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Biomedical subjects

M Soma

Publications and source records attributed to M Soma.

At least 145 records · Page 8Linked to original sources

Heterotransplantation of mixed mesodermal tumor cells in nude mouse--histology of metastatic foci.

The mixed mesodermal tumor has an admixture of carcinoma and sarcoma. The HIRS-BM tumor cell line, derived from the mixed mesodermal tumor, was transplanted into the peritoneal cavity of BALB/c nude mice, and the metastatic foci were examined histologically and karyologically. The HIRS-BM cells produced mixed mesodermal tumors (admixture of adenocarcinoma and rhabdomyosarcoma) resembling the original tumor. The normal interstitial tissue was not present on the boundary of the sarcoma and carcinoma. These results support the combination theory as the cause of mixed mesodermal tumor.

Adenocarcinoma↗

Establishment of HUOCA-II, a human ovarian clear cell adenocarcinoma cell line, and its angiogenic activity.

A cell line designated "HUOCA-II" was established from a human ovarian clear cell adenocarcinoma. The HUOCA-II cells, which were oval, spindle, or polygonal and had neoplastic and pleomorphic features, grew in multiple layers without contact inhibition. The cell line grew fast (population doubling time, 24 hr), and 55 serial passages were carried out within 11 months. The chromosomal number ranged around 46, and no karyological abnormality was found in G-band karyotyping. When heterotransplanted into the subcutis of BALB/c nude mice, HUOCA-II cells produced a poorly differentiated clear cell adenocarcinoma. The tumor angiogenesis factor (TAF) of a molecular weight of about 14,000 was purified from the conditioned medium of HUOCA-II cells, and neovascularization was detected by bioassay with the use of the chorioallantoic membrane of a chick embryo. This TAF also stimulated the growth of endothelial cells in an in vitro culture system.

Adenocarcinoma↗

Plasma catabolism of human apolipoprotein E isoproteins: lack of conversion of the doubly sialylated form to the asialo form in plasma.

Apolipoprotein E (apoE) circulates as a mixture of sialylated and asialylated forms. In this study the catabolic fate and the plasma turnover rate of the different apoE forms have been investigated in vivo in humans. Asialo apoE (E) and doubly sialylated apoE (Ess) were isolated by preparative isoelectrofocusing from the VLDL of subjects homozygous for the E3 allele. 131E3 and 125E3ss were injected simultaneously into three hypertriglyceridemic subjects, and plasma samples were collected up to the sixth day. VLDL were isolated by ultracentrifugation, and the apoE forms were separated by isoelectrofocusing. Gel bands corresponding to E3 and E3ss were cut out and counted for the associated radioactivity. Residence times in plasma for 131E3 and 125E3ss were 0.95 +/- 0.16 and 0.74 +/- 0.16 days, respectively. As determined from the gel count distribution up to 24 hours, no conversion of the injected sialylated form to the correspondent asialylated form was detected.

Aged↗

Establishment and characterization of two human ovarian endometrioid carcinoma cell lines (with or without squamous cell component).

The cell lines designated HMOA and HNOA were established from human ovarian adenoacanthoma and from a mouse graft of human ovarian endometrioid adenocarcinoma, respectively. These cell lines grew well without interruption for over 20 months. The cultured cells of both HMOA and HNOA lines were spindle, polygonal, and columnar, and showed a jigsaw puzzle-like arrangement and a piling-up tendency devoid of contact inhibition. When the HMOA cells were maintained at the confluent stage, the cells formed cysts and/or squamous metaplasia. The chromosome number of both cell lines varied widely and showed aneuploidy, while the modal chromosome number was stable at the diploid range. Both of these cell lines, HMOA and HNOA, were transplanted into the subcutis of BALB/c nude mice and produced well-differentiated adenoacanthoma and poorly differentiated endometrioid adenocarcinoma, respectively. HMOA cells were characterized as producing large amounts of CA125 (ovarian carcinoma marker), in vitro, in the cyst-forming phase. The HNOA cells, however, did not produce CA125.

Adenocarcinoma↗

Establishment and characterization of a human ovarian endodermal sinus tumor cell line--producing specific type of alpha-fetoprotein subfraction.

