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Biomedical subjects

M Matsunaga

Publications and source records attributed to M Matsunaga.

At least 145 records · Page 8Linked to original sources
PubMed1988

Regulation of renin-like enzyme in cultured human vascular smooth muscle cells.

Cultured human arterial smooth muscle cells produced an immunologically specific renin-like enzyme. The renin-like enzyme in the culture medium was mostly an inactive form; the proportion of the active form in the cell was 30 to 75%. Phorbol 12-myristate 13-acetate, N'-O'-dibutylyladenosine 3', 5'-monophosphate and isoproterenol with theophylline increased the renin-like enzyme in the medium and in the cell, dose dependently. Endothelial cell growth supplement also increased the renin-like enzyme produced by cultured vascular smooth muscle cells, and heparin promoted the effects of endothelial cell growth supplement. The existence of the regulation of the renin-like enzyme produced by cultured vascular smooth muscle cells strongly suggests the existence of a local renin angiotensin system in human vascular walls.

Cells, Cultured↗
PubMed1988

The effects of cytokines, antithyroidal drugs and glucocorticoids on phagocytosis by thyroid cells.

The present study was undertaken to examine whether thyrocytes possess phagocytic activity and whether the phagocytic activity is influenced by cytokines, such as interleukin 1, 2 (IL 1, IL 2) and interferon-alpha, -beta, and -gamma (IFN-alpha, beta, and gamma), and drugs, such as methimazole and dexamethasone. Thyroid glands were obtained from patients with Graves' disease. Thyrocytes were prepared by collagenase digestion. Thyrocytes were pre-incubated in the presence or absence of cytokines and drugs at 37 degrees C for 20 h and were further incubated with fluoresceinated latex beads at 37 degrees C for 60 min. The number of phagocytic thyrocytes was determined by FACS IV. Phagocytosis of latex beads was indeed seen within thyrocytes and gradually increased in a time-dependent manner. The rate of phagocytosis in thyrocytes was extremely slow as compared with that in macrophages. Phagocytic activity was detected in thyrocytes from patients with Graves' disease and from normal thyroid tissue adjacent to thyroid cancer. Phagocytosis was inhibited by IL 1, but was enhanced by IL 2. Although the enhanced phagocytosis with IFN-beta was consistently seen, little effect was detected with IFN-alpha and -gamma. Both methimazole and dexamethasone markedly inhibited phagocytosis. These results indicated that thyrocytes had phagocytic properties and that their phagocytic activity was modulated by cytokines, antithyroidal drugs and dexamethasone.

Antithyroid Agents↗
PubMed1988

[A successful treatment of giant carotid artery aneurysm by a detachable balloon technic; a child case].

For the treatment of unclippable giant carotid artery aneurysms, proximal occlusion of the carotid artery is still an accepted treatment by surgical ligation, Selverstone clamp, or detachable balloon. However, proximal artery occlusion should be avoided as far as possible. Use of detachable balloons for proximal artery occlusion in the treatment of giant intracranial aneurysm in children has been reported by several authors, but no report of successfully treated cases of occlusion of the aneurysm without occlusion of the parent artery can be found. On January 1st, 1987, a-5-year old girl was admitted to our clinic with chief complaints of exophthalmos and loss of vision in her left eye. On admission, neurological examination showed palsies of the left oculomotor and abducens nerve and left internal carotid angiogram visualized a giant aneurysm in the cavernous portion. A balloon catheter procedure was carried out under general anesthesia using an intra-arterial catheter technique. A No. 9 French introducer catheter was placed through the femoral artery sheath. No filling of aneurysm without occlusion of the parent artery could be confirmed by angiogram. No. 12 Debrun detachable balloon was then detached. Postoperative course was uneventful. Subsequently, her oculomotor and abducens nerve palsies disappeared. Digital subtraction angiography taken about three months after the procedure showed complete occlusion of the aneurysm. The authors emphasized that the occlusion of the aneurysm using a detachable balloon was also the ideal method for the treatment of the children's giant aneurysm.

Carotid Artery Diseases↗
PubMed1988

Synergy in antigen presentation by thyroid epithelial cells and monocytes from patients with Graves' disease.

