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Biomedical subjects

J Tanabe

Publications and source records attributed to J Tanabe.

At least 55 records · Page 3Linked to original sources
PubMed1995

Acquired von Willebrand disease associated with multiple myeloma; characterization of an inhibitor to von Willebrand factor.

Acquired von Willebrand disease (vWD) has been described in a few patients with multiple myeloma. The present study characterizes an inhibitor of von Willebrand factor (vWF) isolated from a patient with multiple myeloma (IgG-kappa). Multimeric analysis of vWF from this patient's plasma showed a reduction in multimers of all sizes. The inhibitor (IgG) detected only the vWF subunit from plasma of normal individuals. It reacted with intact vWF subunit and a 39/34kDa dispase-digested fragment of vWF (residues; Leu480/Val481-Gly718), but did not react with platelet membrane glycoproteins (GPs) or adhesive proteins. The binding of vWF to GPIb mediated by ristocetin and by botrocetin was inhibited by the patient's IgG with an IC50s of 0.3 mg/ml and 0.48 mg/ml, respectively. The platelet aggregation induced by ristocetin or botrocetin was also inhibited by the IgG. These results indicate that this inhibitor may recognize the binding region of vWF to GPIb. Therefore, the antibody to vWF appears to represent the likely pathophysiological mechanism responsible for the acquired vWD in this patient.

Autoantibodies↗
PubMed1995

Characterization of leukocyte-derived neutrophil chemotactic factor-2 and its possible roles in neutrophil infiltration in allergic inflammation in rats.

This study sought to clarify the responsible chemotactic factor for neutrophils in allergic inflammation in rats. When the leukocytes collected from the pouch fluid 4 h after injection of the antigen solution into the air pouch were incubated, the neutrophil chemotactic activity in the conditioned medium increased time-dependently with higher levels for the leukocytes from the immunized rats than the nonimmunized ones. The chemotactic activity did not result from cytokine-induced neutrophil chemoattractant (CINC) because CINC concentrations in the conditioned medium were low. Neutrophil chemotactic factors in the conditioned medium were separated by isoelectric focusing into two factors, leukocyte-derived neutrophil chemotactic factor (LDNCF)-1 and LDNCF-2. The activity of LDNCF-2 was more than 75% of the total chemotactic activity in the conditioned medium. LDNCF-2 was purified by gel chromatography and reverse-phase HPLC. The N-terminal amino acid sequence (1-20) of the purified LDNCF-2 was identical to the 32-51 amino acid sequence of the pro-form of rat macrophage inflammatory protein (MIP)-2. Higher levels of MIP-2 mRNA in the leukocytes from the immunized rats than that from the non-immunized rats were proved by the reverse transcription-polymerase chain reaction. In vivo, concentrations of CINC in the pouch fluid were low, and did not represent the chemotactic activity in the pouch fluid. These results suggest that LDNCF-2 (MIP-2) is an important chemotactic factor for neutrophils in the allergic inflammation in rats.

Amino Acid Sequence↗
PubMed1995

Leukocyte-derived neutrophil chemotactic factor-2 produced by infiltrated leukocytes in allergic inflammation model in rats is macrophage inflammatory protein-2.

In the air pouch-type allergic inflammation model in rats, leukocytes collected from the pouch fluid 4 h after the antigen challenge produced proteinaceous chemotactic factors for neutrophils. The leukocytes from the immunized rats produced significantly higher amount of the chemotactic factors than that from the non-immunized rats. The major chemotactic factor, leukocyte-derived neutrophil chemotactic factor (LDNCF)-2, was purified and found to be identical with rat macrophage inflammatory protein (MIP)-2 by N-terminal amino acid sequence analysis. Expression of MIP-2 mRNA was higher in the leukocytes from the immunized rats than that from the non-immunized rats. Possible roles of LDNCF-2 (MIP-2) in neutrophil infiltration in the allergic inflammation is discussed.

Amino Acid Sequence↗
PubMed1995

Suppression of interleukin-1 alpha production by protein kinase C activators in human vascular endothelial cells.

