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E Yamaguchi

Publications and source records attributed to E Yamaguchi.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Research trends in molecular genetics of respiratory medicine].

In order to identify necessary or susceptibility genes of respiratory diseases, molecular genetic approaches have been chosen more frequently than before because a tremendous number of anonymous markers over the human genome are now available. However, conventional linkage analysis such as the maximum likelihood method and affected sib-pair analysis have limitations mainly due to heterogeneity of disease genes. Association studies have more power to detect susceptibility genes, however, they tend to yield more false positive results than linkage studies unless corrected for multiple observations. There are some new methods potentially applicable to a genome-wide search for candidate genes. Each method has advantages and disadvantages. Reverse genetics is promising but destined to return to regular biochemical, physiological, and clinical approaches of respiratory medicine.

Disease Susceptibility↗
PubMed1996

[Comparative study on the efficacy of ritipenem acoxil and cefotiam hexetil in chronic lower respiratory tract infections by the double-blind method].

To objectively evaluate the efficacy, safety and usefulness of the newly developed penem oral antibiotic, ritipenem acoxil (RIPM-AC), against chronic lower respiratory tract infections, we conducted a multi-center double-blind comparative study using cefotiam hexetil (CTM-HE) as a control drug. RIPM-AC was orally administered at 200 mg, and CTM-HE at 400 mg, t.i.d. for 14 days, in principle. The results were as follows: The total number of patients enrolled in this trial was 202, of which 151 cases (RIPM-AC group: 75, CTM-HE group: 76) were evaluable for clinical efficacy. 1. The clinical efficacy rates (excellent+good) were 85.3% (64/75) in the RIPM-AC group and 80.3% (61/76) in the CTM-HE group. There was no significant difference between the two groups, hence the clinical equivalency of RIPM-AC to CTM-HE was demonstrated. 2. In the patients enrolled in the evaluation of clinical efficacy, the eradication rates of the causative organisms were 50.0% (13/26) in the RIPM-AC group and 75.0% (18/24) in the CTM-HE group, with no significant difference between the two groups. 3. Side effects were noted in 10 cases (11.0%) of the RIPM-AC group and 10 cases (10.9%) of the CTM-HE group. Abnormal laboratory test findings were observed in 8 cases(9.5%) of the RIPM-AC group and in 14 cases (16.7%) of the CTM-HE group. There were no significant differences between the two groups in the incidence of side effects and abnormal laboratory test findings. In the safety evaluation, RIPM-AC was judged to be safe in 73 cases (80.2%) and CTM-HE in 71 cases (77.2%), with no significant difference. 4. The usefulness rates (markedly useful+useful) were 79.5% (62/78) in the RIPM-AC group and 76.9% (60/78) in the CTM-HE group. There was no significant difference between the two groups. Since RIPM-AC showed clinical efficacy similar to those of CTM-HE and posed no particular safety problems, it is expected to be a useful antibiotic for the treatment of chronic lower respiratory tract infections.

Adult↗
PubMed1995

Cloning of the Candida glabrata TRP1 and HIS3 genes, and construction of their disruptant strains by sequential integrative transformation.

The Candida glabrata (Cg) TRP1 and HIS3 genes have been isolated by complementation of the Saccharomyces cerevisiae (Sc) trp1 and his3 mutants, respectively. Cg TRP1 encodes a polypeptide of 217 amino acids (aa), whose aa sequence is 58% identical to that of Sc TRP1. Cg HIS3 encodes a polypeptide of 210 aa, whose aa sequence is 73% identical to that of the Sc HIS3. Both Cg TRP1 and HIS3 were disrupted by sequential integrative transformation where the Sc URA3 was used as a selection marker for transformation. The resulting auxotrophic strain of his3- and trp1- was used to examine the ability of the Sc genes to complement the Cg mutations; Sc HIS3 and TRP1 complemented the Cg his3- and trp1- mutations, respectively.

Aldose-Ketose Isomerases↗
PubMed1995

Characterization of chitin synthase 2 of Saccharomyces cerevisiae. Implication of two highly conserved domains as possible catalytic sites.

