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Biomedical subjects

M Nagasaki

Publications and source records attributed to M Nagasaki.

At least 19 recordsLinked to original sources
PubMed1995

A new monoclonal antibody (IE8) reactive with dendritically shaped cells in the human tonsil.

A new monoclonal antibody (mAb), 1E8 (IgG1, kappa), was obtained from a hybridoma prepared by fusion of mouse myeloma cells (NS-1) with splenic cells of mice immunized with a human B blastic malignant lymphoma cell line, HPE-Ret-3 (Ret-3). The mAb showed a reactivity unrestricted to a specific cell lineage on flow cytometrical analysis of the reactivity with human lympho-hematopoietic cell lines. In peripheral blood, 1E8 reacted with the cells of all lineage, that is, lymphocytes, monocytes, granulocytes and platelets, even though its intensity was very low by immunohistochemistry. Immunohistochemical examination of human tonsil with 1E8 showed a characteristic staining pattern. Positive cells scattered in follicular (mantle zone and germinal center), parafollicular (T-dependent area), subepithelial and interstitial connective tissue areas. These positive cells seemed to be categorized into dendritically shaped cells (DSC), including dendritic cells (DC) and a subpopulation of macrophages in follicles, interdigitating cells (IDC) and irregularly shaped mononuclear cells. The localization of 1E8 antigen staining was similar to that of integrin CD11c, although its distribution on hematopoietic cell lines did not coincide with that of 1E8 antigen. Immunobiochemical studies showed that 1E8 bound two cell surface proteins with molecular size of 70,000-90,000 and 35,000 Da each. Consequently, 1E8 antigen might be a novel marker of DSC.

Animals↗
PubMed1995

Effects of cholecystokinin (CCK)-JMV-180 on the CCK receptors of rabbit pancreatic acini and gallbladder smooth muscle.

Effects of cholecystokinin (CCK)-JMV-180, a CCK analog, on the CCK receptor functions of isolated rabbit pancreatic acini and gallbladder smooth muscle were studied. When the pancreatic acini were incubated with increasing concentrations of CCK-8, stimulation of amylase release reached a maximum at 3 nM and then declined with the increasing concentration of CCK-8. CCK-JMV-180 also caused a dose-dependent amylase release stimulation, which plateaued and remained unchanged above 300 nM at about 50% of the maximal stimulation by CCK-8. CCK-JMV-180 above 100 nM caused a rightward shift of the downstroke of the dose-response curve for CCK-8 (pA2 = 7.5). In the gallbladder smooth muscle, CCK-8 caused a dose-dependent contraction, but CCK-JMV-180 totally lacked this property. Instead, CCK-JMV-180 caused a rightward shift of the dose-response curve for CCK-8 (pA2 = 7.9). These results suggest that CCK-JMV-180 distinguishes between the CCKA receptors associated with pancreatic exocrine secretion in the acini and those involved in contraction of the isolated gallbladder smooth muscle in rabbits.

Amylases↗
PubMed1994

An autopsy case of acquired immune deficiency syndrome (AIDS) with preceding aplastic anemia.

A case of acquired immunodeficiency syndrome (AIDS) with preceding aplastic anemia is reported. The patient was a 36 year old female who had been diagnosed as having aplastic anemia 10 years before and thereafter had received multiple transfusions. Human immunodeficiency virus (HIV)-seropositivity was revealed 10 months prior to her death, but no particular clinical signs indicating HIV infection, pre-AIDS or onset of AIDS were recognized before serological diagnosis, although the slow progression of leukopenia was noted along with thrombocytopenia. Her general condition deteriorated during the last 10 months accompanied by an acute decrease in the CD4/CD8 ratio. Autopsy revealed full-blown AIDS: systemic aspergillosis, progressive multifocal leukoencephalopathy, Epstein-Barr virus-related B cell lymphoma arising in the diaphragm and severe lymphocyte depletion in the lymph nodes and spleen. Markedly hypoplastic bone marrow was considered to be primarily attributable to the aplastic anemia but the affection of AIDS was not excluded. The possible transmission route of HIV and the effect of the preceding aplastic anemia on the infection and clinical course of AIDS are discussed.

AIDS-Related Opportunistic Infections↗
PubMed1994

Effect of trimebutine on contractile responses in skinned ileal smooth muscle.

The effects of trimebutine on Ca2+ release and modulation of Ca2+ sensitivity of contractile elements induced by carbachol (CCh) were investigated using a tension measuring method in beta-escin-treated skinned smooth muscle of the longitudinal muscle layer of guinea pig ileum. Trimebutine (10-100 microM) concentration-dependently inhibited tension development brought about by Ca2+ release from intracellular stores induced by CCh (10 microM), but did not affect those induced by inositol 1,4,5-trisphosphate (IP3, 25 microM) or caffeine (5 mM). The inhibitory effect was reversible. Trimebutine (100 microM) neither altered the Ca2+ sensitivity of the contractile elements nor affected the effects of GTP gamma S (50 microM) and CCh (100 microM) in potentiating Ca2+ sensitivity of the contractile elements after the Ca2+ storage function had been eliminated by A23187. These results suggest that trimebutine inhibits CCh-induced Ca2+ release by acting at some point during the coupling of muscarinic receptors through a G-protein to phospholipase C and thus reducing the accumulation of IP3.

