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Biomedical subjects

M Soma

Publications and source records attributed to M Soma.

At least 73 records · Page 4Linked to original sources
PubMed1997

[Study of serum thrombomodulin(TM) levels in patients with hyper- or hypo- thyroidism].

We studies a relationship between the serum levels of thrombomodulin(TM) and the thyroid functions. Serum TM levels were measured in 48 patients with Graves' disease, 17 patients with primary hypothyroidism, 7 patients with subacute thyroiditis, 5 patients with painless thyroiditis and 2 patients with systematic Refetoff syndrome. These patients did not have malignant tumor, kidney failure, or blood vessel injury. Control sera were obtained from 42 healthy subjects. Serum levels of TM in patients with untreated Graves' disease were significantly higher(p < 0.001) compared with those in controls. Serum levels of TM in patients with hypothyroidism were not significantly changed as compared with those of controls. There were a positive correlation between the serum levels of TM and FT3 as well as FT4. Serial determinations of the serum levels of TM and thyroid function(FT3, FT4 and TH) in patients with Graves' disease during treatment showed that both the serum levels of TM and thyroid hormones (FT3 and FT4) lowered progressively during treatment. After normalization of serum FT3 and FT4, the serum TM levels returned to normal. However, the serum levels of TM in patients with destructive thyroiditis and Refetoff syndrome were normal in spite of high serum levels of thyroid hormones. These data suggest that an increase in serum levels of TM is not the direct result of thyroid hormones themselves but is the result of the prolonged hypermetabolic state induced by their peripheral activities. Thyroid hormones may stimulate the synthesis or metabolism of TM on the surface of vascular endothelial cells in the patients with Graves' disease.

Graves Disease↗
PubMed1997

Tissue reconstruction of gynecologic tumor cells in the rotation culture system.

Tissue reconstruction of various kinds of gynecologic malignant tumor cell lines was studied using the rotation-culture system. The reconstructed cell aggregates were examined histologically using both light and electron microscopy. Our established cell lines used in this study were uterine cervical epidermoid carcinoma, endometrial adenocarcinoma, ovarian malignant tumor and uterine sarcoma. All of the reconstructed aggregates from each cell line were very similar to the original tumor tissue. In the case of a well differentiated type of adenocarcinoma derived from the ovarian cancers or the endometrial cancers, papillary cell aggregates (grape-like structures) and/or hollow cell ball (gland alveolus-like) structures were observed. The individual cells were adjoined with by desmosomes and well developed microvilli protruded from the free surface of the cells. On the other hand large cell non-keratinizing squamous cell carcinoma cells formed spherical-shaped aggregates that showed a stratified structure similar to pearl formation. Sarcoma cells formed solid clusters while desmosomes or desmosome-like junctions were not detected. Rotation culture is an excellent method to reveal diagnosis of the original tumor and tumorigenesis by investigating a reconstructed tissue from peritoneal effusions because the reconstructed tissue is similar to the original tumor.

Adenocarcinoma↗
PubMed1997

Histogenesis of hollow cell ball structure of ovarian and endometrial adenocarcinoma cells in vivo and in vitro.

Hollow cell ball structure is often found in the ascites of adenocarcinoma patients. How to form a hollow cell ball structure was studied in vivo and in vitro, using the human cell lines derived from ovarian and endometrial adenocarcinomas. The hollow cell ball structure was formed by horizontal rotation culture of 1 x 10(7) single-suspended cells for 24 hours or by transplanting 1 x 10(6) single-suspended cells into the peritoneal cavity of nude mouse for 24 hours. At one month after transplantation hemi-cyst and hollow cell ball structure were formed in the outermost layer of the grafted tumor on the intraperitoneal serous membrane in the nude mouse. And also great number of floating hollow cell ball structure in the ascites were observed. These results suggest that mechanisms of formation of hollow cell ball structure found in the ascites; one by cell aggregate of single cells, sometimes inner cells of cell aggregate fall into necrosis or secretes mucus inside and make a hollow cell ball structure and another by the removed as the hollow cell ball structure grown from hemi-cyst on the surface of intraperitoneal grafted tumor.

