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BACKGROUND Adiponectin is an adipose tissue-specific protein, which possesses anti-atherogenic and antidiabetic properties, yet its plasma levels are decreased in subjects with metabolic syndrome. Although high fat diet has been linked to hypoadiponectinemia, the effect of high-carbohydrate diet on adiponectin levels is not known. Therefore, we studied the effect of high-carbohydrate diet on adiponectin levels in the rat models of hypertension and insulin resistance. METHODS Rats were randomly assigned to the high carbohydrate diet [Sprague-Dawley rats with fructose enriched diet (SDR-F) and spontaneously hypertensive rats with sucrose enriched diet (SHR-S model)] or chow diet (Control group). Rats were followed for 6 weeks (SDR-F model) and 8 weeks (SHR-S model). Body weight, systolic blood pressure, plasma levels of glucose, insulin, triglycerides and adiponectin, were recorded. RESULTS Both models were associated with features of the metabolic syndrome, namely, high insulin levels, increased blood pressure and triglyceride levels. Plasma adiponectin levels did not change in the control groups. In contrast, adiponectin levels increased by 39 and 30% compared to baseline following four and six weeks of fructose enriched diet in SDR (from 3.3+/-0.2 to 4.5+/-0.4 and 4.3+/-0.2 microg/ml, respectively, p

The health hazard of the metabolic syndrome (MS) is increasing, yet there is no effective pharmacologic treatment to this entity as a whole. Recently, hypoadiponectinemia was found to play an important role in the development of MS. We studied the effect of the PPAR-gamma agonist rosiglitazone on adiponectin and the metabolic profile in the fructose-induced hypertensive, hyperinsulinemic, hypertriglyceridemic rat model.Thirty male Sprague-Dawley rats were divided into three groups. Ten were fed standard rat chow for 5 weeks, 10, a fructose-enriched diet for 5 weeks, and 10, a fructose-enriched diet for 5 weeks, with rosiglitazone 10 mg/kg/d added during the last 2 weeks. Blood pressure (BP), oral glucose tolerance test (OGTT), plasma insulin, triglycerides, and adiponectin were recorded, as well as mRNA levels of the adiponectin gene in visceral adipose tissue.Fructose-fed rats developed MS as manifested by the increase in systolic BP (from 139 +/- 3 to 158 +/- 4 mm Hg, P.05), insulin (from 26 +/- 1.6 to 40 +/- 2.5 muU/mL, P.05), triglycerides (from 91 +/- 9 to 304 +/- 24 mg/dL, P.05), and impaired OGTT (area under the curve from 13,894 +/- 246 to 17,725 +/- 700 mg/dL/min). Treatment with rosiglitazone reversed these effects and reduced BP to 133 +/- 7 mm Hg, insulin levels to 30 +/- 2.8 muU/mL, triglycerides to 116 +/- 9 mg/dL, and the OGTT to 15,415 +/- 372 mg/dL/min (P.05 for all variables). In addition, rosiglitazone increased plasma levels of adiponectin fourfold from 4.3 +/- 0.1 to 18.4 +/- 0.6 mug/mL (P.05). This increase was coupled with 3.8-fold increase in adiponectin mRNA in visceral adipose tissue.This study shows for the first time that in an animal model of MS, the insulin sensitizer, rosiglitazone, improves the metabolic profile and increases plasma levels of adiponectin and its gene expression. It is possible therefore that rosiglitazone exerts its beneficial effects by increasing the levels of adiponectin.

Objective There are no guidelines on how to treat patients with excessive hypertension. Anxiety is a common cause of excessive hypertension and therefore antianxiety treatment may be beneficial in these patients. We therefore compared the efficacy and safety of antianxiety treatment with sublingual captopril administration in patients with excessive hypertension and no evidence of acute target organ damage. Methods Thirty-six patients (28 women and 8 men), mean age 60 ± 2 years (range 36 to 85 years) who were referred to the emergency room because of excessive hypertension (>190/100 mm Hg) without evidence of acute target organ damage were randomized to receive either oral diazepam, 5 mg ( n = 17, study group) or sublingual captopril, 25 mg ( n = 19, control group). Blood pressure (BP) and heart rate were recorded hourly for 3 h. Results Both treatments decreased BP significantly (from 213 ± 5/105 ± 3 to 170 ± 8/88 ± 6 mm Hg in the study group, and from 208 ± 5/107 ± 3 to 181 ± 8/95 ± 3 mm Hg in the control group ( P v initial BP). One patient in each group was hospitalized because of sustained excessive hypertension. Conclusions Antianxiety treatment is effective in lowering BP in patients with excessive hypertension. Thus, anxiolytic treatment may be considered in patients with excessive hypertension without acute target organ damage. Further large placebo controlled studies are required to prove the benefit of anxiolytic agents.