Animals↗
PubMed1991

Effects of trimebutine on cytosolic Ca2+ and force transitions in intestinal smooth muscle.

The effects of trimebutine maleate on cytosolic free Ca2+ and force transitions in the guinea-pig taenia cecum were studied by fura-2 fluorometry and tension recording. The addition of 80 mM K+ induced a transient increase in cytosolic free Ca2+ concentration ([Ca2+]i) and tension, followed by a sustained increase. Trimebutine (10 microM) suppressed both [Ca2+]i elevation and tension development. The tonic responses were more potently inhibited than the phasic responses. Phasic components gradually increased as the added K+ increased (10-40 mM). The relationship between the peak increases in [Ca2+]i and tension was not affected by trimebutine (10 microM). This means that trimebutine does not affect the Ca2+ sensitivity of contractile elements. In a high K+ and Ca(2+)-free medium, carbachol (10 microM) or caffeine (30 mM) caused transient [Ca2+]i elevation and tension development in the smooth muscle. Trimebutine (10 microM) decreased the amplitude of both responses. Trimebutine (10 microM) inhibited the spontaneous fluctuations in [Ca2+]i and motility of taenia cecum in the presence of tetrodotoxin (TTX; 0.3 microM). These results suggest that trimebutine has two types of inhibitory actions on intestinal smooth muscle; one, the inhibition of Ca2+ influx through voltage-dependent calcium channels, and the other, the inhibition of Ca2+ release from intracellular storage sites.

Animals↗
PubMed1991

Establishment of a novel cell line with T-lineage phenotype (HPB-MLp-W) from a non-Hodgkin's lymphoma patient.

We report the characterization of a novel human T-cell line, HPB-MLp-W, which was established from blastic cells of a lymph node specimen from a patient with non-Hodgkin's lymphoma. They demonstrated the T-cell association antigens, CD2 and CD4, but no CD3, CD8, CD1, CD5, CD7 nor T-cell antigen receptor on their cell surfaces. They were also positive for Ia and Ki-1 antigen, and negative for CD25 (Tac-1). The cell line HPB-MLp-W had the same pattern of antigen expression as the patient's cells. Southern-blot analysis of DNA showed a rearrangement of the T-cell receptor-alpha and beta genes. To our knowledge, this is a novel cell line with unique T-lineage marker, to be established from a case of non-Hodgkin's lymphoma.

Antigens, CD↗
PubMed1990

Allosteric interaction of trimebutine maleate with dihydropyridine binding sites.

The effects of trimebutine maleate on [3H]nitrendipine binding to guinea-pig ileal smooth muscle membranes and Ca2(+)-induced contraction of the taenia cecum were studied. Specific binding of [3H]nitrendipine to smooth muscle membranes was saturable, with a KD value and maximum number of binding sites (Bmax) of 0.16 nM and 1070 fmol/mg protein, respectively. Trimebutine inhibited [3H]nitrendipine binding in a concentration-dependent manner with a Ki value of 9.3 microM. In the presence of trimebutine (10 microM), Scatchard analysis indicated a competitive-like inhibition with a decrease in the binding affinity (0.31 nM) without a change in Bmax (1059 fmol/mg protein). However, a dissociation experiment using trimebutine (10 or 100 microM) showed that the decreased affinity was due to an increase of the dissociation rate constant of [3H]nitrendipine binding to the membrane. In mechanical experiments using the taenia cecum, trimebutine (3-30 microM) caused a parallel rightward shift of the dose-response curve for the contractile response to a higher concentration range of Ca2+ under high-K+ conditions in a noncompetitive manner. These results suggest that trimebutine has negative allosteric interactions with 1,4-dihydropyridine binding sites on voltage-dependent Ca2+ channels and antagonizes Ca2+ influx, consequently inhibiting contractions of intestinal smooth muscle.

Animals↗
PubMed1989

A novel EBV-related nucleo-cytoplasmic antigen in a null cell-line (HLN-STL-C) reactive to antibodies in the sera from patients with Sjögren's syndrome.

We have established a non-T- and non-B-cell line, HLN-STL-C(STL-C), which harbors the EBV genome, from the lymph node cells of a Japanese ATL patient. This cell line expresses a unique Epstein-Barr virus (EBV)-related nucleo-cytoplasmic (N-C) antigen which is detected by indirect immunofluorescence (IF) with the sera from patients with nasopharyngeal cancer (NPC), infectious mononucleosis (IM) or adult T-cell leukemia (ATL). One of the molecular components of this antigen is proved to be STL-C specific 125 kD molecule by immunoblot analysis (IB). To study the involvement of EBV in Sjögren's syndrome (SS), we examined the reactivity of the N-C antigen with the sera of SS patients by IF and IB. Among 24 cases examined, the sera of 21 cases (87.5%) positively stained the N-C antigen by IF. The staining patterns were divided into two types. Type I, (seven cases) showed positive staining for only N-C antigen, and Type II, (14 cases) was positive for N-C antigen associated with diffuse nuclear staining due to antinuclear antibodies in the SS patient's sera. Only one out of 11 non-Sjögren's patients' sera, which were almost all healthy controls, was positive for N-C antigen in this study. By IB, however, only two out of 15 IF-positive SS patients' sera reacted with STL-C specific 125 kD molecule. These results suggested the presence of heterogenous components in the N-C antigen. Our findings may support the hypothetical conception that EBV plays an etiological role in SS.

