Search PubMed⌕ Search

Biomedical subjects

S Tsuji

Publications and source records attributed to S Tsuji.

At least 361 records · Page 20Linked to original sources
PubMed1998

[A patient with an ACTH-releasing thymic carcinoid tumor presenting with proximal muscle weakness].

We report a 36-year-old man with proximal dominant muscle weakness, thymic tumor, diabetes mellitus, hypokalemia, and increased levels of plasma ACTH and cortisol. The diagnosis of carcinoid tumor was made on the basis of pathological findings in the biopsied specimen of the thymic tumor. The proximal muscle weakness was considered to be due to steroid myopathy resulting from the overproduction of cortisol from the adrenal glands induced by the ectopic ACTH secreted by the thymic carcinoid tumor. Although thymoma in frequently associated with myasthenia gravis, we should also consider carcinoid tumors in patients with a thymic tumor presenting with a proximal muscle weakness.

Adrenocorticotropic Hormone↗
PubMed1998

Electron microscopic localization of acetylcholinesterase activity in the central nervous system: chemical basis of a catalytic activity of Hatchett's brown (cupric ferrocyanide) precipitate revealed by 3,3'-diaminobenzidine.

The chemical basis of the histochemical method for acetylcholinesterase described by Tago et al. was studied. The primary histochemical reaction of Tago's method is performed with diluted Karnovsky's medium, resulting in the in situ formation of Karnovsky's precipitate in minute quantities. The visualization of acetylcholinesterase activity is made in a secondary reaction where diaminobenzidine (DAB) is oxidized in the presence of hydrogen peroxide by the peroxidase-like activity of the histochemical precipitate. Since Karnovsky's precipitate is already known to be a mixture of Cu+3Fe (CN)6 and Cu++2Fe++(CN)6, the catalytic activity of these two complexes was studied in vitro comparatively to cupric ferricyanide (non-histochemical precipitate) and to copper and iron ions participating in the complexes. We showed that only the first two complexes intensely oxidized DAB with or without hydrogen peroxide. Thus, Tago's method is based on the same catalytic activity as Hanker's method (oxidation of DAB using non-diluted Karnovsky's medium without hydrogen peroxide). Since both complexes are able to oxidize DAB without hydrogen peroxide, we propose to describe this catalytic activity as oxidoreductase-like activity. Tago's method was modified for ultrastructural observations by avoiding metal intensification of the DAB precipitate. We obtained fine localization of DAB precipitate in the lumen of endoplasmic reticulum and Golgi apparatus of the neurons of substantia nigra.

3,3'-Diaminobenzidine↗
PubMed1998

Comparative studies on the antiplatelet effects of a humanized anti-platelet glycoprotein IIb/IIIa antibody (YM337) and ReoPro under flow conditions.

Recent clinical studies have shown that the interruption of platelet function appears to be effective for treatment of coronary occlusive diseases. For this purpose, a Fab fragment of humanized anti-platelet glycoprotein (GP) IIb/IIIa monoclonal antibody (YM 337) that exhibited an in vivo antithrombotic effect without prolongation of bleeding time in monkeys was previously characterized. In this study, the effect of YM 337 under physiological flow conditions with high or low shear rate was evaluated. The antiplatelet effects of YM 337 under varying wall shear rates were examined with the whole blood flow system. This technique allows real time visualization of the formation of fluorescence-labeled platelet thrombi on a collagen surface in a parallel plate flow chamber mounted on an epifluorescence microscope. The process of thrombus growth was also recorded in video tape and subjected to computer-assisted image analysis. We found that YM 337 displayed a high shear-preferential antiplatelet effect, while ReoPro, a control anti-GP IIb/IIIa antibody, did not show such shear dependency. The present findings therefore suggest that YM 337 might be a useful antiplatelet agent which can block pathological thrombotic events occurring under high shear, such as in coronary occlusive diseases.

Abciximab↗
PubMed1998

Renaturation of recombinant human neurotrophin-3 from inclusion bodies using a suppressor agent of aggregation.

Escherichia coli has been widely used in the production of recombinant proteins. One of the drawbacks inherent in this method is that the proteins produced in the cells often form inactive inclusion bodies. Usually, the inclusion bodies can be separated from other cell components, solubilized by denaturants such as guanidine hydrochloride or urea, and then renatured through a refolding process such as dilution or dialysis. However, it has been shown that biologically active recombinant human neurotrophin-3 cannot be obtained at high yield by this procedure due to aggregation and precipitation of the protein. We applied the refolding process using the aggregation suppressor L-arginine in the renaturation of neurotrophin-3, and obtained biologically active neurotrophin-3 at high yield from the inclusion bodies. Consequently, about 10 mg of purified neurotrophin-3 was prepared from 1 litre of culture broth.

Amino Acids↗
PubMed1998

[Mucosal microcirculation and angiogenesis in gastrointestinal tract].

