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Biomedical subjects

K Tamura

Publications and source records attributed to K Tamura.

At least 523 records · Page 29Linked to original sources
PubMed1996

Clinicopathological significance of Ki-ras point mutation and p21 expression in benign and malignant exocrine tumors of the human pancreas.

CONCLUSION: The present study suggests that Ki-ras point mutations may play an important role in the early stages of tumorigenesis and that a double mutation has a stronger detrimental effect than a single mutation on the survival after pancreatectomy. BACKGROUND: Previous studies have suggested the important role of Ki-ras point mutations in ras gene codon 12 in the tumorigenesis of pancreatic cancer, but their clinicopathological significance is still unclear. The present study was designed to assess the clinicopathological significance of Ki-ras point mutations, and p21 expression in malignant and benign diseases of the pancreas. METHODS: Oligonucleotide dot-blot hybridization for Ki-ras point mutations in codon 12 and immunohistochemical staining for p21 expression were applied. Cases included 44 primary and 15 metastatic lesions of pancreatic cancer, and 17 benign pancreatic diseases. RESULTS: Ki-ras point mutations and p21 expression were detected in 43 and 19 primary lesions, 9 and 6 metastatic lesions, and four and five benign diseases, respectively. The patients with a single mutation had a better survival after pancreatectomy than those with a double mutation. The patients with a p21(+) GAT mutation showed the worst survival after pancreatectomy compared with other categories of patients.

Adult↗
PubMed1996

Enterobacter kobei sp. nov., a new species of the family Enterobacteriaceae resembling Enterobacter cloacae.

The name Enterobacter kobei sp. nov. is proposed for a group of organisms referred to as NIH Group 21 at the National Institute of Health, Tokyo. The members of this species are Gram-negative, motile rods conforming to the definition of the family Enterobacteriaceae. The DNA relatedness of 23 strains of NIH Group 21 to the representative proposed as the type strain of this species averaged 82% at 70 degrees C, whereas the relatedness to other species within the family Enterobacteriaceae was less than 42%. Because the phenotypic resemblance to Enterobacter cloacae is very close and the DNA relatedness (12-42%) is closer to species of the genus Enterobacter than to other species of the family, the members of NIH Group 21 were placed in the genus Enterobacter. Close phenotypic and genetic relationships were also found between NIH Group 21 and a member of a group of organisms referred to as Enteric Group 69 at the Centers for Disease Control and Prevention (CDC), Atlanta, Georgia, USA. It is suggested that the latter could be regarded as a subspecific rank of E. kobei, though this is subject to study of further strains. The majority of strains of E. kobei were isolated from clinical specimens. A culture of the type strain (NIH 1485-79) has been deposited in the Japan Collection of Microorganisms as JCM 8580.

Bacteriological Techniques↗
PubMed1996

Inhibition of platelet aggregation by endocardial endothelial cells.

We assessed the anti-platelet properties of endocardial endothelial cells (EECs) by measuring platelet aggregation after brief interaction with EECs isolated from the right ventricles of porcine hearts. Platelet aggregation in response to thrombin was significantly inhibited by brief incubation of platelet suspensions over EEC monolayers. Pretreatment of EECs with indomethacin restored platelet reaction but that with L-NAME and hemoglobin (Hb) did not. The PGI2 content of platelet suspensions after interaction with cultured EECs was significantly correlated with the inhibition of platelet aggregation. These results suggest that EECs inhibit platelet aggregation by releasing PGI2.

Animals↗
PubMed1996

Expression of CD26/dipeptidyl peptidase IV in adult T cell leukemia/lymphoma (ATLL).