Chitin synthase 2 of Saccharomyces cerevisiae was characterized by means of site-directed mutagenesis and subsequent expression of the mutant enzymes in yeast cells. Chitin synthase 2 shares a region whose sequence is highly conserved in all chitin synthases. Substitutions of conserved amino acids in this region with alanine (alanine scanning) identified two domains in which any conserved amino acid could not be replaced by alanine to retain enzyme activity. These two domains contained unique sequences, Glu561-Asp562-Arg563 and Gln601-Arg602-Arg603-Arg604-Trp605, that were conserved in all types of chitin synthases. Glu561 or arginine at 563, 602, and 603 could be substituted by glutamic acid and lysine, respectively, without significant loss of enzyme activity. However, even conservative substitutions of Asp562 with glutamic acid, Gln601 with asparagine, Arg604 with lysine, or Trp605 with tyrosine drastically decreased the activity, but did not affect apparent Km values for the substrate significantly. In addition to these amino acids, Asp441 was also found in all chitin synthase. The mutant harboring a glutamic acid substitution for Asp441 severely lost activity, but it showed a similar apparent Km value for the substrate. Amounts of the mutant enzymes in total membranes were more or less the same as found in the wild type. Furthermore, Asp441, Asp562, Gln601, Arg604, and Trp605 are completely conserved in other proteins possessing N-acetylglucosaminyltransferase activity such as NodC proteins of Rhizobium bacterias. These results suggest that Asp441, Asp562, Gln601, Arg604, and Trp605 are located in the active pocket and that they function as the catalytic residues of the enzyme.

Amino Acid Sequence↗
PubMed1995

A follow-up study of patients with cervical cancer after resection, with special emphasis on the incidence of second primary cancers.

The causes of death in long-term survivors after resection of cervical cancer were investigated in a follow-up study of 375 women, focusing especially on the postoperative development of second primary cancers. The 5- and 10-year overall survival rates were 75.0 and 66.0%, respectively, in cases that showed frank invasion, 94.7 and 92.8%, respectively, in those showing microinvasion, and 96.2 and 96.2% respectively, in those showing carcinoma in situ. Multivariate analysis identified patient age and cancer stage at the time of diagnosis as separate factors prognostic for overall survival. During the observation period, 10 patients developed a second primary cancer, but no significantly elevated risk of developing a second primary cancer was demonstrated. However, during the same period, 20 patients also died of noncancerous disease, 9 of this number succumbing to acute myocardial infarction and/or heart failure. These results suggest that patients with cervical cancer may not have an increased risk of developing second primary cancer. It is felt that continued follow-up of long-term cervical cancer survivors should be pursued in order to prevent or arrest the development of noncancerous disease and/or second primary cancer, so that increased prolongation of survival can be achieved.

Adult↗
PubMed1995

Association between high serum total IgE levels and D11S97 on chromosome 11q13 in Japanese subjects.

The genetic linkage of atopy to chromosome 11q13 through maternally derived alleles has been previously reported. Linkage analysis in Japanese families did not confirm the existence of a major gene for atopy at this locus under the model of autosomal dominant inheritance. However, we observed a significant association between serum total IgE levels and genetic markers at this locus both in 14 Japanese atopic families and in 120 unrelated Japanese subjects. We detected eight alleles at the D11S97 locus and eight alleles in the CA/GT repeat region in the fifth intron of the Fc epsilon RI beta gene. A significantly increased frequency of the D11S97/PstI 0.96 kb allele was observed in the chromosomes of the subjects with high serum total IgE levels both in the family study (p < 0.001) and in the population study (p < 0.05). However, multipoint linkage analysis again did not show any evidence for the existence of a major gene regulating atopy on chromosome 11q13 with location scores to -35 under the model of maternal inheritance. Evidence against linkage was confirmed by the non-parametric linkage analysis, using the affected pedigree member method. Also, there was no substitution of isoleucine for leucine in the fourth transmembrane domain of Fc epsilon RI beta (Leu181), which was reported to be responsible for a subset of atopy in the British population. Therefore, the association of serum total IgE levels with chromosome 11q13 indicates that a gene or genes at this locus may contribute to the expression of high IgE levels in the Japanese population as well as in the British population, but the heterogeneity of the genetic regulation of serum total IgE levels is evident between the two populations.

Adolescent↗
PubMed1995

Beta 2 adrenergic receptor gene restriction fragment length polymorphism and bronchial asthma.

