Search PubMed⌕ Search

Biomedical subjects

T Katagiri

Publications and source records attributed to T Katagiri.

At least 37 records · Page 2Linked to original sources
PubMed2001

Construction and characterization of BAC libraries for three fish species; rainbow trout, carp and tilapia.

Bacterial artificial chromosome (BAC) libraries are important tools for genomic research. We have constructed seven genomic BAC libraries from three fish species, rainbow trout (Oncorhynchus mykiss), carp (Cyprinus carpio) and tilapia (Oreochromis niloticus). The two rainbow trout BAC libraries have average insert sizes of 58 and 110 kb. The average size of inserts in the carp BAC library is 160 kb. The average insert sizes of the four tilapia BAC libraries are 65, 105, 145 and 194 kb, respectively. These libraries represent good coverage of each genome (2-64 x coverage). The libraries can be screened by conventional colony hybridization and provide a starting point for the construction of high-density filtres or polymerase chain reaction (PCR) screening approaches. These BAC libraries will facilitate the positional cloning of quantitative trait loci (QTLs) for a variety of economically important traits in these species.

Animals↗
PubMed2001

Successful treatment with cyclosporin A for myelodysplastic syndrome with erythroid hypoplasia associated with T-cell receptor gene rearrangements.

Myelodysplastic syndrome (MDS) with erythroid hypoplasia, a rare form of MDS, has not yet been clearly defined. We report four patients with MDS with erythroid hypoplasia who received immunosuppressive therapy. All were elderly, had severe transfusion-dependent anaemia, morphological evidence of myelodysplasia and a low percentage (3.2-13.6%) of erythroid precursors. Administration of cyclosporin A (CsA) improved their anaemia; all transfusion-dependent patients achieved transfusion-independence. An inverted CD4/8 ratio was seen in three patients who also demonstrated T-cell receptor (TCR)-beta and -gamma gene rearrangements by Southern blotting and clonality by polymerase chain reaction. Treatment with CsA can be an attractive alternative treatment for patients with MDS with erythroid hypoplasia, which may be associated with a clonal abnormality in T cells.

Aged↗
PubMed2001

Involvement of a novel Arabidopsis phospholipase D, AtPLDdelta, in dehydration-inducible accumulation of phosphatidic acid in stress signalling.

Phospholipid metabolism is involved in plant responses to drought and salinity stress. To investigate the role of phospholipase D (PLD) and its product phosphatidic acid (PtdOH) in stress signalling, we isolated a novel PLD cDNA, designated AtPLDdelta, by screening a cDNA library prepared from dehydrated Arabidopsis thaliana. The AtPLDdelta protein, of 868 amino acids, has a putative catalytic domain and a C2 domain that is involved in Ca2+/phospholipid binding. The AtPLDdelta mRNA accumulated in response to dehydration and high salt stress. Histochemical analysis showed that the AtPLDdelta gene is strongly expressed in the vascular tissues of cotyledons and leaves under dehydration stress conditions. Under normal growth conditions, AtPLDdelta was expressed in roots, leaves, stems and flowers but not in siliques. We showed that dehydration stimulates the accumulation of PtdOH. The accumulation of PtdOH in response to dehydration was significantly suppressed in AtPLDdelta antisense transgenic plants. These results suggest that AtPLDdelta may be involved in PtdOH accumulation in the dehydration stress response.

Amino Acid Sequence↗
PubMed2001

Association of the mitochondrial DNA 5178A/C polymorphism with maternal inheritance and onset of type 2 diabetes in Japanese patients.

The mitochondrial DNA 5178A/C (mt5178A/C) polymorphism is associated with longevity and adult onset diseases. We investigated an association of the mt5178A/C polymorphism with the occurrence and clinical features of type 2 diabetes. Two hundred and seventy Japanese patients with type 2 diabetes (181 men and 89 women) and 254 control subjects without diabetes were studied. Patients with mutations at position 3243 in the mitochondrial DNA were excluded. Genotype was determined by the polymerase chain reaction-restriction fragment length polymorphism method. Various clinical features including age at disease onset were compared between the patients with the mt5178A and mt5178C alleles. Mt5178C was observed more frequently in patients with type 2 diabetes than in control subjects (65.9% vs 57.9%, P = 0.058). Clear information about the maternal history of diabetes was obtained from 233 diabetic patients. Patients with a maternal history of diabetes carried the mt5178C allele (58/75, 77.3%) more frequently than did patients without a maternal history of diabetes (100/158, 63.3%; P = 0.032) and control subjects (57.9%; P = 0.002). The mean age at onset of diabetes was significantly lower in patients with mt5178C (47.6 +/- 11.4 years) than in patients with mt5178A (51.5 +/- 10.0 years; P = 0.0073). The mt5178A/C polymorphism may be associated with maternal inheritance of type 2 diabetes and may influence the age at onset through deterioration of mitochondrial function.

