548 research outputs found
Accelerated atherosclerosis in a human immunodeficiency virus infected patient not on highly active anti-retroviral therapy: An autopsy case report
The pandemic spread of human immunodeficiency virus (HIV) has been the greatest challenge to public health in modern times. However today, people infected with HIV are living longer due to highly active antiretroviral therapy (HAART). This has resulted in age related complications like cardiovascular diseases, causing increased morbidity and mortality. The relative contributions of HIV infection versus potential adverse effects of HAART to coronary heart disease risk remains unclear. Recent reports implicate both HIV infection per se and HAART therapy to cause metabolic derangements which are pro-atherogenic. Here, we report a case of HIV infected young patient never exposed to HAART, presenting with accelerated atherosclerosis in aorta, coronary and carotid arteries
Effect of diet on plasma acid-base composition in normal humans
AbstractEffect of diet on plasma acid-base composition in normal humans. Steady-state plasma and urine acid-base composition was assessed in 19 studies of 16 normal subjects who ingested constant amounts of one of three diets that resulted in different rates of endogenous noncarbonic acid production (EAP) within the normal range. Renal net acid excretion (NAE) was used to quantify EAP since the two variables are positively correlated in normal subjects. A significant positive correlation was observed between plasma [H+] and plasma PCO2, and between plasma [HCO3-] and plasma PCO2, among the subjects. Multiple correlation analysis revealed a significant interrelationship among plasma [H+], plasma PCO2, and NAE (r = 0.71, P < 0.001), and among plasma [HCO3-], plasma PCO2, and NAE (r = 0.77, P < 0.001). The partial correlation coefficients indicated a significant positive correlation between plasma [H+] and NAE, and a significant negative correlation between plasma [HCO3-] and NAE, when plasma PCO2 was held constant. These findings indicate that two factors influence the level at which plasma [H+] is maintained in normal subjects: (1) the steadystate rate of endogenous noncarbonic acid production, and (2) the setpoint at which plasma PCO2 is regulated by the respiratory system. Plasma [HCO3-] is also co-determined by these two factors. In disease states, therefore, both factors must be known before a disturbance in acid-base homeostasis can be excluded.Effet du régime sur la composition acido-basique plasmatique chez des sujets humains normaux. La composition acido-basique plasmatique et urinaire à l'équilibre a été déterminée dans 19 études de 16 sujets normaux qui ingéraient des quantités constantes de l'un de trois régimes aboutissant à différents taux de production endogène d'acides non carboniques (EAP) à l'intérieur de la normale. L'excrétion rénale nette d'acides (NAE) a été utilisée pour quantifier l'EAP puisque les deux variables sont positivement corrélées chez des sujets normaux. Une corrélation significative positive a été observée entre le [H+] plasmatique et la PCO2 plasmatique, et entre le [HCO3-] plasmatique et PCO2 plasmatique, parmi ces sujets. Une analyse par corrélations multiples a révélé une interrelation significative entre [H+] plasmatique, PCO2 plasmatique et NAE (r = 0,71, P < 0,001), et entre [HCO3-] plasmatique, PCO2 plasmatique et NAE (r = 0,77, P < 0,001). Les coefficients de corrélation partielle ont indiqué une corrélation significative positive entre [H+] plasmatique et NAE, et une corrélation significative négative entre [HCO3-] plasmatique et NAE, lorsque PCO2 plasmatique était maintenue constante. Ces résultats indiquent que deux facteurs influencent le niveau auqeal [H+] plasmatique est maintenu chez des sujets normaux: (1) le taux de production à l'équilibre d'acides non carboniques endogènes, et (2) le point d'équilibre auquel PCO2 plasmatique est régulée par le système respiratoire. [HCO3-] plasmatique est également codéterminé par ces deux facteurs. Ainsi, dans les états pathologiques, les deux facteurs doivent être connus avant de pouvoir exclure une perturbation de l'homéostasie acido-basique
Time- and exercise-dependent gene regulation in human skeletal muscle
BACKGROUND: Skeletal muscle remodeling is a critical component of an organism's response to environmental changes. Exercise causes structural changes in muscle and can induce phase shifts in circadian rhythms, fluctuations in physiology and behavior with a period of around 24 hours that are maintained by a core clock mechanism. Both exercise-induced remodeling and circadian rhythms rely on the transcriptional regulation of key genes. RESULTS: We used DNA microarrays to determine the effects of resistance exercise (RE) on gene regulation in biopsy samples of human quadriceps muscle obtained 6 and 18 hours after an acute bout of isotonic exercise with one leg. We also profiled diurnal gene regulation at the same time points (2000 and 0800 hours) in the non-exercised leg. Comparison of our results with published circadian gene profiles in mice identified 44 putative genes that were regulated in a circadian fashion. We then used quantitative PCR to validate the circadian expression of selected gene orthologs in mouse skeletal muscle. CONCLUSIONS: The coordinated regulation of the circadian clock genes Cry1, Per2, and Bmal1 6 hours after RE and diurnal genes 18 hours after RE in the exercised leg suggest that RE may directly modulate circadian rhythms in human skeletal muscle