In this review, various aspects of gastrointestinal microcirculation were described. Endothelin-1, vasoconstrictor, is elevated in gastric mucosa, causes gastric ischemia and results in gastric ulceration in human and animals under physical stress. Vasodilators such as NO anticipate the alove actions of endothelin, and thereby protect mucosa from injury. Once ulcer is developed, angiogenesis plays a key role in its healing. Various growth factors, cyclooxygenases-1 and -2, and non-peptide angiogenic factors stimulate this phenomenon and participate in ulcer healing. However, acidic conditions, H. pylori and its product, ammonia, suppress angiogenesis in vitro and in vivo. These evidences may explain why ulcer heals so slowly in gastroduodenal mucosa.

Animals↗
PubMed1998

[Difference between transcortical sensory aphasia following the left frontal lesion and transcortical sensory aphasia following the left posterior lesion].

We assessed the difference between transcortical sensory aphasia (TCSA) following the left frontal lesions (F-TCSA) and TCSA following the left posterior lesions (P-TCSA). All the patients were right-handed and the 7 patients had the lesions in the only frontal lobe and the 10 patients had the lesions only in the left temporo-parieto-occipital regions. We administered pointing tasks, using 90 line drawings representing single nouns. We presented 6 line drawings a pointing board, and we used two kinds of pointing boards: one showed the line drawings each belonging to different categories (random categorized pointing task), the other showed the line drawings each belonging to only either two different categories (two categorized pointing task) and we presented 15 pointing boards each alternatively. The result was that regarding the patients of P-TCSA showed different number of correct answers between the random categorized pointing task and the two categorized pointing task with statistical significance. Regarding the patients of F-TCSA showed no difference between them. The results indicated that disturbance of P-TCSA on the pointing task was the disturbance of semantic process per se. And the disturbance of F-TCSA on the pointing task was that of not only semantic process but also the whole process including comprehending the presented words, searching the line drawings, comparing the line drawings with the presented word and final selection, which demanded persistent multiple memory process consistent with working memory.

Aphasia, Wernicke↗
PubMed1997

[Occupational stress as the cause of psychosomatic and mental disorders].

Occupational stress is caused by occupational or workplace factors, individual factors and social factors. These factors are the cause of many patients having to visit a psychosomatic outpatient clinic. We examined state of employment, type of occupation, type of disease, and factors causing occupational stress of 796 patients visiting our psychosomatic outpatient clinic for the purpose of studying the relation between occupational stress and psychosomatic and mental disorders. The rate of employment was 62.6% for men and 28.1% for women. By type of occupation, there were many office workers, blue-collar workers, and medical staffs except students and housewives. The prevalent diseases were mood disorders, anxiety disorders, and neuromuscular diseases in this order. The most prevalent cause of diseases in male patients (56.3%) was the occupational or workplace factors, while the most prevalent cause of diseases in female patients (42.4%) was the individual factors. These results indicated that almost half of the patients had occupational stress as the cause of their psychosomatic and mental disorders. When treating patients with occupational stress, it is important to work in close cooperation with their superiors or colleagues at work and occupational health physicians, as well as using an ordinary psychosomatic approach.

Adult↗
PubMed1997

Oligomerization of expanded-polyglutamine domain fluorescent fusion proteins in cultured mammalian cells.

Six inherited neurologic diseases, including Huntington's disease, result from the expansion of a CAG domain of the disease genes to produce a domain of more than 40 glutamines in the expressed protein. The mechanism by which expansion of this polyglutamine domain causes disease is unknown. Recent studies demonstrated oligomerization of polyglutamine-domain proteins in mammalian neurons. To study oligomerization of polyglutamine proteins and to identify heterologous protein interactions, varying length polyglutamine-green fluorescent protein fusion proteins were expressed in cultured COS-7 cells. The 19- and 35-glutamine fusion proteins (non-pathologic length) distributed diffusely throughout the cytoplasm. In contrast, 56- and 80-glutamine fusion proteins (pathologic length) formed fibrillar arrays resembling those previously observed in neurons in Huntington's disease and in a transgenic mouse model. These aggregates were intranuclear and intracytoplasmic. Intracytoplasmic aggregates were surrounded by collapsed intermediate filaments. The intermediate filament protein vimentin co-immunoisolated with expanded polyglutamine fusion proteins. This cellular model will expedite investigations into oligomerization of polyglutamine proteins and their interactions with other proteins.

Animals↗
PubMed1997

Localization of the squalene epoxidase gene (SQLE) to human chromosome region 8q24.1.

Squalene epoxidase (EC 1.14.99.7) catalyzes the first oxygenation step in sterol biosynthesis and is suggested to be one of the rate-limiting enzymes in this pathway. We previously isolated the mammalian squalene epoxidase cDNAs and demonstrated the transcriptional regulation of human squalene epoxidase by sterols and inhibitors. The present study was undertaken to determine the chromosomal mapping of the human squalene epoxidase gene (SQLE). PCR evidence localizes human SQLE to chromosome 8 by using the NIGMS (National Institute of General Medical Sciences) Human/Rodent Somatic Cell Hybrid Mapping Panel 2 as template. To refine the localization of human SQLE further, PCR on the Stanford G3 Radiation Hybrid Panel was performed. The result shows that human SQLE is most tightly linked to D8S508, which is reported to be located at 8q24.13-qter (lod score 7.87). Moreover, fluorescence in situ hybridization also maps human SQLE to 8q24.1.

