Biomedical subjects

K Shuto

Publications and source records attributed to K Shuto.

At least 19 recordsLinked to original sources

PubMed2001

Suppression of Ca2+ influx through L-type voltage-dependent calcium channels by hydroxyl radical in mouse cerebral cortical neurons.

In the present study, we investigated the effect of hydroxyl radical (.OH) produced by the Fenton reaction with FeSO(4) to H(2)O(2) on Ca2+ influx by measuring [(45)Ca2+] influx into mouse cerebral cortical neurons in primary culture.OH formed from 3 microM FeSO(4) and 0.01 microM H(2)O(2) significantly reduced 30 mM KCl-induced [(45)Ca2+] influx and this reduction was abolished by .OH scavengers such as N,N'-dimethylthiourea and mannitol. Nifedipine (1 microM), an inhibitor for L-type voltage-dependent Ca2+ channels (VDCCs) showed no additive effect on the reduction of the 30 mM KCl-induced [(45)Ca2+] influx, while the inhibitors for P/Q- and N-type VDCCs showed further suppression of the KCl-induced [(45)Ca2+] influx even in the presence of .OH. Bay k 8644, an activator of L-type VDCCs, dose-dependently stimulated [(45)Ca2+] influx, and this stimulation disappeared in the presence of nifedipine. Similarly, .OH also suppressed significantly [(45)Ca2+] influx induced by Bay k 8644. These inhibitory actions of .OH on the KCl- and Bay k 8644-induced [(45)Ca2+] influx were completely abolished by .OH scavengers. These results indicate that .OH has the activity to suppress Ca2+ influx through L-type VDCCs.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed2001

NMDA receptor activation enhances diazepam binding inhibitor and its mRNA expressions in mouse cerebral cortical neurons.

Effects of N-methyl-D-aspartate (NMDA) on diazepam binding inhibitor (DBI) and its mRNA expression in mouse cerebral cortical neurons were examined. A significant increase in DBI mRNA expression was observed 1 day after the exposure to 0.1 microM NMDA and the maximal expression occurred 2 days after the exposure, whereas transient exposure to 0.1 microM NMDA for 15 min, 1 and 3 h produced no changes in the expression. Similarly, no changes in the expression were found by the concomitant exposure to NMDA and MK-801, a NMDA receptor antagonist, for 72 h subsequent to the incubation with NMDA alone for 3 h. Such NMDA-induced increases in DBI mRNA expression were dose-dependently inhibited by MK-801. Moreover, neuronal DBI content significantly increased by treatment with NMDA, which was completely abolished by MK-801. These results indicate that continuous activation of NMDA receptors is an essential factor for increasing DBI expression in the neurons.

Animals↗

PubMed2000

Mechanism for increase in expression of cerebral diazepam binding inhibitor mRNA by nicotine: involvement of L-type voltage-dependent calcium channels.

We investigated the mechanisms underlying the increase in diazepam binding inhibitor (DBI) and its mRNA expression induced by nicotine (0.1 microM) exposure for 24 h using mouse cerebral cortical neurons in primary culture. Nicotine-induced (0.1 microM) increases in DBI mRNA expression were abolished by hexamethonium, a nicotinic acetylcholine (nACh) receptor antagonist. Agents that stabilize the neuronal membrane, including tetrodotoxin (TTX), procainamide (a Na(+) channel inhibitor), and local anesthetics (dibucaine and lidocaine), dose-dependently inhibited the increased expression of DBI mRNA by nicotine. The nicotine-induced increase in DBI mRNA expression was inhibited by L-type voltage-dependent Ca(2+) channel (VDCC) inhibitors such as verapamil, calmodulin antagonist (W-7), and Ca(2+)/calmodulin-dependent protein kinase II (CAM II kinase) inhibitor (KN-62), whereas P/Q- and N-type VDCC inhibitors showed no effects. In addition, nicotine exposure for 24 h induced [3H]nicotine binding to the particulate fractions of the neurons with an increased B(max) value and no changes in K(d). Under these conditions, the 30 mM KCl- and nicotine-induced 45Ca(2+) influx into the nicotine-treated neurons was significantly higher than those into non-treated neurons. These results suggest that the nicotine-stimulated increase in DBI mRNA expression is mediated by CAM II kinase activation resulting from the increase in intracellular Ca(2+) through L-type VDCCs subsequent to the neuronal membrane depolarization associated with nACh receptor activation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed2000