In human umbilical endothelial cells, treatment with tumor necrosis factor (TNF)-alpha stimulated the production of cell-associated interleukin (IL)-1 alpha. Combined treatment of human umbilical endothelial cells with TNF-alpha and the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol 13-acetate (TPA) suppressed the TNF-alpha-induced production of IL-1 alpha. However, concentrations of 6-keto-prostaglandin F1 alpha in the conditioned medium were increased to a greater extent by combined treatment with TNF-alpha and TPA than by single treatment with TNF-alpha or TPA. Pretreatment with TPA for 15 min was enough to suppress the TNF-alpha-induced IL-1 alpha production. Pretreatment for 15 min with other PKC activators such as aplysiatoxin or teleocidin, also inhibited the TNF-alpha-induced IL-1 alpha production. Stimulation of cell-associated IL-1 alpha production by IL-1 beta or lipopolysaccharide was also inhibited by pretreatment with the PKC activator TPA, aplysiatoxin or teleocidin. However, treatment with the protein kinase inhibitor 1-(5-isoquinoline-sulphonyl)-2- methylpiperazine dihydrochloride (H-7) did not block the inhibitory effect of TPA, aplysiatoxin or teleocidin on the cell-associated IL-1 alpha production stimulated by TNF-alpha, IL-1 beta or lipopolysaccharide, although the PKC activator-induced stimulation of 6-keto-prostaglandin F1 alpha production was counteracted by H-7 treatment. The present work indicates that the production of cell-associated IL-1 alpha stimulated by TNF-alpha, IL-1 beta or lipopolysaccharide is inhibited by treatment with TPA, aplysiatoxin or teleocidin.(ABSTRACT TRUNCATED AT 250 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1995

[Study on conservative treatment of retinoblastoma--effect of intravitreal injection of melphalan on the rabbit retina].

Effects of an intravitreal injection of melphalan on the electroretinogram and on the retinal structure were studied in albino rabbits to establish the non-toxic dose for its intravitreal use. The a-wave, the b-wave, the c-wave, the oscillatory potential and the retinal structure remained unchanged after 10-micrograms injection, but moderately changed after 20-micrograms injection and greatly deteriorated after 90-micrograms injection. A 10-micrograms injection is equal to an intravitreal concentration of about 5.9 micrograms/ml, if evenly diffused in the rabbit vitreous. Considering that colony formation of in vitro retinoblastoma cells is completely suppressed by melphalan at 4 micrograms/ml concentration, an intravitreal application of melphalan could be used as a non-surgical treatment for retinoblastoma.

Animals↗
PubMed1994

A case of Purtscher's retinopathy.

This article describes a case of Purtscher's retinopathy, a syndrome believed to be caused by microembolic infarction of the retina, in a 20-year-old man after remote extraocular trauma. The patient jumped from a 20-meter high building. He suffered multiple crush injuries, but a computed tomographic scan of the brain and orbit was normal. More than 1 month after injury, his visual acuity diminished to light perception in the right eye and counting fingers in the left. The ophthalmoscopic picture was characteristic of Purtscher's retinopathy with cotton-wool exudates and retinal hemorrhages localized to the posterior pole. His vision was improved only slightly 6 months later. Although rare, emergency physicians should be familiar with this entity as a cause of diminished vision associated with extraocular trauma.

Adult↗
PubMed1994

Autoimmune antibody in a patient with idiopathic thrombocytopenic purpura reacted to the platelet low molecular weight glycoproteins and activated platelets.

The authors characterized antiplatelet membrane antibodies in the sera of patients with idiopathic thrombocytopenic purpura (ITP) and cirrhosis of the liver. Antibodies were detected in five of the 22 patients with chronic ITP and in none of the eight patients with cirrhosis of the liver. The authors report a patient with chronic ITP in complete remission. Antibody to platelet glycoproteins (GP), with molecular weights of 55 and 49 kDa, was detected in the serum. The patient's immunoglobulin G (IgG) alone could cause the aggregation of platelet-rich plasma. Anti-GPIIb/IIIa antibody (LJ-CP8) inhibited the aggregation of platelet-rich plasma induced by the patient's IgG in a dose-dependent manner. The F(ab')2 of the patient's IgG had a synergetic effect on the aggregation of PRP induced by adenosine 5-diphosphate. This demonstrates that in ITP, the binding of IgG via its fragment of antigen binding site portion may activate platelets.

Aged↗
PubMed1994

Pharmacological analysis of neutrophil chemotactic factor production by leucocytes and roles of PAF in allergic inflammation in rats.

