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Biomedical subjects

M Yagi

Publications and source records attributed to M Yagi.

At least 91 records · Page 5Linked to original sources
PubMed1998

Effects of chitosan-coated dialdehyde cellulose, a newly developed oral adsorbent, on glomerulonephritis induced by anti-Thy-1 antibody in rats.

The effects of chitosan-coated dialdehyde cellulose (chitosan DAC), a newly developed oral adsorbent for urea and ammonia, were examined in a glomerulonephritis model in rats. Mesangial proliferative glomerulonephritis accompanied with proteinuria was induced by an intravenous injection of anti-rat Thy-1.1 monoclonal antibody (OX-7). The proliferation of mesangial cells and an accumulation of extracellular matrix components such as type I collagen and fibronectin were observed in the glomeruli 9 days after OX-7 injection; these were improved in rats fed a diet containing chitosan DAC (10% content) for 9 days compared with those in rats fed a normal diet. Chitosan DAC treatment decreased the elevated urinary protein and blood urea nitrogen at days 8-9 to the normal levels; the increased fecal excretion of nitrogen might participate in this phenomenon. In addition, chitosan DAC treatment showed an increase in fecal water content associated with a decrease in urinary volume. These therapeutic effects may be due to the reduction of proteinic factor expression and the compensational function of chitosan DAC for kidney. These results suggest that chitosan DAC treatment may be useful for ameliorating mesangial proliferative glomerulonephritis.

Adsorption↗
PubMed1998

[Basic calponin expressing human neuroblastoma cell line of KP-N-YS].

Recent studies have demonstrated that human neuroblastoma (NB) cell lines have at least two morphological appearance of neuroblastic (N-type) and substrate-adhesive (S-type) cells. Our previous study revealed that S-type cells expressed alpha-smooth muscle actin and/or desmin, suggesting the smooth muscle cell characteristics of S-type cells. In the present study, a new human NB cell line, KP-N-YS, was established from bone marrow metastasis of a four-year-old boy with advanced NB, originating from the left adrenal gland. Subsequently N-type cell clone (YS1n) and S-type cell clone (YS2s) was isolated from the parent cell line. Parent and clones cell lines were identified as NB by surface membrane antigen and cytoskeletal protein analysis, and these cell lines were demonstrated as common progenitors by chromosomal analysis. Furthermore the presence of basic calponin were determined by indirect immunofluorescence, Western blot, as well as by RT-PCR (reverse transcriptase-polymerase chain reaction). Our demonstration of basic calponin not in N-type cells, but in S-type cells supports the plausible smooth muscle cell characteristics of this NB cell line.

Antigens, Surface↗
PubMed1998

[Correlation between pyrimidine nucleoside phosphorylase (PyNPase)/platelet-derived endothelial cell growth factor and histological prognostic factor, and influences of 5'-deoxy-5-fluorouridine (5'-DFUR) administration on PyNPase levels. 5'-DFUR Joint Research Group in the Osaka Area for Gastric Cancer].

PURPOSE: Pyrimidine nucleoside phosphorylase (PyNPase), among which thymidine phosphorylase (dThdPase) exists mainly in human tumor tissues, is an enzyme to convert 5'-deoxy-5-fluorouridine (5'-DFUR) to 5-fluorouracil. Recently, it was reported that dThdPase was identical to platelet-derived endothelial cell growth factor, angiogenetic factor. Therefore, we expect that there is possibility of dThdPase being a prognostic factor. METHODS: We investigated for a possible correlation between PyNPase activities in tumor tissues and prognostic factors of histological findings, examined the influences of preoperative oral 5'-DFUR administration to PyNPase levels and investigated for a correlation between HPLC methods and ELISA methods in patients with gastric cancer. RESULTS: Higher levels of PyNPase were observed in patients with advanced t,n,v, and ly factors. PyNPase levels decreased by 5'-DFUR in patients with differentiated cases. A high correlation was found between HPLC and ELISA methods. CONCLUSION: This study suggests that we must investigate possibility of PyNPase being a prognostic factor in more detail.

Antineoplastic Agents↗
PubMed1997

Activation of c-Jun N-terminal kinase during ischemia and reperfusion in mouse liver.

