[Transferrin receptor and erythropoiesis].
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Erythropoiesis↗
Biomedical subjects
Y Kohgo
Publications and source records attributed to Y Kohgo.
Activation of PPARgamma inhibits cell growth and induces apoptosis in human gastric cancer cells.
We investigated the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) and the role of PPARgamma in cell growth in human gastric cancer cells. Reverse transcription-polymerase chain reaction, Northern blot and Western blot analyses showed that a human gastric cancer cell line, MKN45, expressed PPARgamma mRNA and protein. Luciferase assay in MKN45 cells showed that troglitazone, a selective ligand for PPARgamma, transactivated the transcription of a peroxisome proliferator response element-driven promoter. Troglitazone or pioglitazone, selective ligands for PPARgamma, inhibited the growth of MKN45 cells in a dose-dependent manner. Co-incubation of MKN45 cells with troglitazone induced DNA ladder formation. These results suggest that human gastric cancer cells express PPARgamma and that activation of PPARgamma inhibits cell growth and induces apoptosis in gastric cancer cells.
Acyl-CoA Oxidase↗
Stimulation of gastric acid secretion by centrally administered orexin-A in conscious rats.
Orexins are novel neuropeptides that are localized in neurons within the lateral hypothalamus and regulate feeding behavior. The lateral hypothalamus also plays an important role in the central regulation of gut function. We therefore hypothesized that orexins might be involved in the central control of gastric acid secretion. To address this question, we examined the effect of central injection of orexins on gastric acid secretion in rats. Intracisternal injection of synthetic orexin-A but not orexin-B dose-dependently stimulated acid secretion while intraperitoneal administration of orexin-A failed to stimulate acid secretion. Vagotomy or atropine abolished the action by central orexin-A. These data suggest for the first time that orexin-A may act in the brain to stimulate gastric acid secretion by modulating the vagal system. Considering its stimulatory action on feeding, we hypothesize here that orexin-A is a candidate mediator of cephalic phase gastric secretion.
Animals↗
Localization of syndecan-1 in human gastric mucosa associated with ulceration.
Syndecans, cell surface heparan sulphate proteoglycans, are known to function as cell adhesion molecules and as a co-receptor for heparin-binding growth factors that have important roles in tissue homeostasis and repair, but the localization of syndecans in gastric mucosa and their role in gastric ulcer healing are not known. The licalization of syndecan-1, a subfamily protein of syndecans expressed on epithelial cells, was studied in 12 surgically resected human stomachs containing an ulcer or early scar tissue. Localization of syndecan-1 was detected both by immunohistochemistry and by in situ hybridization In non-ulcer sites of gastric mucosa, syndecan-1 protein was expressed at the basolateral surface of foveolar epithelial cells and the cells of intestinal metaplasia, and at the cell surface of stromal plasma cells. In addition, positive dots of syndecan-1 were found in the cytoplasmic area of parietal cells. Foveolar epithelial cells at active stage ulcer margins showed nearly the same intensity of staining as those at non-ulcer site mucosa. By contrast, enhanced staining was obtained in elongated regenerative foveolar cells at the healing ulcer margins and the early scar tissues. The migrating cells on ulcer floors also expressed syndecan-1 protein. The expression sites of syndecan-1 mRNA mostly coincided with those of syndecan-1 protein. These results suggest that syndecan-1 participates in cell adhesion mainly at the foveolar epithelium and plays a role in the healing of gastric ulcers by interacting with heparin-binding growth factors.
Gastric Mucosa↗
Epithelial cell proliferation and gene mutation in the mucosa of gallbladder with pancreaticobiliary malunion and cancer.
