Search PubMed⌕ Search

Biomedical subjects

M Satoh

Publications and source records attributed to M Satoh.

At least 1,027 records · Page 57Linked to original sources
PubMed1986

In vitro production of autoantibodies to U1 ribonucleoproteins by peripheral blood mononuclear cells from patients with connective tissue diseases.

Antibodies to U1 ribonucleoproteins produced by peripheral blood mononuclear cells from patients with connective tissue diseases were measured by a sensitive enzyme-linked immunosorbent assay and by immunoblotting. Mononuclear cells from patients with high-titer serum antibodies spontaneously started secreting IgG anti-U1 RNP antibodies on the second day after culture. The amount of anti-U1 RNP in the culture supernatants reached maximum level on day 8. The most effective production of anti-U1 RNP by B cells was observed when they were cultured in the presence of T cells and adherent cells. Mononuclear cells from patients without anti-U1 RNP antibodies or from normal subjects did not produce a measurable amount of anti-U1 RNP. Treatment of mononuclear cells by cycloheximide resulted in complete inhibition of anti-U1 RNP secretion, which indicates that antibody in the culture supernatants reflects the active biologic phenomenon in vitro. The methods described should be useful in the study of the cellular mechanisms involved in antinuclear antibody production of connective tissue diseases.

Antigens↗
PubMed1986

Involvement of medullary opioid-peptidergic and spinal noradrenergic systems in the regulation of formalin-induced persistent pain.

To confirm that endogenous opioid-peptidergic systems and monoaminergic systems participate in the regulation of pain, the effects of a narcotic antagonist naloxone, inhibitors of enkephalin-degrading enzymes and monoaminergic blockers on persistent pain induced by formalin were investigated. Rats were given formalin into the plantar region of the left hind-paw and the duration of licking responses was measured at periods of 0-10 min (period I), 10-30 min (period II), 30-60 min (period III) and 60-120 min (period IV). Naloxone was administered systemically through mini-osmotic pumps and there was an enhanced licking response at period III and a tendency toward enhancement at period IV. The duration of the licking response at period III was increased when naloxone was given into the fourth ventricle in a dose of 30 nmol/rat, but not when it was injected into the lumbo-sacral subarachnoid space in doses of 30 and 300 nmol/rat. Thiorphan and bestatin injected simultaneously into the fourth ventricle (50 micrograms/rat) depressed the licking response at period III. Intrathecal injection of phentolamine significantly enhanced the licking response at periods I-III and produced a similar, but weaker effect at period IV. Intrathecal injection of propranolol and methysergide did not affect the response. These results suggest that opioid-peptidergic systems in the brain stem and noradrenergic systems in the spinal cord (via alpha-adrenoceptors) participate in the regulation of pain.

Animals↗
PubMed1986

Periodic changes in cycle length of ventricular tachycardia: a Wenckebach type exit block?

A 55-year-old female developed ventricular tachycardia (VT) which showed a Wenckebach periodicity in cycle length. She had had a myocardial infarction about ten years previous and, at age 51, felt fatigability and palpitations. The ECG showed VT. Thereafter, she had had palpitations of short duration two to three times a year. On the last admission she developed fatigability; the ECG showed VT. Lidocaine (100 mg i.v.) did not terminate VT. Procainamide (600 mg) could not terminate the VT, but the rate became slower. Programmed stimulation was given at bedside which effectively terminated VT. Electrophysiologic study induced VT in a reproducible manner. Ventricular tachycardia showed initial fluctuation in cycle length which stabilized at 270 msec. Disopyramide therapy (400 mg/day p.o.) was begun and electrophysiologic study was repeated one week later. VT was again induced but the cycle length was a little longer. A periodic change in cycle length from 328 to 442 msec was repeated. The change in cycle length was uniformly found in surface leads (I, II, V1) and intracardiac electrograms from the right ventricular apex and the His bundle region. No change in QRS complex was found and the periodicity was unrelated to atrial activity. A Wenckebach type exit block was therefore suggested; disopyramide might be responsible for the development of the block. We could not find another such case in the literature.

Bundle of His↗
PubMed1986

Bile ductular cells and the phenotypic heterogeneity of the population of hepatic non-parenchymal epithelial cells induced in rats by chemical carcinogens.

Single doses of diethylnitrosamine, N-hydroxy-2-acetylaminofluorene or N-methyl-N-nitrosourea were administered to rats, before or after obstruction of the common bile duct, and liver sections were stained for alpha-fetoprotein, albumin and glucose-6-phosphatase. In these animals, cells expressing hepatocytic traits were not observed in the resulting expanded population of non-parenchymal epithelial cells. A derivation of non-parenchymal epithelial cells with hepatocytic traits from bile ductular cells is not supported, but not completely ruled out, by these findings. In rats with an obstructed bile duct and administered a single carcinogen dose, serum alpha-fetoprotein was slightly increased, to levels comparable with those occurring after a partial hepatectomy. In these rats, and in partially hepatectomized rats, the cellular source of serum alpha-fetoprotein was not apparent, since no alpha-fetoprotein-positive cells were detected in their liver.

