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S Kawano

Publications and source records attributed to S Kawano.

At least 55 records · Page 3Linked to original sources
PubMed2001

Changes in mRNA levels of alkaline phosphatase and tartrate-resistant acid phosphatase in femur of ovariectomized rats: effects of estrogen and unloading.

Our previous studies demonstrated that estrogen (E2) prevents the development of disuse atrophy of the femur in tail-suspended rats. To elucidate the mechanisms of this E2 action, we investigated the effects of E2 on the expression of alkaline phosphatase (ALP, a marker for bone formation) and tartrate-resistant acid phosphatase (TRAP, a marker for bone resorption) in the femur of ovariectomized and tail-suspended rats. One group of ovariectomized rats received estradiol dipropionate (OVX-E2), and the other the vehicle alone (OVX). Each group was subjected to tail-suspension. After 1, 3, 5 or 7 days of suspension, ALP and TRAP mRNA levels were determined by Northern blot analysis. The ALP mRNA level was not altered by suspension in the OVX group, but it gradually increased in the OVX-E2 group, the highest level being observed at day 5 of suspension. In contrast, TRAP mRNA significantly increased at days 5 and 7 in the OVX group, while it is decreased significantly from day 3 to 7 in the OVX-E2 group. These results indicate that E2 prevents disuse atrophy of the femur in an ovariectomized and tail-suspended rat model by stimulating bone formation and by inhibiting bone resorption.

Acid Phosphatase↗
PubMed2000

Representational difference analysis using myeloid cells from C/EBP epsilon deletional mice.

C/EBP epsilon is a recently cloned member of the C/EBP family of transcriptional factors. Previous studies demonstrated that the expression of this gene is tightly regulated in a tissue specific manner; it is expressed exclusively in myeloid cells. C/EBP epsilon-deficient mice developed normally but failed to generate functional neutrophils and eosinophils, and these mice died of opportunistic infections suggesting that C/EBP epsilon may play a central role in myeloid differentiation. To identify myelomonocytic genes regulated by the C/EBP epsilon gene, we performed representational difference analysis (RDA), a polymerase chain reaction (PCR)-based subtractive hybridization using neutrophils and macrophages from wild-type and C/EBP epsilon knockout mice. We identified a set of differentially expressed genes, including chemokines specific to myelomonocytic cells. Several novel genes were identified that were differentially expressed in normal myelomonocytic cells. Taken together, we have found several genes whose expression might be enhanced by C/EBP epsilon. (Blood. 2000;96:3953-3957)

Animals↗
PubMed2000

Analysis of T wave changes by activation recovery interval in patients with atrial septal defect.

We examined the distributions of the activation recovery interval (ARI), which is correlated with the local action potential duration (APD), to clarify the origin of the repolarization changes in ASD. The ECGs, QRST isointegral maps and ARI isochronal maps of 21 children with ASD from 3 to 5 years old in age were studied in comparison with 21 age-matched normal children. A conventional and 87 unipolar body surface ECG were simultaneously recorded. The ARIs were determined from the first derivatives of the ECG waveforms. Abnormal ST-T patterns were observed in 11 of 21 ASD, but only in two normal children. The QRST maps of a split positive area pattern were seen in 15 of ASD but none of the normal. In the ARI maps, all the normal children exhibited a short-ARI area on the left and a long-ARI area on the right side of the chest. In 19 of ASD, the ARI distribution revealed a leftward extension of the long-ARI area on the anterior chest, a relative shortening on the right anterior chest, and a localized prolonged ARI on the left anterior chest. The results suggest that right ventricular (RV) volume overload in ASD produces a localized prolongation of the APD on the RV epicardium.

Child, Preschool↗
PubMed2000

In vivo conformation of mitochondrial DNA revealed by pulsed-field gel electrophoresis in the true slime mold, Physarum polycephalum.

