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Biomedical subjects

Y Katayama

Publications and source records attributed to Y Katayama.

At least 253 records · Page 14Linked to original sources
PubMed1998

Effect of hyperglycemia on pyruvate dehydrogenase activity and energy metabolites during ischemia and reperfusion in gerbil brain.

The effects of hyperglycemia on brain pyruvate dehydrogenase (PDH) and metabolites (ATP, PCr, and lactate) were investigated at 20 min ischemia, 0, 20, and 60 min, and 4 h reperfusion. During reperfusion, PDH activities were suppressed corresponding to the poor recovery of ATP and PCr concentrations and the increase in lactate concentration in the hyperglycemic group, suggesting that preischemic hyperglycemia may impair metabolism by suppressing PDH activity.

Adenosine Triphosphate↗
PubMed1998

Concentration-dependent actions of a new indene derivative, TN-871, in the enteric nervous system.

Intracellular electrical recordings and fluorimetric measurement of intracellular Ca2+ concentration ([Ca2+]i) were made from enteric neurons of the guinea-pig myenteric and submucosal plexuses to examine the actions of 2-n-butyl-1-(4-methylpiperazinyl)5,6-ethylendioxyindene x 2HCl (TN-871) on neural activity in the single cell. TN-871 affected neuronal electrophysiological properties and synaptic transmission in the enteric nervous system in a concentration-dependent manner; TN-871 at lower concentrations hyperpolarized enteric neurons and/or facilitated synaptic transmission, whereas at higher concentrations it depolarized enteric neurons and/or inhibited synaptic transmission. Experiments with fura-2 showed that TN-871 modulated both resting [Ca2+]i and [Ca2+]i-transient associated with action potentials. Thus, the present results demonstrated that TN-871 at lower concentrations facilitates but at higher concentrations depresses Ca2+-dependent or Ca2+-involving processes, suggesting that TN-871 may affect the Ca2+ dynamics in enteric neurons either directly, indirectly or both.

Action Potentials↗
PubMed1998

Effect of nicardipine, a Ca2+ channel blocker, on pyruvate dehydrogenase activity and energy metabolites during cerebral ischemia and reperfusion in gerbil brain.

The purpose of this study was to determine if nicardipine, a calcium ion channel blocker, affects pyruvate dehydrogenase (PDH) activity and improves energy metabolism during cerebral ischemia and reperfusion. Cerebral ischemia was induced, using the bilateral carotid artery occlusion method, for 60 min followed by reperfusion up to 120 min in gerbils. Nicardipine (1 mg/kg) or saline (vehicle-treated) was given to gerbils 30 min prior to the occlusion of the common carotid arteries. PDH activity and metabolites (ATP, PCr, and lactate) were measured in cortex prior to ischemia, immediately following ischemia, and after each reperfusion period. After 60 min ischemia, PDH activity increased in both groups, and was significantly higher in the nicardipine-treated group. After 20 min reperfusion, PDH activity in the nicardipine-treated group recovered to control levels, whereas, the PDH activity in the vehicle-treated group remained elevated, and was higher than the nicardipine-treated animals. At 60 and 120 min reperfusion, the activities in the vehicle-treated group were significantly below control levels, there were no differences, however, between the two groups. ATP and PCr concentrations were markedly depleted immediately after ischemia in both groups. ATP levels at 20 min reperfusion and PCr levels at 60 min reperfusion were significantly higher in the nicardipine-treated group. Lactate concentrations in both groups increased 7-8 fold, similarly, immediately after ischemia. During reperfusion, the lactate remained elevated in both groups, though the levels in the nicardipine-treated group were lower than those in the vehicle-treated group, but not significantly. Nicardipine treatment normalized PDH activity quickly and improved energy metabolism after reperfusion.

Animals↗
PubMed1998

Bone marrow necrosis in a patient with acute myeloblastic leukemia during administration of G-CSF and rapid hematologic recovery after allotransplantation of peripheral blood stem cells.

Allogeneic peripheral blood stem cell transplantation from an HLA-identical sibling was performed for a 38-year-old male with refractory acute myeloblastic leukemia. The patient was conditioned with total body irradiation (TBI) and high-dose cytosine arabinoside (Ara-C). G-CSF (300 microg/body) was started for priming of residual leukemic cells 24 hr before the beginning of TBI (day -9). However, intolerable generalized bone pain appeared shortly after the start of first dose of G-CSF, and persisted for 3 days in spite of the cessation of G-CSF. Posttransplant hematopoietic engraftment was very rapid. Bone marrow biopsy specimens on day 14 and 30 showed typical bone marrow necrosis histologically. This is the first case of bone marrow necrosis during administration of G-CSF, and our experience suggests that PBSC could repopulate hematopoiesis in spite of severe bone marrow necrosis.

