Singhberg0745

Regular follow-up of spontaneously arrested congenital glaucoma and scleral fixation of intraocular lens is recommended.

Attention-deficit hyperactivity disorder is one of the public neurodevelopmental disorders characterized by impulsivity and restlessness or hyperactivity. This study aimed to assess the prevalence of Attention-deficit hyperactivity disorder and its associated factors among children aged 6 to 17 years in Shewa Robit town, Northeastern Ethiopia, 2020.

A community-based cross-sectional study was conducted among 365 children aged 6-17 years from Feb 1-March 30, 2020, at Shewa Robit town. Systematic random sampling was employed to select study participants. Data were collected by interview using structured and pretested questionnaires. Finally, data was entered using Epi-data 4.2 and analyzed using SPSS version 25. Bivariable and multivariable binary logistic regression analysis was conducted to identify associated factors of attention deficit hyperactivity disorder. Odds ratios with 95% CI were calculated, and variables having a p-value < 0.05 were considered statistically significant.

The prevalence of ficant factors.

Overutilization of advanced diagnostic imaging modalities strains health care systems, especially in resource limited setups. The aim of this study is to identify magnitude of inappropriate Head Computed Tomography scans at Tikur Anbessa Specialized Hospital.

Retrospective cross-sectional study was conducted at Tikur Anbessa Specialized Hospital, Radiology department, among patients getting Head Computed Tomography examinations in the period of August 2018- November 2018. Appropriateness of each scan was assessed using the American College of Radiology Appropriateness Criteria.

