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At least 613 records · Page 34Linked to original sources
PubMed2003

[Primary hyperaldosteronism: report of two cases (normalization of hypertension after adrenalectomy)].

Two cases of Conn Syndrome with high hypertension, who were successful operated, have been prescribed. Retrospective evaluation of both cases suggests that severe and hypocalemic hypertension should motivate the researchers towards primary hyperaldosteronism. Etiology of the disease remains to be an important diagnostic challenge, optimal treatment will vary for each case of primary hyperaldosteronism. For individuals with aldosterone producing tumours the recommended type of treatment will be surgical as in most cases; it results in stabile normalization of RR level and abatement of metabolic dysfunction.

Adolescent↗
PubMed2004

The genetics of sleep disorders.

Most sleep disorders result from complex interactions between genes and the environment. Modern molecular techniques are increasingly applied to determine the contribution of genes to sleep and its disorders. The genetic basis of circadian rhythms has been explored using Drosophila and rodent models. This culminated in the identification of the molecular basis of one autosomal dominant form of familial advanced sleep phase syndrome: mutations in the human period 2 gene. Genetic studies in an autosomal recessive canine model of narcolepsy and in gene-targeted mice have identified the hypothalamic hypocretin (orexin) neuropeptide system as a key target for human narcolepsy. In this case, animal models have provided important clues to a human disorder with complex genetics. The study of the role of genes in the obstructive sleep apnoea syndrome is likely to provide important clues to a phenotype associated with respiratory, cardiovascular, and metabolic dysfunction. This brief review will present the role of genetic factors in the obstructive sleep apnoea syndrome, restless leg syndrome, narcolepsy, and circadian rhythm disorders.

Age Factors↗
PubMed2004

[Experimental study of hemodynamics and oxygen metabolism in pigs with severe acute pancreatitis].

OBJECTIVE: To observe the changes in hemodynamics and oxygen metabolism in pigs with severe acute pancreatitis (SAP) so as to provide a theoretical basis for clinical treatment. METHODS: A porcine model of SAP was reproduced by infusing normal saline (1 ml/kg) of sodium taurocholate (4%) and trypsin (1%) into the pancreatic duct (n=8). Heart rate (HR), central venous pressure (CVP), mean arterial pressure (MAP), pulmonary arterial wedge pressure (PAWP), mean pulmonary arterial pressure(MPAP) and cardiac output were continuously measured with the aid of Swan-Ganz catheter and electrocardiography monitor, and cardiac index (CI) was calculated. Oxygen delivery (DO(2)), oxygen consumption (VODO(2)) and oxygen extraction (ODO(2)ext) were calculated according to the analysis of the blood-gases in arterial and mixed venous blood at 0, 6, 12, 24, 36 hours after taurocholic acid injection, and the result were analyzed. RESULTS: Compared with baseline (0 hour), MAP and CI decreased significantly 12 hours after the acid insult (all P<0.05). Both of partial pressure of artery (PaO(2)) and DO(2) showed a tendency to fall. Compared with 0 hour, PaO(2) decreased significantly at 6, 12, 24 and 36 hours (all P<0.05), and DO(2)at 24 hours (P<0.05). The trends of VO(2) and O(2)ext were consistent, both of them peaked at 6 hours (both P<0.05), then, began to lower, and the difference was statistically significance at 24 hours (both P<0.05). CONCLUSION: There is not only hemodynamic disturbances but also oxygen metabolism dysfunction in pigs with SAP. The pathogenesis of multiple organ dysfunction syndrome might be attributable to the lowering of VO(2) and O(2)ext.

Animals↗
PubMed2005

Increased myocardial N-myristoyltransferase activity in rotenone model of Parkinsonism.

