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Biomedical subjects

N Tsukada

Publications and source records attributed to N Tsukada.

At least 109 records · Page 6Linked to original sources
PubMed1988

Autoradiographic demonstration of gastrin-releasing peptide-binding sites in the rat gastric mucosa.

The location of [125I]iodotyrosyl gastrin-releasing peptide-binding sites in the rat fundic mucosa was studied. Peptide specificity was demonstrated by competitive binding studies using the addition of a large amount of cold gastrin-releasing peptide or substance P. Autoradiography of the stomach tissue was carried out by freeze-drying, embedding in Epon, wet-sectioning with ethylene glycol, and dry-mounting the emulsion film by the wire-loop method to prevent loss of the labeled substance. Specific binding sites of gastrin-releasing peptide were found on D cells, surface mucus cells, and parietal cells, whereas few binding sites were seen on the chief or mucus neck cells.

Animals↗
PubMed1988

In vitro degradation of amyloid material by four proteases in tissue of a patient with familial amyloidotic polyneuropathy.

The effects of 4 proteolytic enzymes, alpha-chymotrypsin, bromeline, collagenase, and lysozyme on amyloid tissue sections from a patient with familial amyloidotic polyneuropathy (FAP) were evaluated. Degradation of amyloid fibrils was significant with alpha-chymotrypsin, moderate with bromeline and collagenase, and slight with lysozyme. All of these proteases except collagenase are used as oral mucolytics in humans. The possibility of their clinical usefulness in the treatment or prevention of the development of FAP is discussed.

Amyloid↗
PubMed1988

[A case of chronic polyneuropathy associated with chronic type B hepatitis].

A case of chronic polyneuropathy associated with chronic type B hepatitis was described. A 31 year-old male was admitted to our hospital with a 2-year history of progressive weakness and sensory disturbances of all limbs. There was past history of acute type B post-transfusion hepatitis after subtotal gastrectomy. On examination there was generalized muscle weakness, particularly in movements of the hands and feet with areflexia. He had a steppage gait. Sensory examination revealed moderately decreased pinprick, light touch, vibration and position sense in the distal portion of all extremities. On admission, hepatitis associated antigen and antibody were negative and positive, respectively. The level of circulating immune complexes was high with the titer of 6.6 micrograms/ml by Clq assay and 16X by Raji cell assay. Liver biopsy revealed fibrosis and periportal inflammatory infiltrate compatible with the diagnosis of chronic viral hepatitis. Sural nerve biopsy showed marked loss of large myelinated fibers and epineural vasculitis with the thickened blood vessel wall and mononuclear cell infiltrates. There have been increasing evidences that extrahepatic manifestations are caused by vasculitis due to HBs antigen-antibody immune complex deposits. On the basis of findings in the literature it seems possible that chronic polyneuropathy may be related to the vasculitis due to HBs antigen-antibody complex deposits after hepatitis B virus infection.

Adult↗
PubMed1987

Isolation of three kinds of human endogenous retrovirus-like sequences using tRNA(Pro) as a probe.

Three kinds of human endogenous retrovirus-like sequences (HuERS-P1, 2 and 3) were isolated from a HeLa cell genomic library using the 3'-half fragment of proline tRNA as a hybridization probe. These elements contained putative primer binding sites complementary to the 3'-terminus of proline tRNA and long terminal repeats (LTRs) characteristic of retrovirus provirus. The LTR sequence of HuERS-P1 consisted of about 690 nucleotides and contained a CAT box, a TATA box and a polyadenylation signal. A complete unit of an Alu family sequence was inserted into the 5'-LTR of one of the clones. HuERS-P2 also contained a TATA box and a polyadenylation signal in its LTR (about 840 nucleotides long), but the LTR sequence of this element was quite different from that of HuERS-P1. Although clone HuERS-P3 contained only the 5'-LTR region, this LTR sequence contained a CAT box, a TATA box and a poly-adenylation signal and was quite similar to the LTR sequence of the recently isolated human retrovirus-related sequence HuRRS-P (Kröger, B. and Horak, I. (1987) J. Virol., 61, 2071-2075). Human and simian DNAs contain 10 to 40 copies of these elements, but mouse DNA does not contain these elements.

Base Sequence↗
PubMed1987

A new model for multiple sclerosis: chronic experimental allergic encephalomyelitis induced by immunization with cerebral endothelial cell membrane.

Multiple sclerosis is considered to be an autoimmune demyelinating disease of the central nervous system. Damage to the blood-brain barrier, of which endothelial cells are the main constituent, occurs in multiple sclerosis, probably due to immunological mechanisms. We report here the results of immune-mediated damage to these cells, produced by immunizing guinea pigs with an endothelial cell membrane fraction. The fraction was obtained from cerebral endothelial cells grown in vitro and was free from myelin basic protein. The immunized animals developed a chronic neurological illness with evidence of delayed hypersensitivity to the cell membrane fraction but not to myelin antigens. Histological examination of the brain in the acute stage showed mononuclear cell infiltrates around blood vessels, while in the chronic phase large areas of demyelination, especially in the periventricular region, were present. This bore a striking similarity to the brain in multiple sclerosis. This may prove to be a useful new animal model for the investigation of the human demyelinating disease.

Animals↗
PubMed1987

Demyelinating neuropathy associated with hepatitis B virus infection. Detection of immune complexes composed of hepatitis B virus surface antigen.

