Search PubMed⌕ Search

Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 433 records · Page 24Linked to original sources

Correlation between intracranial pressure (ICP) and changes in CT images of cerebral hemorrhage.

The relationship between intracranial pressure and CT images was investigated in 80 cases of cerebral hemorrhage that occurred between 1984 and 1990. In traumatic intracerebral hematoma, positive correlation was found between intracranial pressure and both shift of midline structures and volume of hematoma except in the occipital lobe or at the base of the frontal lobe. In nontraumatic intracerebral hematoma, increased intracranial pressure was found to correlate with changes in the configuration of the lateral ventricles, intraventricular hemorrhage, and compression of the basal cisterns and cortical sulci. No correlation between intracranial pressure and hematoma volume was observed, most likely due to the number of elderly patients in the subject population. In nontraumatic subarachnoid hemorrhage, positive correlation existed between increased intracranial pressure and intraventricular hemorrhage as well as Evans' ratio calculated using repeat CT images that were obtained due to disturbances in cerebrospinal fluid circulation. These results suggest that the degree by which intracranial pressure increases in patients with cerebral hemorrhage can be estimated by the changes in CT images.

Adolescent↗

Quantitative cytology of nasal secretions with perennial allergic rhinitis in children: comparison of noninfected and infected conditions.

This study was performed to quantify the number of inflammatory cells in nasal secretions from pediatric patients with perennial allergic rhinitis under noninfected and infected conditions. Nasal secretions were obtained from seven children under both noninfected and infected conditions with perennial allergic rhinitis to house dust mites, and secondary quantitative cytology was performed on the secretions. The number of neutrophils under infected condition was significantly higher than that under noninfected condition (P < .05), whereas the number of eosinophils in infected condition was significantly lower than that in noninfected condition (P < .05). The ratio of eosinophil count to neutrophil count was more than 0.1 in noninfected condition. The ratio was significantly decreased in infected condition (P < .02). These results suggest that the distribution of inflammatory cells in the nasal mucus of children with allergic rhinitis would be modified under infected condition.

Adolescent↗

Studies on the rabies virus RNA polymerase: 2. Possible relationships between the two forms of the non-catalytic subunit (P protein).

We investigated the relationship between the two forms of rabies virus P protein, a non-catalytic subunit of rabies virus RNA polymerase. The two displayed different electrophoretic mobilities as 37- and 40-kDa polypeptides, hence termed as p37 and p40, respectively. Double labeling experiments with [3H]leucine and [32P]orthophosphate demonstrated that p40 was much more phosphorylated than p37. Treatment of the virion proteins with alkaline phosphatase eliminated only p40, and not 37-kDa polypeptide. The p37 was a major product of the P gene, and was accumulated in the infected cell and incorporated into the virion. On the other hand, p40 was apparently detected only in the virion, and little detected in the cells. Treatment of infected cells with okadaic acid, however, resulted in significant accumulation of p40 in the cell, suggesting that p40 was continuously produced in the cell but dephosphorylated quickly. We detected both 37- and 40-kDa products in P cDNA-transfected animal cells, while only a 37-kDa product was produced in Escherichia coli. Incubation of 37-kDa products from E. coli with the lysates of animal cells in vitro resulted in the production of a 40-kDa product, which was also shown to be suppressed by the heparin. From these results, it is suggested that p40 is produced by the hyperphosphorylation of a 37-kDa polypeptide, which depends on certain heparin-sensitive cellular enzyme(s) and occurs even in the absence of the other viral gene products, and that p40 is reverted quickly to p37 in the infected cells, probably being dependent on some virus-induced factor(s).

Amino Acid Sequence↗

Gastric mucosal damage induced by compound 48/80: roles of serotonin and nitric oxide.

