rickets/hypoxia

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[Disorders of oxygen supply and tissue metabolism and their correction in rats with experimental rickets].

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Indices of oxygen supply are studied in preadolescent rats with experimental rachitis. Disturbances in transport, capillary-tissue diffusion and oxygen utilization by tissues of the brain, liver and skeletal muscles correlating with a degree of the rachitis gravity are revealed. It is proved as

Hemoglobin-oxygen affinity in hypophosphatemic rickets.

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In 14 patients with simple X-linked hypophosphatemic rickets, 5 were below the third percentile in height and 9 were between the third and twenty-fifth percentile. Although the mean serum inorganic phosphorus level was only 2.01 +/- 0.65 (normal range for all age groups is 3.8 to 6.0 mg/100 ml),

Nutritional rickets and vitamin D deficiency--association with the outcomes of childhood very severe pneumonia: a prospective cohort study.

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BACKGROUND The association of rickets and vitamin D deficiency (VDD) with pneumonia is well documented, but not with its outcomes. OBJECTIVE To investigate whether rickets and VDD predict the outcomes in very severe pneumonia (VSP). METHODS A prospective cohort study conducted at Al-Sabeen hospital

The hypoxia-inducible factor-1α activates ectopic production of fibroblast growth factor 23 in tumor-induced osteomalacia.

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Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome in which ectopic production of fibroblast growth factor 23 (FGF23) by non-malignant mesenchymal tumors causes phosphate wasting and bone fractures. Recent studies have implicated the hypoxia-inducible factor-1α (HIF-1α) in other

Right ventricular failure and ascites in broiler chickens caused by phosphorus-deficient diets.

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Phosphorus-deficient diets fed to broiler chicks from day 1 to day 21 induced rickets. Some chicks were stunted, but most grew well, though they had increased respiratory rates, high arterial carbon dioxide partial pressure, and low oxygen partial pressure and were polycythemic. Most of the broilers

Reminiscences and reflections.

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Some of Dr. Goldblatt's important contributions during a notable research career of more than 50 years are reviewed. The research on rickets (1922-1932), culminating in the discovery of the antirachitic effect of sterol irradiated with ultraviolet light. The research on cancer (1930-1974),

Redox studies of the epiphyseal growth cartilage: pyridine nucleotide metabolism and the development of mineralization.

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The objective of this investigation was to examine the redox status of chondrocytes in normal and rachitic growth cartilages and to relate energy metabolism to cell maturation and the initiation of mineralization. The redox status was evaluated by chemical analysis and by microfluorimetric scanning

Hsp90 and angiogenesis in bone disorders--lessons from the avian growth plate.

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Thiram-induced tibial dyschondroplasia (TD) and vitamin-D deficiency rickets are avian bone disorders of different etiologies characterized by abnormal chondrocyte differentiation, enlarged and unvascularized growth plates, and lameness. Heat-shock protein 90 (Hsp90) is a proangiogenic factor in

Neonatal iron deficiency causes abnormal phosphate metabolism by elevating FGF23 in normal and ADHR mice.

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Fibroblast growth factor 23 (FGF23) gain of function mutations can lead to autosomal dominant hypophosphatemic rickets (ADHR) disease onset at birth, or delayed onset following puberty or pregnancy. We previously demonstrated that the combination of iron deficiency and a knock-in R176Q FGF23

Regulation of Fibroblast Growth Factor 23 by Iron, EPO, and HIF.

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Fibroblast growth factor-23 (FGF23) is the key hormone produced in bone critical for phosphate homeostasis. Elevated serum phosphorus and 1,25dihydroxyvitaminD stimulates FGF23 production to promote renal phosphate excretion and decrease 1,25dihydroxyvitaminD synthesis. Thus completing

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