Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood vitamin (thiamin, riboflavin, vitamins B6, B12, C, A, and E, folate and beta-carotene), mineral (iron and zinc), alkaline phosphatase and cholesterol levels and hematocrit were assessed in 960 school-age children selected by random sampling from urban and rural regions of Turkey. Nutritional statuses of the children according to each index were compared with respect to age, sex, area and type of settlement. A biochemical deficiency was observed in 20.1% of the children for thiamin, in 89.9% for riboflavin, in 83.4% for vitamin B6, in 23.3% for folate, in 5.9% for vitamin B12, in 43.0% for vitamin C, in 11.6% for vitamin A, in 3.5% for beta-carotene, in 21.8% for vitamin E, in 6.1% for iron, and in 15.7% for zinc. Hematocrit was low in 54.3%. Alkaline phosphatase and cholesterol levels were found to be above normal in 54.6% and 4.9% of the children respectively. It is surmised that a major cause of the deficiencies was an ignorance of good dietary practice. Although the children were found to be relatively short according to the National Center for Health Statistics standards, their normalised weights were within acceptable limits, which suggested a prevalence of stunting but not wasting in this population.
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PMID:Blood vitamin and mineral levels in 7-17 years old Turkish children. 158 3

The plasma concentrations of cortisol and corticosteroid-binding globulin and the adrenal synthesis capacity of cortisol were analysed in 10-week-old healthy and age-matched wasting or unthrifty pigs. Crypt cell multiplication, villus height and intestinal mucosal alkaline phosphatase (ALP) activity were also investigated. Furthermore, the effect of amperozide, a psychotropic drug with specific effects on emotional behaviour, was analysed for its effect on plasma ALP activity and villus height. Although the wasting pigs exhibited an increased cortisol synthesis capacity, there was a decreased plasma concentration of cortisol in these pigs. Furthermore, the plasma cortisol binding capacity was found to be significantly lowered in wasting pigs. There was also a reduced crypt cell proliferation, a reduced villus height and a decreased ALP activity in the ileal mucosa. Treatment with amperozide resulted in a normalisation of plasma ALP activity in unthrifty pigs, indicating a stimulation of body growth. The results indicate that the growth depression of wasting pigs is most probably a chronic stress syndrome caused by the inability of these animals to cope with the events following weaning and mixing.
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PMID:Subclinical characteristics of the wasting pig syndrome. 238 58

The concentrations of calcium and phosphorus and the activity of alkaline phosphatase in serum were evaluated in 42 very-low-birth-weight (VLBW) and 83 low-birth-weight (LBW) infants on the 7th, 21st, and 42nd day of life. 9 VLBW and 16 LBW infants were randomized for measurement of the renal excretion of calcium and phosphorus on the 3rd, 5th, 7th, 21st, and 42nd day of life during human milk feeding and 14 VLBW-infants fed human milk supplemented with 1 mmol NaH2PO4 per 100 ml. All serum parameters were found to be normal. Supplementation of human milk with NaH2PO4 leads to a tendency of higher concentrations of phosphorus than found in VLBW-infants exclusively fed with native human milk, but all differences between the two groups were not significant. VLBW-infants appeared more than LBW-infants to be conserving phosphorus and wasting calcium during human milk feeding. Supplementation of human milk with NaH2PO4 results in higher phosphorus lower calcium excretion in urine of VLBW-infants, but they do not reach the values of LBW-infants. Because the activity of alkaline phosphatase was not different between the feeding groups and in all cases within the normal range a delayed bone mineralisation cannot be assumed in the infants studied. Thus, the phosphorus deficiency which is shown by the renal excretion of calcium and phosphorus in the VLBW-infants can be considered to be latent. In the light of our data the concentration of phosphorus in human milk seems to be too low and the calcium/phosphorus ratio too high for the optimal mineral metabolism in VLBW-infants. The supplementation used improves the situation, but the phosphorus intake seems still too low. Further investigations are needed to detect the optimal phosphorus intake for these infants. The calcium/phosphorus ratio in the urine is a good marker to estimate a latent phosphorus deficiency in VLBW-infants.
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PMID:Calcium and phosphorus homeostasis in very-low-birth-weight infants appropriate for gestational age fed human milk. 324 Mar 2