Pulsed-field gel electrophoresis (PFGE) was used to examine the in vivo and in vitro conformations of Physarum polycephalum mitochondrial DNA (mtDNA). We used plugs containing isolated mitochondria, isolated mitochondrial nucleoids (mt-nuclei), and isolated mtDNA, in addition to whole cells. The mtDNA contained in the myxamoebae, plasmodia, isolated mitochondria, and isolated mt-nuclei was circular, but most of the isolated mtDNA had been site-specifically fragmented and linearized during DNA preparation and storage under low ionic strength conditions. Restriction mapping of Physarum mtDNA by the direct digestion of the isolated mt-nuclei from two different strains, DP89 x AI16 and KM88 x AI16, resulted in the circular form. A linear mitochondrial plasmid, mF, is known to promote mitochondrial fusion and integration of itself into the mtDNA in Physarum. Linearization of mtDNA by the integration of the mF plasmid was demonstrated when we used PFGE to analyze isolated mitochondria from the plasmodial strain DP89 x NG7 carrying the mF plasmid (mF+). The PFGE system can be used not only to determine whether the form of mtDNA is linear or circular but also to analyze the dynamic conformational changes of mtDNA.

Animals↗
PubMed2000

Hematopoietic-specific expression of MEFV, the gene mutated in familial Mediterranean fever, and subcellular localization of its corresponding protein, pyrin.

Familial Mediterranean fever (FMF) is a recessively inherited disorder characterized by recurrent, self-limited attacks of fever and serositis and by infiltration of affected tissues by large numbers of neutrophils. A candidate gene for FMF was identified by positional cloning and named "MEFV." The corresponding protein was named "pyrin." To elucidate the currently unknown function of pyrin, we characterized its tissue distribution, regulation of expression during hematopoietic differentiation, and subcellular localization. Reverse transcription-polymerase chain reaction analysis, followed by hybridization with an internal oligonucleotide, demonstrated expression of MEFV in different populations of peripheral blood cells. Among hematopoietic cell lines, MEFV was almost exclusively expressed in cells of the myeloid lineage. Furthermore, MEFV messenger RNA was strongly expressed within 24 hours of dimethyl sulfoxide-induced granulocytic differentiation of HL-60 cells. Analysis of complementary DNA from human solid tumor-derived cell lines revealed expression of MEFV in several cell lines derived from colon and prostate cancers. Expression of MEFV fused to enhanced green fluorescent protein showed that pyrin localized in distinct patches in the cytoplasm, forming a perinuclear cap. Taken together, MEFV is predominantly expressed in myeloid cells and upregulated during myeloid differentiation, and the corresponding protein, pyrin, is expressed in the cytoplasm. (Blood. 2000;95:1451-1455)

Cells, Cultured↗
PubMed2000

In vitro DNA fragmentation of mitochondrial DNA caused by single-stranded breakage related to macroplasmodial senescence of the true slime mold, Physarum polycephalum.

We found that mitochondrial DNA (mtDNA) isolated from Physarum polycephalum fragmented itself in weak ionic solutions. The mtDNA was dissolved in STE (saline Tris-EDTA: 150 mM NaCl, 10 mM Tris-HCl, 1 mM EDTA), TE (10 mM Tris-HCl, 1 mM EDTA) and DW, and then electrophoresed in an agarose gel. The intact 86-kbp mtDNA band was seen in STE, but several novel bands appeared in TE and DW. In TE, two discrete bands appeared at 6.7-kbp (alpha-band) and 5.0-kbp (beta-band), whereas at least 17 discrete bands were observed in distilled water (DW). These fragmentation patterns were not stoichiometric, as seen when using restriction endonucleases, but were clearly different from the degradation of DNA caused by a physical shearing force or a contaminating nuclease. In this paper, we characterize this in vitro fragmentation of mtDNA from P. polycephalum. We located 19 fragments, including the alpha and beta fragments, on a mtDNA restriction map, and demonstrated that these cleavage sites were S1 nuclease-sensitive regions, which are single-stranded DNA regions such as nicks and gaps in the mtDNA. The alpha and beta fragments are derived from the region encoding ribosomal RNAs (rRNAs) and the ATP synthase (atpA) gene, while the other 17 fragments are not derived from any specific region, but the cleavage sites are located throughout the mtDNA molecule. In P. polycephalum, it is well known that the growth rate of macroplasmodia decreases with aging. Equal amounts of mtDNA from juvenile and aged macroplasmodia were electrophoresed and the frequency of the beta fragment in each sample was measured. The ratio of the beta band to the total signal including background was estimated to be 3.3-4.0% in juvenile macroplasmodia, whereas it increased to 8.3-28.2% in aged macroplasmodia. This result suggests that the in vitro fragmentation of mtDNA is associated with macroplasmodial senescence. The single-stranded breakage of mtDNA of P. polycephalum may accumulate with age.