1. The role of platelet activating factor (PAF) in neutrophil infiltration in air pouch type allergic inflammation in rats was investigated. 2. Neutrophil infiltration into the pouch fluid 8 h after injection of the antigen (azobenzenearsonate-conjugated acetyl bovine serum albumin) solution into the air pouch of immunized rats was inhibited dose-dependently by treatment with PAF antagonists (CV-3988, L-652,731 and Y-24,180) in parallel with the decrease in neutrophil chemotactic activity in the pouch fluid. 3. Four hours after injection of the antigen solution into the air pouch of immunized and non-immunized rats, there was no significant difference between the two groups in the number of total leucocytes, neutrophils, mononuclear cells and eosinophils in the pouch fluid. However, when the infiltrated leucocytes were incubated in medium, chemotactic factor production by leucocytes from immunized rats was greater than that from non-immunized rats. 4. When leucocytes from non-immunized rats were preincubated for various periods in the medium containing 10 or 50 nM of PAF, washed, and further incubated in the medium containing no PAF, chemotactic factor production was not stimulated. 5. The increase in the chemotactic activity in the conditioned medium was not suppressed by the 5-lipoxygenase inhibitor, AA861. In addition, the chemotactic activity in the conditioned medium was not inhibited by the PAF antagonists. 6. Incubation of the infiltrated leucocytes in the medium containing the protein synthesis inhibitor, cycloheximide, inhibited chemotactic factor production in a concentration-dependent manner in parallel with the decrease in uptake of [3H]-leucine into the acid-insoluble fraction of leucocytes. 7. Separation of the chemotactic activity in the conditioned medium by isoelectric focusing revealed that the leucocyte infiltrated into the pouch fluid produce two kinds of factors, viz. leucocyte-derived neutrophil chemotactic factor-i (LDNCF-1) and LDNCF-2 of which pI values are 4-5 and above 8,respectively.8. The results indicate that PAF has no significant role in leucocyte activation to produce chemotactic factors, and that neutrophil chemotactic factors produced by infiltrated leucocytes are not PAF or leukotriene B4 but are produced through a protein synthesis mechanism.9. The mechanism of action of PAF antagonists on neutrophil infiltration into the inflammatory locus is discussed.

Animals↗
PubMed1994

Possible roles of protein kinases in neutrophil chemotactic factor production by leucocytes in allergic inflammation in rats.

1. In an air pouch-type allergic inflammation model in rats, leucocytes that had infiltrated into the pouch fluid collected 4 h after the antigen challenge produced proteinaceous chemotactic factors for neutrophils when they were incubated in the medium. 2. To clarify the mechanism of activation of the infiltrated leucocytes in producing these factors, the effects of protein kinase inhibitors on neutrophil chemotactic factor production were examined. 3. When the infiltrated leucocytes were incubated for 4 h in medium containing the non-selective protein kinase inhibitor K-252a (1-100 ng ml-1, 2.14-214 nM), the tyrosine kinase inhibitor genistein (1-50 micrograms ml-1, 3.7-185 microM), and the more selective protein kinase C inhibitor H-7 (5-100 micrograms ml-1, 13.7-274 microM); neutrophil chemotactic activity in the conditioned medium was decreased in a concentration-dependent manner, but the adenosine 3':5'-cyclic monophosphate (cAMP)-dependent protein kinase inhibitor H-89 (1-1000 ng ml-1, 2.24-2240 nM) showed no effect. 4. Isoelectric focusing of the conditioned medium revealed that the leucocytes produced two neutrophil chemotactic factors, leucocyte-derived neutrophil chemotactic factor (LDNCF) 1 and LDNCF-2. Treatment of the leucocytes with K-252a, genistein, and H-7, but not H-89, inhibited production of both LDNCF-1 and LDNCF-2. 5. These results suggest that activation of tyrosine kinase and protein kinase C, but not cAMP-dependent protein kinase, is responsible for the production of LDNCF-1 and LDNCF-2. 6. The steroidal anti-inflammatory drug dexamethasone and the protein synthesis inhibitor cycloheximide inhibited neutrophil chemotactic factor production in a concentration-dependent manner. Time-course experiments showed that the inhibitory effect by dexamethasone was apparent even 30 min after the incubation.7. Mechanism for inhibiting the production of LDNCF-1 and LDNCF-2 by dexamethasone is also discussed.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

[Comparison of the prevalence of symptoms, elevated serum antibody, antibody types and complications between two outbreaks of influenza in a ward].

We experienced two outbreaks of influenza in the respiratory ward of our hospital in Feb. 1990 and Feb. 1993. Influenza-like symptoms were recognized in 42 of 67 cases (63%) in 1990, and in 22 of 56 cases (39%) in 1993. In the former outbreak, the prevalence of the serum CF titer for anti-influenza antibody was elevated in 25 of 42 cases (60%) (only the A2 antibody titer in 2 cases, B antibody titer in 4 cases in the latter one). Among asymptomatic inpatients, the serum titer was elevated in 3 of 25 cases (12%) in the former outbreak, but in 1 of 8 cases which the serum CF titer for anti-influenza antibody was measured in the latter one. A respiratory complications secondary to influenza were observed in 6 (2 cases pneumonia, 3 cases lower respiratory tract infection, 1 case asthma attack) of 67 cases during the former period, but only 1 of 56 cases during the latter period. In the two outbreaks of influenza in the respiratory ward we found the same results concerning the occurrence of influenza-like symptoms, an elevation of the serum antibody titer, but a significant difference was noted with regard to the phenotype of the prevalent influenza and the occurrence of complications.

