Search PubMed⌕ Search

Biomedical subjects

S Tsuji

Publications and source records attributed to S Tsuji.

At least 577 records · Page 32Linked to original sources
PubMed1995

[Intratumoral LPD deposition within hepatocellular carcinoma without arterial tumor staining].

The dissociation of intratumoral LPD deposition and arterial tumor staining was investigated in 20 cases of hepatocellular carcinoma (HCC) without arterial tumor staining. The intratumoral deposition of LPD injected from the hepatic artery was observed in nine cases of HCC and coincided with the decrease in tumor vascular bed evaluated by photomicroscopic study and arterial portography. LPD deposition was not observed within the 11 other tumors, which were diagnosed as well differentiated HCC. Infusion angiographic CT revealed that the arterial and portal vascular beds were separated from each other. Therefore, arterial tumor staining was insufficient for accurate evaluation of the tumor vascular bed. The vascular bed in cancerous and noncancerous tissue was accurately evaluated by the addition of the contrast enhancements from the hepatic artery and the portal vein.

Carcinoma, Hepatocellular↗
PubMed1995

[Familial myopathy associated with tubular aggregates--report of two siblings].

We reported two siblings with slowly progressive muscle weakness in proximal and peroneal muscles without atrophy, myalgia, cramps, or episodic weakness. The serum creatine kinase level was moderately elevated. The prominent features of their muscle pathology were accumulation of tubular aggregates in type 2 fibers, predominantly in type 2B fibers, and marked type 1 fiber atrophy. Three to eleven % of muscle fibers contained tubular aggregates. Electron microscopic examination revealed accumulation of double-walled tubular structures. Familial myopathy with tubular aggregates as a hallmark of muscle pathology is considered to be a new clinical form of childhood-onset familial myopathies.

Child↗
PubMed1995

[Shear-induced platelet aggregation (SIPA) monitoring of hemostatic effect during platelet transfusion in a patient with Glanzmann's thrombasthenia: a comparison between SIPA and conventional platelet aggregation].

Shear-induced platelet aggregation (SIPA) in a patient with Glanzmann's thrombasthenia was examined during platelet infusion therapy. Prior to platelet infusion, SIPA measured with the modified cone-and-plate type viscometer, as well as ADP-and collagen-induced platelet aggregation measured with the conventional platelet aggregometer, were absent. The patient's SIPA after multiple infusions of platelet, in parallel with the bleeding time and the clinical hemostatic effect, improved to the normal level, while ADP-and collagen-induced platelet aggregation remained abnormal. These observations imply that SIPA is physiologically more relevant than the conventional agonist-induced platelet aggregometry in this type of the disease.

Adenosine Diphosphate↗
PubMed1995

[Estimated production by the official inspection of coal-tar dyes (including dye aluminum lakes) in 1994].

The number of official inspection of coal-tar dyes and their lakes from April in 1994 till March in 1995 were 635 in total. The quantity which passed inspection amounted to 186 ton in Japan. The production of color in each month was summarised in Table 1, and by each producing company in Table 2. The food coal-tar dye produced in the largest quantity was Food Yellow No.4, occupying 40.7% in this period.

Chemical Industry↗
PubMed1995

Gastric mucosal cell proliferation and TGF alpha in the healing of peptic ulcers in human subjects.

We investigated the role of gastric mucosal proliferation and mucosal transforming growth factor-alpha (TGF alpha) in the healing of peptic ulcers in human subjects. During endoscopic observation, mucosal biopsy specimens were taken from the ulcer margin for flow cytometric analysis of the mucosal cell cycle and ELISA for mucosal TGF alpha content. Immunohistochemistry confirmed that biopsy specimens contained proliferating gastric epithelial cells, TGF alpha, and the TGF alpha receptor. When the stage of ulcer healing was categorized according to Sakita and Miwa, mucosal cell proliferation was less at active stages and gradually increased during the healing process. The mucosal TGF alpha level at the ulcer margin was not detectable at the A1 stage but increased to within the normal range during ulcer healing. After re-establishment of the epithelial layer at the site of the ulcer, cell proliferation returned to normal and TGF alpha remained within the normal range. Immunohistochemistry showed coexistence of TGF alpha and its receptor within PCNA-positive proliferating cells. These results suggest that TGF alpha and its receptor play an important role in gastric epithelial cell replication. The increase in TGF alpha at the ulcer margin might indicate a role in stimulation of gastric cell replication during ulcer healing.