We observed 4 patients with the Guillain-Barré syndrome (GBS) type of polyneuropathy and one patient with chronic relapsing polyneuropathy associated with hepatitis B virus infection, and examined the sera, cerebrospinal fluid (CSF) and sural nerve specimens from the patients in search of the pathogenetic factors involved. It was demonstrated that hepatitis B surface antigen(HBsAg)-immune complexes were significantly increased in both the sera and the CSF of the 4 patients with GBS. The serum levels of immune complexes were also closely related to the clinical status of these patients. In all patients, HBsAg-positive labelling of immunofluorescence was found around the endoneural small blood vessels and in the endoneurium. Electron-dense deposits, suggestive of immune complexes composed of hepatitis B virus, were demonstrated in the endoneurium of the patient with chronic relapsing polyneuropathy. These results suggest that HBsAg immune complexes may be of importance in the etiology of GBS or chronic relapsing polyneuropathy associated with hepatitis B virus infection.

Adult↗
PubMed1987

Studies of protease and protease inhibitors in familial amyloidotic polyneuropathy.

Serum levels of 6 protease inhibitors, alpha 1-antitrypsin, Cl inactivator, alpha 2-macroglobulin, antithrombin-3, alpha 1-antichymotrypsin and inter-alpha-trypsin inhibitor were measured in patients with familial amyloidotic polyneuropathy (FAP) and a control group without neurologic disease. No significant differences were observed between the 2 groups. The proteolytic effect of brinase, an enzyme from Aspergillus oryzae, on amyloid tissue sections from patients with FAP was also evaluated. Amyloid fibrils were degraded by brinase, while the tissue structure remained fairly intact.

Amyloid↗
PubMed1987

Anti-endothelial cell antibodies and circulating immune complexes in the sera of patients with multiple sclerosis.

Sera from patients with multiple sclerosis (MS) were examined for anti-endothelial cell antibodies and immune complexes by enzyme-linked immunosorbent assays (ELISAs) using cultured brain endothelial cells and Raji cells respectively. The concentrations of immunoglobulin (Ig) G which bound to cerebral endothelial cells and of immune complexes were significantly increased in the sera of patients with MS, especially those with an exacerbation. The levels of IgG binding to endothelial cells were still increased in the sera of exacerbated MS patients after blocking Fc receptors compared to those of controls. These findings indicate that IgG binding to endothelial cells may be mediated via an immunologically specific antigen-antibody interaction. The results show that anti-endothelial cell antibodies and immune complexes are present in cases of MS and they may play a pathogenetic role in the blood-brain barrier (BBB) damage.

Adult↗
PubMed1987

Chronic relapsing demyelinating polyneuropathy associated with hepatitis B infection.

We studied a patient with chronic relapsing polyneuropathy associated with immune complexes of hepatitis B virus. There were cycles of remission and exacerbation in parallel with liver dysfunction. Immunofluorescent deposits of hepatitis B antigen, immunoglobulin, and C3 component were detected in the vasa nervorum. Ultrastructural study revealed electron-dense deposits that might have been immune complexes composed of hepatitis B virus, both around the endoneural capillary and in the endoneurium. Immune complexes composed of hepatitis B virus may play a role in the pathogenesis of chronic relapsing polyneuropathy.

Adult↗
PubMed1986

Similarities between the Forssman carotid syndrome and experimental allergic encephalomyelitis.

The Forssman carotid syndrome was induced in guinea pigs to study the mechanism of demyelination-like lesions in this animal model and to compare it with experimental allergic encephalomyelitis days after intracarotid injection of rabbit anti-Forssman antibody and chronic lesions at 7-21 days post injection, using routine histological, immunofluorescent, and electron-microscopic techniques. The results were compared to those in a group of guinea pigs with acute or chronic lesions of EAE. The picture was remarkably similar in the two conditions, in regard to localization in the central nervous system (CNS), composition of cellular infiltrates, diameter of lesions produced, myelin loss and axonal degeneration, together with gamma globulin deposition in small vessels in affected areas. The differences were that in the Forssman carotid syndrome, in contrast to EAE, there were no mononuclear cell infiltrates in the acute phase, and no evidence of macrophages invading myelin sheaths was detected. Perivascular lesions consisted of demyelination within infiltrates of mono-nuclear cell in chronic relapsing EAE, but not in the Forssman carotid syndrome. It is suggested that investigation of the CNS may be of benefit in the pathogenetic study of demyelinating disease.

Acute Disease↗
PubMed1986

Anti-endothelial cell antibody and immune complexes in the sera of animals with acute experimental allergic encephalomyelitis and chronic relapsing experimental allergic encephalomyelitis.

Blood-brain barrier (BBB) injury occurs in both acute and chronic relapsing experimental allergic encephalomyelitis (EAE). Sera from animals in which these forms of EAE had been induced were examined for anti-endothelial cell antibodies and immune complexes by enzyme-linked immunosorbent assay (ELISA) using either cultured endothelial cells or Raji cells. IgG binding to endothelial cells was significantly increased in the sera of animals with acute EAE and chronic relapsing EAE, compared to controls. Increased levels of circulating immune complexes were also detected in the sera of some animals with chronic relapsing EAE, especially those in an exacerbation. It is suggested that the anti-endothelial cell antibody and immune complexes detected may play pathogenetic roles in the destruction of the BBB in EAE.

Animals↗