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PubMed1976

Ammonia production by the small intestine of the rat.

1. Slices of duodenum and jejunum produce ammonia from glutamine in vitro. 2. Ammoniagenesis does not increase in response to acidosis or potassium deficiency, two conditions known to cause enhanced ammoniagenesis in the kidney. 3. Gut contains glutaminase 1 as well as gamma-glutamyl transpeptidase. 4. These enzymes do not show any increase during starvation.

Acidosis↗
PubMed2006

Effect of plant growth on dehydration rates and microbial populations in sewage biosolids.

The high water content of sewage biosolids makes them expensive to transport. Two experiments were done to see if it was practical to use transpiration by plants as a low cost method to dehydrate biosolids. (i) To assess biosolids as a growth-medium for plants, maize, beans, pumpkin, forage oats and an annual ryegrass were grown in pots of fresh biosolids. Plant growth varied between species and potassium deficiency was found to be a limiting factor for barley. Roots were slow to penetrate anoxic biosolids in the bottom of the pots. (ii) Dehydration rates were measured in 30 litre boxes of biosolids from two different sources. Boxes were planted with maize or beans, or kept fallow. Despite the high (73-83%) initial water content of the biosolids, plants were susceptible to wilting on warm days which suggested that a significant proportion of the water in biosolids is not freely available to plants. Shrinkage caused a major reduction in biosolids volume in both experiments. When change in volume of the biosolids residue was accounted for, there was a 56% average water loss in planted treatments and 34% water loss in the fallow treatment. This indicates that planting may have some potential as a technique to accelerate dehydration of biosolids. Water contents were not reduced sufficiently to influence biosolids microbial populations.

Dehydration↗
PubMed1973

Transcellular ion flow in Escherichia coli B and electrical sizing of bacterias.

Dielectric breakdown of cell membranes and, in response, transcellular ion flows were measured in Escherichia coli B 163 and B 525 using a Coulter counter as the detector with a hydrodynamic jet focusing close to the orifice of the counter. Plotting the relative pulse height for compensated amplification of a certain size of the cells against increasing detector current, a rather sharp bend within the linear function was found, which did not occur when measuring fixed cells or polystyrene latex. The start current for transcellular ion flow causing the change of the slope is different for the potassium-deficient mutant B 525 in comparison with the wild-type B 163, indicating a change in the membrane structure of B 525 by mutation and demonstrating the sensitivity of the method for studying slight changes in membrane structure in general. The theoretical size distributions for two current values in the range of transcellular ion flow were constructed from the true size distribution at low detector currents, assuming an idealized sharp changeover of the bacterial conductivity from zero to one-third of the electrolyte conductivity.

Cell Biology↗
PubMed1995

Polycystic kidney disease: etiology, pathogenesis, and treatment.

Once viewed as hopelessly incurable disorders and the dustbin for careers in academic medicine, the polycystic kidney diseases have emerged as prime targets of pathophysiologic study and palliative and definitive treatment in the era of molecular medicine. Polycystic kidney disease (PKD) may be hereditary or acquired. The major inherited types are autosomal dominant (AD) and autosomal recessive (AR). ADPKD is caused by at least two (and possibly three) genes located on separate chromosomes, while ADPKD-1 is due to a 14 kb transcript in a duplicated region on the short arm of chromosome 16 very near the alpha-globin gene cluster and the gene for one form of tuberous sclerosis. ADPKD-2 has been assigned to the long arm of chromosome 4. ARPKD is due to a mutated gene on both copies of the long arm of chromosome 6. Cysts originate in renal tubules. Proliferation of tubule epithelial cells modulated by endocrine, paracrine, and autocrine factors is a major element in the pathogenesis of renal cystic diseases. In addition, fluid that is abnormally accumulated within the cysts is derived from glomerular filtrate and, to a greater extent, by transepithelial fluid secretion. Abnormal synthesis and degradation of matrix components associated with interstitial inflammation are additional features in the pathogenesis of renal cystic diseases. The ADPKD genotypes are characterized by bilateral kidney cysts, hypertension, hematuria, renal infection, stones, and renal insufficiency. ADPKD is a systemic disorder; cysts appear with decreasing frequency in the kidneys, liver, pancreas, brain, spleen, ovaries, and testis. Cardiac valvular disorders, abdominal and inguinal hernias, and aneurysms of cerebral and coronary arteries and aorta are also associated with ADPKD. Treatment is supportive: dietary regulation of salt and protein intake, control of hypertension and renal stones, and dialysis and transplantation at the end stage. ARPKD is a relatively rare disease that causes clinical symptoms at birth, with significant mortality in the first month of life. The cysts develop primarily in the collecting ducts because of a failure in the maturation process. Early complications include Potter's syndrome; excessive size of the kidneys, causing respiratory dysfunction; hypertension; and renal insufficiency. Hepatic fibrosis is an associated extrarenal problem that results in significant morbidity in young children and adolescents. Treatment includes supportive care, dialysis, and renal transplantation. Acquired cysts (solitary/simple) are commonplace in older persons. Multiple cysts may be seen in association with potassium deficiency, congenital disorders, metabolic diseases, and toxic renal injury.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Kaliuretic response to aldosterone: influence of the content of potassium in the diet.

