Search PubMed⌕ Search

Biomedical subjects

Y Nishikawa

Publications and source records attributed to Y Nishikawa.

At least 91 records · Page 5Linked to original sources
PubMed1999

[Case report of a long-term home parenteral nutrition patient].

We experienced a patient who received long-term home parenteral nutrition. A 55-year-old woman underwent left adrenalectomy in June, 1992. The histopathological diagnosis was aldosteronism. Abdominal pain and ileus appeared in July, 1993, and an adhesiotomy was conducted. Due to poor appetite and weight loss, fluid was sometimes injected peripherally. After abdominal pain in November, 1996 and April, 1997, the ileus reappeared in July, 1997. A Groshong catheter with a port was then inserted through the subclavian vein to the superior vena cava/right atrial junction. Using this catheter, home parenteral nutrition started. Some time later oral nutrition became possible, but now high calorie parenteral nutrition is continued. The only complications were pain and red skin at the port. A Groshong catheter with port is thus useful for home parenteral nutrition.

Adrenalectomy↗
PubMed1999

Effects of conditioning periaqueductal gray stimulation on responses of thalamic nociceptive neurons to tooth pulp stimulation.

Nociceptive neurons receiving afferent input from the tooth pulp (TP) were recorded from the nucleus ventralis posteromedialis proper (VPM) and intralaminar nuclei of the thalamus in cats anesthetized with urethane and chloralose. The effects of stimulating the periaqueductal gray (PAG), or the nucleus raphe dorsalis (NRD) on responses of thalamic nociceptive neurons were investigated. Eight tooth pulp specific (TPS) and 7 wide dynamic range (WDR) neurons with TP input were observed around the periphery (shell region) of the posterior half of VPM. Following electrical stimulation of either the ventral PAG or the NRD, responses to TP stimulation were inhibited in all TPS and WDR neurons tested. Responses of these neurons to electrical stimulation of trigeminothalamic tract (TTT) fibers in the trigeminal medial lemniscus were also inhibited following PAG/NRD stimulation. These results suggest that PAG/NRD stimulation-produced inhibition of both TPS and WDR neurons may be partially mediated by an ascending antinociceptive mechanism. Intralaminar nociceptive neurons with TP input were observed in the nucleus centralis lateralis (CL), and parafascicularis (Pf). The effects of conditioning electrical stimulation of either the ventral PAG or the NRD on responses of intralaminar nociceptive nerons were studied. Of 15 intralaminar nociceptive neurons tested, 6 neurons were inhibited, 5 neurons were excited and 4 were unaffected following the conditioning stimulus. In neurons in which responses to TP stimulation were inhibited, responses elicited by electrical stimulation of the mesencephalic reticular formation (MRF) were also inhibited. These data suggest that although there is an ascending inhibitory pathway from PAG/NRD to intralaminar nuclei, this system is far less potent compared with the ascending inhibitory system acting upon the VPM.

Analysis of Variance↗
PubMed1999

Functional properties of nociceptive neurons in the nucleus centralis lateralis of the cat thalamus.

We studied functional properties of nociceptive neurons in the thalamic intralaminar nuclei, especially the nucleus centralis lateralis (CL) in urethane-chloralose anesthetized cats. Nociceptive neurons were found in the intralaminar nuclei, i.e. CL, nucleus centralis medialis (CeM) and nucleus parafascicularis (Pf). One third of these nociceptive neurons had their receptive fields throughout the body, including the orofacial area. Namely, they received convergent nociceptive input from the trigeminal and spinal nerve territories. These neurons with widely complex receptive fields were similar to those we found in the middle third of the caudal bulbar reticular formation (RF). Electrical stimulation of the CL antidromically activated about half of the caudal bulbar RF neurons tested. Furthermore, electrical stimulation of the cingulate gyrus antidromically activated some of CL neurons. These findings suggest that most of the CL neurons receiving nociceptive input from throughout the body receive information directly or indirectly via the caudal bulbar RF, and that certain of this information is then conveyed to the cingulate gyrus.

Afferent Pathways↗
PubMed1998

Isolation, purification, and characterization of a collagen-associated serpin, caspin, produced by murine colon adenocarcinoma cells.

