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Biomedical subjects

I Kitajima

Publications and source records attributed to I Kitajima.

At least 91 records · Page 5Linked to original sources
PubMed1992

Working and reference memory in rats in the three-panel runway task following dorsal hippocampal lesions.

Using a three-panel runway task, the influence of dorsal hippocampal lesions on working and reference memory in rats was investigated. Despite 20 postoperative training sessions, rats with hippocampal lesions were unable to perform the working memory task. In the acquisition process of the reference memory task, however, there was no significant difference between hippocampal- and sham-lesioned rats. On the other hand, rats trained preoperatively with a working memory procedure, and then subjected to hippocampal lesions, showed more errors (pushes made on the two incorrect panels of the three panel-gates located at four choice points) than did sham-lesioned rats. The increase in working errors induced by hippocampal lesions was not reduced during 10 subsequent re-training sessions. Hippocampal lesions had no effect on retention of the reference memory performance. The increase in working errors in hippocampal-lesioned rats was significantly reduced by treatment with the cholinesterase inhibitor physostigmine at 0.1 mg/kg and the cholinergic activating drug minaprine at 10 mg/kg. These findings suggest that lesions of the dorsal hippocampus selectively impair the ability to carry out the working memory task whether rats are trained preoperatively or postoperatively, and that the working memory loss in hippocampal-lesioned rats is mediated by lowering of the cholinergic function.

Animals↗
PubMed1991

Induction of inflammatory arthropathy resembling rheumatoid arthritis in mice transgenic for HTLV-I.

Human T cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult T cell leukemia and has also been suggested to be involved in other diseases such as chronic arthritis or myelopathy. To elucidate pathological roles of the virus in disease, transgenic mice were produced that carry the HTLV-I genome. At 2 to 3 months of age, many of the mice developed chronic arthritis resembling rheumatoid arthritis. Synovial and periarticular inflammation with articular erosion caused by invasion of granulation tissues were marked. These observations suggest a possibility that HTLV-I is one of the etiologic agents of chronic arthritis in humans.

Animals↗
PubMed1991

Arthritis in patients infected with human T lymphotropic virus type I. Clinical and immunopathologic features.

Ten patients with chronic inflammatory arthropathy and the human T lymphotropic virus type I (HTLV-I) are described. These patients showed chronic persistent oligoarthritis, associated with proliferative synovitis, in large joints. The place of birth or residence of these patients was within the area endemic for adult T cell leukemia (ATL) and HTLV-I. The age at onset of articular symptoms tended to be higher in these patients than in typical rheumatoid arthritis patients. Anti-HTLV-I antibodies were detected in both sera and synovial fluids from all patients. Western blot analysis revealed antibodies to viral gag proteins (p19, p24, and p28). Atypical lymphocytes with nuclear indentations, consistent with ATL-like cells, were observed in both synovial fluid and synovial tissue. Furthermore, HTLV-I proviral DNA was integrated into the DNA of synovial fluid cells and synovial tissue cells. These findings suggest that HTLV-I might be involved in the pathogenesis of this unique arthropathy.

Aged↗
PubMed1991

Detection of human T cell lymphotropic virus type I proviral DNA and its gene expression in synovial cells in chronic inflammatory arthropathy.

To investigate the pathogenesis of human T cell lymphotropic virus type I (HTLV-I)-associated chronic inflammatory arthropathy (HAAP), we sought to detect proviral DNA in the articular lesions. For the detection of proviral DNA, we used the polymerase chain reaction (PCR). Proviral DNA was detected not only in the peripheral blood mononuclear cells (PBMCs) and synovial fluid cells (SFCs), but also in the T lymphocyte-depleted cultured synovial cells (CSCs). These findings suggest that the infection by HTLV-I might occur in vivo in non-T cells. Furthermore, we detected HTLV-I tax1/rex1 messenger RNA in fresh synovial tissues and CSCs but not in fresh PBMCs and fresh SFCs using reverse transcription and PCR. Immunohistochemically, the CSCs from HAAP patients were also shown to express the HTLV-I antigens. These data indicate that HTLV-I in the non-T synovial cells can be transcribed and expressed. Moreover, the sequences of pXII regions in the CSCs demonstrated 97.5-99.4% homology to that in MT-2 cells, HTLV-I-infected cell line. This confirmed that the PCR-amplified bands reflect HTLV-I itself. These results suggest that this organ-specific inflammation can be attributed to non-T cell virus infection in articular lesions.