BACKGROUND: Beta 2 adrenergic dysfunction may be one of the underlying mechanisms responsible for atopy and bronchial asthma. The gene encoding the human beta 2 adrenergic receptor (beta 2ADR) has recently been isolated and sequenced. In addition, a two allele polymorphism of this receptor gene has been identified in white people. A study was carried out to determine whether this polymorphism is functionally important and has any relation to airways responsiveness, atopy, or asthma. METHODS: The subjects studied were 58 family members of four patients with atopic asthma. Restriction fragment length polymorphism (RFLP) with Ban-I digestion of the beta 2ADR gene was detected by a specific DNA probe with Southern blot analysis. Airways responses to inhaled methacholine and the beta 2 agonist salbutamol, the skin prick test, and serum IgE levels were also examined and correlated to the beta 2ADR gene RFLP. In addition, measurements of cAMP responses to isoproterenol in peripheral mononuclear cells were performed in 22 healthy subjects whose genotype for beta 2ADR was known. RESULTS: A two allele polymorphism (2.3 kb and 2.1 kb) of the beta 2ADR gene was detected in the Japanese population. Family members without allele 2.3 kb (homozygote of allele 2.1 kb) had lower airways responses to inhaled salbutamol than those with allele 2.3 kb. The incidence of asthma was higher in those without allele 2.3 kb than in those with allele 2.3 kb. The beta 2ADR gene RFLP had no relation to airways responses to methacholine and atopic status. cAMP responses in peripheral mononuclear cells of the subjects without allele 2.3 kb tended to be lower than those of the subjects with allele 2.3 kb. CONCLUSIONS: These results suggest that Ban-I RFLP of the beta 2ADR gene may have some association with the airways responses to beta 2 agonists and the incidence of bronchial asthma.

Adolescent↗
PubMed1994

Colonization pattern of vancomycin-resistant Enterococcus faecium.

BACKGROUND: Vancomycin-resistant Enterococcus faecium is increasingly recognized as a serious problem by hospital epidemiologists. Understanding its colonization patterns may help in designing strategies to control its nosocomial spread in the hospital. METHODS: Twenty patients, selected at random, with vancomycin-resistant E. faecium isolated from cultures of various body sites were studied to determine sites of colonization. For 12 of these patients, cultures of environmental surfaces of their rooms and wards were also obtained. RESULTS: Eighteen patients (90%) had vancomycin-resistant E. faecium grown in stool cultures. In five patients (25%), vancomycin-resistant E. faecium was cultured from other sites: groins (four), popliteal fossae (three), mouth (one), and an open wound site (one). Patients with positive cultures from the groins and popliteal fossae also had growth of vancomycin-resistant E. faecium in cultures of diarrhea soiling those sites. No patients had the organism isolated from their nares. Vancomycin-resistant E. faecium grew in cultures obtained from bedside stand tables, over-bed tables, used linen, and bedside rails. CONCLUSIONS: In the 20 patients studied, colonization of vancomycin-resistant E. faecium was limited chiefly to the enteric tract. Absence of colonization of such a secluded area with poor antibiotic penetrability as the nares is encouraging. In our study, vancomycin-resistant E. faecium was isolated from various environmental surfaces from the rooms and wards of patients with vancomycin-resistant E. faecium in their stools.

Administration, Oral↗
PubMed1994

Nocardiosis in 30 patients with advanced human immunodeficiency virus infection: clinical features and outcome.

A total of 30 patients (aged 6-56 years) with nocardiosis and infection due to human immunodeficiency virus type 1 (HIV-1) were identified in our institution between January 1985 and June 1989. Eighteen patients had an AIDS-defining illness before or concurrently with nocardiosis. The mean CD4 lymphocyte count was 109/mm3. Pulmonary nocardiosis in 21 patients, extra-pulmonary nocardiosis in 8, and pulmonary and extrapulmonary nocardiosis in 1 patient was diagnosed. Chest radiographs showed alveolar patterns of infiltrates in 14 patients, reticulonodular patterns in 2, mixed alveolar and reticulonodular patterns in 6, cavitation in 4, and pleural effusion in 3. Of 27 patients treated, the conditions of 22 improved, but the extensive disease in 5 progressed. For 14 patients, recurrence was rapid after their treatment was discontinued. Nocardiosis caused or contributed to the death of 19 patients; in six patients, there was no evidence of nocardial infection at death. Nocardiosis can be a fatal complication of advanced HIV-1 disease. Delayed diagnosis, extensive disease, and early discontinuation of treatment were associated with poor outcome.

AIDS-Related Opportunistic Infections↗
PubMed1994

Analysis of restriction fragment length polymorphism for the HLA-DR gene in Japanese patients with sarcoidosis.