A 45-kDa serpin secreted by a murine colon adenocarcinoma cell line, colon26, was isolated, purified, and characterized. It was found to bind specifically to type I collagen with high affinity and to type III collagen with lower affinity. Immunohistochemical studies of murine embryonic tissues showed a specific distribution of this collagen-associated serpin, named caspin, in relation to the formation of bone, cartilage, teeth, and basement membrane. The expression of caspin in high and low lung metastatic subclones of colon26 cell lines was inversely correlated with their metastatic capacity: low lung metastatic cells secreted higher amounts of caspin than their high lung metastatic counterparts. Caspin also demonstrated high homology with human pigment epithelium-derived factor/early population doubling level cDNA-1, which reportedly induces neuronal differentiation of human retinoblastoma cells and is expressed in association with G0 growth arrest. These findings suggest that caspin/pigment epithelium-derived factor/early population doubling level cDNA-1 is a novel factor that might play a crucial role in embryogenesis and tumor metastasis through binding to the extracellular matrix.

Amino Acid Sequence↗
PubMed1998

Cell growth inhibition by a novel vitamin K is associated with induction of protein tyrosine phosphorylation.

We have shown that a synthetic vitamin K analog, 2-(2-mercaptoethanol)-3-methyl-1,4-naphthoquinone or compound 5 (Cpd 5), potently inhibits cell growth and suggested that the analog exerts its effects mainly via sulfhydryl arylation rather than redox cycling. Since protein-tyrosine phosphatases (PTPases), which have pivotal roles in many cellular functions, have a critical cysteine in their active site, we have proposed PTPases as likely targets for Cpd 5. To test this hypothesis, we examined the effects of Cpd 5 on protein tyrosine phosphorylation of cellular proteins and on the activity of PTPases. We found that Cpd 5 rapidly induced protein tyrosine phosphorylation in a human hepatocellular carcinoma cell line (Hep3B) at growth inhibitory doses, and the effect was blocked by thiols but not by non-thiol antioxidants or tyrosine kinase inhibitors. Cpd 5 inhibited PTPase activity, which was also significantly antagonized by reduced glutathione. Furthermore, the well studied PTPase inhibitor orthovanadate also induced protein tyrosine phosphorylation and growth inhibition in Hep3B cells. These results suggest that inhibition of cellular PTPases by sulfhydryl arylation and subsequent perturbation of protein tyrosine phosphorylation may be involved in the mechanisms of Cpd 5-induced cell growth inhibition.

Carcinoma, Hepatocellular↗
PubMed1998

Circulating platelet-derived endothelial cell growth factor increases in hepatocellular carcinoma patients.

BACKGROUND: Platelet-derived endothelial cell growth factor (PD-ECGF) is an angiogenic factor that is expressed in various cancer tissues. Little is known regarding plasma PD-ECGF levels in patients with chronic liver disease such as chronic hepatitis (CH), cirrhosis, and hepatocellular carcinoma (HCC) with cirrhosis. The expression of PD-ECGF in HCC tissues also remains to be clarified. METHODS: Plasma PD-ECGF levels in patients with chronic liver disease were determined with an enzyme-linked immunoadsorbent assay system using the mouse monoclonal antibodies specific to PD-ECGF. These were cross-sectionally compared among groups of normal persons, CH, cirrhosis, and HCC patients. The HCC patients were classified into two groups based on TNM stage: early and advanced stage disease groups. PD-ECGF expressions in HCC tissues were immunohistologically examined. RESULTS: The plasma PD-ECGF levels from the normal individuals and those with CH, cirrhosis, and HCC specimens were 4.2+/-0.5, 4.3+/-0.6, 4.6+/-1.1, and 6.0 +/-2.5 U/mL, respectively. The plasma PD-ECGF concentration was highest in HCC (P < 0.05). No significant difference was found among the normal subjects, CH, and cirrhosis specimens. Plasma PD-ECGF concentrations were significantly higher in the advanced stage disease HCC group compared with the early stage disease group (6.75+/-2.62 U/mL vs. 4.19+/-0.34 U/mL) (P < 0.05). Immunohistochemical expression of PD-ECGF in HCC cells increased significantly compared with normal liver cells (P < 0.05). CONCLUSIONS: Circulating PD-ECGF plasma level might be a new tumor marker for progression in patients with HCC. Immunohistological findings correspond to elevation of the plasma PD-ECGF in HCC patients. It is possible that increased production of PD-ECGF in HCC cells causes abundant neovascularization.

