Lower-grade glioma (LGG) is a crucial pathological type of glioma. Prokineticins have not been reported in LGG. Prokineticins as a member of the multifunctional chemokine-like peptide family are divided into two ligands: PROK1 and PROK2. We evaluated the role of PROK1 and PROK2 in LGG using TCGA database. We downloaded the datasets of LGG from TCGA and evaluated the influence of prokineticins on LGG survival by survival module. Correlations between clinical information and prokineticins expression were analyzed using logistic regression. Univariable survival and multivariate Cox analysis was used to compare several clinical characteristics with survival. Correlation between prokineticins and cancer immune infiltrates was explored using CIBERSORT and correlation module of GEPIA. We analyzed genes of PROK1 and PROK2 affecting LGG, screened differentially expressed genes (DEGs), interacted protein-protein with DEGs through the STRING website, then imported the results into the Cytospace software, and calculated the hub genes. To analyze whether hub genes and prokineticins are related, the relationship between PROK1 and PROK2 and hub genes was assessed and shown by heat map. In addition, gene set enrichment analysis (GSEA) was performed using the TCGA dataset. The univariate analysis using logistic regression and PROK1 and PROK2 showed opposite expression differences between tumor and normal tissues ( p < 0.05 ). PRO1 and PROK2 expressions showed significant differences in tumor grade, age, Iiscitrate DeHydrogenase (IDH) status, histological type, and 1P/19q codeletion. Multivariate analysis revealed that the up-regulated PROK1 and PROK2 expression is an independent prognostic factor for bad prognosis. Specifically, prokineticin expression level has significant correlations with infiltrating levels of Th1 cells, NK CD 56bright cells, and Mast cells in LGG. We screened 21 DEGs and obtained 5 hub genes (HOXC10, HOXD13, SOX4, GATA4, HOXA9). GSEA-identified FCMR activation, creation of C4 and C2 activators, and CD22-mediated BCR regulation in gene ontology (GO) were differentially enriched in high PROK1 and PROK2 expression phenotype pathway, cytoplasmic ribosomal proteins, and ribosome and were differentially enriched in the low PROK1 and PROK2 expression phenotype pathway. Prokineticins are a prognostic biomarker and the correlation between hub genes and LGG requires further attention.
Background Osteoarthritis (OA) is the most common type of arthritis. OA can cause joint pain, stiffness, and loss of function. The pathogenesis of OA is not completely clear. Moreover, there is no effective treatment, and clinical management is limited to symptomatic relief or joint surgery. This study utilized bioinformatics to analyze normal and OA articular cartilage samples to find biomarkers and therapeutic targets for OA. Methods The GSE169077 gene chip dataset was downloaded from the public gene chip data platform of the National Biotechnology Information Center. The dataset included 6 samples of OA tissues and 5 samples of healthy cartilage tissues. Differentially expressed genes (DEGs) were screened using the R language “limma” function package under the threshold of log 2 [fold change (FC)] ≥2 and a P value <0.05. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) signal pathways of the target genes were enriched and analyzed using the database for annotation, visualization, and integrated discovery (DAVID), and a protein-protein interaction (PPI) network was further constructed using the search tool for the retrieval of interacting genes/proteins (STRING) database. The coexpression relationship of the genes in the module was visualized and screened with Cytoscape. Results A total of 27 DEGs were identified, including 9 downregulated genes and 18 upregulated genes. GO signal pathway enrichment analysis showed involvement in hypoxic response, fibrous collagen trimer, and extracellular matrix structural components. KEGG analysis demonstrated associations with protein digestion and absorption, extracellular matrix receptor interaction, and the peroxisome proliferator-activated receptor signal pathway, among several other pathways. A PPI network was obtained through STRING analysis, and the results were imported into Cytoscape software. The 27 DEGs were sequenced by the cytoHubba plug-in by various calculation methods, and 5 hub genes ( COL1A1, COL1A2, POSTN, BMP1 , and MMP13 ) were finally selected. These genes were analyzed by PPI again and annotated with GO and KEGG in different colors. Conclusions Bioinformatics technology effectively identified differential genes in the knee cartilage tissue of healthy controls and patients with OA, providing opportunities to further explore the mechanism and treatment of OA on a transcriptional level.
We report a case of a Chinese man who developed retroperitoneal haemorrhage almost 1 year after surgery for pelvic fracture (1). To the best of our knowledge, this type of delayed haemorrhaging is rarely observed in clinical practice. We also review the literature to identify the common causes of retroperitoneal haemorrhage in patients undergoing surgery for pelvic fracture and to examine the aetiology of this case.
Neurogenic lower urinary tract dysfunction is a common symptom after spinal cord injury. Here, the case of a 45-year-old male patient who was treated with indwelling urinary catheter during spinal surgery for a fall fracture injury of the T12 thoracic vertebra, associated with decreased muscle strength of both lower extremities, is described. During hospitalization in the rehabilitation department, conventional anticoagulation therapy was administered, and the urinary catheter was removed with the patient urinating by increasing abdominal pressure. At 8 days following urinary catheter removal, the patient was found to have a slight subconjunctival haemorrhage of the left eye, which gradually developed into massive subconjunctival haemorrhage in both eyes. After re-indwelling the urinary catheter, the bilateral subconjunctival haemorrhage gradually improved. No abnormal indicators were found during re-examination of coagulation function and platelet count, and the results of ophthalmological examination were normal. For patients with neurogenic bladder dysfunction associated with spinal cord injury, the risk of bleeding during the anticoagulation period should be carefully assessed to eliminate possible underlying bleeding risk factors (including past medical history and appropriate use of anticoagulant drugs) when considering spontaneous urination through the mode of abdominal pressure.
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