Successful operation for solitary fibrous tumor of the epicardium.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Haga.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
An infant suffered from psoriasiform dermatitis complicated by severe constitutional symptoms. During his 12 months of hospitalization, the symptoms exacerbated periodically despite numerous therapeutic trials. Histologic findings revealed lichenoid psoriasiform dermatitis with striking eosinophilic necrosis of epidermal cells and satellite cell necrosis. Immunohistochemically, CD1+ Langerhans cells had almost disappeared, and CD8+ cytotoxic-suppressor T cells were predominant over CD4+ helper-inducer T cells in the epidermis. These findings in the skin biopsy specimens suggested some similarity to graft-versus-host disease but no known cause of that disorder was proved. Finally, methotrexate was effective. The patient became afebrile, and his skin lesions improved, leaving almost no scarring. This patient seems to have had specific clinical features that do not correspond with any of the known dermatitis. Clinical, histologic, and laboratory findings did not uncover any etiologic factors.
The influence of coronary venous retroinfusion and a vasoselective calcium antagonist felodipine on the microsphere loss in a porcine model of myocardial ischaemia and reperfusion was studied. Sixteen open-chest pigs underwent 45 min of myocardial ischaemia induced by occlusion of the left anterior descending coronary artery followed by 4 h of reperfusion. Either felodipine (felo-retro group, 7 nmol kg-1, n = 6) or the corresponding amount of vehicle (vehicle-retro group, n = 5) was infused retrogradely into the coronary veins over 30 min, starting 5 min before reperfusion. In a third group, the same amount of felodipine was administered intravenously (felo-iv group, n = 5). Myocardial regional blood flow was measured with radiolabelled microspheres (phi = 15 microns) injected before ischaemia to investigate a possible loss during ischaemia. In the felo-retro group, the apparent blood flow in the ischaemic areas, expressed as a percentage of the corresponding values in the non-ischaemic areas (%-flow), were 73 +/- 15, 73 +/- 11 and 75 +/- 19 in the subendocardial, midmyocardial and subepicardial layers, respectively. The corresponding percentage flows were 64 +/- 11, 70 +/- 11 and 62 +/- 9 in the vehicle-retro group and 75 +/- 18, 77 +/- 15 and 76 +/- 11 in the felo-iv group. The differences between the groups were not statistically significant. It is concluded that in this open-chest preparation microsphere loss observed in the ischaemic and reperfused myocardium is not increased by coronary venous retroinfusion or by a concomitantly administered vasodilative agent like felodipine.
Selected immunomodulatory effects of levamisole were studied in patients with asymptomatic metastatic colon cancer and in a preclinical model (CF1 female mice treated with methyl-azoxymethanol acetate) for colon tumors. In the patient population studied, there was no augmentation of cellular cytotoxicity or alteration in lymphocyte subpopulations that participate in these functions. An increase in Fc receptor binding on circulating monocytes was apparent at the 4-week timepoint; however, a corresponding increase in antibody-dependent cellular cytotoxicity was observed in only one of the six patients studied. In most patients, cellular cytotoxicity diminished with time. No significant effects on cellular immunity or carcinogenesis were observed in our murine studies. However, treatment with levamisole did increase circulating immunoglobulin levels and IgM response in mice immunized with the T-dependent antigen keyhole limpet hemocyanin. This parameter was not tested in the human trial. Failure to demonstrate antitumor effects on cellular immunity by levamisole in both human and murine studies suggests that these effects, if they do exist, may involve immunological parameters that were not tested using our methods or that may not be apparent in patients with more advanced malignancy.
Glucagonoma is a rare islet cell tumor of pancreas. Only 122 proven cases have been reported in the English literature so far. Diagnosis of glucagonoma has usually been delayed. The average size of clinically detected glucagonomas was 5.8 cm, and 54.7% of them exhibited metastasis. We describe the case of a 0.7-cm asymptomatic pancreatic glucagonoma. A 45-yr-old female was demonstrated to have a demarcated, small, low echoic mass in the pancreatic head by routine ultrasonography. Table incremental dynamic computed tomography showed a small well-enhanced mass recognized only in an early phase. A 0.7 x 0.7 cm firm nodule on the pancreatic head was excised at operation. Immunohistochemical and ultrastructural studies revealed that this tumor was a glucagon-producing adenoma. This may be the smallest glucagonoma detected by image diagnostics that has been reported in the English literature. Possible early detection of glucagonoma was discussed in this report.
