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Biomedical subjects

T Yanagawa

Publications and source records attributed to T Yanagawa.

At least 109 records · Page 6Linked to original sources

Relationship between degree of polymerization of resin composite and bond strength to Gluma-treated dentin.

The purpose of the present study was to investigate the relationship between shear bond strength (SBS) to dentin and degree of polymerization of resin adjacent to the coupling interface. A hybrid-type resin composite was polymerized on Gluma-treated dentin at thicknesses of 1, 2, 3 and 5 mm, respectively, with seven different light activation times (LAT) from 3 through 180 seconds. SBS of the specimens was determined 10 minutes after the end of light activation. The degree of polymerization of resin close to the dentin interface was determined by Wallace Indentation Depth (WID) of specimens polymerized under the same conditions as the SBS samples, however, separated from the dentin surface by a thin glass plate. Consistent relationships were found for SBS vs. LAT and WID vs. LAT by regression analyses (y = A+B/x). There was a strong linear correlation between SBS and WID (r = -0.93), indicating that the early bond strength to Gluma-treated dentin is a function of mechanical characteristics of resin close to the bonding interface.

Composite Resins↗

[Minimum required number of anesthetists for general hospitals (41-1300 beds) in Japan--analysis of questionnaire, 1992].

BACKGROUND: We have elucidated the deficit of anesthetists in general hospitals excluding university hospitals by assessing the results of questionnaires from 204 institutions in Japan. METHODS: Answers to the questionnaire were computed in average, maximum, and minimum values, using MS-Excel soft ware for statistical analysis. RESULTS: The 204 hospitals were classified into 4 groups; G-1(46)-more than 640 beds, G-2(53)-more than 500 beds, G-3(53)-more than 360 beds, and G-4(52)-less than 359 beds, respectively (parenthesis indicate hospital numbers). The number of cases of anesthesia performed by anesthesiologists were 2055(G-1), 1516(G-2), 1177(G-3) and 959(G-4), respectively. The number of anesthetists per operating table were as follows; 0.62(G-1), 0.62(G-2), 0.58(G-3) and 0.74(G-4), but remarkably low compared to the number of operating theater nurses: 5.49(G-1), 2.96(G-2), 2.82(G-3) and 3.07(G-4). Moreover, the number of emergency cases were as follows; 235(G-1), 187(G-2), 134(G-3) and 125(G-4), respectively. In prolonged surgery over 6 hours, patients were anesthetized with an exchange system or two anesthetists system in 74% of the institutions in G-1. Also, 28-50% of anesthetists in the 4 groups were concerned with intensive care medicine and 0.94-1.54 anesthetists worked in pain clinics with combined operation-theater tasks 1.37-2.49 days per week. In G-1-G-4 institutions, we found that anesthesia cases per year were equivalent to 5 times their bed numbers. CONCLUSION: We concluded that the number of anesthetists should be at least 50% of that of operation-theater nurses. Without increasing anesthesiologists, we cannot expect sophisticated medical care in the 21st century.

Anesthesiology↗

Four novel gene mutations in five Japanese male patients with neonatal or late onset OTC deficiency: application of PCR-single-strand conformation polymorphisms for all exons and adjacent introns [corrected].

Ornithine transcarbamylase deficiency (OTC), the most common inborn error of the urea cycle, shows an X-linked inheritance with frequent new mutations. Southern blots reveal only a small percent of the mutation, but amplification of cDNA or genomic DNA using the polymerase chain reaction (PCR) followed by DNA sequencing, has contributed greatly to overcoming this difficulty. Problems remaining are the limited availability of fresh liver samples for preparation of intact mRNA in the former case, and there are primer sequences for PCR for only some exons in the latter case. Here, we report the structures of intron sequences which are long enough to analyze all exons and adjacent introns of the OTC gene using PCR and PCR single-strand conformation polymorphisms (PCR-SSCP). We carried out a DNA analysis of findings in five Japanese male patients with neonatal or late onset form. Five patients had mutations in the protein coding region. C to G (S192R), A to T (D196V), A to G (T264A), T to C (M268T), and C to T (R277W) substitutions. The first four of these were novel missense mutations and the presence of the mutation was confirmed in the corresponding families.

Asian People↗

A comparative study on T cell receptor V beta gene usages: spleen cells from the non-obese diabetic (NOD) mouse and its non-diabetic sister strain, the ILI mouse, and infiltrating T cells into pancreata of NOD mice.