The association of CD26/dipeptidyl peptidase IV (DPPIV) and human T lymphotropic virus type I (HTLV-I) was studied by two approaches. First, we examined the expression of CD26 in peripheral blood mononuclear cells (PBMC) from the patients with adult T cell leukemia/lymphoma (ATLL), an HTLV-I-related malignancy. The expression of CD26 on the surface of PBMC was decreased in all 20 patients with ATLL compared with those from normal individuals (P < 0.01) and the expression of the CD26 gene transcript was not detectable in seven out of eight patients with ATLL. Then we compared the quantity of viral DNA in CD26-negative (CD26-) and CD26-positive (CD26+) cells obtained from 17 HTLV-I healthy carries by using a polymerase chain reaction method. The CD26-cells had a higher copy number of viral DNA than CD26+ cells. These findings indicate that HTLV-I has in vivo tropism to CD26- cells, suggesting that some phenotypes of ATLL cells reflect the in vivo cellular tropism of HTLV-I.

Adult↗
PubMed1996

Chronic neutrophilic leukemia with dysplastic features mimicking myelodysplastic syndromes.

A 52-year-old male patient with chronic neutrophilic leukemia (CNL) with dysplastic features is described. He had a 2-year history of anemia followed by marked leukocytosis up to 57.5 x 10(9)/l with 88% segmented neutrophils. Bone marrow aspiration and biopsy showed hypercellular marrow with myeloid hyperplasia and 16% myeloblasts. There were also significant morphological abnormalities which included neutrophils with few granules, hypersegmented nucleus or Pelger-Heut anomaly, and micromegakaryocytes. Cytogenetic analysis disclosed a deletion of the long arm of chromosome 7 (7q-). He was diagnosed as having CNL with dysplastic features and was treated conservatively. However, leukemic transformation to acute myelogenous leukemia occurred within a year and he died 16 months after diagnosis. Neutrophilia is a feature not of myelodysplastic syndromes (MDS) but rather of myeloproliferative disorders such as CNL. However, this patient was considered to have MDS with increased proliferation and differentiation of neutrophilic lineage, because of marked myelodysplasia and poor prognosis.

Diagnosis, Differential↗
PubMed1996

A nitric oxide-sensitive electrode: requirement of lower oxygen concentration for detecting nitric oxide from the tissue.

In order to directly detect nitric oxide (NO) liberated from isolated tissue, a practical and convenient method using a nitric oxide-sensitive electrode is described. To avoid the nonselective signal caused by ionic substances, the electrode was covered with three layers but remains permeable for gaseous substances. In a solution bubbled with 20% oxygen (pO2, approximately 150 mm Hg), administration of S-nitroso-N-acetyl-d, l-penicillamine (SNAP) at concentrations greater than 10(-7) mol/L elicited an electrode response. Based on a comparison with the chemical determination of NO released from SNAP, the electrode may be able to detect nitric oxide around nmol/L. At least 30 nmol NO per liter in anoxic conditions was reported to be detected by this electrode (Matsui, 1995). In a specially designed small chamber, the electrode was attached on the surface of endothelial side of the isolated aorta of the guinea pig. When carbachol was added to the chamber, the electrode responded when the solution was bubbled with 20% but not with 40% or 95% of oxygen, suggesting a much faster decomposition of nitric oxide in the presence of higher concentrations of oxygen. The electrode response to carbachol was abolished in the presence of NG-monomethyl-L-arginine or nitro arginine. These results suggest that the electrode method described in this manuscript is suitable for detecting nitric oxide liberated from isolated tissues when comparatively low oxygen levels are present in the physiological salt solution.

Animals↗
PubMed1996

Prevalence, resolution, and determinants of late potentials in patients with unstable angina and left ventricular wall motion abnormalities.

Although transient myocardial ischemia such as exercise-induced ischemia has not been reported to be associated with the occurrence of late potentials, the association of late potentials with more profound ischemic damage, which is represented by reversible but prolonged left ventricular wall motion abnormalities, has not been demonstrated. We prospectively evaluated 37 unstable angina patients who had reversible but prolonged wall motion abnormalities after resolution of chest pain and electrocardiogram (ECG) changes. Signal-averaged ECG (SAECG) and echocardiogram were recorded during the acute phase and before hospital discharge. Late potentials were present in 6 (16 percent) patients on the initial SAECG recording and resolved in all 6 patients on the second recording before hospital discharge. Normalization of inferior left ventricular wall motion abnormality and multivessel disease were observed more frequently in patients with late potentials on the initial recording than in patients without (p < 0.05 and p < 0.05, respectively). In conclusion, late potentials were observed in patients who had reversible but prolonged wall motion abnormalities; these late potentials were resolved with improvement of left ventricular wall motion abnormalities. These results suggest that myocardial ischemia with prolonged wall motion abnormalities is a possible mechanism of the occurrence of late potentials.