Albumins↗
PubMed1986

Antigens associated with various cytotoxic activities of murine peripheral macrophages.

BCG- or glucan-elicited murine peripheral macrophages released a cytotoxin in the presence of loach egg lectin, whereas proteose peptone-, glycogen-, or thioglycollate-elicited or resident macrophages did not. The macrophages that released cytotoxin coincided with those that showed lectin-dependent macrophage-mediated cytolysis (LDMC) in response to loach egg lectin. The cytotoxin released by BCG-elicited macrophages in response to loach egg lectin had a molecular weight of 55 K daltons. The macrophages that released cytotoxin and other cytotoxic macrophages such as those that showed LDMC- and antibody-dependent macrophage-mediated cytolysis (ADMC) were examined by using several antibodies to surface antigens of macrophages. The results showed that murine peripheral macrophages could be divided into three types. Resident macrophages (Type I) which had common macrophage antigens (Mac-1 and B12) showed only LDMC in response to wheat germ agglutinin. Some elicited macrophages (Type II) were asialo GM1-positive and showed both ADMC and LDMC in response to wheat germ agglutinin. Activated macrophages (Type III) showed LDMC in response to loach egg lectin and cytotoxin-release, but had no antigen detectable with monoclonal anti-macrophage antibody (C14). These three types of macrophages were clearly distinguished diagrammatically by their roof-shaped, rocket-shaped and irregular-shaped profiles of activities and antigens. These data suggest that several selected surface antigens of macrophages are associated with distinct cytotoxic stages of peripheral macrophages.

Animals↗
PubMed1986

Five cases of arrhythmogenic left ventricular aneurysm unrelated to coronary occlusion.

Five among 19 cases of sustained ventricular tachycardia (VT) treated in the last two years had left ventricular aneurysms, but the patients denied any previous attack of chest pains that would indicate acute myocardial infarction. Laboratory findings including serum electrolytes were normal and no signs of inflammation were found. Coronary angiograms were normal but the left ventriculograms showed aneurysms in four patients and akinetic to aneurysmal wall motion in one patient. Electrophysiologic studies (EPS) were done in four patients. VT was induced reproducibly by programmed electrical stimulation in three patients and it was terminated by programmed stimulation within 30 seconds. The foci of VT were determined by EPS. One case who showed acceleration of the VT rate following the second induction of VT developed a fulminant course; Adams-Stokes attacks from VT, more than ten times a night in spite of intravenous administration of a large dose of procainamide, were terminated by DC shock. VT was determined to originate from the aneurysm that was resected operatively. In the other two cases, the foci were resected and the intraoperative EPS confirmed the preoperative foci. The postoperative EPS showed no inducibility of VT in three surgical cases. Though the induction of VT may not be indicated in every case of VT, we believe that EPS is required to determine the focus for the operation and to evaluate the precise drug efficacy in rapid VT. It is further stressed that the sustained VT of our patients including the present five, lasted for several hours until it was terminated in the hospital.

Aged↗
PubMed1986

Effect of nifedipine on neuropeptide Y-induced coronary vasoconstriction in anesthetized dogs.

The coronary vasoconstrictor effects of neuropeptide Y (NPY) were confirmed in anesthetized closed-chest dogs. This NPY-induced vasoconstriction was not affected by alpha- or beta-adrenergic blockers and nifedipine given into the perfusion circuit abolished the constriction. After intracoronary nifedipine administration, coronary flow exceeded the control level within 60 sec, then returned to a level between the control value before NPY and the lowest value elicited by NPY after 10 min. When nifedipine was given systemically before NPY, the peak response to NPY was attenuated, suggesting a preventive effect of nifedipine on the NPY-induced coronary vasoconstriction. Since NPY is found in the hearts of many species, including man, NPY may cause coronary vasospasms. An effect on NPY-induced coronary vasoconstriction of nifedipine may be compatible with the beneficial clinical effects of this drug.

Animals↗
PubMed1986

A successful electrical ablation of recurrent sustained ventricular tachycardia in a postoperative case of tetralogy of Fallot.

A 26 year old female patient developed recurrent sustained ventricular tachycardia (VT) after undergoing heart surgery for the third time for chronic pulmonary regurgitation following repair of tetralogy of Fallot. At the last surgery, ventriculotomy was again performed in the outflow tract of the right ventricle. At that time, scar formation and thinning of the cardiac wall were obvious. The surgical result was excellent. Three months later, she lost consciousness. ECG showed VT which was refractory to tolerated doses of antiarrhythmic drugs. Electrophysiologic study showed fragmented activity in the outflow tract of the right ventricle during VT which could be induced and terminated by programmed electrical stimulations. DC energy delivery of 200 Joules to catheter electrodes which recorded local activity 20 msec prior to the onset of the QRS of VT was successful in preventing VT. VT could not be induced by extensive programmed stimulation 1 month later.

