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Biomedical subjects

T Yokochi

Publications and source records attributed to T Yokochi.

At least 109 records · Page 6Linked to original sources

Expression of transglutaminase I in human anagen hair follicles.

The expression of the transglutaminase I in human anagen hair follicles was studied by an immunohistochemical staining. In the bulbar and suprabulbar portions of anagen hair follicles, transglutaminase I was detected on the hair cuticle and the three layers of the inner root sheath. Subsequently, the positive staining became translocated to the inner site of the outer root sheath in the middle part of the hair follicle. In the upper portion of the hair follicle transglutaminase I was detected in the internal part of the outer root sheath and the surface epidermis. Therefore, it was suggested that the expression of transglutaminase I might be closely associated with the terminal keratinization in the anagen hair follicles.

Adult↗

[A case of near total tracheal obstruction from recurrent esophageal carcinoma].

We have treated a 58-year-old man with almost complete tracheal occlusion arising as a result of recurrence of esophageal cancer. Although laser photoresection using partial cardiopulmonary bypass was desirable, neither laser nor cardiopulmonary bypass was available in our hospital. It was then decided to resect the tumor by forceps. In order to prevent bleeding from tumor during such emergency procedure, intratumoral injection of ethanol was preceded and tracheal lumen could be opened successfully. He was managed by insertion of a Dumon silicone stent seven days after the emergency. The result was satisfactory for maintaining the patency of the airway where the stent was placed. Unfortunately the patient died 113 days after the insertion of Dumon silicone stent from massive hemoptysis, which might resulted from the rupture of vessel feeding the tumor or the perforation of aorta involved by the tumor.

Carcinoma, Squamous Cell↗

Discrimination by means of pulsed-field gel electrophoresis between strains of Campylobacter jejuni Lior type 4 derived from sporadic cases and from outbreaks of infection.

The cleavage patterns of the genomic DNA in 42 strains of Campylobacter jejuni Lior type 4, obtained from sporadic cases and from outbreaks of infection were analysed by means of pulsed-field gel electrophoresis (PFGE). The cleavage of DNA with SmaI and SalI restriction enzymes showed 16 distinct fragment patterns in 20 sporadic isolates, indicating that they were heterogeneous. On the other hand, the patterns of 22 isolates derived from two outbreaks showed the same unique restriction patterns, respectively. PFGE may therefore prove useful for subclassifying strains of C. jejuni Lior type 4 and for discriminating between strains derived from sporadic cases and those derived from outbreaks of infection.

Bacterial Typing Techniques↗

A novel form of self tolerance dictated in the thymus of transgenic mice with autoreactive TCR alpha and beta chain genes.

Transgenic (TG) mice with TCR alpha and beta chain genes from a CD4-dependent auto-I-Ak reactive T cell clone were generated. H-2k TG mice had a large number of thymic and splenic CD4 T cells expressing the autoreactive TCR without manifestation of autoimmunity. The cells were not anergic, as they could respond to autologous antigen presenting cells and anti-TCR antibodies in vitro to proliferate and to produce interleukins. Various degrees of down-regulation of CD2 and CD44 was observed in TG mice, indicating the presence of a defective co-stimulatory process in TG T cells. These features indicate that the self tolerance in autoreactive TCR TG mice is due not to clonal deletion and anergy but to a novel mechanism where T cells cannot sufficiently respond to normally existing self ligand in vivo. That such an in vivo unresponsiveness of autoreactive T cells is dictated in the thymus during CD4 T cell differentiation atypical form of positive selection of autoreactive T cells was suggested by the abnormal surface expression of CD69 and HSA.

Animals↗

Localization of apoptosis (programmed cell death) in mice by administration of lipopolysaccharide.

Localization of apoptotic cells by administration of lipopolysaccharide into mice was studied by using the in situ specific labeling of fragmented DNA. This method clearly stained the nuclei of thymocytes at the cortex of the thymus. The nuclei of cells in the bone marrow and in the spleen were also positively stained. It was suggested that the cortex in the thymus is where the LPS-induced programmed cell death occurs.

