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Biomedical subjects

M Matsuda

Publications and source records attributed to M Matsuda.

At least 721 records · Page 40Linked to original sources

[Effect of increase of pulmonary blood flow on segmental pulmonary vascular resistance--with special emphasis on the pulmonary capillary bed].

The decrease of pulmonary vascular resistance with increase of pulmonary blood flow has been attributed to the function of the pulmonary vascular bed, consisting of capillary recruitment or dilatation. However, experimental evidence of a decrease of capillary resistance is lacking. To clarify this phenomenon, we perfused isolated cat lungs with diluted autologous blood and measured pulmonary microvascular pressure while changing pulmonary blood flow rate. We set the initial flow rate to achieve Ppa of 20 cmH2O and changed the flow rate while keeping left atrial pressure (Pla) and alveolar pressure (Palv) constant at 10 cmH2O and 9 cmH2O, respectively. Thereafter, pulmonary flow rate was increased 2 to 3 fold, and pulmonary arterial pressure (Ppa) and venular pressure (Pvo) were measured by venous occlusion method. The initial flow rate was 150 to 270 ml/min and the achieved maximum flow rate was from 300 to 543 ml/min. There was a linear correlation between Ppa, Pvo, and flow rate, in which the slope (rate of increase of pressure with flow) of Ppa was slightly steeper than that of Pvo. We calculated total and segmental pulmonary vascular resistance from the mean pressure-flow relationship. The total and upstream resistance involving arterial and capillary segments decreased hyperbolically with increase in flow rate. The mean upstream resistance decreased about 54%, from 35.20 x 10(-3) (cmH2O/ml/min) at a flow rate of 150 ml/min to 16.27 x 10(-3) (cmH2O/ml/min) at a flow rate of 450 ml/min. The degree of this decrease was similar to the result observed by micropuncture method (Nagasaka, 1990). Downstream resistance, which represents venous resistance, did not change significantly with the flow rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Outcome of patients with primary malignant lymphoma of the brain; relationship to the nucleolar organizer region].

Twelve cases of primary malignant lymphoma of the central nervous system had been treated since April, 1979 to August, 1990. Radiation therapy was completed in ten of them without adjuvant chemotherapy, and the other two patients expired before or during radiation therapy. In spite of good response to the radiation therapy, five of the ten patients died within 2 years. Three cases are alive after more than 5 years, and there has been no recurrence. In eight cases, the number of the argyrophilic proteins of the nucleolar organizer regions (AgNORs) was counted in the formalin-fixed paraffin embedded sections. In those cases with an AgNOR number of 4.0 or higher, prognosis was significantly worse than in the others. AgNOR number may be used as one of the reliable factors in the prognosis of primary malignant lymphoma of the central nervous system.

Adult↗

[Primary malignant lymphoma of the esophagus--a case report].

We report a rare case of primary malignant lymphoma of the esophagus without extraesophageal involvement. A 69-year-old woman was referred to our hospital because of dysphagia. Esophagogram revealed an irregularly marginal ulceration with stenosis at the abdominal esophagus. Endoscopic study showed an ulcerative lesion at the level of 30 cm from the incisor teeth. Esophagocardiectomy was performed. Resected specimen showed a shallow depressed ulceration, 6.5 x 6.0 cm in size, at the lower esophagus. Microscopic examination revealed malignant lymphoma of diffuse, large cell type. No evidence of involvement was found in the dissected lymph nodes and the bone marrow biopsy specimens. She has been well for 4 years and 6 months postoperatively.

Aged↗

Protective activity of adult T cell leukemia-derived factor (ADF) against tumor necrosis factor-dependent cytotoxicity on U937 cells.