We analyzed the usage of T cell receptor (TCR) V beta genes of spleen cells of NOD mice in comparison with those of its non-diabetic sister strain ILI mice which show no insulitis and (ILI x NOD)F1 mice. The quantitative polymerase chain reaction (PCR) method revealed that PCR V beta repertoires of these mice are indistinguishable. This is consistent with our previous observation that ILI mice share the same H-2 class II genes with NOD mice. PCR method also revealed that the V beta transcript of infiltrating T cells into pancreas of NOD mice was not restricted but was rather diverse. The role of TCR repertoire in the development of insulitis was discussed.

Animals↗

Body surface distribution of abnormally low QRST areas in patients with Wolff-Parkinson-White syndrome. Evidence for continuation of repolarization abnormalities before and after catheter ablation.

BACKGROUND: Whether the Wolff-Parkinson-White syndrome (WPW) is associated with repolarization abnormalities is controversial. The QRST isointegral map (I-map) is theoretically independent of the activation sequence and dependent on repolarization properties. There have been no reports concerning the effects of radiofrequency (RF) catheter ablation of accessory pathway (AP) on repolarization properties analyzed by I-mapping. METHODS AND RESULTS: I-maps were constructed from data recorded in 38 patients with WPW to investigate repolarization properties and their body surface distribution in a physiological state, without pharmacological influences, and in 13 ablated patients to elucidate the effects of RF ablation on repolarization properties. Patients were divided into three groups: group A, 15 patients with type A WPW (left-sided AP); group B, 10 patients with type B (right-sided AP); and group C, 13 patients who were successfully ablated. Group C consisted of three subgroups: subgroup CA, 7 patients with type A WPW; subgroup CB, 3 patients with type B WPW; and subgroup CC, 3 patients with concealed WPW. Controls consisted of 608 normals. Although I-maps of WPW were highly (r = .87) correlated with the mean normal I-map, the location of the minimum in groups A and B differed significantly from that in normals. The minimum was located over the upper right anterior chest in normal subjects, over the back in 82% of 22 patients with type A WPW including ablated patients (groups A+CA), and over the mid to lower right anterior chest in 62% of 13 patients with type B WPW including ablated patients (groups B+CB). Groups A+CA and B+CB had an abnormally low QRST area ("-2SD area") over the back and right anterior chest, respectively. The abnormally located minimum and the "-2SD area" were present in 7 of 10 ablated patients with manifest WPW (groups CA+CB). After RF ablation, the distribution of the minimum, initially abnormal, became normal over a period of days or weeks, and the "-2SD area" disappeared over 1 week in all 7 patients. Correlation coefficients between I-maps and the mean normal I-map increased after RF ablation. CONCLUSIONS: (1) WPW is often associated with abnormalities in repolarization properties. (2) Repolarization abnormalities were located over the back in type A WPW and over the right mid to lower chest in type B WPW: (3) The abnormalities remain immediately after RF ablation and gradually normalize. These findings support the concept that ST-T abnormalities in 12-lead ECGs following RF ablation are attributable to "cardiac memory."

Adolescent↗

Human histocompatibility leukocyte antigen-DQA1*0501 allele associated with genetic susceptibility to Graves' disease in a Caucasian population.

Graves' disease (GD) is an autoimmune disease of the thyroid gland. Genes of, or closely associated to, the HLA complex are assumed to contribute to the genetic predisposition to GD. We have previously reported an increased frequency of HLA-DR3/DQ2 in Caucasian patients with GD, and recently the importance of Dw24 encoded by DRB3 gene has been suggested. To further investigate the associations of GD and these genes, 94 unrelated patients with GD and 75 control subjects were typed for HLA-DRB3, -DRB1, -DQA1, and -DQB1, using sequence-specific oligonucleotide probes to analyze polymerase chain reaction amplified DNA (PCR-SSO). Three findings emerged from these studies. 1) The frequency of subjects positive for DQA1*0501 (GD, 73.4% vs. control 42.7%, P = 0.0001, Pc < 0.001, RR = 3.71) was significantly increased among patients. The frequency of DR3 (GD, 34.0% vs. control 17.3%, P = 0.0146, RR = 2.46), which is in tight linkage disequilibrium with DQA1*0501, was also increased; however, it was not significant when the P value was corrected for the number of antigens tested. Neither DQB1 nor DRB3 alleles were significantly increased in frequency. 2) After exclusion of DR3-positive subjects, DQA1*0501 was still significantly increased (GD, 59.7% vs. control 30.6%, P = 0.0012, Pc < 0.01, RR = 3.35) among patients. 3) The distributions of Dw24 and Dw25,26 (Dw25 or Dw26) did not differ between patients and controls on either DR3 positive or negative groups. These findings suggest that DQA1*0501, or a closely associated unknown gene, confers susceptibility to GD, while Dw24 is not directly involved. The importance of DR3, however, remains to be elucidated, because of the fixed linkage with DQA1*0501.