Explore the source record for details and available documents.
A young woman presented with high fever and edema in January, 1984, and was diagnosed as having systemic lupus erythematosus. Prednisolone administration failed to improve her symptoms. In May she was admitted to hospital because of elevated erythrocyte sedimentation rate (ESR), hypoproteinemia, hypogammaglobulinemia, hypocomplementemia, positive antinuclear antibody, elevated immune complex level, and diarrhea. Edema disappeared following administration of diuretics and albumin, although the pathogenesis was still undetermined. In September, she was referred to our institution because of severe watery diarrhea and hypoproteinemia. Endoscopic examination showed a diffuse inflammatory lesion in the duodenum and the colon. Radioisotopic 51Cr-albumin study results were compatible with protein-losing enteropathy. Hypoproteinemia and inflammatory changes of the intestine were improved by antibiotics, suggesting that the inflammatory lesion was caused by bacterial infection. Despite the improvements in clinical symptoms and laboratory findings, the serum IgA level was still low and the thrombocytopenia remained. The morphological characteristics of the megakaryocytes were consistent with idiopathic thrombocytopenic purpura. In May, 1986, the thrombocytopenia deteriorated, causing purpura. Prednisolone was administered again, and this resulted in normalization of the platelet count, although the IgA level remained low. Finally the prednisolone was stopped, and the IgA level gradually recovered, with the improvement of the enterocolitis. The exact pathogenesis of the whole picture in this case is unclear, but an 8-year-long clinical course suggests that the protein-losing was caused by an infectious enterocolitis superimposed on IgA deficiency.
Chimeric 17-1A antibody (IgG1 kappa) was constructed by linking variable region genes of murine monoclonal antibody 17-1A with genes for human kappa light chain and gamma 1 heavy-chain constant regions. This study was undertaken to compare in vitro antibody-dependent cellular cytotoxicity (ADCC) between the chimeric 17-1A (IgG1 kappa) and native murine 17-1A antibody (IgG2a kappa) with human peripheral blood mononuclear cells (PBMNC) against 7 human tumor (1 colon, 6 pancreas) cell lines. ADCC activity was measured by chromium-release assay. When freshly-isolated PBMNC from healthy donors were used for effector cells, significantly higher ADCC activity of chimeric antibody compared to murine antibody at optimal antibody dose (10 micrograms/mL) and lower doses (to 0.6 micrograms/mL) was observed against tumor cells with relatively high 17-1A expression. This high ADCC activity of the chimeric antibody persisted even when freshly-isolated monocyte-depleted PBMNC was used. When interleukin-2 activated PBMNC were used, comparable increases in ADCC were observed with both chimeric and murine antibody. These results suggest that chimeric 17-1A antibody is a more effective mediator of in vitro ADCC activity with human freshly-isolated PBMNC than the native murine antibody and this may be a better choice for clinical cancer trials evaluating possible immunotherapy with monoclonal antibody.
We performed a retrospective analysis of 17 children with photosensitive seizures (PSS) who had been followed for more than 3 years (mean: 9 years). PSS were verified in all patients by simultaneous video-EEG monitoring. The seizures were precipitated by flickering stroboscopes (14 patients) or were induced by patients themselves (3) with head-nodding in front of illumination, blinking at television or close viewing of striped patterns. PSS consisted of myoclonic seizures (eight patients), generalized tonic-clonic convulsions (5), partial seizures (3) or atypical absence (1). According to the International Classification of Epileptic Syndrome, three patients were classified as having severe myoclonic epilepsy in infancy and five as having juvenile myoclonic epilepsy. The remaining nine could not be categorized as any specific epileptic syndrome. Children with age of the onset of epilepsy at 7 years or younger tended to suffer intellectual deficit in addition to intractable seizures.
