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Biomedical subjects

T Yamazaki

Publications and source records attributed to T Yamazaki.

At least 505 records · Page 28Linked to original sources
PubMed1994

Enterococcus faecalis aggravates pyelonephritis caused by Pseudomonas aeruginosa in experimental ascending mixed urinary tract infection in mice.

Mixed urinary tract infection was caused by simultaneous inoculation of 10(4) CFU each of Enterococcus faecalis TN2005 and Pseudomonas aeruginosa P9 into the bladders of CBA/J mice. Both organisms proliferated in the kidneys, and viable cell counts of E. faecalis TN2005 reached a peak level of 4.1 x 10(5) CFU per pair of kidneys within the first 24 h, while P. aeruginosa P9 counts increased more slowly. The number of P. aeruginosa P9 cells peaked at 8.3 x 10(6) CFU per pair of kidneys 5 days after infection. Five days after mixed infection, infiltration of neutrophils into the renal pelvis and renal medulla was observed. Immunohistochemical staining revealed the presence of E. faecalis antigen in the renal medulla. P. aeruginosa antigen was detected mainly in the renal pelvis 5 days after infection and in the renal medulla as well as the renal pelvis 14 days after infection. Mixed infection induced pyelonephritis within 5 days after mixed infection, while it was not observed until 14 days after infection with P. aeruginosa P9 alone. P. aeruginosa P9 inoculated together with E. faecalis TN2005 was more resistant to eradication from the kidneys by beta-lactam antibiotics than P. aeruginosa P9 inoculated alone. These results suggest that E. faecalis TN2005 invades the renal medulla first in mixed urinary tract infection and induces histological changes which lead to aggravation of the pyelonephritis caused by P. aeruginosa P9.

Animals↗
PubMed1994

Effect of lipopolysaccharide on mouse mast cell induction by a splenic cell culture system.

We have previously reported a method of mast cell induction by long-term culture of mouse spleen cells without using exogenous mast cell growth factor (Z.-Q. Hu, T. Yoshida, and T. Shimamura, J. Immunol. Methods 149:173, 1992). Supernatants recovered from the long-term cultures contain endogenous interleukin 3 and soluble stem cell factor. These were assessed by the capacity of the recovered supernatants to foster the growth of a mast cell growth factor-dependent cell line and by neutralizing antibodies. Besides the soluble factors, cell-to-cell contacts mediated by membrane stem cell factor on splenic stromal cells and c-Kit receptors on mast cells also affect mast cell induction. Different lots of fetal calf serum (FCS) were examined to determine a possible trigger for cytokine production. FCS can be divided into mast cell-inducible and noninducible sera by this process. However, not all FCS lots contain mast cell growth factor. The mast cell-inducible lots contain lipopolysaccharide (LPS) confirmed by a Limulus assay. Polymyxin B can neutralize the mast cell induction activity. Non-mast cell-inducible FCS can be converted to inducible FCS by adding exogenous LPS. The results indicate that LPS as a trigger of cytokine production is responsible for mast cell induction.

Animals↗
PubMed1994

In vivo detection of endogenous acetylcholine release in cat ventricles.

To detect and monitor endogenous acetylcholine (ACh) release in the in vivo heart, we applied a dialysis technique to the hearts of anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium and were perfused with Krebs-Henseleit solution containing Eserine (10(-4) M) at 3 microliters/min. Dialysate ACh concentration was measured with high-performance liquid chromatography. In four cats, the response to vagal stimulation was studied. Electrical stimulation of efferent vagal nerves (10 Hz) significantly increased dialysate ACh concentration from 596 +/- 118 (control) to 12,210 +/- 1,661 pM. After stimulation, dialysate ACh concentration significantly decreased to 382 +/- 80 pM below control. The influence of ganglionic blocker was determined in six cats. Control vagal nerve stimulation (10 Hz) increased dialysate ACh concentration from 582 +/- 136 to 9,102 +/- 754 pM. Local perfusion of hexamethonium (10(-4) M) did not affect this nerve stimulation-induced ACh increase (8,611 +/- 1,189 pM), and intravenous administration of hexamethonium (20 mg/kg) prevented this increase (340 +/- 88 pM). We examined the response to vagal nerve stimulation at different frequencies in three cats. Vagal nerve stimulation increased dialysate ACh concentration from a control of 588 +/- 211 to 1,227 +/- 195 pM at 2 Hz, 3,946 +/- 1,059 pM at 5 Hz, and 9,366 +/- 1,873 pM at 10 Hz. Dialysate ACh concentration reflects ACh release from postganglionic vagal nerves innervating the left ventricular myocardium; the dialysis technique permits estimation of relative changes in efferent cardiac vagal nerve activity.