Adult↗
PubMed1998

Changes in TGF-beta receptors of rat hepatocytes during primary culture and liver regeneration: increased expression of TGF-beta receptors associated with increased sensitivity to TGF-beta-mediated growth inhibition.

To clarify the role of transforming growth factor-beta (TGF-beta) and its receptors in hepatocyte growth, we studied the expression of TGF-beta1 and its receptors and the sensitivity to growth inhibition by TGF-beta1 protein in rat hepatocytes derived from resting and regenerating livers. In hepatocytes derived from resting livers, mRNAs for TGF-beta type II receptor (TbetaR-II), insulin-like growth factor-II/mannose 6-phosphate receptor (IGF-II/M-6-PR), and TGF-beta1 increased with time in primary culture. The cell surface TGF-beta receptor proteins (TbetaR-I, II, and III), examined by the receptor affinity-labeling assay using 125I-TGF-beta1, also increased, especially after 48 hr of culture. Hepatocytes were more sensitive to inhibition of DNA synthesis, when the TGF-beta1 protein was added at later times in culture, corresponding to the presence of increased TGF-beta receptors. In hepatocytes from regenerating livers after a partial hepatectomy (PH), an increase of TbetaR-I, TbetaR-II, TbetaR-III, IGF-II/M-6-PR, and TGF-beta1 mRNAs was found, compared with hepatocytes from resting livers. Similarly, using TGF-beta receptor affinity-labeling assay, hepatocytes from PH livers were found to have an increase in TbetaR-I, II, and III proteins, with a peak at 4 days post-PH, compared with hepatocytes from resting livers. When TGF-beta1 protein was added for a short period (6 or 24 hr) after cell attachment to hepatocyte cultures, it inhibited DNA synthesis more effectively in hepatocytes from regenerating compared with resting livers. Our results show that hepatocyte TGF-beta receptors and sensitivity to growth inhibition by TGF-beta1 protein change together and are modulated during liver regeneration, as well as during the conditions of primary culture.

Activin Receptors, Type I↗
PubMed1998

Circulating vascular endothelial growth factor (VEGF) is a possible tumor marker for metastasis in human hepatocellular carcinoma.

Vascular endothelial growth factor (VEGF) is closely related to angiogenesis in various human cancers. However, little is known of its circulating levels in hepatocellular carcinoma (HCC). We examined circulating VEGF levels in chronic liver disease to assess their clinical significance. Plasma VEGF concentrations were determined, by enzyme immunoassay, in patients with chronic hepatitis (CH; n = 36), liver cirrhosis (LC; n = 77), and HCC (n = 86) for a cross-sectional study. Plasma VEGF levels in healthy controls (n = 20) and CH, LC, and HCC patients were 17.7 +/- 5.4 (mean +/- SD), 30.6 +/- 22.8, 34.4 +/- 27.0, and 51.1 +/- 71.9 pg/ml, respectively. The levels were significantly elevated in the HCC group, compared with the control, CH, and LC groups. Plasma VEGF levels in stage I, II, III, IVA, and IVB HCC patients were 27.6 +/- 16.1, 26.5 +/- 13.7, 35.8 +/- 15.3, 45.4 +/- 39.4, and 103.1 +/- 123.2 pg/ml, respectively. The stage IVB patients with remote metastasis showed significantly marked elevation compared with the patients at the other stages. Platelet numbers were weakly correlated with plasma VEGF levels in the HCC group. Plasma VEGF level was highly elevated in patients with HCC, particularly those with metastatic disease. We consider that plasma VEGF is a possible tumor marker for metastasis of HCC. Circulating VEGF may be derived mainly from the large burden of tumor cells, and partly from platelets activated by the vascular invasion of HCC cells.

Adult↗
PubMed1998

Distribution of nociceptive neurons in the ventrobasal complex of macaque thalamus.