Aging↗
PubMed2000

Isolation, characterization, and chromosomal mapping of an ftsZ gene from the unicellular primitive red alga Cyanidium caldarium RK-1.

The FtsZ protein is involved in eukaryote plastid division, but there is little information on its involvement in the plastid-dividing apparatus. To investigate the relationship between FtsZ and the plastid-dividing ring, the ftsZ gene was isolated from the unicellular primitive red alga Cyanidium caldarium RK-1. Comparison of several prokaryotic and eukaryotic FtsZ proteins shows that there are six highly conserved domains in the core region of FtsZ. To determine the chromosomal location of ftsZ, we first determined the electrophoretic karyotype of C. caldarium RK-1. Southern-hybridization analysis combined with CHEF revealed the chromosomes on which the ftsZ gene exist. Northern-hybridization analysis indicated that the C. caldarium RK-1 ftsZ gene is transcribed as a 1.9-kb molecule, and that the transcripts specifically accumulate just before plastid division. Phylogenetic analysis indicated that C. caldarium RK-1 and other eukaryotic ftsZ genes are the descendants of cyanobacterial ftsZ genes, supporting the current agreement that FtsZ is involved in plastid division.

Algal Proteins↗
PubMed2000

A putative mitochondrial ftsZ gene is present in the unicellular primitive red alga Cyanidioschyzon merolae.

Two ftsZ homologues were isolated from the unicellular primitive red alga Cyanidioschyzon merolae (CmftsZ1 and CmftsZ2). Phylogenetic analysis revealed that CmftsZ1 is most closely related to the ftsZ genes of alpha-Proteobacteria, suggesting that it is a mitochondrial-type ftsZ gene, whereas CmftsZ2 is most closely related to the ftsZ genes of cyanobacteria, suggesting that it is a plastid-type ftsZ gene. Southern analysis indicates that CmftsZ1 and CmftsZ2 are both single-copy genes located on chromosome XIV in the C. merolae genome. Northern analysis revealed that both CmftsZ1 and CmftsZ2 are transcribed, and accumulate specifically before cell and organelle division. The results of Western analysis suggest that CmFtsZ1 is localized in mitochondria.

Amino Acid Sequence↗
PubMed2000

Effect of pre-reperfusion residual flow on recovery from myocardial stunning: a myocardial contrast echocardiography study.

