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Biomedical subjects

M Omori

Publications and source records attributed to M Omori.

At least 55 records · Page 3Linked to original sources
PubMed1998

Transforming growth factor-beta1 in plasma and liver of children with liver disease.

Although several liver diseases of childhood, particularly biliary atresia (BA) and cystic fibrosis (CF) liver disease (CFLD) are characterized by hepatic fibrosis, the pathogenesis of this process is incompletely understood. The cytokine transforming growth factor-beta1 (TGF-beta1) has been implicated in hepatic fibrosis in experimental animals, in which both the hepatic expression and plasma concentration of this cytokine are increased. The objective of our study was to determine whether there are similar alterations of TGF-beta1 in patients with hepatic fibrosis secondary to either BA and/or CFLD. The study design was as follows. In study 1, plasma TGF-beta1 was assessed by ELISA in 9 children with BA undergoing liver transplantation, 11 patients with CFLD, and appropriate control subjects. In study 2, hepatic expression of TGF-beta1 protein (assessed immunohistochemically) and hepatic fibrosis were scored semiquantitatively, on a 1-3 scale, by blinded investigators, in archival liver biopsy specimens from 10 children with BA, 10 with CFLD, and from 10 older children with normal hepatic histology, as well as in 4 patients with liver diseases of various etiologies. Simultaneous plasma and liver TGF-beta1 studies were performed in 8 patients with liver disease. Results were as follows. Plasma TGF-beta1 values were inversely correlated with age in healthy subjects (r=-0.54, p < 0.0001). The plasma TGF-beta1 protein of children with BA was decreased (13+/-2 ng/mL) compared with values for healthy children (42+/-6 ng/mL, n=10, p < 0.005). Similarly, the plasma TGF-beta1 concentration in patients with CFLD was also decreased compared with values for children with CF and normal serum liver profiles (n=14) (2+/-1 ng/mL versus 12+/-1, p < 0.05). However, the plasma TGF-beta1 concentration was increased in two patients with other types of liver disease. The hepatic expression of TGF-beta1 was increased in the presence of hepatic fibrosis in all types of liver diseases studied. Forty-six percent of patients had both marked hepatic fibrosis and marked TGF-beta1 labeling; 86% of samples without fibrosis showed no TGF-beta1 labeling, p=0.007. In conclusion, these studies have established the association of hepatic TGF-beta1 protein and hepatic fibrosis in several common liver diseases of childhood. Our data also suggest that, in children, plasma TGF-beta1 does not appear to be a useful marker of hepatic expression of this cytokine.

Adult↗
PubMed1998

Echocardiographic evaluation of cardiac valvular abnormalities in adults with Down's syndrome.

It is well known that congenital heart abnormalities are common in children with Down's syndrome. However there are few studies on cardiac abnormalities in adults with Down's syndrome. Therefore, we estimated cardiac abnormalities by means of echocardiography in 30 institutionalized Japanese adults with Down's syndrome, but without cardiac symptoms. Two-dimensional echocardiography showed an incidence of 26.7% in mitral valve prolapse and 20% increase of echo brightness in the mitral valve. Doppler echocardiography revealed an incidence of 16.7% in mitral valve regurgitation, and 13.3% in aortic valve regurgitation. Thus, even adults with Down's syndrome who are apparently free of cardiac symptoms may be at risk for valvular disease.

Adult↗
PubMed1997

In vitro 1H-magnetic resonance spectroscopy of postmortem brains with schizophrenia.

Some evidence suggests that thalamic dysfunction could explain some of the signs and symptoms of schizophrenia. We measured the absolute concentrations of amino acid metabolites in thalamus, frontal pole, and cerebellar vermis in extracts of postmortem brains from 8 schizophrenics and 10 controls using high-resolution 1H-magnetic resonance spectroscopy. The concentrations of N-acetyl aspartate, glutamate, and valine tended to be reduced in the thalamus of the schizophrenic group. Although it is difficult to ascribe significance to the "tendencies," these data may tend to support other data suggesting decreased thalamic volume or neuronal number in schizophrenia.

Adult↗
PubMed1997

Expression of alpha-fetoprotein and stem cell factor/c-kit system in bile duct ligated young rats.

