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Biomedical subjects

S Satoh

Publications and source records attributed to S Satoh.

At least 343 records · Page 19Linked to original sources
PubMed1997

[A case report of total removal of infected pacemaker leads with cardiopulmonary bypass through right thoracotomy].

A 61-year-old man with septicemia had four infected pacemaker leads, which were impossible to remove using simple traction method. He received CABG previously, and SVG anastomosed to LAD was patent. Redo median sternotomy had a possibility to make damage to SVG. Total removal of infected pacemaker was performed successfully with cardiopulmonary bypass through right thoracotomy.

Cardiopulmonary Bypass↗
PubMed1997

[Chemoradiation for rectal cancer].

Based on the results of the Study Group for Surgical Adjuvant Radiochemotherapy for Rectal Cancer and the Study Group for Surgical Therapy and Combined Irradiation in Rectal Cancer, we examined the clinical aspects of the relatively new field of chemoradiation for rectal cancer and examined improvements in the therapeutic results. Furthermore, we examined the future outlook with particular regard to selection of therapeutic drugs and autonomic nerve preserving operation.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

[Arterial infusion chemotherapy with SMAN CS-Lipiodol for hepatocellular carcinoma evaluation of infusion method].

Forty-four patients with hepatocellular carcinoma were treated with oily anticancer agent SMANCS dissolved in Lipiodol (SMANCS-LPD). The local response rate after the first arterial infusion in all patients was 39%, against 63% in 27 patients with Lipiodol accumulation occupying more than two third of tumor areas. Repeated arterial infusion of SMANCS-LPD did not enhance the therapeutic effect. An infusion of 4mg of SMANCS was ineffective for patients with tumors distributing in bilateral lobes of liver, and 6 mg was recommended for such cases.

Aged↗
PubMed1997

A vesicular variant of bullous pemphigoid with autoantibodies against unidentified 205- and 150-kDa proteins at the basement membrane zone.

We describe a 75-year-old man who developed a vesicular variant of bullous pemphigoid with a distinctive result of immunoblot analysis. Characteristic symptoms consisted of vesiculopapular eruptions with erythematous patches on the arms and legs, many of which fused to form irregularly outlined areas of erythema varying in size. Direct immunofluorescence revealed a linear deposition of IgG at the basement membrane zone of the skin, and indirect immunofluorescence detected circulating IgG autoantibodies at a titre of 1:160, which reacted with the antigens located on the epidermal side of skin split with 1 mol/L NaCl. Immunoblot analysis using epidermal extracts demonstrated the presence of IgG antibodies directed to 150, 205, 240 and 280 kDa proteins as well as to the 180 kDa bullous pemphigoid antigen (BPAG2). All antibodies eluted from nitrocellulose membrane imprints of individual bands with molecular weights of 150, 180 and 205 kDa were found by indirect immunofluorescence to react with the basement membrane zone, whereas those eluted from the bands with molecular weights of 240 and 280 kDa did not. These findings suggest that antibodies directed not only to the 180 kDa BPAG2, but also to 150 and 205 kDa proteins, are involved in the pathogenesis of bulla formation in this patient.

Aged↗
PubMed1997

Serum beta-2-microglobulin in patients with multiple myeloma treated with alpha interferon.

In ten patients with multiple myeloma (MM), serum beta-2-microglobulin (B2M) levels were monitored in order to clarify the influence of alpha interferon (IFN) administration. Despite decreases in M-protein and the absence of renal dysfunction, the levels of serum B2M were sustained above those prior to melphalan-prednisolone and IFN therapy in seven patients with MM for six months. Serum B2M did not increase in ten patients with MM treated only by melphalan-prednisolone. Furthermore, serum B2M levels in a patient who achieved a complete response were sustained above her prior level and returned to normal after cession of IFN therapy. Our study suggests that the serum B2M level is increased by treatment with IFN, and does not prove the condition of the disease.

Adolescent↗
PubMed1996

Disorganization of microtubular network in postischemic liver dysfunction: its functional and morphological changes.