Adult↗
PubMed1998

Casein kinase 2 phosphorylation of recombinant rat osteopontin enhances adhesion of osteoclasts but not osteoblasts.

Osteopontin (OP) is a highly phosphorylated bone matrix protein and contains the RGD cell-binding motif, which mediates cell adhesion through integrin receptors that include alpha(v)beta3. Casein kinase 2 (CK2) is a factor-independent serine/threonine kinase, which may be the predominant physiologically relevant kinase for OP phosphorylation. This study was designed to examine the effects of unphosphorylated recombinant rat OP, and CK2-phosphorylated OP (P-OP), on the adhesion and function of mouse osteoclasts (OC) and osteoblast-like cells (UMR 201-10B and UMR 106-06) in vitro. OP significantly increased OC adhesion compared to plastic alone, and cell attachment was further increased at least twofold on OP phosphorylated with CK2. Attachment was dependent on the integrity of the RGD domain and was completely abolished in the presence of 1 mM RGD peptide. Neither CK2 phosphorylation of mutant OP, in which the RGD was converted to RGE or RAD, nor protein kinase C (PKC) phosphorylation of wild-type OP enhanced OC attachment. An antibody to the beta3 integrin subunit, but not anti-mouse CD44 antibody, specifically blocked the proportion of attachment due to phosphorylation of OP. Actin ring formation in OC was increased by plating cells onto OP, with no further increase by phosphorylation. Both OP and CK2-phosphorylated OP enhanced attachment of the two osteoblastic cell lines, compared to plastic, but in contrast to OCs, there was no significant difference with phosphorylation. Osteoblast attachment was totally blocked by 1 mM RGD peptide, but was not influenced by the beta3 integrin antibody. Plating of UMR 201-10B cells onto OP further increased retinoic acid-induced alkaline phosphatase expression. The results suggest that specific phosphorylation of OP is important for interaction with OCs, compared with osteoblastic cells, and that alternative integrins may be important in the interaction between osteoblastic cells and OP compared with OCs.

Actins↗
PubMed1998

Antioxidant, OPC-14117, attenuates edema formation, and subsequent tissue damage following cortical contusion in rats.

Oxygen free radicals contribute to various kinds of tissue injury processes within the central nervous system. It has been suggested that inhibition of free radical formation has the potential to attenuate secondary neural tissue damage involving ischemia or trauma, and antioxidant therapy may offer a promising approach. In the present study, employing a cortical contusion model in the rat, contusion-induced neural damage, was evaluated by investigating edema formation, behavioral activities and histological changes. The effects of the superoxide radical scavenger, OPC-14117, were also tested to determine how free radicals may contribute to such neural damage. The results demonstrated that cerebral contusion induces a progressive decrease in tissue specific gravity representing edema formation, and behavioral deficits in the Morris water maze test and habituation of exploratory activity. Histological examinations revealed necrotic cavity formation in the cortex and selective neuronal death of the hippocampal CA3 region. These changes were significantly attenuated by OPC-14117, which was administered as a single dose immediately following trauma induction. The above results indicate that oxygen free radicals are involved in contusion-induced edema formation, subsequent tissue damage and cognitive deficits. The superoxide radical scavenger, OPC-14117, has a powerful therapeutic potential for preventing secondary cell damage following traumatic brain injury.

Animals↗
PubMed1998

Pathogenesis of the mass effect of cerebral contusions: rapid increase in osmolality within the contusion necrosis.

The non-hemorrhagic mass effect of cerebral contusions is commonly attributed to vasogenic edema and/or cytotoxic edema (cellular swelling). We propose that a marked increase in osmolality within the contusion necrosis proper, in which the cellular elements uniformly undergo shrinkage, disintegration and homogenation, represents an important and unique mechanism underlying the contusion edema. The present study demonstrates in a rat model of cerebral contusion, that 1) the osmolality of the contused brain tissue increases rapidly, 2) the increase in osmolality is not caused by changes in inorganic ion contents, suggesting a metabolic production of osmoles or release of idiogenic osmoles, and 3) the contused brain tissue strongly attracts water, provided that blood supply is maintained. We suggest that the primary driving force of water accumulation into contused brain tissue is the elevated colloid osmotic potential of contusion necrosis.

