Chandlervaughn0361

In contrast, guanine nucleotide-binding protein G(s) subunit alpha (GNAS) and G protein-coupled receptor 101 (GPR101) mutations can lead to excess growth hormone. Moreover, the deubiquitinase gene USP8, USP48, and BRAF mutations are associated with adrenocorticotropic hormone production. In this review, we describe the genetic and epigenetic landscape of PAs and summarize novel insights into the regulation of pituitary tumorigenesis.Introduction It has been proposed that seizures induce IL-1β biosynthesis in astrocytes and increase blood brain barrier (BBB) permeability, even without the presence of blood borne inflammatory molecules and leukocytes. In the present study we investigate if seizures induce morphological changes typically observed in activated glial cells. Moreover, we will test if serum albumin extravasation into the brain parenchyma exacerbates neuronal hyperexcitability by inducing astrocytic and microglial activation. Methods Epileptiform seizure-like events (SLEs) were induced in limbic regions by arterial perfusion of bicuculline methiodide (BMI; 50 μM) in the in vitro isolated guinea pig brain preparation. Field potentials were recorded in both the hippocampal CA1 region and the medial entorhinal cortex. BBB permeability changes were assessed by analyzing extravasation of arterially perfused fluorescein isothiocyanate (FITC)-albumin. Morphological changes in astrocytes and microglia were evaluated with tridimensional reconstruction and Sholl analysis in the ventral CA1 area of the hippocampus following application of BMI with or without co-perfusion of human serum albumin. Results BMI-induced SLE promoted morphological changes of both astrocytes and microglia cells into an activated phenotype, confirmed by the quantification of the number and length of their processes. Human-recombinant albumin extravasation, due to SLE-induced BBB impairment, worsened both SLE duration and the activated glia phenotype. Discussion Our study provides the first direct evidence that SLE activity per se is able to promote the activation of astro- and microglial cells, as observed by their changes in phenotype, in brain regions involved in seizure generation; we also hypothesize that gliosis, significantly intensified by h-recombinant albumin extravasation from the bloodstream to the brain parenchyma due to SLE-induced BBB disruption, is responsible for seizure activity reinforcement.Background Brainstem cavernous malformations (BSCMs) are a subset of cerebral cavernous malformations with precarious locations and potentially devastating clinical courses. The effects and outcomes of treating BSCMs by microsurgery or gamma knife radiosurgery (GKRS) vary across studies. Methods We searched the Medline, Web of Science, The Cochrane Library, PubMed, and China Biology Medicine disc databases for original articles published in peer-reviewed journals of cohort studies reporting on 20 or more patients of any age with BSCMs with at least 80% completeness of follow-up. Results We included 43 cohorts involving 2,492 patients. Both microsurgery (RR = 0.04, 95% CI 0.01-0.16, P less then 0.01) and GKRS (RR = 0.11, 95% CI 0.08-0.16, P less then 0.01) demonstrated great efficacy in reducing the rehemorrhage rate after treatment for BSCMs. The incidence rates of composite outcomes were 19.8 (95% CI 16.8-22.8) and 15.7 (95% CI 11.7-19.6) after neurosurgery and radiosurgery, respectively. In addition, we found statistically significant differences in the median numbers of patients between neurosurgical and radiosurgical cohorts in terms of symptomatic intracranial hemorrhage (ICH; neurosurgical cohorts median 0, range 0-33; radiosurgical cohorts median 4, range 1-14; P less then 0.05) and persistent focal neurological deficit (FND; neurosurgical cohorts median 5, range 0-140; radiosurgical cohorts median 1, range 0-3; P less then 0.05). Conclusions The reported effects of treating BSCMs by microsurgery or GKRS are favorable for reducing recurrent hemorrhage from BSCMs. Patients in the neurosurgery cohort had a lower incidence of symptomatic ICH, while patients in the radiosurgical cohort had a lower incidence of persistent FND.Background For patients with symptomatic intracranial artery stenosis (sICAS), endovascular treatment has been shown to be feasible and safe in recent studies. However, in-stent restenosis (ISR) risks the recurrence of ischemic stroke. We attempt to elucidate the risk factors for ISR. Methods We retrospectively analyzed 97 patients with sICAS from a prospective registry trial that included 20 centers from September 2013 to January 2015. Cases were classified into the ISR≥ 50% group or the ISR less then 50% group. The baseline characteristics and long-term follow-up were compared between the two groups. Binary logistic regression analyses were identified as an association between ISR and endovascular technique factors. Results According to whether ISR was detected by CT angiography, 97 patients were divided into the ISR group (n = 24) and the non-ISR group (n = 73). The admission baseline features and lesion angiography characteristics were similar, while plasma hs-CRP (mg/L) was higher in the ISR≥ 50% group at admission (8.2 ± 11.4 vs. 2.8 ± 4.1, p = 0.032). Binary logistic regression analysis identified the longer stents (adjusted OR 0.816, 95% CI 0.699-0.953; p = 0.010), balloon-mounted stents (adjusted OR 5.748, 95% CI 1.533-21.546; p = 0.009), and local anesthesia (adjusted OR 6.000, 95% CI 1.693-21.262; p = 0.006) as predictors of ISR at the 1-year follow-up. Conclusions The longer stents, balloon-mounted stents implanted in the intracranial vertebral or basilar artery, and local anesthesia were significantly associated with in-stent restenosis. learn more Further studies are required to identify accurate biomarkers or image markers associated with ISR in ICAS patients. Clinical Trial Registration www.ClinicalTrials.gov, identifier NCT01968122.

Post-traumatic stress disorder (PTSD) is a prevalent, debilitating, and costly psychiatric disorder. Evidenced-based psychotherapies, including Cognitive Processing Therapy (CPT), are effective in treating PTSD, although a fair proportion of individuals show limited benefit from such treatments. CPT requires cognitive demands such as encoding, recalling, and implementing new information, resulting in behavioral change that may improve PTSD symptoms. Individuals with PTSD show worse cognitive functioning than those without PTSD, particularly in acquisition of verbal memory. Therefore, memory dysfunction may limit treatment gains in CPT in some individuals with PTSD.

Here, we present a protocol describing the Cognition and PsychoTherapy in PTSD (CPTPTSD) study, a prospective, observational study examining how cognitive functioning affects treatment response in CPT for PTSD (NCT# 03641924). The study aims to recruit 105 outpatient veterans with PTSD between the ages of 18 and 70 years. Prior to beginning 12 sessions of CPT, Veteran participants will have standardized assessments of mood and functioning and complete a comprehensive neurocognitive battery assessing episodic learning, attention and speed of processing, language ability, executive control, and emotional functioning.