Adenocarcinoma↗
PubMed1996

A nitric oxide synthesis inhibitor decreased prostaglandin production in rat mesenteric vasculature.

Endothelial cells synthesize and release nitric oxide (NO) and prostacyclin (PGI2) which are involved in the regulation of vascular tone and blood pressure. Our objective was to evaluate the effects of inhibiting NO synthesis on vascular prostaglandin (PG) and cyclic nucleotide production, as well as the pressor response to norepinephrine (NE). Isolated mesenteric arterial beds were perfused with Krebs-Henseleit solution containing 100 microM NG-monomethyl-L-arginine (L-NMMA), 100 microM L-arginine (LA), or vehicle. After a 30 min equilibration 0.1, 0.5, 1, or 5 microM NE was infused into the superior mesenteric artery and the perfusion pressure was monitored. The basal perfusion pressure did not differ significantly between groups. The pressure-response curve was shifted to the right in the L-NMMA group vs. the LA and control groups. Perfusion was similarly performed with a Krebs-Henseleit solution containing 100 microM L-NMMA, LA, D-arginine, or vehicle. Perfusates were collected before and after NE infusion for the measurement of PGE2, 6-keto-PGF1 alpha, TxB2, cAMP, and cGMP. In the L-NMMA group the release of PGE2 and 6-keto-PGF1 alpha was decreased, and the release of cGMP was prevented. Production of cAMP did not differ between the four groups before NE infusion, and NE increased cAMP release in the L-NMMA group and controls. The results indicate that inhibition of NO synthesis by L-NMMA enhanced the pressor response to NE, possibly mediated by the decreased cGMP and PGI2 production in resistance vessels.

Animals↗
PubMed1996

Lipoprotein(a) and other lipids after oophorectomy and estrogen replacement therapy.

OBJECTIVE: To assess the effect of surgical menopause and subsequent estrogen replacement therapy (ERT) on lipoprotein(a) [Lp(a)] and common lipids. METHODS: In 24 healthy premenopausal women, lipids (total cholesterol, low-density lipoprotein [LDL] and high-density lipoprotein [HDL] cholesterol, and triglycerides) and gonadotropins (FSH, LH) were measured the day before hysterectomy with bilateral oophorectomy and then after 1, 2, and 3 months. Blood was also drawn after 2, 4, 6, and 15 days to exclude the effect of surgery on Lp(a). In 19 women who volunteered for ERT, the lipid profile was assayed again after 3, 6, and 12 months of treatment. RESULTS: Lipoprotein(a) levels rose significantly over the 3 months after surgery, from a mean +/- standard deviation (SD) 5.7 +/- 6.1 mg/dL to 10.4 +/- 9.2 mg/dL. Total cholesterol and LDL cholesterol levels increased significantly over the first 2 months; HDL cholesterol decreased significantly during the 3 months of follow-up (by 10, 17, and 20%) (P < .001). Plasma triglycerides did not change after surgery. Three months following ERT, Lp(a) and total cholesterol were significantly decreased (28 and 11%, respectively), as was LDL cholesterol (33%) after 6 months. High-density lipoprotein cholesterol increased by 24% after 6 months of treatment, and triglycerides rose significantly in the year of therapy (37%). CONCLUSION: These findings suggest that surgical menopause induces atherogenic changes in the lipid profile in 3 months and that ERT soon reverses them.

Cholesterol↗
PubMed1996

Inhibitory effect of an angiotensin II type 1 receptor antagonist on growth of vascular smooth muscle cells from spontaneously hypertensive rats.

To investigate the role of endogenous angiotensin II (Ang II) in the growth of vascular smooth muscle cells (VSMC), we examined the effect of the novel nonpeptide Ang II type 1 (AT1) receptor antagonist CV-11974 on basal and stimulated-growth of VSMC from normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). CV-11974 inhibited basal DNA synthesis by VSMC from SHR, but not from WKY, in the absence of serum. In the presence of 10% calf serum, DNA synthesis was significantly higher in VSMC from SHR than in cells from WKY, and the inhibitory effect of CV-11974 was attenuated. Ang II dose-dependently stimulated DNA synthesis by VSMC from both rat strains, and this effect was abolished by CV-11974. CV-11974 slightly but significantly suppressed proliferation of VSMC from both rat strains. CV-11974 competitively inhibited the specific binding of 125I-labeled Ang II to VSMC from both rat strains. The angiotensin-converting enzyme inhibitor (ACEI) delapril also reduced basal DNA synthesis by VSMC from SHR, but did not affect proliferation of VSMC from either rat strain. These findings suggest that VSMC from SHR may synthesize Ang II which promotes their basal growth in an autocrine/paracrine manner through the AT1 receptor, and that this system may be associated with the exaggerated growth of VSMC from SHR.

