Remifentanil ameliorates lung injury in neonate rats with acute respiratory distress by down-regulating TIMP1 expression.

Acute respiratory distress syndrome (ARDS) is a critical clinical disease characterized by diffuse inflammation of lung parenchyma and refractory hypoxemia. Remifentanil has been reported to act as an anti-inflammatory antioxidant in a variety of diseases. However, whether Remifentanil has a protective effect in ARDS and its mechanism remains to be further studied. This study was designed to investigate the effects of Remifentanil on ARDS in neonate rats. In this study, we established the model of acute respiratory distress in neonate rats. To study the effects of Remifentanil on ARDS through a series of in vitro and in vivo experiments. Furthermore, the overexpression vector of recombinant tissue inhibitors of metalloproteinase 1 (TIMP1) was injected into the neonate rat before the operation to explore the effect of TIMP-1 overexpression on acute respiratory distress rats through the above experiments. Remifentanil reduced lung injury in rats with acute respiratory distress, reduced inflammation, oxidative stress and tissue cell apoptosis in rats with acute respiratory distress. Remifentanil inhibited the expression of TIMP-1 in rats with acute respiratory distress, and TIMP-1 overexpression inhibited the protective effect of Remifentanil on rats with acute respiratory distress. Remifentanil can reduce lung injury and inflammatory response in young mice with acute respiratory distress and play a protective role by down-regulating the expression of TIMP-1.

A novel device to prevent errors in medication dosing and dispensing.

Erroneous intravenous drug administration has a high probability of causing patient morbidity or mortality during anesthesia. Anesthesiologists are cognizant of this longstanding issue, which has prompted the development of a variety of different protocols and solutions designed to ameliorate the problem and ultimately improve patient outcomes. Unfortunately, no definitive solution has been developed yet. Our invention is a medical device designed to drastically reduce, and hopefully upon further development, refinement and subsequent iterations, completely eradicate the potential for medical errors involving medication misidentification and quantitative errors in anesthetic dosing and dispensing.

Identification of prognostic biomarkers of prostate cancer with long non-coding RNA-mediated competitive endogenous RNA network.

Prostate cancer (PCa) is the second most frequently diagnosed male cancer, and no treatments exist for effective inhibition of metastatic spread of PCa. Long non-coding RNA (lncRNA) plays key roles in pathogenesis and development of various cancers through competing with endogenous RNAs (ceRNAs), but at present research on lncRNA functions in PCa is still very limited. Hence, this aspect was investigated using bioinformatics methods. Firstly, the functional lncRNA-mediated ceRNA network associated with PCa was constructed by the multi-step computational approach. Then the cytoscape software was used to analyze the node degree and betweenness centrality (BC) value of lncRNAs and mRNAs in the interaction. Finally, the lncRNAs were screened in the central region of the network by the node degree and BC value, and the functional enrichment of mRNAs was evaluated with the Gene Ontology (GO) database. In our results, LINC00476, MALAT1, SNHG11, LINC00649, and ILF3-AS1 are the lncRNAs which have the most nodes and higher BC values and considered as prognostic markers in PCa. GO analysis suggested that the function of screened lncRNAs was obviously focused on intracellular receptor signaling pathway, which indicated these lncRNAs might be potential biomarkers for diagnosis, evaluation and gene-targeted therapy of PCa.

Puerarin in inducing apoptosis of bladder cancer cells through inhibiting SIRT1/p53 pathway.

Regulatory effect of puerarin on bladder cancer T24-cell apoptosis and its possible mechanism were investigated. The experimental subjects were divided into the experimental group, the control group and the blank control group, and the cell inhibition rates after treatment were detected, respectively. Then, subjects were further divided into the control group, the puerarin group (treated with puerarin), the agonist group [treated with silent information regulator 1 (SIRT1) agonist SRT1720], the inhibitor group (treated with SIRT1 inhibitor EX527) and the combination group (treated with SRT1720, and then with puerarin). Apoptosis in each group was detected via flow cytometry, and the expression of apoptosis-related proteins, and SIRT1 and p53 proteins in each group was detected via western blotting. Moreover, the expression of SIRT1 and p53 messenger ribonucleic acid (mRNA) was detected via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The inhibition rate of bladder cancer T24 cells was significantly increased after treatment with puerarin at different concentrations. Compared with those in the normal control group, the inhibition rates at 24, 48 and 72 h after treatment with puerarin were significantly increased (p<0.05). Compared with those in the control group, the apoptosis rate of T24 cells was remarkably increased after treatment with different doses of puerarin or EX527, and the expression level of apoptosis-related protein Bcl-2-associated X protein (Bax) was also significantly increased, but the expression level of B-cell lymphoma 2 (Bcl-2) was decreased, and both the protein and mRNA expression levels of SIRT1 and p53 also significantly declined. Compared with those in the puerarin group, the apoptosis rate in the combination group was decreased, and the expression level of apoptosis-related protein Bax was also significantly decreased, but the expression level of Bcl-2 was increased, and SIRT1 and p53 protein expression levels were also remarkably increased. Puerarin can inhibit the proliferation of bladder cancer T24 cells and induce apoptosis, and the possible mechanism is related to the inhibition of SIRT1/p53 signaling pathway.

Mean platelet volume might be an effective indicator of arterial erectile dysfunction.

The aim of our study was to investigate the role of platelet parameters including mean platelet volume (MPV) and platelet count (PC) in the pathogenesis of penile arteriogenic erectile dysfunction (ED) and to evaluate the association between the platelet parameters and arteriogenic ED. There were 244 patients with ED (based on the International Index of Erectile Function [IIEF]-5 ≤21) and 60 healthy controls (IIEF-5 >21) enrolled. All participants were asked to undergo a laboratory examination, and penile vascular function was evaluated using penile color Doppler ultrasonography (pDUS). Among these ED patients, 24 patients with no abnormality on nocturnal penile tumescence (NPT) and 84 with normal vasculature or mixed vascular abnormalities were excluded. The other patients were classified into three groups as follows: control (n = 60), arteriogenic ED (n = 99), and venous leakage (n = 37) groups. MPV and PC were significantly higher in the arteriogenic ED group compared with the venous and control groups (P < 0.05). Receiver operating characteristic curve analysis revealed that the area under the curve for MPV to predict arteriogenic ED was 0.707. MPV ≥9.65 fl was recognized as a cut-off value for potential arteriogenic ED (sensitivity: 47.5%; specificity: 91.7%). A significant inverse correlation was detected between MPV and 10-min peak systolic velocity (PSV) (r = -0.34; P < 0.001) in the arteriogenic ED group. These findings suggest that the MPV might be a powerful indicator to predict and diagnose arteriogenic ED, and MPV may be a marker for ED when using pDUS.