Adolescent↗
PubMed2001

Hyperosmotic stress induces a rapid and transient increase in inositol 1,4,5-trisphosphate independent of abscisic acid in Arabidopsis cell culture.

Phospholipid metabolism is involved in hyperosmotic-stress responses in plants. To investigate the role of phosphoinositide-specific phospholipase C (PI-PLC)-a key enzyme in phosphoinositide turnover-in hyperosmotic-stress signaling, we analyzed changes in inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) content in response to hyperosmotic shock or salinity in Arabidopsis thaliana T87 cultured cells. Within a few s, a hyperosmotic shock, caused by mannitol, NaCl, or dehydration, induced a rapid and transient increase in Ins(1,4,5)P3. However, no transient increase was detected in cells treated with ABA. Neomycin and U73122, inhibitors of PI-PLC, inhibited the increase in Ins(1,4,5)P3 caused by the hyperosmotic shock. A rapid increase in phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) in response to the hyperosmotic shock also occurred, but the rate of increase was much slower than that of Ins(1,4,5)P3. These findings indicate that the transient Ins(1,4,5)P3 production was due to the activation of PI-PLC in response to hyperosmotic stress. PI-PLC inhibitors also inhibited hyperosmotic stress-responsive expression of some dehydration-inducible genes, such as rd29A (lti78/cor78) and rd17 (cor47), that are controlled by the DRE/CRT cis-acting element but did not inhibit hyperosmotic stress-responsive expression of ABA-inducible genes, such as rd20. Taken together, these results suggest the involvement of PI-PLC and Ins(1,4,5)P3 in an ABA-independent hyperosmotic-stress signal transduction pathway in higher plants.

Abscisic Acid↗
PubMed2001

Angiotensin II and serotonin potentiate endothelin-1-induced vascular smooth muscle cell proliferation.

BACKGROUND: Vascular smooth muscle cell (VSMC) proliferation induced by various growth factors has been implicated in a wide variety of pathological processes, including hypertension, atherosclerosis and restenosis after angioplasty. OBJECTIVES: To investigate the interactions among well-known potent vasoconstrictor substances, endothelin-1 (ET-1), angiotensin II (Ang II), and serotonin (5-HT), on VSMC proliferation. METHODS: Growth-arrested rabbit VSMCs were incubated with different concentrations of ET-1 in the absence or presence of Ang II, 5-HT, or both. VSMC proliferation was examined by increases in incorporation of [3H]thymidine into DNA and in cell number. RESULTS: ET-1, Ang II and 5-HT stimulated DNA synthesis in a dose-dependent manner. ET-1 had a maximal effect at a concentration of 0.5 micromol/l (259% of control), Ang II at 1 micromol/l (173%), and 5-HT at 50 micromol/l (205%). When added together, ET-1 (0.1 micromol/l) and Ang II (1 micromol/l) synergistically induced DNA synthesis (341%). When the vasoconstrictors were tested in combination, even non-mitogenic concentrations of ET-1 (0.01 nmol/l) potentiated 5-HT (5 micromol/l)-induced DNA synthesis (404%). Co-incubation of ET-1 (0.01 micromol/l) with Ang II (1 micromol/l) and 5-HT (5 micromol/l) synergistically induced DNA synthesis (566%). These effects on DNA synthesis were paralleled by an increase in cell number. The ETA/B non-selective receptor antagonist, TAK044 (1 micromol/l) and the ETA receptor antagonist, BQ123 (1 micromol/l), but not the ETB receptor antagonist, BQ788 (1 micromol/l), inhibited the mitogenic effect of ET-1 and its interaction with Ang II or 5-HT. In addition, TAK044 (1 micromol/l) or BQ123 (1 micromol/l) along with the angiotensin II type 1 (AT1) receptor antagonist, candesartan (1 micromol/l), the 5-HT2A receptor antagonist, sarpogrelate (10 micromol/l), or both, inhibited the interactions of ET-1 with Ang II or 5-HT. CONCLUSIONS: Our results suggest that Ang II and 5-HT could potentiate ET-1-induced VSMC proliferation. Inhibition of ETA, AT1, and 5-HT2A may be effective in the treatment of VSMC proliferative disorders associated with hypertension, atherosclerosis and restenosis after angioplasty.

