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Articles by F Song
Total Records ( 15 ) for F Song
  P Yao , L Hao , N Nussler , A Lehmann , F Song , J Zhao , P Neuhaus , L Liu and A. Nussler
 

It has been reported that naturally occurring quercetin exerts hepatoprotective effects through heme oxygenase-1 (HO-1) induction. However, the precise mechanism of how ethanol-associated liver damage is counteracted by quercetin-enhanced HO-1 metabolism still remains unclear. To further decipher the protective role of quercetin on ethanol-induced liver damage, we treated human hepatocytes with quercetin and various (end) products of the HO-1 pathway. Our data clearly showed that quercetin treatment attenuated ethanol-induced damage, whereas hemoglobin and zinc protoporphyrin 9 (ZnPP) abolished such effects. Iron-II aggravated ethanol toxicity and was only partially reduced by quercetin. In contrast, carbon monoxide (CO) dose dependently inhibited ethanol-induced cytochrome P450 2E1 (CYP 2E1) activity and hepatotoxicity but had no influence on CYP 2E1 protein expression. Similarly, hemoglobin dramatically stimulated CYP 2E1 activity but not the protein expression in quercetin- and ethanol-cotreated hepatocytes. ZnPP significantly promoted CYP 2E1 protein expression in the presence and absence of CO treatment but inhibited ethanol-induced CYP 2E1 activation following CO incubation in quercetin- and ethanol-cotreated hepatocytes. These results suggested that quercetin virtually attenuated ethanol-derived oxidative damage via HO-1 induction. Heme degradation and CO release may mediate the protective effects through inhibiting ethanol-induced CYP 2E1 synthesis and enzymatic activity, respectively.

  F Song , M Huttunen Lenz and R. Holland
  Background

Existing systematic reviews have concluded that psycho-educational interventions for smoking relapse prevention were ineffective. Our objective was to conduct an exploratory meta-analysis, guided by mechanisms of these complex interventions for preventing smoking relapse.

Methods

Relevant trials were identified from a Cochrane review and by an updated search of MEDLINE and PsycINFO (up to August 2009). We examined theories or mechanisms underlying relapse prevention interventions, and process variables reported in trials. Odds ratios (ORs) for the rate of smoking abstinence at the longest follow-up were pooled in meta-analysis.

Results

Forty-nine trials were included, and interventions were at least partly based on the cognitive-behavioural approach to coping skills training in 41 trials. Only a few trials reported data on process variables. Coping skills training for smoking relapse prevention was effective for community quitters (OR 1.27, 95% CI: 1.08–1.49), and particularly for those who stopped smoking for at least 1 week at baseline (OR 1.52, 95% CI: 1.20–1.93). These findings were interpretable with mechanisms of coping skills training for relapse prevention.

Conclusions

On the basis of post hoc subgroup analyses, coping skills training for smoking relapse prevention is effective for motivated community quitters. This finding has important public health implications and needs to be confirmed by further trials.

 
 
 
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