Alleles↗

Suppression of development of diabetes in NOD mice by lactate dehydrogenase virus infection.

It has been reported that lactate dehydrogenase virus (LDV) selectively infects a subpopulation of macrophages, thereby affecting the immune system. We studied the effects of LDV infection on the development of diabetes in non-obese diabetic (NOD) mice. Five-week-old female NOD mice were infected with LDV (10(8) ID50/mouse) and observed until 23 weeks of age. None of the 21-LDV-infected mice developed diabetes, whereas 10/14 (71.4%) uninfected mice did. Although the subpopulations of T cells and the percentage of Mac1-positive cells in the NOD murine spleen and the number of harvested peritoneal macrophages were unaffected by LDV infection, the proportions of Ia-positive peritoneal macrophages were significantly decreased in LDV-infected compared with uninfected mice (1.1 +/- 0.2%, 6.5 +/- 2.9%; P < 0.01). In LDV-infected NOD mice, insulitis of the same grade as that seen in uninfected NOD mice was observed. In another experiment, 3, 5, 10 or 16-week-old female NOD mice were infected with LDV. None of the mice infected with LDV at 3, 5 or 10 weeks of age developed diabetes and only one of six infected at 16 weeks of age did. These findings indicate that LDV infection suppresses the development of diabetes in female NOD mice by reducing the capacity of Ia-positive macrophages, and suggest that the development of human type 1 diabetes may be suppressed by certain viral infections.

Animals↗

Heparan sulfate as a mediator of herpes simplex virus binding to basement membrane.

Explants of human lip and oral mucosa were infected with herpes simplex virus (HSV) in vitro and the expression of viral antigen was investigated by immunofluorescent antibody staining. Viral antigen was demonstrated in the cells of basal cell layer and lower prickle cell layers. Moreover, an accumulation of viral antigen in the epithelial-mesenchymal junction was observed. To examine the possibility that the basement membrane has an affinity for HSV, the interaction between HSV and major basement membrane components including type IV collagen, laminin, fibronectin, and heparan sulfate was investigated. When tested by a plaque-reduction assay, only heparan sulfate inhibited HSV plaque formation by competing for the virus adsorption to HEp-2 cells. The inhibitory effects of heparan sulfate and heparin were not affected by pre-incubation of these glycosaminoglycans with antithrombin III, whereas de-N-sulfation resulted in a significant reduction of their inhibitory activity. These findings suggest that heparan sulfate is involved in the binding of HSV to the basement membrane and that N-sulfated glucosamine residues of heparan sulfate are essential for HSV binding. The basement membrane may act as a reservoir of HSV in muco-cutaneous tissues.

Antigens, Viral↗

Effect of dibutyryl cyclic adenosine 3',5'-monophosphate on morphological features and biological markers of human salivary myoepithelial cell line in culture.

We have found the emergence of myoepithelial cells (HSG-AZA1) in neoplastic human salivary intercalated duct cell line HSG in culture after treatment with 5-azacytidine. When HSG-ZAZ1 cells were cultured in the presence of N6,O2-dibutyryl cyclic adenosine 3',5'-monophosphate (dB-cAMP), they formed long cytoplasmic processes which were densely packed with ample microfibrils in addition to microtubule bundles. The expression of neuron-specific enolase, synaptophysin, and catecholamine as well as neurofilaments in the treated HSG-AZA1 cells was found by the immunofluorescence staining technique, immunoblotting, immunoelectron microscopy, or catecholamine fluorescence. Both the anchorage-independent and anchorage-dependent growths of HSG-AZA1 cells were suppressed in the presence of dB-cAMP. After the removal of dB-cAMP from the culture, the treated cells returned rapidly to the phenotype and growth rate of the untreated cells. These findings indicate that reversible differentiation into the neuron-like cells of HSG-AZA1 cells occurs in growth medium containing dB-cAMP.

Analysis of Variance↗

Enhanced replication of herpes simplex virus by hexamethylene bisacetamide.

