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Biomedical subjects

M Masuda

Publications and source records attributed to M Masuda.

At least 433 records · Page 24Linked to original sources
PubMed1990

A chronic contained rupture of an abdominal aortic aneurysm complicated with severe back pain.

Chronic contained rupture of an abdominal aortic aneurysm is an uncommon occurrence with the aneurysms usually small-to-moderate in size. Diagnosis may be difficult because patients present with both atypical and chronic symptoms. Pressure erosion of the lumbar spine is presumably a highly significant associated disorder, but an enhanced computed tomographic scan is the most reliable method for the correct diagnosis. We report on a 46-year-old man who developed severe back pain which was initially thought to result from spinal disease. Retrospective review of computed tomographic scans taken two years before admission revealed the beginning of the leakage of the aneurysm. Remarkably, the patient remained stable two years after the rupture.

Aorta, Abdominal↗
PubMed1990

Comparative study of cell saver and ultrafiltration nontransfusion in cardiac surgery.

Hemoconcentration for the establishment of no-donor blood transfusion in open heart surgery was assessed in regard to both the saving of protein and platelets and the exclusion of free hemoglobin. Two different types of hemoconcentrator were compared: the ultrafilter (group I, 6 patients) and the Cell Saver (group II, 6 patients). The total serum protein level, expressed as the percent recovery of the preoperative value, after hemoconcentration was significantly higher in group I (group I versus group II: total serum protein, 118% versus 87% [p less than 0.05]; fibrinogen, 77% versus 50% [p less than 0.01]; immunoglobulin, 83% versus 60% [p less than 0.01]). The platelets also seemed to be well preserved after hemoconcentration in group I. Although the exclusion of free hemoglobin from plasma was inferior in group I compared with group II, the postoperative plasma free hemoglobin level did not increase in group I. We conclude that use of the Cell Saver in nontransfusion cardiopulmonary bypass might cause a severe depletion of various proteins and that the ultrafilter is both safer and more useful if employed routinely.

Adult↗
PubMed1990

Flow cytometric study of injuries in cultured endothelial cells by neutrophils of the inherited cataract rats.

We examined the mechanism of endothelial injuries in the inherited cataract rats (ICR), which have a number of age-associated spontaneous injuries in the aortic endothelium. Cell cycle traverse rate of endothelial cells of ICR was shorter than that of Wistar rats. The rate was estimated from bromodeoxyuridine (BrdU) incorporation into cell nuclei measured periodically after BrdU pulse labeling. Next we established the method for measurement of cultured endothelial cell injury by neutrophils with flow cytometry by assessing the regeneration of injured endothelial cells. By the use of the gate analysis method, contaminated neutrophils were excluded from the analysis. Endothelial cell injury by neutrophils of Wistar rats was detectable at 1 x 10(5) neutrophils (1 neutrophil to 1 endothelial cell) when stimulated with 10 ng/ml phorbol myristate acetate (PMA). Extent of injury increased with an increasing number of neutrophils and the concentration of a stimulator, PMA. We detected endothelial cell injury by ICR neutrophils not only when they were stimulated but also in a resting condition, and ICR neutrophils yielded more injury than Wistar rat neutrophils. Number of adhered neutrophils to endothelial cells and effects of plasma or lymphocytes were the same between two strain rats. Scavengers of hydrogen peroxide and singlet oxygen inhibited the ICR neutrophil-induced endothelial cell injury. These findings indicate that an increase of generation of excited oxygen species from neutrophils, particularly of singlet oxygen, may cause injury of endothelial cells in this specific strain of rats.

Animals↗
PubMed1990

Effect of the preS1 RNA sequence on the efficiency of the hepatitis B virus preS2 and S protein translation.

