Congenital Mesocolic Hernia

Mesocolic hernia is a rare congenital anomaly caused by an error of rotation of the midgut. It may be seen as total encapsulation of the small bowel or a single loop within a hernial sac. It may be asymptomatic or cause life-threatening intestinal obstruction. Symptoms, when present, are often chronic vague abdominal pain and intermittent obstructive episodes. We have encountered a 40-year-old woman with a congenital mesocolic hernia. Abdominal CT provided the diagnosis. She successfully underwent operation and discharged with good condition. Now we present a case of congenital mesocolic hernia with a review of some articles.

Morphologic and Time Dependent Changes of Nitric Oxide Synthesis Following Anoxia and Reoxygenation of the Endothelial Cells of the Umbilical Vein

PURPOSE: In order to clarify the exact role of nitric oxide for a ischemia-reperfusion (I/R) injury, we observed morphologic change of endothelial cells and a time dependent change of nitric oxide synthesis following anoxia and reperfusion injuries. METHODS: The experimental groups were divided into 4 sub-groups: a control group without any treatment, an anoxia group treated with anoxic air (93% N2, 5% CO2, 2% H2) for 50 minutes, a reoxygenation group treated with 100% O2 for 480 minutes, and an allopurinol group treated with allopurinol immediately prior to reoxygenation. Endothelial cells were isolated from a human fetal umbilical vein and cultured in M-199 medium. We observed a morphological change of the endothelial cells with inverted light microscopy and we studied the time dependent change of nitric oxide synthesis with microelectrode following anoxia and reperfusion injuries. RESULTS: Most significantly, the endothelial cells of the anoxia group were more flattened and detached than those of the control group. A more severe detachment of endothelial cells was found in the reoxygenation group than in the anoxia group. There was no significant difference in the morphological change between the allopurinol group and the anoxia group. Additionally, the concentration of NO in the anoxia group (2511.62 428.60 nM/1 105 cells/ml) was lower than that of the control group (3505.14 192.95 nM/1 105 cells/ml) (P<0.005). The NO concentration of thereoxygenation group reached its highest level of 2953.14 90.98 nM/1 105 cells/ml at 180 minutes (P<0.05) and decreased thereafter. There was no significant difference in the NO concentration between the allopurinol and anoxia groups. CONCLUSION: The morphologic damage of endothelial cells in the reoxygenation group was significantly increased as compared with the anoxia group. Nitric oxide syntheses in the reoxygenation and anoxia groups was decreased as compared with the control group.

Morphologic and Time Dependent Changes of Nitric Oxide Synthesis Following Anoxia and Reoxygenation of the Endothelial Cells of the Umbilical Vein

PURPOSE: In order to clarify the exact role of nitric oxide for a ischemia-reperfusion (I/R) injury, we observed morphologic change of endothelial cells and a time dependent change of nitric oxide synthesis following anoxia and reperfusion injuries. METHODS: The experimental groups were divided into 4 sub-groups: a control group without any treatment, an anoxia group treated with anoxic air (93% N2, 5% CO2, 2% H2) for 50 minutes, a reoxygenation group treated with 100% O2 for 480 minutes, and an allopurinol group treated with allopurinol immediately prior to reoxygenation. Endothelial cells were isolated from a human fetal umbilical vein and cultured in M-199 medium. We observed a morphological change of the endothelial cells with inverted light microscopy and we studied the time dependent change of nitric oxide synthesis with microelectrode following anoxia and reperfusion injuries. RESULTS: Most significantly, the endothelial cells of the anoxia group were more flattened and detached than those of the control group. A more severe detachment of endothelial cells was found in the reoxygenation group than in the anoxia group. There was no significant difference in the morphological change between the allopurinol group and the anoxia group. Additionally, the concentration of NO in the anoxia group (2511.62 428.60 nM/1 105 cells/ml) was lower than that of the control group (3505.14 192.95 nM/1 105 cells/ml) (P<0.005). The NO concentration of thereoxygenation group reached its highest level of 2953.14 90.98 nM/1 105 cells/ml at 180 minutes (P<0.05) and decreased thereafter. There was no significant difference in the NO concentration between the allopurinol and anoxia groups. CONCLUSION: The morphologic damage of endothelial cells in the reoxygenation group was significantly increased as compared with the anoxia group. Nitric oxide syntheses in the reoxygenation and anoxia groups was decreased as compared with the control group.

Adrenocortical Carcinoma: Report of two cases

Adrenocortical carcinoma is a rare malignant endocrine tumor which accounts for about 0.05% to 0.2% of all carcinomas. Three clinical patterns can be encountered. In 30% of the cases, a mass syndrome without any clinical evidence of hypersecretion is presented as abdominal pain, a palpable abdominal mass, abdominal distension, and weight loss. In 60% of the cases, an overt clinical syndrome of hypersecretion is of almost purely hypercortisolism in 30% of such cases, vilirization in 22%, feminization in 10%, hyperaldosteronism in 2.5%, and a mixed secretion in 35%. In the remaining 10% of the cases, an adrenal `incidentaloma' is found incidentally during evaluation of the other disease. About 70% to 80% of patients are diagnosed with an advanced stage (III or IV) and metastasis has occured in 20% to 40% of the patients at the time of presentation. Early surgery an with adrenalectomy is the only means of cure. The prognosis is poor with a 5-years survival rate of 16% to 34% due to initial diagnosis at an advanced stage. Recently, we experienced two cases of adrenocortical carcinomas. In case I, a 62-year-old female patient presented with a clinical syndrome of hypercortisolism and had an extensive local invasion of stage IV; in case II, a 49-year-old male patient complained of abdominal pain and distension without any clinical syndrome of hypersecretion and had stage IV liver metastasis.