Animals↗
PubMed1998

[Initial clinical experiences of the ABIOMED BVS SYSTEM 5000 in Japan].

The initial clinical experience of the ABIOMED BVS SYSTEM 5000 in Japan is reported. The system is a paracorporeal pulsatile assist device intended for temporary ventricular support. It consists of a pneumatic drive console, a blood pump, and the atrial and arterial cannulas. The pump is of a dual chamber design, with the upper chamber as a passive, gravity filled resevoir and the lower chamber as a pumping chamber. Since the system is designed to be simple, safe and automatically controlled, no additional personnel is required to control perfusion. This report describes our initial clinical experiences with the ABIOMED BVS SYSTEM 5000 in Japan. This device was used in three patients with post cardiotomy cardiogenic shock and fulminant myocarditis. The first patient developed acute occlusion of left main coronary artery who required emergent surgical revascularization following PTCA and stent implantation. He couldn't wean from CPB and required the insertion of an LVAD. The second case suffered from a cardiac arrest after CABG and could not be resuscitated. The ABIOMED BVS 5000 was inserted and the patient successfully weaned from support. The third patient developed fulminant myocarditis and was supported with the system for 269 hours and was successfully weaned after near complete myocardial recovery. Our initial experience with the ABIOMED BVS SYSTEM 5000 indicates that the system can provide complete cardiac support allowing full recovery from a cardiac variety of causes of dysfunction. The device has the potential to improve the survival rate of patients with severe acute recoverable myocardial damage. It is expected that this device can be a viable tool for treatment of intractable heart diseases.

Adult↗
PubMed1998

Myelodysplastic syndrome with translocation (8;21): a distinct myelodysplastic syndrome entity or M2-acute myeloid leukemia with extensive myeloid maturation?

We report a case of refractory anemia with excess of blasts in transformation with the translocation (8;21), which is frequent in acute myeloid leukemia (AML) but not in myelodysplastic syndromes (MDS). Bone marrow blasts were 1.6% and an extensive myeloid differentiation was noted. Fluorescence in situ hybridization analysis revealed the presence of 21q22 translocations in mature neutrophils, indicating that clonogenic blast progenitors could actively undergo terminal differentiation to mature end cells in vivo. We consider that t(8;21)+ MDS may represent a rare clinical manifestation of M2-AML, in which blast progenitors have an extensive differentiation potential to mature neutrophils without maturation arrests.

Adult↗
PubMed1998

Trapdoor thoracotomy as a surgical approach for aortic arch aneurysm.

Since 1991 ten patients, 9 male and 1 female, with aortic arch aneurysm underwent surgical therapy with trapdoor thoracotomy. The mean age was 67.4 +/- 9.1 (standard deviation) years at operation. In addition to the aortic arch repair, we also performed seven descending aortic replacements. We performed one partial arch replacement, one total arch replacement, and one aneurysmorrhaphy and wrapping of the aortic arch aneurysm. We experienced 1 case of paraplegia, no hospital death, and no long-term mortality.

Aged↗
PubMed1998

Trisomy 12 and t(14;18) in B-cell chronic lymphocytic leukemia.

We report a case of B-cell chronic lymphocytic leukemia (B-CLL) in which trisomy 12 and t(14;18)(q32;q21) were simultaneously detected in the same leukemic clone. Southern blot analysis showed that the BCL2/IgJH rearrangement occurred at the major breakpoint region in the hot spot of the BCL2 gene. Double color fluorescence in situ hybridization analysis using multiple probes indicated that clonal B-cell with t(14;18) represented a subpopulation of the total leukemic cells and that trisomy 12 followed t(14;18) as the cytogenetic aberration in the development of B-CLL. Our findings suggests that both the t(14;18) and the trisomy are secondary chromosomal changes in the leukemogenesis of B-CLL.

Blotting, Southern↗
PubMed1998

Replating potential of colony-forming units of granulocytes/macrophages (CFU-GM) expanded ex vivo by stem cell factor, interleukin (IL)-3, IL-6, granulocyte colony-stimulating factor, erythropoietin with or without thrombopoietin.