Acetylcholine↗
PubMed1994

Localization of Alzheimer amyloid beta protein precursor and its relation to senile plaque amyloid.

The authors examined the ultrastructural localization of amyloid beta protein precursor (APP) in normal human brains immunohistochemically using 3 kinds of APP antisera. The patterns of immunoreaction differed between the antisera used. Antiserum 770, against APP1-770, predominantly labeled the cytoplasm of neurons, whereas antiserum Z31, against the pre-beta region of the APP, labeled astroglial processes intensely and neurons to a lesser extent. Antiserum 1736, against the N terminal of beta protein, labeled both neurons and astrocytes. Vascular smooth muscle cells and some of the endothelial cells in the cerebral arterioles and capillaries were labeled with Z31 and 1736. The APP exists in every cells, while various patterns of immunoreactivity may reflect the difference in the metabolic pathway of APP between cell types.

Aged↗
PubMed1994

Angiotensin II receptor antagonist TCV-116 induces regression of hypertensive left ventricular hypertrophy in vivo and inhibits the intracellular signaling pathway of stretch-mediated cardiomyocyte hypertrophy in vitro.

BACKGROUND: Previous studies have demonstrated that angiotensin II (Ang II) acts as a growth-promoting factor directly on cardiac myocytes and that angiotensin-converting enzyme inhibitor induces regression of hypertrophied hearts both in experimental animals and in humans. These results suggest that the renin-angiotensin system (RAS) is involved in the formation of left ventricular hypertrophy (LVH). To elucidate the role of RAS in the progression of cardiac hypertrophy, we evaluated the effect of an Ang II receptor antagonist on LVH in spontaneously hypertensive rats (SHRs) and investigated the molecular mechanisms by which antagonizing Ang II receptors reduces cell hypertrophy of myocytes using the in vitro model of mechanical stretch. METHODS AND RESULTS: In the in vivo study, we treated SHRs with the nonpeptide Ang II receptor antagonist TCV-116 (0.1, 1, or 10 mg/kg per day) or hydralazine (10 mg/kg per day). Blood pressure was measured by the tail-cuff method, and wall thickness of left ventricle was serially monitored using M-mode echocardiography. Rats were killed at the age of 13, 17, 21, or 25 weeks, and left ventricular (LV) weight, transverse diameter of cardiomyocytes, relative amount of V3 myosin heavy chain (MHC), and degree of interstitial collagen accumulation were examined. Untreated SHRs progressively developed severe hypertension, but treatment with TCV-116 or hydralazine inhibited the increase in blood pressure. Treatment with TCV-116 reduced LV weight, LV wall thickness, transverse diameter of myocytes, relative amount of V3 MHC, and interstitial fibrosis, whereas treatment with hydralazine slightly prevented an increase in LV wall thickness but did not exert significant reduction in other parameters. In the in vitro study, neonatal rat cardiomyocytes were cultured on deformable silicone dishes and mechanically stretched with or without pretreatment of CV-11974 (an active metabolite of TCV-116), and [3H]phenylalanine incorporation, activity of mitogen-activated protein (MAP) kinase, and c-fos mRNA expression were analyzed. Pretreatment of cultured cardiomyocytes with 10(-7) mol/L CV-11974 inhibited an increase in [3H]phenylalanine incorporation, MAP kinase activity, and c-fos gene expression induced by stretch of cardiomyocytes. CONCLUSIONS: The Ang II receptor antagonist TCV-116 induced regression of cardiac hypertrophy and had cardioprotective effects on hypertrophied myocardium in vivo, and antagonizing Ang II receptors inhibited intracellular signaling of stretch-mediated cardiomyocyte hypertrophy in vitro. These results suggest a crucial role of the cardiac RAS in the development of LVH produced by pressure overload.

