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Biomedical subjects

T Matsuse

Publications and source records attributed to T Matsuse.

At least 37 records · Page 2Linked to original sources
PubMed2000

Inhibitory effects of angiotensin-converting enzyme (ACE) inhibitors on oxygen radicals produced by bronchoalveolar lavage cells in young and aged guinea pigs.

We examined the effect of angiotensin-converting enzyme (ACE) inhibitors and age on oxygen radical formation by bronchoalveolar lavage (BAL) cells. Lung-free cells, including pulmonary alveolar macrophages, were harvested from young (4-month-old) and aged (28-month-old) male guinea pigs using BAL. The oxygen radicals produced by BAL cells were measured by a lucigenin-dependent chemiluminescence method using a photon counter. Although spontaneous oxygen radical production by BAL cells from young and aged guinea pigs did not differ, the oxygen radical generation after maximal stimulation with phorbol-myristate acetate (PMA) was greater than that produced without PMA stimulation in both young and aged animals. ACE inhibitors with and without an SH-group (alacepril and lisinopril, respectively) were tested for their effect on oxygen radical formation by BAL cells; both ACE inhibitors inhibited oxygen radical production and generation by BAL cells from both young and aged guinea pigs in a dose-dependent manner. However, the alacepril concentration giving 50% inhibition (IC50) of oxygen radical generation by BAL cells was smaller than the IC50 of lisinopril in both young and aged guinea pigs. These results indicate that ACE inhibitors, in particular those with an SH-group, effectively reduce oxygen radical production by BAL cells from young and aged guinea pigs, and suggest that treatment with ACE inhibitors may be useful for ameliorating oxidant-associated pulmonary disorders in young and aged patients.

Aging↗
PubMed2000

Activin receptors are expressed on human lung fibroblast and activin A facilitates fibroblast-mediated collagen gel contraction.

Activin A is a member of the transforming growth factor-beta superfamily that exerts its diverse biological effects through bindings to activin specific transmembrane serine/threonine kinase receptors. The fibroblast-mediated contraction of a collagen gel is thought to be a model of part of the wound-repair response and tissue contraction. In this study, we found the expression of activin type I receptors (ActR-I and ActR-IB) and type II receptor (ActR-II) on human fetal lung fibroblasts (HFL-1) by RT-PCR and immunocytochemistry. We also examined the effects of activin A on the HFL-1-mediated collagen gel contraction. Activin A stimulated collagen gel contraction in a dose dependent manner and its effect was abolished by an activin-binding protein, follistatin, that specifically suppresses activin A activities. This study demonstrated that ActR-I, ActR-1B and ActR-II are expressed on human fetal lung fibroblast and that activin A regulates fibroblast-mediated collagen gel contraction, suggesting that activin A might contribute to human lung fibroblast activities and structural remodeling observed in pulmonary fibrosis.

Activin Receptors↗
PubMed2000

Association between alpha-1-antichymotrypsin polymorphism and susceptibility to chronic obstructive pulmonary disease.

BACKGROUND: The antiproteases, including alpha-1-antitrypsin, are supposed to prevent lungs from becoming emphysematous. Genetic susceptibility to smoking injury may confer a risk for the development of chronic obstructive pulmonary disease (COPD). METHODS: We have investigated the association between the polymorphism of alpha-1-antichymotrypsin (AACT), one of the antiproteases, and susceptibility to the development of COPD among heavy smokers. Blood samples obtained from both patients with COPD (n = 53) and control subjects (n = 65) at the Tokyo University Hospital, the Juntendo University Hospital and the Tokyo Kenbikyoin Clinic were used for this genotyping assay. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) were performed to genotype the AACT biallelic polymorphism in the signal peptide (-15 alanine to threonine), and the two polymorphisms of the exon (Pro229Ala and Leu55Pro). RESULTS: The proportion of AACT/Ala-15 homozygotes was significantly higher in the COPD patients than in the control subjects (COPD 37.7% vs. control 18.5%). The odds ratio for AACT/Ala-15 homozygotes vs. all other genotypes was 2.7 (95% CI 1.2-6.2) for the COPD group. We could not find any association between the other two polymorphisms and COPD. CONCLUSIONS: Genetic polymorphism in the signal peptide of AACT may be associated with individual susceptibility to the development of COPD, because the AACT/Ala-15 genotype is predominantly found in patients with COPD. It is suggested that AACT/Ala-15 genotype may be less protective against smoking injury.

Adult↗
PubMed2000

Neither IL-1beta, IL-1 receptor antagonist, nor TNF-alpha polymorphisms are associated with susceptibility to COPD.

