Abnormal genes and pathways that drive muscle contracture from brachial plexus injuries: Towards machine learning approach.

In order to clarify the pathways closely linked to denervated muscle contracture, this work uses IoMT-enabled healthcare stratergies to examine changes in gene expression patterns inside atrophic muscles following brachial plexus damage. The gene expression Omnibus (GEO) database searching was used to locate the dataset GSE137606, which is connected to brachial plexus injuries. Strict criteria (|logFC|≥2 & adj.p < 0.05) were used to extract differentially expressed genes (DEGs). To identify dysregulated activities and pathways in denervated muscles, gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and Gene Set Enrichment Analysis (GSEA) were used. Hub genes were found using Cytoscape software's algorithms, which took into account parameters like as proximity, degree, and MNC. Their expression, enriched pathways, and correlations were then examined. The results showed that 316 DEGs were predominantly concentrated in muscle-related processes such as tissue formation and contraction pathways. Of these, 297 DEGs were highly expressed in denervated muscles, whereas 19 DEGs were weakly expressed. GSEA showed improvements in the contraction of striated and skeletal muscles. In addition, it was shown that in denervated muscles, Myod1, Myog, Myh7, Myl2, Tnnt2, and Tnni1 were elevated hub genes with enriched pathways such adrenergic signaling and tight junction. These results point to possible therapeutic targets for denervated muscular contracture, including Myod1, Myog, Myh7, Myl2, Tnnt2, and Tnni1. This highlights treatment options for this ailment which enhances the mental state of patient.

Three-Dimensional Printing to Guide Fenestrated/Branched TEVAR in Triple Aortic Arch Branch Reconstruction With a Curative Effect Analysis.

PURPOSE: To summarize experience with and the efficacy of fenestrated/branched thoracic endovascular repair (F/B-TEVAR) using physician-modified stent-grafts (PMSGs) under 3D printing guidance in triple aortic arch branch reconstruction. MATERIALS AND METHODS: From February 2018 to April 2022, 14 cases of aortic arch aneurysms and 30 cases of aortic arch dissection (22 acute aortic arch dissection and 8 long-term aortic arch dissection)were treated by F/B-TEVAR in our department, including 34 males and 10 females, with an average age of 59.84 ± 11.72 years. Three aortic arch branches were affected in all patients. A 3D-printed model was made according to computed tomography angiography images and used to guide the fabrication of PMSGs. All patients were followed up. RESULTS: A total of 132 branches were successfully reconstructed with no case of conversion to open surgery. The average operation time was 4.97 ± 1.40 hours, including a mean 44.05 ± 7.72 minutes for stent-graft customization, the mean postoperative hospitalization duration was 9.91 ± 4.47 days, the average intraoperative blood loss was 480.91 mL (100-2810 mL), and the mean postoperative intensive care unit monitoring duration was 1.02 days (0-5 days). No deaths occurred within 30 days of surgery. Postoperative neurological complications occurred in 1 case (2.3%), and retrograde type A dissection occurred in 1 case (2.3%). CONCLUSION: Compared with conventional surgery, triple aortic arch branch reconstruction under the guidance of 3D printing is a minimally invasive treatment method with the advantages of accurate positioning, rapid postoperative recovery, few complications, and reliable short- to mid-term effects. CLINICAL IMPACT: At present the PMSG usually depend on imaging data and software calculation. With the guidance of 3D printing technology, image data could be transformed into 3D model, which has improved the accuracy of the positioning of the fenestrations. The diameter reduction technique and the internal mini cuff technique have made a complement to the slimed-down fenestration selection process and the low rate of endoleak. As reproducible study, our results may provide reference for TEVAR in different cases.

Molecular Etiology in Thumb Polydactyly in Mutated GLI3 Mouse Gene.

Sporadic thumb polydactyly with nonfamily inheritance is the most common in clinical work. This study focused on characterization of GLI3 gene function. We constructed the plasmid with p.m948i point mutation of GLI3 and transfected it into mouse embryonic fibroblasts (MEFs) to study the effects and potential mechanism of the mutant gene. The RNA of GLI3 mutant cells was extracted and analyzed by transcriptome sequencing and bioinformatics. Finally, we constructed cbx3 overexpression plasmid, designed siRNA for gene silencing, and transfected it into the MEFs. Cell proliferation and invasion ability of the MEFs were examined. The results showed that there were 2,452 differential expression genes in the MEFs transfected with GLI3 mutant plasmid compared with wild-type MEFs. The results of differential expression analysis showed that the cbx3 gene was significantly up-regulated. Overexpression of cbx3 in MEFs promoted cell proliferation and invasion, while siRNA knockdown of cbx3 expression reduced proliferation and invasion. GLI3 gene mutation in MEFs resulted in cbx3 up-regulation and promoted MEF proliferation and invasion. This study further clarified the potential function of GLI3 in limb development, established a new relationship between gene mutation and polydactyly, and preliminarily clarified the possible signal pathway, all of which have laid a foundation for further study on the etiology of polydactyl.

Clinical potential of miRNA-221 as a novel prognostic biomarker for hepatocellular carcinoma.

miRNA-221 is one of the over 700 kinds of currently known microRNAs (miRNAs) and is up-regulated in multiple tumors, suggesting that it may be a potential carcinogenic miRNA. Few studies have explored the relationship between miRNA-221 and hepatocellular carcinoma (HCC). We performed real-time quantitative polymerase chain reaction (qPCR) to detect miRNA-221 expression in HCC and para-carcinoma tissues and to explore the relationship between abnormal expression of miRNA-221 and clinicopathological features of HCC patients. miRNA-221 expression was significantly higher in HCC tissues than in adjacent tissues (P < 0.001). We analyzed the relationship between miRNA-221 expression level and clinicopathological characteristics of HCC patients. Our results suggested that miRNA-221 expression level was closely related to tumor stage (P = 0.012), number of tumor nodes (P = 0.018), and microvascular invasion (P = 0.010) in HCC patients. The results of survival analysis suggested that HCC patients with up-regulated miRNA-221 expression had a shorter survival time. The high miRNA-221 expression indicates the poor prognosis of HCC patients; thus, miRNA-221 can be regarded an important molecular marker for HCC prognosis.