Angiotensin II↗
PubMed1996

Prevention of cardiac hypertrophy by a sub-antihypertensive dose of the alpha 1-adrenergic antagonist bunazosin in Dahl salt-sensitive rats.

To assess the protective effect of an alpha 1-blocker on the development of cardiac hypertrophy, the selective alpha 1-receptor antagonist bunazosin (2 mg/kg/d, by oral gavage and in drinking water) was given to male Dahl salt-sensitive rats fed a 4% NaCl diet for 7 weeks. Control animals received water only by the same method. Treatment with bunazosin was started when the animals were 7 weeks of age. Blood pressure, pulse rates, and body weight were measured every week during the experiment. Urine was collected for 24 h on the final day of the experiment. All animals were killed by decapitation, blood was collected, and the heart was removed. In both the treated and control groups, time-dependent increase in blood pressure and body weight were observed, and there were no significant differences between the groups in blood pressure or body weight during the experiment. Pulse rate remained unchanged in both groups throughout the experiment. The left ventricular weight/body weight ratio and the left ventricular tissue DNA content were significantly lower in the rats receiving bunazosin than in the control rats. Plasma renin activity, plasma aldosterone, and plasma atrial natriuretic peptide did not differ significantly between the two groups. No significant differences in glomerular filtration rate, urine volume, sodium excretion, urinary metanephrine excretion, and urinary normetanephrine excretion were noted between the two groups. The results indicate that a sub-antihypertensive dose of bunazosin can inhibit the development of cardiac hypertrophy without suppression of the pressure load, suggesting an important role of alpha 1-adrenergic receptors in the pathogenesis of cardiac hypertrophy following the development of hypertension.

Adrenergic alpha-Antagonists↗
PubMed1996

A nitric oxide synthesis inhibitor prevents the ACTH-stimulated production of aldosterone in rat adrenal gland.

The synthesis of nitric oxide (NO) has been demonstrated in the vascular endothelial cells and other tissues including in rat and bovine adrenal gland. To determine whether NO mediates aldosterone production in the adrenals, we evaluated the basal production of aldosterone, and the ACTH or angiotensin II (A II)-stimulated aldosterone in the presence of L-NG monomethyl arginine (L-NMMA) or L-arginine or L-NMMA + L-arginine in isolated rat adrenal capsular tissue by an ex vivo perfusion technique. ACTH increased the release of aldosterone by 40%. Such release of aldosterone was inhibited by L-NMMA, but not by a mixture of L-NMMA and L-arginine. A II stimulated aldosterone release by 40%. The increase in aldosterone release in response to A II was inhibited by L-NMMA or L-arginine. The increase in aldosterone release stimulated by A II was also inhibited by L-NMMA with L-arginine. L-glutamine did not inhibit the A II stimulated aldosterone release. In conclusion, the inhibition of NO synthesis prevented the release of aldosterone stimulated by ACTH, suggesting NO is required for the action of ACTH on aldosterone production.

Adrenal Glands↗
PubMed1996

[Studies on cerebrospinal fluid penetration of cefpirome in adult with meningitis].

A patient with intracerebral hematoma suffered from postoperative bacterial meningitis. Staphylococcus aureus was found from CSF. The organism was multiple drug resistant and refractory to antibiotics including piperacillin (PIPC), cephalexin (CEX), cefotaxime (CTX), ceftazidime (CAZ) and latamoxef (LMOX). It was susceptible to cefpirome (CPR). Treatment with CPR resulted in clinical improvement associated with clearing of the organism from CSF. Serum level of CPR was high enough and CPR penetration into the CSF was satisfactory. The results suggest that CPR is an extremely effective antibiotic for meningitis caused by CPR-susceptible bacteria. Evaluation of the CPR penetration into the CSF of adult meningitis was rarely reported. The result we obtained was important in the treatment for the adult meningitis.