The roles of nitric oxide (NO) and serotonin (5-HT) in the development of gastric mucosal lesions induced by compound 48/80 (48/80) were investigated in rats. Repeated i.p. administration of 48/80 (1 mg/kg) produced damage in the stomach with severe oedema in the submucosa. The lesions induced by 48/80 were prevented by FPL-52694 (a mast cell stabilizer) and methysergide but not tripelennamine. The lesions were also inhibited by simultaneous administration of N(G)-monomethyl-L-arginine (L-NMMA), and this effect was mimicked by inducible NO synthase (iNOS) inhibitors, such as aminoguanidine or dexamethasone and significantly antagonized by coadministration of L-arginine. The mucosal myeloperoxidase activity, thiobarbituric acid reactants and vascular permeability in the stomach were all increased after 48/80 treatment and the changes were also attenuated by cotreatment with L-NMMA. Repeated s.c. treatment with 5-HT (20 mg/kg) provoked similar gastric lesions, which were also prevented by methysergide and iNOS inhibitors, as well as antioxidative drugs, such as allopurinol (a xanthine oxidase inhibitor) and hydroxyurea (a neutrophil-reducing agent). The Ca2 -independent NO synthase (NOS) activity was increased in the gastric mucosa after administration of 48/80 or 5-HT and this change was inhibited by dexamethasone. These results suggest that: (i) the repeated administration of 48/80 induced inflammatory gastric lesions in the rat stomach, mediated by endogenous 5-HT; (ii) NO/iNOS is involved in the pathogenic mechanism of 48/80-induced gastric lesions, in addition to oxyradical formation; and (iii) the deleterious role of NO in this lesion model can be accounted for by a cytotoxic action of peroxynitrite that is formed in the presence of superoxide radicals.

Animals↗

Renal tubular apoptosis after release of ureteral obstruction in the rat kidney.

BACKGROUND: Information concerning the mechanisms underlying recovery from hydronephrosis is limited. The frequency of apoptosis during healing from hydronephrosis was studied using a rat kidney model. METHODS: The presence of apoptosis was studied using an in situ DNA 3' end labeling method, electron microscopy, and agarose gel electrophoresis. RESULTS: The degree of apoptosis in both the medulla and cortex gradually increased during ureteral obstruction as shown by in situ DNA 3' end labeling. Release of the ureteral obstruction resulted in a further increase in the degree of apoptosis in the medulla and cortex. The increase in apoptosis in the medulla was transient and lasted for only 4 days following release, while that in the cortex continued for at least 3 weeks. Apoptosis in the glomerulus was not observed. Electron microscopy revealed cells with aggregated chromatin in compact granular masses that abutted the nuclear membrane. Following release of ureteral obstruction, DNA fragmentation characteristic of apoptosis was visible on agarose gel electrophoresis. CONCLUSION: These results suggest that apoptosis is involved in post-obstructive tubular damage in the rat kidney.

Animals↗

Efficient transfer of the pheromone-independent Enterococcus faecium plasmid pMG1 (Gmr) (65.1 kilobases) to Enterococcus strains during broth mating.

Plasmid pMG1 (65.1 kb) was isolated from a gentamicin-resistant Enterococcus faecium clinical isolate and was found to encode gentamicin resistance. EcoRI restriction of pMG1 produced five fragments, A through E, with molecular sizes of 50.2, 11.5, 2.0, 0.7, and 0.7 kb, respectively. The clockwise order of the fragments was ACDEB. pMG1 transferred at high frequency to Enterococcus strains in broth mating. pMG1 transferred between Enterococcus faecalis strains, between E. faecium strains, and between E. faecium and E. faecalis strains at a frequency of approximately 10(-4) per donor cell after 3 h of mating. The pMG1 transfers were not induced by the exposure of the donor cell to culture filtrates of plasmid-free E. faecalis FA2-2 or an E. faecium strain. Mating aggregates were not observed by the naked eye during broth mating. Small mating aggregates of several cells in the broth matings were observed by microscopy, while no aggregates of donor cells which had been exposed to a culture filtrate of E. faecalis FA2-2 or an E. faecium strain were observed, even by microscopy. pMG1 DNA did not show any homology in Southern hybridization with that of the pheromone-responsive plasmids and broad-host-range plasmids pAMbeta1 and pIP501. These results indicate that there is another efficient transfer system in the conjugative plasmids of Enterococcus and that this system is different from the pheromone-induced transfer system of E. faecalis plasmids.

DNA, Bacterial↗

Effects of diabetes mellitus on the contractile activity of carbachol and galanin in isolated gastric fundus strips of rats.

The role of the cholinergic and peptidergic pathways in the impairment of gastric motility associated with diabetic gastroparesis was assessed at the postsynaptic level using isolated fundus smooth muscle strips. Maximal contractile responses to carbachol and galanin were significantly decreased in fundus strips isolated from rats rendered diabetic by a single intraperitoneal injection of streptozotocin (STZ, 70 mg/kg) 1, 4 and 8 weeks before experiments. We also observed notable decrements in the slopes and Hill's coefficients without conspicuous changes in the EC50 of the respective galanin concentration-response curves measured in strips obtained from STZ animals after 4 and 8 weeks. L-NAME reversed the above-mentioned alterations in an L-arginine-sensitive manner in STZ rats after 4 weeks but not in STZ rats after 8 weeks. The blood plasma nitrite/nitrate levels in STZ animals after 4 and 8 weeks were increased by 44.6 and 61.9%, respectively. Ca2+-independent nitric oxide synthase activity in gastric fundus strips and stomach corpus mucosa from STZ rats after 4 weeks was markedly enhanced by 37.4 and 31.9%, respectively, suggesting an enhanced nitric oxide production. In vivo insulin treatment prevented diabetes-induced alterations in smooth muscle contractility. We conclude that the smooth muscle dysfunction evoked by experimental diabetes causing diminished contractions of fundus strips to carbachol and galanin is at least partly due to the increased nitric oxide synthesis.

