Construction and identification of a mouse spermatocyte-derived cell line with a stable expression of PIAS-NY / 中华男科学杂志

<p><b>OBJECTIVE</b>To construct a lentiviral expression vector of the PIAS-NY gene, and establish a mouse spermatocyte-derived cell line with a stable overexpression of PIAS-NY.</p><p><b>METHODS</b>PIAS-NY was synthesized, amplified by PCR and cloned into the lentiviral vector expression plasmid pGC-FU. After digestion and sequencing, pGC-FU-PIAS-NY, pHelper 1.0 and pHelper 2.0 were co-transfected into 293T cells. Then the lentiviral particles were used to transfect the mouse spermatocyte-derived cells. The expression of the PIAS-NY protein was detected by Western blot.</p><p><b>RESULTS</b>We successfully constructed the lentiviral expression vector pGC-FU-PIAS-NY and established a mouse spermatocyte-derived cell line with a stable overexpression of PIAS-NY.</p><p><b>CONCLUSION</b>The construction of the lentiviral expression vector pGC-FU-PIAS-NY and the obtainment of stably transfected mouse spermatocyte-derived cells have paved the way for further studies on the roles of the PIAS-NY gene in spermatogenesis.</p>

Relationship between Resting Heart Rate and Coronary Syndrome / 中国康复理论与实践

@#Objective To investigate the relationship between resting heart rate (RHR) and coronary heart disease (CHD) and to explore the value of RHR in predicting the occurrence of acute coronary syndrome. Methods 445 patients with CHD were divided into stable angina group and acute coronary syndrome group. RHR, risk factors for coronary heart disease and their correlation were analyzed. Results RHR was higher in the acute coronary syndrome group than in the stable angina group (P<0.01). Logistic regression analysis showed that RHR (OR =1.052, 95% CI: 1.009~1.097, P=0.017), systolic blood pressure (OR=1.027, 95% CI: 1.003~1.053, P=0.031) and hyperglycemia (OR=2.743, 95% CI: 1.207~6.233, P=0.016) were independent risk factors for acute coronary syndrome. Conclusion RHR is an independent risk factor for incidence of acute coronary syndrome.

Applied study of voice function rehabilitation by mucosa tube performed in operation of late laryngocarcinoma / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To study the voice function rehabilitation by mucosa tube performed in operation of late laryngocarcinoma and to improve the survival quality of patients with late laryngocarcinoma.</p><p><b>METHODS</b>Forty-six patients were treated between Oct. 1991 and May 2006, including 41 males and 5 females. The average age of the patients was 54. Seventeen cases were glottic carcinomas (T3N0M0 12, T3N1M0 5), 27 cases were supraglottic carcinomas (T3N1M0 16, T4N1M0 5, T3N0M0 6), 2 cases were pyriform sinus cancer (T4N1M0 2). For those patients with late laryngocarcinoma, who had lost the chance of partial laryngectomy, mucosa tube shaping during the operation could realize voice functional rehabilitation. Only the survive arytenoids of healthy side was preserved, in order to rehabilitate voice, a mucosa tube was sutured using healthy survive arytenoids and a mucosa strip was connected to the trachea and the mucosa of hypopharynx. Survival analysis was performed by using Kaplan-Meier method.</p><p><b>RESULTS</b>Forty-one out of 46 patients obtained almost normal voice and swallow function. The 5-years survival was 76%.</p><p><b>CONCLUSIONS</b>The operation of voice function rehabilitation by mucosa tube performed can get good voice and swallow function to patients with late laryngo carcinoma.</p>

