For the first time, using this novel cell line, we can assay the function of SMN alleles in the complete absence of flwt-Smn.
Emotional processing is a crucial ability in human and impairments in the processing of emotions are considered as transdiagnostic processes in psychopathology. In alcohol use disorder, numerous studies have investigated emotional processing and showed emotional deficits related to the perpetuation of alcohol use. Recent studies have also explored this topic in binge drinking, but few studies are available. In this paper, we explored whether emotional difficulties in binge drinking may be extended to implicit emotion processing.
We compared 39 binge drinkers (BD) and 40 non-binge drinkers who performed a gender categorization task while faces represented emotional expressions of anger, fear, happiness and sadness. Emotional brain responses were assessed thanks to functional magnetic resonance imaging. Emotional versus non-emotional conditions were first contrasted in the whole sample and groups were then compared.
Emotional condition led to differential activations than non-emotional condition, supporting the validity of the paradigm. Regarding group comparisons, BD exhibited higher activations in the left posterior cerebellum (anger processing) and the right anterior cingulate (fear processing) as well as lower activations in the left insula (happiness), the right post-central gyrus, the right cingulate gyrus and the right medial frontal gyrus (sadness processing).
Beyond emotional identification, BD presented differential brain responses following the implicit processing of emotions. Emotional difficulties in binge drinking might be related to a more automatic/unconscious processing of emotions.
Beyond emotional identification, BD presented differential brain responses following the implicit processing of emotions. Emotional difficulties in binge drinking might be related to a more automatic/unconscious processing of emotions.Although ARID1A mutations are a hallmark feature, mutations in other SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling subunits are also observed in endometrial neoplasms. Here, we interrogated the roles of Brahma/SWI2-related gene 1 (BRG1, SMARCA4), the SWI/SNF catalytic subunit, in the endometrial epithelium. BRG1 loss affects more than one-third of all active genes and highly overlaps with the ARID1A gene regulatory network. Chromatin immunoprecipitation studies revealed widespread subunit-specific differences in transcriptional regulation, as BRG1 promoter interactions are associated with gene activation, while ARID1A binding is associated with gene repression. However, we identified a physiologically relevant subset of BRG1 and ARID1A co-regulated epithelial identity genes. Mice were genetically engineered to inactivate BRG1 specifically in the endometrial epithelium. Endometrial glands were observed embedded in uterine myometrium, indicating adenomyosis-like phenotypes. Molecular similarities were observed between BRG1 and ARID1A mutant endometrial cells in vivo, including loss of epithelial cell adhesion and junction genes. Collectively, these studies illustrate overlapping contributions of multiple SWI/SNF subunit mutations in the translocation of endometrium to distal sites, with loss of cell integrity being a common feature in SWI/SNF mutant endometrial epithelia.
Adrenal Cushing syndrome (CS) is a major subtype of CS and has a high surgical cure rate. However, only a few studies have investigated the epidemiology and long-term outcomes of adrenal CS.
We aimed to investigate the nationwide epidemiology, long-term prognosis, and postoperative glucocorticoid replacement therapies of adrenal CS in Korea.
Retrospective cohort study.
A nationwide claim database.
Adrenal CS patients who were defined as having undergone adrenalectomy, a diagnosis code of CS, and not having pituitary gland surgery.
Crude incidence and age-standardized incidence rates, long-term mortality, comorbidities diagnosed preoperatively or developed postoperatively, and the pattern of postoperative glucocorticoid replacement therapy.
From 2002 to 2017, there were a total of 1199 new adrenal CS patients, including 72 patients with adrenocortical carcinoma (malignant adrenal CS), in Korea. The crude and age-standardized incidence rates were 1.51 and 1.27 per million person-years, respectively. The overall standardized mortality ratio was 3.0 (95% confidence interval [CI], 2.4-3.7) for benign adrenal CS and 13.1 (95% CI, 7.6-18.6) for malignant adrenal CS. Adrenal CS patients had a high risk of having coronary artery disease, stroke, metabolic diseases, and depression. A similar proportion of patients were diagnosed with these comorbidities both preoperatively and postoperatively, suggesting a significant residual risk even after adrenalectomy. The median time of postoperative glucocorticoid replacement therapy was 10.1 months, and the major types of glucocorticoids used were prednisolone (66.6%) and hydrocortisone (22.4%).
Adrenal CS is associated with multiple comorbidities even after treatment, which necessitates meticulous postoperative care.
Adrenal CS is associated with multiple comorbidities even after treatment, which necessitates meticulous postoperative care.
White matter injury (WMI) induced by intrauterine inflammation can cause adverse neurological outcomes. Fibrinogen-like protein 2 (FGL2)/fibroleukin is an important trigger of inflammatory responses and is involved in some cerebral diseases. However, the role of FGL2 in intrauterine inflammation-induced WMI remains unclear.
Lipopolysaccharide (LPS) was intraperitoneally injected into wild-type and FGL2 knockout mice to induce intrauterine inflammation. Body weight and brain weight of offspring were monitored. JH-X-119-01 in vitro Major basic protein (MBP) expression was evaluated to demonstrate the myelination of offspring. To investigate the regulatory mechanism of FGL2, cytokine expression, microglial polarization, and the activation of mitogen-activated protein kinase (MAPK) signaling pathway in the offspring were analyzed.
Upon LPS exposure, FGL2 knockout offspring showed a significant increase in body weight loss. MBP reduction induced by LPS was prevented in FGL2 knockout offspring. Expression levels of proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α, and M1 marker CD86 were suppressed, while the expression levels of anti-inflammatory cytokines IL-10 and M2 marker CD206 were increased.JH-X-119-01 in vitro
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