Background The etiology of the metabolic syndrome (MS) includes both genetic and environmental factors. The two most commonly studied animal models of the MS are the high-sucrose diet given to spontaneously hypertensive rats (SHRs) and high-fructose diet given to Sprague Dawley rats (SDRs). This study compares between these two models. Methods The two rat strains were examined; within each group, the rats were assigned to either the high-sugar diet (SDRs with fructose-enriched diet and SHRs with sucrose-enriched diet) or standard rat chow (control group). The rats were followed for 7 weeks. The main MS components (obesity, hypertension, impaired glucose tolerance, hyperinsulinemia, hypertriglyceridemia, and hypercholesterolemia) were measured. Results At baseline systolic blood pressure (SBP), fasting blood levels of triglycerides and insulin, as well as glucose intolerance, were significantly higher among the SHRs compared to SDRs. Following fructose enrichment, SDRs became hyperinsulinemic, hypertriglyceridemic, hypercholesterolemic, hypertensive, and insulin resistant, whereas SHRs responded to sucrose supplementation by a significant elevation in blood pressure and mild worsening of insulin resistance. Endpoint results revealed superiority of sucrose--SHR model in terms of hypertension and superiority of fructose--SDR model in terms of hyperinsulinemia, hypertriglyceridemia, and hypercholesterolemia. Both models showed similar postintervention degree of glucose tolerance. Conclusions The fructose-fed SDR model represents a predominantly environmentally acquired MS, whereas the SHR model is less affected by dietary intervention and better displays the predominantly genetic spontaneous appearance of the syndrome. This fundamental difference should be taken into consideration when choosing an animal model to study the MS.

Background: Terrorist attacks in Israel cause mass events with varying numbers of casualties. A study was undertaken to analyse the medical response to an event which occurred on 17 April 2006 near the central bus station, Tel Aviv, Israel. Lessons are drawn concerning the management of the event, primary triage, evacuation priorities and the rate and characteristics of casualty arrival at the nearby hospitals. Methods: Data were collected both during and after the event in formal debriefings. Their analysis refers to medical response components, interactions and main outcomes. The event is described according to the DISAST-CIR methodology (Disastrous Incidents Systematic AnalysiS Through – Components, Interactions and Results). Results: 91 casualties were reported in this event; 85 were evacuated from the scene including 3 already dead on arrival, 9 severely injured, 14 moderately injured and 59 mildly injured. Six were declared dead at the scene. Emergency medical service (EMS) vehicle accumulation was rapid. The casualties were distributed between five hospitals (three level 1 and two level 2 trauma centres). The first evacuated casualty arrived at the hospital within 20 min of the explosion and the last urgent victim was evacuated from the scene after 1 h 14 min. Evacuation occurred in two phases: the first, lasting 1 h 20 min, in which most of the patients with evident trauma were evacuated and the second, lasting 8 h 15 min, in which most patients presented with tinnitus and symptoms of somatisation. The most common injuries were upper and lower limb injuries, diagnosed in 37% of the total injuries, and stress-related disturbances (anxiety, tinnitus, somatisation) diagnosed in 41%. Conclusion: Rapid accumulation of EMS vehicles, effective primary triage between urgent and non-urgent casualties and primary distribution between five hospitals enabled rapid conclusion of the event, both at the scene and at the receiving hospitals.

The lack of comparative studies of nifedipine and felodipine using 24-h blood pressure (BP) monitoring in the same patients led to the present study evaluating the antihypertensive efficacy and side effects of treatment with slow-release (SR) nifedipine (20 mg twice daily) and extended-release (ER) felodipine (10 mg once daily). In the double-blind study, subjects were randomly assigned to one of two treatment groups : 6 weeks of nifedipine SR (20 mg twice daily) followed by 6 weeks of felodipine (ER) (10 mg once daily with evening matched placebo), or vice versa. Twenty-four-hour ambulatory BP monitoring showed no significant differences in systolic BP (SBP) during the day. There were no significant differences in diastolic BP (DBP) throughout the 24 h, although the frequency of DBP recordings >90 mm Hg was greater during nifedipine (33.1%) than felodipine (27.75%) treatment. The most common side effects were flushing, palpitations, headaches, and ankle edema ; there were no adverse effects on lipid profile or glucose level.

The effect of 20 mg of enalapril with and without 12.5 mg of hydrochlorothiazide on glucose metabolism insulin sensitivity and lipids was evaluated in hypertensive non-insulin-dependent diabetes. Ten mild to moderate hypertensive patients with non-insulin-dependent diabetes mellitus were treated for 8 weeks with 20 mg enalapril once a day, and then divided into two groups of 5 patients each for a second 8 weeks of treatment with enalapril alone or in combination with hydrochlorothiazide, 12.5 mg once a day. Blood pressure, fasting plasma glucose, lipids and insulin, glycosylated hemoglobin, and insulin sensitivity were measured at baseline and after 8 and 16 weeks. Results were analyzed by the ANOVA test for repeated measures and all values are given as mean ± SD. Diastolic blood pressure decreased significantly after the first and second period of enalapril and after the combination of enalapril and hydrochlorothiazide. Glycosylated hemoglobin dropped significantly after the first and second period of enalapril monotherapy. Plasma triglycerides and fasting plasma insulin decreased significantly after the 16 weeks of enalapril. Insulin-mediated glucose uptake increased significantly after 8 and 16 weeks of monotherapy with enalapril. No significant difference was observed in any of the metabolic characteristics, including insulin sensitivity, between the values after 8 weeks of enalapril alone and the final values of the enalapril-treated and the enalapril/hydrochlorothiazide-treated groups. It is concluded that enalapril improves some of the metabolic parameters, including insulin sensitivity, of hypertensive diabetic patients. Despite the small number of hydrochlorothiazide patients, these results lead us to suggest that the coadministration of low-dose hydrochlorothiazide may not adversely affect these parameters, and that enalapril may have blunted the metabolic adverse effect of the diuretic.

