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Biomedical subjects

M Ogata

Publications and source records attributed to M Ogata.

At least 433 records · Page 24Linked to original sources

T-T cell interaction in the in vitro induction of delayed-type hypersensitivity (DTH) responses: demonstration of vaccinia virus-reactive helper T cell activity involved in enhanced induction of DTH responses.

C3H/HeN mice were inoculated i.p. with viable vaccinia virus to generate virus-reactive helper T cell activity. 850R X-irradiated spleen cells from vaccinia virus-primed or unprimed mice as helper cells were stimulated in vitro with either trinitrophenyl (TNP)-modified syngeneic spleen cells (TNP-self), vaccinia virus-infected spleen cells (virus-self), or cells modified with TNP subsequent to virus infection (virus-self-TNP) in the presence of normal C3H/HeN spleen cells (responding cells). After 5 days of culture, effector cells were tested for anti-TNP delayed-type hypersensitivity (DTH) responses by adoptive transfer into footpads of syngeneic C3H/HeN recipient mice together with TNP-self. The results demonstrate that spleen cells from virus-primed mice failed to enhance anti-TNP DTH responses when in vitro stimulation was provided by either virus-self or TNP-self alone. In contrast, spleen cells from vaccinia virus-primed mice, but not from unprimed mice, could augment anti-TNP DTH responses when stimulated by virus-self-TNP. Such a helper activity provided by vaccinia virus-primed mice was shown to be antigen-specific, and mediated by Lyt-1+2-T cells. DTH effector cells enhanced by helper cells were also antigen-specific and Lyt-1+2-T cells. Furthermore, vaccinia virus-reactive helper T cell activity could be applied to augmented induction of anti-tumor DTH responses by stimulation with virus-infected syngeneic fibrosarcoma tumor cells. Thus, these results provide evidence for the role of antigen-specific helper T cells in augmenting the development of DTH responses to cell surface antigens including tumor antigens.

Animals↗

A new hereditary single band variant of the Gc system.

A new single band variant (Gc Ar) or the Gc subtypes not identical with the known Gc variants has been detected in the plasma of a healthy blood donor by isoelectric focusing. Using this technique the variant is represented by a single band which has a similar isoelectric point to the Gc 1C2 anodal band. It is well known that the single band Gc phenotypes remain unaltered after neuraminidase treatment. Nevertheless, the new single band variant (Gc Ar) is altered after neuraminidase treatment as is Gc 2A3. After neuraminidase treatment, the Gc Ar band is affected and moved to the nearby position of the Gc 2 band. Investigation of the proband's family shows that the variant occurs combined with the common alleles Gc 1F, Gc 1S and that it has an autosomal dominant inheritance.

Alleles↗

Stereoselective hydrolysis of 16 alpha-halo-17-keto steroids and long-range substitution effects on the hydrolysis of 16 alpha-bromo-17-ketones and 2 alpha-bromo-3-ketones.

Epimerizations of 16 alpha-chloro- (1a), bromo- (1b), and iodo-3 beta-hydroxy-5-androsten-17-one (1c) by a brief treatment with 0.2 equiv NaOH in aqueous pyridine reached equilibrium between 16 alpha- and 16 beta-halo ketones. 16 alpha-/16 beta-Halo ketone ratios at equilibrium were 1.5 for Cl, 1.25 for Br, and 1.0 for I. Kinetic analysis showed that compounds 1a-c were stereoselectively converted to the corresponding 16 alpha-hydroxy derivative 3 by an SN2 mechanism, in which the order of the apparent reactivity was Br greater than I greater than Cl. The hydrolysis of a number of 16 alpha-bromo-17-ketones and 2 alpha-bromo-3-ketones was carried out. The yields of the corresponding alcohols were found to depend on remote structural features in the steroids.

17-Ketosteroids↗

Operations for cervical spondylotic myelopathy. A comparison of the results of anterior and posterior procedures.