Angiotensin II↗
PubMed2001

Mildly oxidized low-density lipoprotein acts synergistically with angiotensin II in inducing vascular smooth muscle cell proliferation.

OBJECTIVES: Considerable attention has been focused on both mildly oxidized low-density lipoprotein (mox-LDL) and highly oxidized LDL (ox-LDL) as important risk factors for cardiovascular disease. Further, angiotensin II (Ang II) appears to play a crucial role in the development of hypertension and atherosclerosis. We assessed the effect of oxidatively modified LDL and its major oxidative components, i.e., hydrogen peroxide (H2O2), lysophosphatidylcholine (LPC), and 4-hydroxy-2-nonenal (HNE) and their interaction with Ang II on vascular smooth muscle cell (VSMC) DNA synthesis. METHODS: Growth-arrested rabbit VSMCs were incubated in serum-free medium with different concentrations of native LDL, mox-LDL, ox-LDL, H2O2, LPC, or HNE with or without Ang II. DNA synthesis in VSMCs was measured by [3H]thymidine incorporation. RESULTS: Ang II stimulated DNA synthesis in a dose-dependent manner with a maximal effect at a concentration of 1 micromol/l (173%). Ang II (0.5 micromol/l) amplified the effect of native LDL at 500 ng/ml, ox-LDL at 100 ng/ml, and mox-LDL at 50 ng/ml on DNA synthesis (108 to 234%, 124 to 399%, 129 to 433%, respectively). H2O2 had a maximal effect at a concentration of 5 micromol/l (177%), LPC at 15 micromol/l (156%), and HNE at 0.5 micromol/l (137%). Low concentrations of H2O2 (1 micromol/l), LPC (5 micromol/l), or HNE (0.1 micromol/l) also acted synergisitically with Ang II (0.5 micromol/l) in inducing DNA synthesis to 308, 304, or 238%, respectively. Synergistic interactions of Ang II (0.5 micromol/l) with mox-LDL, ox-LDL (both 50 ng/ml), H2O2 (1 micromol/l), LPC (5 micromol/l), or HNE (0.1 micromol/l) on DNA synthesis were completely reversed by the combined use of probucol (10 micromol/l), a potent antioxidant and candesartan (0.1 micromol/l), an AT1 receptor antagonist. CONCLUSIONS: Our results suggest that mox-LDL, ox-LDL, and their major components H2O2, LPC, and HNE act synergistically with Ang II in inducing VSMC DNA synthesis. A combination of antioxidants with AT1 receptor blockade may be effective in the treatment of VSMC proliferative disorders associated with hypertension and atherosclerosis.

Acetylcysteine↗
PubMed2001

Synergistic effect of urotensin II with serotonin on vascular smooth muscle cell proliferation.

