Explore the vast range of titles available.

Dehydration, a condition that characterizes excessive loss of body water, is well known to be associated with acute renal dysfunction; however, it has largely been considered reversible and to be associated with no long-term effects on the kidney. Recently, an epidemic of chronic kidney disease has emerged in Central America in which the major risk factor seems to be recurrent heat-associated dehydration. This has led to studies investigating whether recurrent dehydration may lead to permanent kidney damage. Three major potential mechanisms have been identified, including the effects of vasopressin on the kidney, the activation of the aldose reductase-fructokinase pathway, and the effects of chronic hyperuricemia. The discovery of these pathways has also led to the recognition that mild dehydration may be a risk factor in progression of all types of chronic kidney diseases. Furthermore, there is some evidence that increasing hydration, particularly with water, may actually prevent CKD. Thus, a whole new area of investigation is developing that focuses on the role of water and osmolarity and their influence on kidney function and health.

Background: Excessive fructose intake causes metabolic syndrome in animals and can be partially prevented by lowering the uric acid level. We tested the hypothesis that fructose might induce features of metabolic syndrome in adult men and whether this is protected by allopurinol. Methods: A randomized, controlled trial of 74 adult men who were administered 200 g fructose daily for 2 weeks with or without allopurinol. Primary measures included changes in ambulatory blood pressure (BP), fasting lipids, glucose and insulin, homeostatic model assessment (HOMA) index, body mass index and criteria for metabolic syndrome. Results: The ingestion of fructose resulted in an increase in ambulatory BP (7±2 and 5±2 mm Hg for systolic (SBP) and diastolic BP (DBP), P<0.004 and P<0.007, respectively). Mean fasting triglycerides increased by 0.62±0.23 mmol l−1 (55±20 mg per 100 ml), whereas high-density lipoprotein cholesterol decreased by 0.06±0.02 mmol l−1 (2.5±0.7 mg per 100 ml), P<0.002 and P<0.001, respectively. Fasting insulin and HOMA indices increased significantly, whereas plasma glucose level did not change. All liver function tests showed an increase in values. The metabolic syndrome increased by 25–33% depending on the criteria. Allopurinol lowered the serum uric acid level (P<0.0001) and prevented the increase in 24-h ambulatory DBP and daytime SBP and DBP. Allopurinol treatment did not reduce HOMA or fasting plasma triglyceride levels, but lowered low-density lipoprotein cholesterol relative to control (P<0.02) and also prevented the increase in newly diagnosed metabolic syndrome (0–2%, P=0.009). Conclusions: High doses of fructose raise the BP and cause the features of metabolic syndrome. Lowering the uric acid level prevents the increase in mean arterial blood pressure. Excessive intake of fructose may have a role in the current epidemics of obesity and diabetes.

Use of carbon nanotubes as additives to composite parts for the purpose of increased damping has been the subject of much recent attention, owing to their large surface area per weight ratio which provides for frictional losses at the carbon nanotube–resin matrix interface. This article presents an experimental study to quantify the structural damping in composites due to the addition of carbon nanotubes to thermosetting resin systems with and without fiberglass reinforcement. Carbon nanotubes of varying quantity and morphology are ultrasonically dispersed in epoxy resin and are compression molded to form test samples that are used in forced vibration, free vibration with initial tip deflection, and tension tests to determine their damping ratio, specific damping capacity, and Young’s modulus. Results show increased stiffness and specific damping capacity with the addition of carbon nanotubes and particularly increased frictional loss with increasing surface area to weight ratio. The addition of fiberglass reinforcement to composite samples is shown to reduce the effective damping ratio over plain epoxy samples and carbon nanotube-filled epoxy samples.

Uric acid is strongly associated with cardiovascular and renal disease, but is usually not considered to have a causal role. However, recent experimental, epidemiological, and clinical studies provocatively suggest that uric acid may contribute to the development of hypertension, metabolic syndrome, and kidney disease in some patients. Clinical studies are urgently needed to examine this important possibility.