The biocompatibility of the cardiopulmonary bypass (CPB) circuit, in which an oxygenator is solely heparinized, was assessed by systemic inflammatory reactions as an indicator during CPB. Fourteen patients, 11 males and 3 females, underwent coronary artery bypass surgery and were randomly divided into 2 groups of 7 patients each. For the heparin-coated oxygenator group (Group H), a heparin-coated membrane oxygenator was used in the CPB circuit, and in the control (Group C) an uncoated membrane oxygenator was employed. Systemic inflammatory reactions, such as platelet activation, prostaglandin production, complement activation, and activated granulocyte released substance, were measured prior to, during, and 6 h after CPB. The number of platelets decreased after protamine administration in both groups (14.5 +/- 4.7 x 10(4)/microliters in Group H and 13.8 +/- 8.7 x 10(4)/microliters in Group C) and returned to baseline levels in Group H while it remained decreased in Group C at 6 h after CPB. The platelet factor 4 level was significantly lower in Group H (181 +/- 40 ng/ml) than in Group C (297 +/- 131 ng/ml) after protamine administration. Thromboxane-B2 (TXB2) rose during CPB in both groups; however, there were significantly different levels of TXB2 between the 2 groups at 60 min after CPB (293 +/- 258 pg/ml in Group H versus 408 +/- 120 pg/ml in Group C) and after protamine administration (259 +/- 122 pg/ml in Group H versus 709 +/- 418 pg/ml in Group C). Plasma concentrations of granulocyte elastase were significantly lower in Group H at 30, 60 and 90 min, immediately after, and post-CPB than those of Group C.(ABSTRACT TRUNCATED AT 250 WORDS)
Specific monoclonal antibodies (MoAbs) to Actinobacillus pleuropneumoniae (APP) serotypes 1 and 2 which recognized serotype-specific antigens were produced. It was revealed that the two serotype-specific MoAbs H1-18 and H22-7 recognized O polysaccharides of the lipopolysaccharide (LPS) from APP serotypes 1 and 2, respectively, in the results of antigen analysis by means of SDS-PAGE and Western blotting. Furthermore, ddY mice immunized passively with the above type-specific MoAbs were protected against challenge infection by the homologous serotype of APP at 24 or 48 hr later. However, H1-9 and H3-2 MoAbs recognizing serotype-common protein antigens of APP did not show signs of any protective effect. These results showed that LPS from APP bacterial cells was one of the structural substances in the serotype-specific antigens, and an important component as one of the antigens protecting against the homologous serotype strain.
Apolipoprotein E (apoE) in high density lipoprotein (HDL) fraction (HDL-fr) was determined by the immunofixation method and turbidimetric immunoassay (TIA) after precipitation with phosphotungstic acid/MgCl2 in normolipidemic control subjects and patients with type IV hyperlipemia and hyper HDL-cholesterolemia. Immunofixation assay revealed two major bands of apoE in whole serum: one in the alpha-area and the other in the pre beta-area. ApoE in alpha-area (alpha-apoE) was identical to alpha-apoE in HDL-fr separated by ultracentrifugation but not to alpha-apoE in HDL-fr separated by precipitation (pHDL-fr). alpha-ApoE in pHDL-fr lacked the slower area of the band. Agarose column chromatography and gradient gel electrophoresis indicated that alpha-apoE belongs to early fractionated HDL, and that the precipitatable alpha-ApoE belongs to the higher molecular size HDL alpha-ApoE (%) estimated by immunofixation showed a strong positive correlation with apoE (%) in pHDL-fr. ApoE (%) in pHDL-fr was higher in case of hyper HDL-cholesterolemia and lower in type IV hyperlipemia than in controls, and was inversely correlated with serum triglycerides (TG) and positively with HDL-cholesterol (especially HDL2-cholesterol) in these subjects. It is suggested that the variation of apoE in pHDL-fr depends on the level of HDL2. Also, it may be suggested that apoE in pHDL-fr and precipitatable alpha-apoE belong to low and high molecular HDL2, respectively, and that apoE content in these particles is correlated with HDL2.
Tissue and plasma concentrations of felodipine, a dihydropyridine (DHP) calcium antagonist, retroinfused through the coronary venous system were studied in 27 pigs. The animals underwent 45-min myocardial ischemia followed by 4-h reperfusion. Felodipine (7 nmol/kg body weight) was administered in the coronary vein for 30 min, 5 min before reperfusion. Concentrations of felodipine in the ischemic and nonischemic myocardium and in plasma were determined by gas chromatography. In the ischemic area, felodipine concentration at start of reperfusion was 304 +/- 285, 171 +/- 160, and 52 +/- 47 nmol/kg (mean +/- SD) in the subepicardial, midmyocardial, and subendocardial layer, respectively. Corresponding concentrations in the nonischemic area were 15 +/- 13, 17 +/- 14, and 16 +/- 15 nmol/kg (p < 0.05 vs. ischemic area). Subepicardial concentration was highest at start of reperfusion, whereas concentrations in other layers peaked at the end of retroinfusion. The transmural concentration gradient of felodipine in the ischemic area decreased progressively during the reperfusion period. The nonischemic tissue concentration increased slightly during the reperfusion period. The plasma concentration was very low throughout the study (peak = 3.2 +/- 1.4 nM at 30 min). Coronary venous retroinfusion of felodipine resulted in profound accumulation of the drug, specifically in ischemic myocardium. The plasma concentration was low and did not affect systemic hemodynamics. Coronary venous retroinfusion is considered an advantageous technique for selective drug delivery.