Microtubules in the hepatocytes have been implicated to serve as lines of cytoplasmic transport of secretory materials, but are highly labile structures sensitive to pathological conditions in the cytosol. We examined the role of ischemia/reperfusion-induced cytoskeletal alterations in postischemic liver dysfunction. Rabbit livers were subjected to 60-min warm ischemia followed by 1 h or 24 h of reperfusion. Liver function was assessed by directly measuring hepatic clearance of indocyanine green (ICG), an organic anion whose cytoplasmic transport is assumed to depend on intact microtubules, using near-infrared spectroscopy. Structural alterations of microtubules were observed immunohistochemically using tissue sections stained with monoclonal anti-beta-tubulin antibody. ICG removal from hepatocytes into bile canaliculi deteriorated 1 h but reversed 24 h after reperfusion. Immunohistochemistry showed fragmentation of microtubules at the end of liver ischemia. This cytoskeletal alteration was evident 1 h but was not observed 24 h after reperfusion. Treatment with prostaglandin E1 exerted its beneficial effect by preserving ICG clearance and microtubular network. These results demonstrate that liver ischemia and subsequent reperfusion both affect the organization of microtubular network and suggest that structural disruption of microtubules may be a cause of postischemic liver dysfunction.

Actin Cytoskeleton↗
PubMed1996

Sodium nitroprusside stimulates noradrenaline release from rat hippocampal slices in the presence of dithiothreitol.

It is becoming apparent that nitrogen monoxide (NO) such as nitric oxide has regulatory roles for neuronal cell functions. We examined the role of NO using NO donors on [3H]noradrenaline (NA) release from prelabeled rat hippocampal slices. Sodium nitroprusside (SNP), which had no effect by itself, stimulated [3H]NA release in a dose-dependent manner (ED50 = 0.5 mM) in the presence of dithiothreitol (DTT). The stimulatory effect of SNP with DTT, but not high K+, was observed in an extracellular Ca(2+)-free buffer. The maximal effect of SNP was obtained after incubation for 1-2 h with DTT in buffer at physiological pH (7.4). The simultaneous addition of SNP and DTT to the slices induced a small effect, and the effect of SNP declined after 3.5 h. SNP stimulated cyclic GMP accumulation in the slices without DTT. NaNO2 and 1-hydroxy-2-oxo-3,3-bis(2-aminoethyl)-1-triazene (a generator of nitric oxide), which stimulated cyclic GMP accumulation by themselves, did not stimulate [3H]NA release in the presence and absence of DTT. 3-Morpholinosydnonimine HC1 (a generator of peroxynitrite) had no effect on the release. The stimulatory effect of SNP and DTT on NA release was inhibited 40% by nitric oxide scavengers such as oxyhemoglobin and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxy-3-oxide, although cyclic GMP accumulation induced by NO donors was completely inhibited. These findings suggest that SNP reacts with DTT to produce unknown active species, and that cyclic GMP is not a mediator for SNP-stimulated NA release.

Animals↗
PubMed1996

Angiotensin II-induced renal responses in anesthetized rabbits: effects of N omega-nitro-L-arginine methyl ester and losartan.

Intrarenal arterial infusion of angiotensin II (4 ng/kg/min) reduced renal blood flow, glomerular filtration rate and urinary Na+ excretion (UNaV) without affecting fractional Na+ excretion (FENa) in anesthetized rabbits. Losartan (10 micrograms/kg/min) abolished these angiotensin II-induced renal responses. The renal blood flow, glomerular filtration rate and UNaV responses were potentiated during intrarenal arterial infusion of N omega-nitro-L-arginine methyl ester (L-NAME, 10 micrograms/kg/min). A high dose of L-NAME (50 micrograms/kg/min) also potentiated the renal blood flow and UNaV responses but not the glomerular filtration rate response. Angiotensin II reduced FENa during L-NAME infusion at either dose. In L-NAME-pretreated rabbits, losartan abolished the angiotensin II-induced renal blood flow and glomerular filtration rate responses, but the reduction in FENa still remained. The present study suggests that in the rabbit kidney (1) nitric oxide attenuates the angiotensin II-induced (angiotensin AT1 receptor-mediated) vasoconstriction and (2) angiotensin II can evoke losartan-resistant tubular Na+ reabsorption, but the tubular action is concealed by nitric oxide.

Angiotensin II↗
PubMed1996

Promotion of sleep mediated by the A2a-adenosine receptor and possible involvement of this receptor in the sleep induced by prostaglandin D2 in rats.

