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Biomedical subjects

Susumu Ando

Publications and source records attributed to Susumu Ando.

At least 19 recordsLinked to original sources
PubMed2005

Effect of metal conditioners on polymerization behavior of bonding agents.

This study aimed to determine the influence of metal conditioners on the polymerization behavior of bonding agents. Bonding agents of two-step self-etching primer systems and metal conditioners for adhesion of dental metal alloys were used. Double bond conversion was determined by Fourier transform-ation infrared spectroscopy. The percentage of residual double bonds, including pendant and monomeric double bonds, was calculated by comparing the obtained ratio with that of the uncured bonding agent. The degree of conversion of the bonding agents was obtained by subtracting the remaining double bonds from 100%. ANOVA followed by a Tukey HDS test was performed. Degree of conversion of the bonding agents ranged from 86.0 to 87.8%. When the bonding agents were mixed with metal conditioners or solvents of the metal conditioners, double bond conversion of the bonding agents tended to decrease. Within the limitations of this study, which was far removed from clinical situations, the presence of metal conditioners and remaining solvents had adverse effects on the polymerization reaction of bonding agents. Clinicians should be cognizant of the various factors that can influence bond strength of restorative resins to dentin.

Acetone↗
PubMed2005

Influence of polishing duration on surface roughness of resin composites.

There is a need for effective polishing instruments for resin composite restorations with highly polished surfaces. The purpose of this study was to investigate the influence of polishing duration on surface roughness of light-cured resin composites. Four polishing systems, Compomaster (Shofu), Silicone Points C Type (Shofu), Super Snap (Shofu) and Enhance Finishing and Polishing System (Dentsply/Caulk), were used to polish two commercially available resin composites, Clearfil AP-X (Kuraray Medical) and Lite-Fil II A (Shofu). Resin pastes were condensed into molds (10 mm in diameter, 5 mm in depth) and light irradiated for 40 s. Composite surfaces were ground with # 600 SiC paper followed by polishing with an instrument for 30 s, and the surface roughness was measured every 10 s during polishing procedures. The average surface roughnesses (Ra) were determined using a profilometer. Data were analyzed by Tukey HSD test (P = 0.05). After 30 s of polishing, mean Ra values ranged from 0.07 to 0.50 for Clearfil AP-X, and from 0.11 to 0.57 for Lite-Fil II A. Although the time required for polishing was longer, the surface finish produced by multiple-step polishing systems was superior to that obtained with one-step polishing systems.

Analysis of Variance↗
PubMed2004

Age-related changes in the levels of voltage-dependent calcium channels and other synaptic proteins in rat brain cortices.

Neurotransmitter release from synapses is one of the most important interneuronal signaling in the nervous system. We previously reported that aging decreases depolarization-induced acetylcholine release in rat brain synaptosomes. To investigate the mechanisms underlying the age-related decrements of neurotransmission, we determined the levels of the alpha1 subunit proteins of voltage-dependent calcium channels (VDCCs) and three synaptic proteins that relate to exocytotic processes using synaptosomes prepared from cerebral cortices of young (6-month-old) and aged (27-month-old) rats. Immunoblotting analyses revealed that the protein levels of alpha1A (P/Q-type) and alpha1B (N-type) subunits in aged rats were 38% and 43% lower than the levels of young rats, respectively, but the levels of the alpha1C (L-type) subunit were not different between young and aged. On the contrary, the levels of synaptotagmin-1, synaptophysin and syntaxin were not significantly different between the two age groups in the synaptosomal preparations. These results suggest that synaptic density does not change much in the cerebral cortex in normal aging, and that the reduction of P/Q-type and N-type VDCCs, both of which participate in neurotransmitter release, is one of the causes for the decrease of neurotransmission at aged synapses.

Age Factors↗
PubMed2004

alpha-Sialylcholesterol enhances the depolarization-induced release of acetylcholine and glutamate in rat hippocampus: in vivo microdialysis study.