Adult↗
PubMed1995

The inflammatory reaction in mucosa during healing of gastric ulcers in humans.

To evaluate the inflammatory changes during ulcer healing, we measured myeloperoxidase (MPO) activity and the inflammatory cytokine interleukin-8 (IL-8) in the gastric mucosa of 51 patients with gastric ulcers and 5 normal controls. MPO activity was measured by enzyme assay and IL-8 by ELISA, using biopsy samples taken from the ulcer margin and at 3 and 6 cm from the ulcer. Levels of MPO activity were significantly higher than in normal controls and peaked at the A2 (active) stage, and then gradually decreased and returned to basal levels at the S2 (scarring) stage. The area of increased MPO activity around the gastric ulcer was approximately 6 cm in diameter at the A2 stage, and this area decreased as the ulcer healed. IL-8 levels in gastric mucosa also increased significantly at the A2 stage, and the changes paralleled those of MPO activity during ulcer healing. MPO activity correlated well with the IL-8 level.

Biopsy↗
PubMed1995

[Paraneoplastic cerebellar degeneration--characterization of anti-Yo antibody and underlying cancer].

A group of patients with paraneoplastic cerebellar degeneration (PCD) have shown to produce autoantibody to both neurons and tumor cells (anti-Yo antibody). More than 60% of these patients have shown neurological symptoms and anti-Yo antibody production before the underlying cancers were found, which suggests that the test for anti-Yo antibody is important for the early detection and treatment of cancer. Originally, anti-Yo antibody has been characterized as 1) labelling the cytoplasm of cerebellar Purkinje cells immunohistochemically, 2) binding to the 62 and 34kDa bands on immunoblots of Purkinje cell extracts, 3) being present in female patients with gynecological or breast cancers. Recently, the common binding-epitope of anti-Yo antibody has been reported as leucine-zipper protein. In order to detect the anti-Yo antibody precisely, we examined the immunohistochemical and western blot characters of the recombinant leucine-zipper protein-reactive (anti-Yo) antibody. The results were, 1) sera containing leucine-zipper protein-reactive antibody labels both cerebellar Purkinje cells but some sera might contain other antibodies together with anti-Yo that confuse the immunostaining character of anti-Yo antibody, 2) the antibody binds to 58 kDa band and sometimes co-binds to 34kDa on immunoblots of cerebellar tissue extracts. The underlying cancers are mainly adenocarcinoma in the ovary, fallopian tube, uterus, or breast but occasionally large cel lung and bile duct cancers have been found. Interestingly, a male patient had an antibody similar in character to be anti-Yo antibody immunohistochemically and on immunoblots, that did not recognize leucine-zipper protein and the underlying carcinoma was small cell lung cancer. These results suggest that 1) the diagnosis of anti-Yo antibody should be based on the antibody's reactivity with leucine-zipper protein, 2) some sera with the anti-Yo antibody label other tissues besides the Purkinje cell cytoplasm because of the co-existence of other antibodies seen immunohistochemically and on immunoblots, 3) the search for underlying cancers should not be limited to gynecological or breast carcinomas.

Adenocarcinoma↗
PubMed1995

[A case of complicated form of hereditary spastic paraplegia associated with hypoplasia of the corpus callosum and cataracta].