A 6-hr continuous infusion of 2-[p-(2-carboxyethyl)phenylethylamino]-5'-N-ethylcarboxamidoadenos ine (CGS21680), a selective A2a-adenosine agonist, into the subarachnoid space underlying the ventral surface region of the rostral basal forebrain, which has been defined as the prostaglandin (PG) D2-sensitive sleep-promoting zone, at rates of 0.02, 0.2, 2.0, and 12 pmol/min increased slow-wave sleep (SWS) and paradoxical sleep (PS) in a dose-dependent manner up to 183% and 202% of their respective baseline levels. The increments produced by the infusion of CGS21680 at 0.2 and 2.0 pmol/min were totally diminished when the rats had been pretreated with an i.p. injection of (E)-1,3-dipropyl-7-methyl-8-(3,4-dimethoxystyryl)xanthine (KF17837; 30 mg/kg of body weight), a selective A2-adenosine antagonist. In contrast, the infusion of N6-cyclohexyladenosine (CHA), a selective A1-adenosine agonist, at 2 pmol/min significantly suppressed SWS before causing an increase in SWS, and a decrease in PS was also markedly visible. Essentially the same effects of CGS21680 and CHA were observed when these compounds were administered to the parenchymal region of the rostral basal forebrain through chronically implanted microdialysis probes. Thus, we clearly showed that stimulation of A2a-adenosine receptors in the rostral basal forebrain promotes SWS and PS. Furthermore, i.p. injections of KF17837 at 30 and 100 mg/kg of body weight dose-dependently attenuated the magnitude of the SWS increase produced by the infusion of PGD2 into the subarachnoid space of the sleep-promoting zone, thus indicating that the A2a-adenosine receptors are crucial in the sleep-promoting process triggered by PGD2.

Adenosine↗
PubMed1996

New anterior instrumentation for the management of thoracolumbar and lumbar scoliosis. Application of the Kaneda two-rod system.

STUDY DESIGN: The Kaneda multisegmental instrumentation is a new anterior two-rod system for the correction of thoracolumbar and lumbar spine deformities. This system consists of a vertebral plate and two vertebral screws for individual vertebral bodies and two semirigid rods to interconnect the vertebral screws. Clinical results of 25 thoracolumbar and lumbar scoliosis patients treated with this new instrumentation were analyzed. OBJECTIVES: To evaluate the efficacy of the new anterior instrumentation in correction and stabilization of thoracolumbar and lumbar scoliosis. SUMMARY OF BACKGROUND DATA: Since Dwyer first introduced the concept of anterior spinal instrumentation and fusion for scoliosis, anterior surgery has gradually gained acceptance. In 1976, a useful modification for the anterior spinal instrumentation, which reportedly provided means of lordosation and vertebral body derotation, was described. However, some authors reported a high tendency of the implant breakage, loss of correction, progression of the kyphosis, and pseudoarthrosis as the major complications. To overcome the disadvantages of Zielke instrumentation, the authors have developed a new anterior spinal instrumentation (two-rod system) for the management of thoracolumbar and lumbar scoliosis. METHODS: Anterior correction and fusion using Kaneda multisegmental instrumentation was performed in 25 patients with thoracolumbar or lumbar scoliosis. The average follow-up period was 3 years, 1 month (range, 2 years to 4 years, 7 months). There were 20 patients with idiopathic scoliosis (13 adolescents and seven adults) and five patients with other types of scoliosis, including congenital and other etiologies. All patients had correction of scoliosis by fusion within the major curve, and for 16 of the 25 patients, the most distal end vertebra was not included in the fusion (short fusion). Radiographic evaluations were performed to analyze frontal and sagittal alignments of the spine. RESULTS: The average correction rate of scoliosis was 83%. Over the instrumented levels, the correction rate was 90%. Preoperative kyphosis of the instrumented levels of 7 degrees was corrected to 9 degrees of lordosis. Sagittal lordosis of the lumbosacral area beneath the fused segments averaged 51 degrees before surgery and was reduced to 34 degrees after surgery. The trunk shift was improved from 25 mm before surgery to 4 mm at final follow-up evaluation. The average improvement in the lower end vertebra tilt-angle was 97% in those patients whose lower end vertebra was included in the fusion and 83% in patients whose lower end vertebra was not included in the fusion. Apical vertebral rotation showed an average correction rate of 86%. At final follow-up evaluation, all patients demonstrated solid fusion without implant-related complications. There was 1.5 degrees of frontal plane and 1.5 degrees of sagittal plane correction loss within the instrumented area at final follow-up evaluation. CONCLUSIONS: New anterior two-rod system showed excellent correction of the frontal curvature and sagittal alignment with extremely high correction capability of rotational deformities. Furthermore, correction of thoracolumbar kyphosis to physiologic lordosis was achieved. This system provides flexibility of the implant for smooth application to the deformed spine and overall rigidity to correct the deformity and maintain the fixation without a significant loss of correction or implant failure compared with conventional one-rod instrumentation systems in anterior scoliosis correction.

Adolescent↗
PubMed1996

The action of the cholecystokinin-A receptor antagonist, devazepide, on the digestive system of the chicken.

