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Biomedical subjects

K Usami

Publications and source records attributed to K Usami.

At least 19 recordsLinked to original sources
PubMed2002

CDX2 expression in the stomach with intestinal metaplasia and intestinal-type cancer: Prognostic implications.

CDX2, a transcriptional factor expressed in the intestine, is implicated in the development and maintenance of the intestinal mucosa. Recent studies have demonstrated that CDX2 is expressed in the intestinal metaplasia of the stomach and intestinal-type gastric cancer, while it is not expressed in the normal gastric mucosa. To investigate the role of CDX2 in gastric cancer, we determined CDX2 expression and cell proliferation rate in various types of gastric cancer tissues by immunostaining. Surgically dissected gastric cancer tissues were collected from 40 patients. Consistent with previous reports, CDX2 was expressed in most gastric mucosa samples with intestinal metaplasia (89%, 16/18), although it was not found in the adjacent normal mucosa. CDX2 expression was also detected in 64% (18/28) of intestinal-type gastric cancer cases, whereas it was not observed in the diffuse-type gastric cancer (0/12). Moreover, the CDX2-positive gastric cancer samples showed significantly lower index for Ki-67 immunostaining, indicating reduced cell proliferation rates than in the CDX2-negative samples. Importantly, multivariate analysis for the overall survival rate revealed that the CDX2-positive gastric cancer patients survived significantly longer than the CDX2-negative patients. Even among the intestinal-type gastric cancer cases, the CDX2-positive group showed a lower Ki-67 index and longer postoperative survival than the CDX2-negative group. These results collectively indicate that CDX2 expression in gastric cancer tissues can be a novel prognostic marker for patient survival.

Aged↗
PubMed2000

Effects of pertussis toxin on behavioral responses during different withdrawal periods from chronic cocaine treatment.

1. The role of Gi-proteins on cataleptic responses induced by SCH23390 and haloperidol in chronic cocaine-treated mice was examined by intracerebroventricullor (i.c. v.) and intravenous (i. v.) injections of pertussis toxin (PTX), which catalyzes adenosine diphosphate (ADP)-ribosylation of Gi-proteins. 2. In animals pretreated chronically with cocaine (10 mg/kg, s.c. on alternating days for 21 days), haloperidol (0.1 mg/kg i.p.) exerted an enhanced cataleptic response, but SCH23390 (0.1 mg/kg i.p.) produced an attenuated response at day 1, which converted to a supernormal response, when it was administered 20 days after the last cocaine injection. 3. The attenuated SCH23390 cataleptic response (D1 receptor supersensitivity induced one day after chronic cocaine treatment), was reversed one day after a single dose of PTX, which by itself had no effect, whereas the enhanced haloperidol catalepsy was further enhanced with same dose of toxin. 4. On the other hand, the enhanced SCH23390- and haloperidol-induced cataleptic responses seen during longer withdrawal period (20 days) were potentiated 20 days after a single coadministration of PTX. The stimulatory effects of PTX on the enhanced SCH23390-induced cataleptic response (D1 receptor subsensitivity induced during long-term withdrawal periods from chronic cocaine treatment), may be due to an indirect inhibition of D1 receptors (a synergistic effect) via blockade of postsynaptic dopamine D2 receptors. 5. The postsynaptic D1 receptor supersensitivity and D2 receptor subsensitivity induced one day after chronic cocaine treatment may involve greater Gi-protein ADP-ribosylation in the presynaptic cell body (VTA) than that in the postsynaptic cell body. On the other hand, the subsensitivity of postsynaptic dopamine D1 and D2 receptors (the enhanced SCH23390- and haloperidol-induced cataleptic responses) seen during longer withdrawal periods may mainly involve Gi-protein ADP ribosylation in the postsynaptic cell body, and which may be mediated by a PTX-sensitive muscarinic M2 and/orGABAB receptor activation.

Adenosine Diphosphate Ribose↗
PubMed1998

Layered structure analysis of GMR multilayers by X-ray reflectometry using the anomalous dispersion effect.

As a basic layered structure for giant magnetoresistive (GMR) heads, NiFe/Cu/NiFe/Ta/Si substrate was measured by X-ray reflectometry at Cu Kalpha, Cu Kbeta and Cu K-absorption-edge energies. The accuracy of both the Cu thickness and the interface width between the upper NiFe and the Cu layers was found to improve in the order Cu Kalpha < Cu Kbeta < Cu K-edge. The final thickness and interface width values obtained from Cu Kbeta reflectivity are in good agreement with those from the Cu K-edge. The anomalous-dispersion effect is useful in the more accurate analysis of the layered structure of transition metal multilayers because it causes a large difference in the refractive indices of specific elements near the absorption edge. The Kbeta X-rays, which can be produced from conventional X-ray sources, are also available for the accurate analysis of reflectivity measurements.

Journal Article↗
PubMed1997

Dopaminergic and cholinergic interaction in cataleptic responses in mice.

