Serial measurements of body composition in obese subjects during a very-low-energy diet (VLED) comparing bioelectrical impedance with hydrodensitometry

Bioelectrical impedance analysis (BIA) is a convenient, inexpensive, and noninvasive technique for measuring body composition. BIA has been strongly correlated with total body water (TBW) and also has been validated against hydrodensitometry (HD). The accuracy and clinical utility of BIA and HD during periods of substantial weight loss remain controversial. We measured body composition in moderately and severely obese patients serially using both methods during a very-low-energy diet (VLED). Mean initial weight in these patients was 116 (+/-30) kg (range, 74-196 kg). Mean weight loss was 24 (+/-13) kg with a decrease in fat mass (FM) by HD of kg (p < 0.001) and a decrease in fat-free mass (FFM) of 3.6 kg (p < 0.05). Loss of FFM is best predicted by the rate (kg/wk) of weight loss (r2 = 0.86, p < 0.0001). FFM, as predicted from BIA equations, was highly correlated with FFM as estimated by HD during all testing sessions (r = 0.92-0.98). Although highly correlated, BIA overestimated FFM relative to HD and this difference appeared to be more pronounced for taller patients with greater truncal obesity. Although the discrepancy was no greater during weight-loss treatment, the level of disagreement was considerable. Therefore, the two methods cannot be used interchangeably to monitor relative changes in body composition in patients with obesity during treatment with VLED. The discrepancy between BIA and HD may be caused by body mass distribution considerations and by perturbations in TBW which affect the hydration quotient for FFM (BIA) and/or which affect the density constants for FFM and FM (HD).     

Effect of the intake of different doses of trace elements and their combination with other biologically active substances on iron, copper and manganese metabolism in highly qualified athletes

Investigations conducted on athletes have shown that combinations of trace elements (Fe, Cu and Mn) in biotic doses with vitamins, glutamic acid or dibasol produce a favourable effect on trace element metabolism, and on the body functions. Enrichment of food rations with vitamins only, using no trace elements, drastically increased the secretion of Fe, Cu and Mn from the body. High doses of Fe-containing drugs disturbed Mn balance.     

Phosphate diabetes in patients with chronic fatigue syndrome

Phosphate depletion is associated with neuromuscular dysfunction due to changes in mitochondrial respiration that result in a defect of intracellular oxidative metabolism. Phosphate diabetes causes phosphate depletion due to abnormal renal re-absorption of phosphate be the proximal renal tubule. Most of the symptoms presented by patients with phosphate diabetes such as myalgia, fatigue and mild depression, are also common in patients with chronic fatigue syndrome, but this differential diagnosis has not been considered. We investigated the possible association between chronic fatigue syndrome and phosphate diabetes in 87 patients who fulfilled the criteria for chronic fatigue syndrome. Control subjects were 37 volunteers, who explicitly denied fatigue and chronic illness on a screening questionnaire. Re-absorption of phosphate by the proximal renal tubule, phosphate clearance and renal threshold phosphate concentration were the main outcome measures in both groups. Of the 87 patients with chronic fatigue syndrome, nine also fulfilled the diagnostic criteria for phosphate diabetes. In conclusion, we report a previously undefined relationship between chronic fatigue syndrome and phosphate diabetes. Phosphate diabetes should be considered in differential diagnosis with chronic fatigue syndrome; further studies are needed to investigate the incidence of phosphate diabetes in patients with chronic fatigue syndrome and the possible beneficial effect of vitamin D and oral phosphate supplements.     

The nootropic correction of disorders in learning and memory processes induced by extreme exposures

Experiments on rats demonstrated that the low-intensity electromagnetic field (12.6 cm, 2375 MHz, power density 1 mW/cm2), motion sickness, and electroconvulsive shock provoked the retrograde amnesia in the passive avoidance test. The oxyracetam (100 mg/kg, i.p.), aniracetam (50 mg/kg, i.p.), nooglutil (50 mg/kg, i.p.), meclofenoxate (50 mg/kg, i.p.), pyracetam (200 mg/kg, i.p.), and GABA (200 mg/kg, i.p) prevented the memory-impairing effect of all these extreme factors. On the contrary, the N-acetylglycinamide, semax, and other nootropic drugs were effective only under one or two extreme conditions.     

