Hemorrhagic and Thromboembolic Complications after Bariatric Surgery in Patients Receiving Chronic Anticoagulation Therapy

Background Perioperative management of bariatric surgical patients receiving chronic anticoagulation requires an understanding of potential hemorrhagic and thromboembolic risks. The aim of this study is to evaluate hemorrhagic and thromboembolic complications in morbidly obese patients who are on oral anticoagulation treatment and subsequently undergo laparoscopic bariatric surgery. Methods The medical records of all laparoscopic Roux-en-Y gastric bypass (LRYGB) patients from June 2001 to March 2006 were retrospectively reviewed. In addition, data of patients who received chronic anticoagulation therapy with Coumadin and underwent laparoscopic Roux-en-Y gastric bypass was analyzed. Clinical parameters included length of hospitalization, hemorrhagic complications, thromboembolic complications, conversion rate, reoperation, and blood transfusion. Results During the study period, 1,700 consecutive patients underwent bariatric surgery for the treatment of morbid obesity. Of these, 21 patients were treated with chronic oral anticoagulation; 3 of the 21 (14%) had hemorrhagic complications: one patient had intraluminal hemorrhage and two patients had intraabdominal hemorrhage. Two patients required blood transfusion, and one patient underwent surgical reintervention. None of the 21 laparoscopic operations were converted to open procedures. There were no postoperative mortalities, and there were no thromboembolic events in this series. Conclusions Laparoscopic bariatric surgery can be performed relatively safely in morbidly obese patients who are treated with chronic oral anticoagulation. Even in the presence of bleeding, patients can be successfully treated without the need for reoperation.     

Laparoscopic resection of a retroperitoneal degenerative schwannoma: a case report and review of the literature

Degenerative schwannomas are rare benign tumors. The patient presented in this case report complained of a dull left upper quadrant pain for several months. A computed tomography scan revealed a low-density lesion at the level of T12. The lesion was laparoscopically resected and pathologic examination revealed a degenerative schwannoma.     

Alleviation of acute and chronic graft-versus-host disease in a murine model is associated with glucocerebroside-enhanced natural killer T lymphocyte plasticity

BACKGROUND: Natural killer T (NKT) lymphocytes play a role in graft-versus-host disease GVHD (GVHD). Glucocerebroside (GC) is a naturally occurring glycolipid that plays a role in the immune modulation of NKT lymphocytes. This study aims to determine the effect of GC in murine models of semiallogeneic/acute and chronic GVHD. METHODS: Acute and chronic GVHD were generated by fusion of splenocytes from C57BL/6 to (C57BL/6xBalb/c) F1 mice, and from B10.D2 donor mice into Balb/c, respectively. Recipients were treated daily with GC. Histological and immunological parameters of GVHD were assessed. RESULTS: Treatment with GC significantly alleviated GVHD in both models The beneficial effect of GC was associated with an increase in the intrahepatic/peripheral NKT lymphocyte ratio in the semiallogeneic/acute model. This ratio was decreased in the chronic GVHD model. A significant increase in intrahepatic CD8+ lymphocyte trapping was noted in the semiallogeneic/acute model, whereas the opposite effect was observed in the chronic GVHD model. Administration of GC led to decreased serum interferon-gamma and increased serum interleukin-4 levels in the Th1-mediated model, whereas the opposite effect was observed in the Th2-mediated models. CONCLUSIONS: GC ameliorates GVHD in both Th1- and Th2-mediated murine models, suggesting it is able to differentially affect the immune system. GC may alleviate immunologically incongruous disorders, and may be associated with "fine tuning" of immune responses.     

Human vulnerability to stress depends on amygdala's predisposition and hippocampal plasticity

