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Y Yaoi

Publications and source records attributed to Y Yaoi.

At least 37 records · Page 2Linked to original sources
PubMed1991

Complete primary structure of human collagen alpha 1 (V) chain.

Several cDNA clones, encoding prepropeptide of human collagen alpha 1(V) chain, have been isolated. The prepropeptide (1838 amino acids length) of the alpha 1(V) chain was composed of a putative signal peptide, a large NH2-terminal noncollagenous region, a main collagenous region, and a COOH-terminal noncollagenous region. The signal peptide contained many leucine residues. The NH2-terminal noncollagenous region was much larger than those of the other collagens and had a region homologous to the COOH-terminal domain of laminin A chain, but it did not contain a cysteine-rich region that was maintained in the region of the other collagens. This region also contained probable tyrosine sulfation sites, and short collagenous sequences that were interrupted by three noncollagenous segments. The main collagenous region of the alpha 1(V) chain consisted of 338 repeats of Gly-X-Y-triplet. This region had a high degree (82%) of homology with the amino acids of the collagen alpha 1(XI) chain. The COOH-terminal noncollagenous region resembled that of the alpha 1(XI) chain, too, and 8 residues of cysteine that were important for the formation of the triple helix structure of collagens were observed. These results suggest that the alpha 1(V) chain belongs to the fibrillar collagen relative to the alpha 1(XI) chain, but codon usage of the alpha 1(V) cDNA was clearly different from those of the other fibrillar collagens including the alpha 1(XI), while it was similar to type IV collagen. This result supposes a different evolution of the alpha 1(V) gene from those of the other fibrillar collagens.

Amino Acid Sequence↗
PubMed1991

Insulin binds to type V collagen with retention of mitogenic activity.

The abilities of eight extracellular matrix proteins, fibronectin, vitronectin, laminin, and collagen types I, II, III, IV, and V to bind insulin were examined by binding studies with insulin conjugated with peroxidase. At a physiological pH and ionic strength, type V collagen bound to insulin most strongly. The other types of collagen, laminin, and vitronectin also bound insulin with affinity lower than that of type V collagen. The insulin-binding site of type V collagen was in a 30-kDa CNBr fragment of the alpha 1 (V) chain. Analysis of the amino acid sequence showed that this 30-kDa fragment was identical to the heparin-binding fragment of type V collagen. The insulin-binding sites of laminin and vitronectin were located in the A chain and in the heparin-binding domain, respectively. Insulin bound to type V collagen stimulated the synthesis of DNA by mouse mammary tumor MTD cells, indicating that bound insulin retained mitogenic activity.

Amino Acid Sequence↗
PubMed1991

Inhibition of cell adhesion by type V collagen.

Human umbilical vein endothelial cells grew well in dishes coated with collagen types I, II, III, or IV. However, the same cells tended to detach themselves from dishes coated with type V collagen, and cell proliferation in these dishes was inhibited. Such anti-adhesive activity was partially retained by heat-denatured type V collagen or by its alpha 1 chain, but not by its alpha 2 chain. Several other cell types did not adhere to the type V collagen substratum even in the presence of 10% serum. The cell types strongly inhibited from adhering by type V collagen included Swiss mouse 3T3 cells and their MSV-transformants, BALB/c 3T3 cells and their methylcholanthrene-transformants, NIH 3T3 cells and their ras-transformants, BHK cells, CHO-9 cells, CHO-K1 cells, and mouse melanoma B16-F10 cells. Using Swiss mouse 3T3, we studied the effects of type V collagen on cell adhesion to fibronectin in serum-free medium. When the culture dishes were coated with a mixture of fibronectin with various concentrations of type V collagen, the adhesion of the cells was inhibited depending on the concentration of type V collagen. The inhibition of cell adhesion by type V collagen was competitively overcome by increased concentrations of fibronectin. The activity that interferes with the effects of fibronectin was retained mainly by the alpha 1 chain of heat-denatured type V collagen.

3T3 Cells↗
PubMed1990

Primary structure of the heparin-binding site of type V collagen.

The abilities of collagens, type I, II, III, IV, and V, to bind heparin were examined by heparin-affinity chromatography and binding studies with [35S]heparin. At a physiological pH and ionic strength, only type V collagen bound to heparin. Collagens type I and II showed higher affinities than types III and IV for heparin, but did not bind to a heparin column at a physiological ionic strength. The heparin binding site of type V collagen was located in a 30 kDa CNBr fragment of the alpha 1(V) chain, and the amino acid sequence of this fragment was determined. The 30 kDa fragment contained a cluster of basic amino acid residues, and enzymatic cleavage within this basic domain greatly reduced the heparin-binding activities of the resulting peptides. Thus this basic region is probably the heparin-binding site of type V collagen.

