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Biomedical subjects

H Yasuda

Publications and source records attributed to H Yasuda.

At least 325 records · Page 18Linked to original sources

[A case of sarcoidosis with frequent recurrence of ophthalmoplegia].

A 72-year-old woman was admitted to our hospital with the complaint of recurrent ophthalmoplegia. During three months before her first consultation, she had experienced five episodes of ptosis and diplopia, which had lasted for about 1 month. No significant abnormality was shown with computed tomography (CT), magnetic resonance imaging (MRI) and MR-angiography on her brain. Cerebrospinal fluid was normal. Serum angiotensin converting enzyme (ACE) level was mildly elevated. The enlargement of hilar lymph nodes which showed non-caseating epitheloid granuloma suggestive of sarcoidosis was seen with chest X-ray and CT. A few days after the treatment of 60 mg of prednisolone every other day, ophthalmoplegia disappeared and no recurrence has been observed. Cranial nerve involvement tends to be seen commonly in neurosarcoidosis. By contrast, the nerves innervating the extraocular muscles are rarely involved. Although relapsing course of neurosarcoidosis is well known, no case with frequent recurrence of ophthalmoplegia during a few months has been reported.

Aged↗

[A case of ruptured hepatocellular carcinoma with rapid growth after the interferon therapy in chronic hepatitis].

A 75-year-old man who had had a long history of chronic hepatitis C virus liver disease underwent interferon (IFN) therapy for three months. After three months of the last IFN injection, he presented with a sudden attack of epigastralgia. Abdominal US and CT revealed a tumor about 9 x 10 cm in the right lobe of the liver. Serum AFP level was 8,499 ng/ml. Spontaneous hemoperitoneum due to ruptured hepatocellular carcinoma (HCC) was suspected. Hepatectomy was carried out on 35 days postembolization. Pathological examination revealed HCC of trabecular type. Although the relation between the rapid growth and IFN is not clear, US examination should be performed once a month for the patient.

Aged↗

[Successful surgical correction of endocardial cushion defect in a 64-year-old female patient].

We have experienced a surgical correction of ECD of a 64-year-old female patient. The preoperative left ventriculogram showed typical goose-neck deformity of the left ventricle and mild mitral regurgitation. The correction consisted of repair of the mitral cleft, and patch closure of the ostium primum. Postoperative course was uneventful. The operation of ECD should be recommended even in an older patient.

Cardiac Catheterization↗

Healing of chronic gastric ulcer depends on gastric mucosal prostaglandin synthesis.

In the present study, the role of endogenous prostanoid synthesis in gastric mucosa in the healing of chronic gastric ulcers was investigated. Nineteen patients were divided into two groups in accordance with healing state after one month of treatment with cimetidine only: "healed group" and "unhealed group". Biopsy specimens taken from the mucosa around the ulceration (damaged gastric mucosa) and at a distance from the ulceration (normal gastric mucosa) at endoscopy prior to treatment were homogenized, and the mucosal prostanoid synthesis was determined using [14C]arachidonic acid. The mean value of prostaglandin E2 synthesis in the normal gastric mucosa of the healed group was 60% higher than in that of the unhealed group, but the difference was not significant. However, prostaglandin E2 synthesis in the damaged gastric mucosa of the healed group was 117% higher than in that of the unhealed group. The same tendency was observed for prostaglandin D2 and 6-keto prostaglandin F1 alpha synthesis as for prostaglandin E2. In our study it was demonstrated that there is a good correlation of prostaglandin synthesis in the damaged mucosa with healing of chronic gastric ulceration. Furthermore, our study indicated that prostaglandin synthesis, especially in damaged mucosa, might be important in the healing of gastric ulceration.

6-Ketoprostaglandin F1 alpha↗

Compressed allograft chips for acetabular reconstruction in revision hip arthroplasty.

We report the results of 24 acetabular reconstructions in which cemented polyethylene cups and tamped corticocancellous allografts were used for severe acetabular bone deficiency. Eleven hips had type-II (cavitary) bone deficiency and 13 had type-III (combined) defects. At a mean follow-up of 5.8 years, two components had migrated more than 5 mm and had accompanying radiolucent zones of more than 2 mm width. A radiolucency 5 mm wide was also seen in zone III of an acetabular implant which had not migrated. None of the patients had required revision because of loosening or infection.

Acetabulum↗

Molecular cloning and developmental expression of the alpha-2 tubulin gene of Caenorhabditis elegans.

