Search PubMed⌕ Search

Biomedical subjects

A Ohtsuka

Publications and source records attributed to A Ohtsuka.

At least 55 records · Page 3Linked to original sources

Cytoplasmic delayed neuronal death in the myenteric plexus of the rat small intestine after ischemia.

The present study demonstrates light and electron microscopic changes in neurons in the myenteric plexus of the rat ileum following four-hour ischemia. Macroscopically, an intestinal constriction occurred at the damaged portion at three weeks after ischemia; the segment oral to the constriction markedly swelled at four weeks. In light microscopy, at three weeks after ischemia, the myenteric neurons appeared spongy or foamy, containing many vacuoles in their somatic cytoplasm. At four weeks, the neuronal cytoplasm and nerve fiber bundles had disintegrated to form vacant spaces in the myenteric plexus. The neuronal nucleus of the damaged plexus did not show positive nick-end labeling. In electron microscopy, neuronal cytoplasm revealed degenerative signs already at one week after ischemia: a distended endoplasmic reticulum and swollen mitochondria with fragmentary cristae. The nerve fibers also showed destruction of the mitochondria, and degenerative changes in the postsynaptic sites appeared earlier than the presynaptic terminals. The results suggest that intestinal ischemia causes delayed neuronal death, which differs from the apoptotic process previously demonstrated in the ischemia-damaged brain.

Animals↗

Perineuronal nets of proteoglycans in the adult mouse brain, with special reference to their reactions to Gömöri's ammoniacal silver and Ehrlich's methylene blue.

As our previous studies have indicated, many subsets of neurons in the vertebrate brain possess a sulfated proteoglycan surface coat which reacts to cationic iron colloid and aldehyde fuchsin. The present study demonstrated that this surface coat is supravitally stained with Ehrlich's methylene blue, and doubly with this blue and aldehyde fuchsin, a finding suggesting its being identical to Cajal's superficial reticulum (red superficial) and to Golgi's reticular coating (revetement reticulare). The perineuronal surface coat was further stained with Gömöri's ammoniacal silver, and doubly with this silver and cationic iron colloid. These neurons with such a proteoglycan surface coat usually expressed cell surface glycoproteins which were labeled with lectin Wisteria floribunda agglutinin. Hyaluronidase digestion did not interfere with this lectin labeling of the glycoproteins, methylene blue and Gömöri's ammoniacal silver staining of the surface coat, while it erased the cationic iron colloid and aldehyde fuchsin staining of the surface coat. These findings suggest that the perineuronal proteoglycan surface coat is associated with some additional molecules which are resistant to hyaluronidase digestion and stainable with methylene blue and Gömöri's ammoniacal silver. The possibility is suggested that these molecules might represent "ligand proteoglycans" connecting the perineuronal proteoglycans and cell surface glycoproteins.

Animals↗

[A case of pulmonary arteriovenous fistula associated with cerebellar abscess].

We report a rare case of pulmonary arteriovenous malformation (PAVM) with cerebellar abscess. The patient was 38-year-old woman who admitted to the local hospital for headache and fever. Subsequently, her condition became critical with consciousness disturbance, and hypoxemia. Brain computed tomography (CT) and chest CT revealed cerebellar abscess and PAVM. She was referred to our hospital for the surgery. Pulmonary angiography demonstrated multiple pulmonary arteriovenous fistulas in the right middle lobe and a single nodular pulmonary arteriovenous fistula in the right S8 (10 x 10 mm). After the drainage for the brain abscess, lobectomy of the right middle lobe and the excision of the nodal fistula in the right S8 were successfully performed in the two-staged operation. The patient has done well with no complication and her hypoxemia was improved.

Adult↗

Comparison of the effects of thyroxine and triiodothyronine on protein turnover and apoptosis in primary chick muscle cell cultures.