In urethane-chloralose anesthetized Japanese macaques, the distribution of nociceptive neurons within the thalamic ventrobasal (VB) complex was studied. Nociceptive specific (NS) and wide dynamic range (WDR) neurons were found in the periphery of the contralateral integument compartment of the VB complex. Thus, they formed a shell at the perimeter of this compartment with a somatotopic organization. The compartment consisted of large parts of nucleus ventralis posteromedialis (VPM) and nucleus ventralis posterolateralis, pars caudalis (VPLc). NS neurons were located more caudally than WDR neurons. In the NS zone of VPM, the forehead was represented caudally, and oral structures rostrally. In the ventral NS zone of VPM, there was a sequential representation of the tongue, gum and mandibular skin from the medial to the lateral edge. The hand was represented medially in the NS zone of VPLc, and its representation dominated in the rostral NS zone. There was a sequential representation of the cervical, thoracic, lumbar, sacral and caudal segments mediolaterally along the dorsal VPLc. In the medial half of ventral NS zone of VPLc, the upper body half was represented, and in the lateral half, the lower body half. The foot was represented at or near the medial edge of lateral half. In the rostral WDR zone, the trunk and peripheral face were represented.

Animals↗
PubMed1998

Identification and characterization of the glycoprotein E and I genes of canine herpesvirus.

We have determined the sequence of the gE and gI genes of canine herpesvirus (CHV), DFD-6 strain. The gE ORF codes for a 522 a.a. polypeptide with a signal sequence at the amino-terminus and a trans-membrane domain at the carboxy-terminus. The gI ORF codes for a 259 a.a. polypeptide with a signal sequence but no trans-membrane domain. Comparison with another line of CHV indicated that the DFD-6 gI gene underwent a frame-shift mutation which caused the loss of the trans-membrane domain. Antibodies against the gE and gI polypeptides detected a 94 kDa gE and a broad band of gI (55-62 kDa) in DFD-6 infected cells, respectively. The precursor of DFD-6 gE is modified to the mature form by N-linked glycosylation only in the presence of gI. Together with the fact that the gI- mutant of DFD-6 produced smaller plaques, it is suggested that the truncated DFD-6 gI is functional. The precursor of DFD-6 gI is modified to the mature form by N-linked glycosylation only in the presence of gE.

Amino Acid Sequence↗
PubMed1998

Clinical significance of plasma vascular endothelial growth factor in gastrointestinal cancer.

Circulating vascular endothelial growth factor (VEGF) was measured in gastric and colorectal cancer patients using an enzyme-linked immunosorbent assay (ELISA). Firstly, serum and plasma samples were collected from 20 normal controls to compare the values of VEGF and to determine which specimen type was most suitable for detecting circulating VEGF. Seventeen of 20 normal controls had plasma VEGF levels under the limit of detection (15 pg/ml) and the levels of the remaining three controls were 21, 22 and 38 pg/ml. In contrast, all serum samples indicated high levels of VEGF (mean 238 pg/ml), ranging from 44 to 450 pg/ml. In a time-course test of two normal controls serum VEGF values increased markedly between 30 and 60 min and remained high, whilst plasma VEGF values were low up to 480 min. Thus, plasma samples are more suitable for the measurement of circulating VEGF. Next, plasma VEGF levels were examined in 44 patients with gastric cancer (8 early, 7 advanced without remote metastasis and 29 metastatic), 13 with colorectal adenoma (2 with focal cancer) and 26 with colorectal carcinoma (8 advanced without metastasis and 18 metastatic) before treatment. An extremely high plasma concentration of VEGF was seen in some cancer patients with metastasis. To discriminate these patients, a cut-off level was determined, considering both the distribution of the sample concentration and the upper limit of 95% confidence area of VEGF in the cancer patients without metastasis. The cut-off value was 108 pg/ml and most cancer patients without metastases had VEGF levels below the cut-off value. In 11 of 29 metastatic gastric cancer patients (38%) and 9 of 18 metastatic colorectal cancer patients (50%), plasma VEGF levels were higher than the cut-off value. Survival was also analysed in the patients with metastasis. It was significantly longer in the patients with low VEGF levels (below the cut-off) than in those with high VEGF levels (logrank test, P = 0.042). 34 patients with metastasis (19 gastric cancer and 15 colorectal cancer) were treated with systemic chemotherapy, and their pretreatment levels of plasma VEGF and conventional tumour markers (CEA and CA19-9) were evaluated in relation to response. The response to chemotherapy was significantly higher in patients with low VEGF levels (< or = 108 pg/ml) than in those with high VEGF levels (P = 0.047). Such a difference was not observed with CEA/CA19-9. In conclusion, plasma VEGF is a useful marker for tumour metastasis and patient survival, and a possible predictive factor for the response of patients with gastrointestinal cancer to chemotherapy.