Autosomal dominant, autosomal recessive and X-linked recessive varieties of spastic paraplegia have been recognized. Recently, Japanese patients with complicated form of autosomal recessive hereditary spastic paraplegia (HSP) associated with hypoplasia of the corpus callosum have been reported by Iwabuchi et al. We describe a patient with complicated HSP (Iwabuchi type) and cataracta. A 38-year-old man (his parents were a second cousin) was born uneventfully. His motor development was normal. Motor and mental dysfunctions were noticed during the lower classes of an elementary school. He could ride a bicycle at 18 years old but gradually developed galt disturbance and confined to wheelchair since 35 years. He was admitted to our hospital on February 25, 1994. A neurological examination showed mental retardation, dementia, cataracta, cerebellar ataxia, rigidity, spasticity, severe atrophy of the distal muscles of his extremities, paraparesis, hyperreflexia, positive Hoffmann reflexes and Babinski signs, pes cavus and hammer toes. Brain MRI showed thinning of corpus callosum. Clinical and laboratory findings did not support a diagnosis of metabolic disorders showing spastic paraparesis including adrenomyeloneuropathy, Globoid leukodystrophy, metachromatic leukodystrophy, cerebrotendinous xanthomatosis, Arginase deficiency. We considered that our patient was complicated form of HSP (Iwabuchi et al). However, cataract has not been found in Iwabuchi type of HSP. We discussed here other reports showing cataracta with spastic paraparesis.

Adult↗
PubMed1994

Passive transfer and active immunization with the recombinant leucine-zipper (Yo) protein as an attempt to establish an animal model of paraneoplastic cerebellar degeneration.

Passive transfer of paraneoplastic cerebellar degeneration (PCD) IgG to rodents as well as active immunization with recombinant Yo fusion protein were tried in order to examine the roles of anti-Purkinje cell antibody (anti-Yo antibody) present in the sera and cerebrospinal fluid of patients with PCD in Purkinje cell loss, the hall mark of PCD pathology. On a single injection of PCD IgG to mouse brain, IgG was taken into Purkinje cells and remained there for more than 36 h without Purkinje cell loss. Injection of PCD IgG together with complement or lipopolysaccharide-activated human macrophages or rat mononuclear cells to rats ventricles did not cause Purkinje cell loss. We made a recombinant Yo fusion protein that has the leucine-zipper protein (Yo protein), the common epitope for anti-Yo antibody. Mice immunized with this Yo protein produced high titer antibody against it for more than 3 months, during which time neither neurological symptoms nor Purkinje cell loss occurred. The anti-Yo antibody, with or without complement or activated mononuclear cells, therefore could not be the sole cause of Purkinje cell loss.

Aged↗
PubMed1994

Induction of cholinergic differentiation with neurite sprouting by de novo biosynthesis and expression of GD3 and b-series gangliosides in Neuro2a cells.

The expression of a single glycosyltransferase, GD3 synthase, caused cholinergic differentiation with neurite sprouting. The cells that expressed GD3 were established from Neuro2a cells by transfection of a mammalian expression vector into which were carried a cDNA encoding GD3 synthase and the blasticidin-S-deaminase gene with a SV40 promoter, followed by selection with blasticidin-S-hydrochloride. The blasticidin-S-hydrochloride-resistant colonies derived from the cells transfected with the cDNA encoding GD3 synthase and the clonal cells (N2a-GD3) were spontaneously sprouting neurites but not those derived from cells transfected with only the vector without the cDNA encoding GD3 synthase (N2a-bsr). GD3 expression by N2a-GD3 was confirmed by immunostaining of the cells using the anti-GD3 monoclonal antibody, KM643. N2a-GD3 expressed not only GD3 but also GQ1b, one of the b-series gangliosides, whereas N2a-bsr did not express these gangliosides. Cell proliferation of N2a-GD3 was greatly reduced, as compared with that of N2a-bsr, and, after several passages, it completely stopped. In addition, N2a-GD3 expressed acetylcholine esterase, indicating that the differentiation of Neuro2a cells was induced by expression of GD3 synthase and subsequent modification of the biosynthesis and expression of gangliosides. These results strongly suggest that the de novo synthesis and expression of GD3 and/or b-series gangliosides induce neurite outgrowth and differentiation of Neuro2a cells. Exogenous GM1 stimulated the neuritogenesis of N2a-bsr but not differentiated N2a-GD3, indicating that the mechanism of neurite sprouting in this system may be overlapped en route with that of exogenous GM1.

Acetylcholinesterase↗
PubMed1994

Evolutionary relationships of lactate dehydrogenases (LDHs) from mammals, birds, an amphibian, fish, barley, and bacteria: LDH cDNA sequences from Xenopus, pig, and rat.

