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Biomedical subjects

S Matsuda

Publications and source records attributed to S Matsuda.

At least 559 records · Page 31Linked to original sources

A new blood pressure measuring apparatus equipped with a microcomputer system for conscious rats.

In order to measure the systolic blood pressure of conscious rats without thermal stress, a highly sensitive pulse sensor was developed using a light-emitting diode-photo diode system. The combination of this pulse sensor and microcomputer system led to the development of a six-channel automatic blood pressure measuring apparatus for rats. It can measure the systolic tail arterial pressure of conscious rats at 28-30 degrees C. The relationship between direct carotid arterial pressure (Y) and indirect tail arterial pressure (X) in conscious spontaneously hypertensive rats can be expressed as follows: Y = 0.95X + 19.9 (mm Hg, r = 0.988, 28 degrees C). The new apparatus was also used to confirm the acute hypotensive effects of hydralazine, nifedipine, and pindolol in spontaneously hypertensive rats and the subacute antihypertensive effect of trichlormethiazide in desoxycorticosterone/saline hypertensive rats.

Animals↗

A case of acute myelogenous leukaemia associated with eosinophilia: cytogenetic study of eosinophilic colonies showing the origin of the normal clone.

We describe a case of acute myelogenous leukaemia presenting with remarkable eosinophilia in relapse. Since the patient had chromosomal abnormalities, haemopoietic as well as eosinophilic colonies grown in culture were cytogenetically analysed to determine the origin of the eosinophils. Eosinophilic colonies as well as erythroid bursts revealed a normal karyotype, while a short-term culture of peripheral blood cells in relapse revealed an abnormal karyotype which had been observed before treatment. These data clearly demonstrate that the eosinophilia in this case originated from a normal clone. The cytogenetic analysis of eosinophilic colonies is a useful technique for the definite diagnosis of eosinophilic leukaemia or reactive eosinophilia in patients having marker chromosomes.

Adult↗

Effect of 1 alpha,25-dihydroxyvitamin D3 on proliferation of activated T-cells and established human lymphotropic virus type I-positive T-cell lines.

The effects of 1 alpha, 25-dihydroxyvitamin D3 [1,25-(OH)2D3] on proliferation and de novo DNA synthesis were studied in the following established human leukemia cell lines: lymphoblastic T-cell lines HPB-ALL, CCRF-HSB-2, p12/lchikawa, and HPB-MLT; adult T-cell leukemia- (ATL) and human lymphotropic virus type I (HTLV-I)-infected T-cell lines HUT102, HUT-102B2, MT-1, MT-2, MJ, C2/MJ, KH-2, KH-2Lo, HPB-CTL-1, and ATN-C1; ATL-derived B-cell lines ATL-BK9 and ATL-BK10; lymphoblastic B-cell line Daudi; and myelocytic-monocytic lineage cell lines HL-60 and U937. 1,25(OH)2D3 inhibited proliferation and de novo DNA synthesis of phytohemagglutinin-P-activated T-cells and certain established HTLV-I-positive T-cells. However, it did not inhibit immature lymphoblastic T- and B-cells or ATL-derived B-cells. The degree of inhibition depended on the dose of 1,25(OH)2D3 and the heterogeneity of the established HTLV-I-positive T-cells. KH-2 and subclone KH-2Lo were markedly inhibited, and HPB-CTL-1 was moderately inhibited. Marked inhibition of DNA synthesis in KH-2Lo cells was observed in the proliferative phase of the cell cycle. No inhibition of KH-2Lo proliferation or expression of interleukin-2 and transferrin receptor was noted after removal of 1,25(OH)2D3 from the culture medium. 1,25(OH)2D3 inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced multinucleated cell formation of various HTLV-I-positive T-cell lines and TPA-induced HTLV-I p19 expression in KH-2Lo cells.

Antigens, Viral↗

Induction of preleukemic stage of adult T cell leukemia-like disease in rabbits.

Two HTLV-I-carrying T cell lines were prepared from peripheral lymphocytes of a virus-infected (B/J X Chbb:HM) F1 rabbit, and these cells were inoculated intraperitoneally into 5 newborn F1 rabbits. These animals were killed 3-5 weeks later. Their leukocyte counts were higher than those in normal control animals, with abnormal lymphocytes amounting to 3-5% of total leukocytes. Histological examination showed leukemic infiltration in liver, spleen, lung and kidneys of all these animals. The peripheral lymphocytes at first lacked HTLV-I antigens, but became antigen-positive after in vitro culture. Southern blot analysis of these cells revealed HTLV-I integration patterns different from those of the inoculated cells.

Animals↗

IgA on the surface of erythrocytes from IgA nephropathy patients.

RBCs from one-third of IgA nephropathy patients examined had more IgA1 on their surface than cells from healthy volunteers. The amount of IgA1 on RBCs was estimated to be no more than 30 ng/4 x 10(8) RBCs. The level of IgG on the surface of RBCs from IgA nephropathy patients were the same as those from healthy volunteers. Free IgA1 myeloma protein binds poorly in vitro to RBCs from both an IgA deficient patient and healthy volunteers. Polyethylene glycol precipitate from the sera of IgA nephropathy patients bound to RBCs from an IgA deficient patient. Factor I did not release IgA1 bound to RBCs from IgA nephropathy patients. These results suggest that this binding is mediated through the interaction of IgA1 and RBCs, and that some alteration of the IgA1 molecule (complexes or aggregation) may account for this binding.

Erythrocytes↗