BACKGROUND: Urotensin II (U-II), the most potent vasoconstrictor, and serotonin (5-HT) are known to play an important role in pulmonary hypertension. However, little is known about the effect of U-II and its interaction with 5-HT on vascular smooth muscle cell (VSMC) proliferation. OBJECTIVE: We assessed the interaction between U-II and 5-HT in inducing VSMC proliferation. METHODS: Growth-arrested rabbit VSMCs were incubated in serum-free medium with different concentrations of U-II and 5-HT. VSMC proliferation was examined by the increase in [3H]thymidine incorporation into DNA and cell number. RESULTS: U-II or 5-HT induced [3H]thymidine incorporation in a dose-dependent manner with a maximal effect at a concentration of 50 nmol/l (161%) or 50 micromol/l (205%), respectively. When added together, low concentrations of U-II (50 nmol/l) and 5-HT (1 micromol/l) interacted synergistically in inducing [3H]thymidine incorporation (382%). These effects on [3H]thymidine incorporation were paralleled by an increase in cell number. The G-protein inactivator GDP-beta-S (100 micromol/l), protein kinase C (PKC) inhibitor Ro31-8220 (0.1 micromol/l), Src family tyrosine kinase inhibitor PP2 (1 micromol/l), and mitogen-activated protein kinase (MAPK) kinase inhibitor PD098059 (10 micromol/l) inhibited the mitogenic effects of U-II and 5-HT and also their interaction in inducing [3H]thymidine incorporation. CONCLUSION: Our results suggest that U-II and 5-HT may induce the synergistic interaction in inducing VSMC proliferation via a G-protein-coupled receptor/PKC/Src tyrosine kinase/MAPK pathway, thus contributing to the relatively rapid development of atherosclerosis in hypertensive vascular disease.

Animals↗
PubMed2001

Bone morphogenetic protein 2 stimulates osteoclast differentiation and survival supported by receptor activator of nuclear factor-kappaB ligand.

Bone is a major storage site for TGFbeta superfamily members, including TGFbeta and bone morphogenetic proteins. It is believed that these cytokines are released from bone during bone resorption. Recent studies have shown that both RANKL and macrophage colony-stimulating factor are two essential factors produced by osteoblasts for inducing osteoclast differentiation. In the present study we examined the effects of bone morphogenetic protein-2 on osteoclast differentiation and survival supported by RANKL and/or macrophage colony-stimulating factor. Mouse bone marrow-derived macrophages differentiated into osteoclasts in the presence of RANKL and macrophage colony-stimulating factor. TGFbeta superfamily members such as bone morphogenetic protein-2, TGFbeta, and activin A markedly enhanced osteoclast differentiation induced by RANKL and macrophage colony-stimulating factor, although each cytokine alone failed to induce osteoclast differentiation in the absence of RANKL. Addition of a soluble form of bone morphogenetic protein receptor type IA to the culture markedly inhibited not only osteoclast formation induced by RANKL and bone morphogenetic protein-2, but also the basal osteoclast formation supported by RANKL alone. Either RANKL or macrophage colony-stimulating factor stimulated the survival of purified osteoclasts. Bone morphogenetic protein-2 enhanced the survival of purified osteoclasts supported by RANKL, but not by macrophage colony-stimulating factor. Both bone marrow macrophages and mature osteoclasts expressed bone morphogenetic protein-2 and bone morphogenetic protein receptor type IA mRNAs. An EMSA revealed that RANKL activated nuclear factor-kappaB in purified osteoclasts. Bone morphogenetic protein-2 alone did not activate nuclear factor-kappaB, but rather inhibited the activation of nuclear factor-kappaB induced by RANKL in purified osteoclasts. These findings suggest that bone morphogenetic protein-mediated signals cross-communicate with RANKL-mediated ones in inducing osteoclast differentiation and survival. The enhancement of RANKL-induced survival of osteoclasts by bone morphogenetic protein-2 appears unrelated to nuclear factor-kappaB activation.

Animals↗
PubMed2001

T wave alternans for predicting adverse effects of amiodarone in a patient with dilated cardiomyopathy.

An implantable cardioverter defibrillator (ICD) was used in a 62-year-old man with dilated cardiomyopathy (DCM) because of hemodynamically intolerable ventricular tachycardia (VT). Amiodarone was administered after a second episode of ICD discharge. Three weeks later, incessant VT appeared, and DC discharge failed to terminate it. Microvolt T wave alternans (TWA), measured by a spectral method, was observed in this patient with and without amiodarone administration. The onset heart rate with TWA was lower and the alternans voltage was higher with amiodarone than without it. The effects of amiodarone appeared to be related to the exacerbation of VT and an increased defibrillation threshold. TWA might be useful in predicting the proarrhythmic effects of amiodarone in similar cases.

Amiodarone↗
PubMed2001

The genetic factor in acute myocardial infarction with hypertension.

