S. Sonoda

Genetic study of ossification of the posterior longitudinal ligament in the cervical spine with human leukocyte antigen haplotype.

To evaluate the genetic background of ossification of the posterior longitudinal ligament, the relationship between the presence or absence of ossification and human leukocyte antigen haplotypes was studied in 33 families of patients with ossification of the posterior longitudinal ligament. The study revealed that human leukocyte antigen haplotypes formed certain types of clusters, and that some human leukocyte antigen haplotypes were very rare in the Japanese population, suggesting the involvement of human leukocyte antigen-linked factors in the pathogenesis of ossification of the posterior longitudinal ligament of the cervical spine. In the families of these patients, ossification of the posterior longitudinal ligament was demonstrated by radiography in 56% (10/18) of the siblings. Each of these siblings shared both human leukocyte antigen haplotypes with the patient. None of those who shared only one human leukocyte antigen haplotype with the patient had developed ossification of the posterior longitudinal ligament. From these findings, the presence of both pathogenic human leukocyte antigen haplotypes is considered to be necessary for the development of ossification of the posterior longitudinal ligament, and this genetic predisposition may be activated by multiple factors, including regressive degeneration due to aging and the environment.

Restriction fragment length polymorphism of genes of the α2(XI) collagen, bone morphogenetic protein-2, alkaline phosphatase, and tumor necrosis factor-α among patients with ossification of posterior longitudinal ligament and controls from the Japanese population

Study Design The present study analyzed the restriction fragment length polymorphism patterns of α2(XI) collagen, bone morphogenetic protein‐2, alkaline phosphatase, and tumor necrosis factor‐α genes in patients with ossification of the posterior longitudinal ligament. This study investigates the genetic polymorphism of bone‐induced factors in patients with ossification of the posterior longitudinal ligament and compares it with healthy control subjects. Objectives To clarify the genetic markers linked to ossification of the posterior longitudinal ligament. Summary of Background Data Ossification of the posterior longitudinal ligament is a genetic disease associated with abnormal calcium metabolism involving the posterior longitudinal ligament. Previous genetic studies have not identified the pathologic mechanism of ossification of the posterior longitudinal ligament. Histopathologic studies of ossification of the posterior longitudinal ligament and the animal model, the spinal hyperostotic mouse, have revealed an increase in Type XI collagen and bone morphogenetic protein‐2 expression. Methods Eighteen Japanese patients with ossification of the posterior longitudinal ligament and 51 healthy, unrelated control subjects were investigated for the restriction fragment length polymorphism patterns of COL11A2, bone morphogenetic protein‐2, alkaline phosphatase, and tumor necrosis factor‐α, genes with various restriction endonucleases. Results The gene frequencies of COL11A2 obtained with BamHI (10.0 kb fragment) and HindIII (19.0 kb fragment) observed in patients with ossification of the posterior longitudinal ligament were higher compared with control subjects (0.43 and 0.14, respectively). These differences were statistically significant (BamHI P = 0.018; HindIII P = 0.046). Two new restriction fragment length polymorphism patterns were detected of the bone morphogenetic protein‐2 gene with Mspl and Taql and one already known restriction fragment length polymorphism pattern of the tumor necrosis factor‐α gene with Ncol. However, they were not significantly different from the control subjects. Conclusion Seven restriction fragment length polymorphisms of COL11A2 gene were identified. Two of them (BamHI, 10.0/10.0 kb genotype; HindIII, 19.0/19.0 kb genotype) were significantly different in patients with ossification of the posterior longitudinal ligament.

Expression of a Rat Ovary-independent Mammary Tumor-associated Antigen Defined by a Monoclonal Antibody, TAK-B1

A monoclonal antibody, TAK‐B1, was produced by immunization of BALB/c mice with mammary carcinoma induced in inbred Sprague‐Dawley rats by treatment with 7,12‐dimethylbenz[a]anthra‐cene. TAK‐B1 reacted with ovary‐independent mammary carcinoma cells which had been transformed from ovary‐dependent mammary carcinoma cells, but did not react with original mammary carcinoma cells or with cells from mammary glands exhibiting fibrocystic changes or normal mammary glands. However, TAK‐B1 reacted not only with basal cells of the epidermis and epithelial cells of the bottom portion of crypts of the small intestine in adult rats, but also with basal cells of epidermis in skin and mesenchymal cells around developing hair follicles in fetuses. We therefore classify TAK‐B1 as an ovary‐independent rat mammary tumor‐associated antigen. Immunoelectron microscopic examinations revealed that the antigen recognized by TAK‐B1 was localized in the cell surface membrane of ovary‐independent mammary carcinoma cells. Immunoprecipitation assay revealed that the antigen recognized by TAK‐B1 was composed of M 220,000 protein and four other minor proteins.

Characterization of Macrophages Isolated from the Maternal Surface of Human Term Placenta by a New Method of Urokinase Treatment

Objectives: This study was performed to establish a new method for isolating macrophages from the maternal surface of human term placenta by urokinase treatment and to characterize their immunological functions.