Primary chick muscle cells were treated with physiological level of thyroxine (T4) or triiodothyronine (T3) to examine the effects of the hormones on growth, protein turnover, and apoptosis of the cells. Creatine kinase activity, as an index of differentiation, was increased by both T4 and T3. Even when the conversion from T4 to T3 was blocked by iopanoic acid, T4 increased creatine kinase activity. The rate of protein degradation estimated from [3H] tyrosine release was increased by T3 but not by T4. DNA cleavage and fragmentation, as indices of apoptosis, were induced by T3 but not by T4. These results show that T4 stimulates cell differentiation but not protein degradation and apoptosis in primary chick muscle cells, while all events are stimulated by T3.

Animals↗

A Janus kinase inhibitor, JAB, is an interferon-gamma-inducible gene and confers resistance to interferons.

It has been shown that interferons (IFNs) exert their signals through receptor-associated Janus kinases (JAKs) and signal transducers and activators of transcription (STATs). However, molecular mechanism of regulation of IFN signaling has not been fully understood. We have reported novel cytokine-inducible SH2 protein (CIS) and JAK binding protein (JAB) family genes that can potentially modulate cytokine signaling. Here we report that JAB is strongly induced by IFN-gamma but not by IFN-beta in mouse myeloid leukemia M1 cells and NIH-3T3 fibroblasts. NIH-3T3 cells ectopically expressing JAB but not CIS3 lost responsiveness to the antiviral effect of IFN-beta and IFN-gamma. M1 leukemic cells stably expressing JAB were also resistant to IFN-gamma and IFN-beta-induced growth arrest. In both NIH-3T3 and M1 transformants expressing JAB, IFN-gamma did not induce tyrosine phosphorylation and DNA binding activity of STAT1. Moreover, IFN-gamma-induced activation of JAK1 and JAK2 and IFN-beta-induced JAK1 and Tyk2 activation were inhibited in NIH-3T3 JAB transformants. These results suggest that JAB inhibits IFN signaling by blocking JAK activity. We also found that IFN-resistant clones derived from LoVo cells and Daudi cells expressed high levels of JAB without stimulation. In IFN-resistant Daudi cells, IFN-induced STAT1 and JAK phosphorylation was partially reduced. Therefore, overexpression of JAB could be, at least in part, a mechanism of IFN resistance.

3T3 Cells↗

Expression, structure and chromosomal localization of the human cGMP-binding cGMP-specific phosphodiesterase PDE5A gene.

cGMP-binding, cGMP-specific phosphodiesterase which is encoded by the PDE5A gene plays important roles in cardiovascular system, and is a significant target molecule of therapeutic agents. However, little is known about molecular characteristics of the human PDE5A gene. The 4.4-kb cDNA encoding human PDE5A was isolated from lung and placenta cDNA libraries. The deduced amino acid sequence analysis demonstrated that N-terminal amino acid sequence is dissimilar to that of rat PDE5A [Kotera, J., Yanaka, N., Fujishige, K., Imai, Y., Akatsuka, H., Ishizuka, T., Kawashima, K. & Omori, K. (1997) Eur. J. Biochem. 249, 434-442]. Human PDE5A mRNA is produced in high amounts in various tissues such as pancreas, skeletal muscle, placenta, heart, thyroid, adrenal cortex, testis, small intestine and stomach. In addition, the megakaryocyte-like cell line Dami cells and two types of human vascular smooth muscle cells also produce the mRNA. Over 100-kb chromosomal DNA corresponding to the human PDE5A gene was isolated and analyzed. The human PDE5A gene was revealed to contain 21 exons. Comparison of genomic organization with the rod photoreceptor phosphodiesterase beta-subunit gene (PDE6B), which is another kind of cGMP-specific phosphodiesterase, has shown that the PDE5A and PDE6B genes are very similar in their relative exon intron organization. In particular, the evolutionary relatedness of these genes was suggested in the catalytic domain. Furthermore, chromosomal location of the PDE5A gene was defined as being chromosome 4q26 by fluorescent in situ hybridization analysis.

3',5'-Cyclic-AMP Phosphodiesterases↗

Localization of a serine proteinase inhibitor, B-43, in the bovine pancreas.