The effects of alpha-sialylcholesterol (alpha-SC), a synthetic ganglioside analogue, on synaptic neurotransmission were studied using in vivo microdialysis technique. Application of alpha-SC through a microdialysis probe enhanced high potassium-evoked release of acetylcholine and glutamate in the hippocampal CA3 region of Wistar rats. The experiments using synaptosomes and FM1-43, a fluorescent styryl dye used for studies of neurotransmitter release mechanisms, showed that alpha-SC increased depolarization-induced loss of dye but it did not evoke the dye loss at resting condition. These results indicate that alpha-SC promotes a depolarization-induced exocytotic neurotransmitter release in the brain under in vivo conditions. Application of alpha-SC increased the level of glutamate but not that of acetylcholine, suggesting that alpha-SC affects spontaneous glutamate release and/or transport system at the brain region.

Acetylcholine↗
PubMed2004

Acetyl-L-carnitine supplementation restores decreased tissue carnitine levels and impaired lipid metabolism in aged rats.

The effects of long-term carnitine supplementation on age-related changes in tissue carnitine levels and in lipid metabolism were investigated. The total carnitine levels in heart, skeletal muscle, cerebral cortex, and hippocampus were approximately 20% less in aged rats (22 months old) than in young rats (6 months old). On the contrary, plasma carnitine levels were not affected by aging. Supplementation of acetyl-l-carnitine (ALCAR; 100 mg/kg body weight/day for 3 months) significantly increased tissue carnitine levels in aged rats but had little effect on tissue carnitine levels in young rats. Plasma lipoprotein analyses revealed that triacylglycerol levels in VLDL and cholesterol levels in LDL and in HDL were all significantly higher in aged rats than in young rats. ALCAR treatment decreased all lipoprotein fractions and consequently the levels of triacylglycerol and cholesterol. The reduction in plasma cholesterol contents in ALCAR-treated aged rats was attributable mainly to a decrease of cholesteryl esters rather than to a decrease of free cholesterol. Another remarkable effect of ALCAR was that it decreased the cholesterol content and cholesterol-phospholipid ratio in the brain tissues of aged rats. These results indicate that chronic ALCAR supplementation reverses the age-associated changes in lipid metabolism.

Acetylcarnitine↗
PubMed2004

Synaptic function of cholinergic-specific Chol-1alpha ganglioside.

The function of a cholinergic-specific ganglioside, Chol-1alpha, was investigated. The release of acetylcholine from synaptosomes was inhibited by anti-Chol-1alpha monoclonal antibody but not by monoclonal antibodies against other brain gangliosides tested. Chol-1alpha ganglioside stimulated the high-affinity choline uptake by synaptosomes and consequently enhanced acetylcholine synthesis, resulting in an increased release of acetylcholine from synaptosomes. The memory and learning abilities of rats given anti-Chol-1alpha antibody were remarkably suppressed. These in vitro and in vivo studies suggest that Chol-1alpha ganglioside plays a pivotal role in cholinergic synaptic transmission and participates in cognitive function.

Animals↗
PubMed2004

A case of atrial septal defect complicated by autoimmune hemolytic anemia.

Open heart surgery is rarely performed on patients with heart disease complicated by autoimmune hemolytic anemia (AIHA) with the aid of an artificial heart-lung machine. We successfully performed radical open heart surgery on an atrial septal defect (ASD) patient with the complication of AIHA.

Anemia, Hemolytic, Autoimmune↗
PubMed2003

How does prolonged caloric restriction ameliorate age-related impairment of long-term potentiation in the hippocampus?

Prolonged dietary restriction has been reported to suppress age-induced phenomena. In order to investigate how prolonged caloric restriction reduces age-related deterioration of hippocampal synaptic transmission, we compared the levels of major hippocampal polyunsaturated fatty acids, arachidonic acid and docosahexaenoic acid between 4- and 26-month-old rats. The Ca(2+) responses upon perfusion of NMDA or 30 mM K(+) between 4- and 26-month-old rats with prolonged dietary restriction were also compared using the fluorescent probe Fura-2. A decrease in membrane arachidonic acid is thought to be a major causal factor in the age-related impairment of long-term potentiation. Long-term caloric restriction seems to increase arachidonic acid levels regardless of age. However, there is no significant difference of hippocampal arachidonic acid levels between in freely feeding 4- and 26-month-old rats. Similar results were obtained from the measurement of hippocampal docosahexaenoic acid levels. Under caloric restriction, the 500 microM N-methyl-D-aspartate-induced Ca(2+) response was greatly reduced by aging, while the 30 mM K(+)-induced Ca(2+) response was not affected. In our preliminary data, the amplitude of the population spike after tetanic stimulation did not differ between 4- and 26-month-old rats under caloric restriction, while 50 microM of 2-amino-5-phosphonovaleric acid, a N-methyl-D-aspartate antagonist, markedly inhibited a potentiation of the population spike in 4-month-old rats, but with negligible inhibition in 26-month-old rats. From these results, an age-related impairment of hippocampal excitatory synaptic transmission may not be solely due to the reduction of membrane arachidonic acid. Caloric restriction might prevent age-related reduction in hippocampal synaptic transmission by enhancing non-N-methyl-D-aspartate mechanisms.

