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Biomedical subjects

S Shiokawa

Publications and source records attributed to S Shiokawa.

At least 55 records · Page 3Linked to original sources
PubMed1994

[The comparison of clinical features between early rheumatoid arthritis and established rheumatoid arthritis].

Clinical features between 69 early RA patients (within a year duration) and 79 established RA patients (more than 3 years duration) were compared retrospectively. There were no significant differences about frequencies of morning stiffness (68.2% vs 54.4%) and rheumatoid nodules (20.2% vs 15.2%) between early RA and established RA. There were also no significant differences between two groups about elevation of ESR (92.8% vs 97.4%), positivity of CRP (97.1% vs 94.9%) and rheumatoid factor (RF) (82.6% vs 93.7%), and Lansbury activity index (AI) (mean 68.8% vs 78.8%). After hospitalization and treatment, all clinical indices (ESR, CRP, RF, AI) improved significantly in both groups. There, however, were clinically more "marked improvement" (39.1% vs 16.4%) and "remission" (8.7% vs none) in early RA group. We conclude that by hospitalization and treatment, clinical improvement can be expected in both early and established RA, but to secure satisfactory improvement, early detection and intervention of RA would be recommended.

Adult↗
PubMed1994

Efficacy of additive DMARD therapy in patients with rheumatoid arthritis. Double blind controlled trial using bucillamine and placebo with maintenance doses of gold sodium thiomalate.

OBJECTIVE: To examine the efficacy of the addition of small doses of additional disease modifying antirheumatic drugs (DMARD) to ongoing DMARD treatment [additive DMARD therapy (ADT)]. METHODS: A 3-month prospective, double blind, randomized, placebo controlled study was performed using either 100 mg/day of bucillamine (Buc) or an inactive placebo (P1). Two groups of 12 patients each who had experienced an insufficient benefit from gold sodium thiomalate (GSTM) alone were enrolled in the study. RESULTS: The addition of Buc proved more beneficial than P1 regarding improvement in disease activity (p = 0.0032) and drug usefulness (p = 0.0025). A significant within group improvement was observed in joint swelling count, the Lansbury activity index, erythrocyte sedimentation rate and C-reactive protein. However, the difference in the clinical variables between the 2 groups was minimal. CONCLUSION: The usefulness of ADT was suggested by this trial; however, further confirmation by additional studies is still needed.

Aged↗
PubMed1993

Comparative study of hormonal dynamics in pregnant and nonpregnant cycles during pulsatile subcutaneous administration of human menopausal gonadotropin in anovulatory infertile women.

OBJECTIVE: To assess the clinical relevance of daily hormonal changes for achieving a successful pregnancy in anovulatory infertile women. DESIGN: A comparative study of hormonal dynamics in pregnant and nonpregnant cycles during the pulsatile subcutaneous administration of hMG. Subjects received subcutaneous injection of either 9.375 IU or 14.0625 IU of hMG diluted in 50-microL physiological saline (total daily dose, 150 or 225 IU) at 90-minute intervals by means of a portable peristaltic pump. SETTING: Kyorin University Hospital and Ichikawa General Hospital. PATIENTS: We analyzed 18 pregnant and 42 nonpregnant cycles in 17 patients with secondary hypothalamic/pituitary amenorrhea who conceived after receiving pulsatile hMG treatment. Another 14 women with normal spontaneous ovulation, including 14 pregnant and 15 nonpregnant cycles, served as controls. MEASUREMENTS: Serum concentrations of LH, FSH, E2, and P were measured, and the P:E2 ratio was determined. RESULTS: Serum concentrations of LH and FSH did not differ significantly between the pregnant and nonpregnant cycles. Serum levels of P and E2 were significantly higher during the hMG treatments than those of the spontaneous ovulatory cycles throughout the follicular and luteal phases. Up to the midluteal phase, the P and E2 values in the nonpregnant cycles during the hMG treatments did not differ significantly from those in the pregnant cycles. The P:E2 ratios were comparable between the pulsatile stimulatory cycles and the normal spontaneous ovulatory cycles. However, the P:E2 ratio in the early and midluteal phases was significantly greater in the pregnant cycles than in the nonpregnant cycles. CONCLUSION: The P:E2 ratio in the early and midluteal phases is a more important indicator of hormonal function for implantation than the absolute levels of either P or E2.

Adult↗
PubMed1993

Locally produced angiotensin II induces ovulation by stimulating prostaglandin production in in vitro perfused rabbit ovaries.

