Occurrence of Fusarium spp. and Fumonisins in Stored Wheat Grains Marketed in Iran

Wheat grains are well known to be invaded by Fusarium spp. under field and storage conditions and contaminated with fumonisins. Therefore, determining Fusarium spp. and fumonisins in wheat grains is of prime importance to develop suitable management strategies and to minimize risk. Eighty-two stored wheat samples produced in Iran were collected from various supermarkets and tested for the presence of Fusarium spp. by agar plate assay and fumonisins by HPLC. A total of 386 Fusarium strains were isolated and identified through morphological characteristics. All these strains belonged to F. culmorum, F. graminearum, F. proliferatum and F.verticillioides. Of the Fusarium species, F. graminearum was the most prevalent species, followed by F. verticillioides, F. proliferatum and then F. culmorum. Natural occurrence of fumonisin B1 (FB1) could be detected in 56 (68.2%) samples ranging from 15-155 μg/kg, fumonisin B2 (FB2) in 35 (42.6%) samples ranging from 12-86 μg/kg and fumonisin B3 (FB3) in 26 (31.7%) samples ranging from 13-64 μg/kg. The highest FB1 levels were detected in samples from Eilam (up to 155 μg/kg) and FB2 and FB3 in samples from Gilan Gharb (up to 86 μg/kg and 64 μg/kg).     

Pediatric reference intervals for lipids and apolipoproteins on the VITROS 5,1 FS Chemistry System

OBJECTIVES: Lipid biomarkers are integral in the assessment of dyslipidemia and cardiovascular risk, conditions that have become increasingly prevalent in pediatric populations. A comprehensive set of pediatric reference intervals for traditional or recently established lipid analytes is not currently available. DESIGN AND METHODS: 525 outpatient samples from a pediatric population were categorized into five age groups ranging from 0 to 20 years of age. Groups were further partitioned by gender. Serum or plasma samples were analyzed on the VITROS 5,1 FS Chemistry System for cholesterol and triglycerides by dry-film methods, direct HDL-C and LDL-C by selective detergent elimination, and apolipoproteins AI and B by immunoturbidimetry. Reference intervals were established by non-parametric methods at the 2.5th and 97.5th percentiles. RESULTS: Lipid levels show age- and gender-related differences, particularly during the first year of life and in young adults following puberty. Concentrations of total cholesterol, LDL-C, and apo B were lowest in the 12 months after birth and remained relatively constant throughout childhood, but decreased for males in early adulthood. Triglyceride levels increased gradually throughout childhood and adolescence, and along with cholesterol, the upper limits of these intervals exceeded the recommended concentrations of lipid levels in children. For HDL-C and apo AI, no age- or sex-related differences were found until after puberty when values for males decreased slightly. CONCLUSIONS: Our current reference intervals in children and adolescents provide an important update for lipid markers and suggest earlier incidence of hypercholesterolemia when compared to previous ranges. Increased profiling of lipids is anticipated, and these will aid in the early assessment of cardiovascular risk in pediatric populations.     

The complex nature of the interaction between disease activity and therapy on the lipid profile in patients with pediatric systemic lupus erythematosus

OBJECTIVE: To determine the prevalence of lipid abnormalities at different times and to determine the influence of both the disease and corticosteroid therapy on lipid abnormalities in pediatric patients with systemic lupus erythematosus (SLE). METHODS: Lipid measurements were obtained in an inception cohort of 139 pediatric patients with SLE (114 females). Fasting levels of total cholesterol, triglycerides, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol in the SLE patients were compared with those in age- and sex-matched control subjects. Disease activity levels and medication dosages were obtained at the time of lipid measurements. RESULTS: At the time of diagnosis, the mean levels of total cholesterol, LDL cholesterol, and triglycerides were highest, whereas the mean levels of HDL cholesterol were lowest. The percentage of patients with abnormal triglyceride values was highest at diagnosis, decreased at year 1, and then remained relatively constant thereafter. The mean total cholesterol and LDL cholesterol levels decreased at year 1 as compared with the time of diagnosis and then remained relatively constant. The lowest mean HDL cholesterol levels were found at the time of diagnosis, and these values rose with time. Comparison of lipid levels at different prednisone dosages and disease activity levels revealed that changes in triglyceride levels were mainly associated with changes in disease activity, changes in both total cholesterol and LDL cholesterol levels were associated with changes in the prednisone dosage and not disease activity, and low levels of HDL cholesterol were associated with active SLE, whereas the prednisone dosage was associated with increased levels of HDL cholesterol. CONCLUSION: Factors intrinsic to SLE appear to alter lipid levels. Control of SLE may be the most important factor in improving abnormal lipid profiles, and paradoxically, prednisone therapy may improve abnormal lipid levels.     