Amino Acid Sequence↗
PubMed1989

Serum levels of coagulation-fibrinolysis factors in normal pregnancy, labor and puerperium and in cesarean section delivery.

Plasma levels of fibrinopeptide A (FPA), fibrinopeptide B beta 15-42 (FPB beta 15-42), high molecular weight kininogen (HMW-kg), kinin, prekallikrein and kallikrein inhibitor during pregnancy, labor, cesarean section and puerperium were studied in 170 cases of full term normal delivery and 20 cases of cesarean section delivery with 30 non-pregnant women taken as control. Significant increases of FPA, FPB beta 15-42 and kinin during normal delivery and puerperium were found. There was also a significant increase of FPA in the uterine venous blood during cesarean section. Significant decrease of HMW-kg during normal labor and also significant decrease of prekallikrein and kallikrein inhibitor after cesarean section were also seen. Our findings suggested that the hypercoagulable state during pregnancy is due to the increase of thrombin and plasmin activity, and the kallikrein-kinin system may be related to the onset of labor and post-delivery uterine contraction. Increase of the FPA in the uterine blood promoted localised coagulation activity during cesarean section.

Blood Coagulation Factors↗
PubMed1987

[Combined therapy of bromocriptine, clomiphene citrate and HMG in normoprolactinemic amenorrhea patients who fail to respond to bromocriptine-clomiphene citrate therapy].

The purpose of this study is to investigate the ovulatory effect of the following three methods on 40 patients with normoprolactinemic amenorrhea patients who failed to respond to clomiphene citrate (Cl) alone. Method I is the combined therapy with bromocriptine and Cl (Brc/Cl). Method II is the combined therapy with Brc/Cl and an additional small amount of HMG (less than or equal to 300 IU). Method III is the combined therapy with Brc/Cl and an increased amount of HMG (less than or equal to 1,200 IU) and HCG. The ovulation rate of method I was 57.5% (23/40) in 40 cases, and 55.6% (99/178) in 178 cycles. The pregnancy rate for this method was 23.8% (5/21). Out of the 12 nonrespondent method I cases, 5 additional cases were ovulated by method II and 3 cases were ovulated by method III. The total pregnancy rate was 42.9% (9/21) with these three methods. Seven cases were normal pregnancies, one case was a twin pregnancy and 1 case was an abortion. No other side effects were found in this study. From these results, the combined therapy with Brc/Cl or Brc/Cl + HMG had almost the same ovulatory rate as the HMG-HCG therapy, and fewer side effects.

Adolescent↗
PubMed1987

[Immunohistochemical localization of estradiol in malignant epithelial tumors of the ovary].

Granulosa cell tumors derived from sexcord-stromal cells are thought to be generally estrogen producing neoplasms. However recent reports show that these common epithelial tumors, adenocarcinomas and Brenner tumors, are capable of estrogen activity. We have studied the production of estrogen in common epithelial malignant tumors of the ovary. Two cases of serous cystadeno-carcinomas, five cases of mucinous cystadeno-carcinomas and two cases of endometrioid carcinomas were examined for the presence of estradiol using an indirect immunoperoxidase method. The results were as follows: In all tumors, one case of serous cystadeno-carcinoma, four cases of mucinous cystadeno-carcinomas and one case of endometrioid carcinoma had a positive immunoperoxidase reaction. The incidence of positive reaction showed that mucinous cystadeno-carcinomas were more numerous than others. In positive cases, estradiol localization was recognized in the epithelial cell of mucinous tumors to various degrees, but there was no estradiol localization in admixed goblet like cells. In serous tumors and endometrioid carcinomas also estradiol localization was seen in the cytoplasm. Stromal cells tended to be more weakly positive than epithelial cells. No estradiol localization was detected in any of the spindle cells or fibrinous connective tissues. These results suggest that some common epithelial malignant tumors of the ovary have estrogen activity and estradiol is produced not only in stromal cells but also in epithelial cells.

Adenocarcinoma↗
PubMed1986

[Study of the correlation between gonadotropin- and prolactin-releasing systems in women in the luteal phase and early pregnancy].

