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Y Endo

Publications and source records attributed to Y Endo.

At least 361 records · Page 20Linked to original sources

Incidence of hydatidiform mole in a Tokyo hospital: a 5-year (1989 to 1993) prospective, morphological, and flow cytometric study.

This prospective study reports the incidence of hydatidiform mole (HM) in a population of 13,510 pregnancies in a Tokyo hospital over a 5-year period between 1989 and 1993. During this period all "products of conception" from first- and second-trimester abortions were histologically reviewed, and 76 hydropic placentas were retrieved and analyzed by flow cytometry (FCM). Of 23 specimens originally diagnosed as complete hydatidiform mole (CM), 21 were diploid, and two were aneuploid (nontriploid/tetraploid). Of 22 partial hydatidiform moles (PMs), 20 were triploid, and two were diploid. Of 31 hydropic abortions (HAs), 20 were diploid, nine were triploid, one was tetraploid, and one was aneuploid. As to the correlation between morphology and data of FCM, two PMs were reclassified as HA, and eight HAs as PM, giving a ratio of 1 CM to 1.22 PM (23:28 cases). The incidence of HM was 1:265 pregnancies, (CM, 1:587; PM, 1:483). Only one case (3.6%) of PM was suspected clinically. One specimen of persistent disease occurred following a diploid CM. In our retrospective histological and FCM study in which 172 cases diagnosed as HM were retrieved from surgical pathology files between 1981 and 1991, there were 129 CMs and 43 PMs (CMs:PMs = 3:1). These findings indicate that PM is a common but underdiagnosed condition. Almost all studies in the literature may have severely underreported the incidence of PM. It is suggested that during routine delivery and pathology examination only the most florid PMs are recognized, whereas most with subtler changes go undiagnosed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Atypical polypoid adenomyomas of the uterus.

We performed a clinicopathological immunohistochemical, ultrastructural, and flow cytometric study on six cases of atypical polypoid adenomyoma of the uterus including one with an adenocarcinoma within it. The tumours occurred in nulliparous women aged 22-48 years (average, 33.0 years); three arose in the uterine corpus, and three in the endocervix. Histologically, they were composed of endometrial glands admixed with a stromal component of interlacing bundles of smooth muscle cells. The glands exhibited varying degrees of architectural and cytological atypia. Most of the stromal cells showed strong staining for HHF35, alpha-smooth muscle actin, and vimentin, and some cells contained desmin. Electronmicroscopy, in one case, confirmed the presence of a well-differentiated smooth muscle component. The stromal component may arise as a result of extensive metaplasia of endometrial stromal cells. Uninvolved endometrium showed ciliated cell metaplasia in three patients, and atypical complex hyperplasia in two. One patient had a well-differentiated adenocarcinoma of endometrioid type arising in an endocervical atypical polypoid adenomyoma. All tumours had a diploid DNA content and relatively small S phase fraction (average, 6.23%). The follow-up periods ranged from 4 to 42 months (average, 13.5 months), and all patients were alive and well. Although the histogenesis of atypical polypoid adenomyoma of the uterus remains uncertain, it is suggested that it may arise because of oestrogen-related factors.

Adenomyoma↗

Monoclonality of normal human colonic crypts.

The monoclonality of human colonic crypts was demonstrated by human androgen receptor (HUMARA) gene assay following application of the crypt isolation method. DNA was extracted from an isolated single crypt, Hpa II digestion was performed before polymerase chain reaction (PCR) by primers spanning the HUMARA exon 1 region. The PCR product of a single crypt clearly showed allelic exclusion based on methylation status, while PCR product from a mixture of 40 crypts or colonic mucosa as a whole that included epitheliums and interstitial connective tissue had two bands. This method will facilitate the non-isotopic analysis not only of tumor clonality, but also of the normal structures derived from a single progenitor cell.

Base Sequence↗

Effects of macrophage depletion on the induction of histidine decarboxylase by lipopolysaccharide, interleukin 1 and tumour necrosis factor.

