[Intranodal palisaded myofibroblastome: A rare cause of inguinal lymphadenopathy]. / Le myofibroblastome palissadique intraganglionnaire : une cause rare d'adénopathie inguinale.

INTRODUCTION: Lymphadenopathies are a major cause of consultation in internal medicine, with various causes of diagnosis. Unexplained persistent lymphadenopathy must be biopsied to rule out malignant tumor. CASE REPORT: We report the case of a 53-year-old man, with inguinal lymphadenopathy evolving for more than one year. The patient had no associated symptoms and his blood tests were unremarkable. Due to the progression of the adenopathy and its hypermetabolism on PET-CT, an excisional biopsy was performed. Histological analysis revealed an intranodal proliferation of spindle cells with a palisading pattern. ß-catenine and smooth muscle actin labelling were positive, leading to the diagnosis of intranodal palisaded myofibroblastoma, a benign tumour. CONCLUSION: Intranodal palisaded myofibroblastoma is a rare benign cause of adenopathy, with often inguinal lymph node localization and slow growth and without risk of recurrence after surgical removal.

The HCA National Disease Management Program for coronary disease detection and treatment in women.

The diagnosis and treatment of heart disease in women continues to be one of the greatest challenges facing cardiovascular medicine today. Marked reductions in mortality rates during the past 2 decades did not result in improved outcomes for women. A major rate-limiting step to improving mortality rates for women is early diagnosis and initiation of effective lifesaving therapies for women. In 1999, HCA Healthcare Systems, Inc, Nashville, TN, initiated a coordinated effort among 208 hospitals in 26 states to improve the diagnosis of coronary disease and to target women who should receive aggressive risk factor modification and referral to cardiologists. We describe the initial phases of program development, including employee risk factor screening; citywide health risk assessment; nationwide educational programs for clinicians, staff, and consumers; and a dedicated outcomes assessment program for tracking women at risk for coronary disease. We believe that these efforts provide a venue for optimal care and improved outcomes for women served by HCA facilities.

A retrospective study of 6,671 patients comparing coronary stenting and balloon angioplasty.

OBJECTIVE: To determine whether coronary stenting, compared to percutaneous transluminal coronary angioplasty, reduces the incidence of five clinical endpoints during a six-month follow-up period. BACKGROUND: There is considerable debate concerning whether coronary stents improve clinical outcomes, especially given the rapid growth in the use of coronary stents and their economic impact. METHODS: Study population included a total of 6,671 consecutive patients at 32 hospitals in 16 different states who underwent single or multi-vessel revascularization during 1997. Patients were divided into one of two groups: those who only underwent standard balloon angioplasty (PTCA) for all treated vessels and those who received coronary stents (STENT) in all treated vessels. RESULTS: STENT patients were significantly less likely to have emergency coronary artery bypass surgery (CABG) (p = 0.001) or die during initial procedure (p = 0.034) but were more likely than PTCA patients to be treated for hematoma (p = 0.002) and bradycardia (p = 0.004). After accounting for difference in patient characteristics, risk factors, procedure complications, and number of devices utilized, the estimated odds-ratio indicates that coronary stenting, compared to PTCA, significantly (p < 0.05) reduced adverse outcomes for only one clinical event, myocardial infarction. CONCLUSIONS: Compared to balloon angioplasty patients, coronary stent patients have no statistically significant differences in regard to additional percutaneous coronary intervention or coronary artery bypass during a six-month follow-up period. Since direct cardiac catheterization lab costs associated with coronary stenting is nearly 2.5 times greater than standard balloon angioplasty, our results suggest the cost-effectiveness of coronary stenting, especially for "hard" clinical outcomes, needs to be established.

Specific RNA binding by amino-terminal peptides of alfalfa mosaic virus coat protein.