Here the intestinal helminth infracommunities of 218 double-crested cormorants (Phalacrocorax auritus) from 11 locations in Alabama, Minnesota, Mississippi and Vermont are documented. Trematode infections were present in 98% of hosts; 65% of cormorants carried cestode infections, 4% were infected with acanthocephalans and 66% had nematode intestinal parasites. Parasite infracommunities of hosts collected on wintering grounds had higher richness and diversity than did birds collected on breeding grounds. Differences in parasite richness and diversity between male and female P. auritus were also detected, but not between immature and mature bird hosts. Parasite intensity did not differ by sex, maturity, or between breeding and wintering season. The most common parasite was Drepanocephalus auritus (spathans), which is recognized as a disease agent that negatively impacts the catfish aquaculture industry in the US. Echinochasmus sp. in double-crested cormorants is documented for the first time in the United States. We suggest that the differences observed among parasite infracommunities could be associated with the foraging distances travelled by P. auritus during breeding and wintering seasons, which is limited by allocation of parental care during the breeding season.

Hydrochlorothiazide (HCTZ) is used to manage hypertension and heart failure; however, its side effects include mild hypokalemia, metabolic abnormalities, and volume depletion, which might have deleterious effects on renal and endothelial function. We studied whether HCTZ cause renal injury and/or altered vasoreactivity and if these changes are hypokalemia-dependent. Rats were given a normal diet or a diet moderately low in potassium (K+) with or without HCTZ. Animals fed either a low K+ diet alone or HCTZ developed mild hypokalemia. There was no significant difference in systolic blood pressure in the different treatment groups. All three groups with hypokalemia had mild proteinuria; low K+-HCTZ rats had reduced creatinine clearance. HCTZ-treated rats displayed hypomagnesemia, hypertriglyceridemia, hyperglycemia, insulin resistance, and hyperaldosteronism. No renal injury was observed in the groups without HCTZ; however, increased kidney weight, glomerular ischemia, medullary injury, and cortical oxidative stress were seen with HCTZ treatment. Endothelium-dependent vasorelaxation was reduced in all hypokalemic groups and correlated with reduced serum K+, serum, and urine nitric oxide. Our results show that HCTZ is associated with greater renal injury for the same degree of hypokalemia as the low K+ diet, suggesting that factors such as chronic ischemia and hyperaldosteronism due to volume depletion may be responsible agents. We also found impaired endothelium-dependent vasorelaxation was linked to mild hypokalemia.

Controversy exists over whether an elevated UA is a true cardiovascular risk factor. We hypothesized that the known association between an elevated UA and increased renal vasoconstriction was causal and not secondary. Rats were placed on a low sodium (0.05%) diet with oxonic acid to block endogenous uricase (OA rats); control rats received a low sodium diet alone (LS). OA rats developed modest hyperuricemia (4.0 vs 1.5 mg/dl) and maintained normal renal function (CrCl) at 7 wks. Renal histology showed no crystal deposition; however, mild tubulointerstitial fibrosis was present, with an increase in markers of tubular injury (osteopontin), macrophage infiltration, and collagen III deposition. LS rats maintained normal histology. To better understand the pathogenesis, we examined several vasoactive mediators, and found that OA treated rats had significantly less NOS1 expression in the macula densa, a decrease in medullary NOS3 expression, and an increase in renin staining than LS controls. As these changes are similar to what is observed with cyclosporine (CSA) administration, we examined the effect of an elevated UA in experimental CSA nephropathy. CSA-OA treated rats had an increase in UA compared to CSA alone (5.9 vs 3.2 mg/dl) and significantly worse renal histology at 7 weeks, in terms of tubular damage (osteopontin), macrophages and collagen III deposition. No crystals were demonstrated in the kidneys. CSA rats were similar to OA alone rats with respect to effects on NOS1, NOS3 and renin; however, CSA-OA rats showed greater decreases in NOS1 and NOS3 and a greater increase in renin. Thus, an elevated UA directly causes renal injury through a crystal-independent mechanism that involves alterations in nitric oxide and renin levels; this has significant implications on the role of uric acid in cardiovascular disease, hypertension, and renal disease.