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Biomedical subjects

S Yamada

Publications and source records attributed to S Yamada.

At least 847 records · Page 47Linked to original sources
PubMed1994

Differential effects of dopamine agonists on evoked dopamine release from slices of striatum and nucleus accumbens in rats.

The effects of dopamine receptor agonists on electrically evoked dopamine release from slices of nucleus accumbens were compared with the effects on release from striatal slices in rats. Apomorphine, which has equal potency at the dopamine D2 and D3 receptors, reduced the evoked dopamine release from both regions to the same extent (ED50, 0.42 microM for nucleus accumbens; ED50, 0.46 microM for striatum). Quinpirole or 7-[3H]hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OHDPAT), which are much more potent at the D3 receptor than at the D2 receptor, reduced the evoked dopamine release from the nucleus accumbens (ED50, 0.12 microM for quinpirole; 0.02 microM for 7-OHDPAT) much more than the release from the striatum (ED50, 1.6 microM for quinpirole; 0.55 microM for 7-OHDPAT). These results suggest that the contribution of D3 receptors in nucleus accumbens to regulate dopamine release from dopamine nerve terminals is much greater than in striatum.

Animals↗
PubMed1994

Effects of N-ethylmaleimide on dopamine release in the rat striatum after repeated treatment with methamphetamine.

Effects of N-ethylmaleimide or forskolin on electrically evoked dopamine release were investigated in striatal slices of rats pretreated with methamphetamine. N-Ethylmaleimide and forskolin both enhanced the evoked dopamine release in a concentration-dependent manner. The enhancement by N-ethylmaleimide of spontaneous dopamine release was not abolished by tetrodotoxin; the electrically evoked release was abolished, irrespective of its magnitude. Moreover, N-ethylmaleimide prevented the inhibitory effect of the dopamine receptor agonist, 2-amino-6-allyl- 5,6,7,8-tetrahydro-4H-thiazolo(5,4-d)-azepine dihydrochloride (B-HT 920) and the stimulatory effect of the dopamine receptor antagonist, (-)-sulpiride, on the evoked dopamine release. In contrast, forskolin had no effect on the B-HT 920-induced inhibition and (-)-sulpiride-induced enhancement of the evoked dopamine release. These data indicate that release-modulating dopamine autoreceptors are N-ethylmaleimide-sensitive and forskolin-insensitive. As N-ethylmaleimide has been reported to inactivate Gi protein and to block the regulation of noradrenaline release by alpha 2-adrenoceptors, the present results suggest that N-ethylmaleimide inactivates inhibitory GTP binding proteins to block the regulation by dopamine autoreceptors of evoked dopamine release. Methamphetamine pretreatment, which caused behavioral sensitization to a challenge dose of methamphetamine, attenuated the stimulatory effect of N-ethylmaleimide but not forskolin on the evoked dopamine release. The data indicate that the repeated administration of methamphetamine reduces a function of N-ethylmaleimide sensitive signal transduction system, probably including inhibitory GTP binding protein.

Animals↗
PubMed1994

Effect of opioid peptides on dopamine release from nucleus accumbens after repeated treatment with methamphetamine.

The effect of opioid peptides on extracellular dopamine levels in the nucleus accumbens was compared between rats treated with methamphetamine and saline repeatedly (for 9 days) by using microdialysis. After the period of repeated treatment, the rats in both groups were kept for an additional 9 days without further treatment. Repeated administration of methamphetamine reduced the decreasing effect of dynorphin (10 microM), applied locally in the perfusate, and enhanced the increasing effect of [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAGO, 10 microM) on the extracellular dopamine levels in the nucleus accumbens. It is possible that repeated treatment with methamphetamine leads to attenuation of the inhibition and enhancement of the stimulation of dopamine release from the nucleus accumbens via presynaptic dynorphin- and enkephalin-sensitive receptors, respectively.

Analgesics↗
PubMed1994

Blood vessel invasion and expression of sialyl Lewisx and proliferating cell nuclear antigen in stage I non-small cell lung cancer. Relation to postoperative recurrence.