BACKGROUND: It is commonly assumed that some immunological disorder may play a part in the pathogenesis of sarcoidosis. Previous studies by several groups have shown a significant association with HLA-DR antigens in patients with sarcoidosis. In this study, restriction fragment length polymorphism (RFLP) analysis of the HLA-DR gene was designed to confirm the association at the gene level and to look for a gene rearrangement which may influence susceptibility to sarcoidosis. METHODS: Thirty two unrelated Japanese patients with sarcoidosis were tested for HLA antigens and subjected to RFLP analysis after digestion with Eco RI, Pst I, Bam HI, Pvu II, and Hind III by using an HLA-DR beta cDNA probe. A group of 47 unrelated healthy Japanese subjects served as controls. Frequencies of each restriction fragment were compared between the patients and the control subjects. Correlation between fragment frequencies and clinical features were also analysed. RESULTS: No restriction fragments of HLA-DR beta gene were found specific to the patients with sarcoidosis. The RFLP analysis could detect polymorphism of HLA-DR beta genes that was not distinguishable by conventional serological methods. Several restriction fragments of the DR beta gene were seen only in DRw52 positive individuals, and showed higher frequencies in the patients than in control subjects. The patients with these DNA fragments were likely to have limited stage disease with no ophthalmic involvement. CONCLUSIONS: An association between HLA and sarcoidosis was noted at the DNA level, although no restriction fragments were specific for this disease. RFLP analysis of the HLA gene is a more useful method than the usual HLA typing, and should be the first step in identifying the gene sequence which is connected with susceptibility to sarcoidosis.

Adolescent↗
PubMed1994

Establishing diagnosis of pulmonary malignant lymphoma by gene rearrangement analysis of lymphocytes in bronchoalveolar lavage fluid.

We report the successful application of gene rearrangement analysis to the lymphocytes obtained by bronchoalveolar lavage (BAL) for the diagnosis of pulmonary malignant lymphoma. A 45-yr-old female patient who had been suffering from back pain was shown to have macroglobulinemia and pulmonary infiltrative shadow by chest radiography. Transbronchial lung biopsy revealed a small B-cell infiltrate with monotypic immunoglobulin expression (IgM/kappa light chain), and malignant lymphoma was highly suspected. BAL was performed to evaluate the cell profiles. The phenotyping of lavaged lymphocytes by flow cytometry revealed that the major component of the lymphocytes was CD3-positive T cells, and that CD21-positive B cells accounted for only 10% of all lymphocytes. This result was contradictory to the immunohistochemical population of lymphocytes in biopsied specimens. However, gene analysis of lavaged lymphocytes revealed positive immunoglobulin heavy chain rearrangement and negative immunoglobulin light chain and T-cell receptor rearrangement, suggesting that B cells making up a minor population of lavaged lymphocytes were proliferating monoclonally. Thus, in this case, gene analysis was an effective procedure for detecting the origin of tumor cells and distinguishing monoclonality from reactive accumulations. To our knowledge, this case represents the first reported application of gene rearrangement analysis to cells obtained by BAL. The sensitivity and usefulness of this analysis for the accurate evaluation of pulmonary lymphoproliferative lesions, when applied to BAL cells, should be emphasized.

Bronchoalveolar Lavage Fluid↗
PubMed1994

A patient with chronic hepatitis C who simultaneously developed interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction after alpha-interferon administration.

Following a three-week administration of alpha-interferon (IFN-alpha), a 62-year-old woman with chronic hepatitis C manifested fever and dyspnea and showed diffuse infiltrative opacities on chest roentgenograms. Her laboratory data included results of anemia with reticulocytosis, a decreased complement level and hepatitis with elevated ALP, LDH and gamma-GTP. Because laboratory data also revealed a positive lymphocyte stimulation test for IFN-alpha, this cytokine was considered to be responsible for the development of interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction due to its immunomodulatory effects. Although these three disorders have been reported to develop singly after IFN-alpha therapy, this is the first report of a patient in whom these disorders occurred simultaneously.

Anemia, Hemolytic, Autoimmune↗
PubMed1994

Good's syndrome with a block in the early stage of B cell differentiation and complicated by Campylobacter fetus sepsis.

A 63-year-old man was admitted for Campylobacter fetus sepsis and immunodeficiency syndrome with thymoma (Good's syndrome). Serological examination demonstrated hypoimmunoglobulinemia. Analysis of lymphocyte subsets in the peripheral blood and bone marrow showed marked decreases in the proportion of cells bearing B cell markers. However, there were no abnormalities of cellular immunity. This is a rare case of Good's syndrome in Japan in which the pathogenic mechanism involved a block in the early stage of B cell differentiation. Moreover, this is the first case ever reported of Campylobacter fetus sepsis associated with Good's syndrome.