Animals↗

Increased phosphodiesters in lipopolysaccharide prepared from the polymyxin B-resistant isolate of Klebsiella pneumoniae.

A polymyxin B (PXB)-resistant mutant of Klebsiella pneumoniae O3 was isolated. Lipopolysaccharide (LPS) extracted from the PXB-resistant isolate bound little PXB, although LPS from the parental strain did. The 31P nuclear magnetic resonance (NMR) spectrum of PXB-resistant type LPS showed that it contained much less of the phosphomonoesters and the pyrophosphate esters, and an increased amount of the phosphodiesters, compared to the parental type LPS. The decrease in the binding of PXB might be due to altered phosphate groups on the PXB-resistant type LPS, suggesting that it might explain the PXB-resistance of the mutant.

Drug Resistance, Microbial↗

In vivo production of heat shock protein in mouse peritoneal macrophages by administration of lipopolysaccharide.

The in vivo production of heat shock protein was studied by administration of bacterial lipopolysaccharide (LPS) into mice. Heat shock protein 70 was detected in the extract of adherent peritoneal cells from mice injected intraperitoneally with LPS by using the immunoblotting method. The expression of heat shock protein 70 was found 2 days after injection of LPS and reached its peak 4 days after injection. The intraperitoneal injection of LPS induced the expression of heat shock protein 70, whereas its subcutaneous injection did not. The in vivo production of heat shock protein 70 was inhibited by administration of LPS together with quercetin, an inhibitor of accumulation of heat shock protein 70 mRNA. Tumor necrosis factor alpha enhanced LPS-induced heat shock protein production in vivo. There was a decrease of gamma delta T cells in the peritoneal cavity of mice injected intraperitoneally with LPS. It was suggested that bacterial LPS is a stressful agent which induces the in vivo heat shock protein response, and its administration leads to the production of heat shock protein 70 in peritoneal macrophages.

Animals↗

[Chemical iodination of hormonogenic tyrosine residues of human thyroglobulin is critical for the production of anti-thyroglobulin autoantibody and for the induction of experimental autoimmune thyroiditis in mice].

There is evidence from animal models that the iodine content of thyroglobulin (Tg) may influence its antigenicity in thyroid autoimmunity. To elucidate the effect of iodination of hormonogenic sites of human Tg (hTg) on its autoantigenicity, a synthetic peptide (TB: hTg 2546-2571), containing two hormonogenic tyrosine residues of hTg, and a chemically-iodinated peptide (TB-I) were prepared. We immunized C3H/He (H-2k) mice, a high responder strain to Tg, and BALB/c (H-2d), a low responder strain, with TB or TB-I plus lipopolysaccharide. Lymph node cells from the two strains immunized with TB or TB-I proliferated in response to both TB and TB-I. Anti-Tg autoantibodies were detected in both strains when immunized with TB-I, while immunization with TB failed to produce anti-Tg antibodies. Furthermore, one of the C3H/He mice immunized with TB-I developed diffuse thyroiditis, but BALB/c mice did not. These findings indicate that the iodination of the hormonogenic tyrosine residues of hTg, in other words, the synthesis of mono- and di-iodotyrosine (MIT and DIT) residues, is necessary for the production of anti-Tg autoantibodies in high and low responder mice and for the induction of autoimmune thyroiditis in high responder mice.

Amino Acid Sequence↗

[Patterns of mediastinal and supraclavicular metastases in apical invasive lung cancer--importance of supraclavicular lymph node dissection].

