ObjectiveTo explore the expression of EZH2 and p53 protein in primary prostate cancer (Pca) and its clinical significance.Methods High-throughput tissue microarray technique and immunohistochemistry was used to detect the expression of EZH2 and p53 protein in 48 human prostate cancer specimens without a history of chemo-radiation therapy and 15 cases of benign prostate hyperplasic (BPH) tissues. The pathological characteristics and the relationship of the expression of EZH2 and p53 protein in primary prostate cancer was analyzed. ResultsImmunohistochemical results showed that the positive rates of EZH2 and p53 protein in prostate cancer were 87.50 ％ (42/48) and 33.33 ％ (16/48), respectively, which were significantly higher than that in BPH tissues[13.33 ％ (2/15) and 0 (0/15)](x2=26.429, x2=5.058,P ＜0.05). The expression of EZH2 and p53 protein was significantly related to Gleason score, TNM stage (P ＜0.05), but not to age and serum prostate-specific antigen (PSA) level (P ＞0.05). The positive expression in patients with Gleason＞6 was higher than that with Gleason≤6(P ＜0.05).The positive expression in patients with T3-T4 stage was higher than that with T1-T2 stage(P ＜0.05).Spearman rank correlation showed a significantly positive correlation between EZH2 and p53 protein (r=0.294, P ＜0.05). ConclusionEZH2 and p53 protein may participate in the pathogenesis of prostate cancer.The overexpression of EZH2 and p53 protein could become an index for the evaluation of the level of malignancy and progression of prostate cancer.Furthermore,combining detection of EZH2 and p53 protein may provide a new theoretical basis for the treatment of prostate cancer.

Objective To explore the biphasic effects of simvastatin on vascular smooth muscle cells (VSMCs), which were regulated by sterol regulatory element binding proteins(SREBPs).Methods ① Rat primary VSMCs were cultured,the effects of different concentrations of simvastatin on proliferation and migration of VSMCs were observed, and the expression of SREBP-1 and SREBP-2 mRNA on VSMCs was detected.② Rat models of atherosclerosis were established,and were divided into atherosclerotic injured group (n=6), low concentration simvastatin group (n=6) and high concentration simvastatin group (n=6). Besides, normal control group (sham operation group, n=8) was established. Intragastric group and high concentration simvastation group, respectively, while those in normal control group and atherosclerotic injured group were given same amount of normal saline. Rats were sacrificed 4 weeks later. Plasma lipid levels were examined by enzymic method, ratios of intima/(intima + tunics media) of thoracic aorta and left common carotid artery were determined, and the expression of SREBP-1 and SREBP-2 mRNA on blood vessels was detected by RT-PCR. Results Simvastatin didn't show biphasic effects on the proliferation and migration of VSMCs. Low concentration simvastatin didn't promote the proliferation and migration of VSMCs, while high concentration simvastatin showed inhibition effect on the proliferation and migration of VSMCs, which was dose-dependent and independent of lipid regulation effect by simvastatin. Simvastatin could activate the expression of SREBP-1 and SREBP-2 mRNA of VSMCs. Moreover, high concentration simvastatin could significantly activate the expression of SREBP-1 and SREBP-2 mRNA. Conclusion Simvastatin can inhibit the proliferation and migration of VSMCs by activating SREBPs.

Objective To explore the biphasic effects of simvastatin on vascular smooth muscle cells(VSMCs),which were regulated by sterol regulatory element binding proteins(SREBPs).Methods①Rat primary VSMCs were cultured,the effects of different concentrations of simvastatin on proliferation and migration of VSMCs were observed,and the expression of SREBP-1 and SREBP-2 mRNA on VSMCs was detected.②Rat models of atherosclerosis were established,and were divided into atherosclerotic injured group(n =6),low concentration simvastatin group(n=6) and high concentration simvastatin group(n=6).Besides,normal control group(sham operation group,n=8) was established.Intragastric administration of simvastation of 0.5 mg?kg~(-1)?d~(-1) and 2.5 mg?kg~(-1)?d~(-1) was conducted in low concentration simvastatin group and high concentration simvastation group,respectively,while those in normal control group and atherosclerotic injured group were given same amount of normal saline.Rats were sacrificed 4 weeks later.Plasma lipid levels were examined by enzymic method,ratios of intima/(intima+tunica media) of thoracic aorta and left common carotid artery were determined,and the expression of SREBP-1 and SREBP-2 mRNA on blood vessels was detected by RT-PCR.Results Simvastatin didn't show biphasic effects on the proliferation and migration of VSMCs.Low concentration simvastatin didn't promote the proliferation and migration of VSMCs,while high concentration simvastatin showed inhibition effect on the proliferation and migration of VSMCs,which was dose-dependent and independent of lipid regulation effect by simvastatin. Simvastatin could activate the expression of SREBP-1 and SREBP-2 mRNA of VSMCs.Moreover,high concentration simvastatin could significantly activate the expression of SREBP-1 and SREBP-2 mRNA.Conclusion Simvastatin can inhibit the proliferation and migration of VSMCs by activating SREBPs.

