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Biomedical subjects

N Sakai

Publications and source records attributed to N Sakai.

At least 415 records · Page 23Linked to original sources
PubMed1995

[A case of spinal astrocytoma presenting spinal transverse sign due to hematomyelia].

An unusual case of cervical astrocytoma due to hematomyelia was reported. A 68-year-old man was admitted to our institute because of sudden onset of paraplegia and urinary and bowel disturbance. CT and plain X ray on admission showed no abnormal findings, but emergency MRI revealed a high signal intensity area in Th 8-9 level on T1 weighted image. Preoperative diagnosis was idiopathic hematomyelia and emergency laminectomy was performed. After the dural incision from Th 8-10, the intramedullary hematoma was totally removed, but at the cephalic portion within the hematoma cavity an abnormal tumorous tissue was detected. It was noticed with the bleeding sauce of hematomyelia, and it, too, was totally removed. The microscopic finding concerning the surgical specimen was fibrillary astrocytoma (grade 2), and its vascular component was relatively rich.

Aged↗
PubMed1995

[Krabbe disease (globoid cell leukodystrophy)].

Krabbe disease is an autosomal recessive inherited demyelinating disease, which is deficient in lysosomal enzyme, galactocerebrosidase. Pathophysiological characteristics of this disease are extreme demyelination in white matter and peripheral nerve, existence of globoid cells, absence of accumulation of main substrates, i.e. galactocerebrosidase in tissues and accumulation of psychosine. Molecular basis of this disease including isolation of a cDNA for human and murine galactocerebrosidase and cloning of genome of this gene are reviewed. The trial of gene therapy on twitcher, the mouse model of Krabbe disease, could break through on therapy on this progressive demyelinating disease.

Animals↗
PubMed1995

Hypothermic prevention of nuclear DNA fragmentation in gerbil hippocampus following transient forebrain ischemia.

The protective effect of hypothermia on DNA fragmentation following transient forebrain ischemia in mongolian gerbils was investigated. The DNA fragmentation demonstrated in situ in gerbil hippocampal CA1 was compared between intra- and post-ischemic hypothermia. Intra-ischemic hypothermia prevented the DNA fragmentation in hippocampal CA1 completely, while severe DNA damage was observed in post-ischemic hypothermia group. the degree of DNA fragmentation of hippocampal CA1 in the post-ischemic hypothermia group was equal to that in the ischemic control group. The results suggest that hypothermia during a transient forebrain ischemia exerts a protective effect on the post-ischemic hippocampal damage by preventing the DNA fragmentation in CA1 neurons.

Animals↗
PubMed1995

[A case report of variegate porphyria].

We reported a 30-year-old woman with variegate porphyria. Family history disclosed that her mother had the same skin lesions as the present case. She has had repeated vesicles and brownish pigmentation on her upper extremities since eighteen years of age. Recently she was suffering from common cold, and was treated with drugs. One week later, she started to develop weakness and dysesthesia in all limbs, hallucination, and urinary disturbance. Three weeks later, she was admitted to our hospital because she could not stand any more. On general examination, she had brownish pigmentations and crusts in hands and forearms. Neurologically she had moderate weakness, dysesthesia and hyperreflexia in all limbs. Urine was dark-red. Head and cervical MRI was normal. Nerve conduction studies and somatosensory evoked potentials were within normal limits. Excretion of porphyrins, especially protoporphyrin and X-porphyrin in the feces were markedly increased, and the diagnosis of variegate porphyria was made. Intravenous administration of glucose was effective and her symptoms began to improve in two weeks after her admission. However, recovery of weakness took two months and dysesthesia did not disappear in three months. We considered that her clinical manifestations were caused by involvement of the central and peripheral nervous systems.

Adult↗
PubMed1994

Neural substrates for conditioned taste aversion in the rat.