BACKGROUND: Recurrence in Stage I non-small cell lung cancer was examined with respect to vascular invasion and the immunohistochemical expression of sialyl-dimeric Lewisx (SLX) and proliferating cell nuclear antigen (PCNA). METHODS: One hundred twenty-eight patients with Stage I non-small cell lung cancer who had a curative resection were the subjects of this study. Using tumor tissues fixed in formaldehyde solution, blood vessel invasion (BVI) and lymphatic invasion stained with Victoria blue-hematoxylin and eosin and the immunohistochemical expression of SLX and PCNA were retrospectively studied with respect to postoperative recurrence. RESULTS: By univariate analysis, BVI and SLX and PCNA expression were significantly important factors of disease-free survival (P < 0.01). The disease-free survival of the patients with both BVI and SLX expression was significantly shorter than that of the patients with BVI but negative SLX expression (P < 0.02). In 35 patients with recurrence, tumors with PCNA expression showed a significantly shorter time to recurrence compared with tumors without PCNA expression (P < 0.01). CONCLUSIONS: BVI and SLX expression may be important determinants of recurrence. PCNA may be a determinant of time to recurrence.

Adult↗
PubMed1994

Digital nerve conduction velocity as a sensitive indication of peripheral neuropathy in vibration syndrome.

Digital nerve conduction velocities in the median and ulnar nerves were measured in order to obtain a more accurate indication of peripheral nerve impairment induced by hand-arm vibration. The subjects were 26 patients with vibration syndrome and 28 healthy controls, both groups of about the same age. Two pairs of surface electrodes were attached to the finger and one pair was positioned on the palm, while electrical stimulation was applied to the nerve at the wrist and elbow. Then sensory nerve conduction velocities were antidromically measured within the finger, and also from the wrist to the palm and from the elbow to the wrist. Slowed conduction within the finger was mostly found among the patients. The slowing was also encountered from the wrist to the palm across the carpal tunnel. Abnormalities were observed in the digital nerve segment in about 50-70% of the patients, and in the wrist-to-palm segment in about 10-25% of them. The present study indicates that digital nerve impairment predominantly occurs in the vibration-exposed patients, and that measurement of digital nerve conduction velocity can be a useful objective means to detect peripheral neuropathy in vibration syndrome.

Aged↗
PubMed1994

Distribution of vitronectin in plasma and liver tissue: relationship to chronic liver disease.

To clarify the clinical significance of vitronectin, we compared the concentration of plasma vitronectin with serum fibrous markers and liver function test values in patients with chronic liver diseases. We also evaluated the vitronectin content in the liver by means of enzyme-linked immunosorbent assay and the localization of vitronectin in liver tissue with enzyme immunohistochemistry. In chronic liver disease, the concentration of plasma vitronectin was significantly lower than that in healthy controls, being related to the severity of liver disease. The plasma levels of vitronectin showed no correlation to fibrous markers but a significant correlation with those of serum albumin and prothrombin time. On the other hand, the content of vitronectin in liver tissue was significantly increased in chronic liver disease compared with that in normal controls. In the normal liver, vitronectin was observed in the portal area by light microscopy. In chronic hepatitis and cirrhosis, vitronectin was found in the connective tissue around the portal and central veins and in the areas of piecemeal and focal necrosis. These findings suggested that vitronectin is deposited in injured tissue through the process of repair and fibrosis and plays an important role as an adhesive protein. Moreover, the lower levels of plasma vitronectin in chronic liver disease may be due to its decreased synthesis, deposition or both in injured tissue.

Adult↗
PubMed1994

Osteoclastic resorption of apatite formed on apatite- and wollastonite-containing glass-ceramic by a simulated body fluid.