Ex vivo expansion systems of hematopoietic progenitor cells (HPC) have been extensively studied and their clinical application is under investigation. However, it is not known whether HPC expanded ex vivo will be able to retain their replating potential. CD34+ cells isolated from cord blood were cultured in Iscove's modified Dulbecco's medium supplemented with 10% fetal bovine serum, 1.0% bovine serum albumin, 50 ng/ml stem cell factor, 50 ng/ml interleukin-3 (IL-3), 50 ng/ml IL-6, 100 ng/ml granulocyte colony-stimulating factor, and 3 U/ml erythropoietin for 0, 5, 7, 10, 14, and 21 days. After the expansion cultures, granulocyte/macrophage progenitor cells (CFU-GM) were assayed from each culture by the standard methylcellulose method. After 14 days of culture, CFU-GM-derived colonies were randomly picked up and processed for the replating assay. The fold increase of CFU-GM peaked at day 7 of the expansion culture (29.8 +/- 7.7-fold, n = 5), followed by a decline until day 21. In the replating assay of CFU-GM from freshly isolated CD34+ cells, the mean replating efficiency was 91.2 +/- 4.7%. The replating efficiency decreased gradually with the time of the expansion culture. At day 7 when the fold increase of CFU-GM reached its peak, the replating efficiency had dropped to 47.5 +/- 2.3%, followed by a further decline to 5.3 +/- 3.4% at day 21. Furthermore, the addition of 100 ng/ml thrombopoietin to this expansion system failed to prevent the decline of replating efficiency. These observations suggest that the replating potential of CFU-GM may decrease in the ex vivo expansion system, even when their fold increase reaches its peak. This should be taken into consideration when HPC expanded ex vivo are used in clinical transplantation.

Antigens, CD34↗
PubMed1998

Homozygous missense mutation (band 3 Fukuoka: G130R): a mild form of hereditary spherocytosis with near-normal band 3 content and minimal changes of membrane ultrastructure despite moderate protein 4.2 deficiency.

The characteristics of phenotypic expression were studied in a Japanese family with hereditary spherocytosis and an extremely rare homozygous missense mutation of the band 3 gene (band 3 Fukuoka: G130R). The homozygous unsplenectomized proband was a 29-year-old male with compensated haemolytic anaemia (red cell count 4.21 x 10(12)/l, reticulocytes 278 x 10(9)/l, and indirect bilirubin 44 micromol/l). His red cell band 3 (B3) protein demonstrated a 9.3% reduction and his protein 4.2 (P4.2) level was substantially reduced (45.0%), compared to normal subjects. P4.2 protein was composed mostly of a wild type (72 kD) with a trace of 68 kD peptide. The binding properties of the mutated B3 to normal P4.2 were significantly impaired, which probably resulted in the substantial reduction of P4.2 in this proband, since no abnormalities were detected on the P4.2 gene. Electron microscopy (EM) using the freeze-fracture method demonstrated a mild decrease in intramembrane particles (IMPs) of near-normal size (8 nm in diameter) with no substantial increases in their oligomerization. Their distribution on the membrane P face was almost normal, although most of the IMPs could represent the homozygously mutated B3 protein. EM (quick-freeze deep-etching method) disclosed a skeletal network of near-normal size and size distribution of the skeletal units, suggesting that the mutated B3 protein itself did not have much effect on the skeletal network in situ. Therefore the reduced P4.2 content (45% of that of normal subjects), which remained on the red cell membrane of this proband, appeared to be nearly sufficient for maintaining the normal structure of the skeletal network and IMPs in situ, contrary to the marked abnormalities in both IMPs and the skeletal network in complete P4.2 deficiencies.

Adult↗
PubMed1998

Mechanisms of excitatory amino acid release in contused brain tissue: effects of hypothermia and in situ administration of Co2+ on extracellular levels of glutamate.

