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Biomedical subjects

J E Allison

Publications and source records attributed to J E Allison.

At least 37 records · Page 2Linked to original sources

Structural and functional factors related to testicular neoplasia in feminized rats.

Testicular tumors in King-Holtzman hybrid rats with testicular feminization (tfm) were seen as firm, rounded masses of tissue consisting of Leydig cells, myoid cells, and fibroblast-like cells. The cytoplasm of Leydig cells contained well-developed smooth endoplasmic reticulum, pleomorphic mitochondria with numerous cristae, and many lipid droplets. Mitochondria were numerous and varied in size and shape. Their cristae were in the form of tubules, and lipid-like inclusions were frequently seen in the mitochondrial matrix. Lysosomes, rough endoplasmic reticulum, and Golgi bodies were also scattered in the cytoplasm. An in vitro study showed that more testosterone was produced in the tumor than in the testes of rats with tfm; however, the amount in both was less than normal. Testicular tumor-bearing rats with tfm exhibited slightly higher levels of plasma testosterone than did non-tumor-bearing animals with tfm. Levels in both were significantly higher than normal. Testicular tumor cells growing in culture medium supplemented with luteinizing hormone (LH) contained more protein and synthesized more androgen and DNA than did those growing in culture medium without LH. Observed under the scanning and transmission electron microscopes, the LH-stimulated cells had well-developed cytoplasmic organelles and inclusions and surface specializations such as numerous microvilli, large blebs, and other microextensions. They adhered well to the glass surface. These results indicated that Leydig cells in testicular tumors of rats with tfm had morphologic characteristics of steroid-producing cells. In addition these cells were capable of producing steroids, and this capability was enhanced by the presence of LH.

Androgen-Insensitivity Syndrome↗

Ultrastructural and biochemical characteristics of Leydig cells from newborn androgen-insensitive rats.

Leydig cells of testis of newborn pseudohermaphrodite (tfm) rats have an ultrastructure similar to that of the normal, containing well developed organelles and inclusions. The cytoplasm is filled with smooth endoplasmic reticulum forming a network of interconnected tubules. Lipid droplets are surrounded by cisternae of smooth endoplasmic reticulum and are in close association with pleomorphic mitochondria. Many of the latter are cup-shaped and have tubular cristae and intramitochondrial dense bodies. Essentially, these are characteristics of normal Leydig cells. Accordingly, the production of testosterone by testes from newborn tfm rats is the same as that by testes from normal newborns and adults. However, it is significantly higher than that by testes of tfm adults. Also, the plasma testosterone levels of newborn tfm rats are the same as in the normal newborn, but lower than in normal adults and much lower than in adult tfm animals. Thus, since in the tfm rat the morphology of Leydig cells, androgen production, and maintenance of plasma levels of testosterone are normal in the newborn, but become abnormal with advancing age, it appears that defective androgen action rather than insufficient androgen production is the cause of male pseudohermaphroditism.

Androgens↗

Hormonal factors related to the incidence of testicular tumors in male pseudohermaphrodite rats.

Pieces of testicular tumor from male pseudohermaphrodite (tfm) rats were transplanted between the skin and body wall musculature of 4-day-old female, male, and tfm hosts and to the anterior chambers of the eyes of gonadectomized and intact adult tfm, female, and male hosts. These transplants grew in all hosts except normal males. To determine whether these tumors were hormone-dependent, the levels of circulating gonadotropins were measured in all host types to ascertain which were low in the males and high in all of the others. Prolactin, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels were measured in intact and castrated normal and tfm rats. Normal males had low levels of prolactin, estrogen, LH, and FSH; however, transplants grew well in other hosts with low titers of these hormones. Except for normal males, all hosts had high serum levels of LH. Thus, testicular tumors in tfm rats appear to be LH-dependent.

Animals↗

Reactogenicity and immunogenicity of bivalent influenza A and monovalent influenza B virus vaccines in high-risk children.

Seventy-nine high-risk children were immunized with either commercial, bivalent, split-product influenza A vaccine or purified hemagglutinin-neuraminidase bivalent influenza A vaccine, and 78 of these subjects were immunized with commercial, monovalent, influenza B split-product vaccine. The reactogenicity of all three vaccines was low, and there were no severe reactions. Twenty-nine subjects who received hemagglutinin-neuraminidase vaccine as their initial dose and commercial split-product vaccine as a booster dose had significantly lower antibody responses to influenza A/New Jersey/76 virus than subjects who received two doses of commercial split-product vaccine. The responses of the two groups to influenza A/Victoria/75 virus were comparable. Twenty-four subjects with malignancy who were receiving chemotherapy were compared with a group of subjects matched for age and vaccine preparation. Patients with cancer had significantly lower antibody responses to A/New Jersey/76 virus than patients without cancer. The ultimate responses of patients with cancer to A/Victoria/75 and B/Hong Kong/72 viruses were comparable to those of other patients, but early responses were lower.

Adolescent↗

Pseudohermaphrodite rat: end organ insensitivity to testosterone.

The pseudohermaphrodite rat is characterized by lack of androgen-dependent differentiation. Treatment of these rats with testosterone failed to produce the expected changes in preputial and adrenal gland weights and hexobarbital metabolism. This insitivity of the end organ to testosterone could not be explained by defective formation of dihydrotestosterone.

Adrenal Glands↗