The existence of a facultative hepatic stem cell compartment in bile ductules that participates in the renewal process of epithelial cell populations in the liver is well documented. The present study was undertaken to determine whether the immature bile epithelium responds differently to growth stimulus induced by bile stasis to that seen in the adult animal. In addition, the possible involvement of the growth factor/receptor systems associated with early activation of hepatic stem cells in bile duct proliferation was also examined. Bile duct ligation was used to induce the proliferation of bile epithelial cells. The expression of full-length alpha-fetoprotein (AFP) was used as an indicator for activation of the stem cell compartment. AFP was highly and selectively expressed in small bile ducts 7 days after bile duct ligation in immature rats up to 5 weeks of age. Although no significant increase in the expression of stem cell factor (SCF) c-kit, hepatocyte growth factor (HGF), and transforming growth factor-alpha (TGF-alpha) was observed 7 days after bile duct ligation in adult rats, the expression of all these growth factors was increased in bile duct ligated rats up to 5 weeks of age. These results suggest that the bile ductular epithelium in the young rats responds to bile stasis in a fashion that is phenotypically similar to that seen during early activation of hepatic stem cells in adult liver.

Age Factors↗
PubMed1997

Partial cloning of rat CD34 cDNA and expression during stem cell-dependent liver regeneration in the adult rat.

The sialomucin CD34 is expressed on human and mouse hematopoietic stem cells and is used as an important marker for isolating the hematopoietic stem/progenitor cells. The involvement of hepatic stem cells in liver regeneration under certain conditions in adult rats is now well supported. The objective of the present research was to explore the idea that CD34 might also be expressed on hepatic stem cell progeny. Polymerase chain reaction (PCR)-based cloning of rat CD34 was partially accomplished. During the hepatic stem cell activation (2-acetylaminofluorene/partial hepatectomy [AAF/PH] model), the CD34 transcripts were increased and reached the peak level between 9 and 12 days after partial hepatectomy when the progenitor cells (e.g., oval cells, early hepatocytes in basophilic foci, and intestinal type of cells) are most abundant. Both in situ hybridization and immunohistochemistry, using anti-mouse CD34 antibody, which recognizes the cytoplasmic domain, clearly showed the expression of CD34 on oval cells as well as on endothelial cells of large hepatic vessels. In addition, bile ductular epithelial (BDE) cells both in the AAF/PH model and in normal liver expressed CD34, suggesting a close relationship between BDE cells and the hepatic stem-cell compartment. Taken together, the data indicate that CD34 would, similar to its role in the hematopoietic system, be an important probe for characterizing the cellular biology of the hepatic stem-cell compartment.

2-Acetylaminofluorene↗
PubMed1997

Coexpression of flt-3 ligand/flt-3 and SCF/c-kit signal transduction system in bile-duct-ligated SI and W mice.

Stem cell factor (SCF) and its receptor c-kit constitute an important signal transduction system regulating cell growth and differentiation in hematopoiesis, gametogenesis, and melanogenesis. Recently, we have demonstrated that both SCF and c-kit are expressed in the bile duct epithelial cells of the rat liver and are highly up-regulated during activation of the normally dormant hepatic stem cell compartment. In the present study, we used sl/sld and w/wv mice, which have mutation of either SCF or c-kit, to study the possible involvement of the SCF/c-kit system in the bile duct proliferation. Bile duct ligation was performed to induce the proliferation of bile duct epithelial cells. The transcripts for both SCF and c-kit were clearly increased after bile duct ligation in both control and mutant mice. Moreover, both Sl and W mice responded to the bile duct ligation, similar to the control mice, by developing new bile ducts. Recently, a novel tyrosine kinase receptor, flt-3 receptor, has been identified in the fetal liver. It has been reported that the flt-3 ligand (FL)/flt-3 system can synergize with the SCF/c-kit system and stimulate the proliferation of hematopoietic cells. Therefore, we hypothesized that the FL/flt-3 system might compensate for the compromised SCF/c-kit system in the liver of Sl and W mice. The expression of both FL and flt-3 were significantly increased in bile duct-ligated liver from both normal and mutant mice, and the transcripts for the flt-3 receptor were selectively located on bile duct epithelial cells. Based on these results, we postulate the existence of a compensatory/additive function between the FL/flt-3 and the SCF/c-kit signal transduction systems in hepatic cell biology.

Animals↗
PubMed1996

Intravenous midazolam as a sedative for colonoscopy: a randomized, double-blind clinical trial.

