OBJECTIVETo investigate the effects of micro(mi) RNA-195 on high-glucose induced neonatal cardiomyocyte hypertrophy and to explore the related mechanism.

METHODSThe potential target gene of miRNA-195 (Smad7) was predicted by TargetScan5. 1 software. Cardiomyocytes were isolated from neonatal SD rats and cells were then randomly divided into three groups: cells treated by culture medium containing 5 mmol/L glucose (control group) , by culture medium containing 25 mmol/L glucose (high glucose group) and treated by culture medium containing 25 mmol/L glucose and miRNA-195 inhibitor transfection (miRNA-195 inhibitor group). After 24, 48, or 72 h of in vitro culture, the morphology of cardiomyocytes was examined under phase contrast microscope. Micrographs were captured and the cell surface was calculated. The mRNA expressions of miRNA-195 and myosin heavy chain β (β-MHC), a biomarker for cardiomyocyte hypertrophy, in cardiomyocytes were detected by RT-PCR. The protein expression of Smad7 was determined by Western blot. The concentration of transforming growth factor-β1 (TGF-β1) in the supernatant of culture medium was measured by ELISA.

RESULTSCross-sectional area of cardiomyocytes, expression of miRNA-195 and β-MHC and secretion of TGF-β1 were significantly increased in high glucose-treated cells (P < 0.05 vs. normal control). The protein expression of Smad7 was significantly downregulated in cells exposed to high glucose for 48 h (P < 0.05 vs. normal control). Downregulation of miRNA-195 partly reversed the high glucose-induced effects. The expression of Smad7 was negatively correlated with miRNA-195 in high glucose control group (correlation coefficient: -0.945, P < 0.05).

CONCLUSIONOur results demonstrate that Smad7 could be the target gene of miRNA-195. miRNA-195 might play a crucial role in the development and progression of diabetic cardiomyopathy possibly through downregulating the expression of Smad7 and modulating TGF-β/Smad pathways.

Animals ; Down-Regulation ; Glucose ; Hypertrophy ; MicroRNAs ; Myocytes, Cardiac ; Rats ; Rats, Sprague-Dawley ; Transfection ; Transforming Growth Factor beta1

Objective To study the effects of embryonic neural stem cells transplantion on trauma of red nucleus neu-rons of the rats with spinal cord injury.Methods NSCs in logarithmic phage were labeled with BrdU,a Sprague Dawley rat mode of spinal cord injury (SCI) was developed with electrocircuit control spinal cord injuring device.Thirty SD rats were randomly divided into three groups: sham group,SCI group and NSC group.The NSCs were trans-planted into injured site three days after SCI.Then NSCs labeled with Brdu were detected by immunohistochemisty,rubrospinal tract (RST) neurons were labeled by retrograde transport of the horseradish peroxidase (HRP) from the lesion site,which were taken by damaged axons and remained in the neurons,then the labeled red nucleus (RN) neurons were counted.Hind limb function of experimental rats was evaluated by a blinder observer using BBB open field locomotion rating score.Results BrdU positive NSCs were detected in the spinal cord after transplantation,the number of RST neurons labeled by HRP in NSC group was more than that in SCI group (P <0.01),the BBB score of NSC group was higher than SCI group (P <0.01).Conclusion The transplanted NSCs can survive in the injured site of spinal cord and protect RN,then promote more remarkably functional recovery after SCI.

Objective To access the influence factors of diagnostic delay of endometriosis. Methods We designed a questionnaire of diagnostic delay of endometriosis. From February 2014 to February 2016,400 patients who had dysmenorrhea and diagnosed with endometriosis by surgery in Peking University Third Hospital were surveyed retrospectively. Time and risk factors of diagnostic delay were analyzed.Results The diagnostic delay of 400 patients was 13.0 years(0.2-43.0 years),78.5%(314/400) patients thought pain was a normal phenomenon and didn′ t see the doctor. Patients who suffered dysmenorrhea at menarche experienced longer diagnostic delay than those who had dysmenorrhea after menarche(18.0 vs 4.5 years;Z=191.800,P<0.01).Patients who suffered aggravating dysmenorrhea experienced shorter delay time than those who suffered stable or relieving dysmenorrhea(11.0 vs 12.5 vs 18.0 years;Z=8.270, P<0.05), with the difference statistically significant, single factor analysis shows. Severe dysmenorrhea, deep infiltration endometriosis(DIE), family history of dysmenorrhea or endometriosis, previous surgical history of endometriosis,high stage,with infertility,adenomyoma or other symptoms,could help to shorten diagnostic delay with no significant difference(P>0.05). By multiple logistic regression analysis,the results shown that whether have dysmenorrhea at menarche and clinical diagnosis time were the independent factors affecting delayed diagnosis(P<0.01).Conclusions Diagnostic delay of endometriosis is common and the mean delay time is 13.0 years mainly due to the unawareness of dysmenorrhea. Dysmenorrhea at menarche,clinical diagnosis time and dysmenorrhea intensity are the factors affecting time of diagnostic delay.