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Biomedical subjects

A Imai

Publications and source records attributed to A Imai.

At least 127 records · Page 7Linked to original sources
PubMed1994

Effect of PT-treatment on ANP-mediated inhibition of adenylate cyclase and amylase release in rat parotid gland.

Effects of pertussis toxin (PT) treatment on atrial natriuretic peptide (ANP)-mediated inhibition of adenylate cyclase and amylase release were investigated in rat parotid gland. Adenylate cyclase activity stimulated by GTP gamma S in PT-treated membranes was much larger than that in normal membranes. ANP dose-dependently inhibited adenylate cyclase stimulated by GTP gamma S in control rat parotid membranes, however in membranes prepared from PT-injected (in vivo) rat parotid gland, ANP did not inhibit adenylate cyclase. ANP(10(-7)M) inhibited cAMP accumulation stimulated by forskolin (10(-6)M) in control rat parotid acinar cells by about 34%, however, in PT-treated cells, the inhibitory effect of ANP was attenuated completely. In control cells amylase release stimulated by isoproterenol (10(-6)M) and forskolin (10(-6)M) were also depressed by ANP (10(-7)M) by 27 and 30% respectively. The inhibitory response of ANP on amylase release was completely attenuated by PT-treatment. Gi was detected as a ADP-ribosylated 41-KDa protein by incubation of parotid membranes with PT and [alpha-32P]NAD. In rat parotid gland, these results suggested that ANP mediates adenylate cyclase/cAMP system and consequently reduces amylase release through ANP-C receptor coupled to Gi.

Adenosine Diphosphate Ribose↗
PubMed1994

A putative new proteinous factor negative for stromal growth. Purification and identification from endometrial carcinoma extract.

BACKGROUND: Uterine endometrial carcinoma has been reported to synthesize and secrete some putative mitogens that elicit either a positive or negative proliferation response in endometrial fibroblasts. The purposes of this study were to isolate and to identify the negative growth factor(s) from endometrial carcinoma extract. METHODS: The factor was isolated by a sequence of molecular size exclusion filtration, anion exchange chromatography, gel filtration and Affi-Gel Blue chromatography, followed by NH2-terminal amino acid sequencing. Mitogenicity was determined by [3H]thymidine incorporation into the endometrial fibroblasts. RESULTS: The purification procedure yielded a single active protein band (68 kDa). The protein, purified approximately 20,000-fold, evoked 90% inhibition of [3H]-thymidine incorporation into endometrial fibroblasts in the nanomolar range. This potent growth inhibitor is a previously unidentified protein molecule as revealed by amino acid sequences. CONCLUSIONS: Endometrial carcinoma could produce a new protein that may act as a paracrine factor to suppress the growth of its stroma endometrial fibroblasts.

Amino Acid Sequence↗
PubMed1994

Pathological findings of the facial nerve in a case of facial nerve palsy associated with benign parotid tumor.

The presence of facial nerve palsy associated with an ipsilateral parotid tumor is virtually pathognomonic for a malignant parotid tumor. However, several case reports have documented the occurrence of facial nerve palsy caused by benign parotid lesions. A case of Warthin's tumor causing facial nerve palsy is presented and discussed histologically. To our knowledge, histological examination of the nerve bundles has never before been reported. The histological findings suggest that ischemia of the nerve caused by external compression resulted in facial nerve palsy.

Adenolymphoma↗
PubMed1994

Presence of gonadotropin-releasing hormone receptor and its messenger ribonucleic acid in endometrial carcinoma and endometrium.

In support of a possible clinical use of gonadotropin-releasing hormone (Gn-RH) analogs in the treatment of the endometrial carcinoma, this study was undertaken to establish the presence and characteristics of Gn-RH receptor on endometrial cancer. Materials were human endometrial carcinomas surgically removed and endometrial carcinoma cell lines. Gn-RH receptor was characterized by [3H]Gn-RH binding to plasma membrane preparations. Gn-RH receptor messenger ribonucleic acid (mRNA) was determined by reverse transcription-polymerase chain reaction (PCR) using oligonucleotide primers synthesized according to the published human Gn-RH receptor sequence. Specific Gn-RH binding sites were shown to be present in 16 of 18 well-differentiated and 4 of 7 poorly differentiated adenocarcinoma specimens (Kd = 5.89 +/- 3.59 nM, Bmax = 1.80 +/- 0.95 pmol/mg protein) and cell lines RL95-2 and HHUA with Kd of 2.38 +/- 0.86 nM. The high-affinity binding sites were also detected in six proliferative-phase endometrium (Kd = 4.24 +/- 2.32 nM, Bmax = 2.73 +/- 1.12 pmol/mg protein). Gn-RH receptor mRNA was detected in all endometrial carcinoma and endometrial specimens and cell lines where the specific binding sites were detected, but not in adenomyosis or myometrial samples. The expression of Gn-RH receptor provides a possible point of attack for therapeutic approaches using Gn-RH analogs in this malignancy.