Adult↗
PubMed1998

Epidemiology and properties of heat-stable enterotoxin-producing Escherichia coli serotype O169:H41.

Enterotoxigenic Escherichia coli (ETEC) serotype O169:H41 organisms have become the most prevalent ETEC in Japan since the first outbreak in 1991. It was assumed that the outbreaks were due to clonal spread of this new ETEC serotype. The relationship of 32 strains isolated from 6 outbreaks were examined for biotype, antibiotic susceptibility, enterotoxigenicity, protein banding pattern, lipopolysaccharide banding pattern, plasmid analysis, and ribotyping. Further, the strains were examined by haemagglutination, surface hydrophobicity, and the ability to adhere to HEp-2 cells. The present study suggests that the outbreaks were caused by multiple clones of STp-producing O169:H41 since they showed differences in ribotype and outer membrane protein banding patterns. The strains did not agglutinate human or bovine red blood cells in a mannose-resistant manner. They adhered to HEp-2 cells in a manner resembling enteroaggregative E. coli. Five strains were examined by dot-blot tests for the colonization factor antigens CFA/I, CS1, CS2, CS3, CS4, CS5, CS6, CS7, PCFO159, PCFO166 and CFA/III. Although four strains expressed CS6, no structure for CS6 was identified. A strain that the anti-CS6 MAbs did not react with could adhere to HEp-2 cells in mannose resistant manner; thus, it is unlikely that CS6 play an important role in the adhesion to the cells. Electron microscopy studies of the O169:H41 strains suggested that curly fimbriae, a possible new colonization factor, may be playing an important role in the adhesion of the bacteria to HEp-2 cells. In conclusion, outbreaks due to ETEC O169:H41 were caused by multiple clones, and the strains should be examined in detail for a possible new colonization factor.

Bacterial Adhesion↗
PubMed1998

Construction of canine herpesvirus vector expressing foreign genes using a lacZ-TK gene cassette as a double selectional marker.

An improved method for constructing canine herpesvirus (CHV) recombinants expressing foreign genes by using the lacZ-TK gene cassette as a double selectional marker was developed. A recombinant CHV carrying the lacZ-TK gene at a targeted gene locus was constructed and used as a parental virus for generating new recombinants. The parental virus formed blue plaques and was sensitive to TK-specific drugs, while newly generated recombinants, in which the lacZ-TK gene was replaced with the desired foreign gene, become both resistant to the TK-specific drugs and formed white plaques. Recombinants were isolated by using the combination of drug selection and color selection. This improved method allows construction of recombinant CHV with great ease, because the drug selection can enrich the frequency of recombinant CHV from 0.01-0.1% to 10-80%. This method was employed to construct a recombinant CHV that expressed rabies virus (RV) glycoprotein (G protein).

Animals↗
PubMed1998

Characterization of a human genomic DNA fragment which rescues defective lipid-linked oligosaccharide synthesis in a mutant G258 cell line isolated from the FM3A mouse mammary carcinoma cell line.

The G258 mutant cell line, isolated from the FM3A mouse mammary carcinoma cell line, is temperature-sensitive for both cell growth and asparagine-linked glycosylation due to mutation at a single location. The biochemical defect in the G258 mutant resides in the formation of lipid-linked oligosaccharide, presumably in one of the steps of GDP-mannose-dependent mannosylation (Y. Nishikawa, J. Cell. Physiol. 119, 260-266, 1984; Y. Nishikawa, Biochim. Biophys. Acta 1091, 135-140, 1991). In the present study, we transfected human genomic DNA fragments into the G258 mutant by the radiation hybrid method and isolated transformants (KK-1, -3 and -4) which showed recovery from both temperature-sensitive cell growth and asparagine-linked glycosylation. These transformants contained a common Alu-containing human DNA fragment (1.3 kb) which will be used as a marker for isolating the gene that complements the defect of lipid-liked oligosaccharide synthesis in the G258 mutant.

Alu Elements↗
PubMed1998

Genomic structures and chromosomal location of p91, a novel murine regulatory receptor family.