The gene coding for hepatitis B virus surface antigen consists of preS1, preS2, and S regions. Two species of mRNAs of this gene are transcribed. The larger species covers all three regions and is translated solely into preS1 protein, whereas the smaller one covers the preS2 and S regions and is translated into preS2 and S proteins. This study examines the influence of the 5' upstream sequence lying in the preS1 region on the synthesis of preS2 and S proteins. For this purpose, several expression plasmids were constructed by inserting various portions of the preS1 region between the retroviral LTR promoter and the preS2/S coding region, and preS2/S protein production was examined in the transfected CHL cells. All the transcripts were initiated in the LTR. A sequence located in the region between 102 and 38 nucleotides upstream from the preS2 initiation codon was found to reduce the production of preS2/S proteins probably at the level of translation. Expression of the heterologous chloramphenicol acetyltransferase gene was similarly inhibited when it was placed downstream of the preS1-102/-38 sequence.

Animals↗
PubMed1990

Effects of various cytokines on proliferation of acute lymphoblastic leukemia cells.

We investigated the effects of recombinant human interleukins 1 to 6 (rIL-1 to -6) on the proliferation of blast cells from patients with acute lymphoblastic leukemia (ALL). The 3H-TdR incorporation in the presence of various cytokines was examined in cells from 14 patients: 12 with B-lineage ALL, 1 with T-lineage ALL and 1 with biphenotypic leukemia. In B-lineage ALL, a significant increase in 3H-TdR incorporation was observed in 5/12 cases (42%) in the presence of rIL-1 alpha, in 10/12 cases (83%) with rIL-2, in 9/12 cases (75%) with rIL-3, in 3/6 cases (50%) with rIL-4, in 4/6 cases (67%) with rIL-5, and in 4/12 cases (33%) with rIL-6. The mean stimulation index of the cells showing a positive response was 1.74 for rIL-1 alpha, 3.40 for rIL-2, 2.55 for rIL-3, 1.86 for IL-4, 1.56 for rIL-5, and 2.97 for rIL-6. T-lineage ALL cells were stimulated only in the presence of rIL-2, and biphenotypic leukemia cells were not stimulated by any of the cytokines tested.

Antigens, CD↗
PubMed1990

c-myb gene analysis in T-cell malignancies with del(6q).

Three T-cell malignancies with del(6q) were analyzed for karyotypes and alteration of the oncogene c-myb that is assigned to 6q22-q24. Patients were diagnosed as having non-Hodgkin T-cell lymphoblastic lymphoma, adult T-cell leukemia, and acute T-cell lymphoblastic leukemia, and the deletions of chromosome 6 were del(6)(q21q25), del(6)(q21q23), and del(6)(q21) or del(6)(q21q27), respectively. Tumor cell DNAs were obtained from cultured pleural fluid or from fresh peripheral blood and marrow samples and were analyzed by Southern blot hybridization, using c-myb oncogene probes. Rearrangements, deletions, or amplifications were absent in these tumor DNAs, thereby indicating that the del(6q) breakpoint in these T-cell malignancies was located outside of the c-myb gene. Northern blot analysis revealed the elevated expression of c-myb in the non-Hodgkin lymphoma patient, in accord with lineage characteristics.

Adolescent↗
PubMed1990

Detection and subcellular localization of rabbit platelet phospholipase A2 which preferentially hydrolyzes an arachidonoyl residue.

Like rat platelets, rabbit platelets contain a secretory 14-kDa group II phospholipase A2 [Mizushima, H., Kudo, I., Horigome, K., Murakami, M., Hayakawa, M., Kim, D.K., Kondo, E., Tomita, M., & Inoue, K. (1989) J. Biochem. 105, 520-525]. The present study was undertaken to determine whether or not, in addition to that of the 14-kDa group II enzyme, rabbit platelets exhibit another phospholipase A2 activity. A rabbit platelet soluble fraction was prepared by sonication and centrifugation. When this soluble fraction was subjected to heparin-Sepharose column chromatography, phospholipase A2 activity was detected in both heparin-binding and heparin-non-binding fractions. The activity detected in the heparin-binding fraction appeared to belong to the secretory 14-kDa phospholipase A2, because it bound to anti-human 14-kDa group II phospholipase A2 monoclonal antibody. The activity found in the heparin-non-binding fraction did not appreciably react with the same antibody. When platelets were gently disrupted by the nitrogen cavitation method, the heparin-non-binding activity was mainly recovered in the platelet cytosolic fraction. The heparin-non-binding phospholipase A2 hydrolyzed a phospholipid bearing an arachidonoyl residue at the sn-2 position more effectively than one with a linoleoyl residue. The biochemical features of the activity observed in the heparin-non-binding fraction generally resembled those of human platelet soluble phospholipase A2 [Kim, D.K., Kudo, I., & Inoue, K. (1988) J. Biochem. 104, 492-494].(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Induction of eosinophilic colonies by interleukin-5 on acute myeloblastic leukaemic cells.