Animals↗

Autocrine motility factor in pulmonary adenocarcinomas: results of an immunohistochemical study.

Autocrine motility factors (AMF) have been shown to play an important role in tumor cell migration and metastasis. We have detected AMF expression in tissue specimens from 119 patients with pulmonary adenocarcinoma and examined the relationship between AMF expression, clinicopathological factors and prognosis. AMF expression was correlated with lymph node metastasis and stage. The prognosis of AMF-positive patients was poorer than that of AMF-negative patients. The expression of AMF correlated with more tumor aggressiveness and worse prognosis in pulmonary adenocarcinomas.

Adenocarcinoma↗

Characterization of mouse retinoid X receptor (RXR)-beta gene promoter: negative regulation by tumor necrosis factor (TNF)-alpha.

A genomic clone of mouse retinoid X receptor (RXR)-beta (Rxrb) has recently been isolated and mapped within the H2-K region of the mouse major histocompatibility complex. A putative 250-bp promoter, which is located between Rxrb and H2-Ke4, and may possibly be their common promoter, has also been identified. In order to study the gene regulation of Rxrb, we analyzed the transcriptional function of the Rxrb promoter with chimeric constructs containing the Rxrb promoter fragments fused upstream of a firefly luciferase cDNA, which were transiently transfected into rat GH3 cells. We found that 1) a part of the H2-Ke4 genomic region (1.9-kb), as well as the 250-bp promoter, was transcriptionally active as an Rxrb promoter; 2) tumor necrosis factor (TNF)-alpha significantly repressed the activity of the 250-bp promoter although thyroid hormone, 9-cis retinoic acid, interleukin (IL)-1beta, and IL-6 did not affect the activity; 3) either the change in orientation or point mutations of a consensus NF-kappaB site located in the 250-bp promoter did not affect the repression; 4) SB 203580, a highly specific inhibitor of p38 mitogen-activated protein (MAP) kinase, completely abolished the repression by TNF-alpha. These data suggest that TNF-alpha represses the promoter activity of the 250-bp region, and the repression is mediated by p38 MAP kinase independent of NF-kappaB. We thus have first shown a relation between the retinoic acid receptor and a cytokine TNF-alpha.

Alitretinoin↗

A case of dobutamine-induced coronary arterial spasm with ST-segment elevation.

A 55-year-old Japanese woman demonstrated ST-segment elevation in leads I, aVL, and V3-V6 with chest pain both in an ergometer exercise test and on dobutamine stress echocardiography. Although the baseline coronary arteriogram revealed no organic stenosis, total occlusion of the distal portion of the posterolateral branch of the left circumflex artery was observed during dobutamine infusion with ST-segment elevation and chest pain. This is a rare case of documented dobutamine-induced coronary arterial spasm.

Coronary Vasospasm↗

Doppler echocardiographic assessment and cardiac gene expression analysis of the left ventricle in myocardial infarcted rats.