There is widespread brain pathology in Parkinson's disease (PD), with the primary pathology in the substantia nigra. Oxidative stress is believed to play a role in cell death in PD. Rotenone is a mitochondrial toxin which can produce Parkinson syndrome (PS) in rats. Myristoyl-CoA:protein N-myristoyltransferase (NMT), which catalyzes the co-translational transfer of myristate from myristoyl-CoA to the amino-terminal glycine residue of selected polypeptides, is increased in the myocardium of ischemia-reperfusion rat model myocardium. Animals received rotoneone (n=10) or placebo vehicle (n=6) via Alzet osmotic pumps. Mean cardiac muscle NMT activity of placebo treated (control) rats was 0.608+/-0.366 units/mg protein. Rats with mild or no detectable PS features on rotenone showed slight (mean 0.853+/-0.192) but insignificantly increased activity. Rats that had moderately severe PS features had higher level of NMT activity (mean 1.223+/-0.057), which was borderline significant compared to controls (P=0.066). Rats with severe PS features had the highest NMT activity (1.353+/-0.128) which was significantly greater compared to controls (P=0.003) and to the rats that had equivocal or no motor slowing (P=0.005). Our data show cardiac metabolic dysfunction in a rotenone rat model of PS. The severity of this change correlates with the severity of motor manifestations. Further studies of NMT activity in human PD cases and patients with cardiomyopathy of unknown cause may provide valuable information in these disorders.

Acyl Coenzyme A↗
PubMed1992

Adipsin and an endogenous pathway of complement from adipose cells.

The alternative complement pathway is best known for its role in humoral suppression of infectious agents. We have previously shown that adipose cells synthesize adipsin, the mouse homolog of human complement factor D, and that the synthesis of this protein is reduced in several rodent models of obesity. We show here that adipose cells and adipose tissue also synthesize two other essential components of the alternative pathway of complement, factors C3 and B, and activate the proximal portion of this pathway. This activation occurs in the absence of infectious agents and without triggering the terminal, lytic part of this pathway. We demonstrate the production in vitro of several polypeptides characteristic of complement activation that are known to have potent biological activities, including the anaphylatoxin C3a. Cultured adipocytes require stimulation with cytokines to activate complement, while explanted adipose tissue has no such requirement. The adipose tissue from obese mice is deficient in this localized activation of the alternative pathway. These results indicate that complement activation occurs in a localized site, adipose tissue, in normal mice and is impaired in a state of metabolic dysfunction. This suggests a novel function for the proximal portion of this complement pathway related to adipose cell biology or energy balance.

3T3 Cells↗
PubMed2005

Observations on peripheral microcirculation in young hypertensive patients.

The increase of the peripheral blood flow resistance level is the major hemodynamic parameter in pathophysiology of essential hypertension (HT). The functional and morphological abnormalities of the microcirculation in the early stage, sometimes before the increase of the blood pressure, are intensely explored. Their identification is a proof for the genetical component of the hypertensive disease theory (studies on young male patients). Our purpose is to examine the capillary peripheral bed at the terminal phalanx level using in vivo capillary microscopy on a group of patients that have the risk of developing HT or that already have HT stage I (according to the JNC 7 Report). The nailfold area and the dorsal surface of the phalanx of fingers 3 and 4 were observed, having as a first objective the search for the areas with rare capillaries. Contrary to the data of the existing studies we have not found any case of significant capillary density decrease or of diffuse capillary rarefaction. Seven patients out of the total number of fifteen with HT stage I were identified to have a low vasomotility score. Considering the association of these cases with glucose intolerance (3 cases) and dyslipidemia (4 cases) the capillary functional anomaly could be related to precapillary arteriole modifications (endothelial dysfunction? metabolic status?).

Adult↗
PubMed2006

Impact of malathion on the biochemical parameters of gobiid fish, Glossogobius giuris (Ham).

There is a dearth of information regarding the changes in heart muscle metabolites induced by pesticides. In the present study, the gobiid fish, Glossogobius giuris, was exposed to sub lethal concentrations of (0.05, 0.25 and 0.5 ppm) organophosphorus pesticide, malathion for short duration (24 to 96 hr). The cardiac muscles showed maximum depletion of glycogen and cholesterol content during 72 and 96 hr after treatment with 0.5 ppm malathion. Whereas a slight fluctuation of protein and glycogen content was observed in low concentration (0.05 ppm) of malathion. The levels of protein showed a significant decrease at high concentration (0.5 ppm) when treated for longer duration (96 hr). The present study reports metabolic dysfunction in response to malathion toxicity in the fish.

