Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The latent form of transforming growth factor-beta (TGF-beta) is a component of the extracellular matrix of bone. The active form, when locally injected in vivo, stimulates both inflammation and ectopic bone formation. The present study was undertaken to determine if TGF-beta also stimulated mineralization by isolated rat calvarial osteoblasts cultured in collagen gels. Gels were used because they should mimic in vivo conditions better than classical monolayer culture. Compared to cells in monolayers, osteoblasts cultured in collagen gels exhibited slower growth, but higher alkaline phosphatase activity and mineral deposition. Cultured cells also synthesized the osteoblast-specific marker, osteocalcin. The increase in osteocalcin in cell layers was parallel to the increase in mineral deposition. In the presence of TGF-beta, neither cell growth nor alkaline phosphatase activity increased. Instead, a small decrease occurred in both parameters when compared to untreated cultures. Accumulation of collagen, the major component of the extracellular matrix where mineralization occurs, was similar in untreated and TGF-beta 1-treated cultures. However, 8 pM TGF-beta 1 dramatically suppressed mineral deposition in both types of cultures. Despite TGF-beta 1 stimulating a fourfold increase in lactic acid, the consequent increase in culture medium acidity did not account for the inhibitory effects of TGF-beta 1 on mineralization. These results demonstrate that collagen gel culture is an improved technique over conventional monolayer culture for demonstrating differentiated osteoblast function and sensitivity to TGF-beta 1. TGF-beta 1, at a concentration that has little effect on cell growth, alkaline phosphatase activity, or collagen accumulation, is a potent inhibitor of mineralization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transforming growth factor-beta inhibition of mineralization by neonatal rat osteoblasts in monolayer and collagen gel culture. 779 46

Many systems have been proposed for the encapsulation of bone marrow stromal cells (BMSCs) within degradable hydrogels. Here, we use a novel cyclic acetal-based biomaterial formed from 5-ethyl-5-(hydroxymethyl)-beta,beta-dimethyl-1,3-dioxane-2-ethanol diacrylate (EHD) and poly(ethylene glycol) diacrylate (PEGDA). A cyclic acetal-based hydrogel may be preferred as cyclic acetals hydrolytically degraded into diols and carbonyls as primary degradation products, which may not affect local acidity, unlike other widely investigated polymers. The EHD monomer and PEGDA polymer may be fabricated into a EH-PEG hydrogel by radical polymerization initiated by the ammonium persulfate (APS) and N,N,N',N'-tetramethylethylenediamine (TEMED) system. The objective of this work is to determine whether the components utilized in the fabrication of EH-PEG hydrogels as well as the EH-PEG hydrogels permit BMSC viability, metabolic activity, and osteodifferentiation. Cell viability and metabolic activity were assessed after 30 min, 1 h, and 3 h of exposure to pertinent concentrations of the initiator system (10-20 mM). Osteodifferentiation was assessed by alkaline phosphatase and osteocalcin expression after a short exposure to the initiator system to simulate the encapsulation process. Lastly, cell viability was assessed immediately after encapsulation and after 7 days of culture within the EH-PEG hydrogels. Results indicate that the metabolic activity and viability of BMSCs are minimally affected, and that osteodifferentiation is not significantly affected by the APS-TEMED initiator system. Also, encapsulated BMSCs maintained viability within EH-PEG hydrogels for 7 days. This work demonstrates that the EH-PEG hydrogel is a viable option for the encapsulation and osteodifferentiation of BMSCs.
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PMID:Cyclic acetal hydrogel system for bone marrow stromal cell encapsulation and osteodifferentiation. 1802 39