The purpose of this study was to examine cardiac geometry and function by Doppler echocardiography and to analyze mRNA expression of cardiac phenotype and extracellular matrix in myocardial infarcted rats. Doppler echocardiograms and hemodynamics were measured 2 weeks after myocardial infarction (MI). mRNA levels in the non-infarcted left ventricle (LV) and infarct site were measured by Northern blot analysis. LV internal diastolic dimension was greater in infarcted (MI) than in sham-operated rats (control) (MI 7.2+/-0.3 mm vs control 4.6+0.3 mm, p<0.01). The fractional shortening decreased in MI rats (MI 32+4% vs control 61+/-3%, p<0.01). Peak early filling velocity increased in MI rats (MI 91+/-5 cm/sec vs control 72+/-4 cm/sec, p<0.05), and deceleration rate of the early filling wave was more rapid in rats with MI (MI 25.1+/-2.8 m/sec2 vs control 12.4+/-1.7 m/sec2, p < 0.01). Late filling velocity decreased (MI 16+/-3 cm/sec vs control 35+/-6 cm/sec, p <0.05), resulting in a marked increase in the ratio of early filling to late filling (MI 7.1+/-1.2 vs control 2.5+/-0.4, p<0.01). mRNA levels for beta-myosin heavy chain (beta-MHC), a-skeletal actin, atrial natriuretic polypeptide (ANP), collagen types I and III, and matrix metalloproteinase 2 (MMP-2) in the non-infarcted LV increased significantly by 1.8-, 2.4-, 4.7-, 2.6-, 2.1- (all p<0.01) and 1.4-fold (p<0.05), respectively, compared with sham-operated myocardium. In the infarct site, mRNA levels for transforming growth factor (TGF)-beta1, collagen types I and III, and MMP-2 significantly increased by 3.2-, 11.0-, 9.7-, and 6.3-fold (all p<0.01), respectively, compared with sham-operated myocardium. Myocardial infarcted rat was characterized by cavity dilation and marked abnormalities of systolic and diastolic function, accompanied by a shift of myocytes to fetal phenotype and activation of collagen genes in the non-infarcted myocardium.

Actins↗

Effect of manidipine hydrochloride, a calcium antagonist, on isoproterenol-induced left ventricular hypertrophy.

We examined the effect of a calcium antagonist, manidipine hydrochloride, on cardiac hypertrophy and the expression of the atrial natriuretic peptide (ANP), transforming growth factor beta 1 (TGF-beta 1), and extracellular matrix protein genes in rats with isoproterenol-induced cardiac hypertrophy. Rats were continuously infused with saline or isoproterenol (0.5 mg/kg per day) for 7 days using an osmotic minipump. Treatment with manidipine hydrochloride (once a day at 3 mg/kg) began 1 day before minipump implantation and continued until the end of the experiments (each group; n = 6). After treatment, left ventricular weight was measured and mRNA was extracted and analyzed by Northern blot hybridization. Isoproterenol increased left ventricular weight (2.40 +/- 0.04 g/kg; p < 0.01) without increasing blood pressure. ANP, collagen type I and type III, and fibronectin mRNAs were increased 1.5-(p < 0.01), 1.9- (p < 0.01), 2.7- (p < 0.01), and 3.2-fold (p < 0.01), respectively, by isoproterenol infusion. However, TGF-beta 1, collagen type IV, and laminin B1 and B2 mRNA levels were unchanged by isoproterenol. Manidipine hydrochloride prevented isoproterenol-induced left ventricular hypertrophy (2.26 +/- 0.02 g/kg; p < 0.01) and expression of mRNA of ANP (0.9-fold of the control value; p < 0.01), collagen types I (1.1-fold; p < 0.01) and type III (1.6-fold; p < 0.01), and fibronectin (1.1-fold; p < 0.01). Thus, manidipine hydrochloride prevented cardiac hypertrophy and changes in the expression of genes for ANP and interstitial components of extracellular matrix induced by isoproterenol.

Animals↗

Metaiodobenzylguanidine and heart rate variability in heart failure.

It is assumed that the low-frequency power (LF) of heart rate variability (HRV) increases with progress of congestive heart failure (CHF), therefore positively correlating with cardiac 123I-metaiodobenzylguanidine (MIBG) washout. It is demonstrated here that HRV, including normalized LF, correlated inversely with MIBG washout and positively with the ratio of heart-to-mediastinum MIBG activity in controls and CHF patients, whereas these correlations were not observed within CHF patients. Thus MIBG washout may increase and HRV including normalized LF may decrease with CHF, although the HRV and MIBG measures may not similarly change in proportion to the severity of the cardiac autonomic dysfunction in CHF.

Adult↗

The effect of vasopressin V1- and V2-receptor antagonists on hemodynamics in early and late phase after myocardial infarction in rats.

This study was designed to assess the effect of a nonpeptide vasopressin V1-receptor antagonist, OPC-21268, and a vasopressin V2-receptor antagonist, OPC-31260, on hemodynamics in the early phase and the late phase after myocardial infarction in rats. In the early phase, OPC-21268 (30 mg/kg/day) or OPC-31260 (30 mg/kg/day) was orally administered from day 1 to day 5 after the operation; and hemodynamics were measured at day 5, in the late phase from 10 weeks to 11 weeks and measured at the end of 11 weeks. In the early phase, OPC-21268 reduced the left ventricular end-diastolic pressure (LVEDP) concomitantly with the reduction in systemic blood pressure, but did not change LVEDP in the late phase. OPC-31260 reduced LVEDP and central venous pressure in both phases. OPC-21268 improved hemodynamics only in the early phase and OPC-31260 improved it in both phases.