We have generated a mouse model for hepatic ischemia in which surgical subcutaneous transposition of the spleen allows hepatic ischemia to be applied without affecting other tissues. Using this mouse model we investigated the relationship between the length of ischemic periods in the liver and subsequent liver function; furthermore, we assayed the activation of c-Jun N-terminal kinase (JNK) during ischemia and reperfusion. Although prior to this study only the activated form of JNK was known to be translocated to the nucleus, we found that JNK translocates to the nucleus during ischemia without activation and is then activated during reperfusion. These results suggest a novel mechanism of JNK activation.

Animals↗
PubMed1997

Selective inhibition of platelet-derived growth factor (PDGF) receptor autophosphorylation and PDGF-mediated cellular events by a quinoline derivative.

This report describes the biological effects of our original compound, Ki6783 ((3,4-dimethoxy)-4-phenoxy-6,7-dimethoxyquinoline), a potent and selective inhibitor of platelet-derived growth factor (PDGF) receptor autophosphorylation. This compound strongly inhibited autophosphorylation of the PDGF beta-receptor in cultured rat glomerular mesangial cells (MC) bearing this receptor (IC50 0.1 microM), although it did not inhibit autophosphorylation of other growth factor receptors even at 100 microM. In a cell-free kinase experiment, it showed selective inhibition of PDGF beta-receptor tyrosine kinase. A kinetic study of the compound to this tyrosine kinase revealed a competitive mode of action to ATP. [3H]Thymidine incorporation and cell proliferation of MC were inhibited by Ki6783 in a dose-dependent manner after Ki6783 and PDGF-BB were added to the culture medium. Furthermore, this compound normalized the fibrotic cell shape of v-sis-transformed NIH3T3 cells, which grow in an autocrine manner via the PDGF receptor. These effects could be explained by the inhibition of intracellular signal transduction triggered by PDGF receptor autophosphorylation, in which activation of mitogen-activated protein kinase occurs. These results suggest that Ki6783 is one of the more potent and selective inhibitors of PDGF receptor autophosphorylation and that it may be useful in ameliorating cell abnormalities due to excess action of PDGF and its receptor systems in several diseases.

3T3 Cells↗
PubMed1997

Hypoxia, but not reoxygenation, induces interleukin 6 gene expression through NF-kappa B activation.

Interleukin (IL) 6 is one of major mediators of inflammation, and IL-6 gene activation during hypoxia/reoxygenation has been implicated in the pathogenesis of ischemia/reperfusion injury. However, molecular events involved in IL-6 gene expression during hypoxia/reoxygenation remain to be identified. We have previously shown that NF-kappa B plays an essential and indispensable role in the transcriptional activation of the IL-6 gene induced by various stimuli, including IL-1 and tumor necrosis factor-alpha. We show here that hypoxia, but not reoxygenation, induces the activation of NF-kappa B through the degradation of a major inhibitor of NF-kappa B, I kappa B alpha. This hypoxia-induced NF-kappa B activation resulted in the kappa B-dependent transcriptional activation of the IL-6 gene. Interestingly, the time course of hypoxia-induced NF-kappa B activation was rather slow as compared with those of NF-kappa B activation induced by other stimuli, such as IL-1: a significant NF-kappa B activation was not observed before 1 hr of hypoxia treatment and persisted for up to 7 hr of hypoxia treatment. However, hypoxia-induced NF-kappa B activation was not inhibited by cycloheximide, which indicates that hypoxia directly triggers NF-kappa B activation. Furthermore, while hypoxia is unlikely to generate reactive oxygen intermediates, pretreatment of cells with antioxidants such as N-acetyl cysteine and alpha-tocopherol inhibited NF-kappa B activation induced by hypoxia. Thus, we discuss possible implications of these results for a postulated role of reactive oxygen intermediates in NF-kappa B activation.

Animals↗
PubMed1997

Electrogastrography after operative repair of esophageal atresia.