Adult T cell leukemia-derived factor (ADF) is a human homologue of thioredoxin with many biologic functions including IL-2R induction, growth promotion, thiol-dependent reducing activity, and radical scavenging activity. The regulatory effect of ADF on the cytotoxic activity of TNF was examined by using a human histiocytic lymphoma cell line, U937. When U937 cells were preincubated with recombinant ADF (rADF) (0.1-100 micrograms/ml) at 37 degrees C for 30 min, TNF-dependent cytotoxicity on U937 cells was markedly inhibited. This inhibitory effect was as high as 95% in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay (rADF 100 micrograms/ml) and 85% in the 51Cr-releasing assay (rADF 10 micrograms/ml). After pretreatment of U937 cells with IFN-gamma to augment the sensitivity to TNF, an inhibitory effect of rADF was also found. When U937 cells were washed after preincubation with rADF, resistance to TNF-dependent cytotoxicity was still observed, indicating that rADF inhibited the sensitivity of U937 to TNF-dependent cytotoxicity rather than modifying TNF molecules. Scatchard analysis of TNF receptors on U937 cells using 125I-TNF showed that rADF modulated neither the density nor the affinity of the cell membrane significantly. rADF also reduced the cytotoxicity induced by anti-Fas IgM mAb which shows cytotoxicity quite similar to TNF. rADF (10 micrograms/ml) reduced 90% of the cytotoxicity by anti-Fas IgM mAb, without a detectable change either in Fas Ag expression (MFI 58.1 vs 53.3) or in the degradation of anti-Fas IgM mAb as determined by flow cytometric analysis. These findings indicated that the rADF-induced resistance to the cytotoxic effect of TNF and anti-Fas mAb was not related to the modulation of the TNF receptor or Fas Ag.

Antigens, Surface↗

The effects of denatured sodium hyaluronate on the corneal endothelium in cats.

In an in vivo cat model, wide-field specular microscopy and scanning electron microscopy were used to observe whether heat-denatured sodium hyaluronate causes cell damage to the corneal endothelium. The endothelial cell toxicities of various drugs, including 0.01% benzalkonium chloride, 0.2% chlorhexidine digluconate, and 0.5% lidocaine, mixed with intact or untreated sodium hyaluronate were also investigated. Neither heat-denatured nor intact or untreated sodium hyaluronate alone had any adverse effect on the corneal endothelium in cats, whereas 0.01% benzalkonium chloride and 0.2% chlorhexidine digluconate, mixed with sodium hyaluronate, caused substantial endothelial morphologic changes, which resulted in corneal edema. By comparison, 0.5% lidocaine with sodium hyaluronate was found to have minimal effect on the corneal endothelium in cats. These findings indicate that some chemical contaminant with sodium hyaluronate, not heat-denatured sodium hyaluronate, induces an immediate onset of pseudophakic bullous keratopathy.

Animals↗

The plasminogen activator inhibitor-1 binding site in the kringle-2 domain of tissue-type plasminogen activator.

We have shown that synthetic peptides containing the amino acid sequence Asn-Arg-Arg-Leu, derived from the amino acid sequence of the inner loop of the kringle-2 domain of tissue-type plasminogen activator (tPA), inhibited complex formation between two chain tPA and plasminogen activator inhibitor-1 (PAI-1) by binding to PAI-1. This binding was reversible and was inhibited by not only tPA but also by enzymatically inactive tPA. Quantitative analyses of the interaction of PAI-1 with the peptide containing the Asn-Arg-Arg-Leu sequence indicated that the PAI-1 binding site residues in the inner loop of the kringle-2 domain and is preferentially expressed in two chain tPA.

Amino Acid Sequence↗

Centrally administered NPY stimulated gastric acid and pepsin secretion by a vagally mediated mechanism.

We investigated the possible roles of centrally administered neuropeptide Y (NPY) on gastric secretion, serum gastrin levels and gastric mucosal blood flow in anesthetized rats. Centrally administered NPY dose-dependently stimulated gastric acid and pepsin secretion. The stimulatory effect of intracerebroventricular administration of NPY was more potent than that of intracisternal administration. Centrally administered NPY also increased gastric secretion in the central noradrenaline depleted rats. In contrast, intravenously administered NPY had no influence on gastric secretion. These stimulatory effects were abolished by vagotomy or atropine pretreatment. The serum gastrin levels did not change after central NPY injection. Although intravenously administered NPY slightly increased gastric mucosal blood flow, centrally administered NPY slightly diminished gastric mucosal blood flow. These results indicate that centrally administered NPY markedly influences gastric functions in the rat.

Animals↗

Fibrinogen Kyoto II, a new congenitally abnormal molecule, characterized by the replacement of A alpha proline-18 by leucine.

