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Biomedical subjects

S Tsuji

Publications and source records attributed to S Tsuji.

At least 775 records · Page 43Linked to original sources

[Estimated production by the official inspection of coal-tar dyes (including dye aluminum lakes) in 1990 based on official inspection figures].

The number of official inspections of coal-tar dyes and their lakes from april in 1990 till march in 1991 was 836 in total. The quantity passed amounted to 238 ton in Japan. The production of color for 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 46.2% in this period.

Chemical Industry↗

Identification of a mutation in the arylsulfatase A gene of a patient with adult-type metachromatic leukodystrophy.

To analyze the genetic abnormality in a Japanese patient with adult-type metachromatic leukodystrophy (MLD), we first elucidated the genomic organization of the human arylsulfatase A (ASA) gene and then compared the nucleotide sequences of exons and splice junctions of the mutant ASA gene to those of a normal control. We have identified a new mutation, a G-to-A transition in exon 2, which results in amino acid substitution of Asp for 99Gly. In a transient expression study, COS cells transfected with the mutant cDNA carrying 99Gly----Asp did not show an increase of ASA activity, which confirms that the mutation is a cause of adult-type MLD.

Adult↗

Role of blood ethanol on gastric mucosal injury and gastric hemodynamics.

The present series of studies were performed to test the hypothesis that ethanol in the blood may play a role in the pathogenesis of gastric mucosal injury. Another hypothesis to be examined was that endothelin may be involved in ethanol-induced gastric mucosal injury. Elevated levels of blood ethanol induced by intraperitoneal infusion of ethanol increased vulnerability of the stomach to hydrochloric acid in a dose-dependent manner in rats. This may be due to impaired gastric mucosal hemodynamics and oxygenation as demonstrated by the results obtained by organ reflectance spectrophotometry (decreases in indices of mucosal hemoglobin contents and hemoglobin oxygen saturation). Ethanol infusion caused a dose-dependent increase in gastric vascular resistance in perfused rabbit stomach, which was accompanied by an increased production of endothelin-1. The results suggest that endothelin may be involved in the pathogenesis of ethanol-induced gastric mucosal injury.

Animals↗

[A case of systemic lupus erythematosus complicated with pulmonary hypertension and massive pericardial effusion].

A 22 year-old-female had suffered from polyarthralgia and Raynaud's phenomenon since 1984. In 1986, she was diagnosed as systemic lupus erythematosus (SLE). In April 1988, she was admitted to Kawasaki Municipal Hospital because of fever and dyspnea on exertion (DOE). Physical examination showed high fever, butterfly rash, oral ulcer and elevation of heart sound IIp on auscultation. Laboratory findings revealed that erythrocyte sedimentation rate was elevated to 105 mm/hr. The following values were observed, anti DNA antibody 391 IU/ml, serum IgA 5mg/dl, anti IgA antibody weakly positive. Chest X ray showed CTR 65%. Echo cardiogram showed massive pericardial effusion. 201T1 myocardial SPECT revealed right ventricular pressure over loading. PSL 40 mg/day was started to administer for the massive pericardial effusion due to SLE activities. On 6th of June, right heart catheterization confirmed the pulmonary hypertension (PPA 22 mmHg, Pulmonary artery resistance (PAR) 1163 dyne/sec/cm-5/mm2). By the treatment with PSL, massive pericardial effusion was gradually improved but DOE clinically unchanged. Second right heart catheterization was done on 8th of August. PAR was improved to 895 dyne/sec/cm-5/mm2 but PPA was elevated to 26 mmHg. It is very interesting that PPA was elevated although PAR was improved by PSL therapy. It is considered that the increase in venous return which was caused by improvement of massive pericardial effusion induced conversely the elevation of PPA. Additionally she was complicated with IgA deficiency. It may occur not only by the immunogenetical disorder such as HLA or IgG subclass alteration but also by anti IgA antibody or lymphocytes dysfunction complicated with SLE.

Adult↗

[Intracellular calcium level, lipid peroxidation, and development of gastric mucosal injury in rat hemorrhagic shock].

Although acute gastric mucosal lesions (AGMLs) develop after the mucosal ischemia and reperfusion, precise intracellular mechanism for the development of AGMLs remains unclear. In the present paper, we investigated intracellular calcium level, lipid peroxidation, and gastric mucosal lesion in rat hemorrhagic shock model. We estimated intracellular calcium by measuring phosphorylase a activity in the gastric mucosa. The mucosal phosphorylase a increased during hemorrhagic shock, while it returned to be normal after the reinfusion of shed blood. Although mucosal lipid peroxide and area of AGMLs did not increase significantly during hemorrhagic shock, they increased significantly after the reinfusion. Diltiazem, a calcium antagonist, prohibited both of the increase in mucosal phosphorylase a activity during hemorrhagic shock and the increase in lipid peroxide content and area of AGMLs after the reinfusion of the shed blood. Organ reflectance spectrophotometry revealed that the gastric corpus suffered mucosal ischemia and hypoxia during the hemorrhagic shock. The are of AGMLs had a good correlation with a level of lipid peroxidation in the gastric mucosa. These results suggest 1) that intracellular free calcium in gastric mucosa increases during the mucosal ischemia; 2) that a calcium antagonist prohibits the increased intracellular free calcium during mucosal ischemia; and 3) that a calcium antagonist prohibits the increased mucosal lipid peroxide and the development of AGMLs after the mucosal reperfusion. Thus it is concluded that the increased intracellular free calcium during ischemia plays a key role in the mucosal tissue injury in the ischemia-reperfusion state.