Angiotensin II↗
PubMed1994

Preparation of monoclonal antibodies for immunoblotting human growth hormone receptor and growth hormone-binding protein.

Monoclonal anti-peptide antibodies against the extracellular domain of human growth hormone receptor (hGHR) were prepared. Four monoclonal antibodies (mAbs) reacted with an extracellular domain protein produced by genetic engineering. Among them, GHRP2-88 was the most reactive against hGHRs from human IM-9 cells. The lower limit of detection for immunoblotting using this mAb was about 200 pg hGHR. The GHRP2-88 antibody also reacted with deglycosylated hGHRs from tunicamycin-treated IM-9 cells and with the growth hormone-binding protein (GH-BP) in human plasma.

Antibodies, Monoclonal↗
PubMed1994

A comparative study of the enzymological features of alpha-amylase in the Drosophila melanogaster species subgroup.

A comparative study was done on the enzymological features of alpha-amylase among six sibling species belonging to the Drosophila melanogaster species subgroup. The pH optima were 7.6 for D. melanogaster, D. mauritiana and D. simulans and 7.4 for D. erecta, D. teissieri and D. yakuba. The temperature optima were commonly 37 C in all species studied. However, there are two types of temperature dependence; a strict one as observed in D. melanogaster, D. mauritiana and D. simulans, and a flat one as observed in D. erecta, D. teissieri and D. yakuba. These separations are consistent with the general phylogeny within this species subgroup. The substrate dependence was almost the same in all the species studied. The Vmax and Km were also estimated for each species. We found clear differences in the enzymological features between the species. Thus these differences might reflect an adaptation of the amylase enzyme system to speciation in this species subgroup.

Amylopectin↗
PubMed1994

Molecular analysis of cis-regulatory sequences of the alpha-amylase gene in D. melanogaster: a short 5'-flanking region of Amy distal gene is required for full expression of Amy proximal gene.

The structural locus for alpha-amylase (AMY) in Drosophila melanogaster is duplicated and divergently transcribed. These two genes are designated as Amy-p and Amy-d, respectively. We searched for the cis-acting regulatory elements for full expression of the duplicated Amy-p and Amy-d loci, by injecting plasmid constructs containing sequences from the Amy locus into preblastoderm embryos of an AMY-null strain and measuring exogenous AMY activity produced in transformed host larvae (i.e., the transient expression assay). Relative activities of endogenous amylase isozymes, AMY-1 and AMY-3, in extracts of AMY1,3 larvae of a Canton-S are almost the same. However, three independently isolated Amy-p1 constructs with only the 5' upstream regions of Amy-p1 expressed a very low AMY-1 activity. Two other Amy-p1 constructs with the 5' upstream region of Amy-d3 in addition to that of Amy-p1 produced a high activity. Thus, the 5' upstream region of Amy-d3 is necessary for full expression of Amy-p1. In order to locate cis-regulatory elements within the 5' region of Amy-d3, a series of hybrid constructs including this region were tested to locate them. Our results clearly show that the cis-acting regulatory sequences required for full expression of Amy-p1 are located between the base pairs at -304 and -372 upstream of Amy-d3 gene. In other words, only a short region located upstream of Amy-d3 was found to be necessary and sufficient for the full expression of Amy-p1 in addition to its promoter. This region seems also necessary for the expression of Amy-d3.

Animals↗
PubMed1994

Genetic variation estimated in three Shorea species by the RAPD analysis.

Three species of Shorea (S. leprosula, S. acuminata and S. cursitii) were collected from a natural forest reserve of Malaysia and analyzed for genetic variation using the technique of random amplification of polymorphic DNA (RAPD) by the polymerase chain reaction (PCR). The average number of nucleotide substitutions was estimated. The nucleotide diversities within species were very similar and larger than those found in Drosophila melanogaster. The nucleotide divergences between these species are about 1.5 times the nucleotide diversities within the species, indicating that these species diverged from a common ancestor relatively recently.