The effect of interleukin-5 (IL-5) on blast colony formation of acute myeloblastic leukaemia (AML) cells was studied. IL-5 showed a weak but significant colony stimulatory effect in one out of six cases studied. IL-5 induced eosinophilic colony growth in this case, and chromosomal and histochemical analyses strongly suggested that these eosinophilic colonies were derived from leukaemic blast progenitor cells. To our knowledge, this is the first report that IL-5 induces eosinophilic colonies on fresh AML cells. A possible induction of differentiation of AML blast cells by IL-5 is suggested.

Adult↗
PubMed1990

Enhanced growth of clonogenic cells from acute myeloblastic leukaemia by erythropoietin.

The effect of erythropoietin (Epo) on colony formation by blast progenitors in acute myeloblastic leukaemia other than erythroleukaemia was studied using a blast colony assay. Epo alone did not induce colony formation, but when it was used together with phytohaemagglutinin-stimulated leucocyte-conditioned medium (PHA-LCM) the number of leukaemic colonies significantly increased in nine out of 12 cases studies. Preincubation of Epo with anti-Epo antibody completely abolished this enhancement, indicating that the increase in colony numbers was caused by Epo itself. Cell surface phenotype analysis of colonies produced by Epo plus PHA-LCM showed no increase in percentages of erythroid and megakaryocyte lineages. The addition of Epo also increased the self-renewal capacity of leukaemic blast cells. Fresh leukaemic cells did not express Epo receptors, but they were induced after incubation with PHA-LCM. The present study thus showed that the proliferative response to Epo is not restricted only to the erythroid lineage, but also extends to AML blast cells other than those in erythroleukaemia in the presence of colony stimulating factors.

Antibodies↗
PubMed1990

An increase in polymorphonuclear leucocyte chemotaxis accompanied by a change in the membrane fluidity with age during childhood.

Leucocyte membrane fluidity affects cell deformability as well as the accessibility of receptors and the degree of their exposure on the membrane. These effects modulate the subsequent cellular responsiveness. We have assayed membrane fluidity of polymorphonuclear leucocytes of children, using an excimer-forming lipid technique in flow cytometry, and evaluated its relation to their chemotaxis to a formyl peptide. We report that membrane fluidity and chemotaxis of polymorphonuclear leucocytes are increased with age. These findings may have important implications for the physiological processes in polymorphonuclear leucocyte motility during childhood.

Adult↗
PubMed1990

[A clinical and pathological study on varicella-zoster virus pneumonia].

A 48-year-old male with Adult T-cell leukemia (case 1) and a 57-year-old with acute lymphocytic leukemia (case 2) died of rapid progressive pneumonia and pleuritis. Histopathological findings of the lungs were multifocal hemorrhagic coagulation necrosis, and typical Cowdry type A and full type intranuclear inclusion bodies were observed in alveolar cells, bronchial cells, fibroblast, endothelial cells of small vessels, bronchial gland cells and pleural cells. Antigen against varicella-zoster virus (VZV) was positive in these cells by immunostaining, and the antigen was also demonstrated in other organs such as liver, spleen, pancreas, kidney, adrenal gland, esophagus, stomach, intestine and so on. Furthermore, cytomegalovirus was simultaneously superinfected lungs of both cases, and concomitant candida gastritis (case 1), aspergillus lung abscess and candida liver abscess (case 2) were observed. In the immunocompromised host VZV may involve the visceral organs and death may result from VZV pneumonia.

Bronchi↗
PubMed1990

Construction and characterization of the recombinant Moloney murine leukemia viruses bearing the mouse Fv-4 env gene.

