[Deviations in glycoprotein contents in malignant ascitic fluid and pleural effusions].
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Biomedical subjects
Publications and source records attributed to H Ohtani.
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The protein contents and binding modes of immunoglobulin-amylase complexes were investigated. Amylase staining after immunoelectrophoresis permitted identification of IgA-lambda type in three cases, IgA-kappa type in two cases and IgG-kappa type in one case. The precipitin line of Fab fragment of IgA in four patient's sera after papain digestion was found to have amylase activity. Sucrose density gradient ultracentrifugation studies showed that these complexes were divided into three groups: Group I complexes were dissociated in acid pH, and at pH 7.0 the immunoglobulins, which were isolated at the acid pH, became rebound to serum amylase; Group II complexes were dissociated by acidification, but did not reform at pH 7.0; Group III complexes were unaffected by acidification. We suggest that the immunoglobulin-amylase complexes belonging to groups I and II result from an antigen-antibody reaction. Precipitin curves resulting from the addition of increasing quantities of the patient's serum containing 9 S or 11 S immunoglobulin-amylase complexes to specific antisera revealed that these complexes contained not only monoclonal IgA, but also alpha-1-antitrypsin (alpha 1 AT) and albumin. These IgA complexes could have bound non-specifically to alpha 1 AT and albumin, forming the larger macroamylase complexes.
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A 52 years old female with suspected malignancy was hospitalized because of fever and lymph node swelling. In spite of lymph node biopsy, bone marrow aspiration, blood culture and other diagnostic procedures, no clue to definite diagnosis was obtained. During the course of hospitalization, abscesses with fistulae appeared and tubercle bacilli were demonstrated in the pus from a subcutaneous abscess. Thus, the diagnosis of tuberculosis was established. Finally the patient died of massive bleeding as a result of perforation into thoracic aorta of the zone of necrosis of esophageal wall. It is to be emphasized that tuberculosis should be kept in the list of differential diagnosis of continuous fever.
Cardiac beta-adrenoceptors were studied in membrane fractions from spontaneously hypertensive rats (SHR) and rats with two-kidney, one clip hypertension (2K, 1C HT), using radioligand binding method. beta-Adrenoceptor concentration measured by [3H]-dihydroalprenolol (DHA) binding was significantly lower in cardiac membranes from two months old SHR than those from Wistar-Kyoto rats (WKY) (38.2 +/- 2.6 vs 45.1 +/- 1.8 fmol/mg protein, means +/- SEM, p less than 0.05). Cardiac membranes from 2K, 1C HT rats had also a lower concentration of beta-adrenoceptors than those from the sham-operated control rats at a week after operation (30.9 +/- 2.2 vs 47.8 +/- 1.6 fmol/mg protein, p less than 0.01). But receptor affinity remained unchanged. These reduced concentrations of beta-adrenoceptors were restored to control levels at 12 months old in SHR and at 6 weeks after operation in 2K, 1C HT rats, although age-dependent decrease in beta-adrenoceptor was observed. The decrease in beta-adrenoceptor was associated with increase in plasma noradrenaline levels during the earlier stages of hypertension. But there is no correlation between beta-adrenoceptor concentrations and plasma noradrenaline levels in the chronic stages of hypertension. No significant difference was found in activities of 5'-nucleotidase, which is a marker enzyme of cell membrane, in membrane fractions between the hypertensive hearts and the controls, suggesting that the cardiac hypertrophy is not a determinant factor for change in beta-adrenoceptor. The observed decrease in beta-adrenoceptor concentration may reflect an increase in sympathetic nerve activity during development of hypertension. In the chronic stages of hypertension, additional factors may be involved in the restoration of beta-adrenoceptors.