A new case of heterozygous dysfibrinogenemia characterized by an amino acid replacement in the NH2-terminal region of the fibrin alpha-chain was found in a 27-year-old woman with a bleeding problem. Her one-stage prothrombin time and activated partial thromboplastin time were slightly prolonged, and the purified fibrinogen from this patient had a markedly prolonged thrombin or reptilase time. Release of fibrinopeptides A and B was normal, but the polymerization of fibrin monomers was impaired. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the purified fibrinogen under the reduced condition showed no abnormalities in the apparent molecular weights of its three chains. Reverse-phase high performance liquid chromatography (HPLC) of the lysylendopeptidase-cleaved purified A alpha-chains showed a decrease in one peptide compared with the normal amount and the appearance of an abnormal peptide peak. These peptides were treated with thrombin and further separated on HPLC. Amino acid sequence analysis of the abnormal peptide indicated that A alpha proline-18, the second residue from the NH2-terminus of the fibrin alpha-chain, was replaced by leucine. The synthetic peptide Gly-Pro-Arg-Pro inhibited both thrombin- and reptilase-induced fibrin aggregation, but Gly-Leu-Arg-Pro showed little or no inhibition under the same conditions. The discovery of this abnormal fibrinogen supports the findings that A alpha proline-18 is important as part of the polymerization site in the NH2-terminus of the fibrin alpha-chain. The propositus' mother had the same abnormal fibrinogen. This unique inherited abnormal fibrinogen was designated as fibrinogen Kyoto II.

Adult↗

The specific activity of plasminogen activator inhibitor-1 in disseminated intravascular coagulation with acute promyelocytic leukemia.

In disseminated intravascular coagulation (DIC) with acute promyelocytic leukemia (APL) in the absence of severe infection, marked fibrinolysis was noted in comparison with normal levels of antithrombin III, which is a major inhibitor of the coagulation system. Increased plasminogen activator inhibitor-1 (PAI-1) antigen levels in plasma from patients with septicemia decreased the ratio of the plasma clot lysis rate induced by an anti-alpha 2-plasmin inhibitor monoclonal antibody to the tissue-type plasminogen activator (t-PA) concentration. This decrease was not as prominent in plasma from patients with DIC, especially those with APL. To explore the character of PAI-1 in these plasmas, we measured the specific activity of PAI-1 by determining the ratio of active PAI-1 antigen to t-PA-unbound PAI-1 antigen. To calculate the amount of active PAI-1 antigen, the amount of t-PA/PAI-1 complex before and after the addition of a fixed amount of t-PA to the sample was measured by a sandwich solid-phase enzyme-linked immunosorbent assay using anti-PAI-1 and anti-t-PA monoclonal antibodies. The assay to measure total PAI-1 antigen used three monoclonal anti-PAI-1 antibodies and had similar sensitivities to free active, latent, vitronectin-bound and t-PA-bound PAI-1. The specific activity of PAI-1 decreased in patients with DIC (43.7% +/- 30.6%) and in DIC cases with APL (10.3% +/- 6.0%) in comparison to patients with septicemia (83.7% +/- 20.2%) or normal controls (85.8% +/- 27.3%). In DIC associated with APL, degraded forms of PAI-1 were detected in plasma by immunoblotting. These results suggest that a decrease in the specific activity of PAI-1 and an increase in secondary fibrinolysis result in a hyperfibrinolytic state in DIC patients with APL.

Antibodies, Monoclonal↗

A new congenital abnormal fibrinogen Ise characterized by the replacement of B beta glycine-15 by cysteine.

A new case of heterozygous dysfibrinogenemia characterized by the replacement of NH2-terminal amino acid of fibrin beta-chain was found in a 50-year-old man. Despite a prolonged thrombin time, the propositus' fibrinogen had a normal reptilase time with the normal release of fibrinopeptide A. Release of fibrinopeptide B by thrombin was strongly affected, but a very high concentration of thrombin almost completely released fibrinopeptide B with a normal elution pattern on reversed-phase high performance liquid chromatography (HPLC). Lysylendopeptidase-cleavage of purified B beta-chains analyzed on HPLC showed the decrease of one peptide compared with the normal and the appearance of an abnormal peptide peak. These peptides were treated with thrombin and further separated on HPLC. Amino acid sequence analysis of the abnormal peptide demonstrated that B beta glycine-15, NH2-terminus of the fibrin beta-chain, was replaced by cysteine. These findings will be of particular importance because they strongly support the hypothesis that the NH2-terminal portion of the fibrin beta-chain is involved in the polymerization reaction by thrombin. The propositus' daughter and two sisters had the same abnormal fibrinogen. This unique inherited abnormal fibrinogen was designated as fibrinogen Ise. During these studies, we found that a very high concentration of thrombin cleaves not only the A alpha Arg19-Val20 bond but also the COOH-terminal region of alpha-chains, which results in the generation of further degraded alpha-chains with apparent molecular weights of 44,000 or less.