B-Lymphocyte Subsets↗
PubMed1994

Deficiency of the fourth component of complement (C4): a family case.

In this report, an apparently healthy 38-year-old woman with a remarkably low serum C4 value is described together with other family members who had moderately low serum C4. Plasma C4 typing disclosed that the proband inherited two C4B "null" haplotypes. In addition, Southern blot analysis of the C4 gene indicated that the C4A gene was partially deleted on one of these two haplotypes in the proband. We thus concluded that a de novo deletion on the inherited half-null haplotype was the likeliest cause of the low C4 level.

Adult↗
PubMed1994

[Immunoregulatory role of gamma delta T cell receptor in atopic asthma--association with the IgE response to molds antigen].

To evaluate the role of gamma delta T cells in atopic asthma, we examined the relationship among atopy bronchial asthma, and genetic polymorphism of the gamma chain of T cell receptors (TCR) in families through atopic asthmatic probands. We recruited 5 families (69 subjects). Total serum IgE levels were estimated by a radioimmunosorbent test (IgE RIST). Skin prick tests were done with inhaled allergens consisting of house dust, grass and tree pollens, common molds, and animal danders. Antigen-specific IgE levels in response to these allergens were also measured by multiple antigen simultaneous test (IgE MAST). The atopic phenotype was determined by the presence of a positive skin test, an elevated antigen specific IgE value, an elevated total IgE level, or some combination of these. Although linkage of atopy or bronchial asthma to the gene encoding the gamma chain of TCR was excluded, the lod score between this gene and molds-specific IgE responses was 0.42 at the recombination fraction of 0.1. In an association study, a 19 kb allele of the gamma chain of the TCR gene was found more frequently in asthmatic subjects than in non-asthmatic subjects (p = 0.068). Also, molds-specific IgE responses were significantly associated with this allele (p = 0.018). These findings suggest that molds-specific IgE responses underlying atopic asthma are partly regulated by the gene encoding the gamma chain of the TCR.

Adolescent↗
PubMed1994

[A case of bronchiectasis accompanied by ulcerative colitis (UC) and HTLV-1 associated myelopathy (HAM)].

We report a case of bronchiectasis with marked thickening of the respiratory tract wall occurring in a 37-year-old man with UC and HAM. He was diagnosed as UC at age 20. HTLV-1 was presumably transmitted to this patient by means of a blood transfusion he received at around age 30. On admission, chest X-ray films, tomography and CT-scan revealed dilated lumens and thickened airway walls extending from the trachea to subsegmental bronchi. Pulmonary function tests showed hypoxemia and mixed ventilatory disturbance with a predominantly obstructive component. HAM was diagnosed on the basis of neurological examination and cerebrospinal fluid analysis. A biopsy specimen from the carinal mucosa showed marked T cell infiltration. In these T cells, we detected polyclonal integration of HTLV-1 proviral DNA. Some of the infiltrating T cells showed atypia. In recent times, respiratory diseases other than infiltration of adult T-cell leukemia cells or opportunistic infection have been reported in HTLV-1 carriers and new clinical entities designated as HABA (HTLV-1 associated bronchiolo-alveolar disorder) and HBA (HTLV-1 associated bronchopneumopathy) have been proposed. This case is classified among these new entities, in a broad sense, and is a rare case in that the respiratory disorder is apparently related to UC.

Adult↗
PubMed1994

[Analysis of HLA antigen in Japanese patients with sarcoidosis].

Current clinical investigation of sarcoidosis should be directed toward not only identification of causative agents but also elucidation of the mechanism of the disease susceptibility. For the latter purpose, allotypes of human leucocyte antigen (HLA) are determined under the hypothesis that immune response to antigen peptides is efficiently triggered if the peptides well fit the unique pocket of a given HLA molecule. We have serologically determined HLA allotype in 57 normal controls and 53 patients with sarcoidosis. When assessed by corrected p value, the frequency of DRw52 was significantly increased in the sarcoid patients (79.2% in the patient group vs 50.9% in the control group). This finding has been confirmed by several other studies in Japan. However, as DRw52 and DRw3, DRw5, DRw6, and DRw8 are in strong linkage disequilibrium when determined by a serological method, it has not been elucidated which antigen is most responsible for the disease susceptibility in sarcoidosis. DNA typing of HLA antigens will potentially solve this issue.

HLA Antigens↗