Recently, we found a novel murine cell-surface glycoprotein, designated as p91, expressed mainly in myeloid cells such as macrophages and mast cells. The molecule has six immunoglobulin-like extracellular domains, a transmembrane segment, and a cytoplasmic tail containing four immunoreceptor tyrosine-based inhibition motif (ITIM) or ITIM-like sequences, resembling the structural features of human killer-cell inhibitory receptors (KIR). Here we show that p91 comprises a polymorphic gene family, harboring one potent inhibitory-type p91 and at least two other p91 genes. Tyrosine-phosphorylated, but not nonphosphorylated, synthetic peptides matching the third ITIM and the fourth ITIM-like sequences, respectively, found in the cytoplasmic portion of p91A, the sole inhibitory-type p91, were associated with the tyrosine phosphatases, SHP-1 and SHP-2. In addition, the phosphotyrosyl peptide matching the third ITIM sequence also bound the inositol 5-phosphatase, SHIP. These results support the notion that p91A may function as an inhibitory cell-surface molecule against cell activation. The p91 genes were shown to be clustered in the proximal region of mouse chromosome 7, a syntenic position of human chromosome 19 where the genes for the KIR family are found. A human cDNA clone cross-hybridizing to a murine p91 probe was isolated from a human spleen cDNA library, and was found to code for a molecule quite similar to members of the immunoglobulin-like transcript (or ILT) family. The gene was found to be located on human chromosome 19q13.3-13.4. These results establish the existence of a novel set of potent regulatory receptors in mouse and man, similar but different from the KIR family.

Amino Acid Sequence↗
PubMed1998

Differential effects of N-acetylcysteine on nitroglycerin- and nicorandil-induced vasodilation in human coronary circulation.

We investigated the role of the availability of sulfhydryl groups during vasodilation of the human coronary circulation induced by nitroglycerin and nicorandil. In patients with normal coronary arteries (n = 29) or with coronary artery disease (CAD; n = 26), coronary blood flow (CBF) and epicardial coronary artery diameter after intracoronary administration of 50 microg nitroglycerin or 0.5 mg nicorandil were measured, before and after the intravenous infusion of saline or 100 mg/kg of N-acetylcysteine (NAC). In normal subjects, saline infusion did not alter the nitroglycerin- and nicorandil-induced vasodilation in large epicardial coronary artery. In contrast, NAC potentiated both nitroglycerin- and nicorandil-induced vasodilation. In patients with CAD, nitroglycerin and nicorandil induced less dilation than in normal subjects. NAC augmented the nitroglycerin- and nicorandil-induced vasodilation in the small epicardial coronary artery, but not in the large epicardial segments. In both groups, NAC potentiated the increase in CBF in response to nitroglycerin. However, NAC had no effects on the CBF response to nicorandil. Sulfhydryl availability is at least one determinant of the in vivo responsiveness to nitroglycerin of conductance and resistance vessels in normal human coronary circulation. In patients with CAD, external augmentation of sulfhydryl availability did not affect the depressed response to nitroglycerin in the large epicardial coronary artery. Although nicorandil acts as an NO donor, similar to nitroglycerin, in dilating the epicardial coronary artery, other effects, such as the opening of K(ATP) channel, play a more important role in the nicorandil-induced vasodilation of resistance vessels.

Acetylcysteine↗
PubMed1998

Effects of O-glycosylation inhibitors on the differentiation of HL-60 cells.

The effects of O-glycosylation inhibitors on the growth and differentiation of the human acute promyeloblastic leukemia cell line HL-60 were studied to examine whether the O-glycosylation is needed for HL-60 cells to differentiate into granulocyte-like cells or monocyte-macrophage-like cells. N-Acetyl-alpha-D-galactosaminides, inhibitors of mucin-type oligosaccharide synthesis, and N-acetyl-beta-D-galactosaminides did not affect either growth or differentiation. beta-D-Xylosides, the artificial initiators of glycosaminoglycan synthesis, also were tested. Only 4-methylumbelliferyl-beta-D-xyloside induced HL-60 cells, to differentiate, and they differentiated into granulocyte-like cells, assessed by reduction of nitroblue tetrazolium, Giemsa staining, and esterase double-staining. The aglycon portion of 4-methylum-belliferyl-beta-D-xyloside, 4-methylumbelliferone, caused the differentiation. Thus we could find a new drug that induces the differentiation of HL-60 cells.

Antimetabolites, Antineoplastic↗