Aged↗
PubMed1994

[VEPA and ML-Y1 regimen for elderly non-Hodgkin's lymphoma].

A total of 32 previously untreated patients aged 65 years or older with non-Hodgkin's lymphoma (NHL) were treated with VEPA (vincristine, cyclophosphamide, prednisolone and doxorubicin) or ML-Y1 (doxorubicin, cyclophosphamide, vincristine, methotrexate, bleomycin, procarbazizin and prednisolone). The median age of the patients was 70 years (range 65-77), 19 males and 13 females. The outcome of 16 patients with VEPA and 16 patients with ML-Y1 was retrospectively evaluated. There were no significant differences in response or survival between VEPA and ML-Y1, complete remission rates were 37.5% vs. 31.3% and duration of 50% survival were 20 months and 13 months, respectively. Major side effects of both regimens were myelosuppression, hair loss, nausea, vomiting and peripheral neuropathy. There was no increased toxicity in ML-Y1 but this regimen seemed like VEPA, to be insufficient for NHL in elderly patients. A new intensive regimen should be designed to treat NHL in the elderly patients.

Aged↗
PubMed1994

[Bacterial flora of the respiratory tract in patients with long term tracheostomy--colonization of the lower respiratory tract by Pseudomonas aeruginosa].

Throat secretions (TS) and bronchial secretions aspirated from tracheostomy sites (TSTA) from six subjects with long term tracheostomy were simultaneously collected and then cultured every two weeks from January, 1990, to December, 1992. Isolated bacteria were mainly alpha-streptococci (96.2%) and Neisseria (69.6%) in TS, and Pseudomonas aeruginosa (75.7%) in TSTA. In all cases, P. aeruginosa was isolated from and colonization of the lower respiratory tract by this organism was apparent 24.4 months, on average, after tracheostomy. There were ten episodes of respiratory infection in five cases, eight of which occurred after colonization. P. aeruginosa was the causative organism in seven of these episodes. Findings in patients with long term tracheostomy indicated separate colonization of the upper and lower respiratory tracts and that P. aeruginosa colonized the lower respiratory tract. The colonization of the lower respiratory tract by P. aeruginosa would thus appear to be an important factor inducing respiratory infection.

Adult↗
PubMed1994

[Conservative therapy for retinoblastoma--effect of melphalan on in vitro electroretinogram].

The effect of melphalan (an alkylic anti-cancer drug) on rabbit and human in vitro ERGs was studied to establish the non-toxic concentration of melphalan in chemo-thermotherapy for retinoblastoma. The ERGs were recorded before and 15 min after the perfusate was changed from the control solution to a melphalan-containing solution. Melphalan 10 micrograms/ml and 40 micrograms/ml caused no significant effect on the a-wave, the b-wave, or the oscillatory potential in either the rabbit or the human in vitro ERG. Melphalan 50 micrograms/ml significantly reduced the b-wave, but the change was reversible. Considering the minimum inhibitory concentration of melphalan against retinoblastoma cells on colony assay (4 micrograms/ml), melphalan is one of the most effective drugs for the conservative treatment of retinoblastoma.

Animals↗
PubMed1994

Cold agglutinin disease following allogeneic bone marrow transplantation.

We describe a case of cold agglutinin disease (CAD) following allogeneic bone marrow transplantation. This 36-year-old male developed CAD 3 weeks after allogeneic bone marrow transplantation for chronic myelogenous leukemia. Cyclosporin A and methotrexate had been administered to prevent graft-versus-host disease. Other agents administered included cytomegalovirus hyperimmune globulin and recombinant human G-CSF. Pericarditis preceded the development of CAD. The characterization of cold agglutinin (CA) was monoclonal IgM-kappa with anti-Pr antigen specificity, probably derived from the engrafted donor lymphocytes. The administration of prednisolone led to transient improvement. The CA titer decreased without further treatment 12 weeks after transplant.

Adult↗
PubMed1993

Fibronectin inhibits platelet aggregation independently of RGD sequence.