Adult↗
PubMed1986

A case of atrial septal defect complicating myocardial infarction. Severe heart failure induced by balloon occlusion of ASD.

A 58 year old man with an acute, extensive anterior myocardial infarction was found to also have an atrial septal defect secundum. A cardiac catheterization study showed a large left to right shunt (Qp/Qs: 6.0). Since other clinical findings were not consistent with the prolonged existence of a large shunt, we considered it to be secondary to the myocardial infarction. Balloon occlusion of the ASD was carried out to predict the hemodynamics after the surgical correction, which soon resulted in severe left ventricular failure. Therefore, an operation was not feasible in this case.

Cardiac Catheterization↗
PubMed1986

Association between vibration-induced white finger and hearing loss in forestry workers.

The present investigation was a case-referent study in which age and hours of vibrating tool operation were matched for the cases and referents in an effort to confirm the earlier reported difference in hearing loss between workers with vibration-induced white finger (VWF) and those without VWF. Thirty-seven pairs were formed from 51 men with VWF and 228 without it. The greatest hearing loss was at 4 kHz in both the case and reference groups, as is usually found in typical noise-induced hearing loss. The case group had a higher hearing threshold than the reference group at every frequency, and the difference was significant at 4 and 8 kHz and almost so at 2 kHz. As corroboration for this association, the subjects were divided into three groups by recovery rate of skin temperature 5 min after cold provocation at 10 degrees C for 10 min, a procedure which is one of the valid objective tests for VWF. The subjects with the most delayed recovery reached the highest age-corrected median hearing level at 4 kHz, and those with the promptest recovery marked the lowest. The cause of this increased damage of hearing in relation to VWF is not known. However, the association between VWF and hearing loss is interesting in view of the effects of vibration on parts of the body other than the hand and arm.

Female↗
PubMed1986

Usefulness of fingertip skin temperature for examining peripheral circulatory disturbances of vibrating tool operators.

The data on skin temperature obtained in a cold provocation test (immersing one hand in water at 10 degrees C for 10 min) were analyzed to confirm their usefulness for examining the peripheral circulatory functions of vibrating tool operators. Under room temperatures from 20 to 23 degrees C in winter, the skin temperatures after the end of provocation of the VWF (vibration-induced white finger) group were generally significantly lower than those of the age-matched non-VWF and reference groups, and the non-VWF operators with over 5,000 h of chain-saw experience showed significantly lower skin temperatures 5 and 10 min after provocation than the age-matched referents. In this study skin temperature was used as a screening test for VWF. The highest sensitivity (91.1%) was obtained at 19.0 degrees C at the fifth minute after the end of the provocation, and the highest specificity (93.3%) at 15.5 degrees C at the third minute after provocation, both the sensitivity and specificity being over 70% and the correct diagnosis rate being over 80% among the screening levels.

Cold Temperature↗
PubMed1986

Priming effect of interferons and interleukin 2 on endogenous production of tumor necrosis factor in mice.

The effects of interferons (IFNs) and interleukin 2 (IL 2) on endogenous production of tumor necrosis factor (TNF) were investigated in mice. Production of serum TNF was triggered by iv injection of OK-432 and tested by in vitro cytotoxicity assay. Injection of recombinant IFN-gamma with OK-432 and tested by in vitro cytotoxicity assay. Injection of recombinant IFN-gamma with OK-432 or of IFN-alpha/beta, recombinant IFN-beta, recombinant IFN-alpha A/D or recombinant IL 2 six hours before OK-432 enhanced TNF production about 10-fold, which indicated priming actions of these compounds in TNF production. These findings suggest that these compounds could also be used as priming agents for endogenous production of TNF in cancer patients.

Animals↗
PubMed1986

Endogenous production of TNF in mice long after BCG sensitization.

The effect of tuberculin-antigen protein (PPD: purified protein derivatives) on the priming of tumor necrosis factor (TNF) a long time after sensitization with bacillus Calmette-Guérin (BCG) was investigated in mice. Mice were infected intravenously (i.v.) with 4 X 10(7) colony-forming units (CFU) of BCG per mouse, and the TNF activity triggered by 15 micrograms lipopolysaccharide (LPS) was assayed with time using L-929 cells. The activity was maximal 4 weeks after sensitization and decreased to the control level after 10 weeks. The i.v. injection of 10 micrograms of PPD per mouse enhanced the TNF production triggered by LPS in mice even 10-20 weeks after sensitization. This enhancement was unexpectedly quite transient, being maximal 3 h after PPD treatment. The activity was comparable to that in mice 4 weeks after sensitization of BCG (without PPD). The enhancing effect of PPD was observed in the dose range of 0.1-10 micrograms/mouse, and 10 micrograms of PPD significantly enhanced the TNF activity triggered by even 0.6 microgram LPS. These findings indicate that priming of sensitized animals with some antigens followed by triggering with LPS induces a significant endogenous production of TNF even a long time after antigen sensitization. The possible application of these findings for inducing endogenous production of TNF in human patients by use of tuberculin allergy is discussed.

Animals↗