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OBJECTIVE Non-native English speaking workers with a mild work-related traumatic brain and/or head injury are a vulnerable and underrepresented population in research studies. The researchers present their experiences with recruiting and performing qualitative interviews with non-native English speaking individuals with a work-related mild traumatic brain injury, and provide recommendations on how to better include this vulnerable population in future research studies. This paper presents considerations regarding ethics, recruitment challenges, interview preparation and debriefing, sex & gender and language and cultural issues must be made when working with this vulnerable population. RESULTS The researchers discuss critical issues and provide recommendations in recruiting and engaging with non-native English language workers including ethics, recruitment challenges, interview preparation and debriefing, sex & gender and language, and cultural considerations that must be made when working with this population. The study recommendations advise investigators to spend more time to learn about the non-native English participants in the mild wrTBI context, to be familiar with the vulnerabilities and specific circumstances that these workers experience. By increasing their awareness of the challenging facing this vulnerable population, the intention is to provide better care and treatment options through evidence-based research and practice.BACKGROUND Cytotoxic T lymphocyte-associated antigen-4-Ig (CTLA-4-Ig) competes with CD28 for binding CD80/CD86 on antigen-presenting cells (APCs) to limit T cell activation. B cells are believed to be important APCs in the pathogenesis of autoimmune diseases and express CD80/CD86 after activation; however, relatively little is known about the effect of CTLA-4-Ig on B cells. This study tested the impact of CTLA-4-Ig on human B cell responses. METHODS Human blood B cells were purified from healthy donors and activated in the presence of CTLA-4-Ig or the L6-Ig control protein in vitro. RT-q-PCR and immunofluorescence staining were performed to detect activation marker expression. ELISA was conducted to measure cytokine secretion. The CD80/CD86 levels on the surface of the memory B cells in the blood of 18 patients with rheumatoid arthritis (RA) were detected using immunofluorescence staining. RESULTS CTLA-4-Ig suppressed the expression of Staphylococcus aureus (SAC)-induced CD80, CD86, TNFA, and IL6 in human B cected in the RA patients after abatacept treatment. Blocking CD80/CD86 on B cells by CTLA-4-Ig may hinder T cell activation and associated with the disease activity of RA in vivo. Our findings indicate that CTLA-4-Ig may regulate humoral responses by modulating B cell activation and interfering T cell-B cell interaction.BACKGROUND Pubertal timing is known to be influenced by interactions among various genetic, nutritional, environmental and socio-economic factors, although the ultimate mechanisms underlying the increase in pulsatile GnRH secretion at puberty have yet to be fully elucidated. The aim of our research was to verify the role of KISSR1 (previously named GPR54) and MKRN3 genes on pubertal timing. METHODS We analyzed the DNA sequence of these genes in 13 girls affected by central precocious puberty (CPP) who showed onset of puberty before 8 years of age, and in 6 girls affected by early puberty (EP) between 8 and 10 years of age. RESULTS Direct sequencing of the KISS1R (GPR54) gene revealed two SNPs. One SNP is a missense variant (rs 350,132) that has been previously reported in connection to CPP in Korean girls. The other variant that we found in the GPR54 gene (rs764046557) was a missense SNP located in exon 5 at position 209 of the aminoacid. We identified this variant in only one CPP patient. Automatic sequencing of MKRN3 in all patients revealed three variants in eight subjects. In 6 out of 19 (31.5%) patients (3/13 CPP patients and 3/6 EP patients) we found the synonymous variant c.663C > T (rs2239669). Another synonymous variant (rs140467331) was found in one of our CPP patients, as well as one missense variant (rs760981395) in another CPP patient. CONCLUSION In conclusion, we identified sequence variations of the KISS1R and MKRN3 genes, two of the most frequent genetic causes of ICPP. learn more Our results suggest that these variants might be inducible factors in the pathogenesis of CPP.Recent efforts to describe the human epigenome have yielded thousands of epigenomic and transcriptomic datasets. However, due primarily to cost, the total number of such assays that can be performed is limited. Accordingly, we applied an imputation approach, Avocado, to a dataset of 3814 tracks of data derived from the ENCODE compendium, including measurements of chromatin accessibility, histone modification, transcription, and protein binding. Avocado shows significant improvements in imputing protein binding compared to the top models in the ENCODE-DREAM challenge. Additionally, we show that the Avocado model allows for efficient addition of new assays and biosamples to a pre-trained model.BACKGROUND In the USA, there are several Ehrlichia spp. of concern including Ehrlichia canis, Ehrlichia ewingii, Ehrlichia chaffeensis, Ehrlichia muris eauclarensis, and “Panola Mountain Ehrlichia”. Of these, E. canis is considered the most clinically relevant for domestic dogs, with infection capable of causing acute, subclinical, and chronic stages of disease. Changes in climate, land use, habitats, and wildlife reservoir populations, and increasing contact between both human and dog populations with natural areas have resulted in the increased risk of vector-borne disease throughout the world. METHODS A Bayesian spatio-temporal binomial regression model was applied to serological test results collected from veterinarians throughout the contiguous USA between January 2013 and November 2019. The model was used to quantify both regional and local temporal trends of canine Ehrlichia spp. seroprevalence and identify areas that experienced significant increases in seroprevalence. RESULTS Regionally, increasing sabout prevention of tick exposure.