Animals ; Cardiovascular Diseases ; etiology ; Cerebrovascular Disorders ; etiology ; Homocysteine ; metabolism ; Humans ; Methylenetetrahydrofolate Reductase (NADPH2) ; genetics ; Polymorphism, Genetic

Animals ; Benzodiazepines ; pharmacology ; Ducks ; physiology ; Growth Hormone ; blood ; Insulin-Like Growth Factor I ; metabolism ; Serum ; metabolism ; Weight Gain ; drug effects

Objective:To study the effect of electroacupuncture (EA) at the Pericardium Meridian on the heart function of volunteers with acute hypoxia, and to provide scientific evidence for the acupoints selection along the affected meridian in acupuncture-moxibustion therapy. Methods:Based on a self-control design, eighteen healthy volunteers were recruited in the study. Points from the Pericardium Meridian [Neiguan (PC 6), Ximen (PC 4), Quze (PC 3) and Tianquan (PC 2)], non-Pericardium Meridian point [Shousanli (LI 10)], non-meridian and non-acupoint points [1.0-1.5 cm lateral to Neiguan (PC 6) and Ximen (PC 4), respectively on both sides], and a blank control (only inhaling low-oxygen gas without EA stimulation) were selected to observe, once every week, 10 sessions in total, and only 1 acupoint was observed once. The volunteers inhaled low-oxygen gas mixture (10.8% O2 and 89.2% N2) for 30 min to imitate acute hypoxia. EA was conducted when the gas mixture was inhaled for 10 min and then lasted for 20 min; meanwhile, hemodynamic indexes such as cardiac output (CO), cardiac index (CI), systemic vascular resistance (SVR), systemic vascular resistance index (SVRI), left cardiac work (LCW), left cardiac work index (LCWI) and heart rate (HR) were recorded on a hemodynamic monitor. Results:EA at the acupoints of Pericardium Meridian significantly down-regulated the increased CO/CI, LCW/LCWI, and HR (P<0.05), and significantly up-regulated the decreased SVR/SVRI in hypoxia (P<0.05); EA at other meridian acupoints or at non-meridian and non-acupoint points didn't produce such effects. Conclusion: EA at the Pericardium Meridian can obviously improve the cardiac hyper-activation caused by acute hypoxia in healthy volunteers.

Objective To analyze the gene expression profiles in relation to the migration ability of adult human bone marrow-derived neural stem cells (Md-NSCs), and identify the genetic basis of the high migration potential of Md-NSCs in the central nervous system (CNS). Methods Adult human bone marrow stromal celIs(BMSCs) obtained from adult healthy volunteers were induced to differentiate into Md-NSCs in vitro, and the expressions of the genes related to cell invasiveness and metastasis were investigated by microarray analysis. Quantitative real-time PCR (RT-PCR) was used to verify the microarray results. Results The results of microarray analysis revealed significant overexpressions of the genes MMP1, MMP2, MMP17, ITGA3, RhoB, RhoC and RhoD in the Md-NSCs as compared with the expressions in fresh normal human adult bone marrow cells depleted of red blood cells. Quantitative RT-PCR verified the overexpression ofMMP2 gene by 2.84×100 folds, ITGA3 gene by 2.22×102folds, and RhoC gene by 4.92×100 folds. Conclusion The high migration potential of the Md-NSCs in the CNS is probably associated with the overexpression of the genes that promote cell invasiveness and metastasis. These overexpressed genes are also important oncogenes, and therefore the tumorigenicity of the Md-NSCs warrants further investigation.

Seven compounds were isolated from Onychium japonicum by macroporous resin, silica gel, ODS, Sephadex LH-20 column chromatography and semi-preparative HPLC. Their structures were identified by NMR, MS and other spectroscopic methods as onychone A (1), quercetin (2), quercetin-3-O-α-L-rhamnoside (3), kaempferol-7-O-β-D-glucopyranoside (4), kaempferol-3-O-α-L-rhamnopyranoside (5), (-)-prunin (6), and norathyriol (7). Compound 1 is a novel macrocyclic flavonoid, and all the others are reported from this plant for the first time. In vitro cytotoxic activities of compounds 1-7 were evaluated by MTS testing with five cancer cell lines. Compound 7 exhibited weak cytotoxicity against tumor cell lines A549, SMMC-7721, and SW480.

