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1.
Indian J Cancer ; 2015 Nov; 52(5)Suppl_1: s12-s16
Artículo en Inglés | IMSEAR | ID: sea-169195

RESUMEN

BACKGROUND: The extent of the benefit of erlotinib in the treatment of advanced nonsmall‑cell lung cancer (NSCLC) is still controversial when compared with docetaxel. This meta‑analysis was performed to compare the efficacy of erlotinib with docetaxel for different patients with advanced NSCLC. MATERIALS AND METHODS: We searched Cochrane Library, PubMed, CNKI, and identified 23 randomized controlled clinical trials from 2008 to 2015. According to our further full‑text screening, 6 clinical trials were included in the final meta‑analysis. RESULTS: Six papers were included in this study. The progression‑free survival (PFS), overall survival (OS), objective response rate (ORR), and toxicity were included in our outcomes. The pooled hazard ratio (HR) of PFS was 1.57 (95% confidential index [CI] = 1.47–1.69). The pooled HR of OS was 1.66 (95% CI = 1.43–1.92). The pooled risk ratio of ORR was 0.56 (95% CI = 0.35–0.91). The toxicity analysis showed odds ratio = 1.79 (95% CI = 1.20–2.69). CONCLUSIONS: In terms of PFS, OS, and toxicity the effect of erlotinib in the treatment of advanced NSCLC patients is superior to docetaxel.

2.
Indian J Med Microbiol ; 2015 Apr; 33(2): 262-266
Artículo en Inglés | IMSEAR | ID: sea-159533

RESUMEN

Purpose: To assess whether vancomycin minimum inhibitory concentration (MIC) creeps among clinical isolates of methicillin‑resistant Staphylococcus aureus (MRSA) in a regional hospital in China. Furthermore, to analyze the causes of vancomycin MIC creeps and the relationship between vancomycin MICs and the outcome among patients with MRSA infection. Materials and Methods: All clinical isolates of MRSA from 2006-2010 were retrieved and tested by the broth microdilution procedure to determine their vancomycin MIC. Meanwhile, related patient records were analyzed. Results: While all isolates were susceptive to vancomycin, the percentage of isolates with a vancomycin MIC = 1 mg/L increased significantly from 2006 (37.0%) to 2010 (75.7%). Meanwhile, vancomycin usage density (DDDs/1000 bed‑days) had increased significantly from 2006-2010. Mean linear correlation analysis showed a statistically significant positive correlation (r = 0.905, P < 0.05) between the consumption of vancomycin and the percentage of MRSA isolates with a vancomycin MIC = 1 mg/L. Clinical records revealed high vancomycin MIC was associated with a higher microbiologic failure rate in MRSA bloodstream infections. Conclusions: The data demonstrated vancomycin MIC creep among clinical isolates in our hospital, and the MIC creep may be caused by the increasing usage of vancomycin. Furthermore, the analysis strongly suggested this shift of vancomycin MIC within the susceptible range may be associated with an increasing probability of treatment failure.

3.
Braz. j. med. biol. res ; 42(12): 1173-1178, Dec. 2009. tab, ilus
Artículo en Inglés | LILACS | ID: lil-532296

RESUMEN

This study was designed to investigate the effect of curcumin (diferuloylmethane) on the proliferation and apoptosis of hepatic stellate cells (HSC). The cell line HSC-T6 (1.25 x 10(5) cells/mL) was incubated with curcumin and HSC proliferation was detected by a methyl thiazolyl tetrazolium colorimetric assay. HSC apoptosis was detected by flow cytometry, transmission electron microscope and agarose gel electrophoresis. HSC proliferation was significantly inhibited in a concentration-dependent manner (10.6 to 63.5 percent) after incubation with 20-100 ìM curcumin, compared with a control group. At 20, 40, and 60 ìM, after 24 h of incubation, curcumin was associated with a significant increase in the number of HSC in the G2/M phase, and a significant decrease in cell numbers in the S phase (P < 0.05). At these concentrations, curcumin was also associated with an increase in the apoptosis index of 15.3 ± 1.9, 26.7 ± 2.8, and 37.6 ± 4.4 percent, respectively, compared to control (1.9 ± 0.6 percent, P < 0.01). At 40 ìM, the curcumin-induced apoptosis index at 12, 24, 36, and 48 h of incubation was 12.0 ± 2.4, 26.7 ± 3.5, 33.8 ± 1.8, and 49.3 ± 1.6 percent, respectively (P < 0.01). In conclusion, curcumin inhibits the in vitro proliferation of HSCs in the G2/M phase of the cell cycle and also induces apoptosis in a concentration- and time-dependent manner. The in vivo effect of curcumin on HSCs requires further investigation.


Asunto(s)
Animales , Ratas , Apoptosis/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Curcumina/farmacología , Células Estrelladas Hepáticas/efectos de los fármacos , Línea Celular , Colorimetría , Electroforesis en Gel de Agar , Citometría de Flujo , Células Estrelladas Hepáticas/patología , Microscopía Electrónica de Transmisión , Factores de Tiempo
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