Conditioned taste aversions (CTAs) are well known to be robust and long-lasting instances of learning induced by a single CS (taste)-US (malaise) pairing. CTA can be taken as a general model to search for neural mechanisms of learning and memory. In spite of extensive research on CTAs using a variety of approaches during the last three decades, the neural mechanisms of taste aversion learning still remain unsolved. In this article we propose a model of neural substrates of CTAs on the basis of our recent studies incorporating previous findings by other workers. Our studies mainly included experiments using ibotenic acid injections into various parts of the rat brain as a lesion technique, and c-fos immunohistochemistry in naive and CTA trained rats. CTAs were established by pairing the ingestion of saccharin (CS) with an ip injection of LiCl (US). Behavioral studies have shown that the parabrachial nucleus (PBN), medial thalamus, and basolateral nucleus of the amygdala are essential for both acquisition and retention of CTAs. C-fos studies suggested that association between gustatory CS and visceral US takes place in the PBN. The gustatory cortex (GC) may modify the strength of this association depending on the nature of the CS, viz., novel or familiar. The amygdala is indispensable for the expressions of CTAs. Tastes with hedonic values are stored in the GC in a long-term manner.

Animals↗
PubMed1994

Na(+)-dependent transport of aminopeptidase-resistant sugar-coupled tripeptides in rat intestine.

Aminopeptidase-degradable tripeptide, tyrosylglycylglycine (TGG, a part of aminopeptidase-degradable enkephalines), was coupled with sugars (cellobiose, maltose, lactose, gentiobiose and glucose). These sugar-coupled TGGs were stable enough to be transported from the mucosal to the serosal side in rat everted small intestine, while TGG was not stable enough to be transported. The transport of sugar-coupled TGGs was decreased in the absence of Na+, indicating the Na(+)-dependent transport of sugar-coupled TGG in rat intestine. Cellobiose-coupled TGG and glucose-coupled TGG did not mutually inhibit their transport. It was suggested that the intestinal Na(+)-dependent transporter for disaccharide-coupled tripeptides, which have a pyranose ring, was different from that of monosaccharide-coupled tripeptide, which has no pyranose ring.

Amino Acid Sequence↗
PubMed1994

Somatic mutations of the von Hippel-Lindau tumor suppressor gene in sporadic central nervous system hemangioblastomas.

Hemangioblastoma is one of the benign tumors in the central nervous system. It is often associated with the von Hippel-Lindau (VHL) disease, a well known hereditary tumor syndrome. It is believed that inactivation of both alleles of VHL tumor suppressor gene is essential in the tumorigenic processes in hemangioblastomas associated with VHL disease. The molecular basis for the development of sporadic hemangioblastomas is not known. Here, we analyzed 13 cases of primary sporadic hemangioblastomas for somatic mutations of VHL gene with single strand conformational polymorphism analyses of the tumor DNAs. We detected abnormal single strand conformational polymorphism pattern in 7 tumors (54%). Of these 7 possibly mutated tumors, we successfully characterized 3 tumors by direct sequencing. We were unable to sequence 4 tumors because of the poor quality of DNA obtained from paraffin blocks. Somatic mutations in the 3 tumors were 2 missense mutations and 1 microdeletion. These mutations were observed in 1 tumor in exon 1 and 2 tumors in exon 2. Our results suggest that mutations of VHL tumor suppressor gene are involved in the development of at least 20% of sporadic central nervous system hemangioblastomas.

Base Sequence↗
PubMed1994

Ovarian 3 beta-hydroxysteroid dehydrogenase/delta 5-4-isomerase of rainbow trout: its cDNA cloning and properties of the enzyme expressed in a mammalian cell.

A cDNA clone encoding 3 beta-hydroxysteroid dehydrogenase delta 5-4-isomerase (3 beta-HSD) was isolated from a cDNA library of rainbow trout ovarian thecal cells. Southern hybridization analysis of trout genomic DNA with the cDNA suggested the presence of a single gene encoding 3 beta-HSD in the rainbow trout showing a total genomic size of less than 4 kilobases (kb). The cDNA hybridized to a species of mRNA isolated from rainbow trout ovaries; the 1.4 kb transcripts were most abundant in trout ovaries during the later stages of oogenesis. The trout 3 beta-HSD expressed in non-steroidogenic monkey kidney tumor (COS-1) cells showed a unique enzymatic 3 beta-HSD activity. Dehydroepiandrosterone was a more favoral substrate of the trout 3 beta-HSD than 1- alpha-hydroxypregnenolone. Interestingly, the trout 3 beta-HSD expressed in COS-1 cells exhibited minimal ability to convert pregnenolone to progesterone.