A nucleotide sequence of the mouse Fv-4 env gene was completed. Structural comparison revealed a close relationship of Fv-4 to the ecotropic Cas-Br-E murine leukemia virus isolated from a wild mouse in southern California. Various portions of the env gene of Moloney murine leukemia virus were replaced by the corresponding Fv-4 env sequence to construct recombinant murine leukemia virus clones. Infectivity of these recombinants was checked by the S+L- cell focus induction assay and the XC cell syncytium formation assay. Recombinants bearing the following Fv-4 env sequence retained ecotropic infectivity; the AccI-BamHI and BamHI-BalI regions coding for the N- and C-terminal halves of Fv-4 gp70SU, respectively; and the BalI-NcoI region encoding the cleavage site between gp70SU and p15(E)TM of the Fv-4 env. However, when the Fv-4 sequence was substituted for the p15(E)TM-coding NcoI-EcoRV region or the AccI-EcoRV region covering almost the entire env gene, infectivity was undetectable in our assays. The recombinant clone containing the Fv-4 AccI-EcoRV region, i.e., almost the entire Fv-4 env sequence, was introduced with pSV2neo into NIH 3T3 cells, and a G418r cell line named NIH(Fv4)-2 was isolated. The NIH(Fv4)-2 cell released viral particles that contained reverse transcriptase, Fv-4 env molecules as well as the other viral proteins, and viral genomic RNA. However, proviral DNA synthesis was not detected upon inoculation of this virus in NIH 3T3 cells. The loss of infectivity of the recombinant virus bearing the Fv-4 AccI-EcoRV region appeared to be caused by failure in an early step of replication.

Amino Acid Sequence↗
PubMed1990

Decrease of polymorphonuclear leukocyte membrane fluidity in uremic patients on hemodialysis.

We measured membrane fluidity of polymorphonuclear leukocytes (PMN) from 14 uremic patients on hemodialysis by the excimer-forming lipid technique with pyrenedecanoic acid using flow cytometry. Membrane fluidity of PMN was significantly lower in the uremic patients during the predialysis period. During hemodialysis, progressive normalization in membrane fluidity was observed. Cross-incubation studies indicated that this observation is ascribed to factors in the patients' serum and that they can be removed by hemodialysis. When sera of these patients were fractionated by Sephadex G-25 column chromatography, the specific fraction responsible for a decreased fluidity was found in the low-molecular-weight fraction. Uremic patients have an increased risk of infection, which may be partly due to altered membrane fluidity of their PMN.

Adult↗
PubMed1990

[Limitation of experimental infarct size by levo-carnitine chloride (LC-80), a new mitochondrial function-reactivating agent].

The effect of LC-80 on infarct size induced by 6 hr coronary occlusion was studied in anesthetized dogs. LC-80 at a dose of 100 mg/kg, i.v. was injected 5 min after coronary occlusion and then infused at a rate of 50 mg/kg, i.v./hr until the heart was excised. The two risk areas were determined both by injecting a fluorescent dye (Thioflavin S) into the left atrium (in vivo) and by perfusing the non-occluded coronary bed with Monastral Blue (in vitro). The infarct size was determined by topographically tracing the area of myocardium unstained by triphenyltetrazolium chloride. Four zones such as Zone 1 (normal tissue), Zone 2 (tissue characterized by collateral blood flow), Zone 3a (tissue developing necrosis), Zone 3b (necrotic tissue) were delimited . As a result, (1) LC-80 significantly diminished the incidence of ventricular arrhythmias. (2) LC-80 significantly inhibited the decrease in myocardial free carnitine level in Zone 2 and Zone 3b. (3) LC-80 significantly reduced the infarct size expressed as a percentage of the risk area and increased the size of Zone 2. (4) In the electron microscopic findings, LC-80 showed lesser morphological changes such as swollen mitochondria and intracellular and extracellular edema, especially in Zone 2. (5) LC-80 may be useful for inhibiting the evolution of myocardial ischemic cell death both by the protection of ischemic myocardium and presumably by the increase in the collateral blood flow.

Animals↗
PubMed1990

Decreased fluidity of polymorphonuclear leukocyte membrane in streptozocin-induced diabetic rats.

