Search PubMed⌕ Search

Biomedical subjects

Y Ueda

Publications and source records attributed to Y Ueda.

At least 1,027 records · Page 57Linked to original sources
PubMed1984

[A case report of mastopathy with cartilagenous and osseous metaplasia].

A case of mastopathy with cartilagenous and osseous metaplasia is reported. The patient is a 57-year-old Japanese woman complaining of a tumor measuring around 1.2 cm in diameter near the nipple of the left breast. The xeromammographic diagnosis was adenosis with calcification. Histological examination identified an intracystic tumor composed of papilloma and adenosis with cartilagenous and osseous metaplasia. This is the first Japanese case of its kind.

Breast Neoplasms↗
PubMed1983

Vasoactive intestinal polypeptide (VIP)-containing neurons in the spinal cord of the rat and their projections.

The distribution of vasoactive intestinal polypeptide (VIP)-like immunoreactive structures in the rat spinal cord and their projections were investigated by means of an immunofluorescent method. In the normal rat, a small number of VIP-positive fibers were observed in the superficial layer of the dorsal horn and in the lateral funiculus. With colchicine pretreatment, VIP-positive neurons were demonstrated in the lateral spinal nucleus (lsn) and in the lamina X (Rexed). Transections of the spinal cord at various levels revealed that some of the VIP neurons in the lsn might project to supraspinal areas via lateral funiculus.

Animals↗
PubMed1983

Some of the alpha-NH2-acetylated beta-endorphin-like material in rat and monkey pituitary and brain is acetylated alpha- and beta-endorphin.

There are several studies demonstrating the existence of alpha-NH2-acetylated (N-Ac) forms of beta-endorphin in the intermediate lobe of several species (1,4,6). These include N-Ac-beta-endorphin (1-31), N-Ac-beta-endorphin (1-27) and N-Ac-beta-endorphin (1-26). The existence of N-acetylation of brain beta-endorphin is more controversial (5,6). Using molecular sieving, HPLC, and several radioimmunoassays, either directed at the midportion of beta-endorphin or at only N-acetylated opioids, we have studied brain multiple forms (cf. Akil, 1982). We have noted that little or no acetylation of beta-endorphin-sized material occurs in hypothalamus, and a small amount of N-acetylation appears to take place in the midbrain and the medulla. These results will be described in detail elsewhere (Akil et al., in preparation), but point the fact that processing of beta-endorphin (1-31) in brain is different than either lobe, with the production of beta-endorphin (1-27) and beta-endorphin (1-26) being more predominant in brain terminal areas than in the neuro-intermediate lobe. In the course of these experiments we noted the existence of a smaller-sized material which reacted with our N-acetyl-beta-endorphin antibody. The following study describes the partial characterization of this material as N-Ac-alpha- and N-Ac-beta-endorphin (i.e., the N-acetylated forms of beta-endorphin (1-17) and beta-endorphin (1-16).

Animals↗
PubMed1983

Mechanism of renal excretion of AM-715, a new quinolonecarboxylic acid derivative, in rabbits, dogs, and humans.

The mechanisms of the renal excretion of AM-715, a synthetic antimicrobial agent, were studied in rabbits, dogs, and humans. In both rabbits and humans, AM-715 clearance was greater than creatinine clearance and was profoundly decreased by the administration of probenecid. Thus, in these subjects, AM 715 was cleared by both tubular secretion and glomerular filtration. In dogs, however, the excretion ratio (close to unity), biological half-life, and stop-flow pattern of AM-715 were not affected by probenecid, indicating that the renal excretion of AM-715 took place mostly through glomerular filtration. These results suggest that renal excretion of AM-715 differs with animal species.

Adult↗
PubMed1983

Renal disposition of moxalactam in experimental animals as revealed by stop-flow analysis.

The mechanisms of moxalactam excretion were studied by stop-flow analysis in dogs, monkeys, and rabbits. In dogs, the amount of moxalactam excreted in the urine was almost equal to that estimated by glomerular filtration. There was no specific moxalactam peak corresponding to the p-aminohippuric acid (PAH) peak in the stop-flow patterns of the dogs. The PAH peak disappeared with administration of probenecid, but the moxalactam stop-flow pattern showed no change. In monkeys, no specific moxalactam peak corresponding to the PAH peak could be detected. In the stop-flow pattern of the rabbit, the peak moxalactam concentration corresponded with that of PAH and disappeared with probenecid. These results suggest that in dogs and monkeys renal excretion of moxalactam takes place mostly through glomerular filtration. In rabbits, however, there is a small renal tubular secretory component added to the primary element, glomerular filtration. These observations point to differences in the mechanisms of moxalactam excretion in different animal species.

