Transcutaneous electrical nerve stimulation on acupoints reduces fentanyl requirement for postoperative pain relief after total hip arthroplasty in elderly patients.

BACKGROUND: Transcutaneous electrical nerve stimulation (TENS) is regarded as an effective treatment for various types of pain. However, no randomized controlled trial has investigated TENS on acupoints for postoperative analgesia in elderly patients. This study aim to investigate whether TENS on acupoints has any favorable effect on complementary analgesia after total hip arthroplasty (THA) for elderly patients compared with a sham control treatment. METHODS: Sixty-eight elderly patients requiring THA surgery were enrolled and randomly allocated to one of two groups. Group Acu received true TENS on acupoints (bilateral P6, L14; ST36, GB31 ipsilateral to the surgery site) and Group Sham received sham treatment. All patients received patient-controlled analgesia for two days postoperatively. Analgesia was assessed by postoperative fentanyl requirement and pain intensity using a visual analogue scale (VAS-10 cm). The incidence of analgesia-related side effects, optional medication use and effects of patients' blinding were recorded. RESULTS: Fentanyl consumption in Group Acu was lower than that in Group Sham at 24 h (mean ± SD; 360±117 vs. 572±132 µg; P<0.001) and 48 h (712±184 vs. 1022±197 µg; P<0.001) after surgery. Postoperative pain intensity measured by VAS was similar in both groups. The incidence of opioid-related side effects and rescue medication for postoperative analgesia was significantly higher in Group Sham than in Group Acu. Differences between the groups regarding the effects of patients' blinding were not significant. CONCLUSION: TENS on specific acupoints is an effective and complementary approach to reduce postoperative analgesic requirement in elderly patients after THA.

Gene expression profiling by cDNA array in human hepatoma cell line in response to cisplatin treatment.

Gene expression profiling with cDNA array allows simultaneous analysis of the gene expression pattern of a large number of genes and may enhance the investigation of the molecular mechanisms involved in the treatment of hepatocellular carcinoma with cisplatin. We used cDNA array technology to assess the gene expression profiles related to cell cycle regulation and apoptosis in human hepatoma Hep3B cells in response to cisplatin treatment. In Hep3B cells, apoptosis induced by cisplatin was p53-independent, and was associated with up-regulation of cell cycle regulators, pro-apoptotic genes, growth receptors, and genes involved in signal transduction. These included p33ING1, c-Abl, Bax, insulin-like growth factor binding protein 3, Siva, cyclin D1, RhoA, and Raf-1. Down-regulation of cell cycle regulator CDC2 was observed. Semi-quantitative reverse transcription-polymerase chain reaction and/or Western blot analysis performed on seven of these genes confirmed their upregulation of gene expression. Such global analysis of the cytotoxic response to chemotherapeutic drugs may yield insight into the mechanisms of drug action and allow rational design of more effective treatment strategies.

Induction of apoptosis by cisplatin and its effect on cell cycle-related proteins and cell cycle changes in hepatoma cells.

We investigated cisplatin-induced apoptosis and the effects on cell cycle-related proteins and cell cycle changes. Two human hepatoma cell lines, HepG2 (with wild-type p53) and Hep3B (with deleted p53), were treated with different concentrations of cisplatin. Cisplatin induced apoptosis in both cell lines as assessed by cell morphology, DNA fragmentation analysis,TdT-mediated dUTP nick end labeling assay and flow cytometry. HepG2 cells were more sensitive to cisplatin than Hep3B. Low-dose cisplatin induced a transient G(1) arrest, S phase block and upregulation of p53 and p21(WAF1/CIP1) expression in HepG2, but not in Hep3B cells. With cisplatin at a high dose, both cell lines underwent apoptosis that was accompanied by downregulation of p27(KIP1) and Bcl-x(L). In HepG2, upregulation of p53 and p21(WAF1/CIP1) was observed before apoptosis occurred, suggesting that cisplatin-induced apoptosis in HepG2 might be p53-dependent. Expression of Fas was also increased following cisplatin treatment in HepG2. However, there was no induction of p53, p21(WAF1/CIP1) and Fas observed in Hep3B cells. In conclusion, cisplatin induced apoptosis in hepatoma cells via both p53-dependent and -independent pathways.