RESUMO
Background: Lung ultrasound score (LUS) is a clinical index used to measure lung injury, but its clinical value in patients after cardiopulmonary resuscitation (CPR) remains relatively unknown. The purpose of this study was to investigate the clinical value of LUS in patients after CPR. Methods: This retrospective study included a total of 34 patients older than 18 years with a nontraumatic cause of in-hospital cardiac arrest, who received standard resuscitation and achieved return of spontaneous circulation (ROSC). All patients underwent bedside lung ultrasound examination within half an hour once ROSC was achieved, and LUSs were calculated. The study included patient death as the endpoint event. Results: Compared with the group with lower LUSs, the patients with higher LUSs had a lower oxygenation index, longer duration of CPR, and lower 72 h survival rate. The initial LUS had good clinical value in predicting the secondary outcomes of CPR (adjusted odds ratio (aOR): 1.353, 95% confidence interval (CI): 1.018-1.797, and P = 0.037) and 72 h survival rate of patients who underwent CPR (aOR: 1.145, 95% CI: 1.014-1.294, and P = 0.029). Conclusions: LUS was shown to be helpful and had a prognostic value in patients after CPR.
RESUMO
AIM: To investigate the effects of ginsenoside Rh2 on the human pancreatic cancer cell line Bxpc-3. METHODS: The human pancreatic cancer cell line Bxpc-3 was cultured in vitro and treated with or without ginsenoside Rh2. Growth rates for Bxpc-3 cells were assessed by methyl thiazolyl tetrazolium (MTT) and colony formation assays. Cell cycle changes were analyzed by flow cytometry. Apoptosis was measured by flow cytometry and Hoechst 33258 fluorescence staining. A scratch assay and a Matrigel invasion assay were used to detect cell migration and invasion. Expression of Bax, Bcl-2, survivin, cyclin D1, matrix metalloproteinase (MMP)-2, MMP-9, cleaved caspase-3, caspase-8, and caspase-9 mRNA were determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Bax, Bcl-2, survivin, cyclin D1, cleaved caspase-3, caspase-8 and caspase-9 protein levels were examined by western blotting. Expression of MMP-2 and MMP-9 proteins in culture supernatants were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Rh2 significantly inhibited Bxpc-3 cell proliferation in a dose- and time-dependent manner, as evaluated by the MTT (P < 0.05) and colony formation assays (P < 0.05). Compared to the control group, Rh2 significantly increased the percentage of Bxpc-3 cells in the G0/G1 phase from 43.32% ± 2.17% to 71.32% ± 1.16%, which was accompanied by a decrease in S phase (from 50.86% ± 1.29% to 28.48% ± 1.18%) and G2/M phase (from 5.81% ± 1.19% to 0.20% ± 0.05%) in a dose-dependent manner (P < 0.05), suggesting that Rh2 arrested cell cycle progression at the G0/G1 phase, as measured by flow cytometry. Compared to the control group, cells treated with Rh2 showed significantly higher apoptosis ratios in a dose-dependent manner (percentage of early apoptotic cells: from 5.29% ± 2.28% to 38.90% ± 3.42% (F = 56.20, P < 0.05); percentage of late apoptotic cells: from 4.58% ± 1.42% to 36.32% ± 2.73% (F = 86.70, P < 0.05). Rh2 inhibited Bxpc-3 cell migration and invasion, as detected by scratch wound healing assay and Matrigel invasion assay [percentages of scratch wound healing for 12 h, 24 h and 48 h (control vs experimental group): 37.3% ± 4.8% vs 18.30% ± 1.65%, 58.7% ± 3.5% vs 38.00% ± 4.09% and 93.83% ± 4.65% vs 65.50% ± 4.09%, respectively; t = 6.489, t = 6.656 and t = 7.926, respectively, P < 0.05; the number of cells invading at various concentrations (0 µmol/L, 35 µmol/L, 45 µmol/L and 55 µmol/L): 81.10 ± 9.55, 46.40 ± 6.95, 24.70 ± 6.88 and 8.70 ± 3.34, respectively (F = 502.713, P < 0.05)]. RT-PCR, western blotting or ELISA showed that mRNA and protein expression of Bax, cleaved caspase-3 and caspase-9 were upregulated (P < 0.05), while mRNA and protein expression of Bcl-2, survivin, cyclin D1, MMP-2 and MMP-9 were downregulated (P < 0.05). CONCLUSION: Ginsenoside Rh2 inhibits proliferation, migration and invasion and induces apoptosis of the human pancreatic cancer cell line Bxpc-3.