2-Amino-5-phosphonovalerate↗
PubMed2003

Optimal temperature of continuous lidocaine perfusion for the heart preservation.

OBJECTIVE: During cardiovascular surgery, lidocaine is administered to the cardioplegic system to stabilize cell membranes and prevent arrhythmia. Lidocaine is also commonly used in hypothermia. Both lidocaine and hypothermia are myocardially protective. Under normothermia, lidocaine displays its full pharmacological effects, which are apt, however, to be suppressed under hypothermia. We conducted experiments to determine the optimal temperature for myocardial protection in continuous lidocaine cardioplegia. METHODS: In Langendorff mode, rat hearts were continuously perfused with 1 mMol/l of lidocaine solution at 36 +/- 0.5 degrees C (Group A), 24 +/- 0.5 degrees C (Group B), or 7 +/- 0.5 degrees C (Group C) during preservation. Cardiac function and intracellular calcium concentration were measured during both preservation and reperfusion. Heat shock protein 70 (HSP70) was subsequently analyzed by Western blotting. RESULTS: Rapid cardiac arrest was obtained in Groups A and C. Heart rate recovery was good and ultimately the best in Group B, but worst in Group A. During lidocaine perfusion, the volume of coronary perfusion flow decreased gradually in all groups. After reperfusion, Group A showed only a slight increase in coronary perfusion, While Groups B and C showed a marked increase. Left ventricular contractility showed good recovery in all groups. The calcium concentration increased slightly in Group A, but decreased in Groups B and C. No calcium overload was evident in Group A. The same HSP70 level was detected in all groups. CONCLUSION: Lidocaine used in normothermia does not decrease cardiac metabolism or oxygen consumption, and displays full pharmacological effectiveness in preventing ischemic injury. We found 36 degrees C to be the optimal temperature for heart preservation by coronary perfusion with lidocaine cardioplegia.

Animals↗
PubMed2003

Intracellular calcium increasing at the beginning of reperfusion assists the early recovery of myocardial contractility after diltiazem cardioplegia.

OBJECTIVES: We investigated the ability of diltiazem to prevent myocardial injury by assessing heart function and intracellular calcium concentrations before and after ischemia-reperfusion. METHOD: Isolated rat hearts underwent cardioplegia using the Langendorff perfusion model and were subjected to normothermic global ischemia for 60 minutes. The recovery rates for the heart function (heart rate, coronary flow, left ventricular systolic pressure) after reperfusion were monitored, and the intracellular Ca concentration was measured during ischemia and during the following reperfusion. Experimental groups were divided into three groups according to the diltiazem concentration used in the cardioplegic solution (potassium 20 mmol/l in Ringer's solution): (1) Group A: diltiazem 2.5 mg/l; (2) Group B: diltiazem 5 mg/l; and (3) Group C: no diltiazem. RESULTS: Intracellular calcium concentration increased in all 3 groups during ischemia, but was significantly lower in Group B compared to either Group A or Group C. The heart function was significantly higher for Group A than for Group B or Group C. The hearts in Group B displayed markedly poor recovery in contractility and in heart rate. CONCLUSIONS: Generally, a decrease in intracellular Ca concentration improves the heart function during ischemia and after reperfusion. However, this study showed that some increase in intracellular Ca at the beginning of reperfusion assisted the contractility of rat heart.

Animals↗
PubMed2003

Turnover of myelin lipids in aging brain.