Effects of benidipine hydrochloride on cerebrovascular lesions in salt-loaded stroke-prone spontaneously hypertensive rats: evaluation by magnetic resonance imaging.

We determined possible protective effects of benidipine hydrochloride (benidipine), a dihydropyridine calcium antagonist, on cerebrovascular lesions in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP). The animals were orally treated with benidipine at 1, 3 and 10 mg/kg daily for 7 weeks, and their neurological symptoms, body weight changes, systolic blood pressure and cerebrovascular lesions on magnetic resonance imaging (MRI) were determined at various time points of treatment. Moreover, the brains of the rats that showed cerebrovascular lesions on MRI in the course of treatment or completed 7-week treatment were examined histopathologically. Control rats presented such symptoms as sedation, ataxia and aggressiveness, while their MRI analysis revealed high signals over wide areas from the occipital to frontal cortex and from the corpus callosum to external capsule. These high signal areas corresponded in location to edematous or softening lesions revealed by the histopathological observation. Treatment with benidipine at 3 and 10 mg/kg ameliorated neurological symptoms, significantly suppressing cerebrovascular damages on MRI. Benidipine at 3 mg/kg significantly decreased blood pressure for the first four weeks but it did not thereafter. These findings demonstrate that benidipine can protect salt-loaded SHRSP from cerebrovascular injury as assessed by MRI.

Analysis of Variance↗

PubMed1998

Alterations in [3H]L-N(G)-nitroarginine binding in brain after transient global or transient focal ischemia in gerbils and rats.

We investigated the post-ischemic change in [3H]L-N(G)-nitroarginine binding as a marker of nitric oxide (NO) synthase in the animal brain after transient global ischemia or transient focal ischemia. Transient global ischemia in gerbils was induced for 10 min followed by 1 h to 7 days of recirculation. Transient focal ischemia in rats was induced for 45 min followed by 3 days of recirculation. Following transient global ischemia, [3H]L-N(G)-nitroarginine binding showed a significant increase in the striatum (17-18%) and hippocampal CA1 sector (24%) at 48 and 24 h after recirculation, respectively. The hippocampal CA3 sector also showed a significant elevation (32-40%) in [3H]L-N(G)-nitroarginine binding at 24 and 48 h after global ischemia. Furthermore, the dentate gyrus showed a significant increase (30-32%) in [3H]L-N(G)-nitroarginine binding at 5, 24 and 48 h after global ischemia. Thereafter, a significant reduction in [3H]L-N(G)-nitroarginine binding was observed only in the dentate gyrus 7 days after recirculation. In contrast, [3H]L-N(G)-nitroarginine binding was unchanged in the thalamus throughout the recirculation periods. Histological analysis revealed that transient global ischemia caused severe damage or cellular damage in the striatum and the hippocampal CA1 sector. The hippocampal CA3 sector and thalamus were mildly damaged, whereas the dentate gyrus was morphologically intact. Following transient focal ischemia, a marked elevation (50-52%) in [3H]L-N(G)-nitroarginine binding was found in the regions of the ipsilateral striatum in which severe infarction occurred. Our findings suggest that [3H]L-N(G)-nitroarginine binding increases in the striatum and hippocampus after transient global ischemia or transient focal ischemia. This increase in [3H]L-N(G)-nitroarginine binding may play a pivotal role not only in the pathogenesis of ischemic brain damage, but also in the restoration of injury areas after cerebral ischemia.

