Spermatogenesis is a unique process of cell differentiation, which involves the regulation of a series of complicated post-transcriptional expressions. MicroRNAs (miRNAs) are a class of none-coding RNAs that play important roles in regulating post-transcriptional gene silencing. MiRNAs are expressed in a cell-specific manner in spermatogenesis and participate in the maturation and differentiation of male germ cells. The specifically altered seminal plasma miRNA is closely related with spermatogenic dysfunction and therefore can be used as a novel biomarker for the diagnosis of male infertility. A deeper insight into these specific miRNAs may point a new direction in the studies of the molecular mechanisms of spermatogenesis and spermatogenic dysfunction.
Biomarkers ; Cell Differentiation ; Genitalia, Male ; Germ Cells ; Humans ; Infertility, Male ; Male ; MicroRNAs ; genetics ; RNA Interference ; Semen ; physiology ; Spermatogenesis ; genetics

Actins ; metabolism ; Adult ; Breast ; pathology ; Breast Neoplasms ; metabolism ; pathology ; surgery ; Female ; Humans ; Mammography ; Neoplasms, Muscle Tissue ; metabolism ; pathology ; surgery ; Vimentin ; metabolism

Animals ; Heart Ventricles ; cytology ; Lipid Bilayers ; Potassium Channels ; Sarcolemma ; physiology ; Swine

Norovirus ; chemistry ; genetics ; physiology ; ultrastructure ; Open Reading Frames ; Virus Replication

Adult ; CD56 Antigen ; metabolism ; Carcinoma, Papillary ; diagnosis ; metabolism ; pathology ; surgery ; Endoscopic Ultrasound-Guided Fine Needle Aspiration ; methods ; Female ; Humans ; Male ; Neprilysin ; metabolism ; Pancreatic Neoplasms ; diagnosis ; metabolism ; pathology ; surgery ; Receptors, Progesterone ; metabolism ; Vimentin ; metabolism ; Young Adult ; beta Catenin ; metabolism

Objective To investigate the significance and effect of ultrasonic diagnosis on the autologous bone marrow mesenchymal stem cells (MSC) in angiogenesis. Methods Twenty-four New Zealand rabbits were divided into experiment group (12) and the control group (12). Then rabbit bone marrow MSCs from experiment group were isolated, caltured and marked with Brdu. After ischemic hind limb animal model on all rabbits was set up, autologous bone marrow MSCs were directly injected into the ischemic hind limb muscles in experiment group while same volume normal saline was used in the control group. Two weeks after the implantation of autologous bone marrow MSCs, 2D and color Doppler flow imaging (CDFI) detection were used in rabbit femoral artery of the two groups to observe the inner diameter of the blood vessel, the peak velocity and the acceleration time. The disposition of transplaned cells and the state of angiogenesis in ischemic muscles were assessed using immunofluorescence staining. Results The results of 2D and Doppler ultrasound detection showed the inner diameter of the blood vessel and the peak velocity of the blood current in experiment group obviously higher than that of the control group , and the acceleration time was obviously smaller than that of the control group P<0.01. The immunofluorescence staining showed there were transplanted cells existed in transplanted portion and state of angiogenesis was supurior obviously than that of the control. Conclusions Bone marrow MSCs had the effect to promote angiogenesis. Implantation of autologous bone marrow MSCs was a simple and efficient therapeutic method for the ischemia hind limb. Using high-frequency ultrasound to detect femoral artery may provide a practical and useful method to evaluate the effect on implanted autologous bone marrow mesenchymal stem cells.

Background and purpose: Postoperative chemotherapy targets the metastatic cancer in the remaining lymph nodes, but the heterogeneity in multidrug resistance (MDR) of metastatic cancer cells is a main factor affecting chemotherapeutic efficacy. Recent studies only examined the primary lesion of esophageal squamous cell carcinoma(ESCC). There is no report about heterogeneity between the primary tumor and metastases lymph node. The purpose of this study was to explore the heterogenous expression and clinical signiifcance of multidrug resistance (MDR) associated proteins in primary tumors and metastatic lymph nodes in patients with thoracic ESCC. Methods:The expressions of lung cancer associated resistance protein (LRP), P-glycoprotein (P-gp), topoisomeraseⅡ(TOPO-Ⅱ), thymidylate synthase (TS), glutathione S-transferase-π (GST-π) were examined by immunohistochemistry in primary lesions and corresponding metastatic lymph nodes in 54 patients with thoracic ESCC. The differences between expression of primary lesions and matched metastatic lymph nodes were compared and analyzed in relationship with tissue differentiation degree. Results: The discordant rates of the expression and drug resistance between primary lesions and corresponding metastatic lymph nodes in LRP, P-gp, TS, TOPO-Ⅱ and GST-π were 63.0% and 26.9%, 42.6%and 22.2%, 48.1%and 25.9%, 50.0%and 29.6%, 18.5%and 1.9%respectively. The expression of LRP showed signiifcant difference between the primary tumors and lymph nodes (P=0.026). No signiifcant differences were found for the other four proteins, and GST-πwas expressed in all patients in both the primary tumors and lymph nodes. Protein expression was not associated with degree of differentiation. Conclusion:There is evident of heterogenous expression of MDR associated proteins in metastatic lymph nodes compared to the primary tumors of ESCC. The examination of expression levels of MDR associated proteins in metastatic lymph nodes is helpful to select the postoperative rational chemotherapy plan.

