Humans ; Sympathectomy ; adverse effects ; methods ; Thoracoscopy ; adverse effects ; methods

Humans ; Heart ; Coronary Angiography ; Disabled Persons

Objective To observe the intluence ot chemokine RANTES influence on cardiac allograft acute rejection caused by alloreactive memory CD4+ T cells (Tm) adoptive transfer.Methods Heterotopic heart transplantation (HTx) from Balb/c donors to C57BL/6 recipients was performed by anastomosis of the vessels of the neck.Mice undergoing heterotopic heart transplantation received either adoptive transfer of 1 × 106 CD4+ Tm from the spleen of alloantigen-primed C57BL/6 mice or no cells (control group).After the cardiac transplantation,the mean survival time (MST),mean histologic rank of rejection,relative gene expression and serum concentration of RANTES in the cardiac grafts.Results (1) The percentage of CD4+ Tm was 26.83％ at the spleen of alloantigenprimed mice; (2) The MST was 5.17 ± 0.17 days in the CD4+ Tm+ HTx group versus 7.76 ± 0.21 days at the HTx group (control group) (P＜0.01); (3) The histological tests revealed that mean histologic rank of rejection activity in the sections of cardiac allografts on the day 5 post grafting was grade 3.92 ± 0.08 in the HTx+ CD4+Tm group versus grade 2.67 ± 0.14 in HTx group (P＜0.01) ;(4) The relative gene expression level of RANTES was 2.6 ± 0.21 in the CD4+ Tm + HTx group,significantly higher than in the control group (P＜0.01) ; (5) The serum concentration of RANTES in the CD4+ Tm+ HTx group was 223.6 ± 16.79 pg/mL,higher than in the control group (120.7 ±9.47 pg/mL,P＜0.01).Conclusion Alloreactive CD4+ Tm contribute to the increased expression and secretion of RANTES,and cardiac allograft acute rejection was more extensive in the CD4 + Tm + HTx group.

Adolescent ; Adult ; Anti-Inflammatory Agents ; therapeutic use ; Diagnosis, Differential ; Dipyridamole ; therapeutic use ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Lupus Erythematosus, Systemic ; drug therapy ; Male ; Medicine, Chinese Traditional ; Middle Aged ; Phytotherapy ; Prednisone ; therapeutic use ; Tripterygium ; chemistry

Child ; Humans ; Pneumonia ; diagnosis ; etiology ; Recurrence

Objective To investigate the possible mechanism of curcumin inhibition to murine melanoma growth.Methods Melanoma cell line B16F10 was injected subcutaneously into the outer side of mouse right thigh to establish a melanoma-bearing mouse model.Seven days after the establishing the model, these mice were treated with intraperitoneal injection of curcumin at 50 and 100 mg/kg respectively or RPMI 1640 culture medium as control.Fourteen days later,the mice were killed,tumor weight was calculated;the tumor nuclear factor?B activity and survivin mRNA expression were measured by Western blot and RT-PCR,respectively.Results The tumor weight was significantly lower in the curcumin-treated mice than that in the controls (P

OBJECTIVETo investigate the effects of simvastatin on the proliferation and apoptosis of prostatic epithelial RWPE-1 cells.

METHODSRWPE-1 cells cultured in vitro were treated with simvastatin at 0, 10, 20, and 40 μmol/L for 24, 48, and 72 hours followed by determination of their proliferation by MTT assay, and their apoptosis by flow cytometry. The mRNA and protein expressions of Bcl-2, Bax, and Cx43 were detected by fluorescence quantitative RT-PCR and Western blot, respectively.

RESULTSAfter 72 hours of treatment with simvastatin at 10, 20, and 40 μmol/L, the inhibition rates of the RWPE-1 cells were (21.07 ± 6.41)%, (34.87 ± 9.65)%, and (47.18 ± 10.88)%, respectively, significantly higher than (1.21 ± 0.54)% in the control group (P < 0.05) and in a dose-dependent manner (P < 0.05); the cell apoptosis rates were (0.066 ± 0.016)%, (0.126 ± 0.023)%, and (0.192 ± 0.025)%, respectively, remarkably higher than (0.015 ± 0.005)% in the control (P < 0.05) and also in a dose-dependent manner (P < 0.05); the mRNA and protein expressions of Bcl-2 were decreasing while those of Bax and Cx43 increasing with the increased concentration of simvastatin (P < 0.05). The expression of Cx43 was correlated negatively with that of Bcl-2 but positively with that of Bax.