The cataleptogenic effects of haloperidol, a dopamine D2 receptor antagonist; SCH23390, a D1 receptor antagonist; physostigmine, a cholinesterase inhibitor; and pilocarpine, a muscarinic M1 receptor agonist, were challenged by pretreatment of mice with SKF38393, a dopamine D1 receptor agonist; apomorphine, a dopamine D1/D2 receptor agonist (mainly D2 receptor); pirenzepine, a muscarinic M1 receptor antagonist; and scopolamine, a muscarinic M1/M2 receptor antagonist. The effect of physostigmine and pilocarpine on haloperidol and SCH23390 cataleptic responses was also examined. Each of the challenging agents blocked one or more of the cataleptogenic agents, but only scopolamine blocked all four. Pirenzepine blocked cataleptic responses induced by SCH23390 and pilocarpine, but not those by haloperidol and physostigmine. The results of this study suggest that the action of physostigmine (endogenous acetylcholine) on M2 receptors might be more potent than that on muscarinic M1 receptors. A further interesting observation was that the haloperidol-induced catalepsy was enhanced by physostigmine pretreatment, but not by pilocarpine pretreatment, whereas the SCH23390-induced catalepsy showed the opposite spectrum of enhancement by the two cholinergic agonists. We conclude that, although the four cataleptogenic agents act via the dopaminergic-cholinergic systems, their pharmacological differences may be due largely to the different receptor subtypes that are involved in the mediation of catalepsy produced by each agent. Thus, dopamine receptors not only influence the cholinergic muscarinic receptors, but muscarinic M1 and M2 receptors also might mediate dopamine D1 and D2 receptor responses, respectively. The results suggest that there are, at the least, relationships between muscarinic M1 receptors and dopaminergic D1 receptors, and between muscarinic M2 receptors and dopaminergic D2 receptors. Dopamine D1 and D2 receptors may interact in a synergistic fashion on dopaminergic systems, but act independently of each other in influencing other system such as cholinergic neurons.

Animals↗
PubMed1992

Nerve growth factor suppresses apoptosis of murine neutrophils.

We investigated inhibitory activity of nerve growth factor (NGF) on apoptosis of murine peritoneal exudate neutrophils. During culture for 9 h, apoptotic cells were identified by morphological changes under a light microscope: nuclear pyknosis and chromatin condensation with or without cytoplasmic vacuolation. The apoptotic state was confirmed by DNA fragmentation indicating the endogenous endonuclease activation. When neutrophils were incubated in the presence of NGF, the proportion of cells with the morphological changes was decreased in a dose-dependent manner, and the development of the characteristic DNA fragmentation was restricted. The apoptosis-suppressing activity of NGF was abolished by the addition of anti-NGF monoclonal antibody. These results suggest that NGF may suppress neutrophil apoptosis by preventing the endogenous endonuclease activation.

Animals↗
PubMed1992

Anomalous binding of [3H]N-methyl-quinuclidinyl benzilate methyl chloride to human lymphocyte muscarinic receptors.

Using the muscarinic cholinergic ligand [3H]N-methyl quinuclidinyl benzilate methyl chloride ([3H]NM-QNB), we demonstrated that intact, viable human lymphocytes possess specific muscarinic binding sites. Equilibrium binding studies show that muscarinic acetylcholine receptor are divided into two subtype; high affinity (Ms) and low affinity types (Mw) for the ligand.

Adult↗
PubMed1989

[Changes in muscarinic receptors on lymphocytes in normal aging and Alzheimer's disease].

It has been previously reported that responses of T-lymphocytes to stimulation by phytohemagglutinin declined as age advanced. However, it has not been demonstrated whether receptor binding capacity decreased with age. The potent muscarinic cholinergic antagonist, 3-quinuclidinyl benzilate (QNB) was used to detect the characterization of muscarinic acetylcholine receptors (mAChR) on human lymphocytes. Using techniques developed for the study of mAChR in brain homogenate, direct binding to whole live lymphocytes was shown for the [3H]-QNB. Three age groups of healthy female adults were examined: 42-49 (N = 7), 50-59 (N = 7) and 60-69 years old (N = 8). Moreover, we studied mAChR on lymphocytes from 11 patients (54-65 years old, female) with probable Alzheimer's Disease. Specific binding is saturable, proportional to cell concentration, and can be displaced by atropine. For control subjects (age range 42-69 years old, N = 22), a positive correlation (r = 0.634, alpha less than 0.01) was found between Kd and age. Also positive correlation between Bmax and age was shown to be strong (r = 0.434, alpha less than 0.05), The regression equations are: Y = 3.25X - 109.5 (Kd); Y = 24.7X - 201.8 (Bmax); where, X and Y designate the age of individuals and Kd (or Bmax), respectively. Hence, for patients with Alzheimer's Diseases, the correlation between Kd and age, and between Bmax and age, were weak (r = -0.352, 0.011, not significant, respectively). No significant change in Kd or Bmax was obtained on lymphocytes from patients, compared to age-matched controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Functional changes in muscarinic receptors on lymphocytes in normal aging and Alzheimer's disease].

