Mchughdalby6487

BACKGROUND Due to its eloquent location and potentially devastating neurological consequences, the management of brainstem cavernous malformations (CCMs) attracts considerable debate. There is currently a paucity of Level 1 evidence for their management. The aim of this literature review is to explore the current evidence on the risk-benefit profile of different management options. METHODS A systemic literature search, following the PRISMA algorithm was performed on publications between 2010 and 2018 using the Pubmed database, with the relevant keywords. Only English articles were included. Articles focusing on spinal CCMs and studies with less than 30 participants were excluded. RESULTS A total of 222 search results were reviewed and after removal of duplicates and screening of abstracts, 28 clinical papers comprising 30 or more brainstem CCM cases were included in the study. The heterogeneity of the publications precluded a formal meta-analysis of results. The general consensus is that for CCMs presenting with severe symptoms and/or multiple haemorrhages that reach an accessible pial surface, surgery is considered to be the gold-standard treatment, with some authors suggesting the optimal timing to be within two to six weeks of ictus. For those patients with multiple, deep-seated CCM related haemorrhages that do not reach the pial surface, stereotactic radiosurgery (SRS) can be considered. Conservative treatment is generally considered in incidental cases. Management of brainstem cavernomas of other categories still remains controversial. CONCLUSIONS Due to their highly eloquent location, brainstem CCMs are challenging lesions to manage. Management must be balanced by the risk-benefit profile and tailored to the individual patients and their treating clinicians. This review provides a comprehensive reference considering all treatment options and provides a basis for evidence-based patient counselling. Liraglutide Concomitant treatment with deferoxamine (DFO) protects neural cells from iron and heme-mediated oxidative injury, but also disrupts cell responses to iron loading that may be protective. We hypothesized that DFO treatment and withdrawal would subsequently increase neuronal vulnerability to hemoglobin. Pretreatment with DFO followed by its washout increased neuronal loss after subsequent hemoglobin exposure by 3-4-fold compared with control vehicle-pretreated cultures. This was associated with reduced ferritin induction by hemoglobin; expression of heme oxygenase-1, which catalyzes iron release from heme, was not altered. Increased neuronal loss was prevented by exogenous apoferritin or by continuing DFO or antioxidants throughout the experimental course. Cell nonheme iron levels after hemoglobin treatment were similar in DFO-pretreated and control cultures. These results indicate that DFO deconditions neurons and subsequently increases their vulnerability to heme-mediated injury. Its net effect after CNS hemorrhage may be highly dependent on the timing and duration of its administration. Withdrawal of DFO while heme or iron levels remain elevated may be deleterious, and may negate any benefit of prior concomitant therapy. Autophagy is an intracellular degradation pathway that is highly conserved during the evolution of eukaryotes and is based on lysosome. Under nutritional deficiencies or stress, cells can clear damaged and necrotic organelles and proteins through autophagy to maintain the homeostasis of cells and organisms. Studies have found that abnormal autophagy is closely related to the occurrence and development of neurodegenerative diseases and tumors. In order to further understand the relationship between lysosomes and autophagy, tumorigenesis and drug resistance, the role of autophagy-lysosomal pathway in tumor resistance and related mechanisms and the relationship between drug resistance and hypoxia-induced autophagy are discussed in this paper. Pluripotent cells transiently develop during peri-implantation embryogenesis and have the capacity to convert into three embryonic lineages. Two typical states of pluripotency, naïve and primed, can be experimentally induced in vitro. The in vitro naïve state can be stabilized in response to environmental inductive cues via a unique transcriptional regulatory program. However, interference with various signaling pathways creates a spectrum of alternative pluripotent cells that display different functions and molecular expression patterns. Similarly, human naïve pluripotent cells can be placed into two main levels - intermediate and bona fide. Here, we discuss several culture conditions that have been used to establish naïve-associated gene regulatory networks in human pluripotent cells. We also describe different transcriptional patterns in various culture systems that are associated with these two levels of human naïve pluripotency. BACKGROUND This study aimed to assess the role of fibrinogen (Fib) to albumin (ALB) ratio (FAR) in ankylosing spondylitis (AS) and its association with disease activity. METHODS 135 AS patients and 76 age - and gender - matched healthy controls were collected in this retrospective study. Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) score was used to divide the AS patients into remission group (BASDAI  less then  4) and active group (BASDAI ≥ 4). The association between FAR and BASDAI was evaluated by Spearman correlation. Receiver operating characteristic (ROC) curve was made to determine the area under curve (AUC) value. The prognostic value of FAR in the AS disease activity was tested by multivariate logistical regression analyses. RESULTS AS patients showed higher FAR levels than the controls (P  less then  0.001). FAR was also increased in active group of AS patients than those in inactive group (P  less then  0.001). Spearman analyses showed that FAR was positively related with BASDAI (r = 0.594, P  less then  0.001) in AS patients. ROC curve analyses revealed that the AUC of FAR was higher than ALB and Fib. In addition, the optimal cutoff value of FAR for AS diagnosis was 78.84, with a specificity of 88.2% and sensitivity of 77.0%. Logistical regression analyses showed that FAR (odds ratio = 13.091, 95% confidence interval 4.686-36.571, P  less then  0.001) was a predictor for AS disease activity. CONCLUSIONS FAR was increased in AS and may act as a novel inflammatory parameter for mirroring disease activity in AS.