Objective To investigate the manifestations and genetic mechanisms of male sex reversal syndrome. Methods A 22 year old male patient with 46,XX karyotype was systemically examined and a Y specific sequence tagged site (STS),sY14,was chosen to detect sex determining region of Y (SRY) gene by polymerase chain reaction (PCR). Results This patient shows primary and secondary male sex characters while gonads are hypoplastic and malfunctional.The patent has 46,XX karyotype and SRY gene.Therefore,the patient is diagnosed as 46,XX male sex reversal syndrome. Conclusions Translocation of SRY can bring about 46,XX male sex reversal syndrome,whereas gonads of the patients are hypoplastic and malfunctional because of the absence of other genes on Y chromosome.SRY gene plays an important role in sex determination.

Aged ; Antigens, CD34 ; analysis ; Female ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Proto-Oncogene Proteins c-bcl-2 ; analysis ; Solitary Fibrous Tumors ; metabolism ; pathology

OBJECTIVETo study the effects and mechanism of apigenin on the expression of vascular endothelial growth factor (VEGF) in human breast cancer MDA-MB-231 cells.

METHODSMDA-MB-231 cells were used as the study object. MTT assay was used to detect the effect of apigenin on the cell viability. ELISA was used to determine the protein level of VEGF. RT-PCR was used to detect VEGF at mRNA level. A double luciferase system was used to measure the transcription activity of VEGF. pCEP4-HIF-1alpha was transferred to explore the reversing effect of HIF-1alpha on the inhibitory effect of apigenin on the transcription activity of VEGF. Western blotting was used to detect the time-dependent and dose-dependent effect of apigenin on HIF-lalpha, p-AKT, p-ERK, and p53 expression at protein level.

RESULTSApigenin had no visible inhibitory effect on cell viability. Apigenin reduced the secretion of VEGF, mRNA levels of VEGF and transcription activity of VEGF. Furthermore, the inhibitory effect of apigenin on the transcription activity of VEGF could be reversed by transferring pCEP4-HIF-1alpha into the cells. Additionally, apigenin inhibited the expression of HIF-1alpha and p-AKT, induced the expression of p53, but had no effect on the expression of p-ERK1/2.

CONCLUSIONApigenin can inhibit VEGF expression in breast cancer cells, and this effect may be achieved through decreasing the expression of HIF-1alpha.

Antineoplastic Agents, Phytogenic ; pharmacology ; Apigenin ; pharmacology ; Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; metabolism ; RNA, Messenger ; metabolism ; Transcriptional Activation ; drug effects ; Tumor Suppressor Protein p53 ; metabolism ; Vascular Endothelial Growth Factor A ; genetics ; metabolism

To investigate whether ABL specific tyrosine kinase specific inhibitor STI571 can restore beta1 integrin mediated negative effect on Ph(+) chronic myeloid leukemia(CML), the inhibitory effect of beta 1 integrin activator (beta1 integrin activating antibody 8A2, cytokines such as GM-CSF, G-CSF and SCF) and/or FN on the granulocyte-macrophage colony forming unit (CFU-GM) from 16 patients with Ph(+)CML and 13 normal individuals were examined; the bone marrow mononuclear cells (BMMNC) before and after ABL kinase specific inhibitor STI571 pretreatment (0.1 micro mol/L for 30-60 minutes) were target cells in this study. The roles which VLA4 and VLA5 played in this process were evaluated through blocking assay. The results showed: (1) beta1 integrin activator(s) or FN alone have no effect on CFU-GM from CML or normal bone marrow mononuclear cells before or after STI571 pretreatment, nor STI571 pretreatment itself. (2) The inhibitory effect of beta1 integrin activator(s) plus FN on CML CFU-GM are significantly lower than that on normal CFU-GM. (3) The inhibitory effect of beta1 integrin activator(s) plus FN on CML CFU-GM after STI571 pretreatment is comparable to that on normal CFU-GM. (4) Monoclonal antibody to VLA4 and VLA5 or to total beta1 integrins almost completely abrogate the above effect of STI571. The results suggested enhancing beta1 integrin mediated negative effect on myeloid progenitors in Ph(+)CML is one of the therapeutic mechanisms of STI571 on Ph(+)CML.