Action Potentials↗
PubMed1996

Metabolism, uptake, and transepithelial transport of the diastereomers of Val-Val in the human intestinal cell line, Caco-2.

PURPOSE: The purpose of this study was to determine whether the binding of the diastereomers of Val-Val to the apical oligopeptide transporter(s) could be correlated with their cellular uptake and transepithelial transport. METHODS: The Caco-2 cell culture system was used for all experiments. The binding of the diastereomers of Val-Val was evaluated by determining their ability to inhibit [3H]cephalexin uptake. The stability of the diastereomers was determined in a homogenate of Caco-2 cells and in the apical bathing solution over Caco-2 cell monolayers. The cellular uptake and transepithelial transport properties of the individual diastereomers were studied using Caco-2 cell monolayers. RESULTS: 10 mM concentrations of L-Val-L-Val, L-Val-D-Val, D-Val-L-Val and D-Val-D-Val inhibited cellular uptake of [3H]cephalexin (0.1 mM) by 92%, 37%, 70%, and 18%, respectively. When the cellular uptake of Val-Val diastereomers (1 mM) were evaluated, the intracellular concentrations of L-Val-D-Val and D-Val-L-Val were 15 and 50 times higher, respectively, than that of D-Val-D-Val. The cellular uptake of L-Val-D-Val and D-Val-L-Val was inhibited by Gly-Pro (10 mM) ( > 95%), whereas Gly-Pro had no effect on the cellular uptake of D-Val-D-Val. L-Val-L-Val was not detected in the Caco-2 cells, probably due to its metabolic lability. When the transepithelial transport of the Val-Val diastereomers (1 mM) was determined, L-Val-D-Val, D-Val-L-Val and D-Val-D-Val transport rates were similar. The transepithelial transport of L-Val-D-Val and D-Val-L-Val was inhibited by Gly-Pro (10 mM) 36% and 30%, respectively, while Gly-Pro inhibited carnosine (1 mM) transepithelial transport by 65%. Gly-Pro had no effect on the transepithelial transport of D-Val-D-Val. CONCLUSIONS: These results suggest that the major transepithelial transport route of L-Val-D-Val, D-Val-L-Val and D-Val-D-Val is passive diffusion via the paracellular route. The binding of Val-Val diastereomers to the oligopeptide transporter(s) is a good predictor of their cellular uptake, however, the binding is not a good predictor of their transepithelial transport. It appears that the stereochemical requirements for the transporter that mediates efflux of the peptide across the basolateral membrane may be different from the requirements for the apical transporter that mediates cellular uptake.

Biological Transport↗
PubMed1996

Metabolism, uptake, and transepithelial transport of the stereoisomers of Val-Val-Val in the human intestinal cell line, Caco-2.