Administration, Oral↗

Angiotensin II type 1-receptor antagonist candesartan cilexitil prevents left ventricular dysfunction in myocardial infarcted rats.

The purpose of this study was to analyze the effect of the angiotensin II type 1-receptor antagonist candesartan cilexitil on left ventricular systolic and diastolic function and mRNA expression of contractile proteins, collagen, and Ca2+ handling protein in myocardial-infarcted rats. After myocardial infarction, the animals were randomly assigned to candesartan cilexitil-treated or untreated groups (MI). We performed Doppler-echocardiographic examination and measured the hemodynamics at four and twelve weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. At four weeks in MI, left ventricular end-diastolic dimension increased (Control, 6.2+/-0.6 mm; MI, 8.7+/-0.6 mm; P < 0.01), fractional shortening decreased (Control, 41+/-5%; MI, 16+/-3%; P < 0.01) and E wave deceleration rate increased (Control, 14.3+/-2.0 m/sec2; MI, 23.3+/-2.3 m/sec2; P < 0.01). Candesartan cilexitil significantly prevented these changes. The mRNA expressions of beta-myosin heavy chain, alpha-skeletal actin, atrial natriuretic peptide, and collagens I and III in the non-infarcted left ventricle and right ventricle were increased at four weeks and were significantly suppressed by treatment with candesartan cilexitil. At four weeks, Na+-Ca2+ exchanger mRNA expression was increased, and candesartan cilexitil suppressed this increase. At twelve weeks, sarcoplasmic reticulum Ca2+-ATPase mRNA expression in the infarcted region including the adjacent non-infarcted left ventricle and right ventricle were decreased and candesartan cilexitil restored it to the control level. Candesartan cilexitil prevented the systolic and diastolic dysfunction and abnormal cardiac mRNA expression in myocardial-infarcted rats.

Angiotensin Receptor Antagonists↗

Production of exfoliative toxin A by Staphylococcus aureus isolated from mastitic cow's milk and farm bulk milk.

The production of exfoliative toxins A and B (ETA and ETB) by Staphylococcus aureus isolated from mastitic cow's milk and farm bulk milk was examined by the reverse passive latex agglutination method (RPLA). ETA was detected in 2 (1.2%) of 162 isolates from mastitic cow's milk and in 1 (0.6%) of 166 isolates from farm bulk milk. RPLA titers of these isolates were much lower than in human isolates. No ETB was detected in any of the isolates tested. These ETA-positive isolates belonged to bovine ecovar. They were non-typable using the international phage set for human strains. When these ETA-positive isolates were subcutaneously inoculated into neonatal mice, general exfoliation of the epidermis accompanied by the so-called Nikolsky sign was not recognized. By the immunoblotting and PCR methods, however, ETA and eta gene were recognized in the ETA-positive isolates from mastitic cow's milk and farm bulk milk. These data suggest that ETA is also produced by bovine isolates of S. aureus, but in smaller quantities.

Animals↗

Genetic characterization of parainfluenza virus 3 derived from guinea pigs.

To understand the relationship between novel parainfluenza virus 3 (PIV-3), which has recently been isolated from the lungs of guinea pigs, and other PIV-3 strains, we determined the complete nucleotide sequence of the novel PIV-3 (GPv) genome. A comparison of the nucleotide sequence among PIV-3s, including bovine PIV-3, revealed that GPv is closely related to human PIV-3. The results of the phylogenetic analysis clearly showed that GPv is a lineage of human PIV-3, suggesting that GPv has probably been introduced into guinea pig colonies via infected humans.

Animals↗

Interleukin-1beta administered intracerebroventricularly stimulates the release of noradrenaline in the hypothalamic paraventricular nucleus via prostaglandin in the rat.

We evaluated the effect of intracerebroventricular (i.c.v.) administration of interleukin (IL)-1beta on the rectal temperature and the release of noradrenaline (NA) in the hypothalamic paraventricular nucleus (PVN) of the rat. IL-1beta increased rectal temperature at doses ranging from 300 pg to 300 ng, whereas it, at doses ranging from 3 ng to 300 ng, significantly stimulated the release of NA in the PVN measured by intracerebral microdialysis. The stimulatory effect of IL-1beta on the release of NA was blocked by the subcutaneous injection of indomethacin. These findings suggest that IL-1beta stimulates the release of NA in the PVN via prostaglandin, and that the release of NA in the PVN is not necessarily related to the increase in body temperature.

Animals↗