Animals↗
PubMed2006

Toxicities of antiretroviral therapy in children.

The addition of highly active antiretroviral therapy to the complex regimens used to treat HIV-infected persons has extended the lives of millions. Despite the proven benefits of antiretroviral therapy, adverse events can occur with its use. These reactions can be separated into several distinct categories: mitochondrial dysfunction, metabolic abnormalities, hematologic complications, and allergic reactions. Drug-associated complications can be particularly challenging to treat when they occur in pediatric HIV patients. Care providers who manage HIV-infected children have to be cognizant of these complications when patients present with symptoms because some can mimic manifestations of HIV infection itself. These adverse reactions are neither uncommon nor unexpected, and discontinuation of the inciting agent is not always mandated. But every effort must be made to address them when they do occur so that adequate treatment is given in a timely manner.

Anti-Retroviral Agents↗
PubMed2006

[Dietary management of diabetic pregnancy].

During pregnancy, several metabolic changes are observed which aim to provide optimum substrate, energy and other nutritional requirements to both the mother and the fetus. Maternal nutrition is the only source for most nutrients, influencing neonatal and placenta development, mother's physiological adjustment and also playing a major role in the destiny of the offspring. Over-nutrition or malnutrition are both linked with increased risk of diabetes mellitus in the offspring. Diabetes in pregnancy is the most common and important metabolic dysfunction in pregnancy. This is divided into two types and it is very important to distinguish between them, as each has different nutritional requirements and a different impact on the course of the pregnancy and the development of the fetus. Gestational diabetes mellitus (GDM) is the main type of diabetes in pregnancy, it usually appears in the second half of pregnancy and mainly influences fetal growth rate and can slow systemic development. Most women with GDM are treated with nutritional management alone. Pre-existing diabetes mellitus is present before pregnancy and it's effects begin at fertilization and implantation, and continue throughout pregnancy and thereafter. It involves high risk of early abortion, severe congenital defects and disrupted organogenesis. Although the treatment of pre-existing diabetes is usually a pharmacological one (insulin or oral pharmacological agents), nutritional management is still very important in normalization of glucose levels before and throughout the pregnancy. Fetal morbidity is lower in women with diabetes in pregnancy when optimal glucose control is maintained. Normalization of glucose levels during pregnancy is agreed to be the main factor in preventing poor outcomes in pregnancy. Dietary advice throughout pregnancy include frequent small meals which contain carbohydrates that are not highly processed, rich with slowly absorbed starches and non-soluble polysaccharides and with a low glycaemic index. The recommended daily caloric intake is individually suited to every woman. The main goals of nutritional management are to maintain balanced glucose levels and to provide enough energy and nutrients for all pregnant women, while avoiding ketosis, and minimizing the risk of hypoglycemia (in women treated with insulin). Health care providers should use the window of opportunity of pregnancy to change dietary patterns and to replace them with a healthy lifestyle for both the mother and her family.

Diabetes Complications↗
PubMed2006

Conservation of glycolytic oscillations in Saccharomyces cerevisiae and human pancreatic beta-cells: a study of metabolic robustness.

The present study compares two computer models of the first part of glucose catabolism in different organisms in search of evolutionarily conserved characteristics of the glycolysis cycle and proposes the main parameters that define the stable steady-state or oscillatory behavior of the glycolytic system. It is suggested that in both human pancreatic beta-cells and Saccharomyces cerevisiae there are oscillations that, despite differences in wave form and period of oscillation, share the same robustness strategy: the oscillation is not controlled by only one but by at least two parameters that will have more or less control over the pathway flux depending on the initial state of the system as well as on extra-cellular conditions. This observation leads to two important interpretations: the first is that in both S. cerevisiae and human beta-cells, despite differences in enzyme kinetics and mechanism of feedback control, evolution seems to have kept an oscillatory behavior coupled to the glucose concentration outside the cytoplasm, and the second is that the development of drugs to regulate metabolic dysfunctions in more complex systems may require further study, not only determining which enzyme is controlling the flux of the system but also under which conditions and how its control is maintained by the enzyme or transferred to other enzymes in the pathway as the drug starts acting.