The significant association between pancreaticobiliary malunion (PBM), especially undilated-type PBM, and a high risk of gallbladder cancer is known. Reflux and stasis of pancreatic juice induce various epithelial changes in the gallbladder. Recently, epithelial hyperplasia of the gallbladder was shown to be significantly and frequently associated with undilated-type PBM, and it is suggested that the majority of epithelial hyperplasia may exist at birth or be acquired in early childhood, and thereafter present throughout the lives of PBM patients. Cell kinetic studies demonstrated a significant stepwise increase in cellular proliferative activity from normal gallbladder mucosa, through epithelial hyperplasia to cancer. Epithelial hyperplasia with increased proliferative activity may predispose the mucosa to mutational events, thereby increasing cancer risk in PBM patients. K-ras mutations were frequently detected in gallbladder cancer in PBM patients and in epithelial hyperplasia as well. Epithelial hyperplasia is demonstrated to be an important premalignant lesion of gallbladder cancer. A multistep process of carcinogenesis as a consequence of multiple genetic alterations of oncogenes and tumor suppressor genes has been demonstrated in various organs; however, there is limited information on the molecular mechanism in gallbladder carcinogenesis with PBM. Recent findings support the idea that epithelial hyperplasia plays an important role in gallbladder carcinogenesis with PBM and also support the concept that neoplastic development in gallbladder with PBM also evolves through a multistep process associated with hyperproliferation and genetic alterations.
Adenocarcinoma↗
An inverse correlation between serum leptin levels and hemoglobin A1c in patients with non-insulin dependent diabetes mellitus.
We measured serum leptin concentrations in 70 patients with diabetes mellitus to investigate the relationship between serum leptin levels and glycemic control. A positive correlation between serum leptin levels and body mass index or plasma insulin was obtained as reported previously. The present study also demonstrated an inverse association of serum leptin levels with hemoglobin A1c (HbA1c). Multiple regression analysis revealed that HbA1c was an independent determinant of serum leptin levels. These results suggest that HbA1c may be a factor to influence serum leptin levels and that hyperglycemia for a long period or poorly controlled diabetes may reduce leptin levels.
Adult↗
Proline-rich antimicrobial peptide, PR-39 gene transduction altered invasive activity and actin structure in human hepatocellular carcinoma cells.
PR-39 is an endogenous proline-rich antimicrobial peptide which induces the synthesis of syndecan-1, a transmembrane heparan sulphate proteoglycan involved in cell-to-matrix interactions and wound healing. Previously, we revealed that the expression of syndecan-1 was reduced in human hepatocellular carcinomas with high metastatic potential and speculated that syndecan-1 played an important role in inhibition of invasion and metastasis. It is assumed that a modification of this process with PR-39 and syndecan-1 may result in a new strategy by which it can inhibit the invasion and metastasis. Therefore, we transduced a gene of PR-39 into human hepatocellular carcinoma cell line HLF, which shows a low expression of syndecan-1 and a high in vitro invasive activity, and examined whether this procedure could reduce the invasive activity of tumour cells. In two transfectants with PR-39 gene, the syndecan-1 expression was induced and the invasive activity in type I collagen-coated chamber was inhibited. Moreover, these transfectants showed the suppression of motile activity assayed by phagokinetic tracks in addition to the disorganization of actin filaments observed by a confocal imaging system. In contrast, five transfectants with syndecan-1 gene in the HLF cells revealed suppression of invasive activity but did not alter the motile activity and actin structures of the cell. These results suggest that PR-39 has functions involved in the suppression of motile activity and alteration of actin structure on human hepatocellular carcinoma cells in addition to the suppression of invasive activity which might result from the induction of syndecan-1 expression.
Actin Cytoskeleton↗
Case report: mucinous cholangiocarcinoma featuring a multicystic appearance and periportal collar in imaging.
A case of mucinous cholangiocarcinoma (CC), a rare histological type of CC, featuring unusual images is reported. The patient was hospitalized because of acute development of jaundice and fever. Computed tomography demonstrated multiple cystic lesions in the liver and a band-like low density area parallel to the intrahepatic portal vein, a so-called 'periportal collar'. Endoscopic cholangiography revealed a stricture of the hepatic duct with slight upstream dilatation. Cytology of the bile juice and fine-needle aspiration of the cystic lesion in the liver disclosed mucinous carcinoma. The patient died of multiorgan failure 3 weeks after admission. The autopsied liver showed that multiple mucus lakes were lined with adenocarcinoma cells and signet ring cells were floating in the mucus lakes. The cancer cells had spread along the portal tract and invaded into the hepatic parenchyma.
Adenocarcinoma, Mucinous↗
Genetic polymorphism of aldehyde dehydrogenase 2 in patients with upper aerodigestive tract cancer.
