Potassium dibasic phosphate (PDP) was administered at a concentration of 10% by weight in basal diet to unilaterally nephrectomized Wistar rats previously given 1000 ppm N‐ethyl‐N‐hydroxyethyl‐nitrosamine (EHEN) in the diet for 2 weeks. To study the effect of alkalinization on renal mineralization, some animals concomitantly received 5% potassium citrate (PC). Feeding PDP alone promoted adenomatous hyperplasias, which were regarded as preneoplastic lesions, as well as renal cell tumors in EHEN‐initiated rats, whereas the addition of PC to PDP diets reduced the promoting effect. Histopathology, serum biochemistry and urinalysis indicated retardation of renal calcium crystallization by PC. Two other phosphate salts, sodium phosphate (SP) and calcium phosphate (CP), were also administered. SP showed a slight promoting effect on adenomatous hyperplasias and a 2‐fold increase in the yield of renal cell tumors, while CP induced a clear reduction of both lesions, over EHEN alone. The promoting effects of both PDP and SP and the inhibitory effect of PC were somewhat correlated to 5‐bromo‐2′‐deoxyuridine labeling indices, the degree of nephropathy, and mineralization in the kidney. Immunohistochemically, the nephropathy induced by phosphate salts was not linked to αzu‐globulin. A pathogenesis for renal carcinogenesis is suggested in which nephropathy associated with mineralization enhances the development of renal cell tumors.

The present study was undertaken to explore the cause of postischaemic hypoperfusion through morphological observations of the microstructure of brain cortex capillaries in rats with postischaemic hypoperfusion. Sixteen rats were used. The left middle cerebral artery of each animal was occluded for one hour (n = 8) or 2 hours (n = 8) and was followed by reperfusion for 2 hours. The regional cerebral blood flow (rCBF) of the ischaemia induced brain cortex was monitored continuously during the experiment and the microstructure of the brain cortex capillaries was then observed under electron microscope. Postischaemic hypoperfusion was observed in both ischaemia groups. The rCBF after (1.5 hours of reperfusion was significantly lower in the 2-hour ischaemia group than in the one-hour ischaemia group. The number of endothelial microvilli (MV) per capillary in the one-hour ischaemia group did not differ significantly from the control (the right cortex capillaries), whereas it was significantly higher in the 2-hour ischaemia group (p < 0.05). The ratio of the inner diameter to the outer diameter of capillaries decreased significantly in both ischaemia groups, and the ratio in the 2-hour ischaemia group was significantly lower than that in the one-hour ischaemia group (p < 0.05). Thus the present study statistically revealed that as postischaemic perfusion of the brains decreases, the number of MV increases, and endothelial cells swell more markedly. These microvascular changes seem to represent morphological factors associated with postischaemic hypoperfusion.

To cast light on the mechanisms of drug-resistance, experimental brain tumors were immunohistochemically evaluated for expression of glutathione S-transferase (GST)-alpha, mu, pi, p-glycoprotein and apoptosis-related factors, such as bcl-2 and p53, as well as by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling (TUNEL) method. Rat brain tumors induced by means of prenatal exposure to ethylnitrosourea (ENU) were treated with 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and/or vincristine. Tumors more than 2 mm in size were considered to be drug resistant. The expression of GST-mu was strongly positive in ACNU-treated brain tumors, while p-glycoprotein was overexpressed in vincristine-treated brain tumors. Neither p53 nor bcl-2 expression directly correlated with apoptosis identified by TUNEL method, but tumors lacking apoptotic cells always demonstrated the expression of either GST-mu or p-glycoprotein. These results indicate that tumors resistant to chemotherapy might not be susceptible to induction of apoptosis, and therefore that mechanisms of drug resistance are related to programmed cell death in brain tumors.

A 16-year-old girl presented with a pleomorphic adenoma of the lacrimal gland manifesting as left painless exophthalmos which had persisted for 3 years. Computed tomography revealed a tumor about 15 mm in diameter in the superolateral site of the left orbit. The tumor was removed completely by combined orbitofrontal craniotomy through a transcranial approach. Histological examination demonstrated the growth of tumor cells as glandular cavities or sheets, with myxoid and partly chondroid connective tissue stroma. Pleomorphic adenoma of the lacrimal gland is unusual in adolescents.

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