Amino Acid Sequence↗

[Ca++ antagonist and acute brain ischemia: effects of nilvadipine and nicardipine on middle cerebral artery occlusion in rats].

Effects of calcium antagonists, Nicardipine and Nilvadipine, on neurologic deficits and size of infarct were studied in the rat middle cerebral artery (MCA) occlusion model. Each drug was administered immediately after induction of ischemia, and neurologic grade was evaluated 1 to 24 hours after MCA occlusion. At 24 hours post-occlusion, size of the infarct was compared with that of the control group. In addition, evolution of cerebral infarction was studied at 6 hours and 12 hours post-occlusion by magnetic resonance imaging (MRI). In the Nilvadipine-treated group, neurologic deficits improved more rapidly and the size of infarct was significantly smaller than in the Nicardipine-treated group. MRI showed a progressive extension of cortical infarct in the untreated rat, whereas the infarct size remained unchanged in the Nilvadipine-treated rat. These results suggest the potential therapeutic usefulness of calcium antagonist for acute cerebral ischemia.

Acute Disease↗

Increased production of tumor necrosis factor-alpha by peripheral blood mononuclear cells in the patients with aplastic anemia.

The activity of tumor necrosis factor-alpha (TNF-alpha) in the supernatant of cultured peripheral blood mononuclear cells (PBMC) was measured in patients with aplastic anemia. It was significantly higher in patients with aplastic anemia than in normal controls, both when PBMC were unstimulated or when they were stimulated with PHA. Results from aplastic anemia patients were also significantly higher than patients who had received allogeneic bone marrow transplants. In aplastic anemia patients, the TNF-alpha value produced by PBMC upon stimulation and the platelet count were inversely correlated, as well those patients who had high TNF-alpha values tended to have lower hemoglobin and leukocyte values although this was not significant statistically. These results suggest that the increased production of TNF-alpha by PBMC plays a role in the severe suppression of hematopoiesis in aplastic anemia.

Anemia, Aplastic↗

Fibrinogen date: congenital hypodysfibrinogenemia associated with decreased binding of tissue-plasminogen activator.

A new case of congenital hypodysfibrinogenemia associated with a thrombotic tendency (thrombosis of the peroneal artery, the pulmonary artery and the deep veins of the lower extremities), is reported. Clotting time using Reptilase was significantly prolonged. The low levels of plasma fibrinogen were demonstrated using both thrombin time (Clauss) method (45.0 mg/ml) and radial immunodiffusion technique (106.1 mg/ml). The fibrinogen is also characterized by a defective polymerization of fibrin monomers. Furthermore, the important functional property of this fibrinogen is that the patient's fibrin adsorbs approximately 31-38% of added tissue-plasminogen activator (t-PA) at the time of fibrin formation, whereas control fibrin can adsorb about 79% of added t-PA. This result could provide an explanation for the thrombotic tendency in this patient. This variant fibrinogen appears to have unique characteristics and has been designated as "Fibrinogen Date," according to the city where the proband has lived.

Afibrinogenemia↗

Occult thyroid cancer discovered by fine-needle aspiration cytology of cervical lymph node: a report of three cases.

Three cases of occult thyroid cancer measuring 10, 6, and 3 mm in diameter were discovered by fine-needle aspiration cytology of cervical lymph nodes. In these three cases, thyroid tumors were not palpable, and scintigraphic, echographic, and soft-tissue radiologic examinations demonstrated no abnormalities of the thyroid glands. Cytologically, the presence of intranuclear cytoplasmic inclusions, nuclear grooves, and colloid was characteristic in aspirated materials. Histologically, all three cases were diagnosed as papillary carcinoma. Fine-needle aspiration cytology of cervical lymph node was very useful to find occult carcinoma of the thyroid gland.

Adult↗