1. Our previous work has shown that injection into mice of lipopolysaccharide (LPS) and the cytokines interleukin 1 (IL-1) and tumour necrosis factor (TNF) induces histidine decarboxylase (HDC), the enzyme forming histamine, in various tissues such as liver, lung, spleen and bone marrow, but not in the blood. The induction of HDC also occurs in nude mice and mast cell-deficient mice. On the other hand, haematopoietic cytokines such as IL-3, granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage CSF (GM-CSF) only induce HDC in the haematopoietic organs, i.e. bone marrow and spleen. In the present study, the effect of macrophage depletion on the induction of HDC was examined. 2. On day 1 after a single intravenous injection of a macrophage depletor (liposomes encapsulating dichloromethylene diphosphonate, which is toxic when ingested into macrophages), macrophages were almost completely depleted in the liver and reduced by about 50% in the spleen and bone marrow, but not significantly affected in the lung. On day 3, the degrees of the depletion were similar to those of day 1. In the spleen, macrophages were depleted in the red pulp, and there was a structural destruction. 3. In macrophage-depleted mice, the induction of HDC by LPS, IL-1 alpha or TNF-alpha was not impaired in the liver, and was potentiated in the lung and bone marrow. The induction of HDC was decreased only in the spleen at day 3. 4. HDC was not induced by LPS in the spleen of the adult rat, which is correspondingly inactive in haematopoiesis.5 These results indicate that the major cells in which HDC activity is induced in response to LPS, IL-1 and TNF are not circulating granulocytes, circulating monocytes, T cells derived from thymus, mast cells or phagocytic macrophages. Based on these results, we discuss the possibility that the major cells in which HDC was induced in non-haematopoietic and haematopoietic organs were endothelial cells and haematopoietic precursor cells respectively.

Animals↗

Renal lesion of type Ia glycogen storage disease: the glomerular size and renal localization of apolipoprotein.

In order to investigate the glomerular size and renal localization of apolipoprotein in type Ia glycogen storage disease, a renal biopsy was performed in two proteinuric patients. Histopathological examination of the biopsy specimens revealed focal sclerotic glomerular sclerosis in both patients. The mean glomerular area was 21.6 +/- 11.6 x 10(3) microns 2, indicating enlargement of the glomeruli. Immunohistochemical staining of the specimens for apolipoprotein showed localization of apolipoprotein AI on the inner side of the glomerular capillary wall, and in proximal tubular epithelial cells. In one patient with a history of several episodes of hypoglycemia, treatment with corn starch improved the carbohydrate and lipid metabolic profile and reduced the daily urinary protein excretion from 2.23 to 0.5 g. These results suggest that focal sclerotic glomerular lesions associated with type Ia glycogen storage disease may be related to disorders of carbohydrate and lipid metabolism.

Adult↗

[Inhibition of tumor cell metastasis in chick embryo by beta 1 integrin antisense oligonucleotide].

The antimetastatic effect of integrin beta 1 subunit antisense oligonucleotide on human fibrosarcoma cell (HT-1080) in chick embryo was examined. Phosphorothioate modified antisense oligonucleotide (B1-1) was designed to hybridize specifically to integrin beta 1 subunit mRNA. Pretreatment of HT-1080 cells with B1-1 decreased the metastatic ability in chick embryonic liver and lung, while B1-1 showed no toxicity to HT-1080 nor chick embryo. Western blot analysis showed a reduction of the amount of cell surface integrin beta 1 subunit. B1-1 also inhibited HT-1080 attachment to laminin and fibronectin. These results indicate that the inhibition of tumor cell attachment by antisense oligonucleotide might be a good approach to the prevention of cancer metastasis.

Animals↗

[Comparison of the pattern of integrin expression between primary tumors and liver metastasis of gastric and colorectal cancers].

To investigate the interrelationship between integrin VLA3 overexpression and liver metastasis, immunohistochemical studies of VLA3 were made in 73 cases of gastric cancer (66 cases without liver metastasis, 7 cases with liver metastasis) and 15 cases of colorectal cancer (3 cases without liver metastasis, 12 cases with liver metastasis). The rate of integrin VLA3 expression in 69 primary gastric and colorectal cancers without liver metastasis was 41%, that was higher than that (0%) in the 19 primary tumors of gastric and colorectal cancers with liver metastasis. In contrast, the positive rate for integrin VLA3 staining in 19 cases involving liver metastasis of gastric and colorectal cancers was 58% (11/19), which was higher than that (0%) in primary tumors. These findings suggest that VLA3 may play an important role in the process of liver metastasis of gastric and colorectal cancers.