The excretion of potassium (K+) decreased by 50% (30 v 63 mEq/d, P < .01) when subjects consumed a diet that was low in K+ for 3 days. Although part of this conservation of K+ was achieved in part by suppressing the release of aldosterone, nevertheless providing exogenous mineralocorticoids did not lead to a large kaliuresis when there was a modest degree of K+ depletion. Accordingly, the purpose of this study was to evaluate possible mechanisms for this antikaliuretic response to mineralocorticoids. The renal handling of K+ was examined by independent analysis of the two factors that influence its excretion, the driving force to secrete K+ and the urine volume. This driving force is reflected in a noninvasive fashion by the transtubular [K+] gradient (TTKG). Stimuli to increase the rate of excretion of K+ in subjects on a normal and a low-K+ diet included the administration of 200 micrograms fludrocortisone (9 alpha F), the induction of a high urine flow rate (9 alpha F+furosemide), the induction of bicarbonaturia (9 alpha F+acetazolamide), and the excretion of Cl(-)-poor urine (< 15 mEq/L). On the low-K+ diet, the peak value for the TTKG 3 to 4 hours after 9 alpha F was less than half that while on the normal diet (6.4 v 14, P < 0.01). In contrast, the TTKG was not significantly different on either diet when there was bicarbonaturia or the excretion of a Cl(-)-poor urine (18 v 17 and 17 v 16, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1998

Interventional nutrition for cardiac disease.

Animals with cardiac disease can have a variety of nutritional alterations for which interventional nutrition can be beneficial. Deviation from optimal body weight, both obesity and cachexia, is a common problem in cardiac patients and adversely affects the animal. Methods for maintaining optimal weight are important for good quality of life in dogs and cats with cardiac disease. Providing proper diets to prevent excess intake of sodium and chloride also is important, but severe salt restriction may not be necessary until later stages of disease. Certain nutrient deficiencies may play a role in the pathogenesis or complications of cardiac disease, but nutrients also may have effects on cardiac disease which are above and beyond their nutritional effects (nutritional pharmacology). Supplementation of nutrients such as taurine, carnitine, coenzyme Q10, and omega-3 polyunsaturated fatty acids may have benefits in dogs or cats with cardiac disease through a number of different mechanisms. By addressing each of these areas maintaining optimal weight, avoiding nutritional deficiencies and excesses, and providing the benefits of nutritional pharmacology, optimal patient management can be achieved.

Animals↗
PubMed1997

Structural Novelties in Anionic Cluster Halide Phases. Discrete Tetrahedral A(4)Br(+) Ions in Two New Zirconium Bromide Structures (A = Na-Cs).

Suitable reactions of ABr, Zr, ZrBr(4), and an interstitial Z element in Ta containers at 850 degrees C afford two series of quaternary cluster phases containing A(4)Br(3+) ions. Cubic (A(4)Br)(2)Zr(6)(Z)Br(18) phases occur for various combinations of A = Na-Cs, Z = Be, B, H, Mn. The combination with A = K, Z = B was structurally characterized (inverse fluorite, Fm&thremacr;m, Z = 4, a = 16.191(2) Å). The 15-e cluster exhibits the appropriate magnetic moment, and this decreases toward the diamagnetic 14-electron limit in products with potassium deficiencies, (K(4)(-)(x)())(2)Zr(6)Br(18)B, x </= approximately 0.5. The tetragonal Cs(4)Br[Zr(6)(B)Br(12)]Br(4) (P&fourmacr;2(1)m, Z = 2, a = 12.5482(7) Å, c = 11.5610(9) Å) contains a new type of puckered M(6)Br(16) layers with Cs(4)Br(3+) in tunnels normal to the layers. Both examples of A(4)Br(3+) ions have short central Br-A bonds plus three to nine more distant bromines in neighboring clusters about each A, respectively.

Journal Article↗
PubMed2001

Expression of insulin-like growth factor-I and transforming growth factor-beta in hypokalemic nephropathy in the rat.