Alpha tubulin isotypes are encoded by at least four genes designated alpha-1 to alpha-4 in the nematode Caenorhabditis elegans. We describe here, molecular cloning of the alpha-2 tubulin gene, located on chromosome I, that encodes a protein of 449 amino acids that has high homology to human, mouse and Drosophila alpha tubulins, but relatively lower homology to the yeast alpha tubulins. The alpha-2 tubulin gene is trans-spliced to the SL1 leader sequence. Northern analysis shows that the gene is increasingly transcribed during the early (L1-L3) larval stages but has a lower level of transcription in L4 L4 larvae, adults, and embryos. Using an alpha-2-lacZ fusion gene expression in transgenic animals, we show that the gene is expressed in a tissue-specific manner in the intestine, pharyngeal muscle cells, and a subset of neurons which include a class of DB and VB motor neurons in the ventral nerve cord, posterior touch receptor neurons, PLML, PLMR, in the lumbar ganglia; PVT in the pre-anal ganglion, and ALA in the dorsal ganglion in the head. Our results support the notion that tubulin structure may contribute to the functional specialization of microtubules.

Amino Acid Sequence↗

An animal model of chronic ischemic neuropathy with proliferative changes of nerve microvessel wall.

In order to produce a model of ischemic neuropathy with neural microvascular alterations, sodium laurate was injected into a femoral artery and saline into the contralateral artery at the mid-thigh level in Sprague-Dawley rats aged 11 weeks. In view of the dose-related findings, 0.3 mg sodium laurate dissolved in 0.1 ml saline was used for the main experiment. The laurate-injected leg showed paresis during the experimental period. On day 1-7, various stages of Wallerian degeneration and acute microvascular changes were found. At 1 month, regenerating myelinated nerve fibers (MNFs) were found at the central or total fascicular area mainly in the distal tibial nerve. Morphometric analyses suggested that MNFs other than regenerating fibers are atrophic ones. The proliferative changes of nutrient microvascular walls were striking. The percent of closed epineurial microvessels was significantly larger on the laurate-injected sides and inversely associated with the diameter of MNFs. At 7 months, the attenuation of MNFs was more prominent and microvascular alterations were persistently observed. These pathological findings resemble those of chronic ischemic neuropathy including diabetic neuropathy, suggesting that this neuropathy model might provide some valuable and useful clues for clarifying the pathogenesis of chronic ischemic neuropathy.

Animals↗

Phosphorylation of synthetic vimentin peptides by cdc2 kinase.

Synthetic peptide representing the site Ser-41 in vimentin, Leu-Gly-Ser41-Ala42-Leu-Arg44-Arg-Arg-NH2, and its analogs in which Ala-42 was replaced by various amino acids were tested as substrates for cdc2 kinase. Among them, the analog containing sarcosine as well as proline was an excellent substrate. The result suggests that the N-substituted structure of proline immediately following the site is important for cdc2 kinase phosphorylation. Replacement of Ala-42 by polar amino acids, especially lysine, had negative effects on peptide phosphorylation. The peptides in this study were also assayed with another type of proline-directed protein kinase, tau protein kinase II. The substrate specificity differed essentially from that of cdc2 kinase.

Animals↗

Activin A increases intracellular free calcium concentrations in rat pancreatic islets.

Activin A stimulated insulin secretion in rat pancreatic islets, an effect that was attenuated by reduction of extracellular Ca2+ and abolished by either nitrendipine or verapamil. Activin A increased intracellular the free Ca2+ concentration, [Ca2+]i in fura-2-loaded islets. Activin A-mediated elevation of [Ca2+]i was abolished by the reduction of extracellular Ca2+ or the addition of nifedipine. In addition, activin A did not increase [Ca2+]i in the presence of diazoxide, an opener of ATP-sensitive K+ channels. These results suggest that activin A increases insulin secretion by stimulating Ca2+ entry.

Activins↗

Cloning and functional analysis of the mouse c-kit promoter.

The c-kit protooncogene encodes a tyrosine kinase receptor expressed during ontogeny and adult life by several important and developmentally distinct cell lineages. Mice carrying germ line c-kit mutations exhibit deficiencies in most of these lineages, demonstrating that c-kit function is necessary for their normal development. To facilitate the identification of cis-acting elements which regulate tissue-specific c-kit expression, we cloned and characterized a mouse c-kit promoter which is functional in different cell types. A major c-kit transcription initiation site (TIS), located 58 bp upstream from the translation initiation codon, is utilized in mouse mast cells and in c-kit-positive cells in the mouse cerebellum. The effects of deletions in the 5' flanking region on reporter gene activity identify three short regulatory regions which function in both mouse and human c-kit positive cell lines. The nucleotide sequence of this region does not include CCAAT or TATA boxes but contains consensus binding sites for Sp1, Ap-2 and several short GA-rich elements which resemble binding sites for the ETS-domain proteins.

Animals↗

Dephosphorylation of human p34cdc2 kinase on both Thr-14 and Tyr-15 by human cdc25B phosphatase.

In mammalian cells, p34cdc2 kinase undergoes phosphorylation at threonine-14, tyrosine-15 and threonine-161 in the S and G2 phases of the cell cycle. At the onset of mitosis, the kinase becomes dephosphorylated at threonine-14 and tyrosine-15, resulting in activation. Cdc25 phosphatase has been shown to dephosphorylate tyrosine-15 in vitro, but whether it also does at threonine-14 remains unclear. In this study, we have found that human cdc25B phosphatase dephosphorylates both threonine-14 and tyrosine-15 but not threonine-161.

