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There has been a growing research focus on social determinants to health disparities in general and medication adherence more specifically in low-income Black populations. The purpose of this study was to examine whether prior experiences of racism among Black patients in safety-net primary care indirectly predicts poor medication adherence through increased mental health symptoms and low healthcare provider trust. Two competing models were run whereby mental health leads to provider trust or provider trust leads to mental health in this multiple mediational chain. A group of 134 Black patients (76 men, average age 45.39 years) in a safety-net primary care clinic completed measures of these constructs. Results revealed that in the first model, mental health mediated the relationship between racism and provider trust, and provider trust mediated the relationship between mental health and medication adherence. click here All paths within this model were statistically significant, except the path between provider trust and medication adherence which approached significance. In the second model, provider trust and mental health significantly mediated the relationship between racism and medication adherence, and all direct and indirect paths were statistically significant, though the path between provider trust and medication adherence was omitted. These results may serve as catalysts to assess and attempt to mitigate specific minority-based stressors and associated outcomes within safety-net primary care settings.In 2014, a child with broad combined immunodeficiency (CID) who was homozygous for a private BCL10 allele was reported to have complete inherited human BCL10 deficiency. In the present study, we report a new BCL10 mutation in another child with CID who was homozygous for a BCL10 variant (R88X), previously reported as a rare allele in heterozygosis (minor allele frequency, 0.000003986). The mutant allele was a loss-of-expression and loss-of-function allele. As with the previously reported patient, this patient had complete BCL10 deficiency. The clinical phenotype shared features, such as respiratory infections, but differed from that of the previous patient that he did not develop significant gastroenteritis episodes or chronic colitis. Cellular and immunological phenotypes were similar to those of the previous patient. TLR4, TLR2/6, and Dectin-1 responses were found to depend on BCL10 in fibroblasts, and final maturation of T cell and B cell maturation into memory cells was affected. Autosomal-recessive BCL10 deficiency should therefore be considered in children with CID.Although there is empirical evidence supporting associations between exposure to violence and engaging in physically aggressive behavior during adolescence, there is limited longitudinal research to determine the extent to which exposure to violence is a cause or a consequence of physical aggression, and most studies have not addressed the influence of other negative life events experienced by adolescents. This study examined bidirectional relations between physical aggression, two forms of exposure to violence-witnessing violence and victimization, and other negative life events. Participants were a sample of 2568 adolescents attending three urban public middle schools who completed measures of each construct every 3 months during middle school. Their mean age was 12.76 (SD = 0.98); 52% were female. The majority were African American (89%); 17% were Hispanic or Latino/a. Cross-lagged regression analyses across four waves of data collected within the same grade revealed bidirectional relations between witnessing violence and physical aggression, and between witnessing violence and negative life events. Although physical aggression predicted subsequent changes in victimization, victimization predicted changes in physical aggression only when witnessing violence was not taken into account. Findings were consistent across sex and grades. Overall, these findings highlight the need for interventions that break the connection between exposure to violence and aggression during adolescence.Reduction in diversity of the intestinal microbiome (dysbiosis) is being identified in many disease states, and studies are showing important biologic contributions of microbiome to health and disease. Fecal microbiota transplantation (FMT) is being evaluated as a way to reverse dysbiosis in diseases and disorders in an attempt to improve health. The published literature was reviewed to determine the value of FMT in the treatment of medical disorders for which clinical trials have recently been conducted. FMT is effective in treating recurrent C. difficile infection in one or two doses, with many healthy donors providing efficacious fecal-derived products. In inflammatory bowel disease (IBD), FMT may lead to remission in approximately one-third of moderate-to-severe illnesses with one study suggesting that more durable FMT responses may be seen when used once medical remissions have been achieved. Donor products differ in their efficacy in treatment of IBD. Combining donor products has been one way to increase the potential value of FMT in treating chronic disorders. FMT is being explored in a variety of clinical settings affecting different organ systems outside CDI, with positive preliminary signals, in treatment of functional constipation, immunotherapy-induced colitis, neurodegenerative disease, as well as prevention of cancer-related disorders like graft versus host disease and decolonization of patients with recurrent urinary tract infection due to antibiotic-resistant bacteria. Currently, intense research is underway to see how the microbiome products like FMT can be harnessed for health benefits.Necrotizing enterocolitis (NEC) is a poorly defined disease that primarily affects preterm infants. There has not been much progress in the prevention or treatment of NEC since it became recognized as a common problem in preterm infants. Reasons for this lack of progress include the likelihood that different diseases are being put under the same moniker of "NEC," similar to using "diabetes" for the different diseases it represents. In order to make progress, better delineation of the phenotypes that present as NEC will be necessary to clearly establish their pathophysiology, find specific and sensitive biomarkers, and establish preventative regimens. In this review, we summarize some of the entities that are being called NEC, discuss the pathophysiology of the most classic form of NEC, and provide an overview of how we might proceed in the future to make progress in this field.
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