BACKGROUND: Potassium deficiency (KD) in the rat retards body growth but stimulates renal enlargement caused by cellular hypertrophy and hyperplasia, which is most marked in the outer medulla. If hypokalemia persists, interstitial infiltrates appear and eventually fibrosis. Since early in KD insulin-like growth factor-I (IGF-I) levels in the kidney are elevated, suggesting that it may be an early mediator of the exaggerated renal growth, and as transforming growth factor-beta (TGF-beta) promotes cellular hypertrophy and fibrosis, we examined the renal expression of these growth factors in prolonged KD. METHODS: Rats were given a K-deficient diet or were pair fed or ad libitum fed a K-replete diet for 21 days. Growth factor mRNA levels were measured in whole kidney and protein expression localized by immunohistochemistry. RESULTS: KD rats weighed less than pair-fed controls, while the kidneys were 49% larger. Their serum IGF-I and kidney IGF-I protein levels were depressed, as were their IGF-I mRNA levels in liver, kidney, and muscle. These changes can largely be attributed to decreased food intake. In contrast, kidney IGF binding protein-1 (IGFBP-1) mRNA and TGF-beta mRNA levels were increased significantly. Histology of outer medulla revealed marked hypertrophy and adenomatous hyperplasia of the collecting ducts and hypertrophy of the thick ascending limbs of Henle with cellular infiltrates in the interstitium. Both nephron segments immunostained strongly for IGF-I and IGFBP-1, but only the nonhyperplastic enlarged thick ascending Henle limb cells immunostained for TGF-beta, which was strongly positive. Prominent interstitial infiltrates with ED1 immunostained monocytes/macrophages were present. CONCLUSIONS: These findings are consistent with a sustained role for IGF-I in promoting the exaggerated renal growth of KD and appear to be mediated through local trapping of IGF-I by the overexpressed IGFBP-1, which together with IGF-I can promote renal growth. The selective localization of TGF-beta to hypertrophied nonhyperplastic nephron segments containing IGF-I raises the possibility that TGF-beta may be serving to convert the mitogenic action of IGF-I into a hypertrophic response in these segments. It is also conceivable that TGF-beta may be a cause of the tubulointerstitial infiltrate. Finally, the low circulating IGF-I levels likely contribute to the impaired body growth.

Animals↗
PubMed1991

Two forms of cytochrome P-450(11 beta) in rat zona glomerulosa cells: a short review.

Aldosterone, the major mineralocorticoid hormone, is produced exclusively in the zona glomerulosa of the mammalian adrenal cortex. In the rat species, this zonal specificity of aldosterone biosynthesis appears to be due mainly to the existence of a second form of cytochrome P-450(11 beta), which differs from the major form of the enzyme (molecular weight 51,000) by (1) a lower molecular weight (49,000), (2) a broader range of catalytic activities, which include corticosterone methyl oxidation 1 and 2, (3) an exclusive occurrence in the zona glomerulosa, and (4) a crucial dependence on sodium and potassium intake. The 49K form of the enzyme can be induced by potassium ions in vivo (potassium repletion of potassium-deficient rats) or in vitro (primary cell culture). The biosynthesis of this protein is controlled most likely at the level of transcription. According to indirect evidence, ACTH induces only the 51K form of the enzyme in vitro. Prolonged treatment of rats with a high dose of ACTH has a repressive effect on the 49K form of the enzyme.

Animals↗
PubMed2001

Delay of natural bone loss by higher intakes of specific minerals and vitamins.

For early prevention or inhibition of postmenopausal and age-related bone loss, nutritional interventions might be a first choice. For some vitamins and minerals an important role in bone metabolism is known or suggested. Calcium and vitamin D support bone mineral density and are basic components in most preventive strategies. Magnesium is involved in a number of activities supporting bone strength, preservation, and remodeling. Fluorine and strontium have bone-forming effects. However, high amounts of both elements may reduce bone strength. Boron is especially effective in case of vitamin D, magnesium, and potassium deficiency. Vitamin K is essential for the activation of osteocalcin. Vitamin C is an important stimulus for osteoblast-derived proteins. Increasing the recommended amounts (US RDA 1989), adequate intakes (US DRI 1997), or assumed normal intakes of mentioned food components may lead to a considerable reduction or even prevention of bone loss, especially in late postmenopausal women and the elderly.

Ascorbic Acid↗
PubMed1986

Tetany induced by hypokalemia in the absence of alkalosis.

A 36-year-old patient developed tetany manifested only by a positive Trousseau's sign and with a negative Chvostek's sign 8 weeks after gastric bypass surgery for obesity. The usual causes of tetany (hypocalcemia, hypomagnesemia and alkalosis) were absent. The only possible etiology found was hypokalemia. Previous cases of hypokalemia induced tetany reported were always accompanied by alkalosis. Its absence in our patient makes this case unique and determines that hypokalemia per se in the absence of alkalosis may be a cause of tetany. It is suggested that the Trousseau's sign should be investigated in patients with severe potassium deficiency.

Adult↗