3-Hydroxysteroid Dehydrogenases↗
PubMed1994

Potassium and calcium channel involvement in induction of long-lasting synaptic enhancement by calyculin A, a protein phosphatase inhibitor, in rat hippocampal CA1 region.

In the Schaffer collateral-CA1 pathway in rat hippocampal slices, exposure to calyculin A induced a long-lasting potentiation of the extracellular field potentials with a transient increase in glutamate release. The synaptic enhancement produced by calyculin A was blocked by staurosporine and nicardipine, but not by D,L-2-amino-5-phosphonovalerate. In dissociated CA1 pyramidal cells, calyculin A blocked the action-potential repolarization and fast after-hyperpolarization, and increased spike frequency. These results suggest that calyculin A-induced long-lasting potentiation is triggered by the blockade of Ca(2+)-activated K+ channels, the transient increase of glutamate release and the consequent activation of voltage-gated Ca2+ channels, and is maintained by increases in protein kinases activities.

Animals↗
PubMed1994

Tumorigenicity of BALB3T3 A31 cells transfected with hamster-complement-C1s cDNA.

Hamster-complement-C1s cDNA was inserted into an expression plasmid BCMGSNeo (BCMGSNeoHACS). BALB/c mouse fibroblast A31 cells, which do not produce C1s, were transfected with BCMGSNeoHACS and the transfectants were selected with G418. Normal C1s production by the transfectants was confirmed by Northern and immunoblot analysis and by an esterase assay. To examine the tumorigenicity of the transfectants, 1 x 10(6) cells were injected s.c. into 6-week-old BALB/c nu/nu mice. Three C1s cDNA transfectants (A3CS9, A3CS12, A3CS13) formed tumors whereas both A31 and A31 transfected with the vector alone (A3BCM1 and A3BCM3) did not. The tumors derived from the transfectants showed invasive growth, and many capillaries were observed in the tumors. A tumor derived from A3CS13 was examined immunohistochemically and found to be reactive with an anti-C1s monoclonal antibody. Tumor cells were cultured in vitro again and C1s secreted into the culture medium was examined by immunoblot analysis. C1s synthesized by the tumor cells derived from A3CS13 maintained its biological functions. Tumor cells derived from A3CS9 and A3CS12 cells, however, produced C1s having abnormal disulfide bonds.

3T3 Cells↗
PubMed1994

Changes in the expression of sialyl-Lewisx, a hepatic necroinflammation-associated carbohydrate neoantigen, in human hepatocellular carcinomas.

BACKGROUND: Malignant transformation of cells is associated with the change in their carbohydrate antigens. Sialyl-Lewisx (SLEX) is a necroinflammation-associated carbohydrate antigen (NICA) of liver cells, because it is newly expressed in chronic inflammatory liver diseases. The authors addressed whether this type of carbohydrate antigen shows cancer-associated changes. METHODS: Expression of SLEX and its related structures was studied immunohistochemically using the well characterized monoclonal antibodies in 13 small and 6 advanced hepatocellular carcinomas (HCC). RESULTS: SLEX was negative in 7 small HCC, which were well differentiated histologically. Both negative and positive cells were observed in 6 other small HCC. When positive, SLEX was expressed membranously or cytoplasmically. The membrane positive HCC cells were well differentiated. Cytoplasmic expression was observed in the less differentiated cells. The SLEX-negative cells were associated with any degree of differentiation. In six advanced HCC, the expression of SLEX could also be correlated with their histologic differentiation. HCC expressed sialyl-type 2 chain N-acetyllactosamine (2-NAcLc), but not 2-NAcLc, Lewisx, and Lewisy. CONCLUSIONS: SLEX, a NICA, showed HCC-associated changes that were dependent on the levels of HCC cell differentiation. Suppression and reactivation of alpha 1-3fucosyl-transferase was a possible enzymatic basis for the observed changes.

Adult↗
PubMed1994

Immune complex independent activation of complement, C1s secreted from hamster embryo malignant fibroblasts, Nil2C2 in serum free culture medium.

