ABSTRACT
Background@# Respiratory mechanics are often significantly altered in morbidly obese patients and magnesium sulfate (MgSO4) is a promising agent for managing several respiratory disorders. This study aimed to examine the effects of MgSO4 infusions on arterial oxygenation and lung mechanics in patients with morbid obesity undergoing laparoscopic bariatric surgery. @*Methods@# Forty patients with morbid obesity aged 21–60 years scheduled for laparoscopic bariatric surgery under general anesthesia were randomly allocated to either the control (normal saline infusion) or MgSO4 group (30 mg/kg lean body weight [LBW] of 10% MgSO4 in 100 ml normal saline intravenously over 30 min as a loading dose, followed by 10 mg/kg LBW/h for 90 min). The primary outcome was intraoperative arterial oxygenation (ΔPaO2/FiO2). Secondary outcomes included intraoperative static and dynamic compliance, dead space, and hemodynamic parameters. @*Results@# At 90 min intraoperatively, the Δ PaO2/FiO2 ratio and the Δ dynamic lung compliance were statistically significantly higher in the MgSO4 group (mean ± SE: 16.1 ± 1.0, 95% CI [14.1, 18.1] and 8.4 ± 0.5 ml/cmH2O, 95% CI [7.4, 9.4]), respectively), and the Δ dead space (%) was statistically significantly lower in the MgSO4 group (mean ± SE: −8.0 ± 0.3%, 95% CI [−8.6, −7.4]) (P < 0.001). No significant differences in static compliance were observed. @*Conclusions@# Although MgSO4 significantly preserved arterial oxygenation and maintained dynamic lung compliance and dead space in patients with morbid obesity, the clinical relevance is minimal. This study failed to adequately reflect the clinical importance of these results.
ABSTRACT
Schistosomiasis is a chronic disease with considerable social impact. Despite the availability of affordable chemotherapy, drug treatment has not significantly reduced the overall number of disease cases. Among other mechanisms, the parasite produces PGE2 and PGD2 to evade host immune defenses. To investigate the role of PGE2 and PGD2 in schistosomiasis, we evaluated the effects of L-161,982, Ah6809 [PGE2 receptor antagonists alone or combined with each other] and MK-0524 [PGD2 receptor antagonist] during prepatent Schistosoma mansoni infection. Drugs were administered intraperitoneally an hour before and 24 hours after infection of C57BL/6 mice with 100 Schistosoma mansoni cercariae. L-161,982, Ah6809, their combination and MK-0524 caused partial protection against pre-patent S. mansoni infection which was mediated by biasing the immune response towards Th1 phenotype. These results showed that blockade of PGE2 and PGD2 receptors confers partial protection against pre-patent S. mansoni infection in mice and that they may be useful as adjunctive therapy to current anti-schistosomal drugs or vaccines
Subject(s)
Animals, Laboratory , Dinoprostone , Prostaglandin D2 , Receptors, Prostaglandin E , Receptors, Prostaglandin , MiceABSTRACT
According to a large number of studies, there is a frequent association of congenital heart disease [CHD] and urinary tract anomalies [UTA]. The purpose of this study is to evaluate the advisability of sonographic screening of uropathy in patients with malformative heart disease. The study comprised 180 children. All of these children were investigated for CUD but none were symptomatic in terms of the urinary tract diseases. The patients were divided into 2 groups, group I included 107 patients [59.4%] with a cyanotic CHD and group II included 73 patients [40.5%] with cyanotic CHD. All patients in the study were subjected to echocardiography and sonographic screening for associated uropathy. Out of 180 children, the incidence of UTA detected by sonography was 24/180 [73.3%]. There was no significant difference in the incidence of UTA between those with a cyanotic CHD 14/107 [13.1%] and those with cyanotic CHD 10/73 [13.7%], p=0.15. However, no association between a specific CUD and a particular UTA could be found
Conclusion: sonography should be routinely performed to screen for previously undetected or silent but potentially serious UTA in children with CHD