Objective To investigate the changes in mitoehondrial membrane potential of the rat neurons after acute brain contusion and laceration injuries. Methods Seventy Sprague-Dawley (SD)rats were randomized into the sham injury group(n=10)and brain injury group.The brain injury group was divided into 6 subgroups(n=10)for observation at 1,6,and 24 h and 2,3,and 7 days after acutebrain contusion and laceration injury,which was induced by impact of the brain with a flee-falling object.In the brain slices labeled with fluorescent JC-l staining,the changes in the mitoehondrial membrane potential of the neurons were observed under confocal laser scanning microscopy at the indicated time points.The neuronal apoptosis Was detected using Hoehesd3342 staining and TUNEL assay,and the number of apoptotic neurons was determined under optical microscope.The ultrastructural alterations of the neurons were observed with transmission electron microscopy. Results Compared with that of the sham injury group,the mitoehondrial membrane potential of the neurons decreased significantly 1 h alterthe brain injury(P<0.01),reachingthe lowestlevel at 24 h,and maintained the low level aRerwards.Apoptotie neurons were identified in the brain slices with Hochest33342 staining.One hour after the brain injury,TUNEL assay revealed a small number of positive neurons,which increased significantly at 6 h(P<0.01)and reached the highest level at 48 h.The alteration pattern of the number of the positive neurons showed a 24-h delay in compariSOIl witll that of the mitochondrial membrane potential aRer the brain trauma.Under electronmicroscope.the mitocbondria of the neurons exhibited only slight swelling at l h. and obvious morphological changes of the mitochondria occurred 6 h after the brain trauma,accompanied by chromatin fragmentation,presence of marginal nuclei and broadened nuclear membrane;nuclear condensation and chromatolysis were observed in the neurons 24 h after the brain trauma.Conclusion In rats with acute brain contusion and laceration injuries,the mitochondrial membrane potential of the neurons decreases early(<1h)after the brain injury,which induces apoptosis of the neurons.

Aim To investigate the effect of TaorenHonghua drug pair on intervertebral disc degeneration (IVDD) in rats.Methods Fifty healthy Wistar rats were randomly divided into control group,model group,sham group,meloxicam group and Taoren-Honghua drug pair group,with 10 rats in each group.We established dynamic and static forces imbalance of cervical disc degeneration model or sham surgery in rats.12 weeks later,rats were intragastrically administered with meloxicam,Taoren-Honghua drug pair or saline for 30 days.C4/5 and C6/7 discs were harvested from rats.ABOG staining was used for observation of intervertebral disc morphology,real time PCR for mRNA expressions of type Ⅱ collagen (Col Ⅱ) and type Ⅹ collagen (Col Ⅹ),and immunohistochemical staining for Col Ⅱ and Col Ⅹ.Results Compared with model group,Col Ⅱ expression increased,while Col X expression decreased in chondrocyte of intervertebral disc in Taoren-Honghua-treated group(P ＜ 0.01).Conclusion Taoren-Honghua drug pair could delay the degeneration of cartilage endplate in rat intervertebral disc.

Objective: To explore the survival difference of patients with colon and rectal neuroendocrine neoplasm (NEN) at different stages. Methods: We identified 8 679 patients with colorectal NEN diagnosed between 1988 and 2014 from the Surveillance, Epidemiology, and End Results (SEER) registry, including 5 437 rectal NEN and 3 242 colon NEN ( 1 681 cecum NEN ). Survival curve was drawn by Kaplan-Meier method. Prognostic factors were analyzed by univariate analysis and multivariate Cox regression model. Results: The ratio of male patients with colon and rectal NEN was similar to female (P=0.095). Rectal NEN patients were younger (P<0.001), more highly differentiated (P<0.001), and with earlier stage (P<0.001). Survival analysis showed that the survival of rectal NEN was superior to that of colon NEN, with 10-year tumor-specific survival rates of 86.8% and 44.8% respectively (P<0.001). Multivariate Cox analysis showed that age, gender, marital status, primary tumor site, grade, stage and surgery were independent prognostic factors of colorectal NEN (all P<0.01). The most important factor was stage (HR=3.531), followed by differentiation grade (HR=1.856). Stratified analysis displayed that the survival of rectal NEN in stage Ⅰ, Ⅱ and Ⅳ were better than those of corresponding stage of colon NEN (all P<0.05), but worse in stage Ⅲ (P=0.012). While the survival of rectal NEN were significantly better than those of colon NEN within all stages after excluding 1681 cases of cecal NEN (all P<0.05). Among the patients with well-differentiated NEN, the survival of rectal NEN in stage Ⅰ, Ⅲ and Ⅳ were better than those of corresponding stage of colon NEN (all P<0.05) while there was no significant difference in stage Ⅱ(P=0.169). For poor-differentiated NEN, only the survival of rectal NEN patients in stage Ⅳ (P=0.001) was significant longer than those of colon NEN, while there was no significant difference in stage Ⅰ, Ⅱ and Ⅲ (stage Ⅰ: P=0.760; stage Ⅱ: P=0.181; stage Ⅲ: P=0.313). Conclusions The survival of NEN patients in colon and rectum is different. Cecum NEN should be considered as a separated tumor for prognostic analysis due to its special clinicopathologic characteristics.