Base Sequence↗
PubMed1994

A new methionine antagonist that has antifungal activity: mode of action.

A new antifungal, azoxybacilin (an unusual amino acid with an azoxy moiety) was identified from Bacillus cereus, and its in vitro antifungal activity and mode of action were investigated. Azoxybacilin was active against a broad spectrum of fungi. It was especially active against mycelial fungi, such as Aspergillus, and did not show antibacterial activity. No cross-resistance with antifungals currently on the market was observed. The IC50 values of azoxybacilin antifungal activity against Saccharomyces cerevisiae were significantly greater when amino acids containing sulfur were added to the growth medium, whereas other amino acids were not effective at all. We, therefore, tested the effect of the intermediates involved in the synthetic pathway of these amino acids. The activity markedly diminished when one of the following four intermediates was present in the medium:homocysteine, cysteine, cystathionine or methionine. These four intermediates were the same as those required for the growth of the O-acetylhomoserine sulfhydrylase mutant, S. cerevisiae ONO726, indicating that azoxybacilin would inhibit a step or steps in the sulfur-fixation pathway.

Amino Acids↗
PubMed1994

Involvement of the renin-angiotensin system in the development of left ventricular hypertrophy and dysfunction.

OBJECTIVES: To elucidate the regulation of cardiac gene expression by mechanical stress and to analyse molecular mechanisms associated with the involvement of angiotensin II (Ang II) in the development of cardiac hypertrophy and dysfunction. METHODS: Neonatal rat cardiocytes were cultured in deformable silicone dishes, and mechanical stress was imposed on the cardiocytes by stretching them. In in vivo studies, spontaneously hypertensive rats (SHR) were treated with a non-peptide, specific Ang II type 1 receptor antagonist, TCV 116. RESULTS: Expression of c-fos was rapidly induced, and fetal type genes such as skeletal alpha actin and beta myosin heavy chain genes were re-expressed by stretching. The mechanical stress decreased the expression of Ca(2+)-ATPase in the sarcoplasmic reticulum. With regard to signals for the development of cardiac hypertrophy, mechanical stress evoked c-fos expression via the activation of protein kinase C. The phosphorylation cascade (sequential activation of protein kinase C, Raf-1 kinase, mitogen-activated protein kinase kinase, mitogen-activated protein kinase and S6 kinase), which may be involved in protein synthesis and gene expression, was activated by mechanical stress in cardiocytes. Stretch-induced cardiac cellular hypertrophy was partially inhibited by TCV 116. TCV 116 treatment of SHR reduced left ventricular weight, left ventricular wall thickness, myocyte transverse diameter, V3 myosin heavy chain levels and the interstitial collagen volume fraction. CONCLUSIONS: These results indicate that Ang II may, in part, mediate the stretch-induced hypertrophic growth of cardiomyocytes via the type 1 Ang II receptor.

Animals↗
PubMed1994

[A case of simultaneous bilateral spontaneous pneumothorax].

We present a case of simultaneous bilateral pneumothorax. The patient did not have any symptom and the pneumothorax was detected by health care examination. He was introduced to our hospital and two thoracic drains were inserted into both intrathoracic space as soon as possible. Four days after he was performed a bilateral partial resection of the lung through a bilateral axillary incision. Postoperative course was excellent with almost no pain. The thoracic drains were removed on second postoperative day and the patient discharged on ninth postoperative day.

Adolescent↗
PubMed1994

Involvement of the renin-angiotensin system in the development of left ventricular hypertrophy and dysfunction.

