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Background: Previous studies have suggested that Mycoplasma genitalium is associated with cervicitis and may be a cause of pelvic inflammatory disease. This study attempted to investigate further the possible role of M genitalium in genital symptoms of women attending a sexually transmitted disease (STD) clinic.Goal: To determine the prevalence of and the association of clinical and microbiologic features with M genitalium in women presenting with genital symptoms.Study Design: Between April 1994 and June 1996 a prospective study of 170 consecutive women with abnormal vaginal discharge, with or without urethral itching, dysuria, or pelvic pain, was conducted at the STD clinic at Saint-Louis Hospital in Paris. Information was collected on each subject's characteristics, and a clinical vulvar, vaginal, and cervical examination was performed. Cervical, vaginal, and urethral samples were obtained to identify infecting organisms.Results: DNA of M genitalium was identified by polymerase chain reaction (PCR) at one or more genital sites in 65 women (38%; 95% CI, 31-46%) and was statistically more frequently detected in the vagina (39%) than in the cervix (21%) or urethra (28%) (P = 0.001 and 0.048, respectively). PCR inhibitors were detected in 17 specimens (4%). M genitalium was found in 6/14 (43%) positive for Chlamydia trachomatis, but no significant association between M genitalium and any demographic, clinical, or microbiologic data was noted in univariable or multivariable analysis.Conclusion: This study indicates that M genitalium is frequently encountered in the female genital tract and is not associated with cervicitis or any particular clinical or microbiologic data. [ABSTRACT FROM AUTHOR]

Openers of K+(ATP) channels protect the myocardium from I/R injury. Sulfonylureas are known as potent blockers of K(ATP) channels. We investigated whether 1) mitochondrial permeability transition pore may be involved in the protection afforded by the mitoK+(ATP) opener nicorandil and 2) whether sulfonylureas may prevent this beneficial effect. Anesthetized New Zealand White rabbits underwent 30 min of coronary artery occlusion, followed by 60 (isolated mitochondria) or 240 min (infarct size) of reperfusion. They received an administration of either saline (control) or nicorandil (0.5 mg kg(-1), i.v.) 15 min before ischemia. Each control and nicorandil group was divided in four subgroups pretreated by either saline, glibenclamide (Glib; 1 mg kg(-1)), gliclazide (Glic; 1 mg kg(-1)), or glimepiride (Glim; 5 microg kg(-1)) 10 min before this. Infarct size was assessed by triphenyltetrazolium chloride staining. Mitochondria were isolated from the area at risk for further assessment of the calcium retention capacity. Glibenclamide (35 +/- 8), but neither Glic (61 +/- 9) nor Glim (48 +/- 7), reversed the improvement in calcium retention capacity due to nicorandil (58 +/- 10 vs. 27 +/- 8 nmoles CaCl2 mg(-1) proteins in control). Infarct size reduction by nicorandil (32% +/- 6% vs. 65% +/- 6% of area at risk) was abolished by Glib (55 +/- 5) but not by Glic (37 +/- 3) or Glim (31 +/- 5). These data suggest that 1) the protective effect of nicorandil involves the inhibition of the mitochondrial permeability transition pore and 2) that unlike Glib, second-generation sulfonylureas preserve this cardioprotection.

Background: Brief periods of ischemia performed just at the time of reperfusion can reduce infarct size, a phenomenon called "postconditioning." After reflow, opening of the mitochondrial permeability transition pore (mPTP) has been involved in lethal reperfusion injury. We hypothesized that postconditioning may modulate mPTP opening., Methods and Results: Anesthetized open-chest rabbits underwent 30 minutes of ischemia and 4 hours of reperfusion. Control hearts underwent no additional intervention. Postconditioning consisted of 4 episodes of 1 minute of coronary occlusion and 1 minute of reperfusion performed after 1 minute of reflow after the prolonged ischemia. Preconditioning consisted of 5 minutes of ischemia and 5 minutes of reperfusion before the 30-minute ischemia. An additional group of rabbits received 5 mg/kg IV of NIM811, a specific inhibitor of the mPTP, 1 minute before reperfusion. Infarct size was assessed by triphenyltetrazolium staining. Mitochondria were isolated from the risk region myocardium, and Ca2+-induced mPTP opening was assessed by use of a potentiometric method. Postconditioning, preconditioning, and NIM811 significantly limited infarct size, which averaged 29+/-4%, 18+/-4%, and 20+/-4% of the risk region, respectively, versus 61+/-6% in controls (P< or =0.001 versus control). The Ca2+ load required to open the mPTP averaged 41+/-4, 47+/-5, and 67+/-9 micromol/L CaCl2 per mg of mitochondrial proteins in postconditioning, preconditioning, and NIM811, respectively, significantly higher than the value of 16+/-4 micromol/L per mg in controls (P< or =0.05)., Conclusions: Postconditioning inhibits opening of the mPTP and provides a powerful antiischemic protection.