Colorectal Neoplasms↗

[Chronic subdural hematoma with bleeding tendency; clinical analysis of 11 surgical cases].

Eleven patients with chronic subdural hematoma (CSDH) with bleeding tendency (BT) were surgically treated in the last 12 years. To study the clinical problem of CSDH with BT, 11 surgical cases were divided into 3 groups, Group A; CSDH with primary BT (1 case of hemophilia A), Group B; CSDH with BT secondary to a basic disease (3 cases of leukemia, 2 cases of malignant tumor with DIC, 1 case of chronic renal failure and 1 case of liver cirrhosis), Group C; CSDH with BT by anticoagulants (warfarin) (2 cases of replacement of mitral valve, 1 case of A-C bypass). Evacuation of the hematoma was performed by means of one or two burr holes with irrigation of the hematoma cavity and a drainage tube was placed in the subdural space. The outcome was excellent in Groups A and C. In Group B, two patients with DIC due to gastric cancer and prostatic cancer died, and 3 patients with leukemia recovered dramatically from CSDH, but the poor course of the disease itself resulted in death. The outcome of other patients in Group B was excellent. Since CSDH with BT is often fatal, those patient had usually been treated conservatively. However, from this analysis, we stress that CSDH with BT should be surgically treated after checking the blood conditions carefully to determine whether or not the patient has need for surgery.

Adult↗

Ca2+ ionophore-induced apoptosis on cultured embryonic rat cortical neurons.

The neurotoxicity of ionomycin, a Ca2+ ionophore, was investigated in cultured cortical neurons from embryonic rats. While about 90% of neurons survived 2 h after exposure to ionomycin, the surviving neurons had decreased by about 30 to 40% at 16 h. Both RNA and protein synthesis inhibitors blocked this neurotoxicity. Furthermore, c-Fos immunoreactive neurons increased not only in number but also in the intensity of immunoreactivity. These results suggest that ionomycin-induced neuronal cell death is an active process which requires de novo transcription and translation. In addition, the ultrastructural changes, such as shrinkage of cell body, compaction of nucleus, condensation of chromatin, and membrane blebbing, were observed by electron microscopy. These morphological changes are indexes of apoptosis. Furthermore, DNA fragmentation, a biochemical marker of apoptosis, was also observed. All the results suggest that ionomycin-induced neuronal cell death is apoptotic.

Animals↗

Distribution of angiotensinogen in diseased human hearts.

Extrahepatic synthesis and localization of angiotensinogen (ATN) have been described in animals, thus establishing the tissue renin-angiotensin (RA) system. However, there had been no reports of tissue RA systems in human organs, including the heart. In earlier, we have reported the possibility of ATN synthesis in the human heart using ribonuclease protection assay system. ATN mRNA was detected not only in the liver, but also in both the atrial and ventricular heart tissues, suggesting that ATN is synthesized in the human heart. In this report, we looked for the distribution of ATN in diseased human heart. Northern blot hybridization of cDNA with total RNA extracted from human liver, brain, kidney, atrial and ventricular tissues revealed that ATN mRNA exists in cardiac ventricule. Immunohistochemical studies using a specific antibody to ATN revealed a stronger reaction in the endocardial layer of the human left ventricle, than in the epicardial layer, and intense immunoreactivity in the conduction system and right atrium. This distribution pattern was similar to that of human atrial natriuretic peptide (hANP), which functions a smooth muscle relaxant. Double immunostaining of ATN and hANP demonstrated that all myocytes in the right atrium had immunopositive reactions to ATN, hANP or both of ATN and hANP. Double immunoelectron staining enabled us to show more detailed localization of ATN and hANP; hANP only existed in the specific granules and ATN existed in the myofibril, but not in the granule. Furthermore, our experiments provide evidence of ATN in healthy human hearts and also reveal a widespread immunopositive reaction for ATN in the left ventricle of diseased hearts.