Thirty-one patients with apical invasive lung cancer, who underwent surgical therapy were analyzed. In the patients with palpable nodal metastases in the supraclavicular region, the lymph nodes were dissected through a collar incision in supine position after thoracotomy. In the patients without palpable nodes, the supraclavicular nodes were dissected through the same wound and in the same position after the tumor was resected by the hook or anterior approach. N factor was N0 in eighteen patients, N1 in two patients, N2 in seven patients, and N3 in four patients. The ratio of supraclavicular metastasis was 33.3%. Patterns of mediastinal and supraclavicular metastases were classified into three types. Type I (supraclavicular type): metastasized directly to the supraclavicular nodes via the chest wall, Type II (mediastinal type): metastasized via a common route from hilum to mediastinum, Type III (mixed type): combination of Type I and Type II. Of the nine patients who had N2 or N3 disease uncovered by supraclavicular lymph node dissection, one patient was Type I, six were Type II, and two were Type III. Of the four patients with supraclavicular node metastasis, two had palpable nodes and two histological metastasis. The nodes were metastasized via the chest wall in three patients. Two patients with N3 disease are still alive without recurrence, one patient for eighty-six months and another for twenty months after the operation. Since supraclavicular lymph nodes are local and very near from involved structures of apical invasive lung cancer, dissection of these nodes will provide improved prognosis.

Adenocarcinoma↗

[Chronic empyema associated with large cell carcinoma of lung: case report with review of the literature].

A 71-year-old female was seen with a complaint of chest pain and cough, and a history of tuberculous pleurisy and artificial pneumothorax 40 years ago. The diagnosis of empyema with carcinoma was made by chest X-ray and CT scans. The examination of lung function showed a restrictive disorder. The value of the predicted postoperative FEV1 0.75 l encouraged to perform operation. A left pleuropneumonectomy and combined resections of the invasive portion of the pericardium and left atrium was performed. Histological examination revealed large cell carcinoma of lung (pT 4 N 1 M 0). The literatures are reviewed concerning the thoracic malignant tumor arising in chronic empyema cavity on Japanese cases.

Aged↗

Pulsed-field gel electrophoretic analysis of Campylobacter jejuni DNA for use in epidemiological studies.

The cleavage patterns of the genomic DNA of 42 clinical isolates of Campylobacter jejuni determined by pulsed-field gel electrophoresis (PFGE) were compared with their Lior and TCK serotypes. The fragment patterns of DNA obtained with SalI and SmaI restriction enzymes did not always accord with the corresponding serotypes but strains of the same serotype could be further divided into subtypes by their cleavage patterns. This PFGE method may prove useful for subclassifying C. jejuni.

Campylobacter jejuni↗

A common T-cell epitope between human thyroglobulin and human thyroid peroxidase is related to murine experimental autoimmune thyroiditis.

We have investigated functional common T-cell epitopes between human thyroglobulin (hTg) and human thyroid peroxidase (hTPO) in mice. Four hTg peptides, Tg-P1, Tg-P2, Tg-P3 and Tg-P4, in which 5 amino acid residues are identical to those of hTPO, and 1 hTPO peptide, TPO-P4 relevant to Tg-P4, were prepared. Among these peptides, only Tg-P4 (residues 2730-2743) and TPO-P4 (residues 118-131) were highly antigenic and both peptides shared the common T-cell epitope. In addition, when the spleen cells from mice immunized with mouse Tg (mTg) were restimulated in vitro by Tg-P4 or TPO-P4 as well as by mTg, these cells transferred thyroiditis to naive recipient mice. These findings indicate that this common T-cell epitope between hTg and hTPO is immunogenic and related to the development of murine experimental autoimmune thyroiditis.

Amino Acid Sequence↗

Production of a monoclonal antibody inhibiting the killer activity.

We established the hybridoma producing the monoclonal antibody (mAb) 3C3 by immunizing rats with mouse natural killer (NK)-like cells. The 3C3 mAb seemed to react mainly with T cells and T-lineage cell lines. The 3C3 antigen also seemed to be coincidentally expressed on a part of asialo GM1+ cells from nude mice, suggesting its expression on NK cells. Treatment of effector cells with 3C3 mAb markedly inhibited the killer activity against RL male-1 cells, but less so against YAC-1 cells, in vitro. It is suggested that the cell surface molecule defined by 3C3 mAb was closely associated with the killer activity of T cells and NK cells.

