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T Tatsumi

Publications and source records attributed to T Tatsumi.

At least 55 records · Page 3Linked to original sources
PubMed1996

Effect of ischemic preconditioning on mitochondrial oxidative phosphorylation and high energy phosphates in rat hearts.

The ability of ischemic preconditioning (IP) to protect the myocardium against prolonged ischemia may derive from improved energy balance. We therefore examined myocardial energy metabolism and mitochondrial oxidative phosphorylation in isolated perfused rat hearts which were either subjected (IP group), or not subjected (control group), to preconditioning prior to 30 min sustained ischemia and 30 min reperfusion. Preconditioning was achieved with two cycles of 5 min ischemia followed by 5 min reperfusion. Recovery of myocardial function was significantly greater, and creatine kinase release was significantly lower, in the IP group. Although ATP hydrolysis during the sustained ischemia remained unchanged in both groups, greater preservation of high energy phosphate (eg. ATP and CP) was observed in the IP group after reperfusion. CP content immediately after preconditioning greatly exceeded pre-ischemic values. Lactate production during the sustained ischemia was significantly lower in the IP group, suggesting a decrease in anaerobic glycolysis and a probable attenuation of intracellular acidosis. Oligomycin-sensitive mitochondrial ATPase activity in the control group was significantly decreased both after the sustained ischemia and the reperfusion, but in the IP group it did not change after the preconditioning, sustained ischemia, or reperfusion. Although atractyloside-inhibitable adenine nucleotide translocase activity was markedly decreased during sustained ischemia in both groups, its activity was significantly higher after reperfusion in the IP group. These data suggest that (1) mitochondrial ATPase contributes only slightly to ATP depletion during sustained ischemia, (2) both the CP overshoot phenomenon and the decrease in anaerobic glycolysis can be attributable to cardioprotection during the sustained ischemia, and (3) the preservation of ATPase and adenine nucleotide translocase activities may be a possible explanation for the restoration of high energy phosphates after sustained ischemia-reperfusion injury in the preconditioned hearts of rats.

Adenosine Triphosphatases↗
PubMed1996

Effects of glibenclamide and nicorandil in post-ischaemic contractile dysfunction of perfused hearts in normotensive and spontaneously hypertensive rats.

OBJECTIVE: We have demonstrated previously that nicorandil, an ATP-sensitive potassium channel opener, improved post-ischaemic contractile dysfunction of perfused hearts in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats dose-dependently. This study aimed to characterize the effect of glibenclamide, an ATP-sensitive potassium channel blocker, and nicorandil in post-ischaemic contractile dysfunction of SHR and WKY rats. METHODS: The perfused hearts were subjected to 30 min of global ischaemia and then 30 min of reperfusion. Administration of 10 or 50 mumol/l glibenclamide or of a combination of glibenclamide and 300 mumol/l nicorandil was performed for 10 min before the ischaemia. The left ventricular developed pressure and end-diastolic pressure were measured. RESULTS: Postischaemic contractile function was better in WKY rats than it was in SHR. Neither glibenclamide nor a combination of glibenclamide and nicorandil influenced the postischaemic contractile function or increased the incidence of reperfusion arrhythmias. The recoveries of coronary flow and heart rate after reperfusion were poor and the incidence of reperfusion arrhythmias was low in SHR. CONCLUSIONS: These results suggest that nicorandil improves postischaemic contractile dysfunction via a mechanism involving ATP-sensitive potassium channel opening both in SHR and in WKY rats. The hypertensive hearts were more susceptible to cardiac reperfusion dysfunction, compared with normal hearts.

Animals↗
PubMed1996

Expression of adhesion molecules on myeloma cells.

