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acidosis/proline

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Leht 1 alates 39 tulemused
The middle domain of plasma histidine-proline-rich glycoprotein (HPRG) contains unusual tandem pentapeptide repeats (consensus G(H/P)(H/P)PH) and binds heparin and transition metals. Unlike other proteins that interact with heparin via lysine or arginine residues, HPRG relies exclusively on
Root surface demineralization is widely used as an adjunct to periodontal treatment. To clarify the influence of citric acid root conditioning on periodontal wound healing, the effects of citric acid and associated extracellular acidosis on the viability (MTT assay), attachment and protein synthesis

Lactic acidosis due to pyruvate carboxylase deficiency.

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Two unrelated Canadian Indian infants presented with metabolic acidosis. Lactate, pyruvate, glutamic acid, proline and alanine were greatly elevated in plasma. Urinary excretion of alpha-ketoglutarate and pyruvate was increased. Pyruvate carboxylase activity was very low in skin fibroblasts and
A Canadian Indian family is described in which three of the children were mentally retarded, and had seizures and other neurological abnormalities. They had chronic metabolic acidosis associated with elevated blood levels of lactate, pyruvate, and alanine. Two of the children excreted large amounts
As part of a study on the regulation of renal ammoniagenesis in the mouse kidney, we investigated the effect of chronic metabolic acidosis on glutamine synthesis by isolated mouse renal proximal tubules. The results obtained reveal that, in tubules from control mice, glutamine synthesis occurred at

Regulation of proline oxidase activity by lactate.

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We found that proline oxidase, the first enzyme of the proline degradative pathway, is inhibited by lactate. The Km of the enzyme for proline increases with increasing concentrations of lactate. Since proline can be a source for gluconeogenesis, regulation of proline degradation by lactate may serve
A number of animal models have been developed to investigate calcium oxalate (CaOx) nephrolithiasis. Ethylene glycol (EG)-induced hyperoxaluria in rats is most common, but is criticized because EG and some of its metabolites are nephrotoxic and EG causes metabolic acidosis. Both oxalate (Ox) and

Mechanism of Hyperkalemia-Induced Metabolic Acidosis.

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Background Hyperkalemia in association with metabolic acidosis that are out of proportion to changes in glomerular filtration rate defines type 4 renal tubular acidosis (RTA), the most common RTA observed, but the molecular mechanisms underlying the associated metabolic acidosis are incompletely

Interaction of the S6 proline hinge with N-type and C-type inactivation in Kv1.4 channels.

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Several voltage-gated channels share a proline-valine-proline (proline hinge) sequence motif at the intracellular side of S6. We studied the proline hinge in Kv1.4 channels, which inactivate via two mechanisms: N- and C-type. We mutated the second proline to glycine or alanine: P558A, P558G. These

Acidosis inhibits bone formation by osteoblasts in vitro by preventing mineralization.

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The negative effect of acidosis on the skeleton has been known for almost a century. Bone mineral serves an important pathophysiologic role as a reserve of hydroxyl ions to buffer systemic protons if the kidneys and lungs are unable to maintain acid-base balance within narrow physiologic limits.
The mechanism by which chronic metabolic acidosis (CMA) regulates sodium (Na(+))-chloride (Cl(-)) cotransporter (NCC) in the renal distal convoluted tubules remains unexplored. We examined the role of STE20/SPS1-related proline/alanine-rich kinase (SPAK) and with-no-lysine kinase 4 (WNK4) on
Hyperprolinemia type 2 (HPII) is a rare autosomal recessive disorder of the proline metabolism, that affects the ALDH4A1 gene. So far only four different pathogenic mutations are known. The manifestation is mostly in neonatal age, in early infancy or early
Desmosium styracifolium (D. styracifolium), which is considered as a Chinese herbal medicine, has been reported to treat the kidney stone diseases. However, the potential phytochemically active components and the underlying mechanisms associated with its efficacy in targeting urolithiasis remain to

The effect of birth asphyxia on plasma free amino acids in preterm newborn infants.

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The postnatal plasma amino acid pattern was compared in 16 asphyxiated and 13 non-asphyxiated preterm newborn infants. The lactic acidosis induced by asphyxia was associated with a marked rise in the total amino acid content of the plasma. Among the 17 individual amino acids determined the

Succinyl-CoA ligase deficiency: a mitochondrial hepatoencephalomyopathy.

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This patient presented on the first day of life with pronounced lactic acidosis with an elevated lactate/pyruvate ratio. Urine organic acids showed Krebs cycle metabolites and mildly elevated methylmalonate and methylcitrate. The acylcarnitine profile showed elevated propionylcarnitine and
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