Animals↗

In vivo induction of apoptosis (programmed cell death) in mouse thymus by administration of lipopolysaccharide.

In vivo administration of bacterial lipopolysaccharide to mice induced DNA fragmentation in the thymus. Fragmented DNA was confirmed by agarose gel electrophoresis and laser flow cytometry. DNA fragmentation was predominantly detected in the thymus of young mice, while it was undetectable in the spleen, bone marrow, and lymph nodes. DNA fragmentation in the thymus was roughly dependent on the dose of lipopolysaccharide injected and reached the peak about 18 h after the injection. The addition of lipopolysaccharide to in vitro cultures of thymocytes did not cause DNA fragmentation, suggesting that lipopolysaccharide was unable to induce apoptosis of thymocytes directly. The injection of lipopolysaccharide induced no significant DNA fragmentation in adrenalectomized mice. The injection of anti-tumor necrosis factor alpha antibody together with lipopolysaccharide partially inhibited the appearance of DNA fragmentation in the thymus. On the basis of the fact that DNA fragmentation is one of the characteristics typical in apoptotic cell death, it was suggested that lipopolysaccharide could induce apoptosis in the mouse thymus in vivo. This apoptosis in the thymus might be mediated mainly by the adrenal hormones, but it is likely that tumor necrosis factor alpha might also participate in it.

Adrenalectomy↗

Genetic analysis of double-strand break repair in Escherichia coli.

We had reported that a double-strand gap (ca. 300 bp long) in a duplex DNA is repaired through gene conversion copying a homologous duplex in a recB21 recC22 sbcA23 strain of Escherichia coli, as predicted on the basis of the double-strand break repair models. We have now examined various mutants for this repair capacity. (i) The recE159 mutation abolishes the reaction in the recB21C22 sbcA23 background. This result is consistent with the hypothesis that exonuclease VIII exposes a 3'-ended single strand from a double-strand break. (ii) Two recA alleles, including a complete deletion, fail to block the repair in this recBC sbcA background. (iii) Mutations in two more SOS-inducible genes, recN and recQ, do not decrease the repair. In addition, a lexA (Ind-) mutation, which blocks SOS induction, does not block the reaction. (iv) The recJ, recF, recO, and recR gene functions are nonessential in this background. (v) The RecBCD enzyme does not abolish the gap repair. We then examined genetic backgrounds other than recBC sbcA, in which the RecE pathway is not active. We failed to detect the double-strand gap repair in a rec+, a recA1, or a recB21 C22 strain, nor did we find the gap repair activity in a recD mutant or in a recB21 C22 sbcB15 sbcC201 mutant. We also failed to detect conservative repair of a simple double-strand break, which was made by restriction cleavage of an inserted linker oligonucleotide, in these backgrounds. We conclude that the RecBCD, RecBCD-, and RecF pathways cannot promote conservative double-strand break repair as the RecE and lambda Red pathways can.

Bacterial Proteins↗

Experimental murine model for autoimmune myocarditis using Klebsiella pneumoniae O3 lipopolysaccharide as a potent immunological adjuvant.

Experimental autoimmune myocarditis could be produced in mice by repeated injection of syngeneic heart extract together with Klebsiella pneumoniae O3 lipopolysaccharide (KO3 LPS) as a powerful adjuvant. Histological changes in the cardiac lesions were characterized by infiltration with mononuclear cells in the myocardium, degeneration and loss of myocardial fibers, and replacement of granulation tissues. No such cardiac lesions were produced in mice receiving injections of heart extract alone or KO3 LPS alone. Development of the autoantibody and the delayed type-hypersensitivity (DTH) against syngeneic heart extract was found in mice immunized repeatedly with the mixture of heart extract and KO3 LPS. Moreover, definite cardiac lesions were produced in normal recipient mice by transfer of sensitized spleen cells from hyperimmunized mice. Therefore, it was suggested that those cardiac lesions were caused by the autoimmune mechanism. Our methodology provided a new experimental murine model for autoimmune myocarditis.

Adjuvants, Immunologic↗