Computer Simulation↗
PubMed1991

[Studies of experimental cerebral ischemia with NMR spectroscopy].

In vivo NMR (nuclear magnetic resonance) spectroscopy allows for non-invasive measurement of the intracellular pH and the concentration of different metabolites in defined areas of the brain. Phosphocreatine, ATP and lactic acid are of prime interest in ischaemia research. Moreover, a distinction can be made between glycolysis and the oxidative breakdown of glucose after administering C-13-labelled glucose. Finally, spectroscopy of fluorine-containing inert gases such as Freon-23 allows for measuring cerebral blood flow and for directly relating the metabolic alterations to the changes in cerebral blood flow. Given the non-invasive character of NMR spectroscopy all metabolic process occurring throughout one experiment can for the first time be followed up. Thus metabolic alterations during ischaemia can directly be correlated with post-ischaemic recovery processes. It has been shown with the cerebral ischaemia model in the cat that recovery after circulatory failure rather depends on post-ischaemic changes such as the recirculation rate or the speed of high-energy phosphate formation than on the speed of energy metabolism breakdown or acidosis occurring during ischaemia. The future of nuclear magnetic resonance spectroscopy in experimental ischaemia research certainly lies in the therapeutic range. As the exact extent of ischaemic damage can be determined in each experiment it is possible for the first time to define the effect of a drug substance on metabolic dysfunction in each individual experiment. This method is not only expected to reduce the number of laboratory animals but also to dramatically improve statistical variability compared to group comparisons.

Animals↗
PubMed1991

Rod densitometry in the aging human eye.

Retinal densitometry is a noninvasive physiologic technique used to examine the visual pigments in living human eyes. To assess possible age-related disturbances of rod photopigment kinetics, retinal densitometry was done in 44 eyes of 44 healthy subjects (age range, 12-78 yr). With progressing age, a significant but small increase in photopigment density difference (bleached versus dark adapted eye) and an increase in the time constant of rhodopsin regeneration was found. The increased density difference in rods was consistent with morphologic findings of increased rod outer segment diameter and disc content in older subjects. To explain this change in terms of the decreased specular reflections at the level of the inner limiting membrane was inadequate because age effects were independent of wavelength in the region of 450-550 nm. To control for the effects of ocular stray light from the lens, subjects older than 40 yr with a clear crystalline lens were measured and compared with those with pseudophakia. No statistically significant difference was found between the two groups. Increased rod density difference contrasts sharply with an earlier reported decrease in this parameter for foveal cones. The slowing of the regeneration rate is a phenomenon common to rods and cones. It may be a result of a gradual metabolic dysfunction of the retinal pigment epithelium in older subjects.

Adolescent↗
PubMed1991

[In-vivo 19F-MRS study of 5-fluorouracil (5-FU) metabolism on tumors].

5-Fluorouracil (5-FU) metabolism on tumors was studied by in-vivo 19F-MRS (magnetic resonance spectroscopy). In this study, two kinds of tumors were used, i.e., Yoshida sarcoma implanted subcutaneously to the abdomen of rats and drug-induced tumors in the rats livers. Sequential 19F spectra were obtained just after 150 mg/kg 5-FU injected intravenously. In Yoshida sarcoma, the accumulation of 5-FU was observed and disappearance of 5-FU was slower compared to the normal tissue. However, synthesis of fluoronucleotides (Fnct) could not be detected. In drug-induced liver tumors, the peak of fluoro-beta-alanine (FBAL) was observed. Disappearance of 5-FU and catabolism to FBAL in the liver tumors group were slower compared to the normal liver. Synthesis of Fnct did not increase in the liver tumor group. The results in the liver tumor group are considered to be the confined result of the hepatocytes and tumors cells. It was considered that the delayed catabolism to FBAL in the liver tumor group showed metabolic dysfunction of the liver. Also the synthesis of Fnct in tumors could not be detected by in-vivo 19F-MRS. 19F-MRS method could not detect Fnct in tumors in-vivo. However, the accumulation of 5-FU could be assessed by this method. It is expected that the evaluation of 5-FU pooling in tumors could be used for the index of chemotherapeutic effect.