Animals↗

PubMed1998

Post-ischemic alterations in [3H]FK506 binding in the gerbil and rat brains.

We investigated post-ischemic changes in FK506 binding protein (FKBP) in the brain after transient global ischemia in gerbils or transient focal ischemia in rats. [3H]FK506 was used to label FKBP as a immunophilin. In transient global ischemia, [3H]FK506 binding showed a transient reduction in the frontal cortex only 1 h after recirculation. In the striatum, the dorsolateral part exhibited a significant increase in [3H]FK506 binding 5, 24 and 48 h after ischemia. However, the ventromedial part showed a transient elevation in [3H]FK506 binding 24 h after ischemia. Thereafter, the ventromedial part showed no conspicuous change in [3H]FK506 binding up to 7 days after ischemia. The dorsolateral part also showed no significant change in [3H]FK506 binding 7 days after ischemia. In the hippocampus and thalamus, [3H]FK506 binding was unchanged in the stratum radiatum of the hippocampal CA1 sector, hippocampal CA3 sector, dentate gyrus and thalamus up to 7 days after ischemia. However, the stratum oriens of the hippocampal CA1 sector showed a significant reduction in [3H]FK506 binding 48 h and 7 days after ischemia. A histological study showed that transient cerebral ischemia caused a severe damage in the striatum and hippocampal CA1 sector. In a model of transient focal ischemia, a marked increase in [3H]FK506 binding was also found in the striatum and cerebral cortex where severe infarctions were observed. These results demonstrate that post-ischemic change in [3H]FK506 binding between the striatum and hippocampus may be produced by different mechanisms. Furthermore, our findings suggest that immunophilins may play some role in the pathogenesis of ischemic diseases.

Animals↗

PubMed1998

Postischemic changes of

Sequential alterations of [3H]nimodipine and [3H]ryanodine binding in gerbils were investigated in selectively vulnerable regions, such as the striatum and hippocampus, 1 h to 7 days after 10 min of transient cerebral ischemia. [3H]Nimodipine binding showed no significant changes in the striatum and hippocampus up to 48 h after ischemia. Seven days after ischemia, however, a severe reduction in [3H]nimodipine binding was observed in the dorsolateral striatum, hippocampal CA1 (stratum oriens, stratum pyramidale and stratum radiatum) and hippocampal CA3 sector. On the other hand, [3H]ryanodine binding showed a significant increase in the hippocampus 1 h after ischemia. Five hours after ischemia, a significant reduction in [3H]ryanodine binding was observed only in the hippocampal CA1 sector. Thereafter, the striatum and hippocampus showed no significant alterations in [3H]ryanodine binding up to 48 h after ischemia. After 7 days, a marked reduction in [3H]ryanodine binding was observed in the striatum and hippocampus which were particularly vulnerable to ischemia. These results demonstrate that postischemic alteration in [3H]nimodipine and [3H]ryanodine binding is produced with different processes in the hippocampus. They also suggest that the mechanism for striatal cell damage caused by transient cerebral ischemia may, at least in part, differ from that for hippocampal neuronal damage. Furthermore, our findings suggest that abnormal calcium release from intracellular stores may play a pivotal role in the development of hippocampal neuronal damage. Copyright Rapid Science Ltd

Journal Article↗

PubMed1998

Effect of NG-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, on neurotransmitter receptor systems in aged rats.