Esophageal atresia (EA) is a life-threatening disorder associated with operative complications. Postoperative gastric electrical control activity detected by a non-invasive electrogastrography (EGG) technique was investigated in 13 children aged 1-17 years to clarify whether gastric motility disorders were present. EGG abnormalities were present in 5 patients; persistent dysrhythmias were found in 3. Roentgenographic examinations showed mild gastroesophageal reflux in 3 (60%) of the dysrhythmic patients; 2 others had postprandial dysrhythmias. The mean spectral frequency (MSF) of EA cases with dysrhythmia was significantly higher than that of patients without dysrhythmia in both fasting and postprandial states (P < 0.05). The variability of the peak spectral frequencies (PSFV) in patients with dysrhythmia was significantly higher than in those without dysrhythmia in both fasting and postprandial states (P < 0.05). There were no significant differences in MSF and PSFV between EA patients without dysrhythmia and controls. These results suggest that gastric motor activity may be disordered in patients following operative repair of EA, although they remain asymptomatic. EGG may be a useful screening examination for postoperative gastric functional disorders.

Adolescent↗
PubMed1997

Successful treatment of blunt trauma involving complete laceration of the pancreas and duodenum in a 7-year-old child: report of a case.

The acute onset of peritoneal signs and shock in a 7-year-old boy who had been hit in the epigastrium by a log-seesaw mandated surgical treatment. Enhanced computed tomography (CT) demonstrated complete laceration of the pancreas as well as duodenal injury, and a duodenoduodenostomy with distal pancreaticogastrostomy was subsequently performed. Temporary external drainage of the stomach and distal pancreas led to an uneventful recovery in the early postoperative period. Although the patient's postoperative development was appropriate for his age, the orifice of the distal pancreas spontaneously closed 2.5 years following surgery. We present this report to stress the fact that every effort should be made to preserve the pancreas following abdominal injury in children.

Child↗
PubMed1997

Effect of a glutamine-enriched diet on small bowel allograft during immunosuppressive therapy.

The effect of an orally administered glutamine-enriched elemental diet was examined following orthotopic small bowel allotransplantation using Brown Norway rats as donors and Lewis rats as recipients. The recipients was treated with FK 506 and randomized to receive glutamine-free elemental enteral diet solution (glutamine-free group), glutamine-enriched elemental diet solution containing 7500 mg of glutamine per 100 g diet (glutamine-enriched group) or standard chow (chow group) ad libitum for 7 d. There were no histological changes due to resection. Weight loss in the glutamine-enriched group was significantly less than that of the chow group. Both plasma glutamine levels and the ratio of glutamine to total amino acids in the homogenate of the graft mucosa of the glutamine-enriched group were significantly higher than those of the glutamine-fee group. Villous height and crypt depth were significantly decreased in the glutamine-free group. The BrdU labeling index in the graft epithelium and alkaline phosphatase activity in the homogenate of the graft mucosa of the glutamine-enriched group were significantly higher than those of the glutamine-free group. Therefore, orally administered glutamine-enriched elemental diet appears to promote the regeneration and differentiation of the graft mucosa following small bowel allotransplantation.

Aging↗
PubMed1996

Primary structures of fungal fructosyl amino acid oxidases and their application to the measurement of glycated proteins.

Fructosyl amino acid oxidase (FAOD), which is active toward model compounds of the glycated proteins in blood, N epsilon-fructosyl N sigma-Z-lysine and N-fructosyl valine, was purified to homogeneity from Aspergillus terreus GP1. Though the enzyme did not use glycated proteins directly as its substrate, it used glycated human serum albumin (HSA) when HSA was treated with a protease. Linear relationships between both the concentration and the increase in absorbance and the glycation rate of glycated HSA and the increase in absorbance were observed. cDNAs coding for FAODs were cloned from cDNA libraries of A. terreus GP1 and Penicillium janthinellum AKU 3413. The coding region for both fungal FAODs consisted of 1314 bp encoding 437 amino acids. The sequence of a dinucleotide-binding motif, GXGXXG, was in the deduced N-terminal region and a similar sequence to that the active site of bacterial sarcosine oxidases was found near the C-terminal region of FAOD. The of C-terminal tripeptides SKL and AKL of FAODs from A. terreus and P. janthinellum, respectively, represent typical peroxisomal-targeting signals. Finally, FAOD protein was produced in Escherichia coli transformants in an active form, and at the same level as in the original fungi.

