1 alpha(OH)D3 (ETALPHA) treatment and receptor studies in 16 patients with chronic and myeloproliferative disorders

10 patients with CLL and 2 with CML were treated with gradually increasing doses of 1 alpha(OH)D3, up to 4 micrograms daily during 6 wk. 3 patients with preleukemia and 1 with myelofibrosis were treated with 2 micrograms daily of 1 alpha(OH)D3 for a prolonged period up to 17 wk. The treatment with 1 alpha (OH)D3 did not result in changes of disease parameters in any of the patients under study. Receptor studies for 1,25(OH)2D3 were performed in 8 CLL patients and revealed only 1 patient with increased specific receptor binding capacity. The maximum tolerable dose of 1 alpha(OH)D3 varied individually, but was in the range of 2-4 micrograms daily.     

Comparison of immunohistochemical staining of a mitochondrial protein, lipoamide dehydrogenase, with Fab'-peroxidase conjugates prepared by maleimide or periodate

IgG-maleimide peroxidase, Fab'-maleimide peroxidase, polymer and monomer types of Fab'-periodate peroxidase were prepared from an antibody against rat lipoamide dehydrogenase, a component of the pyruvate dehydrogenase complex which is located in mitochondria. They were examined for immunohistochemical staining of the rat kidney. Fab'-maleimide peroxidase was the best for staining mitochondrial protein. IgG-maleimide peroxidase and the monomer type of Fab'-periodate peroxidase had the same intensity of staining. The polymer type of Fab'-periodate peroxidase could not stain the lipoamide dehydrogenase.     

Biochemical effects of two promoters of hepatocarcinogenesis in rats

The effects of two promoters of hepatocarcinogenesis--phenobarbital and butylated hydroxytoluene (BHT)--on five hepatic biochemical parameters were examined in adult female rats. Phenobarbital given orally in two doses each of 110 mg/kg 21 and 4 hr before the rats were killed caused large increases in hepatic ornithine decarboxylase (ODC) activity and cytochrome P-450 content. Extending the number of phenobarbital treatments to five increased the hepatic enzyme induction and also caused a minor decrease in hepatic glutathione and a small increase in serum alanine aminotransferase activity. Two oral doses of 700 mg BHT/kg (20% of the LD50) caused hepatic DNA damage and induction of both ODC activity and cytochrome P-450 content. When the dose of BHT was reduced from 700 to 140 mg/kg no significant effects on the biochemical parameters were found. Both promoters of hepatocarcinogenesis were identified by their induction of ODC, a marker for promotional potential, but only BHT showed a potential for carcinogenic initiation. The biochemical parameters examined, particularly the alkaline elution technique for DNA damage, ornithine decarboxylase activity and serum alanine aminotransferase, may constitute a useful assay system for examining a compound's potential for carcinogenic initiation, carcinogenic promotion and cellular toxicity.     

Analysis of the activities of a geriatric assessment and rehabilitation unit

In a four month period 228 patients were admitted to the Wakari assessment and rehabilitation unit in Dunedin, New Zealand. One hundred and seventy subjects came from the community, 35 were transferred from the local public hospital, and 23 were readmitted. Median lengths of stay were 13, 26 and 10 days respectively. Assessment of activities of daily living (ADL) dependency on admission and discharge showed a significant improvement in ability by discharge, which correlated closely with place to which subjects were discharged, and with survival. There was 5% inpatients death rate which cumulated to 18%, 23%, 34%, 39% and 46% by six weeks, three months, six months, nine months and one year respectively. High discharge dependency was closely related to poor survival after discharge. Use of domiciliary services did not change because the savings from those who moved into institutions were cancelled out by those who were discharged back to the community being in need of increased social support.