The present study was undertaken to examine the ability of thyrocytes from Graves' patients to present purified protein derivative (PPD) to autologous peripheral blood T cells. Normal human thyrocytes which were pre-cultured with interferon-gamma were able to induce the proliferation of T cells in response to PPD antigen, but unstimulated thyrocytes failed to do. Thyrocytes from Graves' patients on which HLA-DR antigens were expressed have an ability to induce the proliferation of T cells. Thyrocytes from Graves' patients which were pulsed with PPD antigen for 4 h were capable of stimulating proliferation of the T cells. However, the stimulation index of T cells co-cultured with thyrocytes and PPD were significantly lower than that of T cells co-cultured with monocytes and PPD. Sub-optimal numbers of monocytes which by themselves were unable to support T-cell proliferation synergistically augmented antigen presentation by thyrocytes. These results suggest that cellular interactions among thyrocytes, monocytes and T cells may perpetuate immune or autoimmune responses in thyroid tissues from Graves' patients.

Adolescent↗
PubMed1987

Regulation of angiotensin converting enzyme activity in cultured human vascular endothelial cells.

Angiotensin converting enzyme (ACE) of vascular endothelial cells is suggested to control vascular wall tonus through the conversion of angiotensin I (AI) to angiotensin II (AII) and the degradation of bradykinin. To obtain more insight into the pathophysiological significance of ACE of vascular endothelial cells, we studied the regulation of ACE produced by cultured human umbilical vein endothelial cells (EC). Phorbol 12-myristate 13-acetate (PMA) increased the cellular and medium ACE activity, accompanied by a marked morphological change in EC. N'-O'-dibutylyladenosine 3';5'-cyclic monophosphate (db-cAMP) increased only the cellular ACE activity and not the medium ACE activity. The effect of isoproterenol with 0.1mM theophylline mimicked that of db-cAMP. These findings suggest that PMA and cAMP-related agents participate in the control of vascular wall tonus through the positive regulation of ACE produced by vascular endothelial cells.

Bucladesine↗
PubMed1987

Regulated expression of human atrial natriuretic polypeptide gene in mouse L cells.

To investigate whether the human atrial natriuretic polypeptide (hANP) gene is responsive to glucocorticoid, we co-introduced the hANP gene (with SV40 enhancer) with HSV-tk gene into mouse tk- L cells. The transformants with hANP gene with SV40 enhancer expressed hANP specific RNAs. The administration of 1 microM dexamethasone reduced the expressed hANP specific RNAs, especially those that had a physiological initiation site. These results suggest that the hANP gene is really a glucocorticoid responsive gene and may be negatively regulated by glucocorticoid.

Animals↗
PubMed1987

Expression of human atrial natriuretic polypeptide gene in Cos 7 cells.

Cos 7 cells transfected with human atrial natriuretic polypeptide (hANP) gene with SV40 enhancer and replication origin sequences expressed hANP gene. The expressed RNA was indistinguishable from native hANP mRNA and the transcribed protein seemed to be properly processed to alpha-hANP and beta-hANP. This system provides a useful approach to investigate the processing of hANPs and the structure-function relationship of amino acid sequences of hANPs.

Animals↗
PubMed1987

Reduction in the suppressor-inducer T cell subset and increase in the helper T cell subset in thyroid tissue from patients with Graves' disease.