To demonstrate that muscarinic acetylcholine receptor (mAChR) acts as an aging marker, we studied whether receptor binding capacities decreased with age. A potent muscarinic cholinergic ligand, N-methyl scopolamine (NMS), was used to detect how the binding capacities (Kd, Bmax) of the receptor changed with age. Using techniques developed for the study of mAChR in brain homogenate, direct binding to whole live lymphocytes was shown for the [3H]-NMS. Both groups of healthy female adults (40-49 years old, N = 27) and probable Alzheimer's patients (54-71 years old, N = 17) were examined. For the healthy controls, the regression equations are: Y = 12.2X - 272.6 (Kd; r = 0.453, p less than 0.05) Y = 401X - 16,302 (Bmax; r = 0.387, p less than 0.05) in which, X and Y respectively represent the age of individuals and Kd (or Bmax). Hence, for patients with Alzheimer's disease, the correlations between Kd and age, and between Bmax and age, were weak (r = 0.021, 0.032, not significant, respectively). Three age groups from healthy female adults were examined: 40-49 (N = 9), 50-59 (N = 8) and 60-69 years old (N = 10). There were significant differences (p less than 0.05) between age groups 40-49 and 60-69 years old in both Kd and Bmax. Furthermore, significant change (p less than 0.05) with Bmax was obtained in lymphocytes from patients, compared to age-matched controls. These results suggest that muscarinic cholinergic binding by lymphocytes may serve as a useful peripheral marker, reflecting alterations associated with aging.

Adult↗
PubMed1987

Muscarinic cholinergic receptor binding and electrophysiological response to acetylcholine in cultured rat caudate putamen nucleus neurons.

Binding sites with specificity for N-[3H]methylscopolamine ([3H]NMS) are present in homogenates of primary culture neurons from the rat caudate putamen nucleus (CPN). Specific binding is saturable with respect to [3H]NMS. The Scatchard analysis indicates a dissociation constant of 0.6 nM and a density of 7.0 X 10(3) per cell, or 78 fmol/mg protein. In electrophysiological measurements, excitatory postsynaptic currents (EPSCs) in larger cells were increased by pressure application of acetylcholine under voltage clamp condition. The EPSCs may come from neighboring smaller cells with muscarinic acetylcholine receptors.

Acetylcholine↗
PubMed1987

[Effects of phenol and related compounds on erythrocytes and hepatocytes from rats and dipalmitoyl phosphatidylcholine-liposomes].

The effects of phenol, guaiacol and m-cresol on erythrocytes, hepatocytes, dipalmitoyl phosphatidylcholine (DPPC)-liposomes and surface tension were studied at various concentrations. Phenol at 10 mM caused a slight inhibition of hypotonic hemolysis in rat erythrocytes. Guaiacol at 4 and 10 mM and m-cresol at 0.6 to 10 mM caused a significant inhibition of hypotonic hemolysis. In the enzyme leakage from isolated rat hepatocytes, phenol at 0.001 to 0.4 mM and 2 to 10 mM, guaiacol at 2 to 10 mM and m-cresol at 0.001 to 4 mM caused an inhibition in GOT leakage. The leakage of GPT from hepatocytes was inhibited by phenol at 0.4 to 10 mM, guaiacol at 2 to 10 mM, and m-cresol at 0.001 to 4 mM. m-Cresol at 10 mM caused increases in GOT and GPT leakage. The inhibition of phenol and m-cresol on the LDH leakage in hepatocytes were observed at a concentration of 0.001 mM and 0.1 to 1 mM, respectively. Guaiacol or m-cresol at 10 mM caused an increase in LDH leakage. Phase-transition temperature of DPPC-liposomes was depressed by phenol and m-cresol at 1 to 10 mM and by guaiacol at 5 and 10 mM. Guaiacol at 1 and 10 mM and m-cresol at 10 mM caused a depression of surface tension, but phenol caused no change in surface tension. The order of effects on erythrocyte, hepatocyte and DPPC-liposome membranes was m-cresol greater than phenol greater than or equal to guaiacol. In the present study, phenol and its related compound showed a positive correlation between their effects on various membranes and germicidal effects as evaluated by the phenol coefficient, but the effects were not related to a depression of surface tension.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1986

Comparative studies on rat primary cultured and isolated hepatocytes in the evaluation of a therapeutic agents for liver disease.

We have investigated the effect of a therapeutic agent for liver disease, Laennec, on the GOT leakage from freshly isolated and primary cultured rat hepatocytes which were treated with CCl4. By treatment with Laennec together with CCl4, the GOT leakage from isolated hepatocytes increased and that from cultured hepatocytes decreased, compared to those incubated only with CCl4. The results suggest that it is better to use primary cultured hepatocytes than to use freshly isolated hepatocytes to evaluate therapeutic agents for liver disease.

Animals↗