Specific RNA-protein interactions and ribonucleoprotein complexes are essential for many biological processes, but our understanding of how ribonucleoprotein particles form and accomplish their biological functions is rudimentary. This paper describes the interaction of alfalfa mosaic virus (A1MV) coat protein or peptides with viral RNA. A1MV coat protein is necessary both for virus particle formation and for the initiation of replication of the three genomic RNAs. We have examined protein determinants required for specific RNA binding and analyzed potential structural changes elicited by complex formation. The results indicate that the amino-terminus of the viral coat protein, which lacks primary sequence homology with recognized RNA binding motifs, is both necessary and sufficient for binding to RNA. Circular dichroism spectra and electrophoretic mobility shift experiments suggest that the RNA conformation is altered when amino-terminal coat protein peptides bind to the viral RNA. The peptide--RNA interaction is functionally significant because the peptides will substitute for A1MV coat protein in initiating RNA replication. The apparent conformational change that accompanies RNA--peptide complex formation may generate a structure which, unlike the viral RNA alone, can be recognized by the viral replicase.

Beta cell desensitization to glucose induced by hyperglycemia is augmented by increased calcium.

Chronic hyperglycemia has been shown to induce a decrease in beta cell sensitivity to a subsequent glucose challenge. Calcium is a necessary cofactor in the insulin secretory process and glucose elevates cytoplasmic levels. This study was designed to study whether chronic exposure to different extracellular calcium and glucose concentrations would affect the islets' subsequent response to regulatory stimuli. Islets were isolated and cultured in TC 199 plus 10% beta calf serum, glucose (5.5 or 27.5 mM) and calcium (0.5, 2.5 or 4.0 mM) for 48 h. Following culture, the islets were harvested and incubated a second time in the presence of glucose and/or arginine, theophylline, and trifluoperazine (TFP). Some islets were used for insulin content, protein synthesis studies and/or CO2 production from labelled glucose. Islets cultured in a normal glucose environment with low or normal calcium concentration maintained the capacity to respond to a subsequent glucose or arginine challenge. However, islets cultured in a high glucose or high calcium medium failed to respond to a second glucose or arginine stimulus. Theophylline stimulated insulin secretion from both glucose-sensitive and non-sensitive islets, while trifluoperazine inhibited glucose-stimulated insulin secretion in previously sensitive islets and increased insulin secretion in previously non-sensitive islets. The different culture conditions did not alter insulin content, protein synthesis or glucose conversion to labelled CO2. We conclude that chronic exposure to high glucose decreases beta cell responsiveness to glucose and amino acids. Increased extracellular calcium augmented this response. However, the beta cell remained sensitive to theophylline-induced insulin secretion, while TFP paradoxically increased insulin secretion in the glucose-insensitive beta cells. Protein synthesis and glucose oxidation were not affected by culture conditions. Thus we suggest that the glucose-induced desensitization of the beta cells may be due to alterations in the calcium-dependent release mechanism.

Regulation of the hepatic response to glucagon: role of insulin, growth hormone and cortisol.

The hepatic response to glucagon was investigated in five groups of animals: (1) controls; (2) excess growth hormone (GH; tumor-bearing); (3) streptozotocin-induced diabetic; (4) cortisol-treated, and (5) insulin-treated animals. Blood samples were collected from the animal models and hepatocytes were prepared and used for glucagon-binding studies and studies of total glucose production, gluconeogenesis and glycogen determinations. Glucagon binding was elevated in GH-tumor-bearing and cortisol-treated hepatocytes but lower in hepatocytes from diabetic animals. Basal total glucose production wash higher in hepatocytes from diabetic rats but not changed in hepatocytes from GH-tumor-bearing, insulin-treated or cortisol-treated animals. Glucagon significantly stimulated total glucose production in hepatocytes from control, insulin-treated and cortisol-treated but not diabetic and GH tumor models. Gluconeogenesis as evaluated by alanine conversion to glucose was significantly increased in hepatocytes from diabetic and cortisol-treated animals and was significantly lower in hepatocytes from GH-tumor-bearing animals. Glucagon failed to significantly stimulate gluconeogenesis in hepatocytes from diabetic and tumor-bearing animals. Hepatic glycogen content was significantly decreased in diabetic and GH-tumor-bearing animals but not changed in insulin-treated and cortisol-treated animals. We conclude that increased glucagon binding was not always correlated with an increase in glucagon-stimulated glycogenolysis, gluconeogenesis or increased sensitivity to glucagon. Persistent hyperinsulinism may effectively suppress glucagon- or cortisol-stimulated pathways.