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Biomedical subjects

M Minami

Publications and source records attributed to M Minami.

At least 559 records · Page 31Linked to original sources
PubMed1987

Nonunion of the capitate.

A case of nonunion of the capitate of a 13-year-old girl is reported. Autogenous iliac bone grafting obtained union. At the 2-year follow-up, she had no complaints and had full motion of the wrist.

Adolescent↗
PubMed1987

Satisfactory elbow flexion in complete (preganglionic) brachial plexus injuries: produced by suture of third and fourth intercostal nerves to musculocutaneous nerve.

The third and fourth intercostal nerves were sutured to the musculocutaneous nerve to restore flexion of the elbow joint in complete (preganglionic) brachial plexus injuries. Seventeen patients were followed on the average for 5 years and 7 months after surgery. The results were evaluated by means of manual muscle tests and electrical diagnostic tests. Good (grade IV), or better, flexion of the elbow joint occurred in 12 patients over 3 years after the operation.

Adolescent↗
PubMed1987

Treatment of distal radioulnar disorders.

Twenty-nine wrists of 29 patients were treated with three procedures: distal ulnar resection (Darrach's procedure), distal ulnar recession, or hemiresection-interposition arthroplasty. The indications were pain and limitation of motion associated with primary osteoarthritis of the distal radioulnar joint, derangement after distal forearm bone fracture, Madelung's deformity, and distal radioulnar sprain. The age of the patients averaged 48.3 years. Follow-up averaged 1 year and 9 months. Radiographic evaluations were done preoperatively and postoperatively. Relief of pain was good in the wrists treated by Darrach's procedure; however, diminished grip strength and wrist instability occurred. Relief of pain in the wrists treated by distal ulnar recession and hemiresection-interposition arthroplasty was inferior to that of Darrach's procedure; however, postoperative grip strength increased and wrist instability did not occur.

Female↗
PubMed1987

Induction of suppressor T cells by intravenous administration of monoclonal anti-I-A antibody.

Intravenously administered monoclonal anti-I-A antibodies successfully induced suppressor T (Ts) cells specific for alloantigen-specific delayed-type hypersensitivity (DTH) responses in mice. These Ts cells exerted their effects in the effector phase and had no H-2 restrictions. Phenotypic analysis revealed L3T4 antigens on their cell surface but failed to reveal Lyt-2 antigen. Ts cell activity was abrogated by a 30-min incubation with the anti-I-A antibodies used for Ts cell induction. Incubation in the anti-I-A-antibody-coated plate also abrogated the Ts cell activity. Since anti-I-A antibody is idiotypic for the I-A antigen, it is suggested that these Ts cells might express antiidiotypic receptors for I-A antigens. These findings are considered to be consistent with previous observations of hapten-specific systems, in which antiidiotypic Ts cells are inducible by idiotypic antibodies.

Animals↗
PubMed1987

Effect of the substance P antagonist spantide on adrenal sympathetic nerve activity in rats.

In order to elucidate the role of substance P in adrenal nerve activity, the effects of substance P antagonists on tonic activity of the adrenal sympathetic nerve, the response to exogenous substance P and cutaneo-adrenal nerve reflex were investigated in anesthetized rats. Substance P or its antagonist [(Arg1, D-Trp7,9, Leu11)-substance P: spantide] was injected into the subarachnoid space via polyethylene tubing. Intrathecal administration of spantide (0.1-10 micrograms) produced a slight and transient increase in tonic activity of the adrenal nerve. Thereafter, a marked and prolonged decrease in adrenal nerve activity was observed, along with a decrease in arterial blood pressure. Intrathecally administered substance P (0.1-10 micrograms) produced a marked increase in tonic activity of the adrenal nerve in a dose-related manner. This substance P-induced increase in adrenal nerve activity was significantly antagonized by pretreatment with spantide. It was also found that spantide depressed the reflex response in adrenal nerve activity evoked by noxious mechanical pinching of the skin. These findings suggest the possibility that on the spinal level, substance P has an important role in the maintenance of tonic activity of the adrenal nerve and the transmission of nociceptive information to the adrenal nerve in rats.

Adrenal Glands↗
PubMed1987

Central sympathoinhibitory action of a direct-acting vasodilator, budralazine, in anesthetized rats.