We investigated the expression of adhesion molecules including LFA-1 alpha (CD11a), Mac-1 (CD11b), LFA-1 beta (CD18), VLA-beta 1 (CD29), H-CAM (CD44), VLA-4 (CD49d), VLA-5 (CD49e), ICAM-1 (CD54), N-CAM (CD56), LFA-3 (CD58), VNR-beta (CD61), and LECAM-1 (CD62L) on fresh myeloma cells and human myeloma cell lines. By two-color flow cytometric analysis with anti-CD38 antibody, we demonstrated that myeloma cells were located in the strongly CD38-positive (CD38++) fractions. Fresh myeloma cells were obtained from 28 patients with multiple myeloma (MM) and 3 patients with plasma cell leukemia (PCL). All myeloma cells expressed VLA-4 on their surface. Most of the myeloma cells also expressed VLA-5, ICAM-1, and LFA-3, H-CAM was strongly expressed in 3 cases of PCL and 2 cases of aggressive myeloma, and moderately expressed in other MMs. N-CAM was expressed in 68% of MMs, but none of the 3 PCLs. LFA-1 was expressed in two cases of aggressive myeloma, but not expressed in other non-aggressive myelomas. Most of the myeloma cells did not express Mac-1, VNR-beta, or LECAM-1. These results suggest that VLA-4, VLA-5, ICAM-1, LFA-3, and H-CAM are involved in cellular interaction and migration in MM, and that the expression of N-CAM and LFA-1 varies with disease activity in MM.

ADP-ribosyl Cyclase↗
PubMed1996

[Natural killer cell lymphoma having a nodular shadow in the lung as an initial finding, developed to leukemia complicated with hemophagocytic syndrome at the time of relapse].

A 57-year-old female was admitted to Uji hospital for the further evaluation of nodular shadow on her right lung. During the period of admission, she developed cervical lymph node swelling. She was diagnosed as having malignant lymphoma (diffuse, small cleaved cell) by lymph node biopsy. She received combined chemotherapy and obtained partial remission for seven months until she developed fever and pancytopenia. Laboratory data showed increased number of large granular lymphocytes (LGLs) in blood. Bone marrow revealed increased number of LGLs with hemophagocytosis by macrophage. Surface marker analysis revealed LGLs were positive for CD2 CD16, and CD56 and negative for CD3, CD4, CD8, and CD20. T-cell receptor genes beta and gamma were in germ line configuration. Analysis of Epstein-Barr virus genome using termini probe indicated a monoclonal proliferation of LGLs. Reexamination of the biopsy specimen of lymph node revealed LGLs which was negative for CD3 and CD20. The patient was diagnosed as a leukemic phase of natural killer (NK) cell lymphoma complicated with hemophagocytic syndrome (HPS). Serum levels of interferon-gamma, macrophage colony-stimulating factor, granulocyte colony-stimulating factor, and interleukin-6 increased, which might be related to HPS.

Antigens, CD↗
PubMed1995

Gastric ulcer healing and basic fibroblast growth factor: effects of lansoprazole and famotidine.

We examined the effects of lansoprazole and famotidine on gastric basic fibroblast growth factor (bFGF) levels and ulcer healing in patients with gastric ulcer. Sixteen patients with active gastric ulcer were divided into two groups and received treatment with lansoprazole 30 mg/day or famotidine 40 mg/day. They were examined endoscopically at 2, 4, and 8 weeks to measure gastric bFGF levels at the ulcer margin and to assess ulcer healing. Helicobacter pylori infection was determined by a rapid urease test. The two groups were comparable with regard to age, male:female ratio, H. pylori infection rates, and bFGF levels. During treatment, bFGF levels did not change significantly in the famotidine group, whereas they increased by a factor of 2.2 to 2.6 in the lansoprazole group. Cumulative healing rates were also significantly lower in the famotidine group than in the lansoprazole group. These results indicate that lansoprazole increases tissue bFGF levels and promotes gastric ulcer healing in humans.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

Effect of doxorubicin on postrest contraction in isolated rat hearts.

Clinical use of doxorubicin is limited by its cardiotoxicity. In doxorubicin-induced cardiomyopathy, vacuolization of the sarcoplasmic reticulum (SR) has been reported. We investigated whether doxorubicin had a direct action on the sarcoplasmic reticulum (SR) in isolated perfused rat hearts. The left and right atria were trimmed to maintain heart rate (HR) <200 beats/min. Postrest contractions, which are believed to be due primarily to Ca2+ release from the SR, were evoked with a programmable stimulator after variable rest intervals. The amplitude of the postrest contractions increased markedly as the rest interval increased. Doxorubicin (0.1 mM) significantly suppressed this potentiation of the postrest contractions. Furthermore, doxorubicin slowly induced aftercontractions and an increase in left ventricular diastolic pressure (LVDP), phenomena that are usually associated with ouabain intoxication. We conclude that doxorubicin-induced cardiomyopathy may be due to SR dysfunction, leading to intracellular Ca2+ overload.