Over the past 19 years we have operated on 269 patients with myelopathy associated with cervical spondylosis. We report our results in 191 cases which we have followed up for 1 to 12 years (average 31 months). The clinical state before and after operation was recorded using the criteria of the Japanese Orthopaedic Association. Posterior operations gave better results than anterior for the more advanced myelopathies such as transverse lesions, the Brown-Séquard syndrome and the motor syndromes, but the brachialgia and cord syndrome and the central cord syndrome were satisfactorily treated by anterior operations. Of the three anterior and three posterior techniques used, no single one showed an overall superiority. A short duration of symptoms before operation was associated with better results, but these were not influenced by the age of the patients.

Adult↗

An advanced form of familial hypertrophic cardiomyopathy showing massive myocardial fibrosis with intramural small arterial thickening. An autopsy case.

An autopsy case of an advanced form of hypertrophic cardiomyopathy (HCM) showing marked fibrosis with intramural small arterial abnormalities is presented in this report. A 52-year-old woman, who had a positive family history of HCM, was admitted because of palpitations. The chest roentgenogram showed a mildly enlarged cardiac silhouette and the electrocardiogram revealed abnormal Q waves and R wave and T wave abnormalities. The echocardiogram revealed hypokinesis with thinning of the interventricular septum and the anterior wall of the left ventricle. Percutaneous right ventricular endomyocardial biopsies demonstrated moderate interstitial fibrosis with small arterial thickening. At necropsy, the anterior and posterior walls of the left ventricle and the interventricular septum were markedly thinned and showed a massive transmural fibrosis. Moreover, the intramural small arteries, 50-300 microns in diameter, showed marked intimal and medial hypertrophy with proliferation of elastic fibers and smooth muscle cells. From these findings, it is suggested that this was originally a case of HCM which progressed to a decompensated stage because of the abnormal intramural small arteries. The significance of small arterial lesions in HCM is discussed.

Cardiomyopathy, Hypertrophic↗

[Indices of biological monitoring, with special reference to urinalysis of metabolites of organic solvents].

The significance of biological exposure indices, and the methods of biological monitoring of exposure to organic solvents by urinalysis are discussed. The review covers choice of time for urine sampling, correction of the results for urine density, and the urinary concentration of metabolites of non-exposed persons. The method of drawing regression line between concentration of organic solvents in the air and concentration of urinary metabolites in the urine is also described.

Environmental Exposure↗

Effect of tricyclic drugs on mitochondrial membrane.

The effects of tricyclic drugs (clomipramine, imipramine, chlorpromazine and promethazine) on isolated liver mitochondria of rats were examined. All the drugs tested accelerated state 4 respiration. Their stimulative potency at concentrations below 100 microM was in the order of chlorpromazine greater than clomipramine greater than imipramine, promethazine. On state 3 respiration, the chlorine containing drugs had an inhibitive effect at high concentrations, while the other drugs seemed to have a slightly stimulative effect. These drugs stimulated latent ATPase activity of mitochondria. Clomipramine and chlorpromazine inhibited 2, 4-dinitrophenol-stimulated ATPase activity in a dose-dependent fashion. Imipramine also inhibited 2, 4-dinitrophenol-stimulated ATPase activity at high concentrations. Promethazine, however, had almost no effect. All the drugs induced potassium release from mitochondrial vesicles, and their potency was in the order of clomipramine greater than chlorpromazine greater than imipramine greater than promethazine. These results suggest that clomipramine, imipramine, chlorpromazine and promethazine cause impediments in both mitochondrial respiration and ion compartmentation, and that the chlorine containing drugs are more toxic than others on the functions of the mitochondrial membrane.

Adenosine Triphosphatases↗

Adenosine triphosphate restoration and discocytic transformation of stored human erythrocytes.

Erythrocytes in human blood stored for 120 days were collected by centrifugation after dispersion in buffered physiological saline. The aged erythrocytes thus collected were incubated with inosine, adenine, glucose or other media, and their shapes and ATP levels were studied by scanning electron microscopy and a luciferine-luciferase method. The aged erythrocytes incubated in a mixture of adenine and inosine markedly regained their ATP levels, and also showed a marked transformation from spiked spherocytes to normal discocytes. Incubation with inosine alone restored ATP levels of the aged erythrocytes to some extent, but did not result in morphological rejuvenation. Incubation in a mixture of citrate and glucose caused morphological rejuvenation, though it restored ATP levels less effectively than incubation in inosine alone. Incubation with adenine alone neither restored ATP levels nor resulted in morphological rejuvenation of the stored erythrocytes.