Arthritis↗
PubMed1990

Minaprine improves impairment of working memory induced by scopolamine and cerebral ischemia in rats.

Using a repeated acquisition procedure in a three-panel runway apparatus, the effects of minaprine on the impairment of working memory produced by scopolamine, ethylcholine aziridinium ion (AF64A) or cerebral ischemia were investigated in rats. Minaprine (3.2-32 mg/kg IP) as well as idebenone (10-100 mg/kg IP) and physostigmine (0.1-0.32 mg/kg IP) dose-dependently reduced the increase of errors (pushes made on the two incorrect panels located at each choice point) induced by 0.56 mg/kg IP scopolamine. Cerebral ischemia for 5 min caused a significant increase of errors in the runway task. Minaprine at 3.2 and 10 mg/kg administered IP immediately after blood recirculation and again 30 min before the runway test conducted 24 h after ischemia, significantly reduced increases in errors expected to occur after 5 min of ischemia. Physostigmine 0.1 mg/kg similarly attenuated the increase in errors in ischemic rats. However, minaprine at doses up to 32 mg/kg IP failed to reduce the increase of errors induced by AF64A 2.5 nmol injected into the dorsal hippocampus. These findings suggest that minaprine exerts an ameliorating effect on amnesia produced by scopolamine and cerebral ischemia, probably through mediation of its stimulant action on central cholinergic systems.

Animals↗
PubMed1990

WEB 1881 FU ameliorates impairment of working memory induced by scopolamine and cerebral ischemia in the three-panel runway task.

Using a repeated acquisition procedure in a 3-panel runway apparatus, the effect of WEB 1881 FU on impairment of working memory produced either by scopolamine or by cerebral ischemia was investigated in rats and compared with those of aniracetam and Ca hopantenate. Intraperitoneal injection of scopolamine at 0.56 mg/kg significantly increased the number of errors (pushes made on the two incorrect panels of the three panel-gates located at each choice point). WEB 1881 FU at 10-32 mg/kg, p.o., caused a dose-related reduction in the increase of errors expected in the scopolamine-treated rats. Aniracetam at 10-100 mg/kg, p.o., or Ca hopantenate at 100 and 560 mg/kg, p.o., also significantly diminished the increase in errors induced by 0.56 mg/kg of scopolamine. Cerebral ischemia for 5 min significantly increased errors in the 3-panel runway task. WEB 1881 FU at 32 and 56 mg/kg, administered p.o. immediately after blood flow recirculation and again 1 hr before the runway test, conducted 24 hr after ischemia, significantly reduced the increase in errors expected to occur after 5 min of ischemia. Aniracetam at 32 and 100 mg/kg, p.o., similarly diminished the increase in errors in ischemic rats. These findings suggest that WEB 1881 FU has a beneficial effect on memory that has been impaired by scopolamine or by cerebral ischemia.

Animals↗
PubMed1990

[Disturbed formation of dental hard tissues after cyclophosphamide administration].

The changes appeared in the developing dentin and enamel of rat upper incisor after single intraperiotoneal injection of cyclophosphamide (4-8mg/100g body weight) were investigated histologically and microradiographically. 1) Changes appeared immediately after the injection were karyolysis, necrosis and intercellular accumulation of tissue fluid in the preodontoblast layer at the cell proliferating stage and its neighboring pulp tissue, however, no particular change was observed in the adjacent inner enamel epithelium cells. Those changes were more prominent in the labial side than the lingual side and expanded their range with time after the injection and then were replaced gradually by the fibroblasts proliferated. 2) Changes appeared in the dentin secondarily were as follows: a. Hypoplasia of dentin made by the odontoblasts which were at the stage of cell differentiation at the time of the injection. This is probably due to early cessation of dentinoplastic activity. b. Hypoplasia of the dentin induced by the odontoblasts which were at the stage of cell proliferation at the time of the injection. This change was induced by odontoblasts recovered from the changes described in 1). c. Hypomineralization appeared in the dentin which places more incisally than the site of change a and have commenced its matrix formation after the injection. This change did not accompany hypoplasia. d. Slight hypoplasia appeared at the basal side of change b. This change was made by the odontoblasts proliferated after the injection. With time after the injection, "niche" formation became observable at the pulpal surface of dentin due to hypoplasias mentioned above. 3) Osteodentin formation became appear secondarily and expanded its range in the pulp adjacent to the portion of the changes described in 2). Early cessation of dentin described in b and c of 2) is due to cell dysfunction occurred by pressure induced by osteodentin formation. 4) At the developing enamel adjacent to the hypoplastic dentin, no particular change was observed in the progressive mineralization pattern, although distortion of contour of surface or slight hypoplasia were observed.