METHODS: Forty patients, aged between 36 and 60 years, scheduled to undergo colonoscopic removal of colorectal polyps were randomly assigned to receive 0.9% saline solution (n = 20) or 0.05 mg/kg body weight of midazolam (n = 20) intravenously. RESULTS: Midazolam significantly (P < 0.001) increased the tolerance of patients to colonoscopy. It had no significant effect on pulse or systolic blood pressure during endoscopy. Arterial oxygen saturation decreased significantly (P < 0.01) during endoscopy in patients pre-treated with midazolam, but it did not decrease by more than 5%. CONCLUSIONS: Intravenous midazolam is useful as a sedative for colonoscopy, but we recommend continuous oxygen saturation monitoring during endoscopy.

Adult↗
PubMed1996

Precursor-product relationship between oval cells and hepatocytes: comparison between tritiated thymidine and bromodeoxyuridine as tracers.

The expansion and differentiation of oval cells in the acetylaminofluorene (AAF)/partial hepatectomy (PH) model was studied utilizing pulse-chase labeling with both tritiated thymidine ([3H]TdR) and bromodeoxyuridine (BUdR). Animals in which a significant decrease in serum albumin and increase in alanine aminotransferase and bilirubin were observed demonstrated the most prominent differentiation of oval cells into hepatocytes. Administration of [3H]TdR or BUdR, either individually or together, to the animals on day 6 after partial hepatectomy resulted in labeling of the majority of the oval cells by days 7 and 9 after PH. A striking difference in the distribution of [3H]TdR- and BUdR-labeled cells in the double labeling experiments was observed on day 11, at which time the number of [3H]TdR-labeled cells increased 6-fold and that of double labeled cells decreased 2-fold. Furthermore, on day 11 the basophilic foci were weakly positive for BUdR and negative at later time points in animals receiving BUdR alone or together with [3H]TdR. In contrast, the cells in basophilic foci as well as transitional cells were positive for [3H]TdR. Cells heavily labeled with both [3H]TdR and BUdR were present at all time points, indicating an inhibition of the proliferative activity. Pulse labeling of rat liver epithelial cells with BUdR in vitro demonstrated that immunodetection of BUdR was lost after three or more cell divisions. We conclude that the BUdR tagging method is particularly sensitive to label dilution during cell cycling and may not be suitable for establishment of a precursor-product relationship between cell lineages when the progenitor population proliferates more than three times.

2-Acetylaminofluorene↗
PubMed1996

Expression of transforming growth factor alpha/epidermal growth factor receptor, hepatocyte growth factor/c-met and acidic fibroblast growth factor/fibroblast growth factor receptors during hepatocarcinogenesis.

It is widely believed that abnormal production of polypeptide growth factors, together with other molecular alterations, play an important role in neoplastic development. Transforming growth factor alpha (TGFalpha), hepatocyte growth factor (HGF) and acidic fibroblast growth factor (aFGF) are the three major growth factors that contribute to liver regeneration occurring via both hepatocyte replication and oval cell proliferation. It is not clear, however, whether and to what extent these growth factors are also involved in hepatocarcinogenesis. In the present study, the gene expression of TGFalpha, HGF and aFGF and their corresponding receptors was examined by Northern blotting and in situ hybridization during hepatocarcinogenesis induced by the Solt-Farber protocol. All three growth factor/receptor systems, TGFalpha/epidermal growth factor receptor (EGFR), HGF/c-met and aFGF/FGF receptors (flg and bek) were significantly elevated at early time points when oval cells were proliferating. Their respective expression decreased after 1 month and remained at a low level until the development of liver tumors. In all hepatocellular carcinomas (HCC) examined, the transcripts of TGFalpha and aFGF were highly expressed, while those of HGF were low. With regard to the receptor expression in the tumors, EGFR was present at varying levels, c-met was expressed at higher levels and flg increased significantly, whereas bek remained at low levels. These data suggest that TGFalpha and aFGF are the major growth factors involved in the progression of HCC, and that the signal of aFGF is mainly transduced by the receptor flg in HCC. Furthermore, HCC cells were phenotypically very similar to oval cells with regard to the gene expression of growth factor/receptor systems. These results, along with the finding that all the HCC cells are positive for the oval cell antigen OV6, and that cytokeratin 19 is heavily expressed in both tumor and oval cells, strongly suggest that at least some of the HCC induced by the Solt-Farber protocol may be derived from oval cells.

Animals↗
PubMed1996

Expression of leukemia inhibitory factor and its receptor during liver regeneration in the adult rat.