Fibronectin binds to platelet membrane glycoprotein (GP) IIb-IIIa in Arg-Gly-Asp (RGD)-dependent and -independent manner. We have isolated and characterized the 29-kDa dispase fragment of fibronectin. Binding of 125I-fibronectin to thrombin-stimulated platelets was inhibited by the 29-kDa fragment and the GRGDSPA peptide with IC50 values of 1.5 +/- 0.4 and 8.1 +/- 0.9 microM, respectively. The NH2-terminal sequence of this fragment gave this result: Ala-Val-Thr-Thr-Ile-Pro-Ala-Pro-Thr-Asp. This established the position of this peptide within fibronectin as beginning with the residue tentatively designated 1597. Neither the RGDS sequence nor the RGD-independent binding domain of fibronectin (Bowditch, R. D., Halloran, C. E., Aota, S., Obara, M., Plow, E. F., Yamada, K. M., and Ginsberg, M. H. (1991) J. Biol. Chem. 266, 23323-23328) was contained in this fragment. The 29-kDa fragment inhibited ADP-induced aggregation of platelets and binding of fibrinogen to activated platelets. The fragment bound to immobilized GPIIb-IIIa. The 125I-labeled 29-kDa fragment directly bound to thrombin-stimulated platelets with 98,000 +/- 4,600 molecules/platelet (Kd = 4.6 +/- 0.5 x 10(-6) M). Direct binding was inhibited by the unlabeled 29-kDa fragment but was not blocked by either the GRGDSPA peptide or the monoclonal anti-GPIIb-IIIa antibody. These results indicate that the additional RGD-independent binding domain(s) to GPIIb-IIIa are present on fibronectin. This additional binding domain(s) on fibronectin may prevent thrombus formation by interfering with the interaction of fibrinogen with GPIIb-IIIa.

Adenosine Diphosphate↗
PubMed1993

Altered energy metabolism and oxidative injury following endotoxemia in rats with normal or cirrhotic livers.

The release of oxygen-derived free radicals has been implicated in endotoxin-mediated hepatic injury. The effect of hepatic lipid peroxidation on tissue energy reserves in the livers of normal and cirrhotic rats was studied following administration of E. coli endotoxin. Before endotoxin injection, the basal hepatic energy charge was lower and levels of hepatic malondialdehyde (MDA) and total glutathione (GSH) higher in cirrhotic rats than in normal rats. Virtually identical levels of blood endotoxin were obtained in the two groups 24 h after injection of LD50 doses of endotoxin (20 mg/kg and 1 mg/kg in normal and cirrhotic rats, respectively). Hepatic energy charge, tissue blood flow, GSH and glutathione peroxidase (GPX) were consistently or transiently decreased up to 24 h after the injection of endotoxin in both normal and cirrhotic rats. MDA, significantly increased in normal rats 1 h after injection of endotoxin, returned to normal levels 3-12 h after endotoxin administration, but was again elevated at 24 h. Cirrhotic rats did not show any significant change in MDA following endotoxin injection. In normal rats, endotoxin appears to trigger the liberation of free radicals accelerating depletion of hepatic energy reserves, over and above the effect of decreased hepatic blood flow. In contrast, increased lipid peroxidation was not detected in cirrhotic rats despite GSH and GPX consumption during endotoxemia (indicating oxygen radical generation). Cirrhotic livers were apparently protected against oxygen radical injury by higher levels of endogenous GSH and GPX. Reduced hepatic blood flow may be mainly responsible for the alteration in energy metabolism of the cirrhotic liver.

Animals↗
PubMed1993

Anti-fibrinogen antibody mediates fibrinogen binding to platelet membrane glycoprotein IIb-IIIa.

The binding of fibrinogen to platelets requires the agonist activation of platelet membrane glycoprotein IIb/IIIa. We have now found an anti-fibrinogen polyclonal antibody (YCU-R3) that increases the fibrinogen affinity of GPIIb/IIIa-binding function (activation) and subsequent platelet aggregation. The addition of intact IgG, F(ab)2 fragments or Fab fragments induced platelet aggregation. The antibody-mediated fibrinogen binding was specific and saturable. This binding was inhibited by native fibrinogen, the RGDS peptide, the peptide of the C-terminus gamma chain of fibrinogen (gamma 397-411), and the anti-GPIIb/IIIa monoclonal antibody (LJ-CP8). The antibody-dependent fibrinogen binding was similar to that induced by ADP. Moreover, after pretreatment with the anti-fibrinogen antibody and fibrinogen, formalin-fixed platelets bound to fibrinogen saturably. These results suggest that this anti-fibrinogen antibody may function as partial agonist.

Antibodies↗