Bleeding stercoral ulcer with visible vessels: effective endoscopic injection therapy without electrocoagulation.
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Aged↗
Biomedical subjects
A Nishio
Publications and source records attributed to A Nishio.
Colonoscopic clipping closure of a divot after the removal of an impacted chicken bone.
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Colon, Sigmoid↗
The role of thromboxane A2 in regulating porcine basilar arterial tone.
The aim of the present study was to clarify the participation of endogenous arachidonic acid (AA) metabolites in regulating porcine basilar, coronary, pulmonary and mesenteric arterial tones in vitro. A cyclooxygenase inhibitor, indomethacin, relaxed basilar artery but not other arteries examined. Quinacrine (a phospholipase A2 inhibitor), OKY-046 (a thromboxane (TX) A2 synthetase inhibitor) and ONO-3708 (a TXA2/prostaglandin H2 receptor antagonist) produced relaxation in basilar arteries with intact endothelium. Nordihydroguaiaretic acid (a lipoxygenase inhibitor) had no effect on the tone. The amount of TXB2 (a stable metabolite of TXA2) spontaneously released from porcine basilar arteries was 6-10 fold more than those from other arteries. Indomethacin and OKY-046 mostly inhibited the production of TXB2. Endothelial denudation decreased indomethacin-induced relaxation and the amount of TXB2. These results suggest that a vasoconstricting substance(s) is released from endothelial cells and possibly smooth muscle cells in porcine basilar arteries in vitro. The main constricting substance is proposed to be TXA2. On the other hand, several arteries from peripheral vascular beds did not release this vasoconstricting substance.
Animals↗
Femtomolar bradykinin-induced relaxation of isolated bovine coronary arteries, mediated by endothelium-derived nitric oxide.
We reported previously that bradykinin induces endothelium-dependent relaxation at nanomolar (nM) concentrations in isolated bovine coronary arteries with an intact endothelium. Recently we have found that in the presence of 10 microM indomethacin, femtomolar (fM) concentrations of bradykinin induce endothelium-dependent relaxation in some bovine coronary arteries (approximately 10% of the coronary arteries examined). The present study was designed to characterize the relaxation induced by fM bradykinin. Relaxation was completely abolished by repeated application of fM bradykinin, by 100 microM N(omega)-nitro-L-arginine methyl ester and by 10 microM methylene blue. Relaxation induced by nM bradykinin was partly affected by these treatments. Relaxation induced by both concentrations of bradykinin was inhibited by a B2-kinin receptor antagonist, [Thi5,8, D-Phe7]-bradykinin, in a concentration-dependent manner, but not by a B1-kinin receptor antagonist, des-Arg9, [Leu8]-bradykinin. In the presence of 10 microM captopril, an angiotensin-converting enzyme (ACE) inhibitor, all coronary arteries examined in this experiment showed endothelium-dependent relaxation to fM bradykinin. These results show that some bovine coronary arteries relax in response to fM bradykinin, and this response is mediated predominantly by the release of nitric oxide via stimulation of endothelial B2-kinin receptors. The relaxation may be dependent on ACE activity.
Angiotensin-Converting Enzyme Inhibitors↗
Occlusion of the sigmoid sinus after surgery via the presigmoidal-transpetrosal approach.
OBJECT: In this paper the authors report on sigmoid sinus occlusion as a surgical complication in seven of 143 operations in which a presigmoidal-transpetrosal approach was used. METHODS: Five patients (Cases 1-5) developed occlusion within 40 days after surgery, and in the remaining two (Cases 6 and 7) occlusion was detected 5.4 and 6.4 years postsurgery by means of cerebral venography, which was performed in 40 of the remaining 138 patients. Of the two patients with occlusion of the hypoplastic transverse sinus, one (Case 1) did not develop symptoms and the other (Case 2) developed brain edema with transient aphasia. Of the three patients suffering from occlusion of the dominant sigmoid sinus, one (Case 3) developed severe intracerebral hemorrhages and had a poor prognosis; one (Case 4) developed profuse supra- and infratentorial brain edema with consciousness disturbance; and the other (Case 5) developed hemorrhagic infarction in the temporal lobe accompanied by aphasia. Two patients whose sinus occlusion was detected later (Cases 6 and 7) did not develop symptoms and displayed well-communicated transverse sinuses. In Case 7, a dural arteriovenous malformation formed at the site of the sinus occlusion. Laceration of the sigmoid sinus was suspected as the cause of occlusion in Cases 2, 3, and 7; compression of the sinus in Cases 5 and 6, sinus laceration and postoperative dehydration in Case 4; and laceration and compression of the sinus in Case 1. CONCLUSIONS: Differences in the clinical course among these patients were attributed to anatomical variations in the venous system. Occlusion of the sigmoid sinus should be weighed as a potential complication when selecting candidates for the presigmoidal-transpetrosal approach.
