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Biomedical subjects

N Tsukada

Publications and source records attributed to N Tsukada.

At least 127 records · Page 7Linked to original sources
PubMed1985

Muscarinic acetylcholine receptors in rat gastric mucosa. A radioautographic study using a potent muscarinic antagonist, 3H-pirenzepine.

The muscarinic cholinergic innervation of the rat gastric mucosa was investigated by localizing the muscarinic receptors using a tritiated muscarinic antagonist, pirenzepine. Radioautography was performed by freeze drying stomach tissue, which was then embedded in Epon and wet sectioned with ethylene glycol, and dry mounting on emulsion film by the wire-loop method to prevent loss of the labelled substance during fixation and the radioautographic procedure. Light and electron microscopy showed that the specific pirenzepine-binding sites were localized predominantly on parietal cells, chief cells and perivascular plexuses. Analysis of the grain distribution on parietal cells revealed that the silver grains corresponding to the pirenzepine-binding sites were mainly on the basolateral plasma membrane. On the other hand, the surface mucous or mucous neck cells had few pirenzepine-binding sites.

Animals↗
PubMed1985

Search for autoantibodies to endothelial and smooth muscle cells in patients with multiple sclerosis.

The blood-brain barrier (BBB) is disrupted in many of the lesions of multiple sclerosis (MS). Immunologically mediated injury to one of the major components of this barrier, the cerebral capillary, may play a role in the development of the lesion. We therefore examined the sera of 51 cases of MS for the presence of autoantibodies to endothelial and smooth muscle cells, using the indirect immunofluorescent technique. The results were compared to those in other groups of patients with neuroimmunological disorders. We found no anti-endothelial cell antibodies, but autoantibodies to vascular smooth muscle were detectable in 31% of the MS sera tested. They were also present, however, in 30% of sera from cases of myasthenia gravis and in the serum of one of 12 cases of polymyositis. It is considered to be unlikely that antibodies to vascular tissues play any pathogenetic role in multiple sclerosis.

Antibodies, Antinuclear↗
PubMed1985

Peripheral nervous tissue injury induced by galactocerebroside and galactocerebroside immune complexes.

It was demonstrated that New Zealand Albino rabbits sensitized to galactocerebroside had high levels of anti-galactocerebroside antibody and of immune complexes. The rabbits was high titers of immune complexes developed demyelination in the peripheral nerves. Lesion were produced in the peripheral nerves of mice by the i.m. injection of galactocerebroside immune complexes. The lesions were characterized by axonal degeneration, infiltrating macrophages containing myelin debris, and an inflammatory infiltrate of polymorphonuclear and mononuclear cells. Rabbit immunoglobulin and mouse C3 were observed around the endoneural blood vessels. These results suggest that galactocerebroside immune complexes may play a role in the pathogenesis of mouse peripheral nerve lesions, due to the production of vasculomyelinopathy.

Animals↗
PubMed1984

Detection of immune complexes in experimental allergic neuritis.

Circulating immune complexes were assayed in the sera of animals with experimental allergic neuritis (EAN), and immunofluorescent staining and immunohistological examination were performed to clarify the role of immune complexes in the pathogenesis of EAN. The level of immune complexes in the sera of animals with clinical signs of EAN was from 1:32 to 1:64. Control animals showed a titer of immune complexes from 1:2 to 1:4. Animals with EAN showed deposition of immune complexes, which were detected by FITC-conjugated anti-rat IgG or C3-complement, in the vessels of the peripheral nerve. These findings suggest that immune complexes may contribute to the immunopathogenesis of EAN.

Animals↗
PubMed1983

Chronic neuropathy associated with immune complexes of hepatitis B virus.

In 7 patients, including one autopsied case, with neuropathy associated with hepatitis B virus infection, histologic examination of sural nerve biopsies revealed small vessel vasculitis in the vasa nervorum. In all cases, immunofluorescent deposits of hepatitis B surface antigen, immunoglobulin and C3 complement were detected in the vasa nervorum. That these deposits could represent immune complexes composed of hepatitis B virus was supported by the serologic demonstration of high serum-level of immune complexes and by the ultrastructural demonstration of electron-dense deposits around the endoneural capillary and in the endoneurium. The densities of large myelinated fibers were significantly lower than controls (P less than 0.01) in 6 of 7 cases. These results suggest that immune complexes composed of hepatitis B virus might play a significant role in the pathogenesis of endoneural and epineural vascular lesions, through which neuropathy may be induced in patients with hepatitis B virus infection.