Diagnosis, Differential ; Dyspnea, Paroxysmal ; etiology ; physiopathology ; Humans ; Infant, Newborn ; Male ; Meningocele ; complications ; diagnosis ; diagnostic imaging ; physiopathology ; Nasopharynx ; abnormalities ; diagnostic imaging ; Tomography, X-Ray Computed

The effects of interferon-? (IFN-?) on chronic myelogenous leukemia cells were studied in vitro by long-term bone marrow culture(LTBMC). There were no inhibition of cellularity from non-adherent layers and formation of adherent layers, however, CFU-GM from non-adherent layers was inhibited at IFN-? 103U/ml and 104 U/ml groups, when IFN-?was added only at initiation of culture. If IFN-? was continuously added weekly, the cellularity and CFU-GM of non-adherent layers were significantly inhibited, and the formation of adherent layers was inversely associated with the increasing concentration of IFN-?. in addition, Ph(+) cells in non-adherent layers were disappeared early and the percentage of Ph(-) population was increased with the combination of IFN-? and LTBMC. It is concluded that IFN-?selectively inhibits the later CFU-GM of CML cells and the development of stromal cells, the combination of IFN-?and LTBMC might exert a synergically purging effect on Ph(+) CML cells

Animals ; Cell Differentiation ; Cell Movement ; Chemokine CXCL12 ; metabolism ; Endothelial Cells ; pathology ; physiology ; Humans ; Muscle, Smooth, Vascular ; pathology ; physiology ; Receptors, CXCR4 ; metabolism ; Stem Cells ; metabolism ; pathology ; physiology ; Vascular Diseases ; metabolism ; pathology ; physiopathology

Acupuncture Points ; Acupuncture Therapy ; Dilatation, Pathologic ; therapy ; Female ; Halitosis ; therapy ; Humans ; Middle Aged

[ ABSTRACT] AIM:To observe the effect of endogenous nitric oxide synthase ( NOS) inhibitor asymmetric dimeth-ylarginine ( ADMA ) and its signaling pathways on NO levels and skeletal muscle contractility in 4-week running rats. METHODS:The 4 weeks running rat model was established.The twitch tension, tetanic tension and the fatigue test of sole-us muscle induced by electrical stimulation ex vivo were detected.The ATP content, mitochondrial DNA levels and the mR-NA expression of peroxisome proliferator-activated receptor γcoactivator-1α(PGC-1α), nuclear respiratory factor (NRF) were measured to reflect the mitochondrial function and biosynthesis in the skeletal muscle.Serum ADMA concentration was detected by high performance liquid chromatography.The endogenous ADMA enzymes PRMT1 and 2 subtypes of ADMA me-tabolism enzyme DDAH, 3 subtypes of NOS protein expression in the skeletal muscle were determined by Western blot.NOS activity and nitric oxide ( NO) content were analyzed by colorimetric method.RESULTS: Compared with normal control group, the twitch tension, tetanic tension and the anti-fatigue capability of soleus muscle in running group were significantly enhanced, ATP content, mitochondrial DNA content and the mRNA expression of PGC-1αand NRF were significantly in-creased (P<0.01).In addition, the protein expression of constitute type NOS (cNOS) and NOS activity were significantly increased (P<0.01), but the increase in NO content was relatively smaller in soleus muscle in exercise group (P<0.05). Moreover, serum ADMA concentration in running group was increased, while the DDAH2 expression in skeletal muscle was decreased.CONCLUSION:Short-term endurance exercise enhances the twitch tension, tetanic tension and fatigue resist-
ance of soleus muscle.The mechanism may be that increased cNOS expression feedbacks to increase ADMA concentration, thus maintaining the increase in NO synthesis at a relatively low level, and resulting in promoting skeletal muscle mitochon-dria biosynthesis and mitochondrial function.

AIM: To investigate the change of adrenocorticotropic hormone (ACTH) cells and thyroid- stimulating hormone(wn) cells of pars distalls of pituitary gland of morphine dependent dependent rats and its restoration after withdrawal. METHODS: Morphine dependent model of male rats was made by subcutaneous injection of mor- phine and the adstinent model was made after withdrawal. Changes of ACTH cells and TSH cells of pars distails of pituitary gland were detected by immunohistochemistoy survey and image analysis. RESULTS: The intensity of positive staining and the numerical density of ACTH and TSH immunoreactive cells were weakened (P＜ 0.01), after withdrawal from morphine for a short time the changes would exist continuously. CONCLUSION: Morphine may give rise to disorder of endocrine of pituitary gland of male rats, which may incompletely restore after withdrawal for a short time.

Objective To investigate the diagnosis and treatment of sequential diffuse large B-cell lymphoma (DLBCL) after peripheral T-cell lymphoma (PTCL).Methods A case with sequential DLBCL after PTCL was reported,and the characteristics and responses of this case were analyzed.The previous literature was reviewed in order to explain the mechanism and prognosis of such type of disease.Results This patient was diagnosed as PTCL not otherwise specified (PTCL-NOS) definitely,but after a period of treatment,DLBCL was developed as a second tumor.The characteristics and onset interval were just similar to those described in the literature,in which the mechanisms were mentioned as common effects of tumor cell,microenviroment and therapies.This patient got effects through the initial treatment,but considering the poor outcome by former researchers,the prognosis needed to be closely followed up.Conclusion Sequential development of EBV-unrelated DLBCL after PTCL-NOS is very rare,and the mechanism,therapy and prognosis need further investigation.