CDC2 Protein Kinase↗

Modulation of growth of vascular smooth muscle cells by activin A.

Activin A is a homodimeric protein structurally related to transforming growth factor-beta. The present study was conducted to examine the effect of activin A on the growth of rat vascular smooth muscle cells (VSMC) in culture. When serum-deprived cells were incubated with activin A, nuclear labeling of bromodeoxyuridine occurred after a 12-h lag period. The effect of activin A on nuclear labeling was dose-dependent, being maximal at 10(-9) M. Activin A also increased the number of VSMC after 30 h of incubation. Insulin-like growth factor-1 (IGF-1) had only a small effect on nuclear labeling by itself but the effects of IGF-1 and activin A were additive. When quiescent VSMC were treated with activin A for 4 h, the effect of subsequent IGF-1 was markedly enhanced. Furthermore, activin A induced an autocrine production of IGF-1 in VSMC. In contrast to these positive effects on cell growth, activin A was rather inhibitory to the action of IGF-1 in activin-primed cells. In addition, activin A inhibited platelet-derived growth factor-induced nuclear labeling. These results indicate that activin A modifies growth of VSMC by complex mechanisms involving autocrine production of IGF-1 and modification of the action of IGF-1.

Activins↗

Electrophysiological study of dorsal column function in streptozocin-induced diabetic rats: comparison with 2,5-hexanedione intoxication.

Dorsal column function and peripheral motor and sensory conduction velocities (MCV, SCV) were evaluated in experimental diabetic rats and compared with those in 2,5-hexanedione (2,5-HD) intoxicated rats. Hyperglycemia was induced by a single injection of streptozocin, and electrophysiological studies were performed 4 and 12 weeks after the injection. For 8 weeks 2,5-HD was administered daily by drinking water to make the 2,5-HD neuropathy rats. Age-matched rats were used as control. In diabetic rats, gracile surface potentials evoked by electrical stimulation of the lumbosacral trunk remained normal during the experimental period, whereas the N and P waves of the evoked potentials were suppressed and the duration of the N wave was prolonged in the 2,5-HD rats. In 4-week diabetic rats, the antidromic compound action potentials of the gracile tract recorded at the most proximal site of lumbosacral trunk were normal. In 12-week diabetic rats, the gracile tract conduction velocity (GTCV) was decreased, although the duration of these potentials was normal. By contrast, the GTCV was decreased and the duration was markedly prolonged in 2,5-HD rats. These findings might indicate that temporal dispersion of incoming volleys in the gracile tract is increased in 2,5-HD rats, but not in diabetic rats. These results suggest that diabetic myelopathy exists that but the magnitude and progression of this condition are quite different from those of 2,5-HD intoxication, typical dying-back-type neuropathy and that the dorsal column is less vulnerable than the peripheral nerve in diabetes mellitus.

Animals↗

Determination of cyclodextrins in serum by reversed-phase chromatography with pulsed amperometric detection and a membrane reactor.

A high-performance liquid chromatographic method has been developed for the determination of cyclodextrins (CDs) in serum. The method involves solid-phase extraction of CDs, separation on a C18 reversed-phase column using a mixture of water, tetrahydrofuran and methanol as an eluent, eluent pH modification with a cation-exchange membrane reactor surrounded by 1.5 M sodium hydroxide solutions, and pulsed amperometric detection (PAD) with a gold working electrode. The solid-phase extraction on a C18 bonded-silica column was effective for removing the PAD sensitive components in serum. The calibration graphs constructed by internal standard method were linear over the range 6.25-200 pmol of CDs in serum. The detection limits for CDs were about 5 pmol at a signal-to-noise ratio of 3.

Chromatography, High Pressure Liquid↗

C. elegans osm-3 gene mediating osmotic avoidance behaviour encodes a kinesin-like protein.

In the nematode Caenorhabditis elegans, mutants in osm-3 gene are known to be defective in osmotic avoidance, chemotaxis and dauer formation behaviours. To study the molecular basis of these pleiotropic defects we have cloned the osm-3 gene by germline transformation of osm-3 (p802) mutants through microinjection of the wild type genomic DNA. Northern analysis reveals a 3.0 kb transcript corresponding to osm-3. DNA sequencing of the transforming 4.3 kb fragment revealed a kinesin heavy chain-like protein, which contains conserved ATPase and microtubule binding domains. Our results are consistent with the previous EM data on osm-3 (p802) mutants that show an accumulation of dense matrix material in the amphid sheath cytoplasm and a shortened distal segment of the amphid channel cilium. These data suggest a kinesin-like role of the osm-3 product in axonal transport.

Amino Acid Sequence↗