Adult↗
PubMed1996

[Parasagittal meningioma growing in the superior sagittal sinus presenting intracranial hypertension: a case report].

Parasagittal meningiomas often invade the superior sagittal sinus (SSS), but rarely grow inside the SSS as a primary tumor. The authors report a case of parasagittal meningioma growing mainly inside the SSS and presenting papilledema. The SSS is invisible behind the tumor end on the right carotid angiogram but still patent on the left carotid angiogram. The superficial cortical vein on the opposite side works as a collateral pathway. The tumor may have originated from the right wall of the SSS, grew inside the sinus and covered the entrances of the right ascending cerebral veins. V-P shunt was performed after removal of the mass outside the sinus for resolving headache and visual symptoms.

Brain Neoplasms↗
PubMed1995

[Microsatellite polymorphism of muscle glycogen synthase gene and non-insulin dependent diabetes mellitus].

It has been reported recently that A2 allele of muscle glycogen synthase gene determined by Xba I RFLP (restriction fragment length polymorphism) is related to the frequency of NIDDM in Finland. Using PCR-RFLP analysis, we detected no A2 allele in Japanese patients with NIDDM and control. We found a new microsatellite of CA repeat in the human muscle glycogen synthase gene, and the polymorphism of the repeat number was detected by the polymerase chain reaction. Six different alleles were observed, indicating the highly polymorphic nature of this marker. We analyzed the repeat numbers and the genotypes in diabetics and control. The allele frequencies were not significantly different between NIDDM and control. However, the allele frequencies in the patients without high total cholesterolemia was significantly different from those of control. These findings suggest that the muscle glycogen synthase gene or neighboring genes are related to one of the disease genes of diabetes mellitus without high total cholesterolemia.

Adolescent↗
PubMed1995

High glucose increases platelet-derived growth factor production in cultured human vascular endothelial cells and preventive effects of eicosapentaenoic acids.

The regulation of the production of platelet-derived growth factor (PDGF) and the influence of high glucose concentration, eicosapentaenoic acid (EPA) were studied in cultured human umbilical vein endothelial cells (HUE). The PDGF production of HUE increased markedly depending on glucose concentration. However, EPA (3 x 10(-4)M) markedly inhibited PDGF production [27.5 mM glucose group: 123 +/- 3% of control (5.5 mM glucose group), 27.5 mM glucose+EPA group: 104 +/- 5% of control]. These results suggested that a high glucose concentration and a high osmotic pressure-induced increase in PDGF production is involved in the development and progression of diabetic macroangiopathy. As eicosapentaenoic acid inhibits the PDGF production induced by high glucose concentration in HUE, use of this agent may exhibit anti-arteriosclerotic effects.

Cells, Cultured↗
PubMed1995

Restoration of myo-inositol uptake by eicosapentaenoic acid in human skin fibroblasts cultured in high-glucose medium.

The effects of elevated glucose and eicosapentaenoic acid (EPA, C20:5 omega 3) on myo-inositol uptake in human skin fibroblasts (HSF) were evaluated. Myo-inositol incorporation into HSF was dependent on an active transport system via Na(+)-K+ ATPase activity based on the results with Na+ deprivation and ouabain (5 mM). Although glucose (27.5, 55 mM) inhibited 2-[3H] myo-inositol uptake, the addition of EPA (3 x 10(-4) M) prevented glucose-mediated inhibition. Since EPA decreased glucose-mediated inhibition of myo-inositol uptake, this agent might ameliorate some of the devastating functions associated with diabetes.

Cells, Cultured↗
PubMed1995

Effects of long-term treatment with angiotensin-converting enzyme inhibitor on angiotensin II and prostacyclin release from mesenteric arteries in spontaneously hypertensive rats.