Previous data on budralazine, 1-[2-(1,3-dimethyl-2-butenylidene)-hydrazino]-phthalazine, has indicated that it is a direct-acting vasodilating agent that does not produce marked tachycardia. The present study was undertaken to elucidate what effects may be seen on the central sympathetic nerve activity when budralazine is given systemically to rats. Budralazine (0.5, 1.0 and 5.0 mg/kg, i.v.) produced a dose-dependent reduction of mean arterial pressure. At doses of 0.5 and 1.0 mg/kg, budralazine induced bradycardia accompanied with a decrease in cardiac sympathetic nerve activity. Preganglionic adrenal sympathetic nerve activity was also reduced by budralazine (1.0 mg/kg, i.v.). A dose of 0.5 mg/kg of budralazine neither influenced carotid sinus nerve activity nor augmented aortic depressor nerve activity. On the contrary, a high dose of budralazine (5.0 mg/kg) produced simultaneous increases in the heart rate and cardiac sympathetic nerve activity along with a marked suppression of aortic depressor nerve activity. Plasma norepinephrine and epinephrine concentrations were also increased at a dose of 5.0 mg/kg. These findings suggest that budralazine doses of 0.5 and 1.0 mg/kg may reduce the sympathetic outflow that is mediated via central sympathoinhibitory action. Baroreceptor-mediated tachycardia occurred after high dose budralazine (5.0 mg/kg) administration in anesthetized rats.

Animals↗
PubMed1987

Analysis of alloantigen-specific suppressor T cells.

The intravenous administration of allogeneic spleen cells successfully induced two distinct subsets of alloantigen-specific suppressor T cells that function at either the induction phase or the effector phase of alloantigen-specific DTH responses. The induction phase suppressor T cells were found to be Lyt2-, and were not genetically restricted by H-2 region genes. The effector phase suppressor T cells are Lyt2+, and their activity is controlled by genes within the H-2 region. The effector phase suppressor T cells mediate antigen-dependent bystander suppression, provided the appropriate alloantigen is present at the site of the immune responses. This effector phase suppression requires cyclophosphamide-sensitive targets. The results of this study suggest that allospecific suppressor T cells and hapten-specific suppressor T cells have a similar mechanism of action.

Animals↗
PubMed1987

Central sympathoinhibitory action of ketanserin in rats.

The effect of ketanserin on sympathetic efferent nerve activity which was recorded from the postganglionic renal nerve, inferior cardiac nerve and preganglionic adrenal nerve was studied in buffer nerve-intact rats. Intravenous administration of ketanserin (0.05-5.0 mg/kg) produced bradycardia and a reduction of mean arterial pressure dose-dependently. Renal nerve activity and inferior cardiac nerve activity also were reduced by ketanserin. After i.v. administration, baroreceptor afferent nerve activity did not increase, but actually decrease. Moreover, i.v. and i.c.v. administration of ketanserin caused a decrease in preganglionic adrenal nerve activity accompanied with hypotension and bradycardia. Ketanserin (0.5 mg/kg i.v.) and clonidine (3 micrograms/kg i.v.) produced equihypotension and bradycardia. On the other hand, the ketanserin-induced reduction of renal nerve activity was milder than that induced by clonidine. The present findings confirmed that ketanserin has a central sympathoinhibitory action. This central action of ketanserin may play an important role in ketanserin-induced bradycardia and may be partially responsible for ketanserin-induced hypotension.

Animals↗
PubMed1986

The role of adherent accessory cells in the generation of effector suppressor T cells.

The role of accessory cell populations in the generation of effector suppressor (Ts3) cells was studied. By using an in vitro culture system, it was previously determined that the induction of NP-specific effector suppressor activity requires T cells, antigen, and an anti-idiotypic B cell population. We now demonstrate that the generation of Ts3 cells in this system also requires accessory cells. The accessory population appears to play a role in the processing and presentation of antigen. These antigen-presenting accessory cells are required early in the induction phase of Ts3 generation. These accessory cells can present NP coupled to immunogenic or non-immunogenic polypeptide carriers, including polymers of L-amino acids. However, NP coupled to polymers of poorly metabolized D-amino acids fail to induce suppressor T cell generation. Furthermore, the data demonstrate that an H-2 homology must exist between the Ts3 precursors and the antigen-presenting cell population if suppressor activity is to be generated. We also characterize the differential genetic restrictions that govern the induction of Ts3 cells that control suppression of either T cell or B cell responses. The data suggest that although I-J region encoded gene products control the induction and effector phases of suppressor cell activity as measured on T cell responses, the suppression of B cell responses appear to be controlled by I-A gene products. Possible cellular mechanisms that might explain these findings are discussed.

