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Biomedical subjects

K Matsuno

Publications and source records attributed to K Matsuno.

At least 91 records · Page 5Linked to original sources

Country reports from Japan: external quality assessment scheme in Japan.

Several external quality assessment schemes (EQAS) have been conducted in Japan. Results obtained from nation-scale EQAS reveal the current quality of laboratory testing in each laboratory. The largest nation-scale EQAS in Japan is that conducted by the Japan Medical Association. The numbers of participants and of items evaluated have increased in EQAS by JMA over its history of 32 years. Improvement in inter-laboratory differences has been observed for most items in EQAS in recent decades. In 1998, about 2,500 laboratories from throughout the country participated in this surveillance, and 47 items were evaluated. The coefficient of variations for the group of all participants was less than 5% for about one third of all test items. On the other hand, very high variations over 20% were observed for 6 items. Also, inter-method differences exist for many items, which may be or may not be related to matrix effects. Retrospective evaluation of all EQAS data suggests that there is still room for improvement in inter-laboratory differences.

Bacteriological Techniques↗

Quality control and quality assurance of platelet counting.

The accuracy and precision of platelet counting using new automated blood cell analyzers is satisfactory. However, there are several errors in automated platelet counting. Careful review of blood cell histograms and peripheral blood films is necessary to avoid false platelet counts as well as to ensure a good quality control regimen.

Automation↗

Staggered movement of an actin filament sliding on myosin molecules in the presence of ATP.

An actin filament sliding on myosin molecules in the presence of an extremely low concentration of ATP exhibited a staggered movement. Longitudinally sliding movement of the filament was frequently interrupted by its non-sliding, fluctuating movements both in the longitudinal and transversal directions. Intermittent sliding movements of an actin filament indicate establishment of a coordination of ATP-mediated active sites distributed along the filament.

Actins↗

Ameliorative effect of SA4503, a novel cognitive enhancer, on the basal forebrain lesion-induced impairment of the spatial learning performance in rats.

We investigated the effect of successive administrations of SA4503 (1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine dihydrochloride), a novel cognitive enhancer with high affinity and selectivity for the sigma1 receptor subtype, on the cortical cholinergic dysfunction-induced impairment of the spatial learning performance in the Morris water maze (MWM) task in rats. The impairment of the spatial learning performance was produced by the ibotenic acid-induced lesion of the basal forebrain (BF) area in rats. Escape latencies to find the platform during the training trials of the MWM task were significantly prolonged in the BF-lesioned rats compared with the sham-operated rats. Daily treatment with SA4503 (0.1-0.5 mg/kg, P.O./day) for 13 days ameliorated this learning deficit. In the probe trial, BF-lesioned rats reduced the number of times each rat crossed the former platform location during the training trials (goal area) in comparison with sham-operated rats. Successive administrations of SA4503 (0.25 mg/kg, P.O./day) also significantly increased the BF lesion-induced reduction of the number of times each rat crossed the goal area. These results suggest that the successive administrations of SA4503 attenuate the impairment of the spatial learning performance in rats with cortical cholinergic dysfunction, and that SA4503 is useful as a therapeutic drug for Alzheimer's disease.

Animals↗

Beneficial effects of acute and repeated administrations of sigma receptor agonists on behavioral despair in mice exposed to tail suspension.

In an attempt to examine whether sigma receptor agonists alleviate behavioral despair, we investigated the effects of sigma receptor agonists on the tail suspension-induced immobility in mice. The acute and repeated (14 days) administrations of sigma1 receptor agonists, such as 1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine dihydrochloride (SA4503) (1 and/or 3 mg/kg) and (+)-pentazocine (5.6 mg/kg), sigma1/2 receptor agonists, such as 1,3-di(2-tolyl)guanidine (DTG) (3 and/or 5.6 mg/kg), desipramine (7.5 and/or 15 mg/kg), and fluoxetine (10 and/or 20 mg/kg), reduced immobility in mice exposed to tail suspension. N,N-Dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl] ethylamine monohydrochloride (NE-100), a sigma1 receptor antagonist, significantly antagonized the decrease in immobility induced by acute administrations of SA4503 (1 mg/kg) and (+)-pentazocine (5.6 mg/kg). Although not significant, NE-100 showed a tendency to inhibit the DTG (5.6 mg/kg)-induced decrease in immobility. In contrast, repeated administrations of SA4503 (1 and 3 mg/kg), (+)-pentazocine (5.6 mg/kg) or DTG (5.6 mg/kg) failed to affect the increase in body weight. These results suggest that acute and repeated stimulations of sigma, possibly a sigma1 receptor subtype, alleviate behavioral despair, unaccompanied with changes in body weight.

Animals↗

Sigma1 receptor subtype does not interact with stereotyped behaviors in rats.