Chromosome Mapping↗
PubMed1997

Refined genetic location of the chromosome 2p-linked progressive muscular dystrophy gene.

Autosomal recessive progressive muscular dystrophies may be clinically subclassified into limb-girdle muscular dystrophy (LGMD) and distal myopathy (DM), each clinical form being genetically heterogeneous. Genes for LGMD type 2B and Miyoshi myopathy (a form of DM) have been mapped to essentially the same region on chromosome 2p. We described recently a large inbred family with autosomal recessive muscular dystrophy in which the LGMD and the DM phenotypes were manifested in separate affected members, and we assigned the gene for this condition to the same locus as in LGMD2B and Miyoshi myopathy. Here we report extended haplotypes in this family generated from 15 markers located at the region of interest on chromosome 2p13. Key recombinants allowed us to reduce further the candidate region for this polymorphic condition and defined the loci D2S327 and D2S2111 as the most likely boundaries of the mutant gene.

Chromosome Mapping↗
PubMed1997

Lysosomal proteolysis of prosaposin, the precursor of saposins (sphingolipid activator proteins): its mechanism and inhibition by ganglioside.

Saposins A, B, C, and D, which are required for the enzymatic hydrolysis of sphingolipids by specific lysosomal hydrolases, are produced by proteolytic processing of their common precursor protein, prosaposin. Our previous observation suggested that lysosomal cathepsin D may be involved in the proteolysis of prosaposin. Herein we report the involvement of cathepsin D in the proteolytic processing of prosaposin. An antibody against human placental cathepsin D blocked the proteolytic activity toward prosaposin in a human testicular lysosomal protease mixture (glycoprotein fraction). On immunoblot analysis using a monoclonal antibody against human saposin C, cathepsin D showed a similar proteolytic pattern as that of a human testicular glycoprotein fraction and hydrolyzed prosaposin into products of 48 and 29 kDa. The Km and Vmax values were 0.9 microM and 167 nmol/h/mg, respectively. N-Terminal sequence analysis indicated that the 48-kDa band was a mixture of two trisaposins, including domains for saposins A, B, and C and saposins B, C, and D, respectively. A similar study also showed that the 29-kDa band contained two disaposins, including domains for saposins A and B and saposins C and D, respectively. By longer treatment with cathepsin D, disaposins were further processed into mature saposin A and small fragments (14.5-17.5 kDa) containing individual saposins and portions of interdomain sequences. These small fragments were no longer processed by cathepsin D, but trimmed to fragments having similar molecular sizes (10.5-11.5 kDa) to those of mature saposins by a rat lysosome preparation. These findings indicated that cathepsin D is involved in the maturation of saposins but that, in addition to cathepsin D, other proteases appear to be involved in the maturation of saposin B, C, and D in lysosomes. Gangliosides, which specifically form complexes with prosaposin and saposins, inhibit proteolysis of prosaposin by cathepsin D. This finding indicates that prosaposin may be protected from lysosomal proteolysis by forming a complex with gangliosides in vivo.

Animals↗
PubMed1997

A novel monoclonal antibody which reacts with a high molecular weight neuronal cytoplasmic protein and myelin basic protein (MBP) in a patient with macroglobulinemia.

We report on the case of a 70-year-old man with primary macroglobulinemia who showed cranial polyneuropathy and extensive radiculoneuropathy. His serum contained an IgM lambda monoclonal antibody which reacted with both a high molecular weight protein in grey matter and purified myelin basic protein (MBP) on immunoblotting. In an immunohistochemical study, strong immunoreactivity was detected only in the cytoplasm of neurons and weak immunoreactivity was detected in myelin. These findings suggest that this antibody may be related to the pathogenesis of neuronal damage in patients with macroglobulinemia.

Aged↗
PubMed1997

Neuropathology of sporadic amyotrophic lateral sclerosis of long duration.

We performed post-mortem examinations of three patients with progressive neurogenic amyotrophy of long duration. One patient had been clinically diagnosed as having sporadic amyotrophic lateral sclerosis (ALS) and two had been diagnosed with progressive spinal muscular atrophy (PSMA). The disease durations were 10, 17 and 20 years, respectively, and all of the patients died of respiratory failure with no artificial respiratory support. In all of the patients, both the upper and lower motor neuron systems were affected; degeneration of the former was definite, but was milder than that usually encountered in sporadic ALS patients, and the histopathology of the latter was identical to that of sporadic ALS. Light microscopy revealed Bunina bodies, which are characteristic of sporadic ALS, in the remaining anterior horn cells of each patient. In addition, ubiquitin-positive skein-like inclusions were also identified, immunohistochemically, in the remaining anterior horn cells of each patient. Neuron counts indicated that the number of neurons was preserved in Clarke's column in these patients, but was significantly reduced in the intermediolateral nucleus, compared with control subjects. Based on these findings, we think that these three patients, with long disease durations, were affected by essentially the same underlying disease process as that of sporadic, classical ALS. Moreover, we question the neuropathological occurrence of sporadic ALS without involvement of the upper motor neuron system, namely, pure PSMA or lower motor neuron disease.

Aged↗