Amino Acids↗
PubMed1986

The regulatory role of sialic acids in the response of class II reactive T cell hybridomas to allogeneic B cells.

Two different kinds of alloreactive T cell hybridomas were established in previous experiments. One is reactive and the other is nonreactive to allogeneic I-A region-associated membrane antigen (mIa) on B cells. In the present experiments the difference between these hybridomas were analyzed by using representative clones, B cell mIa-reactive clone CB-11.4, and nonreactive clone HTB-9.3. Unresponsiveness of HTB-9.3 clone to allogeneic B cells could not be due to the inability of B cells in interleukin 1 production or the density of mIa molecules on B cells. HTB-9.3 clone could respond to C57BL/6 mouse B cells treated with neuraminidase (Nase), and Nase-treated HTB-9.3 clone could respond to normal B cells from C57BL/6 mouse, indicating that sialic acid on both B cells and HTB-9.3 clone plays a regulatory role in the alloreactivity of the clone. In response to B cells from C57BL/6 mouse, T cells from C3H/He mouse spleen showed similar reactivity to HTB-9.3 clone; that is, T cells could respond to Nase-treated B cells, and Nase-treated T cells to B cells, and T cells primed with C57BL/6 spleen cells in vitro showed similar reactivity to CB-11.4 clone. These results suggest that HTB-9.3 clone represents virgin T cells and CB-11.4 clone-primed T cells at least in alloreactivity. Anti-L3T4a was shown to block alloreactivities of both T cell hybridomas and splenic T cells against B cells more efficiently than against splenic adherent cells. These results suggest that L3T4a on T cell plays more important role in allogeneic response to B cells than to splenic adherent cells.

Animals↗
PubMed1986

Functional analysis of cloned macrophage hybridomas. V. Induction of suppressor T cell responses.

It has been suggested that macrophage-like accessory cells are involved in suppressor T cell (Ts) induction. To further analyze this issue, we obtained several cloned macrophage hybridoma cell lines by somatic cell fusion of the macrophage tumor P388D1 of DBA/2 (H-2d) origin with splenic adherent cells of CKB mice (H-2k). Several cloned lines displayed the serological and functional characteristics of macrophages. We evaluated the ability of these hybridomas to induce third order or effector Ts (Ts3) to suppress the contact sensitivity response against the hapten 4-hydroxy-3-nitrophenyl acetyl (NP). In contrast to the parental P388D1 and two other macrophage hybridomas, one macrophage hybridoma clone, termed 63, when conjugated with NP, induced Ts3, which suppressed contact sensitivity responses against NP but not DNFB, showing that the Ts3 were antigen specific. Macrophage hybridoma 63 could specifically induce Ts3 activity in either H-2k, H-2d, or H-2k/H-2d heterozygous hosts. Thus, macrophage hybridoma 63 functionally expressed major histocompatibility complex-related restricting determinants, and the fusion with cells from a H-2k macrophage donor caused a functional complementation of H-2d-related, Ts-inducing elements. The genetic restriction governing induction of Ts3 was controlled by genes that mapped to I-J region. Furthermore, NP-conjugated macrophage hybridoma 63 could serve as a target for elicitation of suppressor responses after administration of I-Jk, but not I-Jb, restricted suppressor factor. The data suggest that macrophage hybridomas represent a means to dissect heterogeneity within the macrophage population. The data also imply that the I-J determinants expressed on macrophages represent a ligand for the antigen receptor of Ts.

Animals↗
PubMed1986

The differential ability of splenic adherent cells from B6.lpr mice to induce suppressor T cells.

Hapten-coupled splenic adherent cells or resident peritoneal cells from autoimmune B6.lpr mice that are over 5 mo of age fail to induce first-order inducer suppressor T cells (Ts1). However, the same population of hapten-coupled cells can induce both delayed-type hypersensitivity responses and third-order effector suppressor T cells (Ts3). Thus, splenic and peritoneal antigen-presenting cells from B6.lpr mice display a defined defect in the ability to induce certain suppressor T cell responses. The cellular defect in Ts1 induction is controlled by the lpr gene, since age-matched congenic B6 mice do not display this defect. The splenic adherent cell defect is temporarily correlated with the autoimmunity that develops in B6.lpr animals. The antigen-presenting defect in the B6.lpr splenic adherent population for Ts1 induction is reversible by culturing the cells in interferon-gamma. The results are discussed as an illustration of the relationship between experimental models of autoimmunity and defects in a suppressor T cell cascade.

Aging↗