Ramipril is a long-acting nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor introduced for clinical use about a decade ago. Ramipril is a prodrug that undergoes de-esterification in the liver to form ramiprilat, its active metabolite. Ramipril rapidly distributes to all tissues, with the liver, kidneys and lungs showing markedly higher concentrations of the drug than the blood. After absorption from the gastrointestinal tract, rapid hydrolysis of ramipril occurs in the liver. In the therapeutic concentration range, protein binding of ramipril and ramiprilat is 73 and 56%, respectively. Ramiprilat binds to ACE with high affinity at concentrations similar to that of the enzyme and establishes equilibrium slowly. Although ramipril is metabolised by hepatic and renal mechanisms to both a glucuronate conjugate and a diketopiperazine derivative, most of the drug is excreted in the urine as ramiprilat and the glucuronate conjugate of ramiprilat. Elimination from the body is characterised by a relatively rapid initial phase with a half-life of 7 hours and a late phase with a half-life of about 120 hours. No clinically significant pharmacokinetic interactions between ramipril and other drugs have been reported. The drug has been generally well tolerated with the most prevalent adverse effects being dizziness (3.4%), headache (3.2%), weakness (1.9%) and nausea (1.7%). Ramipril is an effective and well tolerated drug for the treatment of hypertension and congestive heart failure in all patients, including those with renal or hepatic dysfunction, and the elderly.

The effect of three calcium entry blockers — verapamil, nifedipine and felodipine — on diuresis, natriuresis, the renin-aldosterone axis, and atrial natriuretic peptide (ANP) levels was studied in 30 previously untreated patients with mild to moderate essential hypertension. All three blockers produced significant antihypertensive effects after 2 and after 24 h. Heart rate tended to decrease, but did not change significantly after verapamil, but increased significantly 1–2 h after nifedipine and felodipine. Plasma renin activity (PRA) did not change significantly with any treatment, and plasma aldosterone decreased with all three agents. ANP levels did not change significantly after verapamil, but increased significantly after nifedipine and felodipine. There was a significant positive correlation between the maximal change in ANP level and urinary sodium after nifedipine and felodipine. The increase in urinary sodium after verapamil was not significant. The role of the direct renal effect of calcium entry blockers in their persistent natriuretic action is discussed, as well as their short-term enhancement of ANP levels, which may account for the initial diuretic and natriuretic effects seen with this class of dihydropiridines.

Whether fluid accumulating in the pleural space is a transudate or an exudate is determined by the widely used criteria of the pleural fluid to serum LDH and protein concentration ratios. Such a distinction is important for limiting the extent of the differential diagnosis of possible causes for this condition. We have found that a pleural fluid to serum total bilirubin ratio can serve the same purpose. The correlation of a bilirubin concentration ratio of 0.6 or more with the presence of an exudate as determined by established criteria is statistically highly significant; and its sensitivity, specificity, positive predictive accuracy, and overall accuracy in relation to etiology and LDH or protein criteria (Light's criteria) are about 90 percent. Hence, the bilirubin criterion is statistically equivalent to the widely accepted LDH and protein criteria. (Chest 1990; 98:141-44) CHF=congestive heart failure; CRF=chronic renal failure

Summary We describe a 19 year old woman with systemic lupus erythematosus on corticosteroid therapy, who developed bilateral, multiple, gas-forming Salmonella enteritidis leg abscesses and osteomyelitis mimicking deep vein thrombosis. The infection was treated successfully by a combination of surgical drainage and intravenous ceftriaxone, followed by prolonged oral pefloxacin. This rare case of gas-producing S. enteritidis emphasizes the difficulty in diagnosing such complications in active systemic lupus erythematosus.

Acute graft-versus-host disease has been described in immunocompromised patients receiving nonirradiated blood products.1 2 3 In addition to the involvement of the skin, liver, and gut typically seen in graft-versus-host disease after bone marrow transplantation,4 these patients have bone marrow involvement that results in pancytopenia. The aplasia observed in graft-versus-host disease is presumably due to recognition by the donor's immune-reactive cells of histoincompatible antigens on the host's hematopoietic precursor cells. Transfusion-associated graft-versus-host disease carries a high mortality rate; most patients succumb to infection.2 Because the onset of transfusion-associated graft-versus-host disease is delayed and because its symptoms are similar to those seen in . . .