Adolescent↗
Purification and characterization of 38-kDa protein in plasma of dietary magnesium-deficient rat.
We have found an increase of a 38-kDa plasma protein level from 10 to 30 days in rats on a magnesium-deficient diet (Mg; 0.001 per cent), using sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE). This 38-kDa protein returned to the control level after feeding the rats a magnesium-sufficient diet (Mg; 0.07 per cent) for 1 week. Purification of the protein by reverse-phase HPLC separated it into two components (p38k-1 and p38k-2). Amino acid analysis showed that these components were both haptoglobin (Hp) beta-chain. Furthermore, hemoglobin-immobilized affinity chromatography analysis confirmed the increase of Hp in magnesium-deficient rat plasma. This is the first demonstration of an increase of Hp in plasma of dietary magnesium-deficient rats.
Amino Acid Sequence↗
Comparative studies of antimitochondrial autoantibodies in sera and bile in primary biliary cirrhosis.
Primary biliary cirrhosis (PBC) is an autoimmune liver disease characterized by destruction of intrahepatic bile ducts. Although the pathogenesis of this disease is still unknown, high titers of antimitochondrial autoantibodies (AMA) have long been recognized in patient sera. However, little is known about the presence of AMA in bile. In this study, we investigated bile and sera from patients with PBC and healthy controls for the presence of AMA and mitochondrial autoantigens. AMA were detected in the bile of 17 of 19 patients (89.4%) with PBC; they were specifically directed against the pyruvate dehydrogenase complex (PDC-E2) in 15 of 19 patients (78.9%), to the branched-chain 2-oxo-acid dehydrogenase complex E2 (BCOADC-E2) in 6 of 19 patients (31.6%), and to the 2-oxoglutarate dehydrogenase complex E2 (OGDC-E2) in 1 of 19 patients (5.3%). In a comparative study of sera from the same patients, anti-PDC-E2 antibodies were found in 19 of 19 patients (100%), anti-BCOADC in 9 of 19 patients (47.3%), and anti-OGDC-E2 in 4 of 19 patients (21.1%) patients. AMA in bile were always found together with antibodies of corresponding specificities in the serum from the same patient. Immunoglobulin (Ig)A AMA were found in the bile of 9 of 19 patients (47.7%) with PBC; they were specifically directed against PDC-E2 in 8 of 19 patients (42.1%) and to BCOADC in 2 of 19 patients (10.5%). Epitope mapping of IgA anti-PDC-E2 antibodies indicated that, like serum autoantibodies, the immunodominant epitope is directed against the inner lipoyl domain of PDC-E2. The prevalence and antigen reactivity of IgA AMA in sera correlated completely with IgA AMA in bile. Autoantibodies against nuclear envelope pore proteins (gp210) were found in 1 of 8 (12.5%) sera of patients with PBC, but not in bile. Furthermore, and of particular interest, we detected the autoantigens, PDC-E2, OGDC-E2, and BCOADC-E2, in the bile of 12 of 19 patients (63.2%), 9 of 19 patients (47.4%), and 9 of 19 patients (47.4%), respectively; PDC-E2 was found in only 1 of 17 (5.9%) disease controls. Although the presence of AMA in bile may merely reflect the presence of these antibodies in sera, the simultaneous detection of mitochondrial autoantigens in bile suggests an increase of mitochondrial autoantigens at inflammatory sites. Such autoantigens, coupled with AMA, may augment the local immune response and disease progression.