Variations in people''s vulnerability to stressful life events may rise from a predated neural sensitivity as well as from differential neural modifications in response to the event. Because the occurrence of a stressful life event cannot be foreseen, characterizing the temporal trajectory of its neural manifestations in humans has been a real challenge. The current prospective study examined the emotional experience and brain responses of 50 a priori healthy new recruits to the Israeli Defense Forces at 2 time points: before they entered their mandatory military service and after their subsequent exposure to stressful events while deployed in combat units. Over time, soldiers reported on increase in stress symptoms that was correlated with greater amygdala and hippocampus responsiveness to stress-related content. However, these closely situated core limbic regions exhibited different temporal trajectories with regard to the stress effect; whereas amygdala''s reactivity before stress predicted the increase in stress symptoms, the hippocampal change in activation over time correlated with the increase in such symptoms. Hippocampal plasticity was also reflected by a modification over time of its functional coupling with the ventromedial prefrontal cortex, and this coupling magnitude was again predicted by predated amygdala reactivity. Together, these findings suggest that variations in human''s likelihood to develop symptomatic phenomena following stressful life events may depend on a balanced interplay between their amygdala''s predisposing reactivity and hippocampal posteriori intra- and interregional plasticity. Accordingly, an individually tailored therapeutic approach for trauma survivors should target these 2 neural probes while considering their unique temporal prints.     

A short-term graphomotor program for improving writing readiness skills of first-grade students.

OBJECTIVE: Children with fine-motor problems and handwriting difficulties often are referred for occupational therapy. The objective of this study was to test the efficacy of a short-term treatment on the fine-motor and graphomotor skills of first-grade students. METHOD: We recruited 52 first-grade students who had scored below the 21st percentile on the Visual-Motor Integration test from schools in a city with a low socioeconomic, mixed (Arab and Jewish) population. The children were randomly divided into an intervention group and a control group. Before and after the intervention, we administered two tests to both groups. RESULTS: Students in the intervention group made significant gains both in the total score on the graphomotor test (Developmental Test of Visual Perception) and on the fine-motor test (Bruininks-Oseretsky Motor Development Scale). CONCLUSION: This study provided preliminary evidence of the efficacy of a short-term graphomotor intervention. The results increased the feasibility of implementing occupational therapy intervention in the Israeli school system, allowing treatment of more children using the same resources.     

Analytical determination of receptor-ligand dissociation constants of two populations of receptors from displacement curves.

The determination of receptor-ligand dissociation constants from displacement data has been restricted until recently to the condition of receptor saturation, in which the concentration of receptor is negligible as compared to the displaced ligand and the displacing ligand used. This restriction has lately been removed since an accurate method has been developed for the determination of the dissociation constants for all experimental conditions for a system that includes a single type of binding site. In many cases, however, there are two types of receptor binding sites that exhibit different affinities toward the ligand. The present study provides an analytic solution for the problem of determination of the two dissociation constants as well as the proportion of the two receptor types. The formal derivation of the equations is described, along with analysis of a displacement simulation. The sensitivity of the method to the ratio between the two dissociation constants is also investigated. The application of the method is demonstrated for the analysis of the binding of beta-adrenergic receptors to the agonist isoproterenol as monitored by the displacement of the beta-antagonist 125I-labeled cyanopindolol.     

Cystatin C takes part in melanoma-microglia cross-talk: possible implications for brain metastasis

The development of melanoma brain metastasis is largely dependent on mutual interactions between the melanoma cells and cells in the brain microenvironment. Here, we report that the extracellular cysteine protease inhibitor cystatin C (CysC) is involved in these interactions. Microglia-derived factors upregulated CysC secretion by melanoma. Similarly, melanoma-derived factors upregulated CysC secretion by microglia. Whereas CysC enhanced melanoma cell migration through a layer of brain endothelial cells, it inhibited the migration of microglia cells toward melanoma cells. CysC was also found to promote the formation of melanoma three-dimensional structures in matrigel. IHC analysis revealed increased expression levels of CysC in the brain of immune-deficient mice bearing xenografted human melanoma brain metastasis compared to the brain of control mice. Based on these in vitro and in vivo experiments we hypothesize that CysC promotes melanoma brain metastasis. Increased expression levels of CysC were detected in the regenerating brain of mice after stroke. Post-stroke brain with melanoma brain metastasis showed an even stronger expression of CysC. The in vitro induction of stroke-like conditions in brain microenvironmental cells increased the levels of CysC in the secretome of microglia cells, but not in the secretome of brain endothelial cells. The similarities between melanoma brain metastasis and stroke with respect to CysC expression by and secretion from microglia cells suggest that CysC may be involved in shared pathways between brain metastasis and post-stroke regeneration. This manifests the tendency of tumor cells to highjack physiological molecular pathways in their progression.