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Biomedical subjects

T Tanabe

Publications and source records attributed to T Tanabe.

At least 397 records · Page 22Linked to original sources

Susceptibility of various animals and cultured cells to exfoliative toxin produced by Staphylococcus hyicus subsp. hyicus.

In piglets inoculated with partially purified exfoliative toxin (pp-shET) produced by Staphylococcus hyicus subsp. hyicus, exfoliation was observed at 12 h after injection. Chickens inoculated with the same dose of pp-shET also showed exfoliation within 30 min of injection. However, exfoliation was not demonstrated in mouse, rat, guinea pig, hamster, dog or cat inoculated with pp-shET until 24 h after injection. In cultured cell lines, especially L-929 and Hep-2, the rounding effect occurred after incubation with pp-shET for 1 h. The rounding effect was also seen in five other cultured cells (NCTC 2544, HeLa/S3, HmLu-1, CHO and BHK-21) 6-24 h after exposure to pp-shET. These round cells survived for 72 h after inoculation and formed a monolayer 24 h after changeover to a toxin-free medium. The rounding effect was observed in cells after the formation of the monolayer, but not before. It was suggested that the rounding effect was not caused by the increase in cyclic AMP in cells inoculated with pp-shET but by the cleavage of intracellular contacts.

Animals↗

Isolation of exfoliative toxin from Staphylococcus hyicus subsp. hyicus and its exfoliative activity in the piglet.

Exfoliative toxin was isolated from the sterile cell-free filtrate of 24 h culture of Staphylococcus hyicus subsp. hyicus strain P-1. The partial purification of exfoliative toxin produced by S. hyicus (shET) was performed by precipitation with 50-80% saturated ammonium sulfate, gel filtration on a Sephadex G-75 column and column chromatography on DEAE-cellulose. Partially purified shET (pp-shET) caused exfoliation in piglets at 8 to 12 h after intradermal or subcutaneous injection. However, heat-treated pp-shET did not cause exfoliation in piglets for up to 24 h after injection. On histopathological examination of the skin at 12 h after injection of pp-shET, an intraepidermal cleavage plane was shown between the stratum corneum and stratum granulosum and at the stratum granulosum.

Animals↗

Adhesion molecules on murine lymphokine-activated killer cells responsible for target cell killing: a role of CD2.

Lymphokine-activated killer (LAK) cells were induced from C57BL/6 mouse spleen cells and the effects of culture time on the expression of cell surface phenotypes and cytotoxic activity of LAK cells were determined. The expression of CD2 remarkably decreased after culture of LAK cells for 30 days, while LFA-1, a principal adhesion molecule in LAK cells, and CD3 were not changed by the culture. LAK cells cultured for 90 days completely lost CD2. In accordance with the decrease of CD2, the cytotoxic activity of LAK cells declined but a certain leven was retained even after the complete loss of CD2. The established LAK cell clones were also strongly positive for the expression of LFA-1 but negative for CD2. When the LAK cell clones were transfected with the CD2 cDNA, they started to express CD2 on their cell surface and to show greater binding ability and stronger cytotoxicity to target tumor cells. These results indicated that CD2 plays a role as an adhesion molecule responsible for target cell killing in murine LAK cells.

Animals↗

Release of esterase from murine lymphokine-activated killer cells in antibody-dependent cellular cytotoxic reaction.

Release of granule enzyme(s) (BLT esterase) in the antibody dependent lymphokine-activated killer (LAK) cell-mediated cytotoxic reaction (LAK ADCC) was studied using LAK cells induced from murine splenocytes and thymocytes, various human tumor cells and relevant monoclonal antibodies (mAbs) to the tumor cells. BLT esterase was not significantly released from LAK cells in direct LAK cell-mediated cytotoxic reactions (LAK CMC). However, cultures of LAK cells and IgG-coated target tumor cells resulted in release of the enzyme concomitantly with target cell lysis, although esterase release proceeded faster than target cell lysis. Anti-LFA-1 mAb showed an inhibitory effect on LAK CMC but not on either LAK ADCC or BLT esterase release in the ADCC. These results indicate that exocytosis of granule enzyme from LAK cells is triggered by stimulation of Fc receptor on LAK cells and that LAK CMC and LAK ADCC differ in their lytic mechanism in terms of the release of BLT esterase.