The present study was undertaken to investigate the role of exogenous and endogenous angiotensin II (Ang II) in ovarian steroidogenesis and production of prostaglandin (PG) in in vitro perfused rabbit ovaries. The addition of 100 or 10 micrograms Ang II at 2-h intervals to the perfusate did not stimulate progesterone production, but significantly stimulated estradiol (E2) production by perfused rabbit ovaries. When the specific antagonist of Ang II, saralasin at 2 x 10(-6) M, was added to the perfusate 30 min before the onset of Ang II administration, Ang II-stimulated production of E2 was significantly blocked. Ang II also significantly stimulated both PGE2 and PGF2 alpha production, while the addition of saralasin to the perfusate significantly inhibited the Ang II-stimulated production of PG. The levels of PGs in ovaries perfused with saralasin plus 100 micrograms Ang II did not differ significantly from those in control ovaries perfused with medium alone. Exposure to human CG (hCG) significantly stimulated production of progesterone and E2 by perfused rabbit ovaries, while the concomitant administration of 2 x 10(-6) M saralasin significantly reduced only E2 production. Addition of saralasin to the perfusate inhibited hCG-stimulated PG production in a dose-dependent manner. The ovulatory efficiency in ovaries treated with hCG alone or hCG plus saralasin was significantly correlated with PG production by perfused rabbit ovaries at 12 h after exposure to hCG. The production of PG stimulated by Ang II was completely reduced by indomethacin treatment during the entire perfusion period. Indomethacin completely blocked Ang II-induced ovulation, but not Ang II-stimulated oocyte maturation. Concurrent administration of staurosporine, a protein kinase C inhibitor, at 10(-6) M significantly inhibited Ang II-stimulated meiotic maturation of ovulated ova and follicular oocytes. In conclusion, these results indicate that Ang II has a direct role in ovarian production of E2 and PG. An intrinsic renin-angiotensin system in the rabbit ovary may act as an intermediary of gonadotropin-stimulated PG production. Locally produced Ang II may induce ovulation in the rabbit ovary, at least in part, by stimulating PG production.

Angiotensin II↗
PubMed1993

Mixed connective tissue disease presenting myasthenia gravis.

We herein describe a 41-year-old female patient with an association of myasthenia gravis (MG) with anti-acetylcholine receptor (AcR) antibody, mixed connective tissue disease (MCTD) and Sjögren's syndrome (SjS). We reviewed the reported association of MG and MCTD, systemic lupus erythematosus, progressive systemic sclerosis, polymyositis and dermatomyositis, and SjS. Since we could find only two patients who fulfilled the diagnostic criteria for MCTD in the previous literature, we concluded that the association of MG and MCTD is rare. We also discuss the coexistence of SjS as one of the underlying pathological conditions for the association of MG and various connective tissue diseases including MCTD.

Adult↗
PubMed1993

Mixed connective tissue disease associated with lupus lymphadenitis.

We have encountered 2 patients with mixed connective tissue disease (MCTD) associated with lymphadenopathy at the outset. Biopsy specimens of enlarged lymph nodes showed massive necrotizing lesions with follicular hyperplasia, which are occasionally observed in the involved lymph nodes of patients with systemic lupus erythematosus (SLE) and called lupus lymphadenitis. Usually, the only histologic finding of an involved lymph node in MCTD is lymphoid hyperplasia. These are the 2nd and 3rd cases of MCTD associated with lupus lymphadenitis. Our cases suggest that histologic studies of the swollen lymph nodes are not helpful in distinguishing MCTD from SLE.

Biopsy↗
PubMed1992

Angiotensin II directly induces follicle rupture and oocyte maturation in the rabbit.

To investigate the possible direct involvement of angiotensin II (Ang II) in ovulation and oocyte maturation, Ang II at 100 or 10 micrograms was administered at 2-h intervals in the in-vitro perfused rabbit ovaries. The addition of Ang II in the perfusate induced ovulation in vitro in the absence of gonadotropin, while ovulation did not occur in any contralateral control ovaries. However, the ovulatory efficiency in the Ang II-treated ovaries was significantly lower than in hCG-treated ovaries. Ang II significantly stimulated the meiotic maturation of ovulated ova and follicular oocytes. Concomitant addition of the specific receptor antagonist of Ang II, saralasin, 30 min before the onset of Ang II administration blocked Ang II-induced ovulation in a complete manner. Although saralasin did not inhibit completely hCG-induced ovulation and oocyte maturation, these results suggest that Ang II produced in the ovary may act locally in the process of ovulation.

Angiotensin II↗
PubMed1992

Intracellular signal transduction in proliferation of synovial cells.

