Drug therapy is one of the efficient methods for prostate cancer treatment. However, drug resistance greatly hindered the treatment of prostate cancer patients. Herein, the mechanisms of drug resistance in prostate cancer have been exhaustively reviewed, and that can provide an alternative strategy and new targets for anti-prostate cancer therapy.

Human immunodeficiency virus (HIV)-1 infection changes transcriptional profiles and regulates. the factors and machinery of the host that facilitate viral replication. Our previous study suggested that the serine/threonine kinase citron kinase (citK) promotes HIV-1 egress. To ascertain if HIV-1 infection affects citK expression in primary cells, peripheral blood mononuclear cells were infected with vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1 vector NL4-3-luc viruses, which resulted in remarkably increased expression of citK. citK overexpression led to a more than two-fold increase in HIV-1 production, whereas a significant decrease was observed when citK was depleted in CD4+ T cells. Infection with HIV-1 pseudoviruses induced increases in the mRNA and protein levels of citK by 2. 5- and 2. 7-fold in HEK293T cells, respectively. By cloning the 5-kb promoter of citK into a luciferase reporter system and transfecting the construct into HEK293T cells, enhanced luciferase activity was observed during HIV-1 infection. Taken together, these data demonstrate that HIV-1 infection upregulates citK expression at the transcriptional level, and thereby renders the host more susceptible to invasion by HIV-1.
CD4-Positive T-Lymphocytes ; virology ; Cloning, Molecular ; Gene Expression Regulation, Enzymologic ; HEK293 Cells ; HIV-1 ; physiology ; Humans ; Intracellular Signaling Peptides and Proteins ; genetics ; Protein-Serine-Threonine Kinases ; genetics ; Up-Regulation ; Virus Replication

Objective To compare the changes of plasma lipid indexes and coronary artery atherosclerotic plaque in TaqI B genotypes in CHD patients with impaired glucose tolerance (IGT) before and after statin therapy. Methods A total of 196 CHD with IGT and 160 controls were included. The changes of plasma lipid indexes and coronary artery atherosclerotic plaque in TaqI B genotypes were analyzed before and after Rosovastatin therapy. Sequenom Mass ARRAY platform was used to detect the CETP TaqI B SNPs. Results The genotype frequency of the B1B1, B1B2 and B2B2 in CHD with IGT group was 35.7%, 48.0% and 16.3% respectively, while in control group was 31.3%, 53.1% and 15.6% respectively. HDL-C, PA and MLA levels increased after Rosuvastatin therapy, while LDL-C, TG, TCH, Lpa, PA, EEMA and PB levels decreased. Conclusions CETP gene polymorphisms TaqI B would have association with the effects of Rosuvastatin therapy in the CHD with IGT.

Objective To investigate the correlation between morning blood pressure surge and Coronary Microvascular Dysfunction.Methods 58 cases of patients with hypertension in our hospital were given 24 h ambu-latory blood pressure monitoring(ambulatory blood pressure monitoring,ABPM).The coronary microvascular dys-function was estimated by the index of microcirculatory resistance(IMR). All cases were given biochemical test-ing,included TCH,TG,HDL-c,LDL-c and SUA.Results According to whether ABMP was arise,the patient were divided into MBPS group(n=21)and the Non-MBPS group(n=37).24 h,day,night and morning peak of systolic blood pressure were significantly higher in the morning peak group than in the average morning peak group. Multiple linear regression analysis showed that,MBPS,24 h average systolic blood pressure,day average systolic blood pressure,night average systolic blood pressure,and age were independent risk factors for coronary artery disease.Conclusion Morning blood pressure surge is closely related to severity of coronary microcirculation dysfunction. It is an independent risk factor for coronary microcirculation dysfunction. To control the blood pres-sure in patients with hypertension effectively can reduce morning peak target organ damage.

Objective To investigate the anti-oxidative effects of alprostadil on contrast-induced nephropathy(CIN)after percuteous coronary intervention (PCI)in patients with chronic kidney disease(CKD).Methods A total of 200 patients with CKD were enrolled in our hospital.According to the random number table was divided into alprostadil 100 cases,100 cases of conventional treatment group.The levels of serum creatinine (Scr),creatinine clearance (eGFR),serum cystatin C (ScysC)and 8-hydroxy-deoxyguanine (8-OHdG)were observed before and after operation at 72 h and 7 d after operation.Results The incidence of CIN in the alprostadil group was significantly lower than that in the conventional treatment group (6% vs 12%,P<0.05).There was no significant difference in the level of Scr,eGFR,ScysC and 8-OHdG between the alprostadil group and the conventional treatment group (P>0.05).The level of Scr in the alprostadil group was significantly lower than that in the conventional treatment group at 72 h and 7 d after operation.The level of eGFR was significantly higher than that of the conventional treatment group (P<0.05).The levels of ScysC and 8-OHdG in the two groups were significantly higher than those before operation at 72 h and 7 d(P>0.05).The levels of ScysC and 8-OHdG in the alprostadil group were significantly lower than those in the conventional treatment group at 72 h and 7 d after PCI(P<0.05).Conclusion Alprostadil may improve the oxidative stress in patients with CKD and provide a preventive effect on CIN.

Human APOBEC3G (hA3G) is a cytidine deaminase which inhibits HIV-1 replication. The HIV-1 accessory protein viral infectivity factor (Vif) counteracts with hA3G by targeting it for proteasomal degradation. In this work, we constructed and optimized molecular models of the hA3G dimer and the hA3G-Vif complex. The molecular modeling study revealed that the loop7 motif of hA3G appears on the interfaces of both the hA3G-Vif complex and the hA3G dimer. Biochemical analysis provided evidence suggesting that binding of Vif to hA3G results in steric blocking of hA3G dimerization, implying that monomeric hA3G serves as a substrate for Vif-mediated degradation. Furthermore, we presented evidence for the important roles of the loop7 motif, especially the central residues within the region, in hA3G dimerization, hA3G--Vif interaction, Vif-mediated hA3G degradation as well as subcellular localization of hA3G. This work highlights a multiple-task interface formed by loop7 motif, which regulates biological function of hA3G, thus providing the feasibility of the strategy of blocking Vif-mediated A3G degradation by targeting the putative site around loop7.