Adult↗
PubMed1981

Mild encephalitogenic activity of basic protein--acidic lipid complex from myelin and detection of immune complexes in experimental allergic encephalomyelitis.

Further biochemical and pathological investigation of basic protein--acidic lipid complex from canine cerebral myelin show the presence of sulfatide, phosphatidylserine, ganglioside and basic protein in the molar ratio of approximately 6 : 3 : 1 : 1 and that it is associated with mild encephalitogenic activity in guinea pigs in comparison to intact myelin and basic protein. Circulating immune complexes were detected in the sera of guinea pigs with clinical signs of experimental allergic encephalomyelitis and immunofluorescent staining showed the deposition of immune complexes of immunoglobulin and complement in vessels of white matter and meninges and in the choroid plexus.

Animals↗
PubMed1981

Immunologic and immunohistochemical study of familial amyloid polyneuropathy.

Amyloid fibril protein was purified from postmortem organs of patients with familial amyloid polyneuropathy. In immunodiffusion tests, the protein reacted with antihuman prealbumin antibody but not with antihuman retinol-binding protein or antihuman immunoglobulin G (IgG). In immunoelectrophoresis, the amyloid fibril protein gave a single line with a slightly faster mobility than prealbumin. Immunohistochemical analysis, using fluorescent and peroxidase-antiperoxidase methods, showed that the amyloid deposits contained antigenic determinants of human retinol-binding protein and IgG but not prealbumin.

Amyloid↗
PubMed1980

[Fabry's disease with malocclusion and acromegalic-appearance: clinical and electromicroscopic studies (author's transl)].

The present case is a 24-years-old man who complained painful attack with numbness in both bilateral shoulder regions and distal extremities. This pain was increased by the stimulations of sunlight and heat. On physical examinations, he had an acromegalic-like-appearance, thick mustache and beard. Malocclusion of the teeth which showed the broad space was found. And skin lesion was not found out. Hypesthesia in bilateral distal extremities was revealed and no other abnormal neurological findings were observed. He was made diagnosis of Fabry's disease by laboratory examinations which were alpha-galactosidase deficiency analysed in leukocytes, increased ceramide trihexosides demonstrated in urinary sediment and electron microscopic findings in the biopsy of the skin and sural nerve. His mother had and decreased alpha-galactosidase activity which levels showed between normal and patient and was speculated to be a carrier. On an electron microscopy, "Zebra body" was observed in fibroblasts, capillary endothelial cells, their pericytes, prineural and Schwann cells. Many of them had a distinct limiting membrane and laminal structure with irregular alterations of light and dark zone. In the cytoplasma of Schwann cells, there were many rough endoplasmic reticulums which were located parallel with alignment and seemed to show the loosed laminal structure with the unclear limited membrane. Occasionally, fusions between irregular laminal structure and rough endoplasmic reticulum were also observed. These findings could be indicated that the formation of Zebra body is related to rough endoplasmic reticulum, because laminal structure which described above is corresponded to pre-Zebra body. In the cytoplasma of the prineural cells, recket-like structure which was seen in histiocytosis X were occasionally observed.

Acromegaly↗
PubMedDate not supplied

An aggressive case of Burkitt's lymphoma with t(8;14) and c-myc rearrangement transformed from CD5+ B-cell lymphoma.

We experienced a case of Burkitt's lymphoma showing an unusual surface phenotype, CD5 expression, at an early stage of the disease. Initially, this patient showed massive abdominal para-aortic lymph node swelling which rapidly developed into leukemic change. Based on the clinical course and cytogenetic features of lymphoblasts in the bone marrow, which showed t(8;14) and c-myc gene rearrangement, the patient was diagnosed with Burkitt's lymphoma. Combination chemotherapy induced short-term remission, but central nervous system (CNS) involvement developed, followed by a regrowth of lymphoma cells in the bone marrow. The bone marrow at the end stage showed monotonous expansion of large cells with conspicuous vacuolation in the basophilic cytoplasm. The initial lymphoma cells showed pan-B markers and were CD5 positive but weakly CD10 positive; however, the lymphoma cells obtained from the bone marrow at the terminal stage did not express CD5. The chromosomal t(8;14) was seen, and identical rearrangement of immunoglobulin heavy chain joining gene and c-myc gene were detected by Southern blot analysis in the bone marrow lymphoblasts throughout the clinical course. This case is evidence that remarkable transformation of CD5-positive lymphoblasts to CD5-negative lymphoblasts occurred in an identical clone of Burkitt's lymphoma.

Aged↗