Turnover rates of myelin membrane components in mouse brains were determined by a method using stable isotope-labeling and mass spectrometry. The half-replacement times based on incorporation rates of newly synthesized molecules for young adult mice were 359 days for cholesterol, 20 days for phosphatidylcholine, 25 days for phosphatidylethanolamine, 94 days for cerebroside and 102 days for ganglioside GM1. The turnover rates of half-lives of myelin components were calculated from the decay curves of initially labeled molecules, and they were about the same as the half-replacement times. Individual components were thus revealed to be metabolized at different rates, and their turnover rates were differently affected by aging. As was observed with phospholipids, myelin pools appeared to be compartmentalized into rapidly and slowly exchanging pools. The turnover rates of cerebroside and GM1 decreased between the young and adult periods and slightly increased in senescence. The latter phenomenon may indicate an enhanced myelin turnover in senescence. The present study reveals the dynamic aspects of myelin membrane turnover during the life span of mouse.

Aging↗
PubMed2003

A study of the myocardial protective effect of rapid cooling based on intracellular Ca, intracellular pH, and HSP70.

OBJECTIVE: It has been reported that rapid cooling of the heart during normothermic coronary circulation at reperfusion after ischemia promotes early recovery of cardiac function due to the positive inotropic effects on the myocardium produced by cooling. The aim of the present study was to investigate the myocardial protective effect of rapid cooling by measuring heat shock protein (HSP) levels and examining the relationship between cardiac function, intracellular Ca concentration, and intracellular pH after rapid cooling. METHODS: Isolated perfused rat hearts were subjected to ischemia for 60 minutes at a myocardial temperature of 37 degrees C. One group of hearts (group R) was subjected to 3 minutes of rapid cooling (</=4 degrees C) 3 minutes after reperfusion was started. The other hearts (group C) were not cooled. Myocardial protection was then compared in the two groups by measuring heart rate, coronary flow, left ventricular contraction, intracellular Ca concentration (fura-2 fluorescence), and intracellular pH (BCECF-AM fluorescence) and examining HSP70 by western blot. RESULTS: (1) Left ventricular contraction was 105+/-0.05% of the pre-ischemia value in group R after rapid cooling, whereas recovery was poor in group C (63+/-2%). (2) The intracellular Ca concentration in group R rose to 141+/-8% of the pre-ischemia value during ischemia, but decreased to 101+/-3% at reperfusion after rapid cooling. In group C, the Ca concentration was 144+/-4% of the pre-ischemia value during ischemia and rose further to 156+/-6% at reperfusion. (3) In group R, the intracellular pH was 6.85+/-0.05 during ischemia and rose after reperfusion was started, but after rapid cooling, decreased again to 7.43+/-0.02 after 60 minutes reperfusion. In group C, the pH was 6.88+/-0.06 during ischemia and rose to 7.90+/-0.09 60 minutes after reperfusion was started. (4) HSP70 was detected in both groups, but the concentration (luminescence) was lower in group R than in group C. CONCLUSION: Rapid cooling reduces myocardial injury by preventing intracellular Ca overload at reperfusion via inhibition of the Na(+)/Ca(2+) exchanger and also decreases the appearance of HSPs, the so-called homeostasis proteins. (Ann Thorac Cardiovasc Surg 2003; 9: 301-6)

Analysis of Variance↗
PubMed2002

Turnover of synaptic membranes: age-related changes and modulation by dietary restriction.

We examined age-related changes in the turnover rates of synaptic membrane components that might underlie the decrease in synaptic functions in senescence. Synaptic membrane constituents were labeled in vivo with deuterium and the disappearance of the deuterated molecules from synaptic membranes was measured by mass spectrometry. The turnover rates of phosphatidylcholine, phosphatidylethanolamine, cholesterol, and synaptophysin were all shown to slow down with aging. Dietary restriction, which is known to retard various aging processes, was found to decrease the turnover rates of membrane lipid species. Consequently, the fatty acid composition in phospholipids remained unchanged in the synaptic plasma membranes of food restricted mice. In contrast, the turnover rate of synaptophysin was accelerated under dietary restriction. This may mean that increased turnover enhances the removal of damaged proteins from membranes.

Aging↗
PubMed2002

Effects of enriched environments with different durations and starting times on learning capacity during aging in rats assessed by a refined procedure of the Hebb-Williams maze task.