Amino Acid Oxidoreductases↗
PubMed1996

Analysis of the megakaryocyte glycoprotein IX promoter identifies positive and negative regulatory domains and functional GATA and Ets sites.

The glycoprotein (GP) Ib-V-IX multisubunit complex binds to von Willebrand factor and mediates the adhesion of platelets to the subendothelium of damaged blood vessels. Expression of the GPIX subunit is required for stability of the complex, and its absence in platelets is associated with the rare bleeding disorder Bernard-Soulier syndrome. Comparative analyses indicate that the four GPIb-V-IX subunits are members of the leucine-rich repeat family and suggest that GPIX resembles a possible primitive progenitor of this group. To characterize GPIX transcriptional regulation, a series of 5' deletion constructs was made linking the GPIX upstream flanking sequence to the luciferase marker gene, and promoter activity was measured in transiently transfected human erythroleukemia cells. This analysis identified two negative regulatory domains between -686 to -423 and -311 to -203 and two positive regulatory domains at -323 to -311 and -151 to -100 relative to the GPIX transcription start site. In addition, site-directed mutagenesis experiments and in vitro gel retardation assays identified Ets and GATA elements at -42 and -65, which positively regulate GPIX promoter activity and specifically bind nuclear factors derived from human erythroleukemia cells. DNase I protection experiments identified a protein-dependent "footprint" and hypersensitive site within the GPIX Ets sequence. These results provide a framework for comparison of the GPIX promoter with others of the GPIb-V-IX system, other megakaryocyte-specific genes, and other members of the leucine-rich repeat family.

Base Sequence↗
PubMed1996

Immunosuppressant FK506 induces interleukin-6 production through the activation of transcription factor nuclear factor (NF)-kappa(B). Implications for FK506 nephropathy.

FK506 is a powerful immunosuppressive drug currently in use that inhibits the activation of several transcription factors (nuclear factor (NF)-AT and NF-kappaB) critical for T cell activation. We show here that, contrary to the situation in T cells, FK506 activates transcription factor NF-kappaB in nonlymphoid cells such as fibroblasts and renal mesangial cells. We further show that FK506 induces NF-kappaB-regulated IL-6 production in vitro and in vivo, in particular in kidney. IL-6 has been shown previously to produce renal abnormalities in vivo, such as mesangioproliferative glomerulonephritis. Similar renal abnormalities were also observed in FK506-treated animals. These results thus suggest a causal relationship between FK506-induced NF-kappaB activation/IL-6 production and some of FK506-induced renal abnormalities.

Animals↗
PubMed1996

The platelet glycoprotein Ib-V-IX system: regulation of gene expression.

Platelet glycoproteins (GPs) Ib-V-IX form the surface receptor for von Willebrand factor, and this receptor-ligand interaction mediates the shear-dependent adhesion of platelets to damaged arterial vessel walls. The receptor is a multicomponent structure consisting of four distinct polypeptides (heterodimeric GPIb: Ib alpha-Mr143k and Ib beta-Mr22k; GPV-Mr83k; GPIX-Mr20k), and each of the four cDNAs and genes has been cloned and characterized. The genes appear to have evolved from a common progenitor genomic sequence related to that encoding GPIX. They share simple structures with few introns and possess common consensus regulatory sequences (GATA, ets, Sp-1) in their 5' flanks. Both the GPIb alpha and the GPIX promoters have been analyzed by transfection of reporter constructs into hematopoietic and nonhematopoietic cells. The promoters function in a tissue-specific fashion, and gel shift and mutational analyses indicate that GATA and ets sequences regulate activity. In the case of the GPIX promoter, footprints confirm the role of the ets-related consensus region. Recent studies of GPIb beta transcriptional regulation suggest that an aberrant polyadenylation signal, located in the 3' end of the gene immediately upstream of the GPIb beta gene, allows in vitro expression of a rare extended fusion transcript encoding both the upstream protein and GPIb beta. Little detailed information is available in regard to expression of the GPV gene. In summary, the genes of the GPIb-V-IX system display features of other megakaryocyte/platelet genes, but the unique regulatory events that direct the selective expression of these genes in megakaryocytes remain to be defined.

