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Various Metabolic (various + metabolic)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Cyclosporine Induces Epileptiform Activity in an In Vitro Seizure Model

EPILEPSIA, Issue 3 2000
Michael Wong
Summary: Purpose: Cyclosporine (CSA) toxicity represents a common cause of seizures in transplant patients, but the specific mechanisms by which CSA induces seizures are unknown. Although CSA may promote seizure activity by various metabolic, toxic, vascular, or structural mechanisms, CSA also has been hypothesized to modulate neuronal excitability directly. The objective of this study was to determine if CSA exerts direct epileptogenic actions on neurons in an in vitro seizure model. Methods: Combined hippocampal-entorhinal cortex slices from juvenile rats were exposed directly to artificial cerebro-spinal fluid (ACSF) containing either (a) 1.0 mM magnesium sulfate (control), (b) 1.0 mM sodium sulfate (low-magnesium), or (c) 1.0 mM magnesium sulfate + CSA (1,000,10,000 ng/ml). Spontaneous and evoked extracellular field potentials were recorded simultaneously from the dentate gyrus (DG) and CA3 hippocampal regions. Evoked synaptic responses were elicited by stimulation of the entorhinal cortex/perforant pathway. Results: CSA elicited spontaneous or stimulation-induced epileptiform activity in the DG or CA3 region of ,40% of slices, consisting of brief repetitive "interictal" discharges or prolonged stereotypical "ictal" discharges. Mean latency to epileptiform activity was ,100 min after onset of CSA application. The interictal discharges were inhibited by the non-NMDA antagonist, NBQX. Similar epileptiform activity was observed in low-magnesium ACSF without CSA. In control ACSF alone, epileptiform activity was not seen, except for rare spontaneous potentials in the DG. Conclusions: Direct effects of CSA on neuronal excitability and synaptic transmission may contribute to seizures seen in clinical CSA neurotoxicity. [source]

Impact of body fat mass extent on cardiac autonomic alterations in women

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2009
J. Sztajzel
Abstract Background, Obesity has been associated with significant abnormalities of the cardiac autonomic regulation. However, the precise impact of increasing body weight on cardiac autonomic function and the metabolic and hormonal contributors to these changes are presently unclear. The aim of our study was to explore in subjects with increasing values of body mass index (BMI) the alterations of cardiac autonomic function and to establish the potential role of various metabolic and hormonal contributors to these alterations. Materials and methods, We investigated time and frequency domain heart rate variability (HRV) parameters taken from 24-h Holter recordings, and several anthropometric, metabolic and hormonal parameters (plasma glucose, insulin, triglycerides, free fatty acids, leptin and adiponectin) in 68 normoglycaemic and normotensive women (mean age of 40 ± 3 years), subdivided according to their BMI into 15 normal body weight (controls), 15 overweight, 18 obese and 20 morbidly obese. Results, Heart rate was increased and HRV was decreased in the morbidly obese group as compared with controls. In overall population, a negative association linked body fat mass (FM) to HRV indices. None of the metabolic and hormonal parameters were significantly related to the HRV indices, after they were adjusted for the body FM. Conclusions, Morbidly obese, normoglycaemic and normotensive young women have increased HR and low HRV, indicating an abnormal cardiac autonomic function and representing a risk factor for adverse cardiovascular events. A decrease of HRV parameters is associated with a progressive increase of body FM. Other metabolic and hormonal factors, characterising obesity, do not show an independent influence on these HRV alterations. [source]

Use of longitudinal data in genetic studies in the genome-wide association studies era: summary of Group 14

GENETIC EPIDEMIOLOGY, Issue S1 2009
Berit Kerner
Abstract Participants analyzed actual and simulated longitudinal data from the Framingham Heart Study for various metabolic and cardiovascular traits. The genetic information incorporated into these investigations ranged from selected single-nucleotide polymorphisms to genome-wide association arrays. Genotypes were incorporated using a broad range of methodological approaches including conditional logistic regression, linear mixed models, generalized estimating equations, linear growth curve estimation, growth modeling, growth mixture modeling, population attributable risk fraction based on survival functions under the proportional hazards models, and multivariate adaptive splines for the analysis of longitudinal data. The specific scientific questions addressed by these different approaches also varied, ranging from a more precise definition of the phenotype, bias reduction in control selection, estimation of effect sizes and genotype associated risk, to direct incorporation of genetic data into longitudinal modeling approaches and the exploration of population heterogeneity with regard to longitudinal trajectories. The group reached several overall conclusions: (1) The additional information provided by longitudinal data may be useful in genetic analyses. (2) The precision of the phenotype definition as well as control selection in nested designs may be improved, especially if traits demonstrate a trend over time or have strong age-of-onset effects. (3) Analyzing genetic data stratified for high-risk subgroups defined by a unique development over time could be useful for the detection of rare mutations in common multifactorial diseases. (4) Estimation of the population impact of genomic risk variants could be more precise. The challenges and computational complexity demanded by genome-wide single-nucleotide polymorphism data were also discussed. Genet. Epidemiol. 33 (Suppl. 1):S93,S98, 2009. © 2009 Wiley-Liss, Inc. [source]

ENDOCRINE REGULATION OF CALCIUM TRANSPORT IN EPITHELIA

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2008
Ramesh C Khanal
SUMMARY 1Calcium (re)absorption occurs in epithelia, including the intestine, kidney, mammary glands, placenta and gills (in the case of fish). 2Calcium is transported across epithelia by two transport mechanisms, paracellular and transcellular, and the movement is regulated by a complex array of transport processes that are mediated by hormonal, developmental and physiological factors involving the gastrointestinal tract, bone, kidney and the parathyroids. 3Clear understanding of the calcium transport pathways and their endocrine regulation is critical for minimizing various metabolic and health disorders at different physiological stages. Here, we first briefly review the calcium transport mechanisms before discussing in detail the endocrine factors that regulate calcium transport in the epithelia. [source]