The expression of surface markers associated with activation and characterization was compared among T cells in thyroid glands and peripheral blood of 10 patients with Graves' hyperthyroidism receiving chronic antithyroid drug therapy, in peripheral blood of 15 patients with untreated hyperthyroid Graves' disease, and in peripheral blood of 21 normal subjects using two-color flow cytometry. In the chronically treated Graves' disease patients, the percentage of activated T cells (HLA-DR+ T cells) among total T cells was significantly higher in thyroid tissue than in peripheral blood, and the increase in percent activated T cells was also significant among both helper/inducer T cell (CD4+ cell) and suppressor/cytotoxic T cell (CD8+ cell) subsets. The percentage of activated T cells in peripheral blood was not significantly different between chronically treated hyperthyroid Graves' patients and normal subjects, whereas the percentage of activated T cells in the peripheral blood from untreated hyperthyroid Graves' disease patients was significantly higher than that in normal subjects or chronically treated hyperthyroid Graves' patients. The percentages of CD4+ cells and CD8+ cells among total T cells were not different between thyroid tissues and peripheral blood in patients with chronically treated hyperthyroid Graves' disease. When CD4+ were further divided into helper T cells (CD4+2H4- cells) and suppressor-inducer T cells (CD4+2H4+ cells) using two-color flow cytometry, the percentage of helper T cells among CD4+ cells was significantly higher in thyroid tissue than in peripheral blood, resulting in an increased ratio of CD4+2H4- cells to CD4+2H4+ cells. The percentage of CD4+2H4+ cells in peripheral blood, however, was not significantly different among untreated and chronically treated Graves' disease patients and normal subjects. From the findings of abnormalities in intrathyroidal T cell subsets, we suggest that the decrease in the function of suppressor T cells within the thyroids of Graves' disease patients may be due to a decrease in CD4+2H4+ cells within thyroid tissue.

Adolescent↗
PubMed1987

Dysfunction of suppressor T cells in thyroid glands from patients with Graves' disease.

To investigate the suppressor function of intrathyroidal (TG) T cells in Graves' disease, the percentage of suppressor T cell subsets and the suppressor function of TG and peripheral blood (PB) lymphocytes in Graves' disease were compared by determining the in vitro production of immunoglobulin G (IgG) in reconstituted mixtures of separated B, CD4+ (helper/suppressor-inducer T), and CD8+ (suppressor/cytotoxic T) cells. TG lymphocytes were obtained by gradient centrifugation of the supernatants of minced thyroid tissues. T Cells were separated by E-rosette formation, and CD4+ and CD8+ cell-rich populations were separated by a panning method using monoclonal anti-CD8 antibody. Mixtures of 5 X 10(4) B (PB1 or TG) cells, 2 X 10(4) CD4+ (PB or TG) cells, and 5 X 10(3) macrophages (PB or TG) were cultured with various numbers of CD8+ (PB) or CD8+ (TG) cells for 7 days with pokeweed mitogen, and IgG synthesis was determined by solid phase RIA. T cell subpopulations were quantitated by a direct immunofluorescence method using monoclonal anti-CD3, anti-CD4, and anti-CD8 antibodies. There was no difference in the percentages of CD8+ cells among total T cells between thyroid glands and peripheral blood from Graves' disease patients [mean PB, 39.8 +/- 9.8% (+/- SD); TG, 42.5 +/- 13.8%; n = 10]. IgG production by mixtures of B and CD4+ cells isolated from peripheral blood was not different from that by cells isolated from thyroid glands [mean PB, 1635 +/- 248 (+/- SE) ng/mL; TG, 1081 +/- 128 ng/mL; n = 19; P = NS]. The nonspecific suppressor activity of thyroid gland CD8+ cells was less than that of CD8+ (PB) cells [percent suppression of IgG production by mixtures of B (PB) and CD4+ (PB) cells, 12.5% vs. 57.0% (P less than 0.01); by mixtures of B (TG) and CD4+ (TG) cells, 5.8% vs. 38.9% (P less than 0.01)]. The suppressor-inducer function of CD4+ (TG) cells was also decreased compared with that of CD4+ (PB) cells. These results suggest that the impairment of suppressor cell activity may lead to excessive production of autoantibody in thyroid glands from patients with Graves' disease.

Adult↗
PubMed1987

Antibodies to brain proteins in a patient with subacute cerebellar degeneration and Lambert-Eaton myasthenic syndrome.

The serum IgG of a 50-year-old woman with lung cancer associated with subacute cerebellar degeneration and Lambert-Eaton myasthenic syndrome showed the antibody activity to rat brain proteins. Using an immunoblotting method, the patient serum reacted with 98 kDa neutral cytoplasmic protein and 68 kDa membrane protein. These proteins were different in molecular weight from those we described previously (Tanaka et al. 1986), which suggests that proteins reacting with serum antibody are variable individually among patients with subacute cerebellar degeneration. These proteins from human brain could not be stained by the patient's serum IgG since these antigen proteins needed to be prepared quickly after death under protease inhibitors and were thought to be easily degraded.