Renal stone disease may ensue from either derangements of urine biochemistries or anatomic abnormalities of kidneys and urinary tract. Genetic, environmental and dietary factors may also cooperate in the pathophysiology of nephrolithiasis. An adequate metabolic evaluation should focus on the urinary excretion of promoters and inhibitors of stone formation as well as on the occurrence of systemic diseases potentially related to secondary nephrolithiasis (i.e., endocrine disturbances, malabsorption, bone diseases). Moreover, metabolic investigations should provide reliable information on patient's dietary habits, guide towards the best therapeutic approach and enable the physician to verify patient's compliance to prescribed therapies.AN EXTENSIVE METABOLIC EVALUATION IS RECOMMENDED IN PATIENTS WITH ACTIVE STONE DISEASE (NAMELY, AT LEAST ONE NEW STONE WITHIN THE LAST TWO YEARS), OR IN THOSE HAVING HAD A SINGLE STONE EPISODE OCCURRED IN PECULIAR CONDITIONS: familial history of disease, childhood, menopause, pregnancy, systemic diseases. Simplified protocols may be adequate in non-active nephrolithiasis or in patients with single stone and no relevant risk factors.In our Stone Centre, a so-called "first level screening" is performed by routine, in order to assess urinary supersaturation with stone forming salts and evaluate the excretion of dietary-related metabolites in urine. Relative blood and urine determinations are reported below.IN VENOUS BLOOD: urea, creatinine, uric acid, Na, K, total and ionised Ca, Mg, P, Cl, alkaline phosphatase, gas analysis. In 24-hr urine samples: urea, creatinine, uric acid, Na, K, Ca, Mg, P, Cl, oxalate, inorganic sulphate, citrate, pH, ammonia and titratable acidity. IN FASTING URINE SAMPLES: Ca, citrate, creatinine, hydroxyproline, Brand's test for cistinuria, urine sediment, urine culture. If the first-level evaluation suggested an abnormal bone turnover, then further determinations are warranted, namely, calciotropic hormones (blood Vitamin D and PTH), markers of bone resorption (urine pyridinium crosslinks, serum crosslaps) and formation (serum osteocalcin) bone mineral density.EVENTUALLY, MORE SOPHISTICATED INVESTIGATIONS ARE REQUIRED TO IMPROVE THE DIAGNOSIS OF PECULIAR DISEASES: serum oxalate and glycolate, urine glycolate and L-glycerate, hepatic AGT activity (primary hyperoxalurias); genetic tests (hereditary nephrolithiasis); acidification tests (renal tubular acidosis).
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PMID:Biochemical evaluation in renal stone disease. 2246 Sep 94

This study examined the effects of the dietary amount and source of protein on bone status in rats. 140 male Wistar rats aged 8 weeks were randomly allocated to 4 groups (n = 35) fed normal-protein (NP, 10% richness) or high-protein (HP, 45% richness) diets based on whey protein (WP) or soy protein (SP) sources for 12 weeks. Plasma urea was 46% higher for the HP compared to the NP diet (p < 0.001). Urinary calcium was 65% higher for the HP compared to the NP and 60% higher for the WP compared to the SP diets (all, p < 0.001). Urinary pH was 8% more acidic in the HP compared to the NP diet (p < 0.001) and 4% in the WP compared to the SP diet (p < 0.01). The plasma osteocalcin concentration was 19% higher for the NP compared to the HP (p < 0.05) and 25% for the SP compared to the WP diets (p < 0.01). Femur ash, metaphyseal and diaphyseal cross-sectional, trabecular and cortical areas were 3% higher in the HP compared to the NP diet (all, p < 0.05). Femur diaphyseal periosteal and endocortical perimeters were also 3% higher in the HP compared to the NP diet (both, p < 0.01). Groups fed the SP diet showed 2% higher femur ash percentage, 7% higher calcium content (both, p < 0.001), and 3% higher diaphyseal cortical area and thickness (both, p < 0.05) than those fed the WP diet. Some interactions were found, such as the greater effects of the SP diet on decreasing the higher plasma urea concentration promoted by the intake of the HP diet (p < 0.001). Under adequate Ca intake, HP diets could better maintain bone properties than NP diets, even with increasing some acidity markers, which could be reduced by the intake of SP sources.
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PMID:Effects of the amount and source of dietary protein on bone status in rats. 2453 97