BACKGROUND: Myocardial contrast echocardiography (MCE) may be used to assess coronary microvasculature in patients with myocardial infarction. Myocardial contrast echocardiography-no reflow suggests poor functional outcome; however, MCE with reflow does not necessarily indicate good myocardial salvage or sufficient functional recovery from myocardial stunning. In this study, MCE was performed to assess the effect of pre-reperfusion residual flow (PRF) on the recovery from myocardial stunning. METHODS AND RESULTS: The size of the occluded bed, an area supplied with an infarct-related artery, was determined by comparing pre- and post-reperfusion MCE images in 40 patients with first acute myocardial infarction. Myocardial contrast echocardiography-no reflow was observed after reperfusion in 8 patients. Significant PRF was not recognizable in any of the 8 patients. The other patients with MCE reflow were subdivided into 2 groups on the basis of the ratio of the area perfused by PRF to that of the occluded bed: 14 patients with the ratio of more than 10% (PRF[+]), and the other 18 patients (PRF[-]). The wall motion score (0, normal to 4, dyskinetic) was obtained in the convalescent stage. RESULTS: (1) Wall motion of the infarct area after day 3 was better in patients with PRF than in patients without PRF. (2) Left ventricular functional improvement in the long term was remarkable in patients with good reflow and PRF(+), modest in patients with good reflow but PRF(-), and not detectable in patients with MCE-no reflow. No significant correlation was found between angiographic collateral grades and PRF. CONCLUSIONS: The presence of residual flow within the infarct area before reperfusion results in not only good myocardial salvage but also rapid functional recovery from myocardial stunning.

Coronary Circulation↗
PubMed2000

Role of mucosal blood flow: a conceptional review in gastric mucosal injury and protection.

The present article overviews the role of gastric mucosal blood flow (MBF) in gastric mucosal injury and protection. The MBF maintains the structure and function of the stomach and, thereby, is closely associated with the pathogenesis and the healing of gastrointestinal lesions. Gastric blood flow was regulated and modified by systemic and also local metabolic factors, such as prostaglandin, leukotrienes and other endogenous chemical mediators, in the mucosa. In the present article, we review the role of endothelin (ET) and nitric oxide (NO) in the development of gastric mucosal injury and protection via mucosal microcirculation. Endothelin-1 was increased under various stressful conditions and caused microcirculatory disturbances resulting in mucosal injury. Inhibitors of NO aggravated mucosal injury induced by ethanol, which produced mucosal congestion. Thus, regionally disturbed gastric circulation is closely associated with the pathogenesis of ethanol- and non-steroidal anti-inflammatory drug-induced gastric lesions. The endothelium-derived vasoactive substances ET and NO regulate gastric mucosal microcirculation and an imbalance of endothelium-derived factors may play an important pathophysiological role in the development of gastric lesions.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Cyclo-oxygenase-2 inhibitors suppress epithelial cell kinetics and delay gastric wound healing in rats.

BACKGROUND AND AIMS: The present study examined the effects of NS-398, a specific cyclo-oxygenase-2 inhibitor, on gastric mucosal cell kinetics and gastric wound healing following acid-induced injury. METHODS: Male Sprague-Dawley rats were fasted for 24 h and then 0.6 mol/L hydrochloric acid (HCl; 1 mL) was administered into the stomach; NS-398 or indomethacin was administered to the animals 10 min after the acid. Levels of constitutive cyclo-oxygenase (COX-1) and mitogen-inducible cyclo-oxygenase (COX-2) in the gastric mucosa were analysed using western blotting and immunohistochemical staining. The grade of the lesion was assessed using planimetry and histological examination, including immunohistochemistry for proliferating cell nuclear antigen (PCNA). RESULTS: Although there was strong expression of COX-1, there was minimal expression of COX-2 in the gastric mucosa. Expression of COX-2 was enhanced mainly in surface epithelial cells and neck cells following HCl administration. Gastric mucosal ulcers and erosions healed within 48 h, during which time the proliferative zone expanded in the control animals. Indomethacin and NS-398 suppressed the expansion of the proliferative zone and delayed the healing of the gastric injury. CONCLUSION: The present study demonstrated that cyclo-oxygenase-2 inhibitors delay gastric wound healing by suppressing expansion of the mucosal proliferative zone. These results provide evidence that cyclo-oxygenase-2 has an important role in gastric mucosal regeneration.

Animals↗
PubMed2000

Expression of cyclooxygenase-2 and nitrotyrosine in human gastric mucosa before and after Helicobacter pylori eradication.