Animals↗
PubMed1995

Recurrent Cushing's disease associated with nephrotic syndrome.

A case of recurrent Cushing's disease with nephrotic syndrome due to membranoproliferative glomerulonephritis (MPGN) is presented. Functional pituitary adenoma recurred 6 years after transsphenoidal pituitary adenomectomy. Due to infiltration into the surrounding tissues, transcranial surgery was performed. However, this failed to induce a remission and thus gamma knife therapy was applied. Histopathological evaluation revealed that the glomerular lesions had progressed to a rather advanced stage of MPGN. Although this association could be coincidental, the recurrence of pituitary macroadenoma might be induced by the cessation of steroid treatment for the nephrotic syndrome.

Adult↗
PubMed1995

Effect of nicorandil on cardiac dysfunction during reperfusion in normotensive and spontaneously hypertensive rats.

The cardioprotective effect of nicorandil, an opener of ATP-sensitive potassium channels, was studied in the isolated perfused hearts of the spontaneously hypertensive rat (SHR) and normotensive Wistar-Kyoto (WKY) rat. The hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion. Controls received no drug. In the nicorandil group, the hearts were treated with 0.03 to 0.3 mmol/L nicorandil for 15 min before ischemia. Left ventricular developed pressure (LVDP) and end diastolic pressure (LVEDP) at 30 min of reperfusion were significantly lower and larger, respectively, in SHR than in WKY rats. Nicorandil improved LVDP and decreased LVEDP at 30 min of reperfusion in both SHR and WKY rats dose-dependently. The hypertensive heart in the early stage is already susceptible to reperfusion-cardiac dysfunction. Nicorandil has a beneficial effect on the post-ischemic dysfunction in both SHR and WKY rats.

Animals↗
PubMed1995

[The volume ratio between squamosal and petrosal air cells divided by Körner's septum].

Pneumatized air cells of the temporal bone are embryologically divided into two portions; the squamosal portion and the petrosal portion. These two portions are anatomically separated by the petrosquamous fissure and petrosquamous lamina, the so-called Körner's septum. In this study, the volumes of the two portions were measured with Target Imaging CT in 5 normal ears (3 subjects) with a clearly recognizable Körner's septum. The combined volume of the two portions, in all CT slices, was also measured. The squamosal portion occupied 32.7% of the total air cell volume, on average, and the petrosal portion was 67.3%. A positive correlation was observed between the total air cell volume of the temporal bone and the volume ratio of the petrosal portion. When the volume of each part was examined according to the CT slice level, from high to low, the maximum volume of the squamosal portion was at the slice level of the epitympanic cavity. The volume of the petrosal portion was prominent at the slice level of the epitympanic cavity and the upper antrum. These results that the petrosal portion plays a more important role than the squamosal portion in pneumatization of the temporal bone. This analysis with Target Imaging CT provides useful information for understanding the middle ear pathology resulting from poor pneumatization of the temporal bone.

Adult↗
PubMed1995

Mobilization of peripheral blood progenitor cells by high-dose Ara C, VP-16 and recombinant human granulocyte colony-stimulating factor: factors affecting progenitor cell yields.

Forty seven patients with hematological malignancies were treated with high doses of cytosine arabinoside (Ara C; 12 g/m2) and etoposide (VP-16), followed by recombinant human granulocyte colony-stimulating factor (rhG-CSF; 50 micrograms/m2). Peripheral blood progenitor cells (PBPC) were collected during rapid leukocyte recovery using a CS-3000 blood cell separator. A blood volume of 9 liters was processed in each apheresis, with 162 apheresis procedures performed. The mean numbers of mononuclear cells (MNC) and colony-forming unit granulocyte-macrophage (CFU-GM) harvested per apheresis were 4.4 x 10(8)/kg and 142.5 x 10(4)/kg, respectively. A sufficient number of CFU-GM for engraftment (> 30 x 10(4)/kg) could be harvested by a single apheresis in 35 of 47 patients (74%). Various factors that influence the collection of progenitor cells were analyzed by univariate and multivariate analyses. The number and duration of previous chemotherapy cycles were the most significant factors affecting CFU-GM yield. In patients with malignant lymphoma, age also had an influence in addition to these two factors. MNC harvested had an impact on CFU-GM yields by univariate analysis. These observations suggest that high-dose Ara C plus VP-16 followed by G-CSF is an effective regimen for harvesting PBPC. PBPC should be collected in the early stage of first-line chemotherapy.