Adenocarcinoma↗
PubMed1994

Influence of atrial natriuretic peptide on cyclic nucleotides and amylase release in rat parotid salivary gland in vitro.

Atrial natriuretic peptide (ANP), sodium nitroprusside and hydroxylamine increased cGMP accumulation in rat parotid acinar cells both in the presence and absence of forskolin but in a different manner. On the other hand, ANP decreased forskolin-stimulated cAMP accumulation, although sodium nitroprusside and hydroxylamine had no effect on cAMP accumulation. Amylase release stimulated by forskolin, dibutyryl-cAMP or isoproterenol was depressed by ANP, whereas sodium nitroprusside and hydroxylamine did not evoke the inhibition of forskolin-stimulated amylase release. These results suggest that the inhibition of cAMP accumulation and of amylase release by ANP were not mediated via cGMP produced by guanylate cyclase-A.

Amylases↗
PubMed1994

Acute myelogenous leukemia in pregnancy: fetal blood sampling and early effects of chemotherapy.

This report documents the acute toxicity of anti-leukemic chemotherapy on the fetus in utero by umbilical blood sampling. A patient with acute myelocytic leukemia diagnosed at the 23rd week of gestation received combination chemotherapy, and carried the pregnancy to successful delivery at the 34th week. During the course of pregnancy, the fetal condition was evaluated by serial real time sonograms and umbilical blood sampling through cordocentesis. Fetal hematopoiesis was preserved against maternal chemotherapeutic agents, and no developmental abnormalities were observed. This is the first attempt to evaluate the acute effects of chemotherapeutic agents on the fetus in utero by real time umbilical cord sampling.

Adult↗
PubMed1994

Gynecologic tumors and symptoms in childhood and adolescence; 10-years' experience.

OBJECTIVES: The advancement of diagnostic imaging evaluations and the earlier occurrence of secondary sexual development prompted us to review our recent experience with genital tract tumors in children. METHODS: We analyzed data for 1938 patients aged less than 18 years who were referred to Gifu University School of Medicine-affiliated Hospitals for the years 1984 through 1993. RESULTS: Of the patients, 145 underwent surgical treatment. Vaginal tumor was seen in 5 patients; 1 endodermal sinus tumor, 1 sarcoma botyroides and 3 Gartner's duct cysts. Two patients with malignant tumor presented only with bloody vaginal discharge; recurrent abdominal pain due to vaginal obstruction was noted in 1 patient with the cyst. Ten had benign tumors in the vulva, presenting with a genital mass. Of 114 ovarian tumors, 3 were diagnosed by antenatal ultrasonographic examinations. Fifty-five had germ cell tumors, 33 had epithelial tumors, and 18 had stromal tumors. The most common symptom was abdominal pain and approximately one-third of girls who complained of abdominal pain had an ovarian tumor. Precocious puberty was noted in 4 girls with stromal tumor. Two of the 23 malignant tumors developed in the vagina and the others originated in the ovary. In 19 patients unilateral salpingo-oophorectomy or local excision was done in an attempt for reproductive organ conservation; 4 cases of advanced stage disease were treated with hysterectomy and/or bilateral salpingo-oophorectomy. Only 3 of the 23 patients with malignant tumor died within 4 years and others are free from disease. CONCLUSIONS: Genital symptoms, even common, alert us to the possibility of a genital tract tumor. The prompt and precise detection of either benign or malignant tumors in children may lead to cure and preservation of fertility with conservative surgery.

Adolescent↗
PubMed1994

Endocrine features in eutestosteronemic women with polycystic ovaries.