B-43, a serine proteinase inhibitor belonging to the ovalbumin branch of the serpin superfamily, was purified and cloned from bovine brain. Since [35S]-labeled B-43 forms SDS-stable complexes with pancreatic serine proteinases, trypsin, alpha-chymotrypsin, and kallikrein, it has been suggested that B-43 is capable of inhibiting these serine proteinases and that B-43 may be present in the pancreas. In the present study, we investigated the localization of B-43 in the bovine pancreas immunohistochemically and examined the effect of B-43 on the amidolytic activities of pancreatic serine proteinases. Strong B-43-like immunoreactivity was localized in acinar cells, especially in the basal sides of the cells where the rough endoplasmic reticulum is located. The nuclei of the subpopulation of acinar cells were also immunoreactive for B-43. The recombinant glutathione S-transferase-B-43 fusion protein inhibited the amidolytic activity of trypsin and, to a lesser extent, alpha-chymotrypsin and kallikrein, but not elastase. These results suggest a role of B-43 in regulating serine proteinases both in the cytoplasm and the nucleus.

Animals↗

Evaluation of disk capture with a splint repositioning appliance: clinical and critical assessment with MR imaging.

OBJECTIVE: The purpose of this study was to evaluate disk repositioning clinically and through use of magnetic resonance imaging after the insertion of a disk repositioning appliance. STUDY DESIGN: Seventy-four patients with 82 temporomandibular joints showing middle to late opening movement click and closing movement click near maximum intercuspation were treated with a mandibular full-coverage repositioning splint. These joints were assessed clinically and by means of magnetic resonance imaging for disk recapture. RESULTS: According to clinical assessment, 75.6% (62/82) of the joints were treated successfully; no click was observed from the splinted mandibular position. When compared with the results of magnetic resonance imaging assessment, clinical assessment showed an accuracy rate of 91.5%, although the incidence of the false negatives was high (40%). CONCLUSIONS: The results of this study showed that about 70% of reducing displaced disks were captured with use of the disk repositioning appliance. And it was also suggested that magnetic resonance imaging is helpful to evaluate disk repositioning therapy.

Adolescent↗

Change of position of the temporomandibular joint disk with insertion of a disk-repositioning appliance.

OBJECTIVE: We report alteration of the temporomandibular joint disk and the condyle position through the construction of a mandibular full-coverage occlusal appliance (often referred to as a disk repositioning appliance). STUDY DESIGN: Forty-five joints with displaced disks with reduction were available for the study. We assessed these joints for disk recapture and the change of disk position with insertion of the appliance using magnetic resonance imaging. RESULTS: Of the 41 joints that had a recaptured disk with insertion of the splint, 25 slid in a posterior direction, although the amount of movement was negligible. No disk slid posteriorly in the joints without splint capture. CONCLUSIONS: On the basis of our results, we conclude that many of the occasionally displaced disks might have moved backward with successful treatment involving a disk-repositioning splint. However, the amount of the movement was negligible.

Adolescent↗

A visual method for analysing bucco-lingual position of artificial posterior teeth. Part 1: use of the ridge crest.

We have developed a visual analysis method to examine the spatial relationship between the edentulous ridges and the bucco-lingual position of the artificial posterior teeth in complete denture fabrication. In this system, a non-contact type shape measurement system is used. We applied this system to the plaster models and the wax dentures of an edentulous patient. Using the measurement data on the upper and lower plaster models, we reconstructed their shape three-dimensionally and determined the points regarded as the ridge crests and the inter-alveolar crest lines in the frontal sections. To generate the upper and lower ridge crest lines which consisted of the points of the ridge crests, interpolation by B-spline curves was applied. Furthermore, the loft surfaces that we regarded as the consecutive inter-alveolar crest lines, were generated between the upper and lower ridge crest lines. The surface models of the plaster models and artificial teeth were displayed on the cathode-ray tube display unit, and the ridge crest lines and the consecutive inter-alveolar crest lines were superimposed on the surface models. This method could be utilized to visualize and examine the bucco-lingual position of the artificial posterior teeth in reference to the inter-alveolar crest lines.

