Bone malformations

Essential to all organisms ac-, tivates numerous enzymes deficiencies in soils lead to infertility in mammals, bone. malformation in growing, I chicks. - v. v.. ) ... 

Early symptoms would be loss of appetite, weakness, weight loss, and bone pains. Later, bone softening and weakening, bone malformation, and poor development of teeth would mean rickets was setting in. 

Cooley s Anemia is a genetic disorder relatively rare in the United States, but found more often among peoples of the Mediterranean area and within a band extending through India and southeast Asia ( 1 ). In addition to severe anemia, the disease causes bone malformation and general deterioration and distruction of the vital organs leading eventually to death. 

The answer is d. (Murray, pp 627-661. Scriver, pp 3897-3964. Sack, pp 121-138. Wilson, pp 287—320.) People with bowed legs and other bone malformations were quite common in the northeastern United States folio-wing the industrial revolution. This was caused by childhood diets lacking foods "with vitamin D and by minimal exposure to sunlight due to the da-wn-to-dusk working conditions of the textile mills. Vitamin D is essential for the metabolism of calcium and phosphorus. Soft and malformed bones result from its absence. Liver, fish oil, and egg yolks contain vitamin D, and milk is supplemented "with "vitamin D by law. In adults, lack of sunlight and a diet poor in "vitamin D lead to osteomalacia (soft bones). Dark-skinned peoples are more susceptible to "vitamin D deficiency. 

Before the introduction of vitamin D-fortified milk, children who spent most of their time indoors often developed rickets. In these vitamin D-deficient children, the most likely explanation for their bone malformations is which of the following ... 

Fetal toxicity has been identified as a sensitive toxic endpoint in rat and rabbit studies involving Octa-BDE. Exposure in the womb resulted in bone malformations and decreased fetal weight in rat and rabbit offspring beginning at doses of 2 mg/kg with fetal death occurring at higher doses" (p.22)... 

Air concentrations of 28.5 mg/m3 for 4 h daily on days 9-12 of gestation caused fetotoxic effects and chromosomal damage to liver cells by day 18 effects included reduced survival, impaired growth, retarded limb ossification, and bone abnormalities. At 2.9 mg/m3, a 9.9% decrease in fetal weight was recorded at 0.26 mg/m3, a 3.1% decrease was measured Oral dosages of 400-600 mg/kg BW on days 7-16 of gestation produces fetal malformations (cleft palate), delayed skeletal ossification, and fetal weight reduction 200-600 mg/kg BW daily for 10 days (DMA) produced fetal and maternal toxicity... 

LD50 of 9.6 mg/kg BW, sc route LD90 (7 days postadministration) of 11.3 mg/kg BW, sc route LD50 of 12 mg/kg BW intraperitoneal route. At 10 mg/kg BW, damage to bone marrow and sperm Single intraperitoneal injection of 1200 mg/kg BW during midgestation results in increased rates of fetal skeletal malformations... 

Azathioprine can be administered both orally and intravenously. It is well absorbed orally and after its rapid conversion to 6-mercaptopurine it is inactivated by xanthine oxidase which converts 6-mercaptopurine to 6-thiouric acid. This final metabolite is then excreted in the urine. In combination with the xanthine oxidase inhibitor allopurinol dose adjustments of azathioprine are needed. Renal disease also raises 6-mercaptopurine concentrations and can make dose adjustments necessary. Azathioprine is still used in organ transplantation programs and for the management of several autoimmune diseases. Its adverse effects include nausea, vomiting, diarrhea and, more seriously, bone marrow suppression and hepatotoxicity. Azathioprine is not thought to cause fetal malformation. 

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