Tumor necrosis factor-alpha (TNF alpha), a product of activated monocytes, induces tissue wasting in certain solid tumors in vivo and in in vitro model systems. Recent studies indicate that TNF alpha also regulates cell replication and expression of differentiated function in a variety of nonneoplastic cell systems. Since monocyte products could accumulate in bone with trauma, inflammation, or other disease states, bone cell activity might be altered by the presence of these pathophysiological molecules. Using cells obtained by sequential enzyme release from fetal rat parietal bone, we find that TNF alpha has acute stimulatory and inhibitory effects on bone cell macromolecular synthesis. Within 24 h of exposure, recombinant human TNF alpha at 0.3-100 nM progressively increases the rate of DNA synthesis in osteoblast-enriched cell cultures up to 3- to 4-fold, and 3-100 nM TNF alpha reduces collagen production and alkaline phosphatase activity by 20-30%. These decreases are not altered by 1 mM hydroxyurea, which blocks the mitogenic effect of TNF alpha by 85-90%. In addition, hydroxyproline levels in the culture medium do not increase relative to the control value after TNF alpha treatment, suggesting that decreased collagen production results from less synthesis rather than increased collagen degradation. Hybridization studies with cDNA encoding the alpha 1-chain of rat type I collagen show that TNF alpha increases type I collagen mRNA to an extent similar to its effect on cell replication. Therefore, TNF alpha appears to inhibit collagen synthesis and alkaline phosphatase activity in osteoblast-enriched cell cultures by mechanisms that are not related to its effects on cell replication.
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PMID:Tumor necrosis factor-alpha inhibits collagen synthesis and alkaline phosphatase activity independently of its effect on deoxyribonucleic acid synthesis in osteoblast-enriched bone cell cultures. 340 90

Whether renal phosphate wasting in X-linked hypophosphatemia (XLH) results from an intrinsic renal or humoral defect remains controversial. In studies of the murine homolog of XLH, harboring the Simian Virus 40 (SV40) large T antigen, we obviated the influence of renal cell heterogeneity and impressed memory by comparing Na(+)-phosphate cotransport in immortalized cells from the S1 segment of the proximal tubule. Cells from SV40 transgenic normal and Hyp mice exhibit characteristics of differentiated proximal tubule cells including gluconeogenesis and alkaline phosphatase activity. Surprisingly, however, we found two distinct populations of cells from the S1 proximal tubule of both normal and Hyp mice. In one, PTH treatment increases cAMP accumulation, while in the other both PTH and thyrocalcitonin enhance cAMP production. Kinetic parameters for Na(+)-phosphate cotransport were similar in both subpopulations of cells from normal (Km, 0.29 +/- 0.03 vs. 0.39 +/- 0.04 mM; Vmax, 4.6 +/- 0.6 vs. 5.2 +/- 0.4 nmol/mg/5 minutes) and Hyp mice (0.33 +/- 0.02 vs. 0.26 +/- 0.04; 6.0 +/- 0.7, 4.8 +/- 0.6). More importantly, phosphate transport in S1 cells of either subpopulation from Hyp mice is no different than that of normals. These data indicate that renal proximal tubule cells from Hyp mice have intrinsically normal phosphate transport and support the hypothesis that a humoral abnormality underlies renal phosphate wasting in XLH.
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PMID:Phosphate transport in immortalized cell cultures from the renal proximal tubule of normal and Hyp mice: evidence that the HYP gene locus product is an extrarenal factor. 750 4

The clinical and pathological features of 22 patients, 11 males and 11 females 17-70 years of age (48.0 +/- 16.0 years), with hepatic tuberculosis were reviewed. Five patients had no evidence of extrahepatic tuberculosis (local form), and 17 had the miliary form. The clinical features of the miliary and local forms were similar with pyrexia, abdominal pain, hepatomegaly and body weight loss as the main manifestations. The biochemical findings were also quite similar in reversed albumin and globulin (A/G) ratio (2.9/3.5 vs. 3.2/3.4 g/dl) and disproportionate elevation of alkaline phosphatase (ALP) in comparison with bilirubin values but lower levels of alanine aminotransferase (ALT) (40.4 +/- 51.0 vs. 170.8 +/- 209.4 U/l; p < 0.05) and ALP (208.5 +/- 138.9 vs. 389.5 +/- 271.1 U/l; p < 0.05) in the miliary form. Patients with the local form had higher albumin (3.2 +/- 0.8 vs. 2.9 +/- 0.7 g/dl), aspartate aminotransferase (AST) (160.4 +/- 221.7 vs. 65.9 +/- 69.7 U/l), and gamma glutamyl-transpeptidase (gamma GT) (217.0 +/- 144.0 vs. 136.0 +/- 92.1 U/l), although the differences were not significant. The histopathological features of the miliary form were also similar to the local form with granuloma, caseation, acid-fast bacilli, fatty change and portal fibrosis as the main findings. The local form revealed more severe signs of hepatocytic damage while the miliary form was more wasting. The results suggest that the miliary and local forms of hepatic tuberculosis had quite similar clinical presentations and pathological features. The biochemical tests suggesting hepatic tuberculosis were reversed A/G ratio and disproportionate elevation of ALP.
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PMID:Hepatic tuberculosis: comparison of miliary and local form. 774 92