Of the 443 Head Computed Tomography scans assessed, 61.6% were done for male patients and the mean age of patients scanned is 35. Children younger than 14yrs of age constituted 17.2%. https://www.selleckchem.com/products/gsk2982772.html No contrast was used in 63.9% of the scans and 64.3% were initial imaging with no prior study for similar indication. Out of the scans evaluated, 11.7% were inappropriate. Headache (38.5%), Seizure (23.1%) and Head trauma (23.1%) were the commonest g appropriateness guidelines should be implemented.Cardiovascular disease (CVD) is still the leading cause of death globally, and atherosclerosis is the main pathological basis of CVDs. Low-density lipoprotein cholesterol (LDL-C) is a strong causal factor of atherosclerosis. However, the first-line lipid-lowering drugs, statins, only reduce approximately 30% of the CVD risk. Of note, atherosclerotic CVD (ASCVD) cannot be eliminated in a great number of patients even their LDL-C levels meet the recommended clinical goals. Previously, whether the elevated plasma level of triglyceride is causally associated with ASCVD has been controversial. Recent genetic and epidemiological studies have demonstrated that triglyceride and triglyceride-rich lipoprotein (TGRL) are the main causal risk factors of the residual ASCVD. TGRLs and their metabolites can promote atherosclerosis via modulating inflammation, oxidative stress, and formation of foam cells. In this article, we will make a short review of TG and TGRL metabolism, display evidence of association between TG and ASCVD, summarize the atherogenic factors of TGRLs and their metabolites, and discuss the current findings and advances in TG-lowering therapies. This review provides information useful for the researchers in the field of CVD as well as for pharmacologists and clinicians.Breast cancer is the most common cause of cancer death among women worldwide. Localized breast cancer can be cured by surgery and adjuvant therapy, but mortality remains high for tumors that metastasize early. Type IV collagen is a basement membrane protein, and breach of this extracellular matrix structure is the first step of cancer invasion. Type IV collagen is found in the stroma of many cancers, but its role in tumor biology is unclear. Here, expression of type IV collagen in the stroma of small breast cancers was analyzed, correlated to clinically used prognostic biomarkers and patient survival. The findings were further validated in an independent gene expression data cohort. Tissue samples from 1,379 women with in situ and small invasive breast cancers (≤15 mm) diagnosed in 1986-2004 were included. Primary tumor tissue was collected into tissue microarrays. Type IV collagen expression in tissues was visualized using immunohistochemistry. Gene expression data was extracted from the Cancer Genome Atlas database. Out of 1,379 women, 856 had an invasive breast cancer and type IV collagen staining was available for 714 patients. In Kaplan-Meier analysis high type IV collagen expression was significantly associated (p = 0.026) with poorer breast cancer specific survival. There was no correlation of type IV collagen expression to clinically used prognostic biomarkers. High type IV collagen expression was clearly associated to distant metastasis (p = 0.002). In an external validation cohort (n = 1,104), high type IV collagen mRNA expression was significantly (p = 0.041) associated with poorer overall survival, with overexpression of type IV collagen mRNA in metastatic tissue. Stromal type IV collagen expression in the primary tumor correlates to poor breast cancer specific survival most likely due to a higher risk of developing distant metastasis. This ECM protein may function as biomarker to predict the risk of future metastatic disease in patients with breast cancers.Background Adrenocortical carcinoma (ACC) is an orphan tumor which has poor prognoses. Therefore, it is of urgent need for us to find candidate prognostic biomarkers and provide clinicians with an accurate method for survival prediction of ACC via bioinformatics and machine learning methods. Methods Eight different methods including differentially expressed gene (DEG) analysis, weighted correlation network analysis (WGCNA), protein-protein interaction (PPI) network construction, survival analysis, expression level comparison, receiver operating characteristic (ROC) analysis, and decision curve analysis (DCA) were used to identify potential prognostic biomarkers for ACC via seven independent datasets. Linear discriminant analysis (LDA), K-nearest neighbor (KNN), support vector machine (SVM), and time-dependent ROC were performed to further identify meaningful prognostic biomarkers (MPBs). Cox regression analyses were performed to screen factors for nomogram construction. Results We identified nine hub genes correlated to prognosis of patients with ACC. Furthermore, four MPBs (ASPM, BIRC5, CCNB2, and CDK1) with high accuracy of survival prediction were screened out, which were enriched in the cell cycle. We also found that mutations and copy number variants of these MPBs were associated with overall survival (OS) of ACC patients. Moreover, MPB expressions were associated with immune infiltration level. Two nomograms [OS-nomogram and disease-free survival (DFS)-nomogram] were established, which could provide clinicians with an accurate, quick, and visualized method for survival prediction. Conclusion Four novel MPBs were identified and two nomograms were constructed, which might constitute a breakthrough in treatment and prognosis prediction of patients with ACC.Barth syndrome (BTHS, OMIM 302060) is a genetic disorder caused by variants of the TAFAZZIN gene (G 4.5, OMIM 300394). This debilitating disorder is characterized by cardio- and skeletal myopathy, exercise intolerance, and neutropenia. TAFAZZIN is a transacylase that catalyzes the second step in the cardiolipin (CL) remodeling pathway, preferentially converting saturated CL species into unsaturated CLs that are susceptible to oxidation. As a hallmark mitochondrial membrane lipid, CL has been shown to be essential in a myriad of pathways, including oxidative phosphorylation, the electron transport chain, intermediary metabolism, and intrinsic apoptosis. The pathological severity of BTHS varies substantially from one patient to another, even in individuals bearing the same TAFAZZIN variant. The physiological modifier(s) leading to this disparity, along with the exact molecular mechanism linking CL to the various pathologies, remain largely unknown. Elevated levels of reactive oxygen species (ROS) have been identified in numerous BTHS models, ranging from yeast to human cell lines, suggesting that cellular ROS accumulation may participate in the pathogenesis of BTHS. Although the exact mechanism of how oxidative stress leads to pathogenesis is unknown, it is likely that CL oxidation plays an important role. In this review, we outline what is known about CL oxidation and provide a new perspective linking the functional relevance of CL remodeling and oxidation to ROS mitigation in the context of BTHS.Ostreolysin A6 (OlyA6) is a 15 kDa protein produced by the oyster mushroom (Pleurotus ostreatus). It belongs to the aegerolysin family of proteins and binds with high affinity to the insect-specific membrane sphingolipid, ceramide phosphoethanolamine (CPE). In concert with its partnering protein with the membrane-attack-complex/perforin domain, pleurotolysin B (PlyB), OlyA6 can form bicomponent 13-meric transmembrane pores in artificial and biological membranes containing the aegerolysin lipid receptor, CPE. This pore formation is the main underlying molecular mechanism of potent and selective insecticidal activity of OlyA6/PlyB complexes against two economically important coleopteran plant pests the western corn rootworm and the Colorado potato beetle. In contrast to insects, the main sphingolipid in cell membranes of marine invertebrates (i.e., molluscs and cnidarians) is ceramide aminoethylphosphonate (CAEP), a CPE analogue built on a phosphono rather than the usual phosphate group in its polar head. Our targeted lipidomic analyses of the immune cells (hemocytes) of the marine bivalve, the mussel Mytilus galloprovincialis, confirmed the presence of 29.0 mol% CAEP followed by 36.4 mol% of phosphatidylcholine and 34.6 mol% of phosphatidylethanolamine. Further experiments showed the potent binding of OlyA6 to artificial lipid vesicles supplemented with mussel CAEP, and strong lysis of these vesicles by the OlyA6/PlyB mixture. In Mytilus haemocytes, short term exposure (max. 1 h) to the OlyA6/PlyB mixture induced lysosomal membrane destabilization, decreased phagocytic activity, increased Annexin V binding and oxyradical production, and decreased levels of reduced glutathione, indicating rapid damage of endo-lysosomal and plasma membranes and oxidative stress. Our data suggest CAEP as a novel high-affinity receptor for OlyA6 and a target for cytolytic OlyA6/PlyB complexes.In recent years, variants in the catalytic and regulatory subunits of the kinase CK2 have been found to underlie two different, yet symptomatically overlapping neurodevelopmental disorders, termed Okur-Chung neurodevelopmental syndrome (OCNDS) and Poirier-Bienvenu neurodevelopmental syndrome (POBINDS). Both conditions are predominantly caused by de novo missense or nonsense mono-allelic variants. They are characterized by a generalized developmental delay, intellectual disability, behavioral problems (hyperactivity, repetitive movements and social interaction deficits), hypotonia, motricity and verbalization deficits. One of the main features of POBINDS is epilepsies, which are present with much lower prevalence in patients with OCNDS. While a role for CK2 in brain functioning and development is well acknowledged, these findings for the first time clearly link CK2 to defined brain disorders. Our review will bring together patient data for both syndromes, aiming to link symptoms with genotypes, and to rationalize the symptoms through known cellular functions of CK2 that have been identified in preclinical and biochemical contexts.