The influence of the cholecystokinin (CCK)-A receptor antagonist, devazepide (DVZ), on the chicken digestive tract was investigated. The passage of food from the crops of birds treated with DVZ was not significantly different from that of the control. DVZ treatment did not inhibit the biliary flow stimulated by the CCK analogue, caerulein. Dispersed chicken pancreatic acini stimulated with CCK were treated with various concentrations of DVZ. At 10-5 M, DVZ completely inhibited amylase release; this concentration was much higher than those reported to have similar effects in mammals. The results suggest that the action DVZ as a CCK antagonist in the chicken is very weak.

Amylases↗
PubMed1996

No association between apolipoprotein E epsilon4 allele and the age of onset in type I familial amyloid polyneuropathy.

It has been shown that the Apolipoprotein E (ApoE) epsilon4 allele increases the risk of developing Alzheimer's disease (AD) and lowers the age of its onset. ApoE has also been suggested to be a common facilitating factor in the different types of amyloidoses. However, the association of ApoE epsilon4 with the onset of disease in various types of amyloidoses has not been extensively investigated. Type I familial amyloid polyneuropathy (FAP) is one form of systemic amyloidosis in which ApoE co-localizes with amyloid deposits. We examined 54 patients with type I FAP and found that there was no significant effect of either ApoE epsilon2 or epsilon4 allele on the age at onset. Our results suggest that ApoE4 is not a facilitating factor in the development of FAP, transthyretin amyloidosis.

Age of Onset↗
PubMed1996

NO donors stimulate noradrenaline release from rat hippocampus in a calmodulin-dependent manner in the presence of L-cysteine.

Nitrogen oxides (NO) such as nitric oxide have been suggested to potentiate neurotransmitter release in a variety of neuronal cells. In this study, we showed that NO donors stimulate the release of noradrenaline (NA) from rat hippocampus both in vivo and in vitro. Co-addition of NO donors (sodium nitroprusside [SNP] or S-nitroso-N-acetylpenicillamine [SNAP]) and thiol compounds (dithiothreitol [DTT] or L-cysteine) stimulated [3H]NA release from prelabeled hippocampal slices. Microdialysis in freely moving rats was used to ascertain the role of NO in control of NA release from the hippocampus in vivo. Co-addition of SNAP and L-cysteine stimulated endogenous NA release within 30 min. The concentration of NA peaked between 30-60 min to almost 3 times basal level. Another thiol compound, glutathione, had no effect on [3H]NA release in the presence of SNP or SNAP. In the presence of SNAP, the effect of L-cysteine was much higher than that of the D-isomer, although SNAP did not show stereospecificity. The effect of SNAP/L-cysteine was rapid and the maximal increase in [3H]NA release was attained 0-1 min after application, which was similar in time course to the effect of KCI. Unlike the release by KCI, SNAP/L-cysteine-stimulated NA release was independent of extracellular CaCl2. However, pretreatment with the calmodulin antagonists W-7 or trifluoperazine significantly reduced the SNAP/L-cysteine-stimulated [3H]NA release. Formation of nitric oxide and activation of guanylate cyclase by nitric oxide were not responsible for SNAP/L-cysteine-stimulated NA release. These findings suggest that NO donors stimulate NA release from the hippocampus in the presence of thiol compounds such as L-cysteine in vivo and in vitro in a calmodulin-dependent, Ca(2+)-and cyclic GMP-independent manner. The physiological roles of thiol compounds such as L-cysteine or glutathione as intermediates of NO are discussed.

Animals↗
PubMed1996

Long-duration xenogeneic extracorporeal pig liver perfusion with human blood.

Hepatic xenografts can tolerate hyperacute rejection owing to their lower susceptibility to humorally mediated injury. We investigated the possibility of long-duration xenoperfusion without immunologically controlling natural antibodies or complements. Pig livers were perfused for 9 h with human blood (Group 1) or pig blood (Group 2). Physiological conditioning and administration of prostaglandin E1 and insulin was characteristic of our system. The portal vein and hepatic artery pressure and bile production did not significantly differ between the two groups. Despite a gradual decrease throughout the perfusion, overall oxygen consumption was significantly higher in Group 1. Liver enzymes were released at higher levels in Group 1. Histological examination revealed intact hepatic architecture in Group 2, while in Group 1 interlobular morphology was severely damaged by endothelial disruption, although hepatic sinusoidal architecture was preserved. It is concluded that, despite biochemically and histologically confirmed tissue injury, graft viability was well-maintained in xenoperfusion even without immunological manipulations.

Alprostadil↗