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Biomedical subjects

Y Sano

Publications and source records attributed to Y Sano.

At least 199 records · Page 11Linked to original sources
PubMed1994

[A case variant asthma with acetylcholine inhalation challenge test].

A 55-year-old male presented with a chief complaint of exertional dyspnea. He had a daughter suffering with bronchial asthma. He had no pertinent past history. He visited the outpatient clinic of a nearby hospital for evaluation of exertional dyspnea, but routine examination results were normal. He was therefore followed up for only about two weeks without treatment. He was sent to our hospital for further analysis. Physical examination revealed clear lung fields but his respiratory rate was 34 per a minute, PaO2 72.9 mmHg and PaCO2 39.7 mmHg. Respiratory function tests, chest XP, chest CT and ECG findings were unremarkable. Pulmonary infarction was ruled out with a pulmonary perfusion scintigram. However, he was hyperreactive to the acetylcholine inhalation challenge test, the respiratory threshold being 625 micrograms/ml. A variant form of bronchial asthma was thus suspected and a bronchodilator was administered. The medication was very effective. After several weeks, his symptoms had clearly disappeared. Therefore, in a case complaining of exertional dyspnea only, bronchial asthma should be ruled out as a possible cause and the acetylcholine inhalation challenge test might be helpful in making the correct diagnosis. Bronchodilator administration should also be considered.

Acetylcholine↗
PubMed1994

[A case of suspected occupational asthma in an orthopedist, due to cast materials containing MDI].

A 38-year-old male presented complaining of an asthma attack. He had a past history of allergic rhinitis and conjunctivitis, family history of bronchial asthma and atopic dermatitis. He was an orthopedist who had been using cast materials containing methylene diphenyl isocyanate (MDI) for one year, and had developed an early asthmatic response while handling the casts. An acetylcholine inhalation test was done and his value was 20000 micrograms/ml. The scratch test for the cast materials was negative though the inhalation challenge test was positive. We suspected that the patient was suffering from bronchial asthma induced by MDI contained in the cast materials. Studies using isocyanates conjugated with human serum albumin were performed. The results were as follows: IgE-RAST negative, ELISA demonstrated the existence of specific IgG for both toluene diisocyanate (TDI) and MDI, as well as IgG4 for both TDI and MDI. The cast contained MDI but not TDI. We therefore considered TDI to be cross-reactant. It was likely that chronic exposure enhancing specific IgG4 and specific IgG might have caused the high IgG4 value. This is the first case of occupational asthma in an orthopedist due to isocyanates.

Adult↗
PubMed1993

Increased fragmentation of urinary fibronectin in cancer patients detected by immunoenzymometric assay using domain-specific monoclonal antibodies.

Monoclonal antibodies (MoAbs) recognizing the distinct domains of human fibronectin had previously been established and they were used to construct several sandwich immunoenzymometric assays (IEMAs) for the structural analysis of fibronectin found in the urine of cancer patients. Urinary fibronectin (UFN) was immunodetectable only with FN12-8 and FN30-8 MoAbs against cell-binding domains and was less reactive with other IEMAs using MoAbs directed to terminal domains, indicating that UFN was almost completely fragmented and consisted mainly of cell-binding regions. The IEMA using MoAbs against cell-binding domains had sufficient immunoreactivities with the antigen fragmented by artificial proteolysis, but these fragments could hardly be detected by other IEMAs. UFN levels were significantly elevated in various cancer patients and extremely elevated in some patients with distant metastasis. It is presumed that UFN fragments which increase in cancer patients are generated by extracellular matrix destruction. Thus UFN levels and the ratio of the fragmented UFN level to the non-fragmented UFN level appear to be informative clinical indicators of tumor malignancy or metastatic ability in cancer patients.

Animals↗
PubMed1993

A novel transposon-like structure carries the genes for pyocin AP41, a Pseudomonas aeruginosa bacteriocin with a DNase domain homology to E2 group colicins.

