Biomedical subjects
Publications and source records attributed to M Okamura.
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The presence of a specific type of cell, highly expressing difucosyl type 2 chain (dimeric Lex; FH-4 antigen), was found in the epiphyseal bone marrow cells of affected joints from patients with active severe rheumatoid arthritis (RA). The antigen was defined by monoclonal antibody FH-4 which was previously found to be directed to the oncofetal marker. The FH-4(+) cell population was identified as myeloid cell lineage with usual morphology specifically found in bone marrow of patients with severe RA, but is virtually absent in the same cell fraction of patients with osteoarthritis, infectious arthritis, and from normal adult subjects.
To assess the interaction and interdependence of left and right ventricular function, ECG-gated radionuclide angiocardiography was performed immediately after cardiac catheterization during right atrial pacing for 11 patients with old myocardial infarction (MI), two with non-obstructive hypertrophic cardiomyopathy, one with aortic stenosis (AS), two with pulmonary infarction (PI), and one with neurocirculatory asthenia (NCA). Absolute left ventricular (LV) volume curves were obtained by the count-based method with attenuation factor corrections. Biventricular pressure and volume curves were digitized and synchronized to end-diastole, and pressure-volume (P-V) loops were constructed throughout a cardiac cycle. The stroke work index (SWI), the work index per min (WI/M) and the contractility index (CNTI) were calculated from the P-V loops. In a patient with NCA, LV end-diastolic volume decreased during rapid pacing, but no significant change in the LV end-systolic P-V relation was recognized. However, the entire right ventricular (RV) P-V loop was shifted toward the left during rapid pacing. In a patient with AS, the LV P-V loop was markedly enlarged and every parameter of LV function was much greater than that of the right ventricle due to increased LV afterload. The areas of RV P-V loops in two patients with PI were larger than those of other patients, because RV pressure was relatively high, and RV volume was increased. It is suggested that RV pressure and volume overloads prevail in patients with PI. In four MI patients with three vessel disease and having collateral circulation, the LV end-systolic P-V relationship was shifted toward the lower right, and every parameter (SWI, WI/M, CNTI) of LV function decreased by rapid pacing. Myocardial ischemia may be induced by rapid pacing stress, causing decreased LV contractility. It was concluded that the P-V loops obtained by RNA and catheterization are clinically useful for estimating the interaction and interdependence between right and left ventricular hemodynamics.
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In order to define the interaction domain on Rhodobacter sphaeroides cytochrome c2 for the photosynthetic reaction center, positively charged lysine amino groups on cytochrome c2 were modified to form negatively charged (carboxydinitrophenyl)- (CDNP-) lysines. The reaction mixture was separated into several different fractions by ion-exchange chromatography on (carboxymethyl)cellulose. Tryptic digests of these fractions were analyzed by reverse-phase peptide mapping to determine the lysines that had been modified. Fraction A was found to consist of a mixture of singly labeled derivatives modified at lysine-35, -88, -95, -97, and -105 and several other unidentified lysines comprising 32% of the total. Although it was not possible to resolve these derivatives, all of the identified lysines are located on the front surface of cytochrome c2 near the heme crevice. The second-order rate constant for the reaction of native cytochrome c2 with reaction centers was 2.0 X 10(8) M-1 s-1, while that for fraction A was 20-fold less, 1.0 X 10(7) M-1 s-1. This suggests that lysines surrounding the heme crevice of cytochrome c2 are involved in electrostatic interactions with carboxylate groups at the binding site of the reaction center. The reaction rates of horse heart cytochrome c derivatives modified at single lysine amino groups with trifluoroacetyl or trifluoromethylphenylcarbamoyl were also measured. Modification of lysine-8, -13, -27, -72, -79, and -87 surrounding the heme crevice significantly lowered the rate of reaction, while modification of lysines in other regions had no effect. This indicates that the reaction of horse heart cytochrome c with the reaction center also involves the heme crevice domain.
We performed immunopathologic studies of the pericarditis present in a patient with mixed connective tissue disease. A large number of nuclear RNP (nRNP) immune complexes (ICs) were found in the pericardial fluid, but not in the serum. The pericardial small vessels had no deposits of IgG. These results suggest that locally formed nRNP ICs were closely associated with the pathogenesis of pericarditis in this patient.
