Background Gastric cancer (GC) is one of the most common carcinomas of the digestive tract, and the prognosis for these patients may be poor. There is evidence that some long non-coding RNAs(lncRNAs) can predict the prognosis of patients with GC. However, few lncRNA signatures have been used to predict prognosis. Herein, we aimed to construct a risk score model based on the expression of five lncRNAs to predict the prognosis of patients with GC and provide new potential therapeutic targets. Methods We performed differentially expressed and survival analyses to identify differentially expressed survival-ralated lncRNAs by using GC patient expression profile data from The Cancer Genome Atlas (TCGA) database. We then established a formula including five lncRNAs to predict the prognosis of patients with GC. In addition, to verify the prognostic value of this risk score model, two independent Gene Expression Omnibus (GEO) datasets, GSE62254 (N = 300) and GSE15459 (N = 200), were employed as validation groups. Results Based on the characteristics of five lncRNAs, patients with GC were divided into high or low risk subgroups. The prognostic value of the risk score model with five lncRNAs was confirmed in both TCGA and the two independent GEO datasets. Furthermore, stratification analysis results showed that this model had an independent prognostic value in patients with stage II–IV GC. We constructed a nomogram model combining clinical factors and the five lncRNAs to increase the accuracy of prognostic prediction. Enrichment analysis based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) suggested that the five lncRNAs are associated with multiple cancer occurrence and progression-related pathways. Conclusion The risk score model including five lncRNAs can predict the prognosis of patients with GC, especially those with stage II-IV, and may provide potential therapeutic targets in future.

Background: Epithelial ovarian cancer (EOC) ranks first for female gynecological tumor-related deaths.Due to the limited efficacy of traditional chemotherapy strategies, potential therapeutic targets are urgently needed. Previous studies have reported a relationship between abnormal spindle-like microcephalyassociated protein (ASPM) and ovarian cancer based on immunohistochemistry (IHC) and bioinformatics analysis. However, the potential role of ASPM in the proliferation of ovarian cancer cells and its molecular mechanism remain to be elucidated. Therefore, we aimed to further investigate the potential role of ASPM and its underlying mechanism in EOC using integrated online databases, clinical samples, and cell models. Methods:We used online databases (Gene Expression Profiling Interactive Analysis, Cbioportal and Kaplan-Meier Plotter) to analyze differential ASPM expression in ovarian carcinoma and explore its prognostic value in ovarian cancer (OvCa) patients. Immunohistochemistry staining based on a clinical tissue microarray (TMA) comprised 75 cases of EOC tissue and 5 cases of adjacent normal ovary tissue was used to detect the ASPM expression and analyze the relationship between ASPM expression and EOC characteristics. Various cell function experiments related to tumorigenesis were performed including the CCK8 assay, 5-ethynyl-2'-deoxyuridine (EdU), colony formation assay and Transwell assay in EOC cell models (A2780 and OVCAR3) with knocked down ASPM by small interfering RNA (siRNA) to observe its role. Finally, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment was conducted to determine the signaling pathways in which ASPM was involved in the pathogenesis of ovarian cancer.Analysis of cell cycle distribution using flow cytometry was further performed to verify the pathways. Results:The expression profile based on data from The Cancer Genome Atlas (TCGA) database confirmed ASPM expression in EOC was higher compared with normal tissue, and further analysis suggested that higher expression was correlated with worse patient prognosis. Immunohistochemical analysis further indicated that ASPM was highly expressed in OvCa tissues and associated with a higher pathological stage, grade, and positive lymphatic metastasis. Cell models with knocked down ASPM by small interfering RNA (siRNA) significantly inhibited proliferation and migration. KEGG pathway enrichment and cell cycle analysis showed that ASPM silencing could inhibit ovarian cancer cell proliferation via synthesis (S) phase arrest.Conclusions: Our study confirmed that ASPM promoted proliferation and caused S phase arrest in EOC cells. ASPM may become a potential molecular marker for early screening and a valuable therapeutic target in EOC.

Introduction Herpes zoster (HZ) is a disease caused by the reactivation of the varicella zoster virus. Postherpetic neuralgia (PHN) is the most common complication of HZ. Aim Repetitive paravertebral block with local anaesthetics and dexmedetomidine for the prevention of PHN in patients with acute herpes zoster. Material and methods 104 patients with acute herpes zoster were randomly divided into two groups. Group Rop received repetitive paravertebral block with 0.25% ropivacaine 20 ml per 72 h three times. Group Dex received repetitive paravertebral block with a mixture of 0.25% ropivacaine 20 ml and dexmedetomidine 20 µg per 72 h three times. Patients were permitted to take tramadol when the visual analogue scale (VAS) ≥ 4. The incidence of zoster-related pain was recorded at 1, 3, and 6 months after the end of treatments; VAS scores and the dose of rescue drug were recorded at 1 week, 2 weeks, 1 month, 3 months, and 6 months after the end of treatments. Results At 1 month post therapy, the incidence of zoster-related pain was 11% in Group Dex, compared with 35% in Group Rop ( p = 0.005). At 3 months post therapy, the incidence of zoster-related pain in Group Dex was still significantly lower than in Group Rop. The VAS scores and the dose of rescue drug in Group Dex were also significantly lower than in Group Rop at each time point ( p < 0.05). Conclusions Repetitive paravertebral block with local anaesthetics and dexmedetomidine in patients with acute herpes zoster can significantly reduce the incidence of zoster-related pain.