To study the effect of cholesterol and 25-OH-cholesterol on cholesterol metabolism in HepG2 cells and the effect of coptisine (Cop) extracted from Coptidis Rhizoma (CR) in reducing and regulating cholesterol. In this study, TC, TG, LDL-c and HDL-c were measured by biochemical analysis; mRNA and protein expressions of LDLR, HMGCR and CYP7A1 were detected by qRT-PCR and Western blot. According to the results, cholesterol and 25-OH-cholesterol inducing could decrease in mRNA and protein expressions of LDLR and CYP7A1, so as to increase TC and LDL-c contents. However, Cop could up-regulate mRNA and protein expressions of LDLR and CYP7A1 and down-regulate that of HMGCR, so as to reduce TC and LDL-c levels. These findings suggested that Cop has potential pharmacological activity for reducing cholesterol, and may reduce cholesterol by regulating mRNA and protein expressions of key genes involved in cholesterol metabolism, such as LDLR, CYP7A1 and HMGCR. This study laid a firm theoretical foundation for developing new natural drugs with the cholesterol-lowering activity.
Berberine ; analogs & derivatives ; pharmacology ; Cholesterol ; metabolism ; Cholesterol 7-alpha-Hydroxylase ; genetics ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Gene Expression Regulation, Enzymologic ; drug effects ; Hep G2 Cells ; Humans ; Hydroxymethylglutaryl CoA Reductases ; genetics ; metabolism ; Receptors, LDL ; genetics ; metabolism ; Triglycerides ; metabolism

Objective To systematically review the effect of traditional Chinese medicine (TCM) in an animal model of lung injury induced by paraquat (PQ),and to provide a theoretical basis for future clinical trials.Methods The Wanfang,CNKI,VIP,PubMed/MEDLINE,EMBASE database (from January 1979 to September 2012) were searched.All papers concerning TCM in animal model of lung injury induced by PQ were retrieved.Study selection and data extraction were performed on the basis of Cochrane systematic review methods.Weighted mean difference (WMD) and 95％ confidence interval (95％CI) with random effects model was adopted to investigate the effect of TCM on lung injury induced by PQ.Results Eighteen papers involving 1 188 rats met our criteria.Meta-analysis showed that TCM could improve the lung coefficiency (WMD-0.07,95％ CI-0.14 to-0.01,P=0.03),reduce lung wet/dry weight ratio (WMD-1.15,95％CI-2.03 to-0.27,P=0.01),increase the serum superoxide dismutase (SOD) activity (WMD 56.08,95％CI 23.46 to 88.70,P=0.000 8),improve plasma glutathione peroxidase (GSH-Px) level (WMD 26.64,95％CI 18.95 to 34.33,P＜0.000 01),and lower serum malondialdehyde(MDA) level (WMD-0.65,95％CI-1.00 to-0.30,P=0.000 2),however there was no significant difference in the level of serum tumor necrosis factor-α (TNF-α) and hydroxyproline (HYP) level between TCM and controls (TNF-α:WMD-25.15,95％CI-54.87 to 4.57,P=0.10; HYP:WMD-0.11,95％CI-2.71 to 0.48,P=0.17).Conclusions These findings demonstrate the efficacy of TCM in animal models of lung injury induced by PQ.However taking account of heterogeneity,the efficacy should be interpreted with caution.

Objective To evaluate the effect of a vasoactive substance urotensin Ⅱ on the expression of type Ⅰ collagen and migration of human skin fibroblasts,and to explore the underlying mechanisms of signal transduction.Methods Fibroblasts were isolated from human foreskin tissues and subjected to primary culture.After a series of subculture,fibroblasts were classified into several groups to be treated with different concentrations (10-10 to 10-6 mol/L) of urotensin lⅡ for 24 hours,urotensin Ⅱ of 10-s mol/L for different durations (0,4,12,24 hours),or pretreated with PD98059 (a mitogen-activated protein kinase kinase inhibitor),nicardipine (a calcium channel blocker) and ciclosporin (a calcineurin inhibitor) of 10-5 mol/L respectively for 30 minutes followed by treatment with urotensin Ⅱ of 10-8 mol/L for 24 hours.The cells receiving no treatment served as the control.Subsequently,enzyme-linked immunosorbent assay was performed to determine the level of urotensin Ⅱ in the supernatant of fibroblasts,and Transwell assay to estimate the migration activity of fibroblasts.Statistical analysis was carried out by t test and analysis of variance.Results Urotensin Ⅱ promoted the expression of type Ⅰ collagen in a time-and concentrationdependent manner.The level of type Ⅰ collagen was increased by 21.2％ (P ＞ 0.05),52.2％ (P ＜ 0.05),84.4％ (P ＜0.05),83.6％ (P ＜ 0.05) and 77.1％ (P ＜ 0.05) in the supernatant of fibroblasts treated with 10-10,10-9,10-8,10-7 and 10-6 mol/L of urotensin Ⅱ for 24 hours respectively,by 23.2％ (P ＞ 0.05),69.5％ (P ＜ 0.05) and 84.1％ (P ＜0.05) in the supernatant of fibroblasts treated with urotensin Ⅱ of 10-8 mol/L for 4,12 and 24 hours respectively,compared with the untreated control fibroblasts.The migration activity was markedly enhanced in fibroblasts treated with urotensin Ⅱ of 10-8 mol/L for 24 hours compared with the control fibroblasts (P ＜ 0.05).PD98059,nicardipine and cyclosporin A inhibited the secretion of type Ⅰ collagen by 18.2％,15.9％ and 19.7％ respectively,and suppressed the migration of fibroblasts by 38.3％ (P ＜ 0.05),20.7％ (P ＜ 0.05) and 81.4％ (P ＜ 0.05) respectively in the groups receiving pretreatment compared with those treated with urotensin Ⅱ alone.Conclusions Urotensin Ⅱ can promote the secretion of type Ⅰ collagen by and migration of fibroblasts,which may be realized through the Ca2+,calmodulin kinase,and mitogen-activated protein kinase pathways.