In order to examine the effect of age and nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), we studied the changes on major neurotransmitter receptor systems in 6 (adult) and 24-month-old (aged) Fischer male rats using receptor autoradiography. L-NAME was administrated intraperitoneally in aged rats once a day for 4 weeks. [3H]QNB (quinuclidinyl benzilate), [3H]HC (hemicholinium-3), [3H]muscimol, [3H]SCH 23390 ([N-methyl-3H]R[+]-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-7-ol-benzazepine), [3H]nemonapride and [3H]mazindol were used as markers of muscarinic acetylcholine receptors, high-affinity choline uptake sites, GABAA (gamma-aminobutyric acidA) receptors, dopamine D1 receptors, dopamine D2 receptors and dopamine uptake sites, respectively. The age-related change in [3H]muscimol binding in the brain was more pronounced than that in [3H]QNB, [3H]HC, [3H]SCH 23390, [3H]nemonapride and [3H]mazindol binding. Chronic treatment (4 weeks) with L-NAME caused no significant changes in [3H]QNB, [3H]muscimol, [3H]SCH 23390 and [3H]nemonapride binding in most areas of aged rat brain, as compared with vehicle-treated aged animals. However, chronic treatment with L-NAME caused a significant reduction in [3H]HC and [3H]mazindol binding in any brain regions of aged rats in comparison with the vehicle-treated aged animals. These results demonstrate that the GABAergic system is more susceptible to aging processes than cholinergic and dopaminergic systems in the brain. Furthermore, our findings suggest that nitric oxide may play some role in the regulation of choline uptake and dopamine uptake systems during aging processes. Copyright 1998 Lippincott Williams & Wilkins

Journal Article↗

PubMed1997

Effect of aging on dopaminergic receptors and uptake sites in the rat brain studied by receptor autoradiography.

We studied the age-related alterations of dopaminergic receptors in the brain of Fisher 344 rats with various age (3 weeks and 6, 12, 18 and 24 months) using in vitro receptor autoradiography. [3H]SCH 23390, [3H]spiperone and [3H]nemonapride, and [3H]mazindol were used to label dopamine D1 receptors, dopamine D2 receptors and dopamine uptake sites, respectively. In immature rats (3 weeks old), [3H]SCH 23390 binding showed a significant increase in most brain regions compared to adult animals (6 months old), whereas [3H]spiperone and [3H]nemonapride bindings showed no significant alteration in any brain areas. In contrast, [3H]mazindol binding showed a significant decline in most brain regions. On the other hand, the age-related alterations in [3H]SCH 23390 binding were not observed in any brain regions. [3H]Spiperone and [3H]nemonapride bindings also showed no significant alteration in the brain during aging, except for a transient alteration in [3H]spiperone binding in the nucleus accumbens and hippocampus of 12 months old rats. However, [3H]mazindol binding showed a significant reduction in most brain areas of 12 months old rats. Thereafter, the age-related reduction in [3H]mazindol binding was observed in most brain regions of 18 and 24 months old rats. The results demonstrate that dopamine uptake sites are more susceptible to the aging process than both dopamine D1 and D2 receptors. Furthermore, our results suggest that dopaminergic receptors and dopamine uptake sites may develop with different patterns and speeds after birth. Our studies may provide valuable information concerning the effect of aging on dopaminergic systems.

Aging↗

PubMed1997

The significance of esophageal variceal pressure in patients with cirrhosis.

We measured the portal circulatory hemodynamic parameters in 10 cirrhotic patients with portal hypertension and esophageal varices to determine the significance of esophageal variceal pressure. In 4 patients (group I), the temporary portal vein occlusion produced significant elevations in both the esophageal variceal pressure and the portal venous pressure. The results of the portal circulatory hemodynamic assessment in this group were consistent with the predominance of the backward flow mechanism. In the remaining 6 patients (group II), however, portal vein clamping resulted in a slightly increased esophageal variceal pressure with an enormous increase in the portal pressure. The forward flow mechanism thus appeared to be predominant in group II. In other words, the results of the pressure measurements were consistent with the functional separation of the hemodynamics in the esophageal varices and portal trunk in group II and the functional hemodynamic continuity in group I. This functional separation between the esophageal varices and the portal trunk in group II might therefore have resulted from the increased blood flow in the lesser splanchnic region.

Blood Pressure↗

PubMed1997

Age-related changes of sodium-dependent D-[3H]aspartate and [3H]FK506 binding in rat brain.

