No abstract

Abstract. During the non-breeding season (April to July), 187 ewes treated wth either an intravaginal sponge impregnated with medroxyprogesterone acetate (MAP) or a controlled internal drug release (CIDRR) device for 9 days and an injection of pregnant mare serum gonadotropin (PMSG) at one day before the cessation of progestogen treatment were inseminated into the uterus by laparoscopy with frozen-thawed semen at fixed-time basis (36, 48 or 60 h after the removal of sponge or device). Insemination was also performed at 18 h after estrus detection as a control. The time to the onset of estrus after CIDRR treatment was significantly (P<0.05) earlier (mean: 24.9 h) than that in ewes treate with MAP sponge (mean: 30.0 h). The percentages of ewes lambing and lambs born per ewe lambing for inseminations at 36, 48 and 60 h were 66.7% and 1.69; 52.0% and 1.31; 46.2% and 1.75 for MAP-treated ewes, and 33.3% and 1.50; 73.9% and 1.53; 40.9% and 1.56 for CIDRR-treated ewes. For control ewes, they were 59.1% and 1.62; and 47.6% and 1.90 for MAP and CIDRR treatments, respectively. There was no significant differences in the lambing rates and prolificacy between MAP and CIDRR treatments and among the insemination times. An optimum time for an intrauterine insemination with frozen-thawed semen appears to be different in the use of MAP sponge (range: 36 to 60 h) and CIDRR (48 h). A significant difference in the lambing rate was found among the sheep farms conducting the present study.

We previously reported that a gene in linkage disequilibrium with HLA-Bw54, DR4, and DRw53 might control the susceptibility to silicosis (K. Honda et al. 1988. N. Engl. J. Med. 319:1610). To further define the HLA-linked gene and other genetic factors for predisposition of silicosis, we determined for HLA-DQ and DP alleles using the polymerase chain reaction and sequence-specific oligonucleotide probes and made a restriction fragment length polymorphism (RFLP) analysis of the fourth component of complement (C4) genes, immunoglobulin lambda variable chain (IGLV) gene, and T-cell receptor alpha and beta genes in 46 Japanese patients with silicosis. The frequency of DQB1*0401 (relative risk [RR] = 2.2, P < 0.02) was increased and that of DQB1*0601 (RR = 0.36, P < 0.01) was decreased in the patients. RFLP analysis of C4 and IGLV genes showed significant association between silicosis and a specific RFLP pattern of C4A3-C4B5 allotype (RR = 2.3, P < 0.05) and that of IGLV 5.3 kb (RR = 0.33, P < 0.003). No other genetic markers showed significant association. Statistical analyses of the associated genetic markers revealed that the HLA-Bw54 was the allele that showed primary association with silicosis and the frequencies of the C4 and HLA-DQ alleles were suggested to be increased due to their linkage disequilibrium with the HLA-Bw54. We conclude that the major gene for silicosis may be mapped near the HLA-B locus.

To investigate genetic factors involved in the pathogenesis of Hashimoto's thyroiditis (HT; goitrous autoimmune thyroiditis), HLA class I and class II antigens were analyzed in both seropositive HT (99 patients) and seronegative HT (43 patients). The frequency of HLA-DRw53 antigen was increased significantly in both seropositive HT (antigen frequency, 0.83; relative risk, 33.3; P less than 0.0002; corrected P less than 0.001) and seronegative HT (antigen frequency, 0.81; relative risk, 3.02; P less than 0.01; corrected P less than 0.05). The etiological fraction values for HLA-DRw53 in seropositive HT and seronegative HT were 0.58 and 0.54, respectively. An increased frequency of HLA-DQw4 and a decreased frequency of HLA-DQw1 were observed in patients with seronegative HT. These data suggest that susceptibility to HT is primarily associated with HLA-DRw53 and that HLA-DQ alleles may control the production of autoantibodies to the thyroid gland. The mode of inheritance of disease susceptibility for HT (controlled by a major gene in linkage disequilibrium with HLA-DRw53) was investigated by the method of Thomson and Bodmer, and it was suggested that disease susceptibility was inherited in a dominant manner.