Antibody independent activation of complement C1s was examined by immunoblot analysis using an antibody against a synthetic peptide of hamster C1s L chain. Approx. 50% of C1s secreted from hamster embryo malignant fibroblasts Nil2C2 was functionally active in its two-chain form in the serum free culture medium. In contrast, no active C1s was found in a culture medium of hamster embryo fibroblasts (HEF). Active C1s was detectable, however, in the culture medium after HEF became a cell line. The immune complex independent activation of C1s was also observed in rat cell lines but not in secondary rat embryo fibroblasts. C1s in a membrane fraction of Nil2C2 was a proenzyme form and was not activated by incubation of the membrane itself suggesting that C1s was activated after secretion. The activation of C1s was not inhibited by human C1 inhibitor (C1-INH), benzamidine or soy bean trypsin inhibitor (SBTI) but was inhibited by leupeptin, nitrophenyl guanidinobenzoate and DFP. Our results suggest that C1s is activated either by a serine proteinase(s) other than those reported to cleave C1s or by an activator which directly stimulates autoactivation of C1s.

Amino Acid Sequence↗
PubMed1994

Incidence and time course of left ventricular dilation in the early convalescent stage of reperfused anterior wall acute myocardial infarction.

The incidence and early process of left ventricular (LV) dilation in 52 patients with reperfused anterior wall acute myocardial infarction (AMI) were assessed. All patients achieved coronary reflow within 24 hours of the onset and had a patent infarct-related artery in the convalescent stage. Left ventriculography was performed at pre-reflow and 25 days (mean) later to determine LV end-diastolic volume (ml) with the area/length method. Short-axis echo images at the midpapillary muscle level were recorded at days 1, 7, 14, and 28 of the AMI. With use of the papillary muscles as the internal landmarkers, the LV wall was divided into the anterior and posterior segments, and length and thickness of each segment were determined. Among 52 patients, 10 (19%) had a > or = 20% increase in end-diastolic volume in the convalescent stage. Echocardiographic studies demonstrated that there were no significant changes in lengths and thicknesses of the anterior and posterior segments during follow-up study relative to his or her baseline value in 42 patients without LV dilation. In the patients with LV dilation, however, the anterior segment exhibited a mean increase of 25% in its length with a mean decrease of 21% in its thickness at day 7 relative to their baseline values, but no progressive expansion was observed after day 7. A mean increase of 7% in the posterior segment length without reduction in its thickness first became evident at day 28.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗
PubMed1994

Krabbe disease: isolation and characterization of a full-length cDNA for human galactocerebrosidase.

Human galactocerebrosidase, the enzyme deficient in Krabbe disease, was purified, through several hydrophobic column steps and gel filtration, 22,650-fold from human lymphocytes. Using information on its N-terminal and internal amino acid sequences, and the polymerase chain reaction method, we cloned a full-length cDNA for the enzyme. The deduced amino acid sequence matched all amino acid sequences determined. The 3780 nucleotide sequence included 2007 nucleotides which encoded a single chain peptide of 669 amino acid residues with a 26 amino acid N-terminal signal peptide and six potential asparagine-linked glycosylation sites. The galactocerebrosidase cDNA detected an about 4 kb mRNA band material in human cultured skin fibroblasts. A nonsense mutation was found at codon 369 (GAA-->TAA) in the coding sequence of cDNA amplified from cultured skin fibroblast mRNA from a patient with typical Krabbe disease.

Amino Acid Sequence↗
PubMed1994

Induction of apoptosis by a dominant negative H-RAS mutant (116Y) in K562 cells.

Recent extensive work on apoptosis has begun to reveal its molecular mechanisms. Several genes that regulate apoptosis have been identified. Among them, the BCL2 gene is considered to be an important gene that inhibits apoptosis. However, there must be other genes, yet to be identified, which suppress apoptosis. It has been suggested that the activation of RAS function by BCR-ABL fusion protein in chronic myelogenous leukemia may be an important mechanism in the BCR-ABL mediated transformation. Therefore, in this study we have investigated whether the suppression of endogenous H-RAS function inhibits the BCR-ABL mediated transforming activity in a K562 human chronic myelogenous leukemia cell line. The induced expression of a dominant negative v-H-RAS mutant (116Y) in K562 cells has resulted in cell death. The morphological characteristics and the detection of fragmented DNA by gel electrophoresis in the dead cells have revealed that this cell death is apoptosis. These results directly indicate that the RAS gene as well as the BCL2 gene has an ability to suppress apoptosis.

Apoptosis↗