An antigenic heterogeneity among IgD myeloma proteins was tested by immunoelectrophoresis and double immunodiffusion in agar with four kinds of anti-delta(Fc) antisera produced by immunization with isolated Fc fragments of IgD myeloma proteins. According to antigenicity of the Fc fragment, IgD myeloma proteins were divided into two different groups. Anti-delta(Fc)-T1 (S.T.) antiserum, absorbed with te Y.S. myeloma protein or serum, either gave a faint precipitin line or failed to react against the isolated IgD myeloma proteins or sera. With the papain-digested IgD myeloma proteins and sera, anti-delta(Fc)-T1 antiserum either gave heavy precipitin lines or failed to react. Of twelve papain-digested sera containing IgD myeloma proteins tested, nine (75%) showed positive precipitin lines using anti-delta(Fc)-T1 antiserum. No relationship was found between the two groups of myeloma proteins with respect to IgD levels. SDS polyacrylamide gel electrophoresis of the IgD myeloma proteins (S.T. and Y.S.) showed no difference in the molecular weights of the whole myeloma proteins, and their light and heavy chains. Polyacrylamide gel electrophoresis of the IgD myeloma proteins (S.T. and Y.S.), after treatment with papain, revealed almost the same patterns.
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In order to evaluate the role of the renin-angiotensin system and the sympathetic nervous system in the maintenance of blood pressure in the sodium-depleted state, the changes of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and plasma noradrenaline (PNA) were examined in unanesthetized dogs after the administration of furosemide. Furthermore, the role of the renin-angiotensin system in the increased sympathetic nerve activity induced by furosemide was assessed by using Sar1-Ile8-angiotensin II, an angiotensin II antagonist. When a dose of 0.8 mg/kg of furosemide was injected intravenously, 3 times every 15 minutes, PRA and PNA were significantly increased with a concomitant increase in PAC. Sar1-Ile8-angiotensin II induced a significant increase in PAC and a slight increase in PRA, while no changes were found in PNA and the mean blood pressure. The increase in PNA induced by furosemide was inhibited dose-dependently by Sar1-Ile8-angiotensin II, through PRA and PAC were further increased. There results suggest that an administration of furosemide induced the increase in PNA and the increase in PNA by furosemide might by mediated by the renin-angiotensin system.
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Plasma catecholamine levels have been used experiemtally and clinically as the indices of the sympathetic nerve activity. We measured plasma catecholamines using high pressure liquid chromatography in rats to assess the significance of plasma catecholamines as an index of the sympathetic nerve activity and its role in hypertension. Pentobarbital anesthesia depressed plasma catecholamine levels, especially plasma adrenaline. Sodium loading for 5 weeks suppressed plasma noradrenaline, while administration of furosemide (1 mg/kg) produced the elevation of plasma noradrenaline. Experimental hypertension, one-kidney and two-kidney types of Goldblatt hypertension and DOCA-salt hypertension, raised plasma noradrenalines both in acute and chronic phases. The infusion of pressor doses of angiotensin II suppressed plasma noradrenaline by the reflex mechanism. Sar1, Ile8-angiotensin II and SQ 14,225 did not suppress plasma cathecholamine elevation due to hemorrhage. L-Hydroxyldopamine produced elevation of plasma catecholamines in experimental nypertension and controls in rats. After adrenal demedullation, plasma noradrenaline was decreased by the administration of 6-hydroxy-dopamine. Acute reduction of circulating blood volume and blood pressure fall produced the elevation of plasma catecholamine, especially plasma adrenaline. In rats, the adrenal medulla plays an important role in the regulation of blood pressure.
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Myofibroblasts were observed in the stroma of breast tumors in all cases examined by electron microscopy; 1 intraductal papillomatosis, 1 papillary carcinoma and 7 infiltrating duct carcinomas. The tubule- or duct-like structure in the tumor tissue were frequently surrounded by myofibroblasts which corresponded to delimiting fibroblasts in the normal breast tissue. In infiltrating duct carcinomas without tubule-like structures, myofibroblasts occurred dispersely in the stroma and they might correspond to fibroblasts in normal connective tissue. A possible role of these myofibroblasts as mesenchymal cells activated in a tumorous condition was discussed.
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