A potential role for mast cells in the of bFGF from normal myocytes during angiogenesis in vivo.

Basic fibroblast growth factor (bFGF) is a potent angiogenic factor produced by cells of mesodermal and neuroectodermal origin. Despite numerous advances, the precise mechanism of bFGF release from cells still remains unknown. Upon release from cells, the protein is stored and protected in the extracellular matrix by binding to heparan sulfate proteoglycans. A number of reports suggest that degrading enzymes secreted by mast cells may play a role in the release of bFGF from connective tissue stores. Additionally, mast cells are believed to play a role in the formation of new blood vessels. In this report, we studied the events involved in neovascularization using a well-characterized model of angiogenesis in rabbits where neovascularization is induced by transfer of a well-perfused rectus abdominis muscle flap to an ischemic limb. Using this model, we demonstrate that bFGF expression is induced in normal myofibers and bFGF is released in the wound fluid at the ischemic/nonischemic interface. The highest concentrations of bFGF were detected on days 14 and 21 postoperation. We also show that the number of mast cells and their degranulation correlate with the release of bFGF from adjacent muscle tissue and the appearance of the growth factor in the wound fluid. There appears to exist a temporal correlation between number of mast cells, their degranulation, and the release of bFGF during angiogenesis in vivo.     

The risk of cardiovascular disease associated with proteinuria in renal transplant patients

Proteinuria in the general population has been shown to be associated with cardiovascular disease, which is the main cause of death in renal transplantation. We investigated the effect of proteinuria on cardiovascular disease after renal transplantation in 532 renal transplant patients with functioning grafts for more than 1 year. Patients were classified into two groups depending on the presence of persistent proteinuria. We analyzed graft and patient survival, posttransplantation cardiovascular disease, and main causes of graft loss and death. Five- and 10-year graft and patient survival rates were lower in the group with proteinuria. The main cause of death was vascular disease in both groups. The presence of posttransplantation cardiovascular disease was higher in the group with proteinuria. Persistent proteinuria was associated with graft loss (RR=4.18), patient death (RR=1.92), and cardiovascular disease (RR=2.45). In conclusion, persistent proteinuria was an independent risk factor for increased cardiovascular morbidity and mortality in renal transplant patients.     

Return to dialysis after renal transplantation. Which would be the best way?

The exact moment to return to dialysis when a graft fails has not clearly been established. Furthermore, there is no agreement with respect to whether the guidelines accepted for patients entering dialysis for the first time are adequate for this subgroup of patients with advanced renal failure, due to the special characteristics of these patients, derived from the immunosuppressive medications they are taking among other accompanying factors. We reviewed a group of renal transplant patients who returned to dialysis and compared them with a group of patients entering dialysis for the first time. Patients with chronic renal failure due to graft failure had a poorer renal function at the time entering dialysis and a more profound anemia. Additionally, complications considered such as the number of hospital admissions during the first year after initiation of dialysis were considerably higher in the group of transplanted patients. We advocate for an earlier referral to the dialysis unit, a more aggressive erythropoietin therapy in the phase of advanced renal failure due to chronic allograft nephropathy, and in selected cases retransplantation before definitive graft loss.     

Mechanism of vascular smooth muscle cells activation by hydrogen peroxide: role of phospholipase C gamma.

BACKGROUND: Hydrogen peroxide (H2O2) formation is a critical factor in processes involving ischaemia/ reperfusion. However, the precise mechanism by which reactive oxygen species (ROS) induce vascular damage are insufficiently known. Specifically, activation of phospholipase C gamma (PLCgamma) is a probable candidate pathway involved in vascular smooth muscle cells (VSMC) activation by H2O2. METHODS: The activation of human venous VSMC was measured as cytosolic free calcium mobilization, shape change and protein phosphorylation, focusing on the role of tyrosine phosphorylation-activated PLCgamma. RESULTS: The exposure of VSMC to exogenous H2O2 caused a rapid increase in cytosolic free calcium concentration ([Ca2+]i), and induced a significant VSMC shape change. Both effects were dependent on a tyrosine kinase-mediated mechanism, as determined by the blockade of short-term treatment of VSMC with the protein tyrosine kinase inhibitor, genistein. Giving further support to the putative role of phospholipase C (PLC)-dependent pathways, the [Ca2+]i and VSMC shape change response were equally inhibited by the specific PLC blocker, 1-(6-((17-beta-methoxyestra-1,3,5(10)trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). In addition, U73122 had a protective effect against the deleterious action (24 h) of H2O2 on non-confluent VSMC. As a further clarification of the specific pathway involved, the exposure to H2O2 significantly stimulated the tyrosine phosphorylation of PLCgamma with a concentration- and time-profile similar to that of [Ca(2+)](i) mobilization. CONCLUSIONS: The present study reveals that H(2)O(2) activates PLCgamma on VSMC through tyrosine phosphorylation and that this activation has a major role in rapid [Ca(2+)](i) mobilization, shape-changing actions and damage by H(2)O(2) in this type of cells. These findings have direct implications for understanding the mechanisms of the vascular actions of H(2)O(2) and may help to design pharmacologically protective strategies.     