The nucleotide sequences of the cDNAs encoding LDH (EC 1.1.1.27) subunits LDH-A (muscle), LDH-B (liver), and LDH-C (oocyte) from Xenopus laevis, LDH-A (muscle) and LDH-B (heart) from pig, and LDH-B (heart) and LDH-C (testis) from rat were determined. These seven newly deduced amino acid sequences and 22 other published LDH sequences, and three unpublished fish LDH-A sequences kindly provided by G. N. Somero and D. A. Powers, were used to construct the most parsimonious phylogenetic tree of these 32 LDH subunits from mammals, birds, an amphibian, fish, barley, and bacteria. There have been at least six LDH gene duplications among the vertebrates. The Xenopus LDH-A, LDH-B, and LDH-C subunits are most closely related to each other and then are more closely related to vertebrate LDH-B than LDH-A. Three fish LDH-As, as well as a single LDH of lamprey, also seem to be more related to vertebrate LDH-B than to land vertebrate LDH-A. The mammalian LDH-C (testis) subunit appears to have diverged very early, prior to the divergence of vertebrate LDH-A and LDH-B subunits, as reported previously.

Amino Acid Sequence↗
PubMed1994

Activation of the alternative pathway of complement by apoptotic Jurkat cells.

Jurkat T cells die of apoptosis upon exposure to anti-Fas mAb. Here we show that although the alternative complement pathway generally does not attack homologous cells, anti-Fas-induced apoptotic Jurkat T cells were attacked antibody-independently by the alternative pathway of human complement and opsonized with iC3b, which is a ligand of the complement receptor type 3 (CR3) of phagocytes. These results suggest that apoptotic cells become the targets of the homologous alternative complement pathway, which facilitates the clearance of apoptotic cells by phagocytes.

Antibodies, Monoclonal↗
PubMed1994

Cloning and expression of Gal beta 1,3GalNAc-specific GalNAc alpha 2,6-sialyltransferase.

A cDNA clone encoding a new type of GalNAc alpha 2,6-sialyltransferase (ST6GalNAc II) with a structure similar to that of a previously cloned GalNAc alpha 2,6-sialyltransferase (ST6GalNAc I; Kurosawa, N., Hamamoto, T., Lee, Y.-C., Nakaoka, T., Kojima, N., and Tsuji, S. (1994) J. Biol. Chem. 269, 1402-1409) was obtained from chicken testes. The predicted amino acid sequence of ST6GalNAc II encodes a protein with type II transmembrane topology, as found for other glycosyltransferases, and showed 32% identity with that of ST6GalNAc I. Transfection of the full length ST6GalNAc II gene into COS cells led to GalNAc alpha 2,6-sialyltransferase activity with a different substrate specificity from that of ST6GalNAc I. Moreover, asialofetuin after treatment with beta-galactosidase did not serve as an acceptor for this enzyme. 14C-Sialylated oligosaccharides obtained from resialylated asialobovine submaxillary mucin with this enzyme were identical to Gal beta 1,3([14C]NeuAc alpha 2,6)GalNAc-ol but not [14C]NeuAc alpha 2,6GalNAc-ol. These results clearly show that the expressed enzyme is a novel type of sialyltransferase that requires beta-galactoside residues linked to GalNAc residues, whereas sialic acid residues linked to galactose residues are not essential for the activity.

Amino Acid Sequence↗
PubMed1994

Structures of the human and mouse growth inhibitory factor-encoding genes.

Growth inhibitory factor (GIF) is down-regulated in Alzheimer's disease (AD) brains. To analyze the mechanism of this down-regulation, we isolated the human and mouse GIF genes. These genes consist of three exons, are approx. 1-kb long and show strikingly high homology to metallothionein-encoding genes. A comparison of the human and mouse GIF showed several conserved sequences, including the putative AP-2, SP-1, TATA-binding protein and metal-responsive elements (MRE). A sequence similar to the human gfa common sequence (hgcs), recently identified as the sequence for an astrocyte-specific transcriptional factor, is present in the promoter of these GIF. Characterization of factors associated with the putative regulatory elements in the promoter of GIF should help in determining the mechanism of the down-regulation of GIF in AD brains.

Alzheimer Disease↗