The genetic determinant for pyocin AP41, a bacteriocin produced by Pseudomonas aeruginosa, has been cloned. The determinant is located on the chromosome flanked by a pair of inverted repeats, forming a transposon-like structure (TnAP41). TnAP41 possesses some features characteristic of the Tn3 family of transposons. Based on a comparison with the structure of the corresponding region of the chromosome of a non-producer strain, we propose that P. aeruginosa has acquired pyocinogeny by the transposition of TnAP41 into the chromosome. The determinant comprises two ORFs encoding the protein subunits responsible for the killing action (the large component) and immunity (the small component). Amino acid sequences of the C-terminus of the large component (the deoxyribonuclease domain) and the immunity protein show remarkable homology to those of E2 group colicins, suggesting that these bacteriocins, which are produced by distantly related species, have originated from a common ancestor.

Amino Acid Sequence↗
PubMed1993

Effects of 5-azacytidine on somatic mutation in a soybean test system.

The mutagenic activity of 5-azacytidine (azaC) was assayed in heterozygous soybean plants (Y11y11), according to the appearance of mutational spots (yellow, dark green and twin) on the leaves. When soybean seeds were treated with azaC at 10-100 micrograms/ml, azaC was found to be significantly mutagenic and to exert heritable effects in the soybean test system. Treatment with azaC increased the frequency of twin spots on the leaves. AzaC would thus appear to cause somatic crossing over as its major effect.

Azacitidine↗
PubMed1993

Evaluation of the antigen specificity of the cellular infiltrate at the delayed type hypersensitivity reaction site with the use of an antigen-specific T cell clone.

Antigen specific T lymphocytes in delayed type hypersensitivity (DTH) test sites were analyzed in cell-transfer experiments. T lymphocytes from B6 mice were transferred into B6PL mice which differ from B6 at the Thy1 allele. When peritoneal exudate cells (PEC) from ovalbumin (OA)-immunized B6 mice were transferred into B6PL mice intravenously, DTH reaction was observed on footpads. A greater number of B6 T cells was identified at the DTH site. OA-reacting B6 T clones were then transferred with antigens into the footpads of B6PL mice. DTH reaction was induced at the footpads. More T cell clones were identified at the DTH test sites than in the control.

Animals↗
PubMed1993

Identification of basophils by immunohistochemistry in the airways of post-mortem cases of fatal asthma.

There is increasing evidence for the role of basophils in the pathogenesis of bronchial asthma. To examine the presence of basophils in the airways of patients with fatal asthma by immunohistochemistry, we stained lung tissues from four post-mortem cases who had died from severe asthmatic attacks and four controls with a monoclonal antibody raised against tryptase (AA-1) and anti-IgE. Mast cells and basophils were identified in the bronchioles as AA-1- and anti-IgE-positive cells, and anti-IgE-positive cells, respectively. Airway mast cells were found beneath the basement membrane, near blood vessels in the submucosa, and adjacent to the submucosal glands, and scattered throughout the muscle bundles. There was a significant increase of mast cells in the asthma group compared with the control group (203.5+/-84.6/mm2, mean+/-s.d. vs 37.7+/-8.7/mm2, P<0.05, n=4). In contrast, basophils were observed in the airway lumen, in the bronchial epithelium and in the submucosa. The number of basophils in the bronchioles was 81.8+/-55.5/mm2 (n = 4); however, basophils were not found at all in the airways of the control group. Although eosinophils, B lymphocytes and macrophages bear low affinity IgE receptors and could react with anti-IgE, the location of these cells in the close sections did not correspond closely with basophils. The presence of basophils in lung tissues obtained from fatal asthma patients supports the view that basophils play a role in the pathogenesis of bronchial asthma.

Adult↗
PubMed1993

Molecular structures and functions of pyocins S1 and S2 in Pseudomonas aeruginosa.