Adolescent↗
PubMed1995

Establishment of a novel myeloma cell line KPMM2 carrying t(3;14)(q21;q32), which proliferates specifically in response to interleukin-6 through an autocrine mechanism.

We established a new human myeloma cell line, KPMM2, which proliferates specifically in response to IL-6 via an autocrine mechanism. The proliferative response of KPMM2 cells to exogenous IL-6 was significantly stimulated in a dose-dependent manner. The growth was markedly inhibited by an anti-IL-6 mAb and an anti-IL-6 receptor (IL-6R) mAb in a dose-dependent manner. KPMM2 cells expressed IL-6 and IL-6R mRNA by RT-PCR. Flow cytometric analysis showed cell surface expression of IL-6R. IL-6 protein was detected in the culture supernatant by ELISA. IL-11, oncostatin M and leukemia inhibitory factor had no effect on the proliferation of KPMM2 cells although interferon-alpha and interferon-gamma inhibited the growth. Furthermore, KPMM2 cells bore a t(3;14)(q21;q32) translocation and this finding is of potential interest for future studies in the light of the nuclear protein BM28 (CDCL1, for cdc-like 1) mapped on 3q21, which plays an important role in the cell cycle. In this report, we demonstrated completely an IL-6-dependent autocrine growth mechanism in KPMM2 cell line. This cell line may be useful to investigate the pathogenesis of multiple myeloma and to evaluate the therapeutic potential of IL-6 blocking agents in vitro and in vivo.

Aged↗
PubMed1994

Hypochlorous acid mobilizes intracellular zinc in isolated rat heart myocytes.

Neutrophil oxidants appear to cause contractile dysfunction in reperfused ischemic myocardium. This "reperfusion injury" may result from the intracellular mobilization of various metals. We examined the ability of hypochlorous acid (HOCl), a highly reactive neutrophil oxidant, to mobilize cellular zinc in cardiac tissue. To monitor cellular zinc concentrations, isolated rat heart myocytes were loaded with N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide (TSQ), a zinc-specific fluorescent chelator. Superfusion of the TSQ-loaded cells with HOCl (50 microM) resulted in a two-fold increase in cellular fluorescence within 15 min, indicating an increase in free Zn2+ concentration. Superfusion of the HOCl-treated cells with ethylene glycol bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), a non membrane-permeant zinc chelator, did not decrease cellular fluorescence. However, superfusion with N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), or dithiothreitol (DTT), two membrane-permeant heavy metal chelators, rapidly diminished fluorescence, suggesting that the increase in TSQ fluorescence was caused by an intracellular increase in free Zn2+. The myocytes retained their rod-shaped morphology throughout these procedures. These data show, for the first time, that HOCl can mobilize intracellular zinc in viable cardiac myocytes. In view of the important intracellular role played by zinc, the mobilization of this metal by oxidants may contribute to the functional alterations observed in reperfused myocardium. Moreover, the ability of TPEN and DTT to complex the HOCl-mobilized zinc suggests that these chelators may be capable of attenuating or reversing these effects.

Animals↗
PubMed1994

Effects of repeated ischemia on release kinetics of troponin T, creatine kinase, and lactate dehydrogenase in coronary effluent from isolated rat hearts.

We studied the release kinetics of cardiac troponin T (TnT) from coronary effluent in a re-stenosis model of 13 isolated rat hearts. After a 20-min period of global ischemia, we reperfused the hearts for 60 min according to the method of Langendorff. A second period of global ischemia was then induced for 5 min (protocol A) or 20 min (protocol B), followed by a second 60-min period of reperfusion. Coronary flow was measured by a timed collection of the coronary effluent. Levels of TnT in the effluent were compared to those of creatine kinase (CK) and lactate dehydrogenase (LD). Levels of TnT increased after the second global ischemia, but no differences were found in the released levels of TnT between protocols A and B. However, the amounts of CK and LD released in protocol B were much greater than those released in protocol A. These studies indicate that the release kinetics of TnT are different from that of CK and LD during reperfusion. It appears that after the initial ischemic damage to TnT, subsequent ischemia causes damage to TnT regardless of the duration of the insult, whereas the damage to sarcolemma is dependent on the duration of the ischemia.

Animals↗