We performed a retrospective study on 7 children in whom the auditory brainstem responses (ABR) showed absence or significantly poor formation of waves II-V. Two patients had degenerative diseases that affected the brains diffusely. In the remaining 5 patients, the symptoms consisted of action tremor (3 patients) or pyramidal signs (2 patients). There were neither clinical signs nor neuroimaging findings suggesting brainstem involvements. The evolutional changes of the ABRs had a good correlation with the clinical course. Absence or significantly poor formation of waves II-V of ABR occurs in various diseases and may not necessarily reflect severe organic brain lesions.
We report herein a rare case of primary esophageal malignant melanoma in a 49-year-old Japanese woman who presented with a 3-week history of dysphagia. Esophagogram and esophagoscopy demonstrated a polypoid tumor in the upper to mid-thoracic portion of the esophagus, and a radical subtotal esophagectomy was performed through a right thoracotomy. Histological and immunohistochemical studies proved this tumor to be a primary esophageal malignant melanoma. She received no postoperative adjuvant therapy and no signs of recurrence have been clinically observed for the 22 months since her operation.
Effects on the ischaemic and reperfused myocardium of felodipine, a vasoselective calcium blocker, retrogradely infused into the coronary vein was investigated in a porcine model. Sixteen open-chest pigs underwent 45 min of myocardial ischaemia by occlusion of the left anterior descending coronary artery followed by 4 h of reperfusion. Either felodipine (felo-retro group, 7 nmol.kg-1: n = 6) or the corresponding amount of vehicle (vehicle group: n = 5) was retroinfused over 30 min starting 5 min prior to reperfusion. In a third group, the same amount of felodipine was administered intravenously (felo-i.v. group n = 5). Myocardial regional blood flow was measured with radioactive microspheres prior to ischaemia and at different times of reperfusion. Infarction size, expressed as a percentage of the area at risk, was significantly reduced to 62 +/- 12% in the felo-retro group as compared to 86 +/- 12% (P < 0.05) and 94 +/- 5% (P < 0.05) in the vehicle and felo-i.v. group, respectively. Following an early hyperaemia, the regional blood flow decreased uniformly in the reperfused myocardium in all three groups and there were no significant differences between the groups at any period of reperfusion. In conclusion, felodipine retroinfused into the coronary vein could salvage ischaemic and reperfused myocardium without affecting the regional blood flow. The mechanism of this protective effect should be explained by factors other than an increased myocardial blood flow during reperfusion.
The effect of the vasoselective calcium antagonist felodipine on myocardial necrosis was studied in 14 anesthetized pigs subjected to 45-min occlusion of the left anterior descending coronary artery (LAD) followed by 24-h reperfusion. Felodipine (7 nmol/kg, n = 7), or the corresponding amount of vehicle diluted in 300 ml saline (n = 7) was infused in the great cardiac vein for 30 min beginning 5 min before onset of reperfusion. Regional myocardial function was measured as percentage of systolic segment shortening (%SS) by sonomicrometry. The recovery in ischemic myocardium was significantly already better among felodipine-treated animals after 30-min reperfusion (mean +/- SD = 9.1 +/- 6.1 vs. 0.1 +/- 3.2%, p < 0.05). The improved recovery in the felodipine group persisted throughout the observation period; %SS was 8.5 +/- 5.9% after 24-h reperfusion. No significant improvement was observed in the vehicle group after 24 h (%SS = 2.7 +/- 2.0%, p < 0.05). The area of the infarct was measured by triphenyl tetrazolium chloride staining. When expressed as percentage of the left ventricle, the infarct was smaller in the felodipine group (8.2 +/- 4.0%) than in the vehicle group (14.6 +/- 3.5%; p < 0.01). The corresponding values for infarct size expressed as percentage of the area at risk was 38.6 +/- 18.9% in the felodipine group and 69.8 +/- 6.7% in the vehicle group (p < 0.01). Peak plasma felodipine concentration was reached 30 min after onset of reperfusion (4.9 +/- 1.2 nM).(ABSTRACT TRUNCATED AT 250 WORDS)