CONCLUSIONSimvastatin inhibits the proliferation of prostate epithelial cells and induce their apoptosis by acting on the gap junctional intercellular communication.

Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Connexin 43 ; metabolism ; Drug Administration Schedule ; Epithelial Cells ; drug effects ; physiology ; Humans ; Hypolipidemic Agents ; pharmacology ; Male ; Prostate ; cytology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; RNA, Messenger ; metabolism ; Simvastatin ; pharmacology ; bcl-2-Associated X Protein ; metabolism

0.05).(4) Significant differences between CC and CIN Ⅰ for p16,CDH1,RASSF1A and TIMP3 genes(P

OBJECTIVETo determine whether oral statins can delay the progression of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS).

METHODSWe conducted a retrospective cohort study of 50-69-year-old males who came for physical examination in our hospital between January 2003 and December 2008. We designed the inclusion criteria, followed them up for 5 years, and investigated the relationship of oral statins with the clinical progression of BPH and LUTS.

RESULTSTotally, 653 men met the inclusion criteria and were included in this study, of whom 283 were treated with oral statins (group 1) while the other 370 with none (group 2). There were no statistically significant differences between the two groups in age and baseline IPSS, Qmax, and prostate volume (PV) (P > 0.05). During the follow-up, 24 cases in group 1 and 35 cases in group 2 were excluded for obvious dys-uria. A gradual increase was observed in IPSS in both groups 1 and 2 year by year from the baseline to the 5th year of follow-up, but significantly lower in the former group (4.27 +/- 1.16, 4.63 +/- 1.05, 5.27 +/- 0.96, 6.41 +/- 1.04, 7.21 +/- 1.21, and 7.93 +/-1.50) than in the latter (4.24 +/- 1.35, 5.26 +/- 1.23, 6.84 +/- 1.20, 8.75 +/- 1.84, 10.82 +/- 3.01, and 12.98 +/- 4.21) (P < 0.01); a gradual decrease was seen in Qmax, though markedly higher in group 1 ([26.56 +/- 2.09], [24.06 +/- 1.94], [21.33 +/- 1.66], [19.24 +/- 1.54], [17.44 +/- 1.53], and [16.27 +/- 1.37] ml/s) than in group 2 ([26.74 +/- 2.40], [23.62 +/- 2.01], [20.63 +/- 1.69], [17.72 +/- 1.48], [14.82 +/- 1.11], and [11.86 +/- 1.24] ml/s) (P < 0.01); and a gradual increase was found in PV, but remarkably smaller in the former group ([19.82 +/- 4.94], [22.60 +/- 4.99], [25.80 +/- 5.20], [27.92 +/- 5.05], [29.11 +/- 5.24], and [29.97 +/- 5.26] ml) than in the latter ([20.21 +/- 4.78], [24.30 +/- 4.98], [28.50 +/- 5.14], [32.84 +/- 4.77], [36.99 +/- 4.78], and [40.90 +/- 4.78] ml) (P < 0.01). Longer medication of statins was associated with better efficacy.

CONCLUSIONOral statins can significantly delay the clinical progression of BPH and LUTS.

Aged ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; therapeutic use ; Longitudinal Studies ; Lower Urinary Tract Symptoms ; drug therapy ; Male ; Middle Aged ; Prostatic Hyperplasia ; drug therapy ; Retrospective Studies

This paper aimed to study phenylpropanoids of Tripterygium hypoglaucum. Twenty-four compounds were isolated from the 70% EtOH extracts of T. hypoglaucum by silica gel column chromatography, reversed phase column chromatography, gel column chromatography, preparative thin layer chromatography, and semi-preparative high performance liquid chromatography. Compounds 1-3 were three new phenylpropionds. Their structures were identified by ultraviolet spectrum, infrared spectroscopy, high resolution electrospray ionization mass spectrometry, and nuclear magnetic resonance data as: threo-2-(4-hydroxy-3-methoxyphenoxy)-3-(4-hydroxy-3-methoxyphenyl)-1,3-propanedol (1), erythro-2-(4-hydroxy-3-methoxyphenoxy)-3-(4-hydroxy-3-methoxyphenyl)-1,3-propanediol (2), erythro-3-(4-hydroxy-3,5-dimethoxyphenyl)-3-ethoxypropane-1,2-propanediol (3). Compounds 4-6, 9, 14, 15, 18, 19, and 21-24 were obtained from Tripterygium genus for the first time. The cytotoxicity assay of cancer cells suggested that compound 20 displayed cytotoxicity on the breast cancer 4T1 cells whose 50% inhibitory concentration was 125.60 μmol·L^-1.