We investigated age-related changes in excitatory amino acid transport sites and FK506 binding protein (FKBP) in 3-week-, and 6-, 12-, 18- and 24-month-old Fischer 344 rat brains using receptor autoradiography. Sodium-dependent D-[3H]aspartate and [3H]FK506 were used to label excitatory amino acid transport sites and immunophilin (FKBP), respectively. In immature rats (3-week-old), sodium-dependent D-[3H]aspartate binding was lower in the frontal cortex, parietal cortex, striatum, nucleus accumbens, whole hippocampus, thalamus and cerebellum as compared to adult animals (6-month-old), whereas [3H]FK506 binding was significantly lower in only the hippocampus, thalamus and cerebellum. 3[H]FK506 binding exhibited no significant change in the brain regions examined during aging. However, sodium-dependent D-[3H]aspartate binding showed a conspicuous reduction in the substantia nigra in 18-month-old rats. Thereafter, a significant reduction in sodium-dependent D-[3H]aspartate binding was found in the thalamus, substantia nigra and cerebellum in 24-month-old rats. Other regions also showed about 10-25% reduction in sodium-dependent D-[3H]aspartate binding. The results indicate that excitatory amino acid transport sites are more susceptible to aging process than immunophilin. Further, our findings demonstrate the conspicuous differences in the developmental pattern between excitatory amino acid transport sites and immunophilin in immature rat brain.

Aging↗

PubMed1997

Effect of nitric oxide synthase inhibitor on age-related changes in second messenger systems and calcium channels in rats.

We investigated the effects of age and nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on protein kinase C (PKC), adenylyl cyclase, calcium/calmodulin-independent cyclic-AMP phosphodiesterase (cyclic-AMP PDE) and voltage-dependent L-type calcium channels in Fischer rat brain using autoradiography. [3H]Phorbol 12,13-dibutyrate (PDBu), [3H]forskolin, [3H]rolipram and [3H]PN200-110 were used to label PKC, adenylyl cyclase, cyclic-AMP PDE and calcium channels, respectively. [3H]Forskolin binding significantly decreased in the striatum, hippocampal CA3 sector, dentate gyrus, hilus, thalamus, substantia nigra and cerebellum of 24-month-old (aged) rats, as compared with 6-month-old (adult) animals. [3H]Rolipram binding also showed an age-related reduction in the thalamus and cerebellum in rats. In contrast, no age-related changes were observed in [3H]PDBu and [3H]PN200-110 binding in the rat brain. Chronic treatment with L-NAME (5 mg/kg, once a day for 4 weeks) showed no significant changes in [3H]PDBu, [3H]rolipram and [3H]PN200-110 binding in aged rat brains. However, this treatment significantly increased age-related decreases in [3H]forskolin binding in the frontal cortex; striatum and hippocampal CA1 sector in rats. The results demonstrate that [3H]forskolin binding in the rat brain is more susceptible to aging processes than [3H]PDBu, [3H]rolipram and [3H]PN200-110 binding. Furthermore, our study shows that chronic treatment with NO inhibitor increases the age associated changes in [3H]forskolin binding in most brain areas of aged rats. These findings suggest that NO may play a key role in the regulation of adenylyl cyclase system during aging processes.

Aging↗

PubMed1997

Effects of vinconate on age-related alterations in [3H]MK-801, [3H]glycine, sodium-dependent D-[3H]aspartate, [3H]FK-506 and [3H]PN200-110 binding in rats.