Leukemia inhibitory factor (LIF) is a polyfunctional cytokine that was discovered in the conditioned medium from Buffalo rat liver cells. In the liver, LIF is known to induce acute phase proteins in the hepatocytes. No comprehensive study has yet been performed on the physiological role of this cytokine during liver regeneration. Thus, we studied the level of expression and cellular distribution of transcripts for LIF, its receptor (LIFR), and signal transducing subunit gp13O during rat liver regeneration after both simple partial hepatectomy (PH) and the oval cell activation induced by the combination of 2-acetylaminofluorene and PH. In addition, the expression of an acute phase protein alpha1-acidglycoprotein was examined. The level of transcripts for LIF and its receptor subunits increased and remained elevated during oval cell expansion. In contrast, after PH, the transcripts were induced only transiently, showing a peak 24 hours after the operation. LIF and receptor subunits were expressed in both parenchymal and nonparenchymal fractions in the 2-acetylaminofluorene/PH model, but the level of expression was most pronounced in the nonparenchymal fraction. In situ hybridization clearly revealed a strong expression of LIF, LIFR, and gp13O in the oval cells and demonstrated only a weak expression in the parenchyma. Interestingly, transcripts of alpha1-acidglycoprotein were exclusively detected in the parenchyma. These results suggest a phenotypic difference between oval cells and hepatocytes in their signaling through gp130. We hypothesize that the LIF/LIFR gp130 system may be involved in the expansion and differentiation of the liver stem cell compartment.

Acute-Phase Proteins↗
PubMed1996

Expression of transcription factors and stem cell factor precedes hepatocyte differentiation in rat pancreas.

Multiple foci of morphologically and functionally differentiated hepatocytes are induced in the pancreas of adult rats subjected to a copper depletion-repletion regimen. Differentiation of hepatocytes in pancreas is preceded by irreversible depletion of over 90% of pancreatic acinar cells. Progressive acinar cell loss during 4-6 weeks of copper deficiency results in the proliferation of oval cells, some of which may serve as the hepatocyte precursor or stem cells. Albumin mRNA is detected in oval cells at 5 and 6 weeks by in situ hybridization at which time no morphologically identifiable hepatocytes are evident in the pancreas. Immunocytochemical analysis demonstrated the presence of stem cell factor (SCF) in proliferating oval cells during 6 weeks of copper depletion, and Northern blot analysis revealed the expression of liver-enriched transcription factors in the rat pancreas during this 4-6-week period of copper deficiency. CCAAT/enhancer binding protein alpha (C/EBP alpha) mRNA was detected first at 4 weeks of copper deficiency. By 5 and 6 weeks of copper deficiency, the expression of mRNAs of C/EBP alpha, beta, and delta, and hepatocyte nuclear factor-3 factor (HNF-3 beta) was markedly enhanced. This enhanced expression of liver-enriched transcription factors and the SCF during oval cell proliferation in the pancreas preceding the expression of albumin mRNA and subsequent differentiation of hepatocyte phenotype further supports the identity of these oval cells as hepatocyte precursors or stem cells.

Albumins↗
PubMed1995

Quantitative EEG in never-treated schizophrenic patients.

To clarify whether patients with schizophrenia still show EEG slowing in the absence of psychopharmacological treatment, EEG was analyzed in 20 acute never-treated schizophrenics and 20 age-matched healthy controls using the computerized wave-form recognition method. Compared to controls, schizophrenics had more fast theta (6-8 Hz) and slow alpha (8-9 Hz) activity, and less fast alpha activity (9-13 Hz). The average EEG frequency at O1 correlated negatively with total and positive symptom scores on the BPRS in the schizophrenic group. These findings confirm that the frequency of alpha rhythm is slowed in schizophrenia and that this slowing is possibly related to the expression of psychopathology in this disorder.

Adult↗
PubMed1995

Isolation and characterization of a mini-collagen gene encoding a nematocyst capsule protein from a reef-building coral, Acropora donei.

Genomic and cDNA clones of a mcol gene encoding mini-collagen (MCOL), a nematocyst capsule protein, have been isolated from a reef-building coral, Acropora donei (Anthozoa). The gene and its flanking regions, comprising 5382 bp and covering three exons and two introns, were sequenced. Exons 2 and 3 together have an open reading frame which can encode a MCOL of 176 amino acids (aa). The coral MCOL has all the characteristic regions present in the four hydra MCOL specified by the four mcol cDNA clones previously isolated from Hydra magnipapillata (Hydrozoa) by Kurz et al. [J. Cell Biol. 115 (1991) 1159-1169], including a central Gly-Xaa-Yaa region and flanking Pro-rich and Cys-repeat regions. This observation suggests that a mcol family is highly conserved in Anthozoa and Hydrozoa, and also that the characteristic regions present in MCOL are essential for the structure and function of these peptides.