Cognitive function as measured by the Hebb-Williams maze task was examined in Fischer 344 male rats that had been exposed to an enriched environment for periods of variable duration and at different starting ages. In one experiment, rats were exposed to environmental enrichment from weaning until the age of 2.5, 15, or 25 months. The results of 12 problems of the Hebb-Williams maze task showed that the enriched rearing condition improved the learning ability in all the age groups; however, factor analysis and ANOVA demonstrated that four of the 12 maze problems were not suitable for detecting the effect of age under different environmental conditions. Reanalysis of the results obtained with the other eight maze problems more clearly revealed both the effects of rearing condition and aging. The latter analysis demonstrated that the learning rate of rats reared under enriched conditions was faster than that of rats reared under standard social conditions. Short-term (3-month) exposure also had positive effects on cognitive function in both adult (11-month-old) and aged (22-month-old) animals. The effect of long-term exposure to an enriched environment starting at weaning was much greater than that of short-term exposure in aged rats, whereas the effects of both long-term and short-term exposure were almost the same in adult rats. These results show that aged animals still have appreciable plasticity in cognitive function, and suggest that environmental stimulation could benefit aging humans as well.

Aging↗
PubMed2002

Animal model of dementia induced by entorhinal synaptic damage and partial restoration of cognitive deficits by BDNF and carnitine.

A rat dementia model with cognitive deficits was generated by synapse-specific lesions using botulinum neurotoxin (BoNTx) type B in the entorhinal cortex. To detect cognitive deficits, different tasks were needed depending upon the age of the model animals. Impaired learning and memory with lesions were observed in adult rats using the Hebb-Williams maze, AKON-1 maze and a continuous alternation task in T-maze. Cognitive deficits in lesioned aged rats were detected by a continuous alternation and delayed non-matching-to-sample tasks in T-maze. Adenovirus-mediated BDNF gene expression enhanced neuronal plasticity, as revealed by behavioral tests and LTP formation. Chronic administration of carnitine over time pre- and post-lesions seemed to partially ameliorate the cognitive deficits caused by the synaptic lesion. The carnitine-accelerated recovery from synaptic damage was observed by electron microscopy. These results demonstrate that the BoNTx-lesioned rat can be used as a model for dementia and that cognitive deficits can be alleviated in part by BDNF gene transfer or carnitine administration.

Aging↗
PubMed2002

Active site of deblocking aminopeptidase from Pyrococcus horikoshii.

New hyperthermostable aminopeptidase from the hyperthermophilic archaeon Pyrococcus horikoshii has acylamino acid releasing (deblocking) activity for acyl (blocked) peptides. Such an enzyme can be used for N-terminal sequencing of acyl peptides. To clarify the active site of the deblocking aminopeptidase, we prepared three mutants in which one of the three possible active site amino acid residues (Asp or Glu) was replaced with their amide derivatives. Activity and cobalt ion dependence of these mutants were examined and compared with those of the native enzyme. The results suggest that all the three possible residues (Asp173, Glu205, and Glu206) participate in the catalytic activity through binding with the cobalt ion.

Amino Acid Sequence↗
PubMed2002

Age-dependent reduction in sialidase activity of nuclear membranes from mouse brain.

Sialidase is an enzyme that cleaves alpha-linked sialic acid residues from sialoglycoconjugates and participates in various cellular functions. In the present study, we characterized sialidase activity in nuclear membranes from mouse brain and examined its age-related changes. A highly purified nuclear membrane preparation from 4-week-old mouse brain contained sialidase activity that hydrolyzed both 4-methylumbelliferyl-alpha-D-N-acetylneuraminic acid (4MU-Neu5Ac) and ganglioside GM3. The specific activities directed toward both substrates were 6.33+/-0.77 and 13.4+/-1.1pmol/mgprotein/min, respectively. Nuclear localization of sialidase activity was confirmed by fluorescent cytochemistry of intact nuclei using 5-bromo-4-chloro-3-indolyl-alpha-D-N-acetylneuraminic acid (X-Neu5Ac) as the substrate. Age-related changes in nuclear sialidase activity in brain tissue were investigated using mice of different ages (i.e. 2-week-, 4-week-, 14-month-, and 26-month-old). Sialidase activity toward 4MU-Neu5Ac had almost identical levels at 2nd and 4th weeks, but thereafter decreased rapidly; the activity at 26 months was about one third of the young levels. Sialidase activity toward GM3 also showed a similar developmental pattern, though the reduction at advancing ages was less than that of activity toward 4MU-Neu5Ac. The present study demonstrates that the activity of nuclear sialidase decreases with aging. The reduced activity of nuclear sialidase may be implicated with alterations of neural cell function during aging.

Aging↗