EFFECTS OF CHANGE IN BODY POSTURE ON PLASMA AND SERUM ELECTROLYTES IN NORMAL SUBJECTS AND IN PRIMARY ALDOSTERONISM
We observed that change in body posture from the supine to the erect position in normal volunteers was associated with a rise in circulating potassium and a fall in sodium concentrations, irrespective of whether the electrolytes were measured in serum or plasma, or whether head-up tilt or ambulation was used. In patients with primary aldosteronism, the fall in serum sodium and rise in serum potassium with ambulation tended to obscure the characteristic electrolyte abnormalities of that syndrome. These changes in potassium and sodium could contribute to the rise in aldosterone secretion on orthostasis. The body posture of patients should be considered in the interpretation of plasma and serum electrolyte levels.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75439/1/j.1365-2265.1981.tb02972.x.pd
Enhanced Uridine Bioavailability Following Administration of a Triacetyluridine-Rich Nutritional Supplement
Uridine is a therapy for hereditary orotic aciduria and is being investigated in other disorders caused by mitochondrial dysfunction, including toxicities resulting from treatment with nucleoside reverse transcriptase inhibitors in HIV. Historically, the use of uridine as a therapeutic agent has been limited by poor bioavailability. A food supplement containing nucleosides, NucleomaxX®, has been reported to raise plasma uridine to supraphysiologic levels
Acute Insulin Stimulation Induces Phosphorylation of the Na-Cl Cotransporter in Cultured Distal mpkDCT Cells and Mouse Kidney
The NaCl cotransporter (NCC) is essential for sodium reabsorption at the distal convoluted tubules (DCT), and its phosphorylation increases its transport activity and apical membrane localization. Although insulin has been reported to increase sodium reabsorption in the kidney, the linkage between insulin and NCC phosphorylation has not yet been investigated. This study examined whether insulin regulates NCC phosphorylation. In cultured mpkDCT cells, insulin increased phosphorylation of STE20/SPS1-related proline-alanine-rich kinase (SPAK) and NCC in a dose-dependent manner. This insulin-induced phosphorylation of NCC was suppressed in WNK4 and SPAK knockdown cells. In addition, Ly294002, a PI3K inhibitor, decreased the insulin effect on SPAK and NCC phosphorylation, indicating that insulin induces phosphorylation of SPAK and NCC through PI3K and WNK4 in mpkDCT cells. Moreover, acute insulin administration to mice increased phosphorylation of oxidative stress-responsive kinase-1 (OSR1), SPAK and NCC in the kidney. Time-course experiments in mpkDCT cells and mice suggested that SPAK is upstream of NCC in this insulin-induced NCC phosphorylation mechanism, which was confirmed by the lack of insulin-induced NCC phosphorylation in SPAK knockout mice. Moreover, insulin administration to WNK4 hypomorphic mice did not increase phosphorylation of OSR1, SPAK and NCC in the kidney, suggesting that WNK4 is also involved in the insulin-induced OSR1, SPAK and NCC phosphorylation mechanism in vivo. The present results demonstrated that insulin is a potent regulator of NCC phosphorylation in the kidney, and that WNK4 and SPAK are involved in this mechanism of NCC phosphorylation by insulin
Improvement in Peripheral Glucose Uptake After Gastric Bypass Surgery Is Observed Only After Substantial Weight Loss Has Occurred and Correlates with the Magnitude of Weight Lost
# 2009 The Author(s). This article is published with open access at Springerlink.com Introduction Altered gut and pancreatic hormone secretion may bolster resolution of insulin resistance after Roux-en-Y gastric bypass (RYGB), but the independent effects of weight loss and hormonal secretion on peripheral glucose disposal are unknown. Methods Two groups of nondiabetic morbidly obese patients were studied: RYGB followed by standardized caloric restriction (RYGB, n=12) or caloric restriction alone (diet, n=10). Metabolic evaluations (euglycemic–hyperinsulinemic clamp, meal tolerance test) were done at baseline and 14 days (both groups) and 6 months after RYGB
Understanding diabetes in patients with HIV/AIDS
This paper reviews the incidence, pathogenetic mechanisms and management strategies of diabetes mellitus in patients with human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS). It classifies patients based on the aetiopathogenetic mechanisms, and proposes rational methods of management of the condition, based on aetiopathogenesis and concomitant pharmacotherapy
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