The cytokines that contribute to airway inflammation, including interleukin-1beta (IL-1beta) and tumour necrosis factor alpha (TNFalpha), might have key roles in the development of chronic obstructive pulmonary disease (COPD). Interleukin-1 receptor antagonist (IL-1RN), the physiological antagonist of IL-1beta, is also known to play a crucial role in several chronic inflammatory diseases. In this study, we investigated the association of the polymorphisms of IL-1beta, IL-1RN and TNFalpha with susceptibility to COPD. To elucidate the genotype of the IL-1beta polymorphisms at position -511 base and at the amino acid residue 105, the IL-1RN polymorphism in intron 2, and TNFalpha polymorphism at position -308, polymerase chain reaction (PCR) and restriction enzyme fragment length polymorphism (RFLP) were performed on blood samples from both patients with COPD (n = 53) and control subjects (n = 65). There were no differences on the allele and genotype frequency of IL-1beta, IL-1RN, and TNFalpha between the two groups. We could not find a significant link between the polymorphism of TNFalpha, which was previously reported to be associated with chronic bronchitis, and COPD. Furthermore, no association between genetic polymorphisms of IL-1beta and IL-1RN and individual susceptibility to COPD was found.

Aged↗
PubMed2000

Effect of ions on antibacterial activity of human beta defensin 2.

Human beta defensin 2 (HBD-2), the most recently discovered human defensin, has been considered to work as a host defense substance against microbial infection. Using Escherichia coli ATCC 25922, we investigated how some cations and anions influenced the antimicrobial activity of HBD-2. This activity, measured in 10 mM phosphate buffer at a concentration of 20 microg/ml, reduced significantly in the presence of 100 and 150 mM sodium or potassium chloride. The reduction was not significantly different when the total amounts of sodium and potassium ions were equal. The kind and the valence of anions (chlorine and sulfate ions) did not affect the bactericidal activity as long as the concentrations of sodium ions were equal. Divalent ions (calcium and magnesium ions) added to 10 mM of Tris buffer significantly inactivated HBD-2 at much lower concentrations (more than or equal to 0.01 mM and 0.05 mM, respectively) than the monovalent ions did. These findings suggest that HBD-2 kills the bacteria through at least two phases, which are affected independently by either monovalent or divalent ions and unaffected by anions.

Anti-Bacterial Agents↗
PubMed2000

Effects of angiotensin-converting enzyme inhibitors on spontaneous or stimulated generation of reactive oxygen species by bronchoalveolar lavage cells harvested from patients with or without chronic obstructive pulmonary disease.

We examined the effects of angiotensin-converting enzyme (ACE) inhibitors on spontaneous or stimulated generation of reactive oxygen species (ROS) by bronchoalveolar lavage (BAL) cells prepared from 6 patients with chronic obstructive pulmonary disease (COPD) and from age-matched control subjects without COPD. The ROS produced by BAL cells were measured by the lucigenin-dependent chemiluminescence method. The application of ACE inhibitors into culture media containing BAL cells inhibited spontaneous and stimulated generation of ROS by BAL cells from COPD patients and control subjects in an ambroxol-concentration-dependent manner. Alacepril, an ACE inhibitor bearing SH-group, inhibited the oxygen radical production and generation by BAL cells from COPD patients in a dose-dependent fashion. Approximately 0.6-0.7 mM of alacepril inhibited 50% of the ROS production by BAL cells from COPD patients, whereas a slightly higher concentration (3 mM) of lisinopril, an ACE inhibitor not bearing an SH-group, was necessary to inhibit the production of ROS. These results suggest that an ACE inhibitor may act as an pulmonary antioxidant in patients with COPD.

Aged↗
PubMed2000

Recombinant adeno-associated virus vectors efficiently transduce foreign gene into bovine aortic endothelial cells: comparison with adenovirus vectors.

Because the features and kinetics of adeno-associated virus (AAV)-mediated gene transfer to endothelial cells (EC) are yet to be ultimately determined, we tested variables pertinent to the efficiency of AAV-mediated gene transfer to bovine aortic endothelial cells (BAEC). The variables with AAV vectors were compared with the better characterized adenovirus (Ad) vectors. There is a dose-response relationship between multiplicity of infection (moi) of AAV or Ad vectors and transduction efficiency in BAEC. The higher moi of AAV vectors achieved more than 80% of transduction efficiency in cultured BAEC. AAV and Ad vectors showed an incubation-time-dependent increase in transduction efficiency of LacZ gene to the BAEC up to 12 h of vector exposure. Although the similar kinetics of transduction efficiency of LacZ gene to BAEC was found in both vectors, the duration of gene expression was longer in AAV vector than that in Ad vectors in vitro. These results indicate that AAV-vector is efficient for gene transfer to EC, and higher moi of vectors or a longer period exposure of vectors to EC can facilitate efficient transduction of a foreign gene into cultured EC. For the duration of gene expression, the AAV vectors may be better than Ad vectors.