Pyocins S1 and S2 are S-type bacteriocins of Pseudomonas aeruginosa with different receptor recognition specificities. The genetic determinants of these pyocins have been cloned from the chromosomes of P. aeruginosa NIH-H and PAO, respectively. Each determinant constitutes an operon encoding two proteins of molecular weights 65,600 and 10,000 (pyocin S1) or 74,000 and 10,000 (pyocin S2) with a characteristic sequence (P box), a possible regulatory element involved in the induction of pyocin production, in the 5' upstream region. These pyocins have almost identical primary sequences; only the amino-terminal portions of the large proteins are substantially different. The sequence homology suggests that pyocins S1 and S2, like pyocin AP41, originated from a common ancestor of the E2 group colicins. Purified pyocins S1 and S2 make up a complex of the two proteins. Both pyocins cause breakdown of chromosomal DNA as well as complete inhibition of lipid synthesis in sensitive cells. The large protein, but not the pyocin complex, shows in vitro DNase activity. This activity is inhibited by the small protein of either pyocin. Putative domain structures of these pyocins and their killing mechanism are discussed.

Amino Acid Sequence↗
PubMed1993

Functional domains of S-type pyocins deduced from chimeric molecules.

Functional domain structures of pyocins AP41, S1, and S2 were assigned by examining the functions of chimeric pyocins and deletion derivatives. Pyocins AP41, S1, and S2 are essentially composed of three domains, the receptor-binding domain, the translocation domain, and the DNase domain, in that order from the N terminus to the C terminus. The alignment of these domains is distinct from that in E2-group colicins with functions similar to those of these pyocins. Pyocins AP41 and S2 have a fourth domain between the receptor-binding and the translocation domains, which is dispensable for their killing functions.

Amino Acid Sequence↗
PubMed1993

The inherent DNase of pyocin AP41 causes breakdown of chromosomal DNA.

Pyocin AP41 degrades the chromosomal DNA in sensitive strains of Pseudomonas aeruginosa but has little effect on RNA, protein, and lipid syntheses. In vitro experiments showed that the carboxyl-terminal part of the large subunit of pyocin AP41 carries an inherent DNase that is responsible for its killing action.

Amino Acid Sequence↗
PubMed1993

Regulation of pyocin genes in Pseudomonas aeruginosa by positive (prtN) and negative (prtR) regulatory genes.

Most strains of Pseudomonas aeruginosa produce various types of bacteriocins (pyocins), namely, R-, F-, and S-type pyocins. The production of all types of pyocins was shown to be regulated by positive (prtN) and negative (prtR) regulatory genes. The prtN gene activates the expression of various pyocin genes, probably by the interaction of its product with the DNA sequences conserved in the 5' noncoding regions of the pyocin genes. The prtR gene represses the expression of the prtN gene, and its product, predicted from the nucleotide sequence, has a structure characteristic of phage repressors and seems to be inactivated by the RecA protein activated by DNA damage. A model for the regulation of the pyocin genes is proposed.

Amino Acid Sequence↗
PubMed1993

Classification and relationships of rice strains with AA genome by identification of transposable elements at nine loci.

We analyzed the presence of p-SINE1 members at five loci in the rice strains belonging to seven species with AA genome in the Oryza genus by the methods including polymerase chain reaction (PCR). Four p-SINE1 members (p-SINE1-r3, r4, r5 and r7) were present at the corresponding loci in all the strains examined. One member (p-SINE1-r6) was, however, not present at the corresponding locus in most of the African strains of O. glaberrima and O. barthii, but was in the other strains. The PCR-amplified fragments containing p-SINE1-r4 in many strains were found to be larger due to insertion of either one of two transposable elements, named Tnr2 and Ret1, within or near p-SINE1-r4, respectively: Tnr2 is 157 bp in length with terminal inverted repeat sequences of about 56 bp; Ret1 is only 13 bp in length with a T stretch at its end. Tnr2 was not present in the corresponding locus in all the strains belonging to O. sativa Japonica and in some strains of O. rufipogon and O. longistaminata, while Ret1 was present only in the two strains of O. longistaminata. These results and previous ones obtained from the analysis of the other two p-SINE1 members (p-SINE1-r1 and r2) in the Wx gene indicate that the elements, such as p-SINE1-r6, Tnr2, Ret1 and p-SINE1-r2, have been inserted into the respective loci during divergence of the rice species with AA genome. The patterns for the presence and absence of the transposable elements at the respective loci enabled us to classify the rice strains with AA genome into ten groups and to infer their relationships.