Autoantibodies↗
A case of a vascular anomaly with peculiar venous drainage.
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Adult↗
Structure of the TCR expressed on a gastritogenic T cell clone, II-6, and frequent appearance of similar clonotypes in mice bearing autoimmune gastritis.
A parietal cell-specific Th1 clone, II-6, which was established from a BALB/c mouse bearing post-thymectomy autoimmune gastritis (AIG), recognizes a peptide of the alpha subunit (alpha891-905) of H+/K+-ATPase and induces gastritis in nu/nu BALB/c mice by adoptive cell transfer. In the present study, the primary structure of the TCR of II-6 was determined as Valpha10-Jalpha c5a-Calpha and Vbeta14-Jbeta2.3-Cbeta2 by cDNA cloning. Using PCR with specific primers, we defined the use of this II-6 TCR in nu/nu mice with transferred II-6 cells and in mice that spontaneously developed AIG by thymectomy on day 3 after birth (d3-Tx). II-6 TCR mRNAs were detected in the gastric mucosa of all of the nu/nu mice, suggesting that II-6 cells indeed home to the gastric mucosa and thereby were directly involved in the destruction of target parietal cells. TCR beta chain mRNAs encoding CDR3 region sequences almost identical with that of II-6 were also found in the gastric mucosa in 43% (six of 14 mice tested) of the d3-Tx AIG mice at 4-12 weeks old by nested RT-PCR. Such a frequent appearance of similar clonotypes in independent individuals suggests that T cells bearing II-6-like TCR including the II-6 itself might be directly involved in, although not essential for, the pathogenesis of AIG in 3d-Tx mice.
Amino Acid Sequence↗
Cyclothialidine analogs, novel DNA gyrase inhibitors.
DNA gyrase inhibitors, cyclothialidines B, C, D and E were isolated from four Streptomycete strains (NR 0659, NR 0660, NR 0661 and NR 0662). Their structures have been elucidated based on the amino acid analysis of the hydrolysates, NMR and HRFAB-MS experiments and shown to be cyclothialidine analogs. The absolute stereochemistry has been determined by the chiral HPLC analysis of the hydrolysates. Cyclothialidines B, D and E are novel and potent inhibitors of DNA gyrase.
Chromatography, High Pressure Liquid↗
Ex vivo study of the effects of dietary magnesium deficiency on the formation and release of NO from endothelial cells and the sensitivity to NO of smooth muscle cells of thoracic aortas isolated from rats.
We found that the contractile responses to phenylephrine (PE) of isolated endothelium-intact thoracic aortas were enhanced by a nitric oxide (NO) synthase inhibitor, nitro-L-arginine (LNAG). and the magnitude of this enhancement was significantly greater in Mg-deficient than control rats. In this study, we used a sandwich method to evaluate the effects of dietary Mg deficiency on the ability of vascular endothelial cells to form and/or release NO and on the sensitivity to NO of vascular smooth muscle cells. Male Wistar rats were fed a Mg-deficient (10 mg Mg/kg diet) or control (700 mg Mg/kg diet) diet for 30 days. With the sandwich method, when endothelium-denuded thoracic aortas from chow fed rats were used as the assay vessels, and endothelium-intact aortas from control or Mg-deficient rats were used as the NO-donor vessels, neither the aortic contractile responses to PE nor the enhancement by LNAG of these responses in control and Mg-deficient rats differed significantly. When endothelium-denuded thoracic aortas from control or Mg deficient rats were used as the assay vessels and endothelium-intact aortas from chow fed rats were used as NO-donor vessels, LNAG enhanced PE-induced contractions to a significantly greater extent in Mg-deficient than control rats. Furthermore, sodium nitroprusside (a NO donor) had a greater relaxant effect on endothelium-denuded thoracic aortas isolated from Mg-deficient than control rats. These ex vivo results suggest that dietary Mg deficiency in rats has little effect on the formation and/or release of NO by aortic endothelial cells. but it does appear to increase the sensitivity to NO of aortic smooth muscle cells.
Animals↗
Ex vivo study of the increased sensitivity to NO of endothelium-denuded thoracic aortas isolated from dietary magnesium-deficient rats.