Aerobic anoxygenic phototrophic bacteria

The aerobic anoxygenic phototrophic bacteria are a relatively recently discovered bacterial group. Although taxonomically and phylogenetically heterogeneous, these bacteria share the following distinguishing features: the presence of bacteriochlorophyll a incorporated into reaction center and light-harvesting complexes, low levels of the photosynthetic unit in cells, an abundance of carotenoids, a strong inhibition by light of bacteriochlorophyll synthesis, and the inability to grow photosynthetically under anaerobic conditions. Aerobic anoxygenic phototrophic bacteria are classified in two marine (Erythrobacter and Roseobacter) and six freshwater (Acidiphilium, Erythromicrobium, Erythromonas, Porphyrobacter, Roseococcus, and Sandaracinobacter) genera, which phylogenetically belong to the alpha-1, alpha-3, and alpha-4 subclasses of the class Proteobacteria. Despite this phylogenetic information, the evolution and ancestry of their photosynthetic properties are unclear. We discuss several current proposals for the evolutionary origin of aerobic phototrophic bacteria. The closest phylogenetic relatives of aerobic phototrophic bacteria include facultatively anaerobic purple nonsulfur phototrophic bacteria. Since these two bacterial groups share many properties, yet have significant differences, we compare and contrast their physiology, with an emphasis on morphology and photosynthetic and other metabolic processes.     

Sites of alcohol and volatile anaesthetic action on GABA(A) and glycine receptors

Volatile anaesthetics have historically been considered to act in a nonspecific manner on the central nervous system. More recent studies, however, have revealed that the receptors for inhibitory neurotransmitters such as gamma-aminobutyric acid (GABA) and glycine are sensitive to clinically relevant concentrations of inhaled anaesthetics. The function of GABA(A) and glycine receptors is enhanced by a number of anaesthetics and alcohols, whereas activity of the related GABA rho1 receptor is reduced. We have used this difference in pharmacology to investigate the molecular basis for modulation of these receptors by anaesthetics and alcohols. By using chimaeric receptor constructs, we have identified a region of 45 amino-acid residues that is both necessary and sufficient for the enhancement of receptor function. Within this region, two specific amino-acid residues in transmembrane domains 2 and 3 are critical for allosteric modulation of both GABA(A) and glycine receptors by alcohols and two volatile anaesthetics. These observations support the idea that anaesthetics exert a specific effect on these ion-channel proteins, and allow for the future testing of specific hypotheses of the action of anaesthetics.     

Stable expression of manganese superoxide dismutase (MnSOD) in insulinoma cells prevents IL-1beta- induced cytotoxicity and reduces nitric oxide production

The fact that insulin-producing islet beta-cells are susceptible to the cytotoxic effects of inflammatory cytokines represents a potential hinderance to the use of such cells for transplantation therapy of insulin-dependent diabetes mellitus (IDDM). In the current study, we show that IL-1beta induces destruction of INS-1 insulinoma cells, while having no effect on a second insulinoma cell line RIN1046-38 and its engineered derivatives, and that this difference is correlated with a higher level of expression of manganese superoxide dismutase (MnSOD) in the latter cells. Stable overexpression of MnSOD in INS-1 cells provides complete protection against IL-1beta-mediated cytotoxicity, and also results in markedly reduced killing when such cells are exposed to conditioned media from activated human or rat PBMC. Further, overexpression of MnSOD in either RIN- or INS-1-derived lines results in a sharp reduction in IL-1beta-induced nitric oxide (NO) production, a finding that correlates with reduced levels of the inducible form of nitric oxide synthase (iNOS). Treatment of INS-1 cells with L-NMMA, an inhibitor of iNOS, provides the same degree of protection against IL-1beta or supernatants from LPS-activated rat PBMC as MnSOD overexpression, supporting the idea that MnSOD protects INS-1 cells by interfering with the normal IL-1beta-mediated increase in iNOS. Because NO and its derivatives have been implicated as critical mediators of beta-cell destruction in IDDM, we conclude that well regulated insulinoma cell lines engineered for MnSOD overexpression may be an attractive alternative to isolated islets as vehicles for insulin replacement in autoimmune diabetes.