Endoscopic microvascular decompression versus microscopic microvascular decompression for trigeminal neuralgia: A systematic review and meta-analysis.

BACKGROUND: To compare the efficacy and safety of full endoscopic or endoscope-assisted microvascular decompression (E-MVD) and microscopic microvascular decompression (M-MVD) for primary trigeminal neuralgia (TN). METHODS: We systematically searched the online database, including PubMed, Embase and Cochrane Library. The search terms used included, but were not limited to, "Trigeminal Neuralgia", "Microvascular Decompression Surgery" and "Endoscope". Postoperative facial pain relief and postoperative complications were considered for meta-analysis. All the outcomes were calculated as odds ratios (ORs) with 95% confidence intervals using R language. RESULTS: A total of three studies involving 442 (E-MVD [218] versus M-MVD [224]) patients were included for analysis in our study. Postoperative facial pain relief (very much improved or much improved) was no difference between the two groups (OR, 0.95;95% CI, 0.57-1.58; I2 = 0%; p = 0.83). In addition, the occurrence of some postoperative complications was not statistically different between the two groups, including CSFleak (OR, 1.35;95% CI, 0.16-11.13; I2 = 0%; p = 0.94), facial paralysis (OR, 0.26;95% CI, 0.03-2.54; I2 = 0%; p = 0.67), hearing loss (OR, 0.87;95% CI, 0.30-2.55; I2 = 32%; p = 0.22), facial numbness (OR, 1.03;95% CI, 0.56-1.87; I2 = 62%; p = 0.10). CONCLUSIONS: Both endoscopic microvascular decompression and microscopic microvascular decompression for trigeminal neuralgia appear to provide patients with equivalent facial pain relief outcomes. Complication rates were also similar between the groups.

Identification of hub genes and biological pathways in glioma via integrated bioinformatics analysis.

OBJECTIVE: Glioma is the most common intracranial primary malignancy, but its pathogenesis remains unclear. METHODS: We integrated four eligible glioma microarray datasets from the gene expression omnibus database using the robust rank aggregation method to identify a group of significantly differently expressed genes (DEGs) between glioma and normal samples. We used these DEGs to explore key genes closely associated with glioma survival through weighted gene co-expression network analysis. We then constructed validations of prognosis and survival analyses for the key genes via multiple databases. We also explored their potential biological functions using gene set enrichment analysis (GSEA) and gene set variation analysis (GSVA). RESULTS: We selected DLGAP5, CDCA8, NCAPH, and CCNB2, as four genes that were abnormally up-regulated in glioma samples, for verification. They showed high levels of isocitrate dehydrogenase gene mutation and tumor grades, as well as good prognostic and diagnostic value for glioma. Their methylation levels were generally lower in glioma samples. GSEA and GSVA analyses suggested the genes were closely involved with glioma proliferation. CONCLUSION: These findings provide new insights into the pathogenesis of glioma. The hub genes have the potential to be used as diagnostic and therapeutic markers.

Mutation in NPPA causes atrial fibrillation by activating inflammation and cardiac fibrosis in a knock-in rat model.

Atrial fibrillation (AF) affects >30 million individuals worldwide. However, no genetic mutation from human patients with AF has been linked to inflammation. Here, we show that AF-associated human variant p.Ile138Thr in natriuretic peptide A (NPPA) encoding the atrial natriuretic peptide (ANP) causes inflammation, fibroblast activation, atrial fibrosis, and AF in knock-in (KI) rats. Variant p.Ile138Thr inhibits the interaction between ANP and its receptor natriuretic peptide receptor A and reduces intracellular cGMP levels. RNA sequencing and follow-up analyses showed that mutant ANP (mANP) activates multiple innate immunity pathways, including TNF-α, NF-κB, and IL-1ß signaling. mANP induces differentiation of cardiac fibroblasts (CFs) to myofibroblasts and promotes CF proliferation and fibrosis. These results suggest that NPPA variant p.Ile138Thr causes AF by activating TNF-α, NF-κB, and IL-1ß signaling, inflammation, and fibrosis. Multiple computational programs suggest that p.Ile138Thr is damaging or deleterious. Based on the 2015 American College of Medical Genetics and Genomics Standards and Guidelines, p.Ile138Thr can be classified as a likely pathogenic variant. Variant p.Ile138Thr was found only in Asian people in the Genome Aggregation Database and Exome Aggregation Consortium database at an averaged frequency of 0.026%. An estimated 1.15 million Asian people carry the variant and might be at risk of AF. The KI rats may provide an inflammation-based, genetic animal model for AF valuable for testing anti-inflammation or other therapies for AF.-Cheng, C., Liu, H., Tan, C., Tong, D., Zhao, Y., Liu, X., Si, W., Wang, L., Liang, L., Li, J., Wang, C., Chen, Q., Du, Y., Wang, Q. K., Ren, X. Mutation in NPPA causes atrial fibrillation by activating inflammation and cardiac fibrosis in a knock-in rat model.