The mechanisms underlying the enhanced relaxant responses to sodium nitroprusside (SNP) associated with magnesium (Mg) deficiency were examined using endothelium-denuded thoracic aortas isolated from rats with dietary Mg deficiency. This enhancement of SNP-induced relaxation was abolished or depressed in the presence of methylene blue (a guanylate cyclase inhibitor). The relaxant responses to 8-bromo cyclic GMP (8-Br cGMP; a membrane-permeable cGMP) of thoracic aortas isolated from Mg-deficient rats were enhanced like those to SNP. These enhanced relaxant responses were depressed by tetraethylammonium (a non-specific K+ channel blocker). Charybdotoxin, a large conductance Ca2+-activated K+ (K[Ca]) channel blocker, inhibited 8-Br cGMP-induced relaxations of aortas from Mg-deficient and control rats. Apamin, a small conductance K(Ca) channel blocker, inhibited 8-Br cGMP-induced relaxations of aortas from Mg-deficient, but not control rats. The relaxant responses to cromakalim (an ATP-sensitive K+ channel opener) of the two groups were not significantly different. These ex vivo results show that dietary Mg deficiency in rats leads to increased sensitivity to NO of endothelium-denuded thoracic aortas in vitro and K(Ca) channel activation via cGMP may be involved in this enhancement.
Animals↗
The vasomotor effects of 5-hydroxytryptamine on equine basilar arteries in vitro.
The vasomotor effects of 5-hydroxytryptamine (5-HT) on isolated equine basilar arteries were studied. 5-HT induced contractions of equine basilar arteries in a concentration-dependent manner, with a pEC50 value (with 95% confidence limits) of 7.35 (7.08-7.62). Similar results were obtained with endothelium-denuded basilar arteries. Contractions were not competitively inhibited by the 5-HT2 receptor antagonist ketanserin at low concentrations of 5-HT. Conversely, at high concentrations of 5-HT, contractions were inhibited by ketanserin in a concentration-dependent manner, with a pA2 value of 8.91 (8.62-9.20). The 5-HT1 and 5-HT2 receptor antagonist methiothepin shifted the concentration-response curve of 5-HT downwards and to the right in a concentration-dependent manner. In the presence of 10(-6) mol/L ketanserin, however, methiothepin antagonized 5-HT-induced contractions competitively with a pA2 value of 7.95 (7.59-8.31). The 5-HT3 receptor antagonist MDL 72222 had no effect on 5-HT-induced contractions. The findings of this study indicate that 5-HT1 and 5-HT2 receptors are located in equine basilar arterial smooth muscle cells, and that stimulation of these receptors results in contraction.
Animals↗
A possible involvement of Fas-Fas ligand signaling in the pathogenesis of murine autoimmune gastritis.
BACKGROUND & AIMS: A Th1 clone, II-6, established from an autoimmune gastritis BALB/c mouse that underwent thymectomy 3 days after birth, recognized a 15 mer peptide constructing the alpha subunit of H+, K(+)-adenosine triphosphatase as antigen and induced gastritis in nu/nu mice by adoptive transfer. The aim of this study was to examine the molecular mechanism of target (parietal cells) destruction in either thymectomized or II-6 cell-transferred nu/nu mice. METHODS: Expression of Fas, major histocompatibility complex class II, and intercellular adhesion molecule 1 molecules on the gastric mucosa of these mice were immunohistochemically examined. In situ DNA fragmentation in these thymectomized or nu/nu mice was tested by the terminal deoxynucleotidyl transferase-mediated digoxigenin-deoxyuridine triphosphate nick end label (TUNEL) method. Moreover, activity of II-6 cells to induce apoptosis was tested by using the 15 mer peptide-pulsed B lymphoma cells, A20.2J, as the target. RESULTS: A portion of parietal cells in gastritis-bearing thymectomized or nu/nu mice at an early stage expressed Fas, major histocompatibility complex class II, and intercellular adhesion molecule 1 molecules and was TUNEL positive. Fas-ligand message was induced on activated II-6 cells and caused DNA fragmentation of the antigen-pulsed A20.2J cells. CONCLUSIONS: Cognate interaction between Fas antigen on the target and Fas ligand on the effector seems to be one possible mechanism for the target cell destruction in organ-specific autoimmune gastritis.