Base Sequence↗
PubMed1993

Diagnosis of rejection in the allografted rat lung: using monoclonal antibodies to T cell subsets for immunologic monitoring.

Early diagnosis of rejection and timely immunosuppression are absolutely important in clinical lung transplantation. We studied surface markers of peripheral blood lymphocytes (PBL), graft infiltrating lymphocytes (GIF) and bronchoalveolar lavage fluid (BALF) in a rat using flow cytometric monitoring to diagnose rejection. Left lung transplantation was performed on Brown Norway (BN) rats and Lewis (LEW) rats in the following groups; Group 1: LEW-LEW (isograft), Group 2: BN-LEW (allograft; no immunosuppression), Group 3: BN-LEW (allograft; treated with Cyclosporine A at a dose of 15 mg/kg/day i.m.). In each group, rats were killed 3, 5, 7 days postoperatively (n = 6 on each day). Monoclonal antibodies investigated in this study were W3/25 (anti-helper T lymphocyte), OX8 (anti-suppressor/cytotoxic T lymphocyte), and OX39 (anti-interleukin 2 receptor). Histological classification of rejection in Group 2 showed vascular phase at 3 days, alveolar phase at 5 days, and destructive phase at 7 days, respectively. No evidence of rejection was found in Group 1 or 3. In Group 2, W3/25 positive cell proportion in GIL and BALF significantly decreased as the rejection progressed, but OX8 positive and OX39 positive cell proportion increases were significantly greater than in Groups 1 and 3 as the rejection progressed. These results lead us to speculate that the studies of T cell subsets in GIL and BALF lymphocytes are useful for diagnosis of rejection in lung transplantation.

Animals↗
PubMed1993

Pharmacokinetic characterization of menaquinone-4 in dogs by sensitive HPLC determination.

A simple and sensitive assay method for a pharmacokinetic study of Menaquinone-4 in dogs was established using HPLC with fluorescence detection following extraction with organic solvent. The quantification limit of this method was 1 ng/ml of plasma. A new oily solution formulation of Menaquinone-4 was administered orally to nonfasted dogs at doses of 0.4, 4 and 40 mg/kg. The plasma concentrations reached maximum levels at 1 to 1.5 h after dosing, and then decreased slowly. AUC values up to 24 h after administration were almost dose-proportional. Menaquinone-4 was also administered to dogs in soft-capsules, for comparison with a conventional hard-capsule oral formulation and an intravenous lecithin formulation. The mean AUC for oral dosing in the soft-capsule formulation was 13.5% of that for intravenous dosing in lecithin, and was 4.6 times higher than that for oral dosing in hard-capsules. Additional dosing in fasted dogs indicated that the AUC in pre-fed dogs was about 4 times higher, suggesting that feeding before giving Menaquinone-4 raises the bioavailability. Overall Menaquinone-4 was absorbed rapidly after administration in non-fasted dogs and dose-proportional bioavailability was obtained among the doses of 0.4 to 40 mg/kg. Higher plasma concentrations were observed after administration in the soft-capsule formulation rather than in the hard-capsule formulation. These findings suggest that the soft-capsule formulation would show a good pharmacokinetic profile for elderly patients with osteoporosis.

Administration, Oral↗