PURPOSE: The purpose of this study was to determine the stereospecificity of the apical oligopeptide transporter(s) for the stereoisomers of Val-Val-Val and to determine whether the interaction of these molecules with this transporter(s) could be correlated with their cellular uptake and/or transepithelial transport. METHODS: The interactions of these stereoisomers with this transporter(s) were evaluated by determining their ability to inhibit [3H]cephalexin uptake into Caco-2 cells. The metabolism of these stereoisomers was determined in a homogenate of Caco-2 cells and in the apical bathing solution over Caco-2 cell monolayers. The cellular uptake and transepithelial transport properties of these stereoisomers were studied using the Caco-2 cell monolayers. RESULTS: The L-L-L tripeptide was totally degraded within 1 h in the Caco-2 cell homogenate and within 2 h when applied to the apical side of a Caco-2 cell monolayer. In contrast, 36.7 +/- 1.3% and 69.7 +/- 0.9% of L-Val-L-Val-D-Val remained after 2 h in the cell homogenate and in the apical bathing solution, respectively. The other six stereoisomers of Val-Val-Val were completely stable in the Caco-2 cell homogenate. Five of the stereoisomers (L-L-L, L-L-D, L-D-L, D-L-L, D-D-L) significantly inhibited the cellular uptake of [3H]cephalexin (91%, 62%, 14%, 45%, 16%, respectively). The other stereoisomers had no effect on the [3H]cephalexin uptake. When the cellular uptake of the stereoisomers was determined, the D-L-L and L-D-L tripeptides showed the highest intracellular concentrations (1.32 +/- 0.25 and 0.62 +/- 0.20 nmol/mg protein after a 2-h incubation, respectively). In contrast, the intracellular concentrations of the other stereoisomers were less than 0.1 nmol/mg protein. Moreover, the cellular uptake of the D-L-L and L-D-L tripeptides was inhibited by Gly-Pro by 82% and 68%, respectively, whereas Gly-Pro showed moderate to no inhibitory effect on the cellular uptake of the other stereoisomers. The permeability coefficients of the stereoisomers across the Caco-2 cell monolayers were very low (1.8 to 3.1 x 10(-7) cm/sec) and almost identical. Gly-Pro had no effect on their transepithelial transport. CONCLUSIONS: These results suggest that the interaction of the Val-Val-Val stereoisomers with the apical oligopeptide transporter(s) could be a good predictor of their cellular uptake. However, since the major transepithelial transport mechanism of Val-Val-Val stereoisomers is passive diffusion via the paracellular route, the binding of these molecules to the oligopeptide transporter(s) is not a good predictor of their transepithelial transport. It appears that the stereochemical requirements for the transporter that mediates permeation of the peptide across the basolateral membrane may be different from the requirements for the apical transporter that mediates cellular uptake.

Biological Transport↗
PubMed1996

Pro-gastrin-releasing peptide (31-98) as a tumour marker of small-cell lung cancer: comparative evaluation with neuron-specific enolase.

We attempted to clarify whether serum levels of a carboxy-terminal fragment of ProGRP, ProGRP(31-98), could serve as a more accurate tumour marker in patients with SCLC than neuron-specific enolase (NSE). ProGRP(31-98) and NSE were measured retrospectively in 101 newly diagnosed untreated patients with SCLC, 111 with non-small-cell lung cancer (NSCLC) and 114 patients with non-malignant lung diseases. ProGRP(31-98) and NSE levels were determined using a sandwich enzyme-linked immunosorbent assay. Sensitivity in SCLC patients was 72.3% for ProGRP(31-98) and 62.4% for NSE. Comparing the area under curve (AUC) of 'receiver operator characteristics' of ProGRP(31-98) with that of NSE, ProGRP(31-98) was the more powerful marker in the diagnosis of SCLC (P = 0.0001). Serum levels of ProGRP(31-98) were higher in the 40 patients with extensive disease than in the 61 patients with limited disease (P = 0.0082). ProGRP(31-98) was significantly higher in patients with pure small-cell carcinoma than in patients with mixed small-cell/large-cell carcinoma (P = 0.02). In serial measurement in 16 patients responding to treatment, a high degree of correlation was noted between the decrease in serum ProGRP(31-98) levels and clinical response during the second week after treatment (P = 0.0045). These results indicate that the determination of serum ProGRP(31-98) levels plays an important role in the diagnosis and treatment of SCLC patients.

Biomarkers, Tumor↗
PubMed1996

Randomised trial for the prevention of delayed emesis in patients receiving high-dose cisplatin.

