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1.
Practical Oncology Journal ; (6): 535-539, 2014.
Article in Chinese | WPRIM | ID: wpr-499179

ABSTRACT

Objective To explore the effect of mediastinal drainage on the treatment for intra -thoracic anastomotic leak in esophageal cancer patients after esophagectomy .Methods One hundred and thirty -four e-sophageal cancer patients underwent esophagectomy and a mediastinal drainage tube was routinely placed intro -operatively ( observation group ) .Other 150 esophageal cancer patients underwent esophagectomy without mediasti -nal drainage were retrospectively set as control group .The following factors in the two groups were compared:in-cidence of anastomotic leak,and mortality rate,incidence of respiratory failure,incisional infection,rate and dura-tion of moderate or high fever ( T≥38℃) , duration of antibiotic use , duration of anastomotic leak healing and length of hospital stay of anastomotic leak patients .Results There was no significant difference in incidence rate of anastomotic leak between observation and control groups .There was no death ,no respiratory failure in observa-tion group;rate of chest incisional infection in observation group was 18.2%(2/11).Mortality rate,respiratory failure rate and chest incisional infection rate in control group were 33.3%(3/9)、44.4%(4/9)and 77.8%(7/9)respectively.Incidence and duration of moderate or high fever (36.4%and 2.3 ±1.2d respectively)in obser-vation group were significantly lower than those in control group (100 % and 8.6 ±2.3 d respectively)(P<0.05).Duration of antibiotic use,duration of leak healing and length of hospitalization (9.6 ±3.2 d,23.6 ±5.5 d and 22.6 ±5.7 d respectively)were significantly shorter than those in control group (21.3 ±6.8 d,38.3 ±8.4 d and 38.5 ±9.6 d,P<0.05)respectively).Conclusion Although mediastinal drainage could not prevent anasto-motic leak in patients underwent esophagectomy ,it could definitely decrease death and respiratory failure resulted from anastomotic leak .Mediastinal drainage could also decrease severity of intrathoracic infection caused by anas -tomotic leak and shorten the duration of leak healing .

2.
Chinese Journal of Lung Cancer ; (12): 399-404, 2006.
Article in Chinese | WPRIM | ID: wpr-339374

ABSTRACT

<p><b>BACKGROUND</b>With the development of patch clamp and molecular biology technique, and the application of them in the investigation of tumor cellular membrane ion channnel, the ion channel is becoming the hot spot of the tumor base research gradually. The aim of this study is to investigate the electrophysiological properties of human lung adenocarcinoma cell line A-549 and the role of K+ channel in inhibition of cell proliferation by the recombinant mutant human tumor necrosis factor (rmhTNF).</p><p><b>METHODS</b>Ionic currents were recorded using the whole-cell patch clamp recording technique. The proliferation activity of A-549 cells was measured by MTT assay. The cell cycle and apoptosis rates of the carcinoma cells were measured by flow cytometric analysis (FCM).</p><p><b>RESULTS</b>Whole-cell patch clamp recording revealed a voltage-gated K+ current in A-549 cells, which could be blocked by the K+ channel blocker, TEA and CsCl. The amplitude of K+ current was markedly diminished in all cells incubated with different concentration of rmhTNF (P < 0.01). Obvious inhibitive effect of rmhTNF on proliferation of the cells was found in vitro in a dose-dependent manner (P < 0.01), the maximal inhibitory rate was 38.68% when the concentration was 400U/mL. The rmhTNF inhibited the cell cycle shifting from G1 phase to S phase and promoted apoptosis as determined by FCM analysis. The proportion of G1 cells increased from 53.02% to 72.93%, and the apoptosis rate increased from 2.08% to 8.68%. The difference were significant between the control and the high concentration groups ( 200U/mL and 400U/mL) (P < 0.01).</p><p><b>CONCLUSIONS</b>rmhTNF exerts its cytotoxic effects on A-549 cells through inhibiting cell cycle shifting and inducing apoptosis. The K+ channels on the A-549 cell membrane can be blocked by rmhTNF partly, and the effect of inhibiting proliferation and activating apoptosis on A-549 cells is a result of depression of the K+ channel.</p>

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