Computer Graphics↗

Chick skeletal muscle proteolysis in vitro increased by corticosterone.

Six-day-old chick skeletal muscle (extensor digitorum longus) was incubated in the presence of corticosterone (CTC; 0, 3, 30, and 300 ng/ml) for 2 h at 37 degrees C. Tyrosine and N (tau)-methylhistidine releases, as indices of total muscle and myofibrillar proteolysis, were increased by CTC but with different dose responses, indicating an independent regulation of myofibrillar and non-myofibrillar protein degradation.

Animals↗

Light and electron microscopic detection of anionic sites in the rat choroid plexus.

Electron microscopy of ultrathin sections stained with cationic iron colloid revealed that, in the choroid plexus of the rat brain ventricles, the luminal surface and fenestral diaphragm of the capillary endothelium as well as the basement membranes of the endothelium and epithelium are strongly anionic or intensely negatively charged. The iron colloid reaction to these anionic sites was erased by treatment with hyaluronidase or digestions with chondroitinase ABC/heparitinase/keratanase. These results indicate that sulfated proteoglycans provide such anionic sites of the choroidal capillaries. Discussion suggested that the negative charge on the luminal surface of the capillary endothelium prevents the adhesion of blood cells to capillary walls and also prevents endothelial adhesion by their repelling each other. It was further discussed that the negatively charged endothelial fenestrae and basement membranes may act as a charge barrier to inhibit the passage of anionic molecules.

Animals↗

Typology of abdominal arteries, with special reference to inferior phrenic arteries and their esophageal branches.

Origins and distribution of the human inferior phrenic arteries were studied by dissecting 68 Japanese adult cadavers. The inferior phrenic arteries were usually observed as paired (left and right) vessels. Their origins were summarized as follows: a) the aorta itself (85/138 cases, 61.6%), b) the ventro-visceral arteries (celiaco-mesenteric system of the aorta) including the celiac trunk (39/138 cases, 28.2%) and the left gastric artery (4/138 cases, 2.9%), and c) the latero-visceral arteries (adreno-renal system of the aorta) including the middle adrenal artery (4/138 cases, 2.9%) and the renal artery (6/138 cases, 4.3%). The left and right arteries occasionally originated in common trunk from the aorta, celiaco-mesenteric system or adreno-renal system (22/138 cases, 15.9%). A typological diagram explaining these variations is given. The inferior phrenic arteries, especially the left ones, sometimes issued visceral or esophageal branches. This fact indicates that the inferior phrenic arteries are homologous with the celiac trunk and mesenteric arteries. It is further discussed that the celiac trunk and mesenteric arteries are originally paired vessels, through introduction of our previous typological diagram of the abdominal arteries.

Abdomen↗

Coexistence of rare arteries in the human celiaco-mesenteric system.

Some rare anomalies of the celiaco-mesenteric system were observed postmortem in a Japanese adult male: a) The left gastric, common hepatic, splenic and superior mesenteric arteries arose independently from the abdominal aorta. b) The anterior inferior pancreaticoduodenal artery of the superior mesenteric artery issued a hepatic artery which ascended along the anterior surface of the pancreas and gave off the right gastroepiploic, right gastric and cystic arteries. c) The common hepatic artery gave off an anastomosing branch to the superior mesenteric artery. d) The left gastric artery gave off the left accessory hepatic artery. e) The splenic artery issued the accessory middle colic artery. f) The left inferior phrenic artery gave off the esophageal branch. These anomalies are discussed in light of a typological system which we proposed in a previous paper for the celiaco-mesenteric system.

Abdomen↗

Mast cells in osteoarthritic and rheumatoid arthritic synovial tissues of the human knee.