Amino Acid Sequence↗
PubMed1995

Serial proton magnetic resonance spectroscopy in a patient with the interval form of carbon monoxide poisoning.

Serial proton magnetic resonance spectroscopy (1H-MRS) studies were performed from immediately after the appearance of sequelae in a patient with the interval form of carbon monoxide (CO) poisoning. The volume of interest was set over the frontal lobe white matter. In the early period a persistent increase in choline was found, which was thought to reflect the course of progressive demyelination. The appearance of lactate and decrease in N-acetylaspartate reflected the point at which neuron injury became irreversible. These were followed later by the finding of irreversible changes on MRI and single photon emission computed tomography. The findings suggest that 1H-MRS may be a useful modality to determine neuron viability and prognosis early in the course of the interval form of CO poisoning.

Brain Diseases↗
PubMed1995

Effect of vitamin A deficiency on the integrity of hepatocytes after partial hepatectomy.

The effect of vitamin A deficiency on hepatic regeneration in male and female rats was studied after partial hepatectomy. A fourfold increase in the number of positive dUTP end-labeled nuclei was observed in the deficient animals as early as 30 minutes after partial hepatectomy and their number reached a peak by 8 hours after the operation. The bile duct cells were both morphologically and biochemically intact at all time points. Administration of retinyl palmitate 1 hour before partial hepatectomy significantly reduced the number of positive nuclei, and treatment with retinyl palmitate 24 or 48 hours before the operation reduced the number of positive cells to the level observed in control vitamin A-supplemented rats. The level of transcripts for c-jun, c-fos, c-myc, and transforming growth factor-beta 1 were increased for an extended period of time in livers of deficient animals, whereas the expression of both p53 and max were unchanged. Immunocytochemistry demonstrated the presence of latent transforming growth factor-beta 1 in cells showing evident apoptotic or necrotic changes in their nuclei. This study demonstrates the importance of vitamin A for the survival of hepatocytes both in intact vitamin A-deficient liver and after partial hepatectomy, whereas the ductal cells appear to be less sensitive to vitamin A deficiency.

Animals↗
PubMed1994

Inhibitory effects of (-)-epigallocatechin gallate on spontaneous hepatoma in C3H/HeNCrj mice and human hepatoma-derived PLC/PRF/5 cells.

The inhibitory effect of (-)-epigallocatechin gallate (EGCG), a main constituent of Japanese green tea, on spontaneous hepatoma in C3H/HeNCrj mice was investigated. A total of 72 mice were divided into three groups; the control group without EGCG, and two experimental groups receiving 0.05% (w/w) or 0.1% EGCG in drinking water. EGCG reduced the incidence of hepatoma-bearing mice from 83.3% (control) to 56.0% (0.05% EGCG) and 52.2% (0.1% EGCG), and also reduced the average number of hepatomas per mouse from 1.83 (control) to 0.72 (0.05% EGCG) and 0.91 (0.1% EGCG) at week 65. Ridit analysis of the distribution of the number of hepatomas in each group revealed that EGCG significantly increased the rate of mice without hepatoma in the two EGCG groups as compared to the control. EGCG did not affect body weight gain, food consumption or any serum biochemical parameter. EGCG inhibited the growth and secretion of alpha-fetoprotein by human hepatoma-derived PLC/PRF/5 cells without decreasing their viability. These results indicate that EGCG may be a practical, nontoxic preventive agent against human hepatoma.

Animals↗
PubMed1994

Molecular cloning and nucleotide sequence of the beta-galactosidase gene from Enterobacter cloacae GAO.

The gene encoding a beta-galactosidase from Enterobacter cloacae GAO was cloned and expressed in Escherichia coli. The nucleotide sequence of the insert of a positive clone had an open reading frame of 3084 bp that encoded a polypeptide of 1028 amino acid residues with a calculated molecular mass of 116,677 daltons. The amino acid sequence of beta-galactosidase deduced from the nucleotide sequence, especially the sequence around the putative active site and of the fourteen regions, showed significant homology to beta-galactosidases of other microorganisms, E. coli, Klebsiella pneumoniae, Lactobacillus bulgaricus, and Clostridium acetobutylicum.

Amino Acid Sequence↗