Infection due to the Mycobacterium avium complex (MAC) is the most common opportunistic disease of bacterial origin among patients with AIDS in the United States. The incidence of disseminated disease due to MAC (DMAC) has risen dramatically in recent years. The risk of developing DMAC increases as the CD4+ lymphocyte count declines to < 100/mm3. Preliminary analyses of several studies suggest that gender, racial or ethnic group, and individual risk factors for human immunodeficiency virus infection do not influence the incidence of DMAC but that prior Pneumocystis carinii pneumonia, the development of severe anemia, or the interruption of antiretroviral therapy may increase risk. Both the respiratory and the gastrointestinal tracts probably serve as portals of entry for MAC. Colonization may potentiate the risk of DMAC but does not always precede dissemination. Patients with AIDS and DMAC have a shorter duration of survival than do those with AIDS but without DMAC. While treatment for DMAC may extend survival, no well-controlled, prospective, randomized clinical trial has documented this point. Most patients with AIDS and DMAC have disseminated multiorgan disease; the most frequently described symptoms include fever, night sweats, weight loss or wasting, diarrhea, and abdominal pain. The most commonly identified laboratory abnormalities are anemia and elevated serum levels of alkaline phosphatase. Localized disease syndromes related to MAC infection occur less often.
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PMID:Disease due to the Mycobacterium avium complex in patients with AIDS: epidemiology and clinical syndrome. 820 73

An intrinsic phosphate (Pi) transport defect in the proximal tubule (PT) presumably underlies X-linked hypophosphatemic rickets. We recently reported normal Pi transport in the S1 segment of the Hyp mouse PT. Whether Pi wasting results from an abnormality in the S2 or S3 segment remains unknown. Thus, we compared Pi transport in S2 and S3 immortalized cells from transgenic (simian virus 40) normal and Hyp mice. These cells display biochemical features of PT cells, including alkaline phosphatase- and hormone- stimulated cAMP activity as well as gluconeogenesis. Moreover, kinetic studies in S2 cells reveal a similar Km[0.26 +/- 0.03 (+/-SEM) vs. 0.22 +/- 0.03 mM] and maximum velocity (Vmax; 5.5 +/- 0.66 vs. 5.9 +/- 0.72 nmol/mg x 5 min) in normal and Hyp mice, respectively. Km and Vmax were also similar in cells from the S3 segment; however, the Vmax values in S3 cells in normal and Hyp mice (2.8 +/- 0.45 and 3.0 +/- 0.56 nmol/mg x 5 min) were reduced in both animal models compared to those in S2 cells (P < 0.001), whereas the Km values in S3 cells from normal and Hyp mice (0.10 +/- 0.02 and 0.11 +/- 0.04 mM) were increased relative to those in S2 cells (P < 0.001). These data indicate that Pi transport throughout the PT of Hyp mice is intrinsically normal. Such observations exclude the presence of a nascent defect in renal Pi transport in the kidneys of Hyp mice and support the hypothesis that a humoral abnormality underlies X-linked hypophosphatemic rickets.
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PMID:Normal phosphate transport in cells from the S2 and S3 segments of Hyp-mouse proximal renal tubules. 860 7

Two sexually mature marmosets (Callithrix jacchus) showing clinical signs similar to those seen in wasting marmoset syndrome (weight loss, decreased muscle mass, and alopecia) were evaluated for clinical and anatomic pathologic changes. The most prominent clinical pathologic alterations included macrocytic normochromic anemia, hypoproteinemia, hypoalbuminemia, elevated serum aspartate aminotransferase and alkaline phosphatase levels, and previously unreported changes of thrombocytosis. The principal gross and histopathologic finding was chronic colitis, which appeared to be the most important contributing factor to the development of wasting syndrome in these marmosets.
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PMID:Clinical pathologic changes in two marmosets with wasting syndrome. 899 97

Although current theory holds that the murine homologs of X-linked hypophosphatemia represent mutations of two closely linked genes with distinct pathophysiological consequences, insufficient data are available to support this hypothesis. We investigated whether an intrinsic defect in renal sodium (Na+)-dependent Pi cotransport truly distinguishes gy from hyp mice. We compared Pi transport in immortalized cells from S1 and S2 segments of the renal proximal convoluted tubule (PCT) of normal and gy mice. Cells from both murine models exhibit characteristics of differentiated PCT cells including gluconeogenesis, alkaline phosphatase activity, and parathyroid hormone (PTH)- and thyrocalcitonin (TCT)-dependent adenosine 3',5'-cyclic monophosphate production. More importantly, kinetic studies reveal that cells from the PCT of gy mice have intrinsically normal Pi transport and support the hypothesis that, as in hyp mice, a humoral abnormality is likely responsible for the renal Pi wasting in this mouse model. These observations are consistent with the conclusion that gy and hyp mice do not represent mutations of two closely linked genes but rather two separate mutations of the same gene.
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PMID:Phosphate transport in renal cell cultures of gy mice: evidence of a single defect in X-linked hypophosphatemia. 924 98


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