Animal models of cognitive dysfunction

The increased life expectancy in industrialised countries in the last half century has also brought to a greater incidence of neurological disorders, including neurodegenerative diseases and developing in a rather long time. In this respect, Alzheimer's disease (AD), for the large incidence, and the dramatic loss of autonomy caused by its cognitive and behavioural symptoms represents one of the main challenges of modern medicine. Although AD is a typical human disease and probably includes several nosographic entities, the use of animal models may contribute to understand specific aspects of pathophysiology of the disease. The most widely used animal models are rodents and non-human primates. In this review different animal models characterised by impaired cognitive functions are analysed. None of the models available mimics exactly cognitive, behavioural, biochemical and histopathological abnormalities observed in neurological disorders characterised by cognitive impairment. However, partial reproduction of neuropathology and/or cognitive deficits of Alzheimer's disease (AD), vascular dementia and dementia occurring in Huntington's and Parkinson's diseases, or in other neurodegenerative disorders may represent a basis for understanding pathophysiological traits of these diseases and for contributing to their treatments.     

Mechanism of complement activation during extracorporeal blood-biomaterial interaction: effects of heparin coated and uncoated surfaces

In vitro studies with miniaturized rotating circuits and heparinized human blood, as well as long-term extracorporeal membrane oxygenation with either heparin coated (HBS) or uncoated surfaces connected to adult sheep, were performed comparing the impact on complement activation in blood and on surfaces. Analysis of surface bound complement proteins revealed significantly reduced binding of activated C3 and C5b-9 to HBS in vitro, compared with uncoated surfaces, which was probably due to more HBS bound complement inhibitors (C1-Inhibitor, factor H) being present. This was reflected by significantly reduced activation of the alternative pathway (C3bBbP) and terminal complex (SC5b-9) by HBS but slightly increased levels of classic pathway complex (C1rs-C1-inhibitor). These results were confirmed during in vivo study by analysis of hemolytic complement function, activation specific C3 derived split products, and surface bound complement proteins. Increased binding of complement regulators to HBS appears to effectively reduce complement activation by biomaterials, leading to improved long-term biocompatibility.     

Closing the anion gap: contribution of D-lactate to diabetic ketoacidosis

BackgroundA high anion gap in diabetic ketoacidosis (DKA) suggests that some unmeasured anions must contribute to the generation of the anion gap. We investigated the contribution of d-lactate to the anion gap in DKA.MethodsDiabetic patients with and without DKA and high anion gap were recruited. Plasma d-lactate was quantified by HPLC. Plasma methylglyoxal was assayed by liquid chromatography-tandem mass spectrometry.ResultsThe plasma fasting glucose, β-hydroxybutyrate, and blood HbA1c levels were highly elevated in DKA. Plasma anion gap was significantly increased in DKA (20.59 ± 6.37) compared to either the diabetic (7.50 ± 1.88) or the control group (6.53 ± 1.75) (p < 0.001, respectively). Moreover, plasma d-lactate levels were markedly increased in DKA (3.82 ± 2.50 mmol/l) compared to the diabetic (0.47 ± 0.55 mmol/l) or the control group (0.25 ± 0.35 mmol/l) (p < 0.001, respectively). Regression analysis demonstrated that d-lactate was associated with acidosis and anion gap (r = 0.686, p < 0.001).ConclusionsPlasma d-lactate levels are highly elevated and associated with metabolic acidosis and the high anion gap in DKA. Laboratory monitoring of d-lactate will provide valuable information for assessment of patients with DKA.     

Increased plasma methylglyoxal level, inflammation, and vascular endothelial dysfunction in diabetic nephropathy

Objectives

To investigate the association of plasma levels of methylglyoxal (MG) and markers of inflammation/endothelial dysfunction with diabetic nephropathy (DN).

Design and methods

Plasma levels of MG, cytokines, and adhesion molecules were measured in type 2 diabetic patients (T2DM), T2DM patients with DN, and the controls.

Results

Plasma MG levels in DN were significantly higher than those in T2DM and the controls (312 ± 135 vs. 212 ± 73 and 312 ± 135 vs. 147 ± 78 nmol/L, respectively, P < 0.001). The plasma levels of MG were positively correlated with the fasting glucose, HbA1c, and urinary albumin/creatinine ratio (r = 0.754, P < 0.05). Plasma levels of IL-6, TNF-α, and adhesion molecules were markedly increased in DN compared to T2DM patients and the controls.

Conclusions

Increased plasma levels of MG, cytokines, and adhesion molecules are associated with DN. These markers may be useful in predicting the development of DN.