We attempted to assess the association between hyperandrogenemia and inappropriate gonadotropin secretion in women with polycystic ovaries (PCO). Thirty-one patients diagnosed as PCO by ultrasonography were divided into two subgroups: 17 with high serum total testosterone (T) level (> or = 0.5 ng/ml) and 14 with normal serum total T level (< 0.5 ng/ml). Both subgroups presented for the complaints of oligomenorrhea and/or hirsutism. The control group consisted of 15 women with regular ovulation for reference data collection. The PCO subjects with normal T, but not those with high T, revealed remarkable depletion of sex hormone binding globulin (SHBG), as compared with control. The PCO subject groups with high and normal serum T did not differ with respect to estrogen level, androgen level, follicle-stimulating hormone and prolactin levels, and SHBG concentration. Solely serum luteinizing hormone (LH) level was observed to be higher in those with high T, as typical features, than another subgroup or control. These data suggest that an increase in bioactive T as a result of decrease in serum SHBG or LH elevation may contribute to ovarian dysfunction in the patient with PCO.

Adult↗
PubMed1994

Possible evidence for estrone-specific binding sites in human uterine endometrial carcinoma.

Estrone (E1), a principal estrogen in postmenopausal women, may have profound consequences in the maintenance and progression of hormone-sensitive endometrial carcinoma. This study was designed to investigate the specific binding sites for E1 in the tumor and in the normal endometrium. The binding of [3H]E1 to the cytosolic fraction and KCl-soluble nuclear fraction from 3 endometrial carcinomas showed saturation kinetics with an apparent equilibrium dissociation constant of approximately 37 and 50 nM, respectively. The specific binding site of E1 was also found in 3 normal endometria. However, the binding capacity in the endometrial carcinoma increased to 1.5-fold of that in the normal endometrium. E2 did not affect [3H]E1 binding to any subcellular fraction from endometrial carcinoma specimens. These findings demonstrate the presence of specific binding sites for E1 in human endometrial carcinoma. The endometrial carcinoma growth may be mediated, at least in part, by E1 and its binding site interaction.

Binding Sites↗
PubMed1994

Lack of evidence for aromatase expression in human ovarian epithelial carcinoma.

It is controversial whether ovarian epithelial carcinoma possesses steroidogenic enzymes. We investigated aromatase expression in ovarian epithelial carcinoma, and compared it with the normal ovary and placenta. Samples were obtained from an ovarian carcinoma cell line SK-OV-3, ovarian tumour tissues from four patients with epithelial carcinoma and one patient with dysgerminoma. Aromatase enzymatic activity was measured in microsome fractions by quantitating 3H2O released from [1-3H] androstenedione and [3H]oestrone converted from [1,2,6,7-3H] androstenedione. Aromatase messenger ribonucleic acid (mRNA) was determined by reverse transcription-polymerase chain reaction (RT-PCR) using oligonucleotide primers synthesized according to the published human aromatase gene sequence. No aromatase activity was detected in either of two mucinous cystadenocarcinoma specimens or in SK-OV-3 cells, while aromatization proceeded with apparent Michaelis-Menten kinetics in the normal ovaries and placentas. The apparent Km value was 200 nmol/L for the ovary. Aromatase mRNA was detected in dysgerminoma, and the normal ovary and placenta, but not in any of three mucinous cystadenocarcinoma specimens, one serous cystadenocarcinoma specimen and SK-OV-3 cells. These results for both enzyme activity and gene expression suggest that the human ovarian epithelial carcinoma lacks aromatase. The demonstration of absence of aromatase gene expression raises the possibility that aromatase activity in ovaries bearing epithelial carcinoma may be associated with hyperplastic stromal rather than tumour cells.

Adenocarcinoma↗
PubMed1994

Expression of gonadotropin-releasing hormone receptor in human epithelial ovarian carcinoma.

We have previously demonstrated the presence of gonadotropin-releasing hormone (Gn-RH) messenger ribonucleic acid (mRNA) in epithelial ovarian carcinoma. In this study, the expression of Gn-RH receptor (Gn-RHR) was investigated in human ovarian carcinoma and human ovarian carcinoma cell line. Gn-RHR was determined by [3H]Gn-RH binding assay. Gn-RHR mRNA was determined by reverse transcription-polymerase chain reaction using oligonucleotide primers synthesized based on published human Gn-RHR sequence. Specific Gn-RH binding sites were shown to be present in plasma membrane isolated from five ovarian mucinous cystadenocarcinoma samples and one serous cystadenocarcinoma (Kd = 15.3 +/- 8.08 nmol/L). Gn-RHR mRNA was detected in four mucinous cystadenocarcinoma specimens, one serous cystadenocarcinoma, and SK-OV-3 cells, but not in white blood cells. These results suggest that Gn-RH may play an autocrine regulatory role in the growth of ovarian carcinoma.