We immersed mirror-polished apatite- and wollastonite-containing glass-ceramic (A-W GC) disks in a simulated body fluid (SBF) for 5 days to form bonelike apatite on their surface. Neonatal rabbit bone cells were cultured on these or on plain A-W GC disks for 10, 24, and 48 h. We observed the substrates by scanning electron microscopy after treating them with pronase E plus EDTA to remove all cells except osteoclasts. Osteoclasts with a non-motile appearance formed no lacunae on the plain A-W GC, whereas on the bonelike apatite formed on A-W GC by the SBF, actively moving osteoclasts made many tracklike resorption lacunae. These were evident even after 10 h of culture and became more extensive after longer culture periods. The bonelike apatite was therefore a more suitable medium than plain A-W GC for maintaining osteoclast activity. This study demonstrated in vitro osteoclastic resorption of bonelike apatite formed on A-W GC by an SBF. It suggests that the apatite layer, through which a surface-active ceramic bonds to bone in vivo, can be resorbed by osteoclasts and subjected to bone remodeling.

Animals↗
PubMed1994

In situ localization of transforming growth factor-beta 1 mRNA in the rat kidney with Masugi nephritis.

Masugi nephritis was induced in rats by the administration of nephrotoxic duck serum and, in their kidneys, the distributions of transforming growth factor-beta 1 (TGF-beta 1) mRNA, TGF-beta 1, and macrophage antigenic marker were investigated. Kidney specimens were obtained at 3, 7, and 14 days after the injection. By in situ hybridization, TGF-beta 1 mRNA was found to be localized in the cells of mesangial region from the early stage of nephritis. By the immunohistochemical stainings, TGF-beta 1 was found to be localized in the cells of distal convoluted tubulus throughout the experiments and the macrophage antigenic marker was found to be localized in the occasional cells which were different from that contained TGF-beta 1 mRNA. Our data indicate that TGF-beta 1 mRNA is expressed by the resident glomerular cells and not by the migrating macrophages in rat kidney with Masugi nephritis.

Animals↗
PubMed1994

Characteristics of paralytic shellfish poisoning toxins derived from short-necked clams (Tapes japonica) in Mikawa Bay.

A "red tide" bloom of Alexandrium tamarense occurred in Mikawa Bay in April 1991. In association with this, paralytic shellfish poisoning toxin was detected in short-necked clams by mouse bioassay. High performance liquid chromatography analysis demonstrated large quantities of the N-sulfocarbamoyl toxins, C1, and C2 (approximately 90% of the total toxins), whose latent potency was confirmed by treatment with boiling at low pH.

Animals↗
PubMed1994

Isolation and characterization of mutants of pseudorabies virus with deletion in the immediate-early regulatory gene.

Pseudorabies virus (PrV) immediate-early regulatory protein (IE180) is a potent and promiscuous activator of viral and cellular gene transcription. A mutant with deletion in the IE180 gene is expected to be useful for elucidating the functions of IE180. In this study, we constructed such mutants. Initially, transformants that express IE180 were established from PK-15 and Vero cells by transfection with the IE180 gene of the wild-type PrV. Two types of the deletion mutant could be obtained by using those transformants. One type was the deletion mutant, represented by AY64, in which the IE180 gene was replaced by insertion of the modified Escherichia coli lacZ gene, which was inserted under the control of the IE180 promoter. The other type, represented by AY1030, was a mutant produced from the former type by subsequent deletion of the lacZ gene. The deletion mutants of both types could replicate in the transformants with the IE180 gene, but not in the parent cells. On the other hand, the lacZ gene in AY64 was functional under the control of the IE180 promoter and could express beta-galactosidase (beta-gal) in not only the transformants but also the parent cells, indicating that the IE180 promoter of the mutants can fulfill the intended function in inoculated cells. The parent cells infected with the AY64 expressed only beta-gal, but neither infectious virus nor viral products relating to PrV. The deletion mutants constructed in this study appeared to provide a helpful model for investigating the functions of the IE180-homologs of other herpesviruses as well as IE180 itself, since PrV has only one IE gene. The applicability of the deletion mutants as a useful and safe vector for the introduction of foreign genes into various cells and animals was discussed.

