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Watanabe Heritable Hyperlipidemic (WHHL) and cholesterol-fed New Zealand White (CH-FED NZW) rabbits were sacrificed at 15 months of age or after 16 weeks of cholesterol feeding, respectively. During the experimental period, the arterial walls of both the CH-FED NZW and WHHL rabbits were exposed to similar amounts of cholesterol and the lesions which developed at the aortic arch had similar intimal thicknesses, total lipid and cholesterol content. However, the lesions of the WHHL rabbits morphologically resembled human plaques, and contained lipid in the form of smectic liquid crystalline droplets and cholesterol monohydrate crystals. The CH-FED NZW rabbits had lesions which were fatty streak-like, containing liquid crystalline cholesteryl ester droplets but few crystals. The aortic arch intimas of the CH-FED NZW rabbits contained significantly more cholesteryl ester, and less unesterified cholesterol and triglyceride, than those of the WHHL rabbits. The intimal compositions of the two rabbit models did not overlap. Analysis of the compositions predicted precipitation of cholesterol monohydrate crystals in the WHHL but not the CH-FED NZW. The physical state of the deposited cholesterol esters was similar in both with about half being in smectic liquid crystalline form at body temperature. Since the size and total lipid content of the lesions of the CH-FED NZW and WHHL rabbits were similar, we suggest that the greater time of exposure to hypercholesterolemia was important in the formation of cholesterol monohydrate crystal-containing plaques in the aortic arch of the WHHL rabbits.

Neuronal cells expressing neural cell adhesion molecule (N-CAM) accumulate the largest N-CAM component (N-CAM 180) at cell - cell contact sites. To test whether this accumulation is induced by interactions at the surface membrane, latex beads coated with several purified adhesion molecules or extracellular matrix (ECM) components were co-cultured with neuroblastoma cells. Beads coated with L1, N-CAM, the L2/HNK-1 carbohydrate epitope-carrying molecules from adult mouse brain or laminin from Engelbreth-Holm-Swarm (EHS) sarcoma did not induce an accumulation of N-CAM 180 or L1 at sites of contact suggesting that these molecules are not directly involved in N-CAM 180 accumulation or that their mobility is required for this process. Beads coated with ECM components of the PF-HR9 cell line induced accumulation of N-CAM 180 at sites of contact with neuroblastoma cells. Accumulation was seen at cell bodies of undifferentiated and differentiated neuroblastoma cells, as well as on neurites and growth cones of differentiated neuroblastoma cells. Accumulation of the neural adhesion molecule L1 was also seen, but less prominently and reproducibly. These observations suggest that molecules of the ECM can directly or indirectly, e.g. via molecules linked to N-CAM 180 on the cell surface, induce accumulation of N-CAM 180.

In 652 patients with ureteral stenoses treated in the last 23 years we found 12 (1.8%) patients with rare benign and 5 (0.7%) patients with rare malignant diseases resulting in ureteral stenoses. Causes, clinical symptoms, diagnostic procedures and pathohistological findings are analysed and discussed with emphasis on the pathohistological diagnosis. Operative procedures are demonstrated and long term follow-up studies presented.

Administration of 3 microg dexamethasone at day 8 of incubation into the allantoic cavity resulted in various embryopathies in embryos by the 15th day of incubation. Chicken alpha-foetoprotein (chAFP) and serum albumin concentrations, when examined at the 12th day of incubation, were below the corresponding controls (P<0.01), whereas total serum protein was only slightly lower, On day 15 chAFP concentrations were similar to those of the controls, serum albumin values were markedly reduced and total serum protein was significantly decreased. The results suggested a selective reduction of serum albumin synthesis in the 15-day-old chick embryo. Following administration of 2 IU insulin on the first day of incubation, into the yolk sac, one third of the embryos developed embryopathies. ChAFP, serum albumin and whole serum protein values were unchanged on either the 12th day or 15th day of incubation. Inoculation of 100 microg adrenaline into the allantoic cavity on the sixth day of incubation resulted in embryopathies in only a few instances. ChAFP total serum protein values were not affected. However, serum albumin concentrations were significantly lower on the 12th day, but not on the 15th. The responses to L-thyroxine were both time- and dose-dependent. Inoculation of 2 microg thyroxine on the second day of incubation resulted in few embryopathies. ChAFP levels were significantly lower on the 12th and 15th day of incubation. In contrast, serum albumin and total serum protein concentrations were normal at both times. Similar results were obtained when 2 microg of thyroxine were administered at the third day of incubation. Thus in order to inhibit selectively chAFP synthesis, administration of 2 microg thyroxine on day 2 or 3 of incubation is suggested. When 10 microg thyroxine were injected on day 8 of incubation, 80% of the embryos showed embryopathies on day 12 of incubation. ChAFP and serum albumin levels were markedly depressed. The concentration of total serum protein was significantly decreased on day 12 but less so, though still significantly, on day 15. These results demonstrate the possibility to influence selectively chAFP and serum albumin synthesis, thereby facilitating studies on chemically induced teratological, including pathophysiological, processes in the avian embryo.