The purpose of this study was to investigate the correlation between gonadotropin (Gn) and prolactin (PRL) releasing activities on the hypothalamo-pituitary axis in the luteal phase of the normal menstrual cycle and in the early gestational period. The plasma levels of LH-beta subunit (LH-beta) following an intravenous bolus of 100 micrograms LHRH did not change significantly in early pregnancy. The plasma PRL levels, as well as the Gn levels, were significantly elevated (p less than 0.05) after the administration of 100 micrograms LHRH in the luteal phase, but did not rise in early pregnancy. The intravenous bolus of 10mg metoclopramide (MCP) had no effect on plasma LH-beta, LH, FSH, estradiol or progesterone in the luteal phase or early pregnancy. The plasma PRL levels remained significantly (p less than 0.001) elevated after the administration of MCP. However, there was no significant difference between PRL response to MCP in the early pregnant and luteal phase groups. In the luteal phase, we could show the correlation between Gn and PRL releasing mechanisms on hypothalamo-pituitary axis, which could not be found in early pregnancy.

Estradiol↗
PubMed1986

Prolactin-releasing system in maternal, fetal, and amniotic compartments during labor.

The effect of a dopamine antagonist on prolactin concentrations was studied in maternal, fetal plasma, and amniotic fluid in term gestation. Twenty-three women with normal full-term pregnancies received 10 mg metoclopramide intravenously during labor. The prolactin levels in maternal plasma increased significantly after metoclopramide. However, the prolactin levels in amniotic fluid and fetal plasma did not change significantly after administration of this drug. Although the increased values of prolactin in maternal plasma were significantly correlated with metoclopramide concentrations after metoclopramide injection, there was no correlation between these two values in amniotic fluid. The authors conclude that the prolactin-releasing system in amniotic fluid is independent of the maternal hypothalamopituitary axis.

Adult↗
PubMed1985

[Effect of dopaminergic agents on the endocrine profile in labor and early puerperium].

The purpose of this study was to investigate the prolactin (PRL) releasing mechanism of the hypothalamo-pituitary axis during labor and early puerperium. Ten full-term gravidas during labor and 42 women in early puerperium were examined in this study. The plasma PRL levels rose significantly (p less than 0.001 approximately 0.05) after an intravenous bolus of 10mg metoclopramide (MCP). The peak values for PRL increase were 609.3 +/- 194.1ng/ml during labor and 447.0 +/- 62.3ng/ml in early puerperium. However, there were no significant differences in PRL response to MCP between these two groups. The plasma PRL levels dropped significantly (p less than 0.001 approximately 0.01) after an oral administration of 2.5mg bromocriptine (BRC), and the PRL release from the pituitary by MCP was suppressed significantly (p less than 0.001) by pretreatment with BRC in the puerperium. In addition, no significant changes in plasma 17 beta-estradiol (E2), progesterone (P) and cortisol levels could be observed after MCP. We concluded that the control mechanism of PRL secretion remained unchanged during labor and early puerperium.

Bromocriptine↗
PubMed1984

Growth-inhibitory glycopeptides obtained from the cell surface of cultured chick embryo fibroblasts.

Cell surface glycopeptides were obtained from cultured chick embryo fibroblasts (CEF) by digestion with Pronase E, and a fraction exerting growth-inhibitory activity on CEF was isolated by high performance gel permeation chromatography. The active fraction, tentatively termed cell surface glycopeptide-2 (CSGP-2), was soluble in 5% trichloroacetic acid (TCA) or 75% ethanol. It inhibited the growth of CEF reversibly at 10-20 micrograms sugar/ml, but did not inhibit BALB/c mouse 3T3, SV40-transformed 3T3, and human diploid cells at similar concentration. The growth-inhibitory activity of CSGP-2 was reduced or lost after digestion with neuraminidase or oxidation with sodium metaperiodate. Cellulose acetate electrophoresis revealed that CSGP-2 was a mixture of sialoglycopeptides. A similar growth inhibitor was also isolated from chicken embryonic tissues.

Animals↗
PubMed1984

The prolactin-releasing mechanism of the hypothalamo-pituitary axis in pregnancy.

The purpose of this study was to investigate the prolactin (PRL)-releasing mechanism of the hypothalamo-pituitary axis in pregnancy. Forty-six gravidas in the first and second trimesters received bromocriptine (BRC), 2.5 mg orally, metoclopramide (MCP), 10 mg intravenously, or thyrotropin-releasing hormone (TRH), 500 micrograms intravenously. Additionally, BRC was given orally to another 42 gravidas 60 minutes prior to the intravenous injection of MCP or TRH. The plasma PRL levels decreased significantly after BRC and remained significantly elevated after MCP or TRH administration. However, there were no significant differences of PRL response to these agents between the first- and second-trimester groups. The PRL release from the pituitary by MCP or TRH was suppressed significantly by pretreatment of BRC in the gravidas. We concluded that the control mechanism of PRL secretion remained unchanged in the first and second trimesters.

Adult↗