To evaluate the long-term effects of an angiotensin-converting enzyme inhibitor (ACEI) on vascular angiotensin II (AII), eicosanoid production and vascular reactivities, we treated spontaneously hypertensive rats (SHR) with alacepril for 6 weeks and perfused the isolated mesenteric arterial bed which contains resistance vessels. Alacepril significantly lowered the arterial blood pressure. Changes in perfusion pressure in response to norepinephrine (NE) were attenuated, and isoproterenol-stimulated AII release from the perfused mesenteric arterial beds was inhibited in the alacepril-treated SHR. Vasodilation induced by acetylcholine (Ach) and prostacyclin (PGI2) release was significantly increased in the vasculature of the alacepril-treated SHR. Alacepril exerted no effect on cyclic GMP (cGMP) formation, but increased cAMP formation in the vasculature. These findings suggest that ACEI inhibits AII formation and facilitates PGI2 production in the resistance vessels, which leads to blunting of the pressor response to NE and improvement of endothelial function in SHR. These humoral and mechanical changes in the vasculature may contribute to the depressor and organ protective effects of ACEI.

Acetylcholine↗
PubMed1995

Enhancement effect of carteolol on the clonidine-induced vasodilation of rat mesenteric arteries.

It has demonstrated that carteolol can increase the endothelium-dependent vasodilation induced by alpha-2 adrenergic agonist. In order to evaluate the effect of carteolol, and to clarify the mechanism, we examined the effects of 10 microM carteolol on the vasodilation induced by increasing doses (10(-7)-10(-4) M) of clonidine in perfused rat mesenteric arteries preconstricted with 100 microM phenylephrine. Clonidine elicited a dose-dependent vasodilation of the mesenteric arteries preconstricted with phenylephrine. Carteolol enhanced the vasodilation induced by higher doses (10(-5) and 10(-4) M) of clonidine, although carteolol itself exerted no direct vasodilating effect. On the other hand, 10 microM propranolol or 10 microM metoprolol did not augment the clonidine-induced vasodilation. In the presence of 100 microM NG-monomethyl L-arginine (LNMMA), an analogue of L-arginine, the enhancement of the clonidine-induced vasodilation by carteolol was abolished. This inhibition by LNMMA was restored with 300 microM L-arginine, but not with 300 microM D-arginine. These results suggest that carteolol enhances the clonidine-induced vasodilation by an endothelial-related mechanism mediated by the release of endothelium-derived nitric oxide in resistance vessels.

Animals↗
PubMed1995

Characteristics and expression of transforming growth factor-beta receptor subtypes on vascular smooth muscle cells from spontaneously hypertensive rats.

OBJECTIVE: To investigate the characteristics and expression of transforming growth factor (TGF)-beta receptor subtypes on vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. METHODS: The effects of TGF-beta 1 on DNA synthesis were evaluated by [3H]-thymidine incorporation into quiescent VSMC plated at high (5 x 10(4) cells/cm2) or low (5 x 10(3) cells/cm2) cell density. Specific binding of TGF-beta to VSMC was assessed by incubation of the cells with [125I]-TGF-beta 1. Affinity labelling of receptor subtypes was achieved by exposure of the cells to [125I]-TGF-beta 1 and cross-linking with disuccimidyl suberate. RESULTS: VSMC from SHR displayed a biphasic DNA synthesis response to TGF-beta 1 at high cell density, with DNA synthesis stimulated by low concentrations of TGF-beta 1 but not by high concentrations, whereas at low cell density there was a small increase in DNA synthesis in response to TGF-beta 1. TGF-beta 1 inhibited DNA synthesis in VSMC from WKY rats at both high and low cell densities. Binding assays revealed that VSMC from SHR had a larger number of TGF-beta receptors and a higher affinity for TGF-beta at high and at low cell densities. The affinity labelling with [125I]-TGF-beta 1 revealed the presence of receptor subtypes with relative molecular masses of 280-300, 85, 70, 60 and 50 x 10(3) on vascular smooth muscle cells from both rat strains at high cell density. The abundance of the 85 x 10(3) molecular mass receptor subtype was greater in VSMC from SHR. The 85 x 10(3) molecular mass receptor subtype was not detected on VSMC from either strain at low cell density. CONCLUSION: The present results suggest a different expression of TGF-beta receptor subtypes on VSMC from SHR and WKY rats. These differences may account for the exaggerated proliferative response of VSMC from SHR to TGF-beta.

Animals↗