Animals↗
PubMed1991

[Brain imaging and schizophrenia].

Brain structures and brain function have been investigated by the new brain imaging techniques for more than ten years. In Psychiatry, these techniques could afford a new understanding of mental diseases. In schizophrenic patients, CAT scanner and RMI pointed out statistically significant ventricular enlargements which are presently considered as evidence for abnormalities in brain maturation. Functional imaging techniques reported metabolic dysfunctions in the cortical associative areas which are probably linked to the cognitive features of schizophrenics.

Brain↗
PubMed1990

The relation of clinical catastrophes, endogenous oxalate production, and urolithiasis.

A dose-related toxicity syndrome of renal, cerebral, and liver dysfunction; metabolic acidosis; and deposition of calcium oxalate crystals in tissues is reported in association with various apparently unrelated treatments for a wide range of diseases. The parenteral nutrient xylitol, the hyperosmolar agent glycerol, the polysorbate emulsifiers (e.g., in vitamin E preparations), the anesthetic methoxyflurane, and possibly the experimental hypoglycemic agent dichloroacetate all produce a toxicity syndrome very similar to that of ethylene glycol poisoning. In long-term, high-dose oral toxicity studies with rodents, these or similar agents also produce calcium oxalate bladder stones and bladder tumors. Studies with both unlabeled and labeled agents in humans and animals and in vitro experiments with purified enzymes, tissue homogenates, and isolated hepatocytes have provided both strong circumstantial and direct evidence for the existence of minor pathways of carbohydrate metabolism and of oxidative dealkylation and dehalogenation reactions in drug biotransformations that link these agents to endogenous oxalate production. Because urinary oxalate is now considered to be a critical factor in stone formation and because it is increasingly accepted that 80-90% of urinary oxalate is produced endogenously, it is now possible to formulate pathways that link oxalate production with dietary macronutrients. Therapeutic modifications of diet, in vivo hormonal milieu, and intracellular metabolic controls in relation to endogenous oxalate production may provide new forms of treatment for urolithiasis.

Animals↗
PubMed1990

[Papaverin--effective in therapy of pruritus of atopic dermatitis?].

Patients suffering from atopic dermatitis show increased phosphodiesterase activity in leucocytes. As a result, the level of intracellular c-AMP is reduced, which can produce a number of metabolic dysfunctions: We found strong evidence that an enhanced release of several inflammation mediators can favor itching, which in turn promotes the development of eczema, since it induces reflectory scratching. In order to solve the question whether papaverine as a phosphodiesterase inhibitor might offer a new approach in the systemic therapy of itching, we performed a placebo-controlled study on 51 patients with atopic dermatitis, who were orally treated with papaverin-HCl over 8 weeks. However, we did not observe any improvement of itching or eczema during treatment. Some other recently developed phosphodiesterase inhibitors are discussed.

Administration, Oral↗
PubMed1989

[A study on the pathogenesis of hepatolenticular degeneration using an in vitro model].

Hepatolenticular degeneration (HLD) as an autosomal recessively inherited disease has been known to be associated with by copper metabolic dysfunction. Its primary genetic defect is still not clear. The average copper content of HLD cells was found to be approximately threefold as much as that of normal cells in the authors previous studies. Cultured fibroblasts were used to serve as an in vitro model to investigate the primary molecular defects. The distribution of intracellular copper in the proteins of HLD cells were examined. The cell lysates were fractionated by gel chromatographic filtration. The copper concentration of the column fractions revealed that the copper binding character was altered in HLD cells. A decreased ratio of copper to proteins was observed in cytoplasmic proteins having a molecular weight greater than 300,000. There was more copper specifically bound to the lower molecular weight compounds in the HLD cells. The results of this laboratory technology suggested that this might serve as a method for establishing the early diagnosis of this disease.

Cells, Cultured↗