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Quinn Klemmensen posted an update 6 months, 3 weeks ago
The development of Sjögren’s syndrome (SS) is accompanied by B cell hyperproliferation and mutation. Our previous study identified aberrant expression of BST-2 (also known as Tetherin/CD317) in B cells from either the peripheral blood or infiltrated salivary glands. However, the roles of BST-2 in the regulation of B cell activation remain unknown. In this study, we identified that BST-2 can respond to BAFF simulation but not to other B cell simulators in neoplastic B cell lines. A CCK-8 assay, an EdU assay and Annexin V/PI staining indicated that BST-2 inhibition attenuated BAFF-enhanced proliferation and survival in both Raji cells and Daudi cells. Screening of BAFF-related signaling in neoplastic B-lymphoid cells indicated that BST-2 was involved in the regulation of NF-κB signaling upon BAFF simulation. However, inhibition of NF-κB by JSH-23 significantly reduced the proliferation and survival of Raji and Daudi cells under both normal and BAFF-simulated conditions. Collectively, our results indicate that BST-2/Tetherin is a BAFF-responsive membrane factor involved in the regulation of NF-κB signaling, thereby assisting in the proliferation and survival of neoplastic B-lymphoid cells. Our study provides a potential molecular mechanism underlying aberrant overactivation of B cells upon SS development.Increasing evidence suggests that microglial polarization plays an important role in the pathological processes of neuroinflammation following subarachnoid hemorrhage (SAH). Previous studies indicated that milk fat globule-epidermal growth factor-8 (MFG-E8) has potential anti-apoptotic and anti-inflammatory effects in cerebral ischemia. However, the effects of MFG-E8 on microglial polarization have not been evaluated after SAH. Therefore, the aim of this study was to explore the role of MFG-E8 in anti-inflammation, and its effects on microglial polarization following SAH. We established the SAH model via prechiasmatic cistern blood injection in mice. Double-immunofluorescence staining, western blotting and quantitative real-time polymerase chain reaction (q-PCR) were performed to investigate the expression and cellular distribution of MFG-E8. Two different dosages (1 and 5 μg) of recombinant human MFG-E8 (rhMFG-E8) were injected intracerebroventricularly (i.c.v.) at 1 h after SAH. Brain water content, neurolog the protein levels of the integrin β3/SOCS3/STAT3 pathway. rhMFG-E8 inhibits neuronal inflammation by transformation the microglial phenotype toward M2 and its direct protective effect on neurons after SAH, which may be mediated by modulation of the integrin β3/SOCS3/STAT3 signaling pathway, highlighting rhMFG-E8 as a potential therapeutic target for the treatment of SAH patients.Lead is a known reproductive, developmental, and neurological toxicant. Workers with a high likelihood of being exposed to lead at work may inadvertently transport lead home from work, known as “take-home exposure.” This is concerning for many workers for whom a workplace intervention is not feasible because their worksites and employers often change, rendering centralized strategies insufficient. This study aimed to better understand the connection between lead in the home of workers living with children and work in construction (n = 23), while other occupations were used as a comparison group (janitorial n = 5, autobody n = 2). Thirty workers living in disadvantaged communities in the Greater Boston area were recruited in 2018-2019 through collaboration with non-profits and worker unions with expertise working with low-income or immigrant workers. Construction workers that performed renovations, bridge constructions, welding, metal work, and demolitions were prioritized during recruitment. During a visit tosample size is needed to verify findings. Results provide evidence that work-related factors are important to consider when assessing home exposures, and that take-home exposures for workers in lead high-risk jobs such as construction may be an important source of exposure in the home prime for public health intervention at work, home, and community levels.
Substantial research has investigated the adverse effects of traffic-related air pollutants (TRAP) on human health. Convincing associations between TRAP and respiratory and cardiovascular diseases are known, but the underlying biological mechanisms are not well established. High-resolution metabolomics (HRM) is a promising platform for untargeted characterization of molecular mechanisms between TRAP and health indexes.
We examined metabolic perturbations associated with short-term exposures to TRAP, including carbon monoxide (CO), nitrogen dioxide (NO
), ozone (O
), fine particulate matter (PM
), organic carbon (OC), and elemental carbon (EC) among 180 participants of the Center for Health Discovery and Well-Being (CHDWB), a cohort of Emory University-affiliated employees.
A cross-sectional study was conducted on baseline visits of 180 CHDWB participants enrolled during 2008-2012, in whom HRM profiling was determined in plasma samples using liquid chromatography-high-resolution mass spectrometry withatures. The results were encouraging of further use of HRM and MWAS approaches for characterizing molecular mechanisms underlying exposure to TRAP.
Little is known about radiofrequency electromagnetic fields (RF) from mobile technology and resulting dose in young people. We describe modeled integrated RF dose in European children and adolescents combining own mobile device use and surrounding sources.
Using an integrated RF model, we estimated the daily RF dose in the brain (whole-brain, cerebellum, frontal lobe, midbrain, occipital lobe, parietal lobe, temporal lobes) and the whole-body in 8358 children (ages 8-12) and adolescents (ages 14-18) from the Netherlands, Spain, and Switzerland during 2012-2016. The integrated model estimated RF dose from near-field sources (digital enhanced communication technology (DECT) phone, mobile phone, tablet, and laptop) and far-field sources (mobile phone base stations via 3D-radiowave modeling or RF measurements).
Adolescents were more frequent mobile phone users and experienced higher modeled RF doses in the whole-brain (median 330.4mJ/kg/day) compared to children (median 81.8mJ/kg/day). selleck products Children spent more time using tablets or laptops compared to adolescents, resulting in higher RF doses in the whole-body (median whole-body dose of 81.