Viral-like brain inflammation during development causes increased seizure susceptibility in adult rats.

Viral infections of the CNS and their accompanying inflammation can cause long-term neurological effects, including increased risk for seizures. To examine the effects of CNS inflammation, we infused polyinosinic:polycytidylic acid, intracerebroventricularly to mimic a viral CNS infection in 14 day-old rats. This caused fever and an increase in the pro-inflammatory cytokine, interleukin (IL)-1beta in the brain. As young adults, these animals were more susceptible to lithium-pilocarpine and pentylenetetrazol-induced seizures and showed memory deficits in fear conditioning. Whereas there was no alteration in adult hippocampal cytokine levels, we found a marked increase in NMDA (NR2A and C) and AMPA (GluR1) glutamate receptor subunit mRNA expression. The increase in seizure susceptibility, glutamate receptor subunits, and hippocampal IL-1beta levels were suppressed by neonatal systemic minocycline. Thus, a novel model of viral CNS inflammation reveals pathophysiological relationships between brain cytokines, glutamate receptors, behaviour and seizures, which can be attenuated by anti-inflammatory agents like minocycline.

Caesarean section rates in teaching hospitals of Tehran: 1999-2003.

To determine the trends of caesarean section in teaching hospitals of Tehran University of Medical Sciences, a retrospective analysis was performed on the obstetric data from 3 hospitals in a 5-year period. The caesarean section rate increased from 35.4% of deliveries in 1999 to 42.3% in 2003. The data showed that there was a steady increase in elective operations that might explain the rise in overall caesarean section rate.

Caesarean section rates in teaching hospitals of Tehran: 1999-2003

To determine the trends of caesarean section in teaching hospitals of Tehran University of Medical Sciences, a retrospective analysis was performed on the obstetric data from 3 hospitals in a 5- year period. The caesarean section rate increased from 35.4% of deliveries in 1999 to 42.3% in 2003. The data showed that there was a steady increase in elective operations that might explain the rise in overall caesarean section rate

Ultra-low dose naltrexone potentiates the anticonvulsant effect of low dose morphine on clonic seizures.

Significant potentiation of analgesic effects of opioids can be achieved through selective blockade of their stimulatory effects on intracellular signaling pathways by ultra-low doses of opioid receptor antagonists. However, the generality and specificity of this interaction is not well understood. The bimodal modulation of pentylenetetrazole-induced seizure threshold by opioids provide a model to assess the potential usefulness of this approach in seizure disorders and to examine the differential mechanisms involved in opioid anti- (morphine at 0.5-3 mg/kg) versus pro-convulsant (20-100 mg/kg) effects. Systemic administration of ultra-low doses of naltrexone (100 fg/kg-10 ng/kg) significantly potentiated the anticonvulsant effect of morphine at 0.5 mg/kg while higher degrees of opioid receptor antagonism blocked this effect. Moreover, inhibition of opioid-induced excitatory signaling by naltrexone (1 ng/kg) unmasked a strong anticonvulsant effect for very low doses of morphine (1 ng/kg-100 microg/kg), suggesting that a presumed inhibitory component of opioid receptor signaling can exert strong seizure-protective effects even at very low levels of opioid receptor activation. However, ultra-low dose naltrexone could not increase the maximal anticonvulsant effect of morphine (1-3 mg/kg), possibly due to a ceiling effect. The proconvulsant effects of morphine on seizure threshold were minimally altered by ultra-low doses of naltrexone while being completely blocked by a higher dose (1 mg/kg) of the antagonist. The present data suggest that ultra-low doses of opioid receptor antagonists may provide a potent strategy to modulate seizure susceptibility, especially in conjunction with very low doses of opioids.

Is normal beta-hCG regression curve helpful in the diagnosis of persistent trophoblastic disease?

OBJECTIVE: The aim of this study was to evaluate the probable usefulness of normal beta-human chorionic gonadotropin (beta-hCG) regression curve in the diagnosis of persistent trophoblastic disease (PTD). METHODS: A log-value regression curve was developed from the means and 95% confidence limits of serial weekly serum beta-hCG titers of 43 patients with uneventful complete hydatidiform moles and 14 patients, who were previously confirmed as PTD. RESULTS: All 14 PTD patients (100%) had abnormal values, beyond normal range, within 4 weeks. beta-hCG was in its upper values, compared to normal regression curve at 2.29 +/- 0.19 weeks. This was earlier than plateau or rise detection at 4.21 +/- 0.33 weeks (P < 0.001). Within 3 weeks of evacuation, 13 of 14 (92.86%) PTD patients' beta-hCG values exceeded the normal range, whereas only six of 14 (42%) showed a rise or plateau. CONCLUSION: Our finding indicates that the normal beta-hCG regression curve may be useful for quicker detection of PTD than the plateau or rise of level.