Animals↗
PubMed1994

Pseudorabies virus immediate-early regulatory protein IE180 expressed by recombinant baculovirus is functional.

IE180, an immediate-early regulatory protein of pseudorabies virus, is required to activate viral early and late genes and is essential for viral growth. We constructed a recombinant baculovirus expressing IE180 in SF21AE insect cells. IE180 expressed by the recombinant migrated on gels as a single band with a molecular weight of 180 kDa and reacted with anti-IE180 peptide serum in Western blotting assay. Immunofluorescence using anti-IE180 peptide antibody demonstrated the accumulation of IE180 in cytoplasm of SF21AE cells infected with the recombinant virus. The IE180 produced in the insect cells was introduced into mammalian Vero cells infected with a PrV mutant with deletion of the IE180 gene by a cell-fusion technique. The growth of the deletion mutant in the fused cells was confirmed by infective assay and immunodetection of the progeny virus. This indicates that the IE180 expressed by the recombinant baculovirus is functional as a transactivator.

Animals↗
PubMed1994

High-affinity specific [3H]tamsulosin binding to alpha 1-adrenoceptors in human prostates with benign prostatic hypertrophy.

The binding of a novel radioligand, [3H]tamsulosin, to human prostatic membranes with benign prostatic hypertrophy (BPH) has been characterized. [3H]Tamsulosin rapidly associated with its binding sites in human prostatic membranes with BPH, and the binding reached steady state by 30 min at 25 degrees C. The rate constants for association and dissociation of [3H]tamsulosin binding were calculated to be 0.21 +/- 0.05/nM per minute and 0.01 +/- 0.004/min, respectively. The specific binding of [3H]tamsulosin in human prostatic membranes was saturable and of high affinity (Kd = 0.04 +/- 0.01 nM). The density of [3H]tamsulosin-binding sites (Bmax) was 409 +/- 28 fmol/mg protein. The Kd and Bmax values for [3H]tamsulosin binding in human prostates were significantly lower than those for [3H]prazosin binding. [3H]tamsulosin binding was remarkable for its significantly lower degree of nonspecific binding. Six alpha-adrenoceptor antagonists competed with [3H]tamsulosin for the binding sites in the rank order: tamsulosin > WB4101 > prazosin > S-(+)-isomer > naftopidil > yohimbine. The binding affinities (pKi) of these antagonists for [3H]tamsulosin binding in human prostates closely correlated with their pharmacological potencies (pA2) in prostates. In conclusion, [3H]tamsulosin selectively labels alpha 1-adrenoceptors in human prostates, and thus may become a useful radioligand for the further analysis of these receptors.

Adrenergic alpha-Antagonists↗
PubMed1994

Hydrocephalus: is impaired cerebrospinal fluid circulation only one problem involved?

Hydrocephalus is a complex disease of the brain as a whole, and imbalance between cerebrospinal fluid (CSF) formation and absorption is not the sole mechanism involved in its pathophysiology. In the absence of a lymphatic system in the central nervous system, open communication between CSF and interstitial fluid (ISF) of the brain may contribute to maintaining homeostasis of the brain, keeping the microchemical environment in good balance. Membranes or cell layers separating CSF from ISF of the brain do not provide impermeability, so the CSF communicates with ISF across the ependymal layer and the pial surface of the brain. In contradiction of the classical theory, the CSF one may obtain at the cisterna magna, for instance, is different from the newly formed CSF out of the choroid plexus, because it has been modified by the free communication between CSF and ISF spaces as the CSF descends along the neural axis. Free flow of water and some smaller molecules provides a bidirectional movement of water and other materials, and this must play an important role in brain volume control. The significance of this role should not be overlooked in regard to the pathophysiology of hydrocephalus.

Animals↗
PubMed1994

Combined oral administration of etoposide and arabinofuranosylcytosine-5'-stearylphosphate enhances the antitumor effect against P388 ascites tumors.