Animals↗
PubMed1983

Interactions of beta-lactam antibiotics and antineoplastic agents.

The in vitro interactions of four beta-lactam antibiotics and five antineoplastic agents were examined with 100 clinically isolated strains of four species of gram-negative bacilli. Generally, by the checkerboard dilution method, beta-lactam antibiotics, when tested in combination with mitomycin C, bleomycin, or 5-fluorouracil, showed synergistic action, whereas when tested in combination with carboquone, they showed antagonistic action. Almost no combinations of adriamycin showed the interactions. Among beta-lactam antibiotics, piperacillin was more frequently synergistic than cefoperazone, cefazolin, or carbenicillin when tested in combination with each antineoplastic agent against various species.

Anti-Bacterial Agents↗
PubMed1983

Functional heterogeneities among concanavalin A-activated OKT4+ and OKT8+ cells by using autologous erythrocyte rosette technique.

Normal human peripheral blood T lymphocytes activated by concanavalin A (Con A) were fractionated into OKT4+ and OKT8+ populations by complement-dependent cell lysis using OKT8 and OKT4 antibodies, respectively. By using the preferential ability of some, but not all, Con A-activated T cells to form rosettes with autologous erythrocytes, each population was further divided into autorosetting cells and nonautorosetting cells, and thus Con A-activated OKT4+ autorosetting, OKT4+ nonautorosetting, OKT8+ autorosetting, and OKT8+ nonautorosetting cells were obtained. The immune regulatory function of these populations was then investigated using a pokeweed mitogen-driven B cell plaque-forming cell system. These studies demonstrated that (a) autorosetting cells can exert potent suppressor activity regardless of their phenotypes of OKT4+ and OKT8+ antigens, and fail to help B cell differentiation; suppressor function mediated by these cells is radiosensitive; moreover, receptors for autologous erythrocytes may constitute either the interleukin 2 (IL2) receptors themselves or a component of an IL2 receptor-effector complex involved in modulating the growth signal that IL2 transmits to T cells; (b) OKT4+ nonrosetting cells serve adequately as radioresistant helper cells, but are devoid of suppressor cells; and (c) OKT8+ nonrosetting cells are found to lack either suppressor or helper activity, suggesting that they may belong to a T lymphocyte subset distinct from the subsets related to immune regulation. The results lead us, therefore, to the conclusion that there may exist functional heterogeneities among both the OKT4+ and OKT8+ populations; these heterogeneities can be dissected by virtue of the autologous erythrocyte rosette technique.

Antibodies, Monoclonal↗
PubMed1983

A defect in the suppressor circuits among OKT4+ cell populations in patients with systemic lupus erythematosus occurs independently of a defect in the OKT8+ suppressor T cell function.

The autologous mixed lymphocyte reaction (MLR) is thought to be part of a regulatory role of T cells on B cell function. OKT4+, but not OKT8+, cells can proliferate in response to autologous non-T cells. Moreover, the OKT4+ cell population activated early in the course of autologous MLR functioned as inducer cells for the differentiation of B cells, whereas later in the response, the activated OKT4+ cells were particularly enriched in suppressor cells. A part of the autologous MLR appears to be an important pathway for the activation of feedback suppression mechanisms among cells contained within the OKT4+ populations. Patients with systemic lupus erythematosus (SLE) were studied with regard to the following OKT4+ cell functions in vitro after activation in the autologous MLR: a) proliferative response, and b) helper and suppressor activities for differentiation of B cells. A marked reduction in the proliferative response of OKT4+ cells was observed in SLE patients. SLE OKT4+ cells activated in the autologous MLR could function as helper cells but could not exert any suppressor activity. This OKT4+ cell abnormality was present regardless of the disease activity, and occurred in the absence of autoantibodies including anti-T cell antibodies. Instead, SLE anti-T cell antibodies could preferentially eliminate cells bearing the OKT8+ phenotype characteristic of suppressor cells in populations of normal T cells. These results suggest that the defect in the suppressor circuits among OKT4+ cell populations is intrinsic to SLE lymphocytes and that the OKT8+ suppressor T cell defect is caused by antibodies produced by the B cells of SLE patients.

Adult↗