This study assessed the contribution of polymorphisms of angiotensin II (AngII) receptors and bradykinin B2 (BK-B2) receptor to hypertension and acute myocardial infarction (AMI) in a Japanese population: 150 subjects with essential hypertension, 150 subjects with AMI with/without hypertension, and 150 healthy, age- and sex-matched controls. Polymorphisms of the AngII type 1 receptor (1166 A/C) and type 2 receptor (3123 C/A), and the BK-B2 receptor (-58T/C, exon 1) were analyzed and significant differences of genotypes and allelic frequencies in the AngII type 2 receptor C/A and BK-B2 receptor -58T/C were found between the essential hypertension and control subjects. Further, a significantly higher incidence of the C allele of the BK-B2 receptor was seen in AMI subjects with hypertension compared with those without hypertension. Genetic variations in the AngII and BK-B2 receptors could prove to be significant pathophysiological mechanisms affecting essential hypertension and AMI, and genetic differences appear to be a new risk factor for these conditions.

Adult↗
PubMed2001

Genetic background in patients with acute myocardial infarction.

The renin-angiotensin system is believed to play important roles in the development of acute myocardial infarction, and gene polymorphisms may also be involved. To investigate the genetic background in patients with acute myocardial infarction, we performed a case control study in a Japanese population. The study included 150 patients with acute myocardial infarction and 150 healthy, age- and sex-matched controls. We examined polymorphisms of angiotensin II type 1 receptor (1 166 A / C), type 2 receptor (3123 C / A), and bradykinin B2 receptor (-58 T / C) in these subjects. The allelic frequencies of angiotensin II type I receptor C and angiotensin II type 2 receptor A were significantly higher in the acute myocardial infarction subjects than in the control subjects, and this tendency was more significant in the younger patients. The combined ratios of angiotensin II type 1 receptor C and type 2 receptor A alleles in patients under 64 years old were significantly higher than in their older counterparts. However the total numbers of conventional coronary risk factors (hypertension, hypercholesterolemia, diabetes mellitus, and smoking) in individual subjects were not significantly different between younger and older patients. These polymorphisms were found to be involved in the development of acute myocardial infarction, particularly in the younger patients, and it was concluded that the incidence of acute myocardial infarction might be reduced by management from the genotypes.

Aged↗
PubMed2001

Brain specific human genes, NELL1 and NELL2, are predominantly expressed in neuroblastoma and other embryonal neuroepithelial tumors.

NELL1 and NELL2 encode cysteine-rich amino acid sequences including six epidermal growth factor-like motifs, which contain signal peptides at the N-terminals. The deduced amino acid sequences of both genes are 55% identical and their cysteine stretch structures are conserved. NELL1 is expressed in the brain and kidney, whereas NELL2 is expressed specifically in the brain. The cell lineage expressing NELLs in the nervous system was investigated in established cell lines and central nervous system tumor tissues obtained from patients by Northern blot and reverse transcriptase-polymerase chain reaction analyses. NELL1 and NELL2 were predominantly expressed in neuroblastoma cell lines and little expressed in glioblastoma cell lines. NELL1 and NELL2 were also expressed in central neurocytoma, medulloblastoma, and some astrocytic tumors. Immunohistochemical analysis revealed that NELL2 protein was localized in the cytoplasm of neurons. These results suggest that NELL2 is predominantly expressed in the neuronal cell lineage in the human nervous system. NELL1 is expressed mainly in tumors in the neuronal cell lineage.

Aged↗
PubMed2001

[CD56- and CD4-positive non-Hodgkin's lymphoma of probable T-cell origin].

A 65-year-old man was admitted with swelling of the right neck and bilateral inguinal lymph nodes. Endoscopic examination revealed no nasal infiltration. Pathological examination of a neck lymph node biopsy specimen revealed peripheral T-cell lymphoma according to the Revised European-American Classification of Lymphoid Neoplasms (REAL). The phenotype of the lymphoma cells was CD56+, CD16-, CD2+, surface CD3-, cytoplasmic CD3+, CD4+, CD8-, CD5+, CD7- and CD45RO+. May-Giemsa staining demonstrated no azurophilic granules in the lymphoma cells. Immunohistopathologic examination showed negativity for TIA-1 and granzyme B, and rearrangement of the TCR C beta 1 gene was also noted. These findings strongly suggested that this was a T-cell lymphoma. The patient received 8 courses of CHOP chemotherapy plus sobuzoxane. This led to a marked decrease of lymph node swelling, and currently the patient is still in remission. According to the REAL classification, T/NK-cell lymphomas are included among the peripheral T cell tumours, and seem to constitute a heterogeneous group of neoplasms. Although some cases of CD4+ CD56+ lymphoma have been reported, the present case appears to be the first example to show TCR gene rearrangement and negativity for TIA-1 and granzyme B. Since the classification of T/NK-cell lymphoma is still controversial, accumulation of such cases may help to better define T/NK-cell neoplasms.

