Transmesocolic internal herniation: a rare case of small bowel obstruction, “the Marrakesh hernia”

Internal hernias, including paraduodenal (traditionally the most common), pericecal, foramen of Winslow, and intersigmoid hernias, account for approximately 0.5–5.8% of all cases of intestinal obstruction and are associated with a high mortality rate, exceeding 50% in some series. We report an extremely rare case of an internal abdominal hernia, through the right mesocolon, in a young woman with a right colon with no peritoneal fixation. This hernia was revealing by abdominal pain, nausea, and vomiting. The diagnosis of internal hernia was suggested by computed tomography (CT), but the exact type of internal hernia was confirmed by surgical exploration. The postoperative course was uneventful and the patient fully recovered after 3 days. The patient is free from symptoms and from recurrence, after 12 months of follow-up.     

Elaidic acid sustains LPS and TNF-α induced ICAM-1 and VCAM-I expression on human bone marrow endothelial cells (HBMEC)

ObjectivesElaidic acid, the predominant trans-fatty acid in industrially hydrogenated oils, exists on high levels in Iranian hydrogenated oils and margarines. This study was undertaken to investigate the effect of elaidic acid and its cis-counterpart oleic acid on expression of ICAM-1 and VCAM-1 on human bone marrow endothelial cells (HBMECs).Design and methodsHBMEC were pre-treated with TNF-α or LPS for induction of the adhesion molecules expression, and then treated with elaidic acid or oleic acid. Soluble and cell associated forms of ICAM-1 and VCAM-1 were quantified by ELISA and Western blot.ResultsOur findings indicated that oleic acid suppresses VCAM-1 and ICAM-1 expression on HBMEC near to the basal level. Conversely, elaidic acid maintained the level of VCAM-1 and ICAM-1 up-regulated by TNF-α or LPS.ConclusionsIt is suggested that elaidic acid could keep the HBMEC at the stimulated phenotype. These findings provide further support on the detrimental effects of elaidic acid in promotion and induction of cardiovascular diseases (CVD).     

Locking sliding knots in laboratory model of thoracoscopic repair of esophageal atresia

Aim

The study aimed to assess feasibility and strength of locking sliding knots, in comparison to intracorporeal square knots, in a thoracoscopic model of esophageal atresia (EA).

Methods

A simple thoracoscopic model of EA was created, and inside this model, 26 sliding knots were used to suture a soft drain together. In all cases, ten 5-0 monofilament sutures were used for this “anastomosis.” The drain is then mounted on a motorized digital tensometer, and the knots with the best tension profile were retested 4 more times to obtain an average. The tensometer measured the knots' strength by producing a constant and increasing weight on the sutured EA model and continuous readings were taken by integrated computer software. The point, at which either the knot slipped, broke, or the drain disrupted, was taken as the maximum load tolerated by the sliding knots. Knot pushers were not required for any of these knots.

Results

Of the 26 sliding knots, only locking sliding knots tolerated reasonably high tensions. However, when comparing these knots to the standard square knot, only Giant and Field knots had similar tension readings. Field knot was found to be very complex and therefore impractical with 5-0 suture material, leaving Giant knot as the only knot with favorable results.

Conclusions

Locking sliding knots and particularly Giant knot could have an enormous impact in minimally invasive surgery of neonatal conditions and can potentially replace intracorporeal knots. Giant knot is faster to tie and thus could reduce surgeon's fatigue during complex procedures.     

The change in attitude and knowledge of health care personnel and general population following trainings provided during integration of mental health in Primary Health Care in Iran: a systematic review

Background  

Mental health has been integrated in the primary health care program in small cities and villages of Iran in a national level since the late 1980s. We performed a systematic review of literature to investigate the effect of education on change in attitude and knowledge of mental health care providers and the population covered in the program during the recent two decades in Iran.     

Prolonged ethanol administration depletes mitochondrial DNA in MnSOD-overexpressing transgenic mice, but not in their wild type littermates

Alcohol consumption increases reactive oxygen species formation and lipid peroxidation, whose products can damage mitochondrial DNA (mtDNA) and alter mitochondrial function. A possible role of manganese superoxide dismutase (MnSOD) on these effects has not been investigated. To test whether MnSOD overexpression modulates alcohol-induced mitochondrial alterations, we added ethanol to the drinking water of transgenic MnSOD-overexpressing (TgMnSOD) mice and their wild type (WT) littermates for 7 weeks. In TgMnSOD mice, alcohol administration further increased the activity of MnSOD, but decreased cytosolic glutathione as well as cytosolic glutathione peroxidase activity and peroxisomal catalase activity. Whereas ethanol increased cytochrome P-450 2E1 and mitochondrial ROS generation in both WT and TgMnSOD mice, hepatic iron, lipid peroxidation products and respiratory complex I protein carbonyls were only increased in ethanol-treated TgMnSOD mice but not in WT mice. In ethanol-fed TgMnSOD mice, but not ethanol-fed WT mice, mtDNA was depleted, and mtDNA lesions blocked the progress of polymerases. The iron chelator, DFO prevented hepatic iron accumulation, lipid peroxidation, protein carbonyl formation and mtDNA depletion in alcohol-treated TgMnSOD mice. Alcohol markedly decreased the activities of complexes I, IV and V of the respiratory chain in TgMnSOD, with absent or lesser effects in WT mice. There was no inflammation, apoptosis or necrosis, and steatosis was similar in ethanol-treated WT and TgMnSOD mice. In conclusion, prolonged alcohol administration selectively triggers iron accumulation, lipid peroxidation, respiratory complex I protein carbonylation, mtDNA lesions blocking the progress of polymerases, mtDNA depletion and respiratory complex dysfunction in TgMnSOD mice but not in WT mice.