Therapy effects of fenofibrate on alcoholic fatty liver and drug-induced fatty liver in rats / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the fat decreasing effects of fenofibrate on alcoholic fatty liver and drug-induced fatty liver in rats.</p><p><b>METHODS</b>Alcoholic fatty liver and drug-induced fatty liver rats models were established. The two kinds of rats with fatty liver were seperatedly divided into fenofibrate treatment group (80 mg/kg daily) and control group without treatment. Rats were killed after four weeks, then the levels of serum triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL) and malondialdehyde (MDA), hepatic lipase (HL), lipoprotein lipase (LPL) both in serum and liver tissue were measured according to the Test Kits. Histopathological changes in liver was dyed with HE and observed under light microscope.</p><p><b>RESULTS</b>After treatment by fenofibrate, in the serum of rats with alcoholic fatty liver, the level of TG decreased significantly (1.07 mmol/L 0.06 mmol/L vs 1.56 mmol/L 0.29 mmol/L, t=5.115, p<0.001), while the level of TC had no alteration. The levels of MDA both in serum and liver tissue decreased (1.10 nmol/L 0.22 nmol/L vs 1.26 nmol/L 0.21 nmol/L, t=0.592, p<0.05; 5.92 nmol/g 1.24 nmol/g vs 7.42 nmol/g 1.22 nmol/g, t=3.477, p<0.05, respectively), while the levels of HL, LPL in serum and liver tissue increased significantly (Serum: 0.053muEq/ml/h 0.006muEq/ml/h vs 0.037 muEq/ml/h 0.006muEq/ml/h, t=-5.086, p<0.001; 0.018 muEq/ml/h 0.004 muEq/ml/h vs 0.014muEq/ml/h 0.004muEq/ml/h, t=-2.485, p<0.05. Liver tissue: 0.075muEq/ml/h 0.010muEq/ml/h vs 0.065muEq/ml/h 0.007muEq/ml/h, t=-2.437, p<0.05; 0.022 muEq/ml/h 0.014 muEq/ml/h vs 0.008 muEq/ml/h 0.002 muEq/ml/h, t=-2.876, p<0.05). Fat content in liver decreased (26.01 mg/g 1.69 mg/g vs 71.45 mg/g 2.66 mg/g, t=-43.224, p<0.001). The pathological changes of liver in fenofibrate-treated rats with alcoholic fatty liver were improved. For the drug-induced fatty liver rats, fenofibrate treatment group had no difference from the untreated control group.</p><p><b>CONCLUSION</b>Fenofibrate can significantly decrease the fat content in liver tissue of rats with alcoholic fatty liver, as well as ameliorating liver pathological changes. But fenofibrate has no effect on drug-induced fatty liver.</p>

The effect of finofibrate and simvastatin on the serum free fatty acids of alcoholic fatty liver in rats / 中国药理学通报

AIM To investigate the effect of fenofibrate and simvastatin on the serum free fatty acids of alcoholic fatty liver in rats. METHODS The rat model of alcoholic fatty liver was reproduced by chronic ethanol ingestion plus olive oil diet. The model rats were divided into three groups as follows: finofibrate treatment group(finofibrate 80 mg?kg -1 po, once a day),simvastatin treatment group (simvastatin 4 mg?kg -1 po, once a day)and control group without either above-mentioned treatment. Experimental rats were treated for four weeks and then sacrificed for blood sampling. Serum free fatty acids were analyzed by gas chromatography. RESULTS Fenofibrate significantly ameliorated the decrease in polyunsaturated fatty acids induced by ethanol [oleic acid:(38.212?7.788) ?g?L -1 vs (31.620?6.142) ?g?L -1,linoleic acid:(37.269?8.065) ?g?L -1 vs (30.254?9.063) ?g?L -1,arachidonic acid:(11.646?2.601) ?g?L -1 vs (9.012?1.236) ?g?L -1] accompanied by the improvement of the fat infiltration of the liver, but demonstrated no effect on the increase in serum saturated fatty acids by ethanol. In the contrast, simvastatin can aggravate the decrease in polyunsatrurated fatty acids and significantly increase the levels of satrurated fatty acids in serum induced by ethanol along with the pathological aggravation of alcoholic fatty liver. CONCLUSION The results of present study revealed that fenofibrate and simvastatin exerted different effect on the serum free fatty acids of alcoholic fatty liver. Polyunsatrurated fatty acids in the serum play an important role in the pathogenesis and treatment response of alcoholic fatty liver.