Adult↗
PubMed1989

Contribution of peripheral opioid receptors to the trimebutine-induced contractions of the proximal colon in anesthetized rats.

In this study we investigated the involvement of opioid receptors in the contractile response to trimebutine using with the proximal colon of anesthetized rats. Trimebutine (3 mg/kg i.v.) enhanced spontaneous contractions of the proximal colon in anesthetized rats. The contractile response was partially inhibited by intravenous administration of an opioid antagonist, naloxone at 1 approximately 30 micrograms/kg, but was hardly depressed by intracisternal administration of naloxone (30 micrograms/kg). Morphine (30 micrograms/kg i.v.) evoked colonic contractions which were abolished by intravenous naloxone (30 micrograms/kg). These results suggest that the colonic contractions evoked by trimebutine in anesthetized rats are, in part, mediated by peripheral opioid receptors.

Anesthesia↗
PubMed1988

An autopsy case of disseminated histoplasmosis probably due to infection from a renal allograft.

An autopsy case of a 52-year-old Japanese male, who died of disseminated histoplasmosis, is reported. He had received a cadaveric renal allograft 4 years prior to death. The donor was a 33-year-old American negro male, who had resided in Texas. The patient had been treated with immunosuppressive drugs after renal transplantation, and mycotic pneumonia developed 3 months before death. At autopsy, acute necrotizing lesions composed of histiocytes were observed in the transplanted kidney, lungs, prostate gland and various lymph nodes. Abundant yeast-like fungal elements, measuring 2-5 micron in diameter, were engulfed by the histiocytes, and were identified as Histoplasma capsulatum by the immunoperoxidase method. The transplanted kidney was considered to have been the source of the infection.

Cadaver↗
PubMed1988

[An autopsied case of a malignant lymphoma with a severe nephrotic syndrome overlapped by cirrhotic glomerulosclerosis].

A 52-year-old man, who had been diagnosed as having alcoholic liver cirrhosis, presented a chronic nephritic syndrome due to hepatic glomerulosclerosis. Ten months before death, massive proteinuria exceeding 40 g/day was noted. A renal biopsy revealed diffuse mesangial sclerosis, associated with an IgA deposition consistent with hepatic glomerulosclerosis. Although the nephrotic syndrome subsided with immunosuppressive therapy, he died of hepatic failure. Postmortem examinations disclosed a diffuse, medium-size B-cell lymphoma, involving the peritoneal and retroperitoneal organs and an IgA-positive plasmacytosis. His massive proteinuria seems to have been caused by the paraneoplastic syndrome of a malignant lymphoma.

B-Lymphocytes↗
PubMed1987

Intrahepatic portosystemic venous shunt: occurrence in patients with and without liver cirrhosis.

Portosystemic venous shunt within the hepatic parenchyma is rare, and its cause is disputed. Only 12 cases have been reported in the literature. Four new patients are presented here, all of whom had cerebral manifestations due to elevated blood-ammonia levels. One patient, initially misdiagnosed as having a psychiatric disorder, had multiple small portohepatic venous shunts in the peripheral hepatic parenchyma that were believed to be congenital in origin. The other three patients with clinical evidence of cirrhosis and portal hypertension had large tubular shunts between the posterior branch of the portal vein and the inferior vena cava. Shunts of this type were considered to be the collateral pathways developed in the hepatic parenchyma as a result of portal hypertension. The diagnosis of intrahepatic portosystemic venous shunts was established by angiography in all four patients. Sonography and CT failed to show the multiple small shunts, but did provide diagnostic information concerning the large tubular shunts. Intrahepatic portosystemic venous shunt can be the cause of hepatic encephalopathy. One should be familiar with the typical radiographic manifestations of this condition to prevent misdiagnosis as a psychiatric or neurologic disorder.

Aged↗
PubMed1986

Initial pulmonary artery involvement in Takayasu arteritis.

Although the pulmonary artery is involved in many cases of Takayasu arteritis, few cases have been reported in which the pulmonary artery was initially involved. Two such cases are reported here. Both of these cases had been initially diagnosed as chronic pulmonary embolism. The importance of considering Takayasu arteritis in cases of chronic pulmonary arterial obstruction of unknown cause is emphasized. Bronchial-pulmonary artery communication and coronary-bronchial artery communication in Takayasu arteritis are also discussed.

Adult↗