A cell line was established from an endodermal sinus tumor of the ovary from a 57-year-old Japanese woman, obtained on July 22, 1982. Histological study of the resected tumor revealed a mixture of reticular, solid and cystic patterns, being consistent with the characteristic feature. The cell line, designated as human Akimoto endodermal sinus tumor (HAEST), was subcultivated over 50 times during 29 months. The cells were spindle or columnar in shape and showed pleomorphic and neoplastic features. The modal chromosome number was stable at diploid range and the marker, large acrocentric, chromosome was identified. The cells were transplanted into the cheek pouch of hamsters and produced an endodermal sinus tumor. alpha-Fetoprotein subfractions in the conditioned media were studied by a modified method of lectin affinity crossed-line immunoelectrophoresis, and we found that the HAEST cells produced concanavalin A nonreactive subfraction, lentil lectin weakly reactive subfraction, phytohemagglutinin-E reactive subfraction and phytohemagglutinin-E nonreactive subfraction, which were predominantly synthesized by the fetal yolk sac, at an early stage of gestation. From these findings, we concluded that the HAEST was indeed an endodermal sinus tumor cell line. This line is expected to have a wide application for various laboratory studies.

Animals↗

Increased release of prostaglandins from the mesenteric vascular bed of diabetic animals: the effects of glucose and insulin.

To study prostaglandin (PG) metabolism in peripheral vascular beds, PGs and TxB2 released from perfused mesenteric tissues were measured in both normal and streptozotocin (STZ)-induced diabetic rats. The release of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), thromboxane B2 (TxB2) and prostaglandin E2 (PGE2) was significantly increased in mesenteric vascular beds from diabetics in comparison with control rats. The 6-keto-PGF1 alpha/TxB2 ratio was decreased in diabetics. In order to clarify the mechanism of this imbalanced synthesis of eicosanoids, we infused buffer with 500 mg/dl glucose which was similar to the concentration of blood glucose in the diabetic rats. In response to this high glucose concentration, TxB2 released into the effluent from the mesenteric beds of normal animals was increased to the diabetic level. The release of the other PGs was not changed significantly. The 6-keto-PGF1 alpha/TxB2 ratio was decreased in control rats perfused with buffer containing 500 mg/dl glucose. We also investigated the effect of insulin (50 and 100 microU/ml) in the diabetic mesenteric vascular beds, but there were no changes in prostaglandin or TxB2 release. These data suggest that a high glucose level may have an important role in regulating TxA2 synthesis and in modulating the balance between PGI2 and TxA2 in diabetes. It is postulated that an increase in the micro-circulation of PGI2 may partially be protective against the progression of angiopathy.

6-Ketoprostaglandin F1 alpha↗

Histogenesis and tissue reconstruction of mixed mesodermal tumor.

The clonal cell lines designated as HIRS-BMS and HIRS-BMA were established from HIRS-BM (multipotent primitive cells which differentiated into rhabdomyosarcoma and adenocarcinoma cells) by a single cell plating method. The HIRS-BMS was a rhabdomyosarcoma cell line composed of elongated fibrous cells which contained myoglobin. The HIRS-BMA was an adenocarcinoma cell line composed of round cells. The tissue reconstruction of these cell lines was studied in vitro (rotation culture system) and in vivo (transplantation into hamster cheek pouch). The HIRS-BMS cells produced rhabdomyosarcoma, both in vitro and in vivo, and the HIRS-BMA produced poorly differentiated adenocarcinoma, in vitro and in vivo. The mixture of HIRS-BMS and HIRS-BMA produced a mixed mesodermal tumor resembling the original tumor. These results support the theory of a combined tumor as a cause of mixed mesodermal tumor.

Adenocarcinoma↗

In vitro inhibition of rat arterial smooth muscle cell growth by extractive sulfated mucopolysaccharides.

The effect of a sulfated mucopolysaccharide mixture of known composition, extracted from pig duodenum, was studied on the proliferation of rat arterial smooth muscle cells cultured from rat aorta. Cell growth, stimulated by fetal calf serum, was monitored by direct cell count and by determination of the mitotic index. The extractive mixture was studied in comparison with commercial heparin, with heparin with different electrophoretic mobilities in barium acetate and with dermatan and heparan sulfates. Heparins and the extractive mucopolysaccharide mixture inhibited cell growth measured at various time intervals, and in their presence the proliferation of smooth muscle cells plateaued at lower cell densities. Dermatan and heparan sulfates were either inactive or significantly less effective than the other mucopolysaccharides. A short preincubation (3 h) of smooth muscle cells with the extractive mixture, followed by incubation with the growing medium with no mucopolysaccharides added, slowed the cell growing rate, suggesting an interaction of the mixture components with the cell surface.

Animals↗

Effects of dietary saturated, N-6 and N-3 polyunsaturated fats on blood pressure and prostaglandins outflow from perfused mesenteric vascular bed in rats.