In the present study, we clearly showed that the sigma1 receptor subtype did not interact with the induction of stereotyped behaviors in rats. Namely, (+)-N-allylnormetazocine [(+)-SKF-10,047] (5.0, 10.0, and 20.0 mg/kg, SC), a traditional sigma receptor ligand that has affinities for the sigma1 receptor subtype and the N-methyl-D-aspartate (NMDA)/phencyclidine (PCP) receptor channel complex, markedly produced PCP-like stereotyped behaviors, such as head weaving, turning, and backpedaling, in rats. On the contrary, 1-(3,4-dimethoxyphenyl)-4-(3-phenylpropyl)piperazine dihydrochloride (SA4503), a potent and selective sigma1 receptor agonist, did not produce these behaviors. Additionally, PCP-induced stereotyped behaviors were significantly augmented by (+)-SKF-10,047, but not by SA4503. We thus suggest that the induction of PCP-like stereotyped behaviors elicited by (+)-SKF-10,047 closely interacts with NMDA/PCP receptor channel complex but not with the sigma1 receptor subtype.

Animals↗

Activation of sigma1 receptor subtype leads to neuroprotection in the rat primary neuronal cultures.

The mechanisms of sigma (sigma) receptor ligands-induced neuroprotective effects are controversial because both sigma receptors and phencyclidine (PCP) binding sites of the N-methyl-D-aspartate (NMDA) receptor channel complex have been reported to contribute to these neuroprotective effects. Thus, to clarify the role of sigma receptor in the neuroprotective effects, we examined the effects of 1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine dihydrochloride (SA4503), a novel sigma1 receptor agonist with negligible affinity for the NMDA/PCP receptor channel complex, on the hypoxia/hypoglycemia- and exogenously applied NMDA-induced neurotoxicity in the rat primary neuronal cultures. A selective sigma1 receptor agonist, SA4503, significantly suppressed the hypoxia/hypoglycemia-induced neurotoxicity in the cultures, whereas this agonist failed to inhibit the NMDA-induced neurotoxicity. Similarly, (+)-pentazocine ((+)-PTZ), a prototype sigma1 receptor agonist, inhibited the hypoxia/hypoglycemia-induced neurotoxicity, whilst it did not affect the NMDA-induced toxicity in the cultures. These neuroprotective effects of SA4503 and (+)-PTZ were partially blocked by N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]ethylamine monohydrochloride (NE-100), a putative sigma1 receptor antagonist. These results suggest that the sigma1 receptor subtype plays an important role in the sigma receptor ligands-induced neuroprotective effects via the regulation of excitatory amino acids (EAAs) release from the presynaptic sites.

Animals↗

Dynamics of time and information in dynamic time.

Time is intrinsically locally asynchronous, dynamic in itself, and self-organizing in having locally asynchronous time precipitate further asynchronous time while leaving behind globally synchronous time. The resulting global synchronism is skewed in locally asynchronous time, while being vertical to the effected globally synchronous time. Information is a dynamic attribute of time and can be represented as a skewed synchronism in locally asynchronous time. Information originates in the communication among asynchronous times of a local character.

Information Science↗

The relativist stance.

The two mindsets of absolutism and relativism are juxtaposed, and the relational or relativist stance is vindicated. The only 'absolute' entity which undeniably exists, consciousness has the reality of a dream. The escape hatch from this prison is relational, as Descartes and Levinas found out: Unfalsified relational consistency implies exteriority. Exteriority implies infinite power which in turn makes compassion inevitable. Aside from ethics as a royal way to enlightenment, a new technology called 'deep technology' may be accessible. It changes the whole world in a demonstrable fashion by manipulation of the micro frame--that is, the observer-world interface.

Information Theory↗

Purification and some properties of IMP dehydrogenase of Bacillus cereus.

IMP dehydrogenase was purified from a crude extract of B, cereus cells. The molecular mass of the purified enzyme was estimated to be 56 kDa by SDS-PAGE and 225 kDa by gel filtration. The optimum pH of the enzyme was about 9.5. The first seven residues at N-terminus of the enzyme was determined to be Met-Trp-Glu-Ser-Lys-Phe-Val. The enzyme showed a significant specificity for inosine nucleotides among 15 purines and pyrimidines tested, but not acted on other purines and pyrimidines including inosine. Among 11 metal ions and 3 enzyme inhibitors tested, Al3+ activated the IMP dehydrogenase. The enzyme activity was strongly inhibited by Zn2+ and Fe3+.

Ammonium Sulfate↗

Human deltex is a conserved regulator of Notch signalling.

A fundamental cell-fate control mechanism regulating multicellular development is defined by the Notch-signalling pathway. Developmental and genetic studies of wild type and activated Notch-receptor expression in diverse organisms suggest that Notch plays a general role in development by governing the ability of undifferentiated precursor cells to respond to specific signals. Notch signalling has been conserved throughout evolution and controls the differentiation of a broad spectrum of cell types during development. Genetic studies in Drosophila have led to the identification of several components of the Notch pathway. Two of the positive regulators of the pathway are encoded by the suppressor of hairless [Su(H)] and deltex (dx) genes. Drosophila dx encodes a ubiquitous, novel cytoplasmic protein of unknown biochemical function. We have cloned a human deltex homologue and characterized it in parallel with its Drosophila counterpart in biochemical assays to assess deltex function. Both human and Drosophila deltex bind to Notch across species and carry putative SH3-binding domains. Using the yeast interaction trap system, we find that Drosophila and human deltex bind to the human SH3-domain containing protein Grb2 (ref. 10). Results from two different reporter assays allow us for the first time to associate deltex with Notch-dependent transcriptional events. We present evidence linking deltex to the modulation of basic helix-loop-helix (bHLH) transcription factor activity.