To determine whether cure of Helicobacter pylori infection influences the expression of COX-2 and nitrotyrosine in the distal stomach of humans, biopsy specimens were examined immunohistochemically. H. pylori infection was determined using a rapid urease test, culture and histology. Positive staining of COX-2/nitrotyrosine in the epithelium was expressed as the percentage of stained cells to the total epithelial cells. There was a significant increase in COX-2/nitrotyrosine staining in H. pylori -positive subjects compared with H. pylori -negative subjects. Cure of the infection resulted in a significant decrease in both COX-2/nitrotyrosine staining in all patients (52.1+/-12.1% vs 15. 4+/-7.2%, P<0.001; and 57.3+/-13.6% vs 36.1+/-18.0%, P<0.01, respectively). However, immunoreactivity of COX-2/nitrotyrosine was observed in all cases with intestinal metaplasia even after the cure of H. pylori infection.Thus, cure of H. pylori infection may decrease the risk of gastric carcinogenesis due to COX-2 and NO-related compounds in gastric mucosa but not in those patients with intestinal metaplasia.

Adult↗
PubMed2000

Endothelin-1 and right-sided heart failure in rats: effects of an endothelin receptor antagonist on the failing right ventricle.

The development of pulmonary hypertension (PH) causes right-sided heart failure. We investigated whether chronic treatment with the endothelin-A- (ETA) receptor antagonist BMS-193884 in rats with monocrotaline- (MCT) induced PH improves right-sided heart failure. Administration of BMS-193884 (100mg/kg) was commenced on the day before treatment with MCT. At 19 days, hemodynamics were measured under anesthesia and hearts were removed. The right ventricular systolic pressure (RVSP), an indicator for pulmonary hypertension, was remarkably elevated in the PH group compared with the normal control group. BMS-193884 effectively prevented this elevation. The central venous pressure, an indicator for right-sided heart failure, was markedly increased in the PH group. This increase was reduced to the normal level by BMS-193884. In the failing right ventricle of the PH group, the expression of atrial natriuretic peptide (ANP) mRNA, which is a molecular marker for the failing heart, was markedly increased. BMS-193884 greatly prevented this increase. The present study suggests that ET-1 contributes to the right-sided heart failure caused by PH and that an ETA-receptor antagonist is a beneficial drug which improves both hemodynamics and cardiac gene expression in the failing right ventricle.

Animals↗
PubMed2000

Induction of cyclooxygenase-2 in rat gastric mucosa by rebamipide, a mucoprotective agent.

Recent studies indicate an expression of mitogen-inducible cyclooxygenase (COX-2) in gastric mucosa. Rebamipide, a mucoprotective agent enhances prostaglandin (PG) synthesis. The present study was designed to clarify the mechanism for rebamipide-induced mucosal protection. Male Sprague-Dawley rats were administered 5, 15, or 50 mg/kg/day rebamipide for 14 days. The expression of constitutive cyclooxygenase (COX-1) and COX-2 in gastric mucosa was determined using Western blot analysis. Another series of rats was used to examine 1) the levels of PGE(2) in stomach with and without pretreatment with a COX-2 inhibitor; 2) the protective action of rebamipide against gastric damage caused by 0.6 N HCl; and 3) the effects of a COX-2 inhibitor on rebamipide-induced gastric mucosal protection. COX-2 expression was enhanced, whereas COX-1 expression did not change significantly in the gastric mucosa of rats after treatment with rebamipide. The gastric mucosal PGE(2) was higher in the rebamipide groups than in the vehicle-treated group. Rebamipide also suppressed gastric damage induced by HCl in a dose-dependent manner. A COX-2 inhibitor blocked the rebamipide-induced increase in mucosal PGE(2), and mucosal protection induced by rebamipide. The results indicate that rebamipide induces COX-2 expression, increases PGE(2) levels, and enhances gastric mucosal defense in a COX-2-dependent manner. Thus, COX-2 has an important role in the effects of rebamipide on gastric mucosal protection.

Alanine↗