Animals↗
PubMed1990

[Unknown cause of familial neuromuscular disease with infiltration of cytotoxic/suppressor T cells].

We report two brothers, aged 68 and 61 years respectively, who had an unclassified familial neuromuscular disease with infiltration of cytotoxic/suppressor T cells in muscle biopsies. The elder brother was in good health and active during child and adulthood until the age of 65 when muscle atrophy in the quadriceps muscle was noted. His muscle weakness and atrophy progressed relatively rapidly in the course of a few years. The muscle symptoms predominated in the under extremities at the initial stage, later to be generalized, sparing the facial muscles. The serum creatine kinase (CK) was 145 mu/ml (normal 5-80 mu/ml). EMG revealed myopathic changes. A biopsy taken from biceps muscle showed extensive inflammatory cellular infiltrations among fibers and in the perimysium. The infiltrated cells were identified to be cytotoxic/suppressor T cells. The younger brother first noticed diminished bulk in quadriceps muscle bilaterally at the age of 59. The muscle symptoms were similar to those seen in his brother. Serum CK was 520 mu/ml. EMG showed myopathic changes except for fibrillation potentials in the biceps. A biopsy taken from quadriceps muscle revealed the similar findings of his brother. The classification of these cases is a controversial subjects. We differentiated quadriceps myopathy, limb-girdle muscular dystrophy and myositis, which we couldn't classify. So at this point we reported these cases as unknown cause of familial neuromuscular disease.

Aged↗
PubMed1989

Nasu-Hakola disease (membranous lipodystrophy). Clinical, histopathological and biochemical studies of three cases.

We report 3 cases of Nasu-Hakola disease found in 2 families. These cases had identical clinical features with progressive spastic paraplegia and severe dementia after adolescence. They had no history of any skeletal symptoms, but roentgenographs of their bones presented characteristic evidence of polycystic osteodysplasia. All cases revealed not only manifestations of this condition in the central nervous system, but also peripheral neuropathy with axonal degeneration. The membranous structures in the adipose tissues appeared histochemically to be composed of a kind of compound glycolipid or glycoprotein. Histopathologically, the biopsied rectum showed the infiltration of many histiocytes in the mucosa and ultrastructurally, the granules in these histiocytes showed many membrane-bound vacuoles of different sizes. Interestingly, the histochemical reactivity of the material in the granules was very similar to that of membranous structures in adipose tissues. In the biochemical analysis of lipids in affected adipose tissues, no marked abnormalities were found in the patients. Nasu-Hakola disease is not a typical form of lysosomal storage disease, because lysosomal enzyme activities remain normal and there is no accumulation of urinary oligosaccharides and lipids, no vacuolation of lymphocytes, and no hepatosplenomegaly. However, histochemical findings suggest that the lysosomes may be secondarily involved in this disease, and that the formation of membranous structures might be related to the disturbance of glycolipid or glycoprotein metabolisms.

Adipose Tissue↗
PubMed1989

Immune dysfunction in hypophosphatemic vitamin D-resistant rickets: immunoregulatory reaction of 1 alpha(OH) vitamin D3.