OBJECTIVES: To elucidate the regulation of cardiac gene expression by mechanical stress and to analyse molecular mechanisms associated with the involvement of angiotensin II (Ang II) in the development of cardiac hypertrophy and dysfunction. METHODS: Neonatal rat cardiocytes were cultured in deformable silicone dishes, and mechanical stress was imposed on the cardiocytes by stretching them. In in vivo studies, spontaneously hypertensive rats (SHR) were treated with a non-peptide, specific Ang II type 1 receptor antagonist, TCV 116. RESULTS: Expression of the c-fos gene was rapidly induced, and fetal type genes such as skeletal alpha actin and beta myosin heavy chain genes were re-expressed by stretching. The mechanical stress decreased the expression of Ca(2+)-ATPase in the sarcoplasmic reticulum. With regard to signals for the development of cardiac hypertrophy, mechanical stress evoked c-fos expression via the activation of protein kinase C. The phosphorylation cascade (sequential activation of protein kinase C, Raf-1 kinase, mitogen-activated protein kinase kinase, mitogen-activated protein kinase and S6 kinase), which may be involved in protein synthesis and gene expression, was activated by mechanical stress in cardiocytes. Stretch-induced cardiac cellular hypertrophy was partially inhibited by TCV 116. TCV 116 treatment of SHR reduced left ventricular weight, left ventricular wall thickness, myocyte transverse diameter, V3 myosin heavy chain levels and the interstitial collagen volume fraction. CONCLUSIONS: These results indicate that AngII may, in part, mediate the stretch-induced hypertrophic growth of cardiomyocytes via the type 1 Ang II receptor.

Actins↗
PubMed1994

Mast cells display natural suppressor activity partially by releasing transforming growth factor-beta.

We have previously reported a method for inducing natural suppressor (NS) cells by long-term culture of normal adult mouse spleen cells. The NS cells were further identified as mucosal or immature mast cells by morphology, cytochemistry, histochemistry and function. A cloned immature mast cell line was also confirmed to have NS activity. As NS cells, the cell line suppressed non-specifically the plaque-forming cell (PFC) response. The NS cell-free supernatant was partially enriched by chromatography and some fractions suppressed the PFC response and thymocyte proliferation. Heat treatment of the fractions failed to deplete the suppressive activity. The fractions were confirmed, by immunoblotting analysis, to contain transforming growth factor (TGF)-beta. Recombinant human TGF-beta was also able to suppress the PFC response and thymocyte proliferation. Neutralizing anti-TGF-beta reversed the suppression by both human TGF-beta and the fraction. From the above results, it is clear that mast cells displayed NS activity, at least partially, through the release of TGF-beta.

Animals↗
PubMed1994

[A case of thoracoscopic pulmonary lobectomy for lung cancer].

A case of thoracoscopic right lower pulmonary lobectomy is reported. A 79-year-old man was admitted to our hospital after the accidental finding of a right pulmonary growth. A computed tomography (CT) scan of the thorax confirmed the presence of a neoplasm, 2.5 cm in diameter, at the posterior-basal segment of the right lower lobe. Considering the general condition of the patient and the characteristics of the lesion, we decided to perform a assess the possibility of a thoracoscopic lobectomy instead of the traditional posterolateral approach. The pulmonary artery was dissected with the new endoscopic cherry dissector, and ligated with the polyester suture material and Endo Clip then dived with Endo scissors. The lower pulmonary vein was dissected with this endoscopic cherry dissector and divided with Endo GIA 30 clamping the new thoracoscopic De Bakey type vascular clamp. The specimen was extracted through the minimal thoracotomy (15 cm). The postoperative course was uneventful with minimal postoperative pain, and the patient was discharged after complete surgical recovery with excellent functional and cosmetic results.

Aged↗
PubMed1994

[Genetic alterations of human colorectal cancer].

Genetic alterations of several oncogenes and tumor suppressor genes are associated with human colorectal carcinogenesis. Especially in mutations, the K-ras, p53, APC and DCC gene frequently occurred, and these gene alterations seem to have important roles in colorectal carcinogenesis. We investigated 28 human colon cancer specimens obtained from surgery and five human colon cancer cell lines by PCR-SSCP assay, PCR-OSH assay, RT-PCR or sequencing method. Forty percent of cancers from surgical specimens had Ki-ras 2 (codon 12/13), p53 (Exon 5-8), APC (MCR) gene mutations, and fifty-seven percent of them had lower expression of DCC gene that of normal matched colon mucosa of the same patient. G to A transition was the most frequent in K-ras mutational spectrum in this case; 25% of patients had both k-ras and p53 gene point mutations. Form the results, we concluded that it in colorectal carcinogenesis for both K-ras and p53 gene point mutations might not necessary occur.

Colonic Neoplasms↗