Objective To observe the expression of growth factors (vascular endothelial growth factor [VEGF],stromal cell-derived factor-1 [SDF-1 ],basic fibroblast growth factor [bFGF],insulin-like growth factor [IGF-1],transforming growth factor-β [TGF-β],platelet-derived growth factor [PDGF],brain derived neurotrophic factor [BDNF],glial cell line-derived neurotrophic factor [GDNF] and nerve growth factor [NGF]) in rat ischemic brain tissues after intravenous implantation of bone marrow stromal cells (BMSCs) and/or endothelial progenitor cells (EPCs). Methods Healthy adult Wistar rats were randomly divided into 4 groups:vehicle group,BMSCs transplantation group,EPCs transplantation group and BMSCs combined with EPCs transplantation group (n=20). The rats were subjected to middle cerebral artery occlusion (MCAO),and 24 h after that,they were intravenously transplanted with either 3×106 BMSCs,EPCs,BMSCs/EPCs or 1 mL physiological saline.Seven d after transplantation,real time-PCR and Western blotting were employed to detect the expressions of VEGF,SDF-1,bFGF,IGF-1,TGF-β,PDGF-BB,BDNF,GDNF and NGF. Results The mRNA expressions of bFGF,VEGF and BNDF in the BMSCs/EPCs transplantation group were significantly higher as compared with those in the other groups (P＜0.05).BMSCs transplantation group enjoyed the highest mRNA levels of NGF,GDNF and TGF-β among all the groups, significantly higher as compared with those in the other groups (P＜0.05),followed by BMSCs/EPCs transplantation group.EPCs transplantation group enjoyed the highest mRNA levels of PDGF,IGF-1 and SDF-1,significantly higher as compared with those in the other groups (P＜ 0.05), followed by BMSCs/EPCs transplantation group. Conclusion BMSCs combined with EPCs implantation can promote the functional rehabilitation in rats after focal cerebral ischemia, which provides new way for improving the transplantation success rate.

OBJECTIVEThis study was designed to examine the in vitro effects of fenvalerate on steroid production and steroidogenic enzymes mRNA expression level in rat granulosa cells.

METHODSUsing primary cultured rat granulosa cells (rGCs) as model, fenvalerate of various concentrations (0, 1, 5, 25, 125, 625 micromol/L) was added to the medium for 24 h. In some cases, optimal concentrations of 22(R)-hydroxycholesterol (25 micromol/L), Follicle stimulating hormone (FSH, 2 mg/L), or 8-Bromo-cAMP (1 mmol/L) were provided. Concentrations of 17 beta-estradiol(E2) and progesterone (P4) in the medium from the same culture wells were measured by RIA and the steroidogenic enzyme mRNA level was quantified by semi-quantitative RT-PCR.

RESULTSFenvalerate decreased both P4 and E2 production in a dose-dependent manner while it could significantly stimulate rGCs proliferation. This inhibition was stronger in the presence of FSH. Furthermore, it could not be reversed by 22(R)-hydroxycholesterol or 8-Bromo-cAMP. RT-PCR revealed that fenvalerate had no significant effect on 3 beta-HSD, but could increase the P450scc mRNA level. In addition, 17 beta-HSD mRNA level was dramatically reduced with the increase of fenvalerate dose after 24 h treatment.

CONCLUSIONFenvalerate inhibits both P4 and E2 production in rGCs. These results support the view that fenvalerate is considered as a kind of endocrine-disrupting chemicals. The mechanism of its disruption may involve the effects on steroidogenesis signaling cascades and/or steroidogenic enzyme's activity.

3-Hydroxysteroid Dehydrogenases ; analysis ; metabolism ; 8-Bromo Cyclic Adenosine Monophosphate ; pharmacology ; Animals ; Base Sequence ; Cells, Cultured ; Dose-Response Relationship, Drug ; Estradiol ; analysis ; metabolism ; Female ; Follicle Stimulating Hormone ; pharmacology ; Granulosa Cells ; cytology ; drug effects ; metabolism ; Hydroxycholesterols ; pharmacology ; Nitriles ; pharmacology ; Progesterone ; analysis ; metabolism ; Pyrethrins ; pharmacology ; RNA, Messenger ; analysis ; metabolism ; Rats ; Steroids ; metabolism