In order to elucidate the mechanisms of release of EAAs and their excitotoxicity in cerebral contusion, cortical contusion was produced in the rat parietal cortex, and the changes in extracellular levels of EAAs in the central and peripheral areas of contusion were investigated using microdialysis. The cortical contusion induced a rapid increase in dialysate concentration of glutamate ([Glu]d) from a baseline level of 4.6+/-2.8 microM to a maximum level of 36.3+/-12.8 microM. This elevation of glutamate was significantly attenuated by mild hypothermia (32 degrees C for 90 min, comprising 20 min before and 70 min after the injury induction) in the peripheral area of contusion (p < 0.01) but not in the central area. Histological evaluations revealed that the hypothermia reduced the necrosis volume of contusion to 38.3% of that in the normothermic control (p < 0.01). In situ administration of Co2+, an inhibitor of Co2+-dependent exocytotic release of EAAs from the nerve terminals, via the microdialysis system, also attenuated the [Glu]d elevation following cortical contusion, in the peripheral area of contusion (p < 0.01) but not in the central area. These findings indicate that cerebral contusion involves heterogeneous and complex mechanisms of EAA release into the extracellular space. The release of EAAs in the contusion core was nonsensitive to hypothermia and Co2+ administration, suggesting that such EAA release was related to primary disruption of the cell membrane or vascular wall by the physical force of the head trauma, resulting in leakage of EAAs from the metabolic pool in the cytosole or blood stream. In contrast, in the peripheral area, the effectiveness of hypothermia and Co2+ administration implied a presynaptic mechanism of EAA release, which consisted, at least in part, of Ca2+-dependent exocytotic EAA release from depolarized nerve terminals. The EAAs released in the contusion core may diffuse towards a peripheral direction and act on the postsynaptic receptors, causing neuronal depolarization. Such a diffusion-reaction process appears to induce additional release of EAAs from the depolarized nerve terminals. Hypothermia may block this diffusion-reaction process and eventually reduce the contusion volume.

Animals↗
PubMed1998

Phylogeny and photosynthetic features of Thiobacillus acidophilus and related acidophilic bacteria: its transfer to the genus Acidiphilium as Acidiphilium acidophilum comb. nov.

Phylogenetic analyses based on 16S rDNA sequences and genomic DNA-DNA relatedness showed that the sulphur-oxidizing facultative chemolithotroph Thiobacillus acidophilus was closely related to members of the genus Acidiphilium, which is a group of strictly aerobic, heterotrophic acidophiles now categorized into aerobic photosynthetic bacteria. Lipophilic pigment analyses revealed that zinc-chelated bacteriochlorophyll a and carotenoids occurred in appreciable amounts in T. acidophilus and all established species of the genus Acidiphilium. PCR experiments showed that T. acidophilus as well as Acidiphilium species contained puf genes, encoding the photosynthetic reaction centre proteins and the core light-harvesting complex of the purple bacteria. There were high similarities between T. acidophilus and Acidiphilium species in the primary structure of their reaction centre proteins deduced from the nucleotide sequence data. The phylogenetic tree of the reaction centre proteins was in agreement with the 16S rDNA sequence-based phylogenetic tree in the relationship between T. acidophilus and Acidiphilium species and between the Acidiphilium cluster and other purple photosynthetic bacteria. Based on these results, together with previous phylogenetic and phenotypic information, it is proposed to reclassify T. acidophilus (Guay and Silver) Harrison 1983 as Acidiphilium acidophilum comb. nov. The type strain is ATCC 27807T (= DSM 700T).

Bacteriochlorophylls↗
PubMed1998

Follow-up study of hypervariable region sequences of the hepatitis C virus (HCV) genome in an infant with delayed anti-HCV antibody responses.

An infant born prematurely and infected with hepatitis C virus (HCV) one month after birth was followed for 4.5 years. The patient did not produce detectable anti-HCV antibodies until two years after the onset of hepatitis. Before seroconversion, a single clone of HCV, as determined by quasispecies of the hypervariable region (HVR) of the HCV genome, was almost exclusively found in the serum. After seroconversion, however, another distinct lineage of HCV clones replaced it within half a year. As HCV infection persisted further in the presence of anti-HCV antibodies, many derivatives of both sequence lineages emerged to exhibit the typical quasispecies feature of HVR sequences. Neither seroconversion nor the changes in HVR sequences influenced the serum aminotransferase titers.

Aging↗
PubMed1998

Improvement with disodium cromoglycate of neutrophil phagocytosis and respiratory burst activity in a patient with hyperimmunoglobulin E syndrome.

We report a case of hyperimmunoglobulin E syndrome (HIE) complicated by neutrophil deficiency which was successfully treated with oral administration of disodium cromoglycate. A 48-year-old Japanese man with HIE developed Streptococcus pneumoniae meningitis. Laboratory tests after the meningitis revealed persistent neutropenia (300-800/mm3) and defects of phagocytosis and bacterial killing by neutrophils. Administration of disodium cromoglycate was started, and neutrophil counts gradually increased to 1200-1600/mm3. The impaired neutrophil activities returned to normal. The patient improved clinically; during the 2-year treatment, he had only two brief episodes of the common cold. Disodium cromoglycate may have potential clinical use in the treatment of cases of HIE even with neutrophil deficiency.

Cromolyn Sodium↗