Cataracts in the Norwegian Buhund-current prevalence and characteristics.

OBJECTIVE: To evaluate prevalence and characteristics of cataracts in the Norwegian Buhund breed 20 years after high reported prevalence of especially pulverulent nuclear cataracts (PNCs). ANIMALS STUDIED: Two hundred and fifty Norwegian Buhund dogs in Norway, Sweden, and Denmark (117 males and 133 females) with previously unknown eye health status were included. Forty-five dogs had multiple examinations (two to six times over a 6-year period). Median age was 4.4 years [0.2-15.2] at first examination and 5.3 years [0.2-15.2] at last examination. PROCEDURES: All dogs underwent regular screening for inherited eye diseases. RESULTS: At the last observation of each dog, 52.4% were affected by PNC, categorized as minimal (33 of 250 dogs; 13.2%), mild (31 dogs; 12.4%), moderate (38 dogs; 15.2%), or pronounced (29 dogs; 11.6%). Moderate or pronounced changes were only seen in older dogs, and progressive changes were identified in some of the re-examined dogs. Some dogs, free of lenticular changes at early examinations, were affected by PNC at re-examinations. The odds for finding PNC increased with dog's age up to approximately 8 years. Presumably inherited cataracts other than PNC were found in 53 dogs (21.2%) with cortical (17.6%) and posterior polar (6.4%) locations as the most common ones. CONCLUSIONS: The high prevalence of PNC in the breed reported 20 years ago persists. PNCs are not always visible in young dogs, and the rate of progression varies. The prevalence of other types of cataract is also high, but cataracts rarely cause loss of vision in this breed.

Response of malignant B lymphocytes to ionizing radiation: gene expression and genotype.

The human malignant B-lymphocyte cell lines Reh and U698 show arrest in G2 phase after ionizing radiation (IR), but only Reh cells arrest in G1 phase and die by apoptosis. We have used cDNA microarrays to measure changes in gene expression at 2, 4 and 6 hr after irradiation of Reh and U698 cells with 0.5 and 4 Gy in order to begin exploring the molecular mechanisms underlying the phenotypic changes. We also investigated whether gene expression changes could be caused by possible aberrations of genes, as measured by comparative genomic hybridization. Reh cells showed upregulation of CDKN1A that likely mediated the G1 arrest. In contrast, U698 cells have impaired function of TP53 protein and no activation of CDKN1A, suppressing the arrest in G1. The G2 arrest in both cell lines was likely due to repression of PLK1 and/or CCNF. IR-induced apoptosis in Reh cells was probably mediated by TP53 and CDKN1A, whereas a high expression level of MCL1, caused by gene amplification, and activation of the NFKB pathway may have suppressed the apoptotic response in U698 cells. Genes suggested to be involved in apoptosis were activated long before this phenotype was detectable and showed the same temporal expression profiles as genes involved in cell cycle arrest. Our results suggest that differences in functionality and/or copy number of several genes involved in IR-regulated pathways contributed to the phenotypic differences between Reh and U698 cells after IR, and that multiple molecular factors control the radiation response of malignant B lymphocytes.