We investigated some steps in the signal transduction pathway leading to the proliferation of synovial cells. 12-o-tetradecanoyl phorbol-13-acetate (TPA) which is known to stimulate phospholipid- and Ca(2+)-dependent protein kinase (C-kinase) enhanced the proliferation of synovial cells. The proliferation of synovial cells induced by interleukin-1 beta. Tumour necrosis factor alpha and granulocytes/macrophages colony stimulating factor, was inhibited by a potent C-kinase inhibitor, H7. These findings strongly suggested that the signal transduction pathway leading to proliferation of synovial cells is transmitted via C-kinase activation. Prostaglandin E2, which is known to stimulate adenylate cyclase, leading to the elevation of intracellular c-AMP level, inhibited the proliferation of synovial cells. This effect could also be mimicked by the addition of a cell permeable c-AMP analog, dibutyryl c-AMP or theophylline. Studies suggest that the feedback signal for proliferation of synovial cells was transmitted through c-AMP. We therefore conclude that signals for stimulation and inhibition of synovial cell proliferation are transmitted through different pathways.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Direct effect of gonadotropin-releasing hormone agonists on the rabbit ovarian follicle.

OBJECTIVE: To determine if gonadotropin-releasing hormone agonist (GnRH-a)-induced oocyte maturation and degeneration can be attributed to the direct actions on the follicle. DESIGN: Mature rabbit follicle culture. INTERVENTIONS: The mature follicles were cultured with human chorionic gonadotropin (hCG) (100 ng/mL), buserelin acetate (10(-9) to 10(-6) M), leuprolide acetate (10(-9) to 10(-6) M), or buserelin acetate (10(-7) M) with a GnRH antagonist (10(-8) to 10(-6) M) for 14 hours. MAIN OUTCOME MEASURES: The percentage of oocytes achieving germinal vesicle breakdown, the oocyte degeneration rate, prostaglandins (PG) production by mature follicles, and the frequency of fertilization and embryonic development. RESULTS: Gonadotropin-releasing hormone agonist induced the meiotic maturation of follicle-enclosed oocytes in a dose-dependent manner while concomitantly increasing oocyte degeneration. The simultaneous addition of GnRH antagonist inhibited significantly GnRH-a-induced oocyte maturation and PG production by the mature follicles. Furthermore, a GnRH antagonist reversed the oocyte degeneration rate that had been increased by GnRH-a. The rates of normal fertilization and early embryonic development were significantly reduced in the oocytes matured by GnRH-a as compared with those matured by hCG. CONCLUSIONS: Gonadotropin-releasing hormone agonist acts directly on mature rabbit follicles to trigger the oocytes to undergo meiotic maturation, but oocytes matured in vitro by GnRH-a are not necessarily cytoplasmically mature.

Animals↗
PubMed1992

Protein kinase C mediates gonadotropin-releasing hormone agonist-induced meiotic maturation of follicle-enclosed rabbit oocytes.

The present study was undertaken to determine the effects of a protein kinase C inhibitor, staurosporine, on gonadotropin-releasing hormone agonist (GnRHa)-induced oocyte maturation and follicular prostaglandin (PG) production, and the response to direct activators of protein kinase C using rabbit mature follicle culture. Treatment of mature follicles with GnRHa (buserelin and leuprolide acetate) neither stimulated nor inhibited cAMP accumulation in both the follicle and oocyte. Exposure to staurosporine at 10(-6) M 60 or 15 min before GnRHa (buserelin) administration reduced significantly the meiotic maturation of follicle-enclosed oocytes induced by GnRHa at 10(-7) M. However, staurosporine addition coincident with the agonist or thereafter did not inhibit meiotic maturation. Staurosporine suppressed GnRHa-induced meiotic maturation in a dose-dependent manner, whereas hCG-stimulated oocyte maturation was not inhibited. Similarly, staurosporine administered 60 min before exposure to GnRHa suppressed GnRHa-stimulated PG production by mature follicles. The active phorbol esters, 10(-6) M 12-0-tetra-decanoyl phorbol 13-acetate (TPA) and 10(-6) M 4 beta-phorbol 12,13-didecanoate (4 beta-PDD) stimulated meiotic maturation whereas the biological inactive isomer, 4 alpha-PDD, did not. The kinetics of germinal versicle breakdown of follicle-enclosed oocytes in the presence of active phorbol esters paralleled that of GnRHa-treated oocytes. Furthermore, the concomitant addition of staurosporine at 10(-6) M to the culture medium inhibited significantly (p less than 0.05) TPA-induced meiotic maturation. These data demonstrate that GnRHa stimulated both the meiotic maturation of follicle-enclosed oocytes and follicular PG formation via a mechanism other than the cAMP-mediated process.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaloids↗
PubMed1992

Possible involvement of lipoxygenase products in human corpora lutea.

