Douglashendricks0504

Conjunctival congestion has been reported as the most common ophthalmic manifestation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, affecting 18.4%-31.6% of patients with corona virus disease 2019 (COVID-19). Orbital inflammatory disease has been rarely reported in association with COVID-19 infection, with only 2 case reports of adolescent patients having been recently published. We present a unique case of orbital myositis in a 10-year-old boy who tested positive for SARS-CoV-2 infection in the absence of typical systemic COVID-19 manifestations. Although it is uncertain whether SARS-CoV-2 infection triggered the inflammation or was coincidental, the possible association of the events is concerning.

To formally assess the content, intent, and authorship of the most popular Instagram hashtags related to pediatric ophthalmology.

Public Instagram posts with over 20 likes, using one or more of 6 vision therapy (VT) hashtags and containing English content were identified. A categorical classification system was used to analyze each post for the target audience post owner, primary intent of post, diagnosis addressed, whether advice was provided, and whether references to studies were provided.

A total of 1,766 Instagram posts were analyzed. Half were made by VT clinics or therapists (50%), and only 14 posts were made by physicians (0.8%). The majority were self-promotional. Statistically significant relationships between post owner and intent, post owner and diagnosis, and the provision of advice and diagnosis were found.

Although VT Instagram posts are dominated by self-promotion and advertisements, social media provides an outlet for patients and parents to seek support and information. Ophthalmologists have yet to discuss VT on Instagram.

Although VT Instagram posts are dominated by self-promotion and advertisements, social media provides an outlet for patients and parents to seek support and information. Ophthalmologists have yet to discuss VT on Instagram.

Pharmacologic agents targeting bile acid signaling show promise for treating nonalcoholic steatohepatitis (NASH). However, clinical findings suggest that new treatment strategies with enhanced therapeutic efficacy and minimized undesired effects are needed. This preclinical study investigates whether combining an apical sodium-bile acid transporter (ASBT) inhibitor GSK233072 (GSK672) and fibroblast growth factor-15 (FGF15) signaling activation improves anti-NASH efficacy.

Mice with high fat, cholesterol, and fructose (HFCFr) diet-induced NASH and stage 2 fibrosis are used as a NASH model. GSK672 or AAV8-TBG-FGF15 interventions are administered alone or in combination to HFCFr diet-fed mice.

The combined treatment significantly enhances therapeutic efficacy against steatosis, inflammation, ballooning, and fibrosis than either single treatment. Mechanistically, the synergistic actions of GSK672 and FGF15 on inhibiting gut bile acid reuptake and hepatic bile acid synthesis achieve greater magnitude of bileGF15 signaling activation produce metabolic changes that partially mimic the bariatric surgery condition whereby lipid malabsorption and increased FGF15/19 signaling synergistically mediate weight loss and metabolic improvement. Further clinical studies may be warranted to investigate whether combining ASBT inhibitor and FGF19 analogue enhances anti-NASH efficacy and reduced treatment-associated adverse events in humans.Cathelicidins are an important antimicrobial peptide family and are expressed in many different vertebrates. They play an important role in the innate immune system of the host. However, amphibian cathelicidins are poorly understood. In this study, the cDNA of the cathelicidin gene was obtained from the skin transcriptome of tiger frog (Hoplobatrachus rugulosus). The predicted amino acid sequence of tiger frog cathelicidin (HR-CATH) comprises a signal peptide, a cathelin domain, and a mature peptide. Epigenetics inhibitor The HR-CATH amino acid sequence alignment with other frog cathelicidins showed that the functional mature peptide is highly variable in amphibians, whereas the cathelin domain is conserved. A phylogenetic tree analysis showed that HR-CATH is most closely related to cathelicidin-NV from Nanorana ventripunctata. HR-CATH was chemically synthesized and its in vitro activity was determined. It had high antibacterial activity against Vibrio parahaemolyticus, Staphylococcus aureus, and the pathogenic bacterium Aeromonas hydrophila. HR-CATH damaged the cell membrane integrity of A. hydrophila according to a lactate dehydrogenase release assay and was able to hydrolyze the genomic DNA from A. hydrophila in a dose-dependent manner. Furthermore, in RAW264.7 cells (mouse leukemic monocyte/macrophage cell line), HR-CATH induced chemotaxis and enhanced respiratory burst. Our study shows that amphibian cathelicidin has antimicrobial activity and an immunomodulatory effect on immune cells.This cross-cohort study aimed to (1) determine a network-based molecular signature that predicts the likelihood of inadequate response to the tumor necrosis factor-ɑ inhibitor (TNFi) therapy, infliximab, in ulcerative colitis (UC) patients and (2) address biomarker irreproducibility across different cohort studies. Whole-transcriptome microarray data were derived from biopsies of affected colon tissue from 2 cohorts of infliximab-treated UC patients (training N = 24 and validation N = 22). Response was defined as endoscopic and histologic healing at 4-6 weeks and 8 weeks, respectively. From the training cohort, genes with RNA expression that significantly correlated with clinical response outcomes were mapped onto the Human Interactome network map of protein-protein interactions to identify a largest connected component (LCC) of proteins indicative of infliximab response status in UC. Expression levels of transcripts within the LCC were fed into a probabilistic neural network model to generate a classifier that predicts inadequate response to infliximab. A classifier predictive of inadequate response to infliximab was generated and tested in a cross-cohort, blinded fashion; the AUC was 0.85 and inadequate response was predicted with a 90% positive predictive value and 82% sensitivity. Genes separately identified from the 2 cohorts that correlated with response to infliximab appeared distinct but mapped onto the same network region of the Human Interactome, reflecting a common underlying biology of response among UC patients. Cross-cohort validation of a classifier predictive of infliximab response status in UC patients indicates that a molecular signature of non-response to TNFi therapies is present in patients' baseline gene expression data. The goal is to develop a diagnostic test that predicts which patients will have an inadequate response to targeted therapies and define new targets and pathways for therapeutic development.