Tumors causing humoral hypercalcemia of malignancy (HHM) were implanted to athymic nude rats. In one of these rat models transplanted with uterine cancer (UCC), a complete reproduction of human HHM syndrome was achieved: hypercalcemia, hypophosphatemia with increased urinary phosphate and cyclic AMP excretion, and suppressed serum 1,25-dihydroxy-vitamin D (1,25(OH)2D) level. In another hypercalcemic nude rat model implanted with oral cavity cancer (OCC), all the features were similar except for markedly elevated serum 1,25(OH)2D. Hypercalcemia disappeared by surgical removal of the tumors in both models, confirming the humoral mechanisms for causing these features. Furthermore, in UCC tumor-bearing rats, hypophosphatemia, increased renal phosphate excretion, and reduced serum 1,25(OH)2D concentration were already present when these rats were only marginally hypercalcemic. These results raise the possibility that the changes in renal tubular phosphate handling and vitamin D metabolism in HHM are not secondary to hypercalcemia but are due to direct effects of the humoral factor(s) that cause this syndrome. Extracts of both tumors exhibited stimulation of cyclic AMP production in osteoblastlike cells, UMR 106, which could be almost completely inhibited by parathyroid hormone (PTH) antagonist, human PTH(3-34). By comparing the nature and characteristics of humoral factor(s) from UCC and OCC models, mechanisms responsible for causing these abnormalities can be explored. Thus, these nude rat models can be useful for elucidating the underlying mechanism of the development of HHM.

Wedescribe here a case of a manwith Kartagener's syndrome, whose parents were cousins each other, associated with infundibular pulmonic stenosis, chronic renal failure and azoospermia. These combined abnormalities have not been previously reported in one patient with Kartagener's syndrome, as far as English literatures are concerned.

Wepresent a case of primary plasma cell leukemia with Bence Jones proteinuria. After combination chemotherapy, leukemic cells and the urinary levels Bence Jones protein were decreased. Small lytic bone lesions were detected only in the skull. Typical plasma cells were rarely seen in peripheral blood on the hyperleukocytic phase, however they were increased in the advanced stages. The most important diagnostic sign was persistent expression of CD38antigen on leukemic cells throughout the entire course of the illness and these leukemic cells expressed very late antigen-4 (VLA-4) but not VLA-5. (Internal Medicine 32: 565-568, 1993)

We used an Avidin-Biotin peroxidase complex (ABC) immunoperoxidase technique to evaluate the localization of IL-6 of human bone marrow cells in multiple myeloma (MM). The cellular distribution of IL-6 was determined at light and electron microscopic levels. The author's study indicated that cytoplasmic IL-6 was detected only in the myeloma cells of bone marrow cells. Immunoelectron microscopic (immuno-EM) study showed positive reactivity mainly in the perinuclear space (PNS), well-developed rough endoplasmic reticulum (RER), and Golgi area.