We investigated the effects of age and (+/-)-methyl-3-ethyl-2,3,3a,4-tetrahydro-1 H-in-dolo[3,2,1-de] [1,5] naphthyridine-6-carboxylate hydrochloride (vinconate), an indolonaphthyridine derivative, on calcium channels, neurotransmitter receptor systems and immunophilin in Fischer rat brain using quantitative receptor autoradiography. [3H]MK-801, [3H]glycine, sodium-dependent D-[3H]aspartate, [3H]FK-506 and [3H]PN200-110 were used to label N-methyl-D-aspartate (NMDA) receptors, glycine receptors, excitatory amino acid transport sites, FK-506 binding proteins (FKBP) and voltage-dependent L-type calcium channels, respectively. [3H]Glycine and sodium-dependent D-[3H]aspartate binding significantly decreased in the frontal cortex, parietal cortex, striatum, nucleus accumbens, hippocampus, thalamus, substantia nigra and cerebellum of 24 month old rats in comparison with 6 month old animals. In contrast, [3H]MK-801, [3H]FK-506 and [3H]PN200-110 binding showed no significant changes in the brain of 24 month old rats. Intraperitoneal chronic treatment with vinconate (10 and 30 mg/kg, once a day for 4 weeks) dose-dependently ameliorated the significant reduction in [3H]glycine and sodium-dependent D-[3H]aspartate binding in the brain of 24 month old rats. These results demonstrate that glycine receptors and excitatory amino acid transport sites are more susceptible to aging processes than NMDA receptors, immunophilin and voltage-dependent L-type calcium channels. Furthermore, our findings suggest that vinconate may have a beneficial effect on age-related changes in glycine receptors and excitatory amino acid transport sites.

Aging↗

PubMed1997

Effect of cerebral ischemia on dopamine receptors and uptake sites in the gerbil hippocampus.

Dopamine D1 and D2 receptors and uptake sites were studied in the gerbil hippocampus, parietal cortex and thalamus 1 h to 7 days after 10 min of cerebral ischemia using the occlusion of bilateral common carotid arteries. [3H]SCH23390 ([N-methyl-3H]R[+]-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-7-ol-be nzazepine) and [3H]mazindol were used as markers of dopamine D1 receptors and uptake sites, respectively. [3H]Nemonapride was used to label dopamine D2 receptors. No obvious alteration in [3H]SCH23390 and [3H]mazindol binding was found in the hippocampus up to 48 h after ischemia. These bindings showed a significant reduction in the hippocampus after 7 days of recirculation. In contrast, [3H]nemonapride binding was unaffected in the hippocampus during the recirculation periods. The parietal cortex and thalamus also exhibited no significant changes in [3H]SCH23390, [3H]nemonapride and [3H]mazindol binding after ischemia. MAP2 (microtubule-associated protein 2) immunoreactivity was unchanged in all regions up to 48 h after ischemia. Thereafter, a marked loss of MAP2-immunoreactive neurons was observed in the hippocampal CA1 and CA3 neurons 7 days after recirculation. These findings were consistent with histological observations with cresyl violet staining. Our results demonstrate that dopamine D1 receptors and dopamine uptake sites in the hippocampus are susceptible to cerebral ischemia, whereas dopamine D2 receptors in this region are particularly resistant. Furthermore, these findings suggest that dopamine transmission may not be major factor in producing ischemic hippocampal damage.

Animals↗

PubMed1997

Age-related changes in [3H]nimodipine and [3H]rolipram binding in the rat brain.