Aged↗
PubMed2001

Adult T-cell leukemia showing different immunophenotypes in invaded organs.

We report here a case of adult T-cell leukemia (ATL) who presented acute renal failure and skin eruption. Renal and skin biopsies showed diffuse invasion of ATL cells. Furthermore, the surface phenotype of tumor cells taken from the bone marrow (BM) or peripheral blood (PB)(CD4-CD8-) differed from that of cells taken from the kidney or skin (CD4+CD8-). These findings suggested that CD4-CD8-ATL cells in the BM and PB had differentiated to CD4+CD8- cells in the kidney and skin.

Acute Kidney Injury↗
PubMed2001

[Morphological and histological studies of in-stent restenosis in seven types of stents implanted in porcine coronary arteries].

OBJECTIVES: Differences in the mechanism of restenosis after stenting between coil and tubular stents were examined in porcine coronary arteries using histological and immunohistochemical methods. METHODS: Twenty-four pigs underwent balloon-induced injury in the left anterior descending coronary artery. Two weeks later, seven different stents clinically available in Japan (Coil stents: GR I, GR II, Wiktor, Cordis; Tubular stents: gfx, Multilink, Palmaz-Schatz) were implanted in the injured site. Four weeks after the stent implantation, the pigs were sacrificed for histological examination and for morphometrical analysis of the lumen, neointima, media and adventitia. Immunohistochemical studies using anti-proliferating cell nuclear antigen (PCNA), anti-alpha-smooth muscle actin and anti-macrophage antibody were also performed. RESULTS: The coil stents formed eccentric, and the tubular stents formed concentric neointimal proliferation. Although there was no difference in the area of neointima between the stents, the area of lumen in the tubular stents was bigger than that in the coil stents (p < 0.01), because the vascular area was bigger in the tubular stents (p < 0.05). Immunohistochemical examination found many PCNA-positive cells in the proliferated neointima, especially in the area around the stent strut. Many of these cells around the stent strut were positively stained by anti-macrophage antibody. Other cells positively stained for PCNA were confirmed as smooth muscle cells. CONCLUSIONS: Tubular stents maintained a wider lumen than coil stents, because negative remodeling after stenting was less in the tubular stents. Implantation of stents with less negative remodeling is very important to prevent restenosis after stenting.

Actins↗
PubMed2000

CD45 is required for CD40-induced inhibition of DNA synthesis and regulation of c-Jun NH2-terminal kinase and p38 in BAL-17 B cells.

Stimulation of B cell antigen receptor (BCR) may induce proliferation, differentiation, or apoptosis, depending upon the maturational stage of the cell and the presence or absence of signals transmitted via coreceptors. One such signal is delivered via CD40; for instance, ligation of CD40 rescues B cells from BCR-induced apoptosis. Here we show that, in contrast to WEHI-231 cells, CD40 ligation did not reverse BCR-induced growth inhibition in the BAL-17 mature B cell line and CD40 ligation itself inhibited proliferation. This inhibitory signaling was not observed in CD45-deficient cells. Further analyses demonstrate that transfection of dominant-negative form of SEK1 or treatment with SB203580 strongly reduced CD40-induced inhibition of BAL-17 proliferation, suggesting a requirement for c-Jun NH2-terminal kinase and p38 in CD40-induced inhibition of proliferation. Interestingly, CD40-initiated activation of c-Jun NH2-terminal kinase and p38 was enhanced and sustained in CD45-deficient cells, and these phenotypes were reversed by transfecting CD45 gene. However, CD40-mediated induction of cell surface molecules was not affected in CD45-deficient cells. Taken collectively, these results suggest that CD45 exerts a decisive effect on selective sets of CD40-mediated signaling pathways, dictating B cell fate.

Animals↗