Animals↗
[A case report of transaortic mitral valve replacement in Marfan's syndrome].
One-stage operation was successfully performed in 30-year-old male with annulo aortic ectasia and mitral valve regurgitation secondary to Marfan's syndrome. The replacement of the mitral valve was performed through aortic root. The transaortic mitral valve replacement employed here should prove useful for similar cases requiring reconstruction of aortic root and replacement of mitral valve simultaneously in Malfan's syndrome.
Adult↗
Stability of free Mg2+ concentration and increased concentration of free Ca2+ in vascular smooth muscle cells during dietary magnesium deficiency in rat.
Intracellular free calcium and magnesium ion concentrations ([Ca2+]i and [Mg2+]i respectively) were estimated in thoracic aorta smooth muscle strips isolated from magnesium-deficient and control rats using fura-2/AM and mag-fura-2/AM, respectively. Adult male Wistar rats were fed a magnesium-deficient diet (10 mg Mg/kg diet) or a control diet (700 mg Mg/kg diet) for 30 days. Plasma magnesium level in magnesium-deficient rats was half of that in control rats at 30th day. Therefore, thoracic aorta strips, denuded of endothelium, were loaded with fura-2/AM or mag-fura-2/AM in the presence of 0.5 or 1.0 mM Mg2+, and [Ca2+]i or [Mg2+]i was measured under the same Mg2+ conditions. The [Ca2+]i in the aorta strips isolated from magnesium-deficient rats in the presence of 0.5 mM Mg2+ (254.9 +/- 13.1 nM) was approximately three times greater than in those from control rats in the presence of 1.0 mM Mg2+ (86.5 +/- 9.2 nM). The [Mg2+]i was not significantly different between the two groups at either Mg2+ level. The muscle tension and [Ca2+]i increased after [Mg2+]o was exchanged from 1.0 to 0.5 mM; however, [Mg2+]i showed no change. The total calcium content increased and total magnesium content decreased in thoracic aorta strips isolated from magnesium-deficient rats. These results suggest that [Mg2+]i is stable, but that [Ca2+]i increases in vascular smooth muscle cells of thoracic aortas isolated from dietary magnesium-deficient rats.
Animals↗
Myasthenia gravis, acute transverse myelitis, and HTLV-I.
We present the unusual case of a 49-year-old female carrier of HTLV-I with myasthenia gravis who presented with acute transverse myelitis. Laboratory data suggested a recent infection with varicella zoster virus and demyelination by an autoimmune process in the central nervous system. Adult T-cell leukemia-like cells were observed in the cerebrospinal fluid. T-cell-mediated immune responses modulated by HTLV-I infection may be involved in the pathogenesis of myasthenia gravis and acute transverse myelitis in this case.
Acute Disease↗
Mechanisms of the enhanced contractile response to a low concentration of phorbol 12,13-dibutyrate in thoracic aorta isolated from rats with dietary magnesium deficiency.
The mechanisms underlying the enhanced contractile response to phorbol 12,13-dibutyrate (PDBu) were examined in de-endothelialized thoracic aortas isolated from rats with dietary magnesium (Mg) deficiency. PDBu (1.0 nM)-induced contractions were significantly larger in Mg-deficient rats than in the controls. The contraction was completely inhibited by nifedipine, removal of external Ca2+ or by l-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7). PDBu (1.0 nM) and phorbol 12-myristate 13-acetate (1.0 microM) significantly decreased the KD value and increased the Bmax for the binding of [3H]PN200-110 to the aortas. The degree of the decrease in the KD value was significantly greater in Mg-deficient rats than in the controls. The PDBu-induced decrease in the KD value was abolished by H7. These results suggest that activation of protein kinase C by phorbol esters may participate in the activation of L-type Ca2+ channels, which increases both the affinity of [3H]PN200-110 binding and the magnitude of the external Ca(2+)-dependent contraction. Dietary Mg-deficiency may enhance these processes.
Animals↗