Faecal incontinence in patients with a sphincter defect: comparison of sphincteroplasty and sacral nerve stimulation.

AIM: Sphincteroplasty (SP) is used to treat faecal incontinence (FI) in patients with a sphincter defect. Although sacral nerve stimulation (SNS) is used in patients, its outcome in patients with a sphincter defect has not been definitively evaluated. We compared the results of SP and SNS for FI associated with a sphincter defect. METHOD: Patients treated by SNS or SP for FI with an associated sphincter defect were retrospectively identified from an Institutional Review Board approved prospective database. Patients with ultrasound evidence of a sphincter defect were matched by age, gender and body mass index. The main outcome measure was change in the Cleveland Clinic Florida Faecal Incontinence Score (CCF-FIS). RESULTS: Twenty-six female patients with a sphincter defect were included in the study. The 13 patients in each group were similar for age, body mass index, initial CCF-FIS and the duration of follow-up. No differences were observed in parity (P = 1.00), the rate of concomitant urinary incontinence (P = 0.62) or early postoperative complications. Within-group analysis showed a significant reduction of the CCF-FIS among patients having SNS (15.9-8.4; P = 0.003) but not SP (16.9-12.9; P = 0.078). There was a trend towards a more significant improvement in CCF-FIS in the SNS than in the SP group (post-treatment CCF-FIS 8.4 vs 12.9, P = 0.06). Net improvement in CCF-FIS was not significantly different between the groups (P = 0.06). CONCLUSION: Significant improvement in CCF-FIS was observed in patients treated with SNS but not SP patients. A trend towards better results was seen with SNS.

Expression of a mutated phospholipase A2 in transgenic Aedes fluviatilis mosquitoes impacts Plasmodium gallinaceum development.

The genetic manipulation of mosquito vectors is an alternative strategy in the fight against malaria. It was previously shown that bee venom phospholipase A2 (PLA2) inhibits ookinete invasion of the mosquito midgut although mosquito fitness was reduced. To maintain the PLA2 blocking ability without compromising mosquito biology, we mutated the protein-coding sequence to inactivate the enzyme while maintaining the protein's structure. DNA encoding the mutated PLA2 (mPLA2) was placed downstream of a mosquito midgut-specific promoter (Anopheles gambiae peritrophin protein 1 promoter, AgPer1) and this construct used to transform Aedes fluviatilis mosquitoes. Four different transgenic lines were obtained and characterized and all lines significantly inhibited Plasmodium gallinaceum oocyst development (up to 68% fewer oocysts). No fitness cost was observed when this mosquito species expressed the mPLA2.

Effects of N-acetylcysteine in hepatic ischemia-reperfusion injury during hemorrhagic shock.

This article seeks to standardize an experimental model of liver ischemia-reperfusion in rats following hemorrhagic shock modulated by N-acetylcysteine (NAC). Twenty-seven adult Wistar rats were randomized into three groups: the HS-IR-Garm underwent hemorrhagic shock with selective hepatic ischemia followed by reperfusion; the HSIR + NAC-G, the same procedure plus NAC; and the control group, only venous catheterization. Blood was withdrawn for 10 minutes until MABP reached 35 mm Hg, which was maintained for 1 hour. The blood was then reinjected as required to maintain MABP at that level. Ringer's lactate solution was infused in a volume equivalent to three times the shed blood, over a period of 15 minutes. Half of the shed blood was reinfused over 5 minutes. HSIR + NAC-G received 150 mg/kg of NAC, during treatment of the shock, and again 10 minutes before reperfusion and continued for 30 minutes. Finally, both groups were subjected to 40 minutes of warm selective hepatic ischemia and reperfusion for 1 hour. Data were analyzed by nonparametric tests (P < or =.05). Liver enzyme levels were higher in HS-IR-G (DHL = 6094 +/- 1688, AST = 746 +/- 175, and ALT = 457 +/- 90) than in HSIR + NAC-G group (DHL = 2920 +/- 284, AST = 419 +/- 113, and ALT = 253 +/- 26). The values in the control group were lower than both experimental groups (DHL = 965 +/- 173, AST = 163 +/- 42, and ALT = 82 +/- 28). Our data showed that liver ischemia-reperfusion injury following hemorrhagic shock produces important hepatic damage and that NAC reduces injury in this rat model.