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Changes in vascular endothelial function, blood coagulation and cardiac function indexes after the implantation of a permanent cardiac pacemaker in patients with bradycardia were investigated. A total of 53 healthy people and 117 patients with bradycardia in Jining First People's Hospital from January 2015 to August 2017 were selected. Factor VIII: coagulation (FVIII:C), von Willebr and factor (vWF), antithrombin activity (AT:A), D-dimmer (D-D), thrombomodulin (TM), tissue factor (TF), left ventricular ejection fraction (LVEF) and left ventricular end-systolic volume (LVESV) in the non-pacemaker group and the pacemaker group were significantly different from those in the control group (P<0.05), in which FVIII:C, vWF, D-D, TM, TF and LVESV were significantly higher than those in the control group, while LVEFs were significantly lower than that in the control group. After the implantation of a pacemaker, the FVIII:C, vWF, fibrinogen (FIB), D-D, TF and LVESV in patients were significantly higher than those before implantation (P<0.05), while the LVEF was significantly lower than that before implantation (P<0.05). In addition, in different pacemaker groups, there were no significant differences in blood coagulation and vascular endothelial indexes, but differences in cardiac function levels were obvious, in which LVEF in dual-chamber (DDD) pacemaker group was significantly higher than that in ventricular inhibited (VVI) pacemaker group, and LVESV in the former was significantly lower than that in the latter (P<0.05). Finally, here was no significant difference in the quality of life of patients implanted with different pacemakers (P>0.05), but the quality of life of patients in the DDD pacemaker group was better than that of patients in the VVI group. Therefore, implanting pacemakers in patients with bradycardia affects vascular endothelial function, blood coagulation, and cardiac function indexes in patients, and complications become less after the implantation of DDD pacemakers. [ABSTRACT FROM AUTHOR]

The aim of the present was to assess whether serum thymidine kinase 1 (STK1) concentration is a useful biomarker for the screening of benign prostatic hyperplasia (BPH) or prostate malignancy. Serum samples were collected from 123 patients with prostate carcinoma prior to surgery, biopsy or androgen deprivation therapy and at 3, 6 and 10 months following the procedure. A total of 205 patients with BPH and 266 healthy controls were also utilized. STK1 concentration and total prostate-specific antigen (PSA) were measured in patient serum by use of commercial assays. The pathological specimens (obtained from surgery or biopsy) were assessed according to Gleason scores (GS). STK1 concentration and total PSA were significantly higher in patients with prostate carcinoma compared with patients with BPH and healthy individuals. Furthermore, STK1 concentration was associated with Gleason score, while total PSA was not. However, no association was identified between STK1 concentration and total serum PSA. A receiver operating characteristic analysis was performed on STK1 concentrations among patients with prostate carcinoma. The results demonstrated that the sensitivity and specificity were high, with an area under the curve (AUC) of 0.97. Although the sensitivity and specificity of total PSA were also high, the AUC value was relatively low (0.74). The results indicated that STK1 concentration is a more reliable prognostic biomarker than total PSA in respect to the GS system. Additionally, since STK1 concentration is associated with Gleason score, the use of biopsies to determine Gleason score may be replaced to some extent by the STK1 concentration test, thus reducing the discomfort of patients from which biopsies are obtained. [ABSTRACT FROM AUTHOR]

Depression has been well established as an independent predictor of mortality and cardiac morbidity rates in patients with coronary artery disease (CAD). Evidence has shown that single nucleotide polymorphisms located in pre-microRNA (miRNA) or mature miRNA may modify various biological processes and affect the process of carcinogenesis, and the downregulation of neuronal nitric oxide synthase 1 (NOS1) can induce depression. It has been shown that NOS1 is the target gene of miR-146a, and that the rs2910164 G/C polymorphism can downregulate the expression of miR-146a. In the present study, computational analysis was used to identify the target of miR-146a, and a luciferase reporter assay system was used to validate NOS1 as a target gene of miR-146a. In addition, U251 cells were treated with miR-146a mimics/inhibitors to verify the negative regulatory association between miR-146a and NOS1. Reverse transcription-quantitative polymerase chain reaction analysis and western blot analysis were used to estimate the mRNA expression of NOS1 and the expression of miR-146a. The results showed that the ‘seed sequence’ was located within the 3′-untranslated region of NOS1 by searching an online miRNA database (www.mirdb.org), and the luciferase reporter assay confirmed that NOS1 was a direct target gene of miR-146a. It was also found that the mRNA and protein expression levels of NOS1 in U251 cells treated with miR-146a mimics and NOS1 small interfering RNA were substantially downregulated, compared with cells treated with the scramble control. The cells treated with miR-146a inhibitors showed increased expression of NOS1. In addition, the presence of a minor allele of the rs2910164 polymorphism was significantly associated with risk of depression in patients with CAD. Taken together, the findings indicated a decreased risk of depression in the patients with CAD who were carriers of the miR-146a rs2910164 C allele, and this association may be attributed to its ability to compromise the expression of miR-146a, and thereby increase the expression of its target gene, NOS1. [ABSTRACT FROM AUTHOR]