Animals↗

Molecular cloning of two species of cDNAs for human alpha-N-acetylgalactosaminidase and expression in mammalian cells.

Two species of cDNAs for human alpha-N-acetylgalactosaminidase were isolated from a human fibroblast cDNA library. The two species differ each other by a 70 bp insertion in the coding region. Transient expression study in COS cells demonstrated that only the cDNA without the 70 bp insertion expressed alpha-N-acetylgalactosaminidase activity. Analysis of mRNA species utilizing polymerase chain reaction revealed that the majority of the mRNA does not contain the 70 bp insertion, and the mRNA containing the 70 bp insertion is present only in a minor amount in human brain.

Acetylglucosaminidase↗

Evoked potential studies in mitochondrial encephalomyopathy.

Evoked potentials were studied in a patient with a mitochondrial encephalomyopathy revealing a defect of nicotinamideadenine dinucleotide dehydrogenase and cytochrome C oxidase in the mitochondria of a muscle biopsy specimen. The biopsy specimen showed myopathic changes with ragged-red fibers and markedly decreased cytochrome C oxidase in the muscle fibers. Subcortical somatosensory evoked potentials to median nerve stimulation were normal in the peak latencies of N9, N11, and N13. Cortical somatosensory evoked potentials to median nerve stimulation revealed significantly delayed peak latencies of N20, P20, P25, and N26, although N16 latency was normal. In particular, the interpeak latency between N16 and N20 was significantly delayed. In topographic maps, N20 and P20 were delayed in the peak latencies with normal scalp distributions. Dysfunction of somatosensory cortex indicated by the delay of cortical somatosensory evoked potentials may be related to a cortical mitochondrial abnormality. The absence of responses to auditory stimulation within 10 milliseconds could be related to the dysfunction of peripheral acoustic nerves.

Adult↗

Isolation of temperature-sensitive CHO-K1 cell mutants exhibiting chromosomal instability and reduced DNA synthesis at nonpermissive temperature.

Twenty-five temperature-sensitive (ts) mutants were isolated from Chinese hamster CHO-K1 cells after mutagenization with N-methyl-N'-nitro-N-nitrosoguanidine. Of 13 complementation groups identified, nine exhibited chromosomal instability at a nonpermissive temperature. They were classified into three major classes according to inducibility of sister chromatid exchange (SCE) and/or chromosomal aberration (CA): class 1 resulted in predominant SCEs, class 2 manifested both SCEs and CAs, and class 3 exhibited higher induction of CAs. Flow cytometric analysis of the mutants exhibiting chromosomal instability indicated that many of the mutants were arrested in the S or S to G2 phases of the cell cycle at the nonpermissive temperature, accompanied by a decrease in the rate of DNA synthesis. These results imply that ts defects are related to some points in DNA replication and might be responsible for the induction of SCEs and/or CAs at the nonpermissive temperature.

Animals↗

High reproducibility of regional abnormalities on interictal 123I-IMP SPECT brain scans in adults with partial epilepsy.

The reproducibility of two N-isopropyl-(iodine 123) p-iodoamphetamine (123I-IMP single photon emission computed tomography (SPECT) scans both taken during interictal periods was studied in 13 adult patients with partial epilepsy who had normal CT scans. The frequency of the seizures and the nature of the ictal symptoms were virtually unchanged during the interval between the two SPECT scans performed in each case. In 8 (72.7%) of 11 patients who had abnormal images consisting of focal hypofixation images of 123I-IMP, i.e. zones of decreased regional cerebral blood flow on the first scans, complete or partial regional reproduction of the SPECT abnormalities was observed. This high reproducibility supports the usefulness of SPECT scans in the regional diagnosis of epileptic foci.

Amphetamines↗

Stability of messenger RNA in postmortem human brains and construction of human brain cDNA libraries.

We studied stabilities of poly(A)(+)-RNA in postmortem mouse and human brains for up to 12 hours. The yields of total RNA were not changed significantly during postmortem periods either in mouse brains or human brains. Cell-specific cDNA probes were used to evaluate postmortem stability of poly(A)(+)-RNA in each cell type in the central nervous system. We used neuron-specific enolase (NSE), S-100 beta (S-100), and myelin-associated glycoprotein (MAG) for molecular markers of neuron, astrocyte, and oligodendrocyte, respectively. There was no detectable degradation of mRNAs coding for NSE, S-100, and MAG during the postmortem periods on Northern blot hybridization analyses. These results indicate that intact mRNAs expressed in neuron, astrocyte, or oligodendrocyte can be isolated from postmortem brains for up to 12 hours after death. Using poly(A)(+)-RNA thus isolated from two postmortem human brains, we constructed directional cDNA libraries and demonstrated the presence of full-length cDNAs for NSE, S-100, and MAG on Southern blot hybridization analysis. The present data should encourage studies on altered gene expressions in human brain in various neurologic diseases.

Aged↗