Despite recent advances in control of acute emesis following cisplatin-based chemotherapy regimens, delayed emesis remains a significant cause of treatment-related morbidity and factors associated with delayed emesis have not yet been evaluated. A prospective randomised trial was conducted to compare the efficacy and toxicity of granisetron, dexamethasone plus prochlorperazine with granisetron alone in controlling cisplatin-induced delayed emesis and to identify the important factors that influence its occurrence and severity. Seventy cisplatin-naive patients with inoperable solid tumors participated in the trial. Patients who received 80 mg m-2 or 100 mg m-2 of cisplatin were randomly assigned to receive either granisetron 40 micrograms kg-1 intravenously (i.v.) on day 1, dexamethasone 20 mg i.v. on days 2 and 3 and prochlorperazine 5 mg orally thrice daily on days 1-5 or granisetron 40 micrograms kg-1 i.v. on day 1 alone. There was no difference in their acute antiemetic efficacy. A combination regimen was more effective than granisetron alone in preventing delayed symptoms, with superior rates of complete plus major responses of 77% vs 51% (P = 0.0460). Treatment arm was the only determinant factor for the occurrence of delayed emesis (P = 0.0101).

5-Hydroxytryptophan↗
PubMed1996

Monoclonal antibody specific to bovine lens epithelial cell membrane: preparation of a lens epithelial cell-selective immunotoxin.

The lens opacity directly decreases visual acuity. To date, neither prophylactic nor pharmacologic treatments have been effective in stopping or decreasing lens opacity. Although extracapsular cataract extraction followed by intraocular lens insertion is considered to be an effective treatment, postoperative proliferation of lens epithelial cells (LECs) disturbs the vision again. In the present study a monoclonal antibody (MAb) directed against bovine LECs was generated. The MAb (XC3-2-B1H9) reacted specifically with the cell membrane of LECs. No other tissues in bovine eyes, such as the cornea, iris, ciliary body, choroid, retina, or the sclera, or any other major bovine organs, such as lung, liver, spleen, and kidney, were associated. The specificity of XC3-2-B1H9 was confirmed both by immunohistochemistry and by immunoblotting. This MAb cross-reacts with dog LECs. Based on immunoblot analysis, XC3-2-B1H9 recognizes the band with a Mr of about 160 kD of the water-insoluble fraction of LECs. The subclass of these MAbs is IgG1 as determined by immunodiffusion. This MAb has the capacity to act as a component of an immunotoxin to target the LECs.

Animals↗
PubMed1996

Inhibition by acetylsalicylic acid, a cyclo-oxygenase inhibitor, and p-bromophenacylbromide, a phospholipase A2 inhibitor, of both cirrhosis and enzyme-altered nodules caused by a choline-deficient, L-amino acid-defined diet in rats.

Effects of inhibitors of arachidonic acid (AA) metabolism on the development of fatty liver, cirrhosis, glutathione-S-transferase placental form (GST-P)-positive nodules and the generation of 8-hydroxydeoxyguanosine (8-OHdG) and thiobarbituric acid-reactive substances (TBARS), caused by a choline-deficient, L-amino acid-defined (CDAA) diet, were examined in male Fischer 344 rats by feeding CDAA diets supplemented with the inhibitors for 12 and 30 weeks. Acetylsalicylic acid (ASA) (at doses of 0.1 and 0.2%) and p-bromophenacylbromide (BPB) (0.1 and 0.2%) were used as inhibitors of, respectively, cyclo-oxygenase and phospholipase A2, and quercetin (QU) (0.75 and 1.5%) and nordihydroguaiaretic acid (NDGA) (0.1 and 0.2%) as inhibitors of lipoxygenase. None of the inhibitors affected the development of fatty liver caused by the CDAA diet. ASA at a doe of 0.2% almost completely prevented the appearance of cirrhosis, GST-P-positive nodules, 8-OHdG and TBARS in seven out of 11 (63.7%) rats. BPB at a dose of 0.2% also exerted inhibitory effects on all of these lesions but to a lesser extent than ASA. QU and NDGA exerted inhibitory effects limited to the GST-P-positive nodule case. The results indicate that a perturbed AA metabolism, particularly of the cyclo-oxygenase pathway, derived secondarily from depletion of labile methyl groups or phosphatidylcholine, might play key roles in the cirrhosis, hepatocarcinogenesis and oxidative stress caused by a CDAA diet. The results also indicated a possible involvement of the lipoxygenase pathway in hepatocarcinogenic processes.