Angiotensinogen↗

The ribosomal RNA identity elements for ricin and for alpha-sarcin: mutations in the putative CG pair that closes a GAGA tetraloop.

alpha-Sarcin is a ribonuclease that cleaves the phosphodiester bond on the 3' side of G4325 in 28S rRNA; ricin A-chain is a RNA N-glycosidase that depurinates the 5' adjacent A4324. These single covalent modifications inactivate the ribosome. An oligoribonucleotide that reproduces the structure of the sarcin/ricin domain in 28S rRNA was synthesized and mutations were constructed in the 5' C and the 3' G that surround a GAGA tetrad that has the sites of toxin action. Covalent modification of the RNA by ricin, but not by alpha-sarcin, requires a Watson-Crick pair to shut off a putative GAGA tetraloop. Either the recognition elements for the two toxins are different despite their catalyzing covalent modification of adjacent nucleotides in 28S rRNA or there are transitions in the conformation of the alpha-sarcin/ricin domain in 28S rRNA and one conformer is recognized by alpha-sarcin and the other by ricin A-chain.

Base Sequence↗

Expression of type-IV collagenases in human tumor cell lines that can form liver colonies in chick embryos.

Chick embryo has been used as a model system for evaluating the metastatic potential of tumor cells. We have previously demonstrated that expression of the tissue inhibitor of matrix metalloproteinase-I (TIMP-I) gene can suppress liver colonization of tumor cels in chick embryo, probably by inhibiting the activity of matrix metalloproteinases (MMP) produced by tumor cells. In an attempt to identify MMP associated with liver colonization, we examined 24 human tumor cell lines for their potential to form metastatic colonies in chick-embryo liver after the cells had been inoculated into the chorioallantoic membrane (CAM) vein. We compared the results with the mRNA expression of MMP (MMP-I, MMP-2, MMP-3, MMP-9) studied previously. Three of 8 cell lines from mesenchymal tumors (fibrosarcoma HT1080, osteosarcomas SK-ES and MNNG/HOS) and 2 of 16 cell lines from epithelial tumors (gastric carcinoma KKLS and bladder carcinoma T24) proliferated in the livers. MMP-2 and MMP-9 were the enzymes whose transcripts were more frequently expressed in these 5 metastatic cell lines (MMP-1; 2/5, MMP-2; 4/5, MMP-3; 0/5, MMP-9; 3/5), but other cell lines that did not form liver colonies expressed the transcripts at lower frequency (MMP-2; 7/19, MMP-9; 3/19). Although either or both MMP-2 and MMP-9 transcripts were expressed in 4 of the 5 metastatic cell lines, they were undetectable in T24 cells. However, induced expression of both enzymes was detected by immunostaining in the T24 cells colonized in the liver. Thus, type-IV collagenases expressed by tumor cells may play a role in facilitating colonization in chick embryos.

Animals↗

Molecular cloning of murine pig-a, a gene for GPI-anchor biosynthesis, and demonstration of interspecies conservation of its structure, function, and genetic locus.

Many membrane proteins are anchored to the cell membrane by glycosylphosphatidylinositol (GPI). The core structure and biosynthesis of the GPI anchor are well conserved in eukaryote cells. We previously cloned a human PIGA gene that participates in GPI anchor biosynthesis. We have now cloned complementary and genomic DNA of Pig-a, the murine homologue of PIGA, and compared its function and gene structure with those of PIGA. The deduced amino acid sequence of mouse PIG-A is 88% identical with that of human PIG-A. Transfection of Pig-a cDNA complemented the defects of both a PIG-A-deficient murine cell line and a PIG-A-deficient human cell line, demonstrating that functions of mouse and human PIG-A are conserved. Like human PIGA, the chromosomal Pig-a gene has six exons and spans approximately 16 kb. Moreover, Pig-a was mapped to X-F3/4, which is syntenic to human Xp22.1, where PIGA is located. Thus, murine Pig-a provides a good animal model to study paroxysmal nocturnal hemoglobinuria, a disease caused by a somatic mutation of PIGA. Database analysis demonstrated that a yeast gene, SPT14, is homologous to Pig-a and PIGA and that these genes are members of a glycosyltransferase gene family.