BACKGROUND: Alcohol consumption is one of the major risk factors of the upper aerodigestive tract (UADT) cancers, and combined cancers are frequently discovered in the patients with UADT cancer. The association between esophageal cancer and alcohol-related metabolizing enzymes is well studied, but only a few examinations about the association between head and neck cancer and the enzymes were performed. METHODS: Fifty-two patients with UADT cancer (head and neck cancer in 25, esophageal cancer in 19, and multiple cancers in 8) were examined in the alcohol habit and in the polymorphisms of aldehyde dehydrogenase 2 (ALDH2) and cytochrome P-4502E1. RESULTS: Patients with multiple cancers had significantly higher ethanol consumption than the other two groups (p < 0.001). The frequency of ALDH2*1/2*2 heterozygote was significantly lower (p = 0.009) in patients with head and neck cancer (5/25) than patients with esophageal cancer (11/19). The allele frequency of P-4502E1 did not show a significant difference between the groups (p = 0.700). CONCLUSIONS: These results demonstrated the difference in the frequency of ALDH2 heterozygote between the patients with esophageal cancer and patients with head and neck cancer.
Aged↗
Increase of serum des-gamma-carboxy prothrombin in alcoholic liver disease without hepatocellular carcinoma.
The purpose of this study is to determine serum des-gamma-carboxy prothrombin (DCP) levels in benign liver diseases by a new sensitive method, and to demonstrate the elevation of serum DCP in alcoholic liver disease (ALD) without hepatocellular carcinoma (HCC). Median values of serum DCP were 16.2 mAU/ml (range: 3.2 to 1570 mAU/ml) in ALD and 16.7 mAU/ml (1.2 to 75.4 mAU/ml) in viral liver disease (VLD). Using the cut-off value of 40 mAU/ml as a tumor marker for HCC, 21% (11/52) was positive in ALD and 2% (1/57) was positive in VLD (p = 0.0014, Fisher's exact probability test), and 27% (9/33) was positive in alcoholic liver cirrhosis and 3% (1/39) was positive in viral liver cirrhosis (p = 0.0042, Fisher's exact probability test). The positive rate of DCP was significantly (p < 0.001, Spearman's rank correlation test) correlated with the severity of liver disease in ALD. Serum vitamin K level was not decreased in cases with ALD. In a demonstrable case, serum DCP was decreased after abstinence and was increased again after the beginning of ethanol intake, suggesting the involvement of ethanol to the elevation of serum DCP in ALD. In conclusion, serum DCP was significantly elevated in ALD, compared with VLD, although the mechanism of the elevation of DCP was not clarified. Ethanol intake may act, in part, on the increase of serum DCP in ALD.
Aged↗
alpha-Fetoprotein-producing adenocarcinoma of the pancreas presenting focal hepatoid differentiation.
We report a rare case of pancreatic carcinoma producing alpha-fetoprotein (AFP), showing focal hepatoid differentiation in metastatic lymph nodes. A 65-yr-old female was admitted because of abdominal pain. The serum AFP was measured at 16,170 ng/mL. Radiological examinations revealed a mass measuring 6 cm in diameter in the body and tail of the pancreas. A right supraclavicular lymphadenopathy was found and biopsied. Light microscopy showed a tumor consisting of a portion of a hepatoid area and well-differentiated adenocarcinoma, which was suggestive of a hepatoid adenocarcinoma. Immunohistochemical analysis showed that the tumor cells expressed AFP, alpha 1-antitrypsin (AT) and albumin. Although the pathological diagnosis of the primary pancreatic tumor was not obtained, this appears to be the first case of hepatoid adenocarcinoma of the pancreas.
Adenocarcinoma↗
[Histological findings of TTV-positive non-B non-C chronic hepatitis patients].
TT virus has been reported in association with patients with acute and chronic liver disease of unknown etiology. In order to estimate the pathogenesis of TTV, we investigated the liver histology in the patients of TTV-positive chronic hepatitis. The findings frequently observed in TTV-DNA positive cases were changes in liver parenchyma such as focal necrosis, hepatocyte degeneration or fatty change of various degree. On the other hand, degree of chronic inflammation in portal areas such as lymphocyte infiltration, piecemeal necrosis or fibrosis were relatively mild, which might suggest the good prognosis in TTV-positive cases. However, we could not find any differences in liver histology between TTV positive and negative patients.