Animals↗

Establishment of mouse lymphokine-activated killer cell clones and their properties.

To assess the properties of lymphokine-activated killer (LAK) cells, we established mouse LAK cell clones from LAK cell lines induced from C57BL/6 mouse spleen cells. Although these clones expressed similar phenotypes to the parent LAK cells, Lyt-2 was expressed in a restricted portion of the clones. All clones were found to express T3 CD2 and T cell receptor (TcR) alpha beta on their cell surface. Rearrangement patterns of TcR beta were the same among the clones derived from the same parent cell line but differed in those from different cell lines as determined by using C beta 1 and J beta 2 probes. The molecules responsible for LAK-target cell binding were examined by using a monoclonal antibody (mAb) against lymphocyte function associated antigen 1 (LFA-1). This mAb (termed KBA) showed inhibitory effects on both LAK-target cell binding and cytolytic activity of LAK cell clones, indicating a principal role of LFA-1 in LAK cell clones. The magnitude of perforin mRNA expression in LAK cell clones was unrelated to their cytolytic activities.

Animals↗

Augmentation by tumor necrosis factor alpha of the systemic therapeutic effect of lymphokine-activated killer cells in adoptive immunotherapy of murine tumor.

The therapeutic effect of a combined modality of lymphokine-activated killer (LAK) cells and tumor necrosis factor alpha (TNF alpha) on MBL-2 tumor in C57BL/6 mice was studied. Murine LAK cells induced from splenocytes by interleukin 2 (IL2) could lyse MBL-2 target cells in vitro. but no enhancement of the LAK activity was found by the treatment of LAK cells with TNF alpha in vitro. However, the treatment of MBL-2 with TNF alpha enhanced the sensitivity to LAK cells. Moreover, administration of TNF alpha to mice bearing solid MBL-2 tumor led to increased tumor vascular permeability within 1 h, and resulted in the enhanced accumulation of systemically transferred LAK cells in tumor tissue. Based on these results, we treated MBL-2-bearing mice with TNF alpha and then with LAK cells 1 h later. No therapeutic effect was observed when tumor-bearing mice were treated with TNF alpha alone or LAK cells plus IL2. However, adoptive immunotherapy using LAK cells and TNF alpha had therapeutic effects, i.e., growth inhibition of tumor nodules and prolongation of survival. These results indicated that appropriately timed pretreatment of tumor-bearing mice with TNF alpha augmented the anti-tumor efficacy of LAK cells.

Animals↗

Immunocytochemical and immunochemical detection of a 32 kDa nonamelogenin and related proteins in porcine tooth germs.

Porcine tooth germ was investigated immunochemically and immunocytochemically using antibodies against a synthetic N-terminal peptide fragment from a 32 kDa nonamelogenin found in the inner (old) secretory enamel. In immunochemical preparations, these antibodies reacted to many proteins of differing molecular weights, especially to 140 kDa, 89 kDa, 56 kDa, 45 kDa, and 32 kDa proteins. Analysis of the layers of enamel suggested that the 140 kDa and/or 89 kDa proteins, both of which were found in newly formed enamel, were the parental proteins secreted by the ameloblasts, and that they were degraded to produce 32 kDa and other low molecular-weight proteins associated with progressive mineralization. In immunohistochemical preparation, immunoreactivity at the differentiation stage was detected initially over the amorphous dense material or fine fibrils around calcified globules in predentin, while the stippled material was devoid of immunoreactivity. The amorphous dense material seemed to give rise to a continuous layer of initial enamel. At the matrix formation stage, the immunoreactivity of immature enamel just beneath the putative secretory face of the Tomes' processes was intense. From the surface of the enamel matrix to a depth of about 100 microns, immunoreactivity of prism sheaths was weaker than that of enamel prisms, producing a reverse honeycomb pattern. In the enamel matrix deeper than 100 microns, immunoreactivity was weak and homogeneously distributed. The Golgi apparatus and secretory granules of the secretory ameloblasts showed immunoreactivity. These results suggest that the likely parent proteins of the 32 kDa nonamelogenin protein, i.e., the 140 kDa and/or 89 kDa proteins, play a significant role in the calcification of the enamel matrix.