Amino Acid Sequence↗

Adrenalectomy increases local cerebral blood flow in the rat hippocampus.

The present study examined the effect of glucocorticoid manipulations on local cerebral blood flow in the hippocampus. We measured local cerebral blood flow in the hippocampus at 1-h intervals over a 1-day period in freely moving rats, by means of the H2 clearance method, before and after sham adrenalectomy, adrenalectomy or adrenalectomy with corticosterone replacement. We also measured local cerebral blood flow in the prefrontal cortex before and after adrenalectomy. Four weeks after the adrenalectomy, hippocampal blood flow at each time of day was an average of 47% greater than before the operation, showing diurnal variation as before. After the sham adrenalectomy or adrenalectomy with corticosterone replacement, hippocampal blood flow did not change significantly with respect to either its level or its diurnal variation. Local cerebral blood flow in the prefrontal cortex increased by only 19% after adrenalectomy. The present study demonstrates that adrenalectomy causes a remarkable increase in hippocampal blood flow, probably due to a lack of corticosterone.

Adrenalectomy↗

Studies of effects of anticancer agents in combination with/without hyperthermia on metastasized human bladder cancer cells in chick embryos using the polymerase chain reaction technique.

Cultivated T24 cells derived from a human bladder cancer were inoculated into the chorioallantoic membrane vein of chick embryos. Hyperthermic treatment was performed following injection of anticancer agents 3 days after the inoculation of the T24 cells. DNA samples were obtained from the livers of the chick embryos, and the polymerase chain reaction technique was used to amplify a DNA fragment specific to the human beta-globin gene. The Southern hybridization method was used to evaluate the inhibitory effects of anticancer agents in combination with/without hyperthermia on T24 cells metastasized to the liver. The hyperthermia exerted an inhibitory effect on the growth of the T24 cells in the livers of the chick embryos, and this was dependent on the thermal dose. The antitumor effects of hyperthermia performed at 42.5 degrees C for 20 min and at 43.0 degrees C for 10 min were evidenced by 69.2% an 82.0% inhibition of the growth of the metastasized T24 cells, respectively, as compared with the growth of untreated T24 cell. Hyperthermia performed at 42.5 degrees C for 10 min alone produced 26.7% tumor growth inhibition, and these conditions for hyperthermia were subsequently used as a criterion for evaluating the effects of its combination with various anticancer agents. Adriamycin (20 micrograms/egg) alone, mitomycin C (10 micrograms/egg) alone, carboplatin (10 micrograms/egg) alone, and cisplatin (10 micrograms/egg) alone produced 13.5%, 58.9%, 27.3%, and 29.1% tumor growth inhibition, respectively. Adriamycin and mitomycin C applied in combination with hyperthermia showed additive inhibitory effects on the growth of the metastasized T24 cells in this chick embryo model.

Animals↗

Immunohistochemical expression of manganese superoxide dismutase in hepatocellular carcinoma, using a specific monoclonal antibody.

The expression of manganese superoxide dismutase (Mn-SOD) was studied immunohistochemically, using a specific monoclonal antibody, in surgically resected hepatocellular carcinoma (HCC) and noncancerous tissues from 47 patients (2 with well-differentiated HCC, 36 with moderately differentiated HCC, 8 with poorly differentiated HCC, and 1 with undifferentiated carcinoma). Cancer cells in 44 patients (93.6%) were positive for Mn-SOD. The staining pattern of cancer cells was mostly homogeneous in well-differentiated HCC, whereas it was heterogeneous in poorly differentiated HCC. Moreover, strongly positive immunoreactivity was observed in noncancerous liver tissues in all patients, especially in normal hepatocytes surrounding HCC, regenerative small hepatocytes in the tumor boundary, and mononuclear inflammatory cells in the necroinflammatory lesions. The positive immunoreactivity for Mn-SOD in patients with HCC appears to reflect increased production of the enzyme protein.

Adult↗