We investigated immunologic function in six cases with hypophosphatemic vitamin D-resistant rickets (VDRR) before and after treatment with 1 alpha-hydroxycholecalciferol (1 alpha(OH) vitamin D3). All cases suffered frequent episodes of infection, which tended to be more severe in the older patients. OKT9-, OKT10-, and OKM1-positive cells and adenosine deaminase (ADA) were significantly increased, whereas numbers and activity of natural killer (NK) cells were lower than normal before treatment. After administration of 1 alpha(OH) vitamin D3, however, the susceptibility to infection apparently decreased, and NK cell number and activity increased in all patients. ADA was also significantly decreased and remained in the normal range after treatment. These results suggest that vitamin D plays a role in the impaired immunoregulatory functions of NK cells in VDRR. Furthermore, ADA may be one parameter reflecting this immunologic impairment.

Adenosine Deaminase↗
PubMed1989

[The effect of body respirator on the desaturation during the night in Duchenne muscular dystrophy].

Recently body respirator (BR) has been used to control respiratory failure in patients with late stage Duchenne muscular dystrophy (DMD). We examined the effect of BR using a pulse oximeter. Arterial oxygen saturation (SaO2) for the night (21:00-7:00) was monitored in 15 DMD patients (5 cases without BR, 3 cases with BR partially for the night and 6 cases with BR all night long) and the desaturation (SaO2 less than 90%) time was followed three times (Jan. '87, Nov. '87, Apr. '88) in each patient. Desaturation time did not increase in 4 cases without BR. But in one case without BR it increased so much that we decided to put the patient on BR. In 3 cases with BR partially for the night, desaturation was well controlled when they used BR. No marked increase of desaturation was found in 4 cases with BR all night long. 2 of these cases were changed from cuirass type BR to jacket type BR and were getting on satisfactorily. Thoracic cage expansion of jacket type was larger than that of cuirass type, and it was found that jacket type was valuable. Also, we investigated the cause of desaturation by recording SaO2, nasal flow, thoracic cage motion and abdominal motion at the same time by making use of a polygraphy. The result showed that the main cause of desaturation was the resistance of thoracic cage motion against BR. And we think research and development is needed.

Adolescent↗
PubMed1988

Ultrastructural demonstration of Maclura pomifera agglutinin binding sites in the membranocystic lesions of membranous lipodystrophy (Nasu-Hakola disease).

This paper reports three cases of membranous lipodystrophy (Nasu-Hakola disease) in two families and studies the carbohydrate components of membranocystic lesions in all three cases, using twelve kinds of lectins labelled by horseradish peroxidase (HRP). Maclura pomifera agglutinin (MPA), which specifically binds alpha-D-galactose residues, strongly stained typical membranocystic lesions, whereas the other lectins did not. However, Helix pomatia agglutinin (HPA), which specifically binds to N-acetyl-D-galactosamine (GalNAc), stained the membranes of degenerated adipose cells. These were thought to appear during the initial or early stage of the membranocystic lesions. This suggests that a change of carbohydrate residues occurs during the formation of the membranocystic lesions. We also investigated the lectin binding sites at the ultrastructural level using MPA-HRP colloidal gold (CG) conjugate. In the well developed membrane, CG particles were arranged regularly along the minute tubular structures. On the other hand, there were a few irregularly spaced CG particles on the thinner membranes and also on the membranes of the degenerating adipose cells. No CG particles labelled the cell membranes of normal adipose cells. The presence of alpha-D-galactose residues in the membranocystic lesions is demonstrated for the first time at the electron microscopic level.

Adipose Tissue↗
PubMed1988

Immunological studies of HTLV-I associated myelopathy.

We report the immunological studies of 50 cases with a chronic progressive myelopathy associated with elevated antibodies to human T-cell lymphotropic virus type I (HTLV-I) and adult T-cell leukemia-like cells (HAM). These are as follows: (1) T-cell activation; (2) increase of the OKT4/OKT8 ratio, due mostly to increased inducer/helper T cells and/or decreased suppressor/cytotoxic T cells; (3) decrease of natural killer cell numbers and activity; and (4) increase of immunoglobulins (IgG, IgA). Our results provide evidence that autoimmune events may participate in the pathogenesis of HAM and may be relevant in the hypothesis of common immune mechanisms between HAM and HTLV-I positive tropical spastic paraparesis.

Adult↗