 2 , as would be expected, the efficiency of metal-centred emission decreases to 0.02% for Yb III and 0.05% for Nd III . The ability to control 1 O 2 generation through the excitation wavelength indicates that incorporating 2,2'5',2"-terthiophene resulted in access to multiple sensitization pathways. These energy pathways were unravelled through transient absorption spectroscopy. © 2020 WILEY-VCH Verlag GmbH &amp; Co. KGaA, Weinheim.Although there appears to be an overall trend of diminishing oral manifestations of HIV infection, evidence is emerging on the increased incidence of concomitant parotid gland enlargement and xerostomia. Furthermore, several case narrations and a limited series have suggested a possible association of sialolithiasis with highly active antiretroviral therapy, mostly involving the parotid gland. The aim of this report is to present a patient with a giant sialolith of the submandibular gland following a 27-year intake of various antiretrovirals for HIV infection and review the relevant literature. © 2020 Special Care Dentistry Association and Wiley Periodicals, Inc.Culture bump theory provides a practical and goal-oriented framework for addressing cultural differences that can impact communication and patient care. Differences in language and culture, coupled with a lack of knowledge or competency regarding these differences, often contribute to 'culture bumps' between healthcare providers and patients. Interpreters serve the unique role of 'cultural brokers', going beyond bridging the linguistic divide to close cultural gaps. Research from the perspective of interpreters focused on culture bumps and cultural competency within genetic counseling sessions is lacking. We aimed to assess interpreters' experiences with significant 'culture bumps' in genetic counseling sessions, obtain interpreters' perspectives regarding genetic counselors' gaps in cultural competency, and explore interpreters' perceptions of the impact of cultural competency on the genetic counseling sessions. Spanish and Polish interpreters experienced in working in person with genetic counselors were rec). link2 Further research is necessary to explore these concepts within other languages and cultures, as well as to determine the most appropriate methods for implementing these suggestions for improvement. © 2020 National Society of Genetic Counselors.The human FcγRs interact with antigen-complexed IgG ligands to both activate and modulate a powerful network of inflammatory host-protective effector functions that are key to the normal physiology of immune resistance to pathogens. More than 100 therapeutic monoclonal antibodies (mAbs) are approved or in late stage clinical trials, many of which harness the potent FcγR-mediated effector systems to varying degrees. This is most evident for antibodies targeting cancer cells inducing antibody-dependent killing or phagocytosis but is also true to some degree for the mAbs that neutralise or remove small macromolecules such as cytokines or other immunoglobulins. The use of mAb therapeutics has also revealed a "scaffolding" role for FcγR which, in different contexts, may either underpin the therapeutic mAb action such as immune agonism or may trigger catastrophic adverse effects. The still unmet therapeutic need in many cancers, inflammatory diseases or emerging infections such as SARS-CoV-2, requires increased effort on the development of improved and novel mAbs. A more mature appreciation of the immunobiology of individual FcγR function and the complexity of the relationships between FcγRs and antibodies is fuelling efforts to develop more potent "next-gen" therapeutic antibodies. Such development strategies now include focused glycan or protein engineering of the Fc to increase affinity and/or tailor specificity for selective engagement of individual activating FcγRs or the inhibitory FcγRIIb or alternatively, for the ablation of FcγR interaction altogether. This review touches on recent aspects FcγR and IgG immunobiology and its relationship to the present and future actions of therapeutic mAbs. This article is protected by copyright. All rights reserved.Parkinson's disease (PD) is the second most common neurodegenerative disease. Eigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, is known to exert a beneficial effect on PD patients. Although some mechanisms were suggested to underlie this intervention, it remains unknown if the EGCG-mediated protection was achieved by remodeling gut microbiota. In the present study, 0.1 mM or 0.5 mM EGCG was administered to the Drosophila melanogaster with PINK1 (PTEN induced putative kinase 1) mutations, a prototype PD model, and their behavioral performances, as well as neuronal/mitochondrial morphology (only for 0.5 mM EGCG treatment) were determined. According to the results, the mutant PINK1B9 flies exhibited dopaminergic, survival, and behavioral deficits, which were rescued by EGCG supplementation. Meanwhile, EGCG resulted in profound changes in gut microbial compositions in PINK1B9 flies, restoring the abundance of a set of bacteria. link3 Notably, EGCG protection was blunted when gut microbiota was disrupted by antibiotics. We further isolated four bacterial strains from fly guts and the supplementation of individual Lactobacillus plantarum or Acetobacter pomorum strain exacerbated the neuronal and behavioral dysfunction of PD flies, which could not be rescued by EGCG. Transcriptomic analysis identified TotM as the central gene responding to EGCG or microbial manipulations. Genetic ablation of TotM blocked the recovery activity of EGCG, suggesting that EGCG-mediated protection warrants TotM. Apart from familial form, EGCG was also potent in improving sporadic PD symptoms induced by rotenone treatment, wherein gut microbiota shared regulatory roles. Together, our results suggest the relevance of the gut microbiota-TotM pathway in EGCG-mediated neuroprotection, providing insight into indirect mechanisms underlying nutritional intervention of Parkinson's disease. © 2020 The Authors. The FASEB Journal published by Wiley Periodicals, Inc. on behalf of Federation of American Societies for Experimental Biology.