Using flow cytometry with the excimer-forming lipid technique with pyrenedecanoic acid, we measured membrane fluidity of polymorphonuclear leukocytes (PMNs) from 20 streptozocin (STZ)-induced diabetic rats. Diabetes mellitus was induced in male Sprague-Dawley rats (body wt 243 +/- 11 g) with an injection of 25 mg/kg i.v. STZ. Membrane fluidity of PMNs was significantly lower at 2 wk after the STZ injection when serum glucose reached the plateau (31.1 +/- 5.8 mM), and after 3 wk, membrane fluidity remained unchanged. In 7 STZ-resistant rats for which serum glucose was less than 10 mM at 2 wk after the STZ injection, gradual normalization in membrane fluidity was observed. PMN membrane fluidity at each week correlated inversely with respective serum glucose levels 1 wk previously (r = -0.76) but not with serum lipid levels. Cross-incubation studies ascribed this observation to factors in the diabetic rat serum. Glycosylated protein, which was separated from diabetic rat serum, decreased membrane fluidity of control rat PMNs. Human diabetic subjects have an increased risk for infection, which may be due partly to altered membrane fluidity of their PMNs.

Animals↗
PubMed1990

A new serum-free culture system for leukemic colony assay.

A new serum-free assay system for leukemic colony formation (leukemic colony-forming units, L-CFU) was established, and, utilizing this system, the colony-promoting activities of recombinant human colony-stimulating factors (rhCSFs) and the effectiveness of CSFs on cellular self-renewal capacity were investigated. The serum-free assay system included deionized bovine serum albumin (1%), cholesterol (7.8 micrograms/ml), and ASF 101 medium. The plating efficiencies obtained by culturing with phytohemagglutinin-stimulated leukocyte-conditioned medium (PHA-LCM) ranged from 0.01% to 1.35% in this system. Spontaneous colonies were observed in 9 out of 13 cases studied. Recombinant human granulocyte CSF (rhG-CSF), rh granulocyte-macrophage CSF (rhGM-CSF), rh interleukin 3 (rhIL-3), and rh interleukin 1 (rhIL-1) stimulated colony formation in 10, 9, and 6 out of 13, and 5 out of 11 cases, respectively. The magnitude of stimulation by each CSF ranged from 6% to 145%, 21% to 200%, 0% to 1229%, and 14% to 182% of PHA-LCM, respectively. In eight cases, blast colony assays in serum-free and serum-containing cultures were simultaneously performed. The magnitudes of responsiveness of each CSF differed in the two assay systems; this indicated some effect of fetal calf serum. The value of self-renewal capacity was also examined and compared with that in serum-containing culture. Self-renewal capacity could be maintained with a serum-free culture system. It showed marked variation from case to case, and there was no correlation between the primary colony formation and the self-renewal capacity in both culture systems. Taken together, the development of a completely serum-free culture system was found to be efficient as evaluated by a L-CFU colony assay.

Blood↗
PubMed1990

[Surgical treatment of constrictive pericarditis].

Since 1957, 30 patients with constrictive pericarditis have been treated surgically in Kyushu University Hospital. The surgical approaches were the left anterolateral thoracotomy in 17 patients (group I); the median sternotomy without cardiopulmonary bypass (CPB) in 6 patients (group II); and the median sternotomy with CPB in 7 patients (group III). The hospital mortality was 3.3 percent. The mean postoperative follow-up period was 11.7 years (longest 30 years). The actuarial survival rate at 5 years postoperatively was 88% in total cases (100% in group I, 82% in group II and 52% in group III), 88% at 10 years, 75% at 15 years and 67% at 20 years. Several patients in group III, who underwent complete pericardiectomy using CPB showed severe congestive heart failure and arrhythmia postoperatively. The comparative study between an poor result group (patients who died within 10 years post-operatively) and a good result group (patients who survived more than 10 years postoperatively revealed that preoperative hepatomegaly, atrial fibrillation and the interval between the onset of symptoms and the pericardiectomy influenced the survival rate significantly. These results suggested that pericardiectomy using CPB was a safe method for removing the calcified pericardium in the patient with severe constrictive pericarditis. However, a careful long term follow-up was necessary for the patient with severe myocardial damage even though the complete pericardiectomy was performed.

Adolescent↗