Adult ; Aged ; Aged, 80 and over ; Antiviral Agents ; therapeutic use ; Carcinoma, Hepatocellular ; epidemiology ; virology ; Female ; Hepatitis B ; drug therapy ; epidemiology ; Humans ; Liver Neoplasms ; epidemiology ; virology ; Male ; Middle Aged ; Retrospective Studies ; Young Adult

Objective To study the imaging apperances and the diagnostic value of conventional magnetic resonance imaging (MRI) and diffusion-weighted imaging (DWI) in differentiating histopathological types of small hepatocellular carcinoma (sHCC).Methods 40 sHCC confirmed by histopathology were classified into 4 groups according to their degree of differentiation:well (n=6),well-moderate (n=5),moderate (n=27) and moderate-poor (n =2).All patients received conventional MRI and DWI (1.5T,b =0 and 600 s/mm2) before the operation.The ADC values of the sHCC were measured and compared.Results On T1WI,32 lesions showed hypointensity,4 hyperintensity (well) and 4 isointensity (well-moderate =2,moderate =2).On T2WI,hyperintensity was observed in 39 lesions and isointensity in 1 lesion (well).Steatosis in the sHCC was seen in 17 of 40lesions (17/40,42.5 ％,well=4,well-moderate=1 and moderate=12).A pseudocapsule was seen in 67.5 ％ sHCC (27/40,well=4,well-moderate=3,moderate=18 and moderate-poor=2).32 lesions showed hypervascularity on arterial phase,and 8 lesions showed hypovascularity (well=3,moderate =4,moderate-poor=1).On DWI,37 lesions showed hyperintensity,except for 3 lesions with welldifferentiated sHCC which showed isointensity (50％,3/6).The mean ADC values±S.D.of sHCC in the well,well-moderate,moderate and moderate-poor groups were (1.757 ± 0.337) × 10-3,(1.917±0.574)×103,(1.816±0.545)×103 and (1.723±0.217)×10-3,respectively.There were no significant differences among the 4 groups.Conclusion The imaging appearances of wellmoderate,moderate and moderate-poor sHCC on conventional MRI were classical which make diagnosis easy.Hyperintensity on DWI contributed to diagnosis.However,the imaging appearances of some well-differentiated sHCC were atypical.The lesions could be isointensity or hyperintensity on DWI.The combination of conventional MRI and DWI contributed to better diagnosis of sHCC,especial for atypical sHCC.

Objective To observe the effect of ginsenoside Rb1,the most abundant ginsenoside in ginseng root,on differentiation and lipolysis of 3T3-L1 cells and to explore its anti-diabetic mechanism.Methods 3T3-L1 preadipoeytes were induced under standard differentiation process in the presence of 0.1,1,10,100?mol/L ginsenoside Rb_1 for 6 days.Oil red O staining,measurement of triglyceride contents and glucose uptake assay were performed.The expressions of mRNA and protein of PPAR?2,C/EBP?,ap2,glucose transporter (Glut) 1,and Glut4 were analysed with quantitative real time-PCR and Western blot.The binding affinity of Rb_1 to PPAR?-LBD was evaluated by Surface Plasmon Resonance (SPR).Lipolysis of adipocytes was examined by the measurement of glycerol released from adipoeytes treated with Rb_1 for 1 h.Results Ginsenoside Rb_1 facilitated differentiation of 3T3-L1 preadipoeytes in a dose-depondent manner.10?mol/L ginsenoside Rb_1 increased lipid accumulation by about 56%.Treatment of differentiating adipocytes with 10?mol/L ginsenoside Rb_1 increased the expressions of PPAR?2 and C/EBP?mRNA and protein,as well as mRNA expression of ap2,one of their target genes.After treatment of differentiating adipoeytes with Rb_1,basal and insulin-mediated glucose transport augmented significantly accompanied by up-regulations of mRNA and protein level of Glut4,but not of Glutl.SPR showed Rb_1 could bind to PPAR?which suggested Rb_1 was a ligand of PPAR?.Ginsenoside Rb_1 inhibited basal lipolysis in adipoeytos in a dose-dependent manner.However,it did not affect isoproterenol-stimulated lipolysis.Conclusion As a PPAR?ligand,ginsenoside Rb_1 promotes adipogenesis,inhibitas basal lipolysis and inereasos basal and insulin-mediated glucose transport in cultured adipoeytes.Therefore,anti-diabetic and insulin-sensitizing activity of ginsenosides is,at least in part,involved in the enhancing effect on PPAR?2 and C/EBP?expressions,hence promoting adipogenesis and glucose uptake,and inhibiting lipolysis in adipocytes.