Hexamethylene bisacetamide (HMBA) is a potent inducer of differentiation of tumor cells. The effect of HMBA on cell growth and replication of herpes simplex virus (HSV) was investigated in HEp-2 epidermal cells, IMR-32 neuronal cells, K562 myeloid cells, Daudi Burkitt lymphoma cells, and CCRF-CEM T-lymphoid cells. The growth of HEp-2 and IMR-32 cells was not affected by HMBA at concentrations from 0.5 through 2 mM. The growth of K562, Daudi, and CCRF-CEM cells was inhibited by HMBA at concentrations from 1 through 5 mM. When HSV-infected cells were incubated with 0.5 through 5 mM HMBA, a dose-dependent increase in virus yield was observed in HEp-2 and IMR-32 cells, but not in the other cell lines. These findings indicate that HMBA enhances the replication of HSV in epidermal and neuronal cells and that HMBA therapy may be responsible for the development of herpetic lesions.

Acetamides↗

Herpes simplex virus type 1 and type 2 infection in human oral mucosa in culture.

To examine the sensitivity of human oral mucosa to herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infection, human gingival mucosa explants were infected with either HSV-1 or HSV-2 in vitro and the expression of virus specific antigen was examined by the immunofluorescent antibody technique. HSV-2 antigen was found in the basement membrane, basal cell layer and lower prickle cell layer. This finding was consistent with the HSV-1 infection. Electron microscopic study revealed the presence of nucleocapsids and enveloped virus particles in the basal cells of HSV-2-infected organ cultures. These findings indicate that human gingival mucosa is sensitive to infection with HSV-2, as well as HSV-1, and that the virus may replicate in the undifferentiated epithelial cells of mucosal epithelium.

Adolescent↗

The suppressive effect of anti-asialo GM1 antibody on low-dose streptozotocin-induced diabetes in CD-1 mice.

To elucidate the role of natural killer (NK) cells in the pathogenesis of diabetes in streptozotocin-induced diabetes, we examined whether treatment with anti-asialo GM1 antibody prevents the occurrence of diabetes in CD-1 mouse model. Anti-asialo GM1 antibody was injected intraperitoneally 2-3 times a week starting three days before the first streptozotocin injection. In controls, rabbit immunoglobulin or saline was injected instead of anti-asialo GM1 antibody. Three of twelve anti-asialo GM1 antibody-treated mice developed diabetes, however eight of eight (100%) rabbit immunoglobulin injected mice and 20 of 23 saline-injected mice developed diabetes. The incidence of diabetes in the anti-asialo GM1 antibody-injected group was significantly higher than in the two control groups (p less than 0.01, p less than 0.01, respectively). The NK-cell activities of spleen cells from anti-asialo GM1 antibody-treated mice were significantly lower than in control mice. Flow-cytometry analysis demonstrated that anti-asialo GM1 antibody-positive cells had disappeared from spleens of anti-asialo GM1 antibody-injected mice but no suppression of T-lymphocytes could be demonstrated. These results suggest that NK cells play a role in the pathogenesis of streptozotocin-induced diabetes in CD-1 mice.

Animals↗

Anti-asialo GM1 antibody suppression of cyclophosphamide-induced diabetes in NOD mice.

To elucidate the role of natural killer (NK) cells in the pathogenesis of diabetes in the non-obese diabetic (NOD) mouse, we examined whether or not cyclophosphamide-induced diabetes occurs in NOD mice intraperitoneally (i.p.) injected with anti-asialo GM1 antibody. Two weeks after a single intraperitoneal injection of cyclophosphamide, none of the 24 NOD mice which had previously been treated with antiasialo GM1 antibody, 2-3 times per week for either 2 or 3 weeks, had developed indications of diabetes such as glycosuria or a high plasma glucose level. On the other hand, signs of diabetes were found in 10 of 24 control NOD mice injected with normal rabbit Ig instead of anti-asialo GM1 antibody (p less than 0.01). The NK cell activities of spleen cells from anti-asialo GM1 antibody-treated mice were significantly lower than those of control mice (p less than 0.01). Flowcytometry analysis demonstrated that anti-asialo GM1 antibody-positive cells had disappeared from the spleens of anti-asialo GM1 antibody-injected mice but no suppression of CD8+ and CD4+ cells could be demonstrated. These observations suggest that NK cells are involved in the development of diabetes in NOD mice.

Animals↗

Effect of hexamethylene bisacetamide and cyclosporin A on recovery of herpes simplex virus type 2 from the in vitro model of latency in a human neuroblastoma cell line.