Amino Acid Sequence↗

Significance of membrane glycoproteins in platelet interaction with oxidized low-density lipoprotein.

The significance of three platelet membrane glycoproteins, (CD62p, CD63, and CD36) was studied in platelet interaction with native and copper-oxidized plasma low-density lipoproteins (LDL). Native LDL acquired platelet-activating ability only after oxidation. Flow-cytometric studies showed that CD62P and CD63 were rapidly expressed on platelets at a low concentration of oxidized LDL, indicating that they are more sensitive markers than platelet aggregation for detection of platelet activation by oxidized LDL. CD36 was found to be contributing to the binding and activation of platelets with oxidized LDL, but not to the binding of platelets with native LDL. Although the presence of oxidized LDL in plasma is known, its effect on platelet function remains to be studied.

Antigens, CD↗

Notch inhibition of E47 supports the existence of a novel signaling pathway.

E47 is a widely expressed transcription factor that activates B-cell-specific immunoglobulin gene transcription and is required for early B-cell development. In an effort to identify processes that regulate E47, and potentially B-cell development, we found that activated Notch1 and Notch2 effectively inhibit E47 activity. Only the intact E47 protein was inhibited by Notch-fusion proteins containing isolated DNA binding and activation domains were unaffected-suggesting that Notch targets an atypical E47 cofactor. Although overexpression of the coactivator p300 partially reversed E47 inhibition, results of several assays indicated that p300/CBP is not a general target of Notch. Notch inhibition of E47 did not correlate with its ability to activate CBF1/RBP-Jkappa, the mammalian homolog of Suppressor of Hairless, a protein that associates physically with Notch and defines the only known Notch signaling pathway in drosophila. Importantly, E47 was inhibited independently of CBF1/RPB-Jkappa by Deltex, a second Notch-interacting protein. We provide evidence that Notch and Deltex may act on E47 by inhibiting signaling through Ras because (i) full E47 activity was found to be dependent on Ras and (ii) both Notch and Deltex inhibited GAL4-Jun, a hybrid transcription factor whose activity is dependent on signaling from Ras to SAPK/JNK.

3T3 Cells↗

Reduction of cisplatin toxicity and lethality by sodium malate in mice.

The effects of oral treatment with sodium malate, an active ingredient of Juzen-taiho-to, on the nephrotoxicity, bone marrow toxicity, hepatotoxicity and gastrointestinal toxicity caused by i.p. administration of 9 doses of 3.0 mg/kg/d cisplatin (CDDP) (on days 3, 4, 5, 6, 7, 8, 10, 11 and 12) were examined in ddY mice inoculated with sarcoma 180 (S-180) cells on day 1 of the study. The CDDP-induced increases in blood urea nitrogen, serum creatinine, serum glutamic-oxaloacetic transaminase, serum glutamic-pyruvic transaminases and relative stomach weight and the decreases in food intake and body weight were inhibited nearly to the control levels without reducing the antitumor activity of CDDP against S-180 by the oral treatment with sodium malate of 12 doses of more than the equimolar amount of CDDP (on days 3, 4, 5, 6, 7, 8, 10, 11, 12, 13, 14 and 15). However, the CDDP-induced decreases in white blood cell and platelet counts and relative spleen and thymus weight could not be inhibited completely by combination with sodium malate, even at a dose of twice the equimolar amount of CDDP. The sodium malate-induced reduction of CDDP-induced nephrotoxicity and hepatotoxicity was observed after oral administration, as well as with i.p., s.c. and i.v. administration, and the effect was almost the same for each route of administration. Sodium malate also reduced the toxicity induced by high doses of CDDP (4.5, 6.0, 7.5, 9.0 and 12.0 mg/kg/d) at doses of twice the equimolar amount of CDDP. Sodium malate at a dose of 10.68 mg/kg/d (twice as high as carboplatin, CBDCA) did not reduce the nephrotoxicity, bone marrow toxicity, hepatotoxicity and gastrointestinal toxicity caused by i.p. administration of 9 doses of 15.0 mg/kg/d CBDCA on days 3, 4, 5, 6, 7, 8, 10, 11 and 12 in ddY mice inoculated with sarcoma 180 (S-180) cells on day 1 of the study. From this study, it was suggested that sodium malate could become a useful agent for the reduction of CDDP-induced toxicity, particularly nephrotoxicity and hepatotoxicity.

Animals↗