Effects of the dietary administration of saturated fat and of n-6 and n-3 polyunsaturates on blood pressure, prostaglandin metabolism in small vessels, tissue fatty acid distribution and urinary PGE2 excretion were compared. Rats were divided into three groups. Diets contained 10% hydrogenated coconut oil (HCO), 10% safflower oil (SFO) or 10% cod liver oil (CLO) added to a basic fat free diet for 10 weeks. Systolic blood pressure was increased in the CLO group animals. Urinary PGE2 excretion was decreased in the HCO and CLO groups as compared to that in the SFO group animals. PGE2, 6-keto-PGF1 alpha and thromboxane (Tx) B2 outflow from isolated perfused mesenteric arterial beds were extremely decreased in the CLO group animals, and to a lesser extent in the HCO group as compared to the SFO animals. In the tissue phospholipid, 20:3n-9/20:4n-6 ratios were increased in the HCO group indicating essential fatty acid deficiency, and n-6 and n-3 polyunsaturates were elevated in the SFO and the CLO group animals respectively. Arachidonic acid concentration was highest in the SFO group, while there was no significant differences between the HCO and the CLO group. These results suggest that dietary fatty acid manipulation affects urinary PGE2 excretion and PGI2, PGE2 and TxA2 synthesis in mesenteric arterial beds and also changes the tissue fatty acid distribution. Furthermore, n-3 polyunsaturates caused an extreme reduction of 2-series PGs synthesis in small resistance vessels.

Animals↗

Prostaglandins and thromboxane outflow from the perfused mesenteric vascular bed in spontaneously hypertensive rats.

To clarify the metabolism of PGE2, prostacyclin (PGI2) and thromboxane A2 (TxA2) in small vessels in spontaneously hypertensive rats (SHR), we removed superior mesenteric vascular beds from 10 week old SHR and age matched normotensive controls (WKY). The mesenteric artery was perfused with Krebs-Henseleit buffer and samples of effluent collected every 15 minutes during 3 hours perfusion for analysis of PGE2, 6-keto-PGF1 alpha (a stable metabolite of PGI2) and TxB2 (a stable metabolite of TxA2) by specific radioimmunoassays. Levels of all three arachidonic acid (AA) metabolites, PGE2, 6-keto-PGF1 alpha and TxB2, in the mesenteric effluent were significantly reduced in SHR as compared to WKY. TxB2 was detected in all samples throughout the perfusion. 6-keto-PGF1 alpha/PGE2 ratios and TxB2/PGE2 ratios were significantly increased in SHR. 6-keto-PGF1 alpha/TxB2 ratios in the first four samples were significantly decreased in SHR as compared to WKY. These data suggest that there may be reduced availability of PG precusor AA and unbalanced synthesis of PGs in small vessels in SHR. Both may have relevance to the development of hypertension in the animals.

Animals↗

Magnesium deficiency in the rat increases tissue levels of docosahexaenoic acid.

The effects of magnesium deficiency on tissue levels of total lipids and fatty acids were evaluated. Sprague-Dawley rats were fed a magnesium-deficient diet for 14 wk with controls being pair-fed to the deficient rats. Compared to the controls, serum and 24-h urinary magnesium levels were markedly lower in the magnesium-deficient rats. Serum cholesterol and total phospholipids were significantly higher in the magnesium-deficient rats than in the controls. Edema and polycystic degeneration of the kidneys were present in the magnesium-deficient rats. Kidney total phospholipids and triacylglycerols were significantly lower in the magnesium-deficient rats than in the controls. The main change in tissue fatty acid composition in magnesium deficiency was the higher docosahexaenoic acid (22:6n-3) in serum, liver and aorta than in controls. The possible relationship of these findings to human alcoholism is discussed.

Animals↗

The effects of hydrogenated coconut oil, safflower oil, and evening primrose oil on development of hypertension and sodium handling in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) were fed a basal regular diet (BD) or three different fat-supplemented diets which contained 10% hydrogenated coconut oil (HCO), 10% safflower oil (SFO), or 10% evening primrose oil (EPO). The rats received these four different diets from 4 weeks to over 24 weeks of age. The development of hypertension in SHR was significantly retarded in the EPO-supplemented animals. The blood pressure was lower in the SFO group animals as compared with the BD and HCO groups, but this did not reach significance. Sodium excretion rate in young SHR was increased in the EPO group compared with the HCO and SFO groups, and the urinary K/Na ratio was decreased in the EPO group compared with the HCO and EPO groups. Water intake and urine volume were increased in the SFO group as compared with the HCO and EPO groups. Sodium concentration in erythrocytes was decreased in the rats receiving SFO. Pressor responses to norepinephrine and angiotensin II were enhanced in the EPO and SFO groups as compared with the basal chow group. These data suggest that a dietary supplementation of EPO which contains a substantial amount of gamma-linolenic acid consistently lowers blood pressure in SHR. The mechanism is uncertain, but the effects on sodium handling may in part be responsible for the retardation of the development of hypertension. There was a difference between the EPO and the SFO groups in sodium--water handling, and to some extent in the blood pressure development in SHR.

Angiotensin II↗