The goal of the present work was to examine whether hexamethylene bisacetamide (HMBA) and cyclosporin A affect the recovery of herpes simplex virus type 2 (HSV-2) from an in vitro model of HSV-2 latency in human neuroblastoma cell line IMR-32. IMR-32 cells were infected with HSV-2 at a multiplicity of infection of 0.1 plaque-forming units/cell and were cultured at 40 degrees C for 14 days, resulting in the establishment of a model of HSV-2 latency in IMR-32 cells. When the cultivation temperature was shifted down from 40 to 37 degrees C, recovery of virus growth began to occur after an incubation period of 2 days. During the time of shift-down of the incubation temperature, the latently infected cells were further cultured at 37 degrees C in the presence or absence of 5 mM HMBA or 0.5 micrograms/ml cyclosporin A, which does not affect stability of HSV-2 nor proliferation of IMR-32 cells. Consequently, the rate of HSV-2 recovery from the latently infected cells cultured in the presence of 5 mM HMBA was significantly increased, as compared with the untreated controls. In addition, the DNA methylation level of the latently infected IMR-32 cells cultured in the presence of HMBA was significantly decreased when compared to the level in the untreated controls. On the other hand, the cultivation of the latently infected cells in the presence of 0.5 micrograms/ml cyclosporin A resulted in a significant decrease in the rate of HSV-2 recovery. These findings indicate that the recovery of HSV-2 from the model of latency in IMR-32 cells is enhanced by HMBA treatment, which induces a significant decrease of total genomic DNA methylation level, and is inhibited by cyclosporin A treatment.

Acetamides↗

Induction of cells with phenotypic features of neuronal cells by treatment with dibutyryl cyclic adenosine 3',5'-monophosphate in a human parotid gland adenocarcinoma cell line in culture.

A human parotid gland adenocarcinoma cell line, with an intercalated duct cell phenotype of the salivary gland and expression of vasoactive intestinal polypeptide and amylase, was cultivated in the presence of dibutyryl cyclic adenosine 3',5'-monophosphate (dB-cAMP). Morphological changes occurred; cells formed long cytoplasmic processes densely packed with ample microfibrils, as well as microtubules, and grew in a netlike appearance. In addition, it has been found by the immunofluorescence staining technique, immunoblotting, or immunoelectron microscopy that the cells treated with dB-cAMP express neurofilaments, neuron-specific enolase, synaptophysin, and HNK-1 antigen, as well as the alpha- and beta-chains of tubulin, whereas these antigens are not detected in untreated cells. The expression of vasoactive intestinal polypeptide detected diffusely in the cytoplasm of untreated cells was restricted to the cell membranes during the cultivation of cells in the presence of dB-cAMP, while expression of amylase persisted in the treated cells in a fashion similar to that in untreated cells. Moreover, both anchorage-independent and anchorage-dependent growth of the cells was markedly suppressed in the presence of dB-cAMP. After removal of dB-cAMP from the culture, the treated cells returned rapidly to the phenotype and growth rate of the untreated cells. These findings indicate that reversible conversion into cells with phenotypic features of neuronal cells of a human parotid adenocarcinoma cell line occurs in growth medium containing dB-cAMP.

Adenocarcinoma↗

Cytophagic histiocytic panniculitis evolving into total lipodystrophy.

A 15-year-old boy had persistent fever with severe neutropenia, thrombocytopenia, coagulation disorder, and marked elevation of lactate dehydrogenase values. A diagnosis of cytophagic histiocytic panniculitis was made after repeated skin biopsies. Three years after onset, he gradually lost 20 kg in body weight, and both skin and bone marrow specimens revealed degenerative changes of fatty tissue without any inflammatory cells. These findings suggest that total lipodystrophy syndrome results from the inflammatory destructive process of adipose tissue. To our knowledge, our report is the first to show, in a series of histologic studies, that an inflammatory destructive process may be involved in some cases of total lipodystrophy syndrome.

Adolescent↗

Coexpression of intermediate-sized filaments in sialadenoma papilliferum and other salivary gland neoplasms.

The neoplastic cells present in a sialadenoma pappiliferum were found by immunoperoxidase method and immunofluorescent staining technique to co-express 3 different types of intermediate-sized filaments (IFs) defined by monoclonal antibodies to cytokeratin, vimentin and desmin. When other salivary gland tumors such as 18 pleomorphic adenomas, 15 adenolymphomas, 2 oxyphilic adenomas, 7 mucoepidermoid tumors, 5 acinic cell tumors, 8 adenoid cystic carcinomas and 6 adenocarcinomas were examined immunohistochemically for the expression of IFs, no tumors with all 3 types of IFs observed in sialadenoma papilliferum were found.

Adenocarcinoma↗