Base Sequence↗
PubMed1994

Inhibition by prolactin of membrane-associated phosphatidylinositol kinase of human endometrial fibroblast.

Certain malignant tumors synthesize and secrete a putative peptide mitogen, which elicits a potent proliferative response in their supporting stromal cells. We recently demonstrated that prolactin (PRL) binds to human endometrial fibroblasts and inhibits mitogenicity of an endometrial carcinoma extract (Imai A, et al. Proc Soc Exp Biol Med 203:117-122, 1993). In this report, we have studied inhibitory regulation by PRL of phosphatidylinositol (PtdIns) kinase activity associated with plasma membranes isolated from human endometrial fibroblasts. Incubation of the isolated plasma membrane with [gamma-32P]ATP and exogenous PtdIns caused [32P]phosphate incorporation into PtdIns phosphate (PtdInsP); 95% of the 32P-labeled PtnInsP was accounted for by PtdIns 4-P. The PtdIns phosphorylation by membrane preparations was selectively stimulated in a dose-dependent manner by vanadate, in parallel with an elevated autophosphorylation of endogenous membrane proteins. Concomitant exposure of the membrane preparations to PRL led to a remarkable inhibition of the vanadate-responsive PtdIns phosphorylation and protein autophosphorylation. This inhibition was dependent on PRL dose, and half-maximal effect occurred at a concentration 1-10 nM of PRL. Degradation of the produced PtdInsP in the plasma membranes was not affected by PRL. Similar inhibition of PtdIns kinase activities were observed in membranes prepared from cells that had been pretreated in vivo with PRL prior to assay in vitro. These findings demonstrate that PtdIns kinase activity associated with protein autophosphorylation is suppressed by PRL in plasma membrane isolated from endometrial fibroblasts. The inhibition of vanadate-responsive PtdIns kinase by PRL suggests an involvement of this enzyme in the antimitogenic action of the hormone on human endometrial fibroblasts.

1-Phosphatidylinositol 4-Kinase↗
PubMed1993

Endodermal sinus tumor of the vagina in an infant: magnetic resonance imaging evaluation.

Endodermal sinus tumor is a rare and highly malignant lesion. This report documents the clinical findings and magnetic resonance imaging (MRI) of an uncommon case of the endodermal sinus tumor arising in the vagina of a 6-month-old infant. MRI was extremely accurate in delineating the possible extent and location of the vaginal lesion. This is the first report to demonstrate MRI of vaginal endodermal sinus tumor.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1993

Presence of gonadotropin-releasing hormone and its messenger ribonucleic acid in human ovarian epithelial carcinoma.

OBJECTIVE: The purpose of this study was to investigate the expression of gonadotropin-releasing hormone messenger ribonucleic acid and the presence of gonadotropin-releasing hormone in human ovarian carcinoma known to have gonadotropin-releasing hormone binding sites and to be affected by gonadotropin-releasing hormone analog. STUDY DESIGN: Human ovarian carcinomas surgically removed and human ovarian carcinoma cell lines were examined. Gonadotropin-releasing hormone was determined by a radioimmunoassay and a bioassay. Gonadotropin-releasing hormone messenger ribonucleic acid was determined by reverse transcription polymerase chain reaction using oligonucleotide primers synthesized according to the published human gonadotropin-releasing hormone sequence. RESULTS: Gonadotropin-releasing hormone was shown to be present in extracts of ovarian mucinous cystadenocarcinoma sample (0.8 +/- 0.12 pg/mg of protein) and ovarian adenocarcinoma cell line SK-OV3 (0.92 +/- 0.17 pg/mg of protein) but not in the normal ovary and placenta. Two of two extract samples from individual cases evoked dose-dependent phosphoinositide breakdown in rat granulosa cells similar to that caused by authentic gonadotropin-releasing hormone. Gonadotropin-releasing hormone messenger ribonucleic acid was detected in two of two mucinous cystadenocarcinoma specimens, one of one serous cystadenocarcinoma, and SK-OV3 cells but not in the dysgerminoma, mucinous cystadenoma, and normal ovary and placenta. CONCLUSION: The demonstration of gonadotropin-releasing hormone and its messenger ribonucleic acid raises the possibility that gonadotropin-releasing hormone may play an autocrine regulatory role in the growth of ovarian carcinoma.

Adenocarcinoma↗