The distribution and density of mast cells in the normal and diseased synovial membranes were investigated. The mast cell count (MCC) in the osteoarthritic (OA) synovium (36.9 +/- 26.9 cells/mm2) was significantly higher than that in the rheumatoid arthritic (RA) synovium (18 +/- 12.3 cells/mm2). There was a marked positive correlation between the MCC and the volume of joint fluid in OA (r = 0.544). There was a marked negative correlation between the MCC and the volume of joint fluid in RA (r = -0.478). The synovial inflammatory score had a poor correlation with the MCC in OA (r = 0.377) and RA (r = 0.305). No correlation was noted between MCC and age, sex, roentgenographic grades, disease duration, C-reactive protein or leucocyte number in synovial fluid. Our data suggests, thus, that mast cells could be involved in the pathogenesis of inflammatory diseases of the synovium, especially in the mechanism of hydroarthrosis.

Adult↗

Vitamin E reduces glucocorticoid-induced growth inhibition and lipid peroxidation in rats.

This experiment was conducted to study the effects of vitamin E on growth inhibition and lipid peroxidation in rats treated with different levels of corticosterone (CTC). Rats (Sprague-Dawley strain, 5 weeks of age) were divided into two groups: control group receiving a basal diet containing 60 mg DL-alpha-tocopheryl acetate/kg diet, and vitamin E group receiving the same diet supplemented with 5,000 mg tocopherol. After 6 days, rats of both diet groups were further divided into three groups by dose levels of CTC treatment (0, 25, and 100 mg CTC/kg body weight/d). CTC was administered to the rats by subcutaneous injection for 4 d. Growth was dose-dependently inhibited by the CTC treatment. Feeding the vitamin E diet significantly (p < 0.05) improved growth retardation. Feed efficiency was lowered by CTC treatment, while this was significantly (p < 0.05) minimized by feeding the vitamin E diet. Lipid peroxidation (TBARS) in the liver was elevated by the CTC treatment (p < 0.001) when the rats were fed the basal diet. The increment in TBARS was significantly (p < 0.001) reduced by vitamin E. The activities of glutathione S-transferase (GST) and superoxide dismutase (SOD) were significantly reduced by the CTC treatment in a dose-dependent manner in both dietary groups. Feeding vitamin E significantly (p < 0.001) improved the reduction in GST activity. The SOD activity showed some tendency. The present results demonstrate the effectiveness of vitamin E in improving growth retardation in glucocorticoid-treated rats and suggest that reductions in increased lipid peroxidation due to CTC may be an important factor of the action of vitamin E.

Animals↗

Vitamin E reduces glucocorticoid-induced oxidative stress in rat skeletal muscle.

The purpose of this study was to investigate the effect of vitamin E on oxidative stress in the skeletal muscle of glucocorticoid-treated rats. Male Sprague-Dawley rats (5 weeks of age) were fed a basal diet or a diet supplemented with vitamin E (5,000 mg DL-alpha-tocopheryl acetate/kg diet) for 10 d. The rats of both diet groups received subcutaneous injections of corticosterone (CTC) (0, 25, and 100 mg/kg body weight/d) during the final 4 d. Weights of the extensor digitorum longus and gastrocnemius (GAST) muscles were dose-dependently reduced by CTC. However, the muscle weight losses in rats fed the vitamin E diet were smaller than those in rats fed the basal diet. Protein carbonyl content in the GAST muscle, which was determined as an index of oxidatively modified protein, was increased by 100 mg of CTC, and the increment was significantly (p < 0.01) reduced by vitamin E supplement. Hyperglycemia was induced by 100 mg of CTC, but it was not affected by vitamin E. Lipid peroxide (TBARS) in plasma and in GAST muscle was elevated by 100 mg of CTC, and vitamin E significantly (p < 0.001) suppressed the formation of TBARS in the muscle. The change in TBARS paralleled that in protein carbonyl. These results show that CTC leads to oxidative stress in rat skeletal muscles and that vitamin E has roles in reducing the oxidative stress which causes muscle atrophy.

Animals↗