We investigated the antitumor effect of oral administration of etoposide and arabinofuranosylcytosine-5'-stearylphosphate (C18PCA) against P388 ascites tumors in B6D2F1 mice. Etoposide (25 mg/kg) and C18PCA (5 mg/kg) were given orally on days 1-5 after tumor inoculation. The median life span of the mice treated with etoposide or C18PCA alone was 19.5 and 18 days, respectively. The combination of both drugs significantly extended the median life span to 33 days. To clarify this enhancement of the increase in median life span, we examined intracellular deoxyribonucleoside triphosphate (dNTP) pools, cell-cycle distribution, DNA fragmentation, and the time course of the plasma drug concentration. Etoposide had no effect on intracellular dNTP pools in this experimental system, whereas treatment of cells with C18PCA or with the combination of both drugs resulted in a significant increase in dTTP pools to values ranging from 1.8- to 2.0-fold higher than the control levels. There was a significant increase in cells in the S + G2/M phase when cells had been treated with both etoposide and C18PCA. Agarose-gel electrophoresis of the extracted DNA revealed that C18PCA enhanced the fragmentation of DNA, with a length of about 180 bp being induced by etoposide. The plasma peak levels of etoposide (1000 nM) and ara-C (50 nM) were observed at 20 and 30 min after the simultaneous administration of both drugs, respectively. The plasma etoposide level gradually decreased to 10% of the peak level at 240 min after administration. On the other hand, the plasma concentration of ara-C was maintained at above 20 nM at 240 min. These observations suggest that C18PCA and etoposide act on P388 murine leukemic cells by accumulating cells in the S + G2/M phase. Even if the plasma concentration of ara-C is low, the repair of DNA damage by etoposide may be hindered in the presence of ara-C following an increase in DNA fragmentation.

Administration, Oral↗
PubMed1994

Regulating factors of liver regeneration after hepatectomy.

The factors regulating liver regeneration were studied by measuring changes in the liver volume and serum hepatocyte growth factor (HGF) levels after hepatectomy. Changes in the liver volumes were studied in 68 hepatectomized patients, including (A) hepatoma patients who had chronic hepatitis or liver cirrhosis (n = 44) and (B) metastatic liver cancer patients who had normal liver parenchyma (n = 24). The hepatic volume increased by 13.8% of the remnant hepatic volume in group A and by 49.1% in group B. The examined factors included the percentage of resected liver volume (%RLV) and the results of laboratory tests. Regression analysis showed that in group A, both %RLV (beta = 0.46) and the serum total bilirubin (T-Bil) level (beta = -0.33) correlated significantly with the extent of liver regeneration and that in group B, only %RLV (beta = 0.78) correlated significantly with the regeneration. Serum HGF levels after hepatectomy were studied in 21 hepatectomized patients, including 11 hepatoma patients and 10 patients with some types of metastatic liver cancer. Serum HGF levels increased significantly after surgery in all 21 patients. Regression analysis, however, showed that the change in HGF was related to liver cirrhosis (beta = 0.46) and to the maximal postoperative T-Bil level (beta = 0.51) but not to the extent of liver regeneration after hepatectomy. These results suggest that liver regeneration is regulated primarily by factors relating to the percentage of the resected liver parenchyma and that serum HGF levels do not directly relate to liver regeneration after surgery.

Aged↗
PubMed1994

Analysis of the VNTR locus D1S80 in a Japanese population.

A population study on the VNTR locus D1S80 was carried out in a sample of 377 unrelated Japanese individuals living in and around Gifu Prefecture (central region of Japan). A total of 29 different alleles was distinguished. Alleles 18, 24 and 30 were found to be the 3 most common alleles in this population sample and their frequencies were 0.147, 0.200 and 0.162, respectively. Out of the 435 possible phenotypes, 120 were observed. The observed heterozygosity was 0.88 and the power of discrimination was 0.98. No significant deviations from Hardy-Weinberg equilibrium could be found in this Japanese population sample.

Alleles↗