Acetophenones↗
PubMed1996

Prognostication of proximal femoral growth disturbance after Perthes' disease.

Disturbance of proximal femoral growth associated with Perthes' disease was investigated retrospectively with the use of serial radiographs of 48 patients with unilaterally affected hips. Two types of proximal femoral growth abnormalities--moderately disturbed (6 patients) and severely disturbed (13 patients)--were observed and classified based on resultant femoral length shortening and femoral head deformity of affected hips. Proximal femoral growth disturbance after Perthes' disease was dependent on age at clinical onset: patients whose age at onset was greater than 8 years had a poor prognosis. Future femoral length shortening and femoral head deformity were also found to correlate with the extent of epiphyseal and physeal involvements and the acetabular coverage of the femoral head at the stage of regeneration of involved epiphysis. The current results raised the possibility that the severity of proximal femoral growth disturbance and abnormal growth patterns could be prognosticated based on the extent of epiphyseal and physeal involvements and on the lateralization of femoral head estimated on radiographs during the early stages of Perthes' disease.

Adolescent↗
PubMed1996

Impaired compensatory adaption to B-cell mass reduction in young spontaneously hypertensive rats (SHR).

The aim of this study was to examine the effect of insulin resistance on B-cell function and replication. To this end insulin-resistant spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY) as a control were subjected to 90% pancreatectomy (Px) or sham operation at the age of 4 weeks. Islet function and regeneration were examined 4 weeks after surgery. Plasma glucose levels were higher in SHR than in WKY 4 weeks after Px (488 +/- 30 vs. 395 +/- 31 mg/dl; p < 0.01). In sham-operated animals, plasma glucose responses to intravenous injections of glucose (0.5 g/kg body weight) were much higher in WKY than in SHR, while plasma insulin responses were greater in SHR than in WKY. There was no insulin response to glucose in either strain of Px rats. In sham-operated rats, the insulin content of the remnant equivalent pancreas (4.6 +/- 0.8 vs. 3.0 +/- 0.3 micrograms; p < 0.05) and whole pancreas (62.2 +/- 2.8 vs. 53.3 +/- 2.1 micrograms; p < 0.05) were greater in SHR than in WKY. However, the insulin content was lower in SHR than in WKY (1.9 +/- 0.3 vs. 2.5 +/- 0.7 micrograms; p < 0.05) 4 weeks after Px. Fibrotic degeneration of pancreatic islets was greater in Px-SHR than in Px-WKY. These data suggest that the B cells of SHR are more vulnerable to reduction of islet mass than those of WKY. A diminished capacity for islet cell regeneration in SHR may be linked to insulin resistance presented in this animal model of hypertension.

Adaptation, Physiological↗
PubMed1996

Serotyping and categorisation of Escherichia coli strains isolated between 1958 and 1992 from diarrhoeal diseases in Asia.

A total of 3065 strains of Escherichia coli isolated between 1958 and 1992 from patients with diarrhoea in different countries were examined for virulence factors by hybridisation with biotinylated DNA probes for genes that coded for production of heat-labile and heat-stable enterotoxins, enteroinvasiveness, production of verotoxins and attaching-and-effacing factor and were serotyped. Of the 3065 strains, 1998 were placed into one of four pathogenic categories by their virulence factors: 1057 enterotoxigenic E. coli (ETEC) comprising 30 O-groups, 73 serovars and 137 untypable strains; 132 enteroinvasive E. coli (EIEC) comprising 11 O-groups and 13 serovars; 64 verotoxin-producing E. coli (VTEC) comprising 11 O-groups, 17 serovars and 13 untypable strains; and 745 enteropathogenic E. coli (EPEC) comprising 34 O-groups, 92 serovars and 91 untypable strains. The remaining 1067 strains did not hybridise with any of the DNA probes used. About half the number of O-groups recognised were not restricted to a single pathogenic category, although the combinations of O- and H-antigens were different in each category.

Asia↗