Adult↗
Discordant expression of myeloid antigens and myeloperoxidase in a case of t(8;21) positive AML expressing CD7.
We describe a case of acute myeloid leukemia (AML) showing myeloperoxidase (MPO)-positive and myeloid antigens negative. Although the leukemic cells showed few granules in May-Grünwald Giemsa staining, cytochemical MPO staining revealed that most of the blast cells strongly reacted with MPO. The leukemic cells did not express myeloid antigens (CD13, CD33), nor B-lymphoid or T-lymphoid antigens on the cell surface using flow cytometry, however. The cells did express CD34 and CD7. Discordant expression of MPO and myeloid antigens was also confirmed by electron microscopic MPO staining and by immunocytochemistry using a streptoavidin-biotin alkaline phosphatase labeling technique. Cytogenetic studies showed 46, XX, t(8;21) (q22;q22), del (9) (q22) in the bone marrow cells. In addition, AML1/ETO chimeric mRNA was detected from these cells. We summarize eight reported cases of MPO positive and myeloid antigens negative AML. Five of nine cases including our case had the same chromosomal abnormality of t(8;21) (q22;q22) and showed better prognosis than the other cases.
Adult↗
Esophageal tunnel formation after endoscopic variceal sclerotherapy.
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Diagnosis, Differential↗
Proliferative potential and K-ras mutation in epithelial hyperplasia of the gallbladder in patients with anomalous pancreaticobiliary ductal union.
BACKGROUND: Recent studies have shown that anomalous pancreaticobiliary ductal union (APBD) is an important risk factor for the development of gallbladder carcinoma. Epithelial hyperplasia of the gallbladder is one of the characteristic changes, but it is not clear whether epithelial hyperplasia is a premalignant lesion that could lead to cancer in APBD patients. METHODS: Twenty-four APBD patients were classified into two types: patients with bile duct dilation (dilated type) (n 13) and patients without dilation (undilated type) (n = 11). Resected gallbladders obtained from APBD patients and control patients without APBD were examined histologically and with immunohistochemical techniques for the detection of p53 and Ki-67 (as a cell proliferation marker). K-ras mutations were examined using polymerase chain reaction-restriction fragment length polymorphism and direct DNA sequence analysis. The patients were also classified, according to extent of epithelial hyperplasia, as having high grade or low grade hyperplasia. RESULTS: Fifteen (63%) of 24 APBD patients had epithelial hyperplasia of the gallbladder, whereas no patients without APBD exhibited this lesion. The incidence of epithelial hyperplasia was significantly higher in the gallbladders of undilated-type APBD patients (91%) than in those of dilated-type patients (38%) (P < 0.01). Three of 24 APBD patients (13%) had gallbladder carcinoma, and 2 of the 3 gallbladder carcinomas (67%) were accompanied by diffuse epithelial hyperplasia of the gallbladder. Among 21 nonneoplastic gallbladders, diffuse epithelial hyperplasia was observed in all (100%) of the undilated-type APBD and in 4 (33%) of 12 dilated-type APBD (P < 0.001). High grade hyperplasia was observed in 7 of 11 patients (64%) with undilated-type APBD and 2 of 13 patients (15%) with dilated-type APBD (P < 0.05). The incidence of high grade hyperplasia increased with age among patients older than 35 years. Ki-67 labeling index (LI) was significantly higher in hyperplastic mucosa than in control gallbladder mucosa. High grade hyperplasia had a significantly higher Ki-67 LI than low grade hyperplasia (P < 0.001). Two (22%) of 9 high grade hyperplasia cases had K-ras mutations, whereas none of 6 low grade hyperplasia cases had. The types of K-ras mutations in codon 12 were GTT (Val) and GAT (Asp) in each case of hyperplasia; these were identical to those of concomitant carcinomas. Neither hyperplastic nor normal mucosa exhibited p53 overexpression. CONCLUSIONS: The results of this study suggest that hyperplasia of the gallbladder mucosa in APBD patients is an early change that, because of the increased proliferative activity and presence of K-ras mutations, could be considered a premalignant lesion of the gallbladder. An increased cell population of epithelial hyperplasia may predispose the mucosa to mutational events, resulting in an increased risk for the development of gallbladder carcinoma in APBD patients.
Adolescent↗
Acarbose-induced hepatic injury.
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Acarbose↗