Adenoviridae↗
PubMed2000

[Sleep apnea syndrome and hypertension using desaturation index].

To examine the roles of obstructive apnea (OA) and central apnea (CA) in oxygen desaturation on hypertension and sleep apnea syndrome (SAS), we performed a sleep study on 41 elderly subjects (mean age 69.5 +/- 6.8 years, male:female = 31:10). Nocturnal oxygen desaturation was documented with a pulse oximeter and apneas (OA and CA) were diagnosed on the basis of results of respiratory inductive plethysmography and oronasal flow. Significant desaturation (SDS, greater than 5% drop in SpO2 from baseline value) and desaturation index (DI; epsilon SDS (%) x duration (hour)) were calculated using the continuous nocturnal monitoring system with a pulse oximeter. We defined central type apnea above 50% as the central type group (n = 8, mean age 58.6 +/- 2.9, mean BMI 21.3 +/- 1.0, male:female = 7:1), and obstructive type and mixed type apnea above 50% as the obstructive type group (n = 21, mean age 70.0 +/- 3.2, mean BMI 25.3 +/- 1.0, male:female = 17:4). Other subjects were assigned to the control group (n = 12, mean age 64.3 +/- 2.3, mean BMI 23.8 +/- 1.2, male:female = 7:5). The DI (delta 5%) of the central type was 0.34 +/- 0.17, and that of the obstructive type was 1.78 +/- 0.7 showing a significant increase in the latter compared to the control group (p < 0.02). The DI (< 90%) of the central type was 0.14 +/- 0.07, and that of the obstructive type was 1.72 +/- 0.75, and that of the obstructive type was significantly greater than in the control group (p < 0.05) and central type (p < 0.05). There were 4 cases (33.3%) with hypertension in the control group and 4 cases (50.0%) with hypertension in the central type group, but there were 15 cases (71.4%) with hypertension in the obstructive type group. Hypertensive prevalence in the obstructive group was significantly more than in the control group (p < 0.05). No significant difference in body mass index or age were seen in the obstructive group and control group. There was a significant correlation between mean blood pressure and apnea index (AI). The AI of the hypertensive group was significantly higher than that of the normotensive group (p < 0.001). These results suggest that subjects with significant obstructive apneas may be at greater risk for hypertension than subjects with central apneas and that hypertension in the pathogenesis of SAS may be related to the severity of apneas rather than oxyhemoglobin desaturation.

Adult↗
PubMed2000

[A case of very late onset overlap syndrome of systemic sclerosis and systemic lupus erythematosus].

A 88-year-old woman was admitted with appetite loss and dehydration in April 1999. She first noticed finger swelling in May 1996 and systemic sclerosis (SSc) was diagnosed in February 1997 on the basis of a clinical picture of low-grade fever, diffuse skin thickening, Raynaud's phenomenon, and pulmonary fibrosis. Retrospectively pulmonary fibrosis could have been identified on chest X ray film in September 1995. Although her appetite loss and dehydration were improved by hydration, pleural effusion continued. After detailed examinations, anti-topoisomerase 1 (Scl-70) antibody, anti-Sm antibody, and an anti-double-stranded DNA antibody (dsDNA) were found in her serum. However, the other antibodies to anti-SS-A, SS-B, Jo-1, and RNP were not detected. These results suggest that this elderly case was a very late onset overlap syndrome of systemic lupus erythematosus (SLE) and SSc. Thus, the pleural effusion in this case may have been caused by SLE-associated pleuritis. Although the late onset elderly cases with overlap syndrome are very rare, SLE, SSc, and their combination can be found in aged patients over 80 years old. SLE and SSc should be carefully considered for the differential diagnosis of pleural effusion and skin thickening even in elderly patients.

Aged↗
PubMed2000

[The relationship between adhesion molecules and hypoxia].

Hypoxia is an essential developmental and physiological stimulus that plays a key role in the pathophysiology of heart attack, cancer and other major causes of mortality. Recently studies have shown that hypoxia itself may directly activate NFk-B. NFk-B sites are also present in the promoter of the ICAM-1 gene. Therefore, it is possible that hypoxia could directly activate the ICAM-1, through activation of NFk-B. Hypoxia-inducible factor 1 is the only known mammalian transcription factor expressed uniquely in response to physiologically relevant levels of hypoxia. In the another cause of the induction of adhesion molecules with hypoxia adhesion molecules are induced by the inflammatory cytokine(IL-1, TNF alpha) that caused with anoxia/reperfusion. The adhesion molecules induced by hypoxia play one of the key rolls of the various diseases. For example the level of cICAM-1 in OSAS patients were increased. These observations suggest that OSAS-induced hypoxia activate adhesion molecules, resulting in the important risk factor of cardiovascular disorders.

Animals↗