Ageing is associated with changes in neurotransmission which might be correlated with abnormal calcium metabolism. Because there is evidence that nimodipine can enhance the learning abilities of ageing animals and rolipram can enhance the excitability of neurons, providing a functional basis for cognition-enhancing activity, age-related alterations in the binding of voltage-dependent L-type calcium channels and calcium/calmodulin-independent cyclic adenosine monophosphate-selective phosphodiesterase (cyclic-AMP PDE) were studied in 3-week- and 6-, 12-, 18- and 24-month-old Fisher 344 rats by use of receptor autoradiography. [3H]Nimodipine and [3H]rolipram were used to label the voltage-dependent L-type calcium channels and calcium/calmodulin-independent cyclic-AMP PDE, respectively. [3H]Nimodipine binding showed no obvious change in all brain areas of 12- and 18-month-old rats, as compared with 6-month-old animals. In 24-month-old rats, however, [3H]nimodipine binding increased significantly in the striatum and hippocampal CA3 sector. In contrast, [3H]rolipram binding showed no significant change in most brain areas during ageing, except for a transient change only in the hippocampal CA1 sector of 12-month-old animals. [3H]Nimodipine and [3H]rolipram binding showed a significant increase in some brain areas of 3-week-old rats compared with 6-month-old animals. The results indicate that in rats voltage-dependent L-type calcium channels are more susceptible to ageing processes than calcium/calmodulin-independent cyclic-AMP PDE. Our data also demonstrate that voltage-dependent L-type calcium channels and calcium/calmodulin-independent cyclic-AMP PDE might play roles in developmental processes. These findings might help further elucidation of the relationship between age-related neurological deficits and behavioural pharmacology including cognitive function.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1997

[Evaluation of CTA for arterial infusion chemotherapy for liver metastasis from colorectal cancer].

To compare between the arterial blood supply of metastatic liver tumor and effects of intrahepatic arterial infusion chemotherapy (IHAC), we examined 8 patients with 27 liver metastasis from colorectal cancer. They were treated with ADM/lipiodol/5-FU/LV (19 nodules) or 5-FU/LV (8 nodules). To evaluate the arterial blood supply, CT arteriography (CTA) was performed, which classified tumors into 3 grades. Grade (Gr) 0; almost no enhancement, Gr1: less than one-third of tumor, Gr 2; less than two-thirds; Gr 3 over two-thirds (no case). As a result, 3 of NCs and 3 of PDs were Gr 0, 7 of MRs, 3 of NCs and 2 of PDs were Gr 1, and CR, PR and 7 of MRs were Gr 2. These results suggest that the arterial blood supply is necessary for a better response of IHAC and CTA is effective to forecast the response to IHAC.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1996

Effects of cerebral ischemia on dopamine receptors in the gerbil striatum.

Dopamine D1 and D2 receptors and uptake sites were studied in the gerbil striatum and frontal cortex 1 h to 7 days after 10 min of cerebral ischemia caused by occlusion of the bilateral common carotid arteries. [3H]SCH23390 ([N-methyl-3H]R[+]-8-chloro-2, 3,4,5-tetrahydro-3-methyl-5-phenyl-7-ol-benzazepine), [3H]nemonapride and [3H]mazindol were used as markers of dopamine D1 receptors, D2 receptors and uptake sites, respectively. A significant reduction in [3H] SCH23390 binding was found in the striatum from 48 h after ischemia. In contrast, during the recirculation periods, [3H]nemonapride and [3H]mazindol binding was mostly unaffected in this region which was the most vulnerable to ischemia. The frontal cortex, where ischemic neuronal damage was mild, also showed no significant changes in [3H]SCH23390, [3H]nemonapride and [3H]mazindol binding after ischemia. Thus, cerebral ischemia that was associated with cell loss in the striatum resulted in a selective reduction of dopamine D1 receptors and not D2 receptors. No changes in dopamine D1 or D2 receptors were observed in frontal cortex. If massive dopamine release occurs with cerebral ischemia, it is not reflected by modification in the number of uptake sites located on dopamine terminals.

Animals↗

PubMed1996

A new sealing device (Sandwich-disc) for rapid recreation of pneumoperitoneum during laparoscopic assisted surgery.

We have developed a new device which enables rapid sealing of a minilaparotomy during laparoscopic assisted surgery to recreate an airtight condition. This device consists of a center rod and two discs (7 cm in diameter) which form an airtight condition by compressing the inner and outer surfaces of the abdominal wall. Advanced laparoscopic procedures requiring both pneumoperitoneum and minilaparotomy are facilitated with the use of this device. This new device is called the Sandwich-disc: Takasago Medical Industry Co., Ltd.

Colonic Neoplasms↗