The present study was undertaken to determine the ability of cultured luteal cells from human corpora lutea to secrete progesterone (P4) and prostaglandins (PGs), and to assess the effects of the products of the lipoxygenase pathway on luteal P4 production. Luteal cells responded to human chorionic gonadotropin (hCG) with a significant increase (2- to 7-fold) in P4 production. Arachidonic acid significantly stimulated PGE2 synthesis by luteal cells in a dose-dependent manner. Both basal PGE2 production and the responsiveness to arachidonic acid were maintained for 8 days. In contrast, both PGF2 alpha and 6-keto-PGF1 alpha production abruptly declined as the culture proceeded. However, the addition of hCG did not further stimulate the accumulation of the 3 PGs assayed. In the subsequent experiment, 5-hydroxyeicosatetraenoic acid (5-HETE) and the reaction products of soybean lipoxidase of arachidonic acid (AA-LIP) were utilized for evaluating the involvement of the lipoxygenase pathway in luteolysis. The addition of 5-HETE dose-dependently inhibited P4 production by the cultured luteal cells. Although treatment with either arachidonic acid or lipoxidase alone had no effect on P4 production, AA-LIP significantly reduced P4 production in the presence or absence of hCG. These results suggest that the products of the lipoxygenase as well as of the cyclo-oxygenase pathway may be important in regulating the life span and function of human corpora lutea.

Adult↗
PubMed1992

Possible involvement of leukotrienes in human luteal function.

The present study was undertaken to assess the ability of human corpora lutea to produce leukotriene B4 (LTB4). The maximum capacity of luteal cells to secrete progesterone was attained on day 4, and both the basal production and the responsiveness to hCG decreased thereafter. In contrast, the production of LTB4 by cultured luteal cells was significantly reduced on day 4, but increased thereafter. The basal concentration of LTB4 produced by luteal cells varied from 75 to 590 pg/10(5) cells/2 days. LTB4 production appeared to decrease concomitantly with increased-progesterone production in cultured luteal cells. Exposure to hCG decreased significantly LTB4 production by cultured luteal cells on day 4. An inhibitor of the lipoxygenase pathway, nordihydroguaiaretic acid (NDGA), inhibited LTB4 production in a dose-dependent manner. However, NDGA did not affect basal progesterone production by the cultured luteal cells. A significant inverse relationship existed between the accumulation rates of progesterone and LTB4 in the luteal cells. Furthermore, the addition of LTB4 inhibited progesterone production in a dose-dependent manner in both the presence and absence of hCG. In conclusion, LTB4 could be synthesized by human corpora lutea in vitro, and correlated inversely with the secretion rates of progesterone. These data suggest that LTB4 produced locally in the corpus luteum may be an important regulator in human luteal regression.

Adult↗
PubMed1991

Multicentric reticulohistiocytosis associated with subclinical Sjögren's syndrome.

A case of multicentric reticulohistiocytosis in a 60-year-old Japanese woman associated with subclinical Sjögren's syndrome is presented. The clinical features along with the light microscopic studies are commented. Partial improvement of the skin lesions and tendon sheath swelling was achieved after treatment with cyclophosphamide but the patient's general condition remained unchanged. Taking the rarity of multicentric reticulohistiocytosis into account, coexistence of these two conditions in the present and previously reported cases suggests that an autoimmune mechanism may play a part in the pathogenesis of multicentric reticulohistiocytosis.

Cyclophosphamide↗
PubMed1991

Effects of colony-stimulating factors on proliferation and activation of synovial cells.

Joint synovium of patients with rheumatoid arthritis plays an important role in initiation and progress of joint diseases. Proliferation and activation of synovial cells, including macrophages, are modulated by various cytokines and arachidoic acid metabolites. Two kinds of cytokines; granulocyte/macrophage colony-stimulating factors (GM-CSF), and monocyte/macrophage colony-stimulating factor (M-CSF) induce the proliferation or activation of monocyte/macrophages, and their progenitor cells or other stromal cells in bone marrow. We investigated the effects of GM-CSF and M-CSF on synovial cells. GM-CSF stimulated the proliferation of synovial cells and its effect was enhanced by the presence of indomethacin, like that of a potent stimulator of synovial cells, interleukin-1 beta (IL-1 beta). But GM-CSF did not induce the production of IL-1 beta. M-CSF neither stimulated the proliferation of synovial cells nor induced production of IL-1 beta by synovial cells. It was suggested that GM-CSF played some role in the proliferation of synovial cells of the joints.

Cell Division↗