Adenine↗

The mechanism of tolerance induction of tumor-specific delayed-type hypersensitivity responses by intravenous inoculation of tumor cells.

C3H/HeN mice were inoculated intravenously (iv) with 10(6) 10000-R X-irradiated syngeneic MCH-1-A1 fibrosarcoma cells 3 times at 4-day intervals (pretreatment). Spleen cells from these pretreated or normal mice were sensitized in vitro to MCH-1-A1 tumor cells and effector cells generated after 5 days of culture were assayed for delayed-type hypersensitivity (DTH) responses by an adoptive transfer into footpads of syngeneic recipient mice together with MCH-1-A1 cells. Normal spleen cells stimulated with MCH-1-A1 tumor cells generated appreciable anti-MCH-1-A1 DTH responses, whereas spleen cells from the above pretreated mice failed to induce anti-MCH-1-A1 DTH responses. These pretreated spleen cells did not inhibit the generation of DTH responses when co-cultured with normal spleen cells as responding cells. Since vaccinia virus-reactive helper T cells are capable of enhancing DTH responses against antigens co-expressed on vaccinia-infected cells, their ability to augment anti-MCH-1-A1 DTH responses from the pretreated spleen cells upon stimulation with vaccinia-infected MCH-1-A1 cells was investigated. The results demonstrate that under conditions in which enhanced anti-MCH-1-A1 DTH responses were obtained by supplementing vaccinia helper T cells, these vaccinia-helpers were not able to generate any significant DTH responses from the pretreated spleen cells. These results indicate that iv inoculation of tumor cells suppresses the generation of tumor-specific DTH responses not by inducing suppressor cell activity, but rather by inhibiting DTH effector clones themselves.

Animals↗

[A clinical study of calcium pyrophosphate dihydrate crystal deposition disease].

Clinical features of calcium pyrophosphate dihydrate crystal deposition disease (CPPD c.d.d.) were studied and the following results were obtained. The prevalence of CPPD c.d.d. was 9.7% in 300 persons aged 50 or older, who stayed or worked at an old-age home. The most common type of CPPD c.d.d. was the asymptomatic type. Comparative studies between the patients with CPPD c.d.d. and subjects without it revealed that scoliosis of the lumbar spine, osteoarthritis-like changes of the knee, subchondral bone cyst and patella wrapped around the femur were statistically more frequent in the former. The clinical study of 50 patients with CPPD c.d.d. revealed calcification not only in the articular cartilage but also in periarticular tissues and ligamentum flavum. The histological study demonstrated frequent destructive changes of the tissues around the site of CPPD crystal deposition. Formation of CPPD crystals appeared to be initiated by degenerating chondrocytes and metaplastic chondrocytes.

Age Factors↗

[The augmentation of tumor-specific immunity by T-T cell interaction].

The present study establishes a tumor-specific immunotherapy model based on the principle of T-T cell interaction mechanism responsible for augmenting the induction of anti-tumor-specific effector T cells. In this model, high incidence of tumor regression was observed in hosts bearing transplantable or autochthonous tumors when these hosts, in which hapten-reactive helper T cells had been generated, received an injection of haptenic solution into the growing tumor mass. This indicated a role of hapten-reactive helper T cells in regressing the tumor. In consideration clinical application of this tumor-specific immunotherapy model, we have also tried to investigate the use of more appropriate haptenic compounds and have succeeded in synthesizing a noble haptenic compound cross-reactive with BCG, a haptenic muramyl dipeptide (MDP) derivative. The results demonstrated that prepriming of BCG and subsequent immunization with syngeneic tumor cells (mitomycin C-treated) modified with the haptenic MDP derivative resulted in the enhanced induction of tumor-specific immunity. Further investigation is in progress to establish a new tumor-specific immunotherapy model by utilizing this haptenic MDP derivative.

Animals↗