Chromosome Mapping↗
PubMed1996

Anti-interferon activity of adenovirus-2-encoded VAI and VAII RNAs in translation in cultured human cells.

The mode of anti-interferon action of VAI and VAII RNAs of adenovirus type 2 (Ad2) was studied by transfecting interferon-alpha (IFN-alpha)-treated KB cells in culture with a plasmid construct containing the VAI or VAII RNA gene and an SV40 promoter-chloramphenicol acetyltransferase (CAT) gene construct as reporter (pSV2-CAT). The longer the treatment of KB cells with IFN-alpha (2,000 IU/ml) lasted, the higher was the inhibition of CAT expression. A maximum of 76% inhibition was attained without pronounced cytotoxicity during 48 h of treatment. The earlier the VAI RNA gene was transfected, the higher was the enhancement of CAT expression. CAT activity increased from 113 to 157% in normal cells and 200-400% in IFN-alpha treated cells, as compared with the corresponding controls without VAI RNA transfection. The level of CAT mRNA was neither appreciably decreased by IFN-alpha treatment, nor detectably increased by VAI or VAII RNA. The effect of VA RNA thus appeared to be on translation rather than on transcription. The relative constancy of the level of CAT mRNA indicated that IFN-alpha inhibition of CAT expression was not due to the activation of RNase L, but due mainly to translational repression. The level of VAII RNA expressed was only 9-13% of that of VAI RNA. Nevertheless, VAII RNA gene transfection stimulated CAT activity to 112% of the control in non-IFN-alpha-treated cells, and 126-182% in IFN-alpha-inhibited cells. When IFN-alpha treatment was started late after VAI RNA cotransfection, CAT expression increased to 169% which was higher than the expression in cotransfected control cells without IFN-alpha treatment. The enhanced level of CAT activity was in remarkable contrast to the IFN-alpha inhibited level of 25% without VA RNA co-transfection when IFN-alpha was added upon seeding. The enhanced CAT activity in cells treated late with IFN-alpha could be ascribed to higher levels of VA RNAs.

Adenoviruses, Human↗
PubMed1996

Four cases of selenium deficiency in postoperative long-term enteral nutrition.

Because selenium is seldom added to formulations for enteral nutrition (EN), postoperative patients who are supported with EN are at risk for selenium deficiency. This report describes four cases of suspected selenium deficiency in long-term EN. Two patients underwent pancreaticoduodenectomy, one underwent total gastro-pancreatectomy, and one underwent esophageal resection and reconstruction with jejunal autotransplantation. They all developed malabsorption syndrome within 2 yr after operation. Enteral nutritional support with an elemental diet was provided continuously for 7-11 yr. Over the past 1-2 yr they experienced increasing bilateral muscular pain and weakness in the legs, gait disturbance, palpitation, and shortness of breath. Investigation for possible trace element deficiency revealed very low levels of selenium in the blood. After 10-20 d of supplementation with daily intravenous administration of selenious acid 0.16 mg/d (100 micrograms/d of selenium), their blood levels of selenium rose and their symptoms resolved. They were then continued on a maintenance regimen of oral sodium selenite 0.13 mg/d (60 micrograms/d of selenium).

Aged↗
PubMed1996

Mediastinal yolk sac tumor in a young girl: case report and review of the literature.

The authors report a rare case of a female infant who underwent successful treatment of a mediastinal yolk sac tumor. Therapy included four cycles of preoperative PVB (cisplatinum, vinblastine, bleomycin), complete surgical resection of the tumor, and one postoperative cycle of PVB and four cycles of VAC (vincristine, actinomycine, cyclophosphamide) chemotherapy. The successful treatment of this tumor depends on preoperative chemotherapy to reduce the size, followed by complete surgical excision with subsequent postoperative chemotherapy. Recent improvements in the treatment of mediastinal yolk sac tumors are discussed.

Antineoplastic Combined Chemotherapy Protocols↗