Ameloblasts↗

[Surgical management of congenitally corrected transposition of the great arteries].

From 1962 to 1990, we have experienced 12 patients with congenitally corrected transposition of the great arteries (CTGA). Associated cardiac defects were present in all cases, most frequently ventricular septal defect (100%), and pulmonary stenosis (67%), Palliative procedures were done in 5, corrective operations in 6. One patient underwent corrective procedure 27 years after palliation. The hospital mortality rate was 8% (1/12), and 1 late death (8%) was seen in this series. In most cases, we approached the defect through the mitral valve, and the deLeval method was very useful in placing stitches along the trabecular septum. AV conduction disturbance could be avoided in 5 of 6 patients who underwent the closure of ventricular septal defect. Pulmonary stenosis was relieved by valvotomy and/or infundibulectomy, or implantation of an extracardiac conduit according to their anatomy. Cardiac function of systemic ventricle (morphologic right ventricle) were well preserved in the case undergoing intracardiac repair and also in the palliative cases. Careful observation is needed in these cases.

Adolescent↗

[Clinical investigation on the adjunctive method in the surgery of thoracic aortic aneurysms--comparison of the temporary bypass and partial extracorporeal bypass].

Since 1980, two different operative strategies were employed during resection to provide distal aortic perfusion by temporary bypass (Group "TB", 39 patients) or partial extracorporeal bypass (Group "PEC", 39 patients) in the operation for the thoracic descending aortic aneurysms or the dissecting aortic aneurysms with DeBakey type III. No significant differences were found in the patient population or the operative procedures between two groups. Mean bypass flow in Group "PEC" was 1850 +/- 70 (ml/min), which is significantly higher than in Group "TB" (1000 +/- 240 ml/min). However, there were no significant differences in the distal aortic pressure between two groups, which was due to administration of vasodilators. Platelet counts in Group "PEC" were significantly lower in the postoperative courses, probably caused by the use of roller pumps or suckers. The incidence of the postoperative renal dysfunction was almost the same in two groups. Cardiac functions during temporary bypass were suppressed by the aortic cross-clamping, therefore, it is necessary to evaluate the cardiac function preoperatively in employing this method. Partial extracorporeal bypass has the disadvantages of the requirement for full heparinization, but it can be indicated to almost all cases, even to the patients with poor cardiac function. It also has the advantage to maintain the distal perfusion in the unexpected intraoperative situations. The method of distal aortic perfusion should be determined by patient-related and disease-related factors.

Aged↗

[Successful surgical treatment of a case of corrected transposition in situs inversus with associated anomalies].

A 33-year-old female with corrected transposition (situs inversus) with ventricular septal defect (VSD), atrial septal defect (ASD), and pulmonary stenosis (valvular and subvalvular) was operated successfully. Closure of ASD and infracristal VSD was performed through right atrial approach. In order to get complete exposure of VSD, a part of anterior leaflet of mitral valve was detached temporally. An external conduit was interposed between the morphologic left ventricle and the main pulmonary artery to relieve pulmonary stenosis. Postoperative course was uneventful except a transient complete heart block for a day. Several technical aspects of the radical operation were discussed including VSD closure method to avoid damaging the atrioventricular conducting tissues and reconstructive procedure of morphological left ventricular outflow.

Abnormalities, Multiple↗