Antibodies↗
PubMed1987

The effects of nifedipine and captopril on renal function in patients with essential hypertension: comparison with sodium nitroprusside.

In comparison with a nonspecific vasodilator, sodium nitroprusside (SNP), we intended to deduce the characteristics of nifedipine (NIF) and captopril (CAP) in the treatment of hypertension. Ten patients with essential hypertension were hospitalized and kept on a constant sodium diet (10 g NaCl/day). Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured before and after the respective administration of SNP (0.9 +/- 0.5 mcg/kg/min), NIF (17 +/- 5 mg), and CAP (85 +/- 24 mg). SNP significantly reduced the mean blood pressure (MBP), the renal vascular resistance index (RVRI), urine volume (UV), urinary excretion of sodium (UNaV), and significantly raised active renin concentration (ARC), plasma norepinephrine (NE), and the heart rate (HR). RBF, GFR, and plasma epinephrine (E) were not changed. Compared with SNP, NIF significantly raised RBF, UV, UNaV, and fractional excretion of sodium (FENa) and significantly reduced RVRI. The differences between the increases in ARC, NE, and HR by NIF and those by SNP were not significant. GFR and E were not changed by NIF. Although CAP did not reduce MBP as much as SNP did, the increase in RBF by CAP was significantly greater than that by SNP. Changes in GFR, UV, UNaV, FENa, and E by CAP were not different than those by SNP. CAP increased ARC and did not raise E, NE, and HR. In conclusion, compared with SNP, NIF significantly raised RBF, UV, UNaV, and FENa and significantly reduced RVRI. On the other hand, the renal response to CAP was not very much different from the response to SNP. The characteristics of CAP were the suppressed sympathetic response to the decrease in blood pressure.

Adult↗
PubMed1987

Chromosome aberrations and clinical features of adult T cell leukemia-lymphoma not associated with human T cell leukemia virus type I.

Chromosome aberrations and clinical features of three patients with adult T cell leukemia-lymphoma (ATL) not associated with human T cell leukemia virus type I (HTLV-I) are described. From their clinical features, two patients were diagnosed as acute type and one patient was diagnosed as chronic type, which later converted to acute crisis. Clonal and many chromosomal abnormalities were observed before therapy in the two acute type cases and at relapse in the chronic type case. Karyotype aberrations, including trisomy 3, trisomy 7, trisomy 21, del(6)(q21), del(10)(p13), 14q11 translocation, and loss of X chromosome, all of which are frequently found in HTLV-I associated ATL, were also seen in these cases of HTLV-I-negative ATL.

Acute Disease↗
PubMed1987

The remarkable proliferation of helper T cell subset in response to autologous thyrocytes and intrathyroidal T cells from patients with Graves' disease.

We have studied cellular interactions among thyrocytes, intrathyroidal T cells and peripheral blood T cells from Graves' patients. In the autologous mixed lymphocyte reaction of Graves' patients, CD4+ cells were able to proliferate vigorously against autologous non-T cells, whereas CD8+ cells responded weakly to non-T cell stimulators. Furthermore, the proliferative response of the CD4+ 2H4+ suppressor-inducer T cell subset was increased like that of the CD4+ 2H4- helper T cell subset. In contrast to peripheral blood non-T cell stimulators, thyrocytes and intrathyroidal T cells had the ability to activate the CD4+ 2H4- helper T cell subset but were not able to cause proliferation both of CD4+ 2H4+ suppressor-inducer T cell and CD8+ suppressor/cytotoxic T cell subsets. The marked reduction in proliferative responses of CD4+ 2H4+ cells and CD8+ cells could not be attributed to a difference in kinetics or altered response to variable number of stimulator cells. On the basis of these findings, it is suggested that the concentration of the helper T cell subset may be progressively increased and suppressor circuits may be unable to be activated in thyroid tissues. These abnormalities in cellular interactions may induce the excessive production of autoantibodies.

Adolescent↗