Objective To examine the association between tea drinking and the risk of lung cancer in Chinese population.Methods All relevant published articles in Chinese and English literature database were identified.Meta-analysis was conducted.Combined odds ratio (OR) and 95％ confidence interval (CI) were calculated to estimate the associations and dose-response relationship between tea drinking and the risk of lung cancer.Results Twelve studies were included.An inverse association with lung cancer was observed on tea drinkers when compared to non-tea drinkers (OR=0.66,95％CI:0.49-0.89).Conclusion Tea drinking might serve as a protective factor on lung cancer in the Chinese population.

BACKGROUNDThe long-term effects of bone marrow-derived cells (BMC) transplantation in patients with acute myocardial infarction (AMI) have not been established. The present meta-analysis of randomized controlled trials with follow-up ≥ 2 years was performed to investigate the long-term effects of BMC therapy in patients after AMI.

METHODSSpecific terms were used to conduct a systematic literature search of MEDLINE, EMBASE, the Cochrane Library and the Cochrane Central Register of Controlled Trials, and the China Biological Medicine Disk database from their inception to March 2012. A standardized protocol was used to extract information, and random effect model was used to analyze all data except major adverse events.

RESULTSFive trials comprising 510 patients were included. Compared with controls, BMC therapy significantly improved left ventricular ejection fraction (LVEF) (4.18%, 95%CI: 2.02% to 6.35%, P = 0.0002), while mildly but not significantly reduced left ventricular end-systolic volume (-4.47 ml, 95%CI: -10.92 to 1.99, P = 0.17) and left ventricular end-diastolic volume (-2.29 ml, 95%CI: -9.96 to 5.39, P = 0.56). Subgroup analysis revealed that significant improvement of LVEF induced by BMC therapy could be observed in patients with baseline LVEF ≤ 42%, but disappeared in those with baseline LVEF > 42%. There were trends in favor of BMC therapy for most major clinical adverse events, though most differences were not significant.

CONCLUSIONSIntracoronary BMC infusion in patients with AMI seems to be safe and may further improve LVEF on top of standard therapy; especially the beneficial effects could last for long term. The findings need to be validated in the future.

Acute Disease ; Bone Marrow Transplantation ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; physiopathology ; surgery ; Randomized Controlled Trials as Topic ; Ventricular Function, Left

OBJECTIVETo investigate the influence of fluorosis on nicotinic acetylcholine receptors (nAChRs) in protein and gene levels in SH-SY5Y cells and the mechanism of the receptor modification.

METHODSSH-SY5Y cells, a human neuroblastoma cell line, were incubated with different concentrations of fluoride or with antioxidant for 48 hours. The functions of cells were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) method, and protein oxidation detected by carbonyl content; the alpha3 and alpha7 nAChR subunits in protein level were measured by Western blotting and in mRNA level by RT-polymerase chain reaction (RT-PCR).

RESULTSIn high-dose group as compared to the control, the decreased MTT (49%), increased protein oxidation (72%), and lower expression of alpha3 (51%) and alpha7 (47%) nAChR subunit proteins were obviously observed in SH-SY5Y cells. There were no changes in expression of nAChR subunit mRNAs between the cells treated with fluoride and those un-treated in controls. Prior treatment with antioxidant resulted in preventing the decrease of nAChR protein in cells exposed to the high doses of fluoride.

CONCLUSIONFluorosis should result in damage of cells and the declined expression of nAChRs in protein levels, but no influences on gene expression of the receptors in human neuroblastoma neurons. The decreased nAChR proteins might be involved in the mechanism of oxidative stress induced by fluorosis.

Cell Line, Tumor ; Fluoride Poisoning ; metabolism ; Fluorides ; toxicity ; Humans ; Neuroblastoma ; metabolism ; pathology ; Protein Processing, Post-Translational ; drug effects ; Proteins ; metabolism ; RNA, Messenger ; biosynthesis ; genetics ; Receptors, Nicotinic ; biosynthesis ; genetics