Background and Purpose-Chronic kidney disease (CKD) is increasingly recognized as an independent risk factor for cardiovascular disease and stroke. Our aim was to examine the association between estimated glomerular filtration rate (GFR) and stroke outcome and to assess whether CKD and its severity affect stroke outcome in a large cohort of unselected patients with acute stroke. Methods-We examined the association between baseline estimated GFR and CKD and 1-year outcomes in 821 consecutive patients with acute stroke (ischemic or hemorrhagic). GFR was estimated by 2 methods: the Modification of Diet in Renal Disease and the Mayo Clinic quadratic equation. An estimated GFR rate Յ60 mL/min/1.73 m 2 defined CKD. Results-Odds ratios (95% CI) for death across levels of estimated GFR based on both equations were estimated. CKD was present in 36% (nϭ291)

ABSTRACT. Objective. Between October and November 2003, several infants with encephalopathy were hospitalized in pediatric intensive care units in Israel. Two died of cardiomyopathy. Analysis of the accumulated data showed that all had been fed the same brand of soy-based formula (Remedia Super Soya 1), specifically manufactured for the Israeli market. The source was identified on November 6, 2003, when a 5.5-month-old infant was admitted to Sourasky Medical Center with upbeat nystagmus, ophthalmoplegia, and vomiting. Wernicke's encephalopathy was suspected, and treatment with supplementary thiamine was started. His condition improved within hours. Detailed history revealed that the infant was being fed the same formula, raising suspicions that it was deficient in thiamine. The formula was tested by the Israeli public health authorities, and the thiamine level was found to be undetectable (<0.5 g/g). The product was pulled from the shelves, and the public was alerted. Thiamine deficiency in infants is very rare in developed countries. The aim of this study was to report the epidemiology of the outbreak and to describe the diagnosis, clinical course, and outcome of 9 affected infants in our care.Methods. After the index case, an additional 8 infants were identified in our centers by medical history, physical examination, and laboratory testing. The group consisted of 6 male and 3 female infants aged 2 to 12 months. All were assessed with the erythrocyte transketolase activity assay, wherein the extent of thiamine deficiency is expressed in percentage stimulation compared with baseline (thiamine pyrophosphate effect [TPPE]). Normal values range from 0% to 15%; a value of 15% to 25% indicates thiamine deficiency, and >25% indicates severe deficiency. Blood lactate levels (normal: 0.5-2 mmol/L) were measured in 6 infants, cerebrospinal fluid lactate in 2 (normal: 0.5-2 mmol/L), and blood pyruvate in 4 (normal: 0.03-0.08 mmol/L). The diagnostic criteria for thiamine deficiency were abnormal transketolase activity and/or unexplained lactic acidosis. Treatment consisted of intramuscular thiamine 50 mg/day for 14 days combined with a switch to another infant formula.Results. Early symptoms were nonspecific and included mainly vomiting (n ‫؍‬ 8), lethargy (n ‫؍‬ 7), irritability (n ‫؍‬ 5), abdominal distension (n ‫؍‬ 4), diarrhea (n ‫؍‬ 4), respiratory symptoms (n ‫؍‬ 4), developmental delay (n ‫؍‬ 3), and failure to thrive (n ‫؍‬ 2). Infection was found in all cases. Six infants were admitted with fever. One patient had clinical dysentery and group C Salmonella sepsis; the others had mild infection: acute gastroenteritis (n ‫؍‬ 2); upper respiratory infection (n ‫؍‬ 2); and bronchopneumonia, acute bronchitis, and viral infection (n ‫؍‬ 1 each). Two infants were treated with antibiotics. Three infants had neurologic symptoms of ophthalmoplegia with bilateral abduction deficit with or without upbeat nystagmus. All 3 had blood lactic acidosis, and 2 had high cerebrospinal fluid lactate levels. Patient 1, our index case, wa...

Abstract-The most known risk factor for nonalcoholic fatty liver disease (NAFLD) is the metabolic syndrome. In this study, we characterized changes in liver pathology, hepatic lipid composition, and hepatic iron concentration (HIC) occurring in rats given fructose-enriched diet (FED), with and without therapeutic maneuvers to reduce blood pressure and plasma triglycerides. Rats were given FED or standard rat chow for 5 weeks. Rats on FED were divided into 4 groups: receiving amlodipine (15 mg/kg per day), captopril (90 mg/kg per day), bezafibrate (10 mg/kg per day) in the last 2 weeks, or a control group that received FED only. FED rats had hepatic macrovesicular and microvesicular fat deposits develop, with increase in hepatic triglycerides (ϩ198%) and hepatic cholesterol (ϩ89%), but a decrease in hepatic phospholipids (Ϫ36%), hypertriglyceridemia (ϩ223%), and hypertension (ϩ15%), without increase in HIC. Amlodipine reduced blood pressure (Ϫ18%), plasma triglycerides (Ϫ12%), but there was no change in hepatic triglycerides and phospholipids concentrations. Captopril reduced blood pressure (Ϫ24%), plasma triglycerides (Ϫ36%), hepatic triglycerides (Ϫ51%), and hepatic macrovesicular fat (Ϫ51%), but increased HIC (ϩ23%), with a borderline increase in hepatic fibrosis. Bezafibrate reduced plasma triglycerides (Ϫ49%), hepatic triglycerides (Ϫ78%), hepatic macrovesicular fat (Ϫ90%), and blood pressure (Ϫ11%