Scrotal cystic hygroma in a 13-year-old boy

We describe a patient with cystic hygroma, in a rare location (scrotum). The hygroma was diagnosed incidentally after injury to the scrotum in a 13-year-old boy. The diagnostic methods used, the characteristics of this type of tumor, its treatment and its clinical course are described. We suggest that cystic hygroma be taken into account in the differential diagnosis of other more frequent causes of scrotal masses.     

The Prevalence of Groin Pain After Metal-on-Metal Total Hip Arthroplasty and Total Hip Resurfacing

Background  

Groin pain after total hip arthroplasty (THA) or total hip resurfacing arthroplasty can be troubling for patients and surgeons. Potential sources of pain include infection, loosening, metal hypersensitivity, or impingement of bony structures or the iliopsoas tendon.     

Evaluation of the Rebound Hernia Repair Device for Laparoscopic Hernia Repair

Background:

The characteristics of the ideal type of mesh are still being debated. Mesh shrinkage and fixation have been associated with complications. Avoiding shrinkage and fixation would improve hernia recurrence rates and complications. To our knowledge, this is the first study of a device with a self-expanding frame for laparoscopic hernia repair.

Methods:

Six Rebound Hernia Repair Devices were placed laparoscopically in pigs. This device is a condensed polypropylene, super-thin, lightweight, macro-porous mesh with a self-expanding Nitinol frame. The devices were assessed for adhesions, shrinkage, and histological examination. Laboratory and radiologic evaluations were also performed.

Results:

The handling properties of the devices facilitated their laparoscopic placement. They were easily identified with simple x-rays. The mesh was firmly integrated within the surrounding tissue. One device was associated with 3 small adhesions. The other 5 HRDs had no adhesions. We noted no shrinkage or folding. All devices preserved their original size and shape.

Conclusions:

At this evaluation stage, we found that the Rebound Hernia Repair Device may serve for laparoscopic hernia repair and has favorable handling properties. It prevents folding and shrinkage of the mesh. It may eliminate the need for fixation, thus preventing chronic pain. The Nitinol frame also allowed radiologic evaluation for gross movement. Further studies will be needed to evaluate its clinical application.     

Sub-exemplar shape tuning in human face-related areas

Although human face recognition performance shows high selectivity, even for unfamiliar faces, the neuronal circuitry underlying this high performance is poorly understood. Two extreme alternatives can be considered: either a "labeled-line" principle, in which subtle changes in face images lead to activation of differently tuned neuronal populations, or a coarse coding principle, where the high face selectivity is coded by the relative activation of broadly tuned neurons. In this study, we set to parametrically examine the shape and selectivity profile of face-related visual areas. To that end, we applied the functional magnetic resonance (fMR)-adaptation paradigm. Unfamiliar face stimuli were morphed into sets ranging from identical faces, through subtle morphing, to completely different exemplars. The fusiform face area (FFA) revealed high face sensitivity, so that even facial images perceived as belonging to the same individual (<35%) were sufficient to produce full recovery from adaptation. Interestingly, the psychophysical detectability of facial differences paralleled the release from fMR-adaptation. These results support the labeled-line model where high sensitivity to face changes is paralleled by narrow tuning of neuronal populations selective to each face image, and they suggest that fMR-adaptation is closely related to behavior. The results bear strong implications to the nature of face-related neuronal responses.     

Use of a Roux Limb to Correct Esophagogastric Junction Fistulas after Sleeve Gastrectomy

Laparoscopic sleeve gastrectomy (LSG) can be complicated, in the early postoperative course, by an esophagogastric junction (EGJ) leak with very serious consequences. A 48-year-old woman developed an EGJ leak 3 days after LSG surgery and was treated with conservative measures. Finally, 6 weeks after the original surgery, a Roux limb was brought to the EGJ and anastomosed side-to-end to the fistula. At the beginning, the Roux limb was the only functioning outlet and finally, 2 months later, both pathways (the gastric sleeve and the Roux-en-Y) are patent at 3 months after surgery. The Roux limb resolved a dangerous EGJ leak after a LSG.     

The G93C mutation in superoxide dismutase 1: clinicopathologic phenotype and prognosis

BACKGROUND: Twenty percent of familial amyotrophic lateral sclerosis (ALS) is caused by mutations in the superoxide dismutase 1 gene (SOD1). Few data exist on their clinicopathologic phenotypes. OBJECTIVES: To determine the clinical and pathologic phenotype associated with the G93C mutation in SOD1 and to compare survival in familial ALS related to this mutation with survival in other ALS subgroups. DESIGN: Retrospective study. SETTING: Tertiary referral center for neuromuscular disorders. PATIENTS: Twenty patients with the G93C mutation for whom clinical data were available and 1 patient with pathologic data. MAIN OUTCOME MEASURES: Characteristics and survival compared with other ALS subgroups, adjusting for known prognostic factors. RESULTS: The G93C mutation was associated with a purely lower motor neuron phenotype without bulbar involvement. Presence of the mutation independently predicted longer survival compared with other ALS subgroups. Pathologic examination showed degeneration of the anterior horn, spinocerebellar tracts, and posterior funiculi, with minimal involvement of corticospinal tracts and no degeneration of brainstem motor nuclei. Survival motor neuron gene copy number had no significant influence on age at onset or survival in patients with the G93C mutation. CONCLUSIONS: These findings add to the knowledge of SOD1-related familial ALS and demonstrate further clinicopathologic variability between different SOD1 mutations. Finally, they demonstrate the independent prognostic value of the G93C mutation.