Long non-coding RNAs correlate with genomic stability in prostate cancer: A clinical outcome and survival analysis.

BACKGROUND: Long non-coding RNAs (lncRNAs) participate in the regulation of genomic stability. Understanding their biological functions can help us identify the mechanisms of the occurrence and progression of cancers and can provide theoretical guidance and the basis for treatment. RESULTS: Based on the mutation hypothesis, we proposed a computational framework to identify genomic instability-related lncRNAs. Based on the differentially-expressed lncRNAs (DElncRNAs), we constructed a genomic instability-derived lncRNA signature (GILncSig) to calculate and stratify outcomes in patients with prostate cancer. It is an independent predictor of overall survival. The area under the curve = 0.805. This value may be more significant than the classic prognostic markers TP53 and Speckle-type POZ protein (SPOP) in terms of outcome prediction. CONCLUSIONS: In summary, we conducted a computation approach and resource for mining genome instability-related lncRNAs. It may turn out to be highly significant for genomic instability and customized decision-making for patients with prostate cancer. It also may lead to effective methods and resources to study the molecular mechanism of genomic instability-related lncRNAs.

TACR2 is associated with the immune microenvironment and inhibits migration and proliferation via the Wnt/ß-catenin signaling pathway in prostate cancer.

BACKGROUND: The tachykinin receptor 2 (TACR2) is encoded by the tachykinin receptor correlation gene. Recent microarray analysis for prostate cancer suggests that TACR2 expression is associated with clinical phenotype and disease-free survival among patients with prostate cancer. RESULTS: TACR2 protein levels were lower in prostate cancer tissues than in adjacent normal prostate tissue. TACR2 expression significantly correlated with clinical stage, Gleason scores, and survival outcomes. TACR2 expression positively correlated with mast cells and negatively correlated with M2 macrophages. Overexpression of TACR2 promoted the migration and proliferation of prostate cancer cells by regulating the Wnt signaling pathway. CONCLUSIONS: The TACR2-Wnt/ß-catenin signaling pathway is critical in prostate cancer. TACR2 may affect tumor cells' occurrence and development by changing the content of immune cells in the tumor microenvironment. These findings suggest that TACR2 may be a candidate molecular biomarker for prostate cancer therapy.

Postoperative Cerebral Embolism After video-assisted thoracoscopic left upper lobectomy : A Case Report and Literature Review.

Postoperative cerebral embolism after left upper or lower lobectomy caused by the thrombus in the pulmonary vein stump (PVS) is a rare complication. However, it is still unclear how the cerebral embolism develop after lobectomy, and how can we prevent further embolism after thrombus removal. We present a case of a 55-year-old man without cardiovascular disease history suffering cerebral embolism 2 days after left upper lobectomy. Patient underwent endovascular thrombectomy and discharged hospital 10 days later with proper recovery. No thrombus was detected in an enhanced pulmonary CT after 1 month of aspirin intake, but the length of PVS was measured.

The Chinese prescription lianhuaqingwen capsule exerts anti-influenza activity through the inhibition of viral propagation and impacts immune function.

BACKGROUND: Lianhuaqingwen Capsule (LH-C) is a traditional Chinese medicine (TCM) formula used to treat respiratory tract infectious diseases in Chinese. The aim of this study was to determine the antiviral activity of LH-C and its immunomodulatory effects on viral infection. METHOD: The in vitro cytotoxicity and antiviral activity of LH-C was determined by MTT and Plaque reduction assays. Time course study under single-cycle virus growth conditions were used to determine which stage of viral replication was blocked. The effect of LH-C on the nuclear export of the viral nucleoprotein was examined using an indirect immunofluorescence assay. The regulation to different signaling transduction events and cytokine/chemokine expression of LH-C was evaluated using Western blotting and real-time RT-PCR. After virus inoculation, BALB/c mice were administered with LH-C of different concentrations for 5 days. Body-weight, viral titers and lung pathology of the mice were measured, the level of inflammatory cytokines were also examined using real-time RT-PCR. RESULTS: LH-C inhibited the proliferation of influenza viruses of various strain in vitro, with the 50% inhibitory concentration (IC50) ranging from 0.35 to 2 mg/mL. LH-C blocked the early stages (0-2 h) of virus infection, it also suppressed virus-induced NF-kB activation and alleviated virus-induced gene expression of IL-6, IL-8, TNF-a, IP-10, and MCP-1 in a dose-dependent manner. LH-C treatment efficiently impaired the nuclear export of the viral RNP. A decrease of the viral titers in the lungs of mice were observed in groups administered with LH-C. The level of inflammatory cytokines were also decreased in the early stages of infection. CONCLUSIONS: LH-C, as a TCM prescription, exerts broad-spectrum effects on a series of influenza viruses, including the newly emerged H7N9, and particularly regulates the immune response of virus infection. Thus, LH-C might be a promising option for treating influenza virus infection.

Nanotechnology-based approaches for antibacterial therapy.

The technique of antimicrobial therapy action is to stop or slow the growth of bacteria that can kill people, animals, and crops. The most widely used antibacterial agents are antibiotics. Even though these antimicrobial medications are quite effective, there are still certain barriers or challenges in using them effectively. To solve these issues, new antimicrobial drug molecules that don't have side effects or resistance are needed. These days, antimicrobial drugs placed in nanosized vehicles, or nanomedicine, made of different metal and metallic oxides as well as of polymer, carbon or lipid-based may be used to address these issues with conventional therapy and delivery techniques. This review focuses on the importance of nanotechnology in antimicrobial therapy, nanoparticles (NPs) used in this therapy, their mode of action, and the recent advancement in nanotechnology for antimicrobial therapy.

Indolethylamine-N-Methyltransferase Inhibits Proliferation and Promotes Apoptosis of Human Prostate Cancer Cells: A Mechanistic Exploration.

Indolethylamine-N-methyltransferase (INMT) is a methyltransferase downregulated in lung cancer, meningioma, and prostate cancer; however, its role and mechanism in prostate cancer remain unclear. By analyzing The Cancer Genome Atlas (TCGA)-PRAD, we found that the expression of INMT in prostate cancer was lower than that of adjacent non-cancerous prostate tissues and was significantly correlated with lymph node metastasis Gleason score, PSA expression, and survival. Combined with the GSE46602 cohorts for pathway enrichment analysis, we found that INMT was involved in regulating the MAPK, TGFß, and Wnt signaling pathways. After overexpression of INMT in prostate cancer cell lines 22Rv1 and PC-3, we found an effect of INMT on these tumor signal pathways; overexpression of INMT inhibited the proliferation of prostate cancer cells and promoted apoptosis. Using the ESTIMATE algorithm, we found that with the increase of INMT expression, immune and stromal scores in the tumor microenvironment increased, immune response intensity increased, and tumor purity decreased. The difference in INMT expression affected the proportion of several immune cells. According to PRISM and CTRP2.0, the potential therapeutic agents associated with the INMT expression subgroup in TCGA were predicted. The area under the curve (AUC) values of 26 compounds positively correlated with the expression of INMT, while the AUC values of 14 compounds were negatively correlated with the expression of INMT. These findings suggest that INMT may affect prostate cancer's occurrence, development, and drug sensitivity via various tumor signaling pathways and tumor microenvironments.