Two hundred twenty-six specific pathogenfree male and female F344 rats were exposed to nickel sulfide inhalations for 78 weeks (5 days/wk, 6 hr/day) and observed for an adiditional 30-week period. For the same amount of time, 214 rats were exposed to filtered room air and served as controls. Rats exposed to nickel sulfide showed a significantly higher incidence of pulmonary hyperplastic and neoplastic lesions originating from the bronchial and bronchiloo-alveloar segments. The overall incidence of lung tumors in the animals treated with nickel sulfide was 14 percent compared with 1 percent in the controls. Pulmonary inflammatory reactions were also greatly increased. Injection of an agent (hexachlorotetra-fluorobutane) that induced lung infarction did not increase the proportion of animals having lesions, nor did it alter the type of lesions found in animals exposed to nickel sulfide.

The herbicide 2,4,5-trichlorophenoxyacetic acid is teratogenic and fetocidal in two strains of mice when administered either subcutaneously or orally and in one strain of rats when administered orally. The incidences of both cystic kidney and cleft palate were increased in the C57BL/6 mice as well as the incidence of cleft palate in the AKR mice. The incidence of cystic kidney was also increased in the rats. In addition, an increase in the ratio of liver weight to body weight in the mouse fetus and the occurrence of hemorrhagic gastrointestinal tract in the rat fetus suggest that this compound also has fetotoxic properties.

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T h e serum concentrations o f calcium, albumin a n d p a r a t h y r o i d hormone ( P T H ) a n d t h e plasma levels of ionized calcium were determined in 1 2 4 healthy subjects, 89 patients w i t h p r i m a r y h y p e r p a r a t h y r o i d i s m ( H P T ) , 23 o f whom had t h e syndrome o f multiple endocrine neoplasia t y p e 1 (MEN-1) a n d 43 patients who h a d hypercalcaemia o f other causes t h a n HPT (non-H P T ) , in most cases d u e t o widespread malignancies. T h e total serum calcium was c o r r e c t e d f o r t h e serum albumin concentration (CaM). Healthy females over t h e age o f 50 h a d h i g h e r CaM, t h a n y o u n g e r females a n d t h e women o f all ages also had, h i g h e r serum PTH levels t h a n males. For all s t u d y g r o u p s b o t h t h e i n t r a -a n d i n t e r -d i u r n a l variations were small f o r all t h e studied variables. Discriminant f u n c t i o n a n d optimal discriminatory limits were calculated w i t h the help o f computer programs. A consideration o f all t h e i n d i v i d u a l s in t h e discriminant analysis, revealed t h a t measurements o f CaM alone separated most HPT patients b o t h from t h e healthy subjects a n d from t h e non-HPT patients. However, when o n l y those who had b o r d e r l i n e values ( d e f i n e d as CaM between 2 . 4 5 a n d 2 . 7 5 mmol/l) were included it t u r n e d o u t t h a t measurements o f ionized calcium m a r k e d l y improved t h e delineation o f mild HPT from t h e healthy subjects a n d that, in addition, PTH measurements helped t o exclude those w i t h non-HPT hypercalcaemia.T h e optimal discriminatory levels o f serum calcium were calculated as t h e levels w h i c h caused t h e minimum loss in terms o f misclassification when attention was paid t o the r e l a t i v e importance o f false positive t o false negative classifications and t o t h e prevalence o f HPT. T h e optimal d i s c r iminatory level f o r serum calcium f o r a weighting r a t i o between false positive t o false negative of 1:1, a n d a prevalence of HPT o f 1 &, was calculated t o be 2 . 6 8 mmol/I a n d f o r a prevalence o f 50 % 2 . 5 6 mmol/I. In t h e l a t t e r situation a w e i g h t i n g r a t i o o f 1O:l f o r false positive t o false negative gave a level o f 2 . 6 3 mmolll while a w e i g h t i n g r a t i o o f 1 : 1 0 corresponded t o a n optimal d i s c r i m i n a t o r y level o f 2 . 4 7 mmol/I.

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The induction of lymphomas in C57BL mice by methylcholanthrene, urethan, or diethylnitrosamine was accompanied by the development of murine leukemia viral antigen in most of the lymphoid tumors. The cell-free transmission of lymphomas induced by methylcholanthrene and the development of antibody to murine leukemia virus prior to the detection of overt lymphoma in these mice suggest that unmasking of a latent leukemia virus is an indigenous actuating cause of the lymphomas.

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