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In order to analyze the molecular mechanisms of cell adhesion during development, proteins on the surface of chick embryonic neural cells were compared with proteins released after placing these cells in culture. One of the components released into culture, F1 (molecular weight, M, 140,000), was derived by proteolytic cleavage of a cell surface precursor with a molecular weight of at least 240,000.Another proteinj F2, recovered Cell adhesion has attracted the attention of biologists in a variety of fields because it reflects some of the most fundamental aspects of metazoan physiology. Several attempts have been made to analyze cell adhesion, but as yet its physical basis remains unknown. The main conclusion that can be drawn from these studies (1-5) is that adhesion is a complex phenomenon that in some way includes molecular ligation of cell surfaces. In view of this complexity, an experimental approach requires an analysis of (a) the structure of molecules expressed at and released from the cell surface; (b) the specific interactions among these molecules; (c) the relationship of the properties of these molecules to cell-cell binding in kinetically defined assays; and (d) the relationship of this binding to tissue formation.In this paper, we describe the application of this approach to the study of adhesion among dissociated retinal and brain cells from chick embryos. These studies suggest that proteolytic alteration of a major cell surface protein results in the appearance of determinants required for the initial formation of bonds between both retinal and brain cells. A model of the activation and ligation steps has been formulated and the overall control of adhesion during the development of these two tissues is discussed in terms of this model. Isolation of Proteins F1 and F2 from Retina. Retinas from 10-day embryos were cultured either as intact tissue in medium with Trasylol, or as cell monolayers in medium with 5% serum. Supernatants from cultures of intact tissue (TCS) were collected after 24 hr and centrifuged to remove debris. Cells in monolayer cultures were washed and incubated for 24-48 hr in medium without serum but with Trasylol, after which the monolayer culture supernatant (MCS) was collected and centrifuged. MATERIALS AND METHODSAfter a 30-fold concentration by ultrafiltration through Amicon PM-10 membranes, MCS and TCS from 400 retinas were passed through DE-52 DEAE-cellulose (Whatman) columns in 0.01 M Tris-HCl-0.4 M KCl, pH 7.2, to remove nucleic acids, and fractionated on a 0.5 X 10 cm column of DE-52 in 0.01 M Tris, pH 7.2, with a linear gradient from 0.01 to 0.4 M KCl. Fractions containing the F1 or F2 proteins (see Fig. 1) were identified by analytical polyacrylamide gel electrophoresis, pooled, and further separated by preparative gel electrophoresis on 1 cm X 10 cm cylindrical gels of 6.5% acrylamide in Tris-glycine buffer (6). F1 and F2 were located by scanning the gels at 280 nm with a Gilford spectrophotometer and eluted from the appropriate gel slice by electrophoresis (...

Immunoglobulin free light chain (FLC) kappa (κ) and lambda (λ) isotypes exist mainly in monomeric and dimeric forms. Under pathological conditions, the level of FLCs as well as the structure of monomeric and dimeric FLCs and their dimerization properties might be significantly altered. The abnormally high fractions of dimeric FLCs were demonstrated in the serum of patients with multiple myeloma (MM) and primary systemic amyloidosis (AL), as well as in the serum of anephric patients. The presence of tetra- and trimolecular complexes formed due to dimer-dimer and dimer-monomer interactions was detected in the myeloma serum. Analysis of the amyloidogenic light chains demonstrated mutations within the dimer interface, thus raising the possibility that these mutations are responsible for amyloidogenicity. Increased κ monomer and dimer levels, as well as a high κ/λ monomer ratio, were typically found in the cerebrospinal fluid from patients with multiple sclerosis (MS). In many MS cases, the elevation of κ FLCs was accompanied by an abnormally high proportion of λ dimers. This review focuses on the disease-related changes of the structure and level of dimeric FLCs, and raises the questions regarding their formation, function, and role in the pathogenesis and diagnosis of human diseases.

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