We measured U1-RNP: anti-U1-RNP immune complexes (U1-RNP ICs) in patients with mixed connective tissue disease (MCTD) and systemic lupus erythematosus (SLE) to examine the clinical significance of circulating U1-RNP ICs. The level of U1-RNP ICs in 11 patients with MCTD was significantly higher than that in 22 normal subjects and there was a close correlation between the level of U1-RNP ICs and the clinical disease activity index of MCTD. In contrast, the level of U1-RNP ICs in 31 patients with SLE was not significantly higher than that in normal subjects and that was not correlated with the clinical disease activity index of SLE or the renal histologic activity index of lupus nephritis. We conclude that U1-RNP ICs are present in sera of patients with MCTD and SLE, and that the level of U1-RNP ICs may be closely associated with clinical disease activity in patients with MCTD.
Twenty-nine of the 129 patients with RP seen at the Mayo Clinic between 1943 and 1984 had renal involvement. These patients were older, had arthritis and extrarenal vasculitis more frequently, and had a significantly worse survival rate than those without renal involvement. Renal biopsies were obtained in 11 of these 29 patients. The predominant lesions were mild mesangial expansion and cell proliferation, and segmental necrotizing glomerulonephritis with crescents. Small amounts of electron-dense deposits, predominantly mesangial, were noted on electron microscopy. Immunofluorescence revealed faint deposition of C3 and/or IgG or IgM, predominantly in the mesangium. Autopsies were obtained in 13 of the 47 patients who had died. Information regarding the renal pathology was available in 10 of these 13 autopsies. At the time of the initial evaluation at the Mayo Clinic, 6 of these 10 patients had evidence of renal involvement. At autopsy, none of these 10 patients had evidence of active renal vasculitis or segmental necrotizing glomerulonephritis, but 8 of the 10 patients exhibited variable degrees of vascular and glomerular sclerosis, segmental mesangial proliferation, tubular loss, and interstitial lymphocytic infiltrates. These observations expand the limited information available in the literature, which is based on 11 previously published case reports of renal involvement in RP. In only a few of our patients and previously reported patients were the manifestations of the disease limited to the systems characteristically involved in pure RP. The frequent coexistence of other autoimmune and connective tissue diseases supports the role of immune mechanisms in the pathogenesis of this syndrome. Deposition of immune complexes is likely to play a role in the pathogenesis of the glomerular lesions associated with RP. Administration of corticosteroids alone is sufficient to induce a complete remission in some cases, while in others the addition of a cytotoxic agent is necessary to control the activity of the disease or to spare corticosteroid side effects and maintain a remission. Immunosuppression-related infectious complications and undetected relapses after discontinuation of immunosuppressive therapy are largely responsible for the morbidity and mortality observed in these patients.
Serum levels of alpha (alpha) and gamma (gamma)-interferons (IFN) were measured in 30 patients with untreated systemic lupus erythematosus (SLE) with a solid-phase, sandwich immunoradiometric assay using specific monoclonal antibodies. The serum levels of alpha-IFN were higher in patients with SLE than in normal subjects, and correlated with the clinical activity index (rs = 0.60, P less than 0.01), but not with renal histological activity. The serum level of alpha-IFN correlated with the serum level of immune complexes (r = 0.46, P less than 0.01) and the number of peripheral lymphocytes inversely (r = -0.49, P less than 0.01). Serum gamma-IFN levels were also higher in patients with SLE than in control subjects but no correlations were found between it and either clinical activity, renal histological activity or various laboratory parameters. Serum levels of both alpha-IFN and gamma-IFN were higher in SLE patients with erythema than in those without. These results suggested that serum levels of alpha-IFN were more closely related to clinical activity of SLE than were those of gamma-IFN, and that peripheral lymphocytes were probably not the source of the elevated serum IFN-alpha concentration.
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In an attempt to find a reliable method to assess fever in patients with systemic lupus erythematosus (SLE), a multifactorial analysis was applied to the routine laboratory examinations, including white blood cell count (WBC) and serum globulin fraction concentrations. During 74 febrile episodes, 49 SLE patients showed increased disease activity and the remaining 25 febrile episodes were due to intercurrent infection. The two different groups of fever episodes were clearly separated by a principal component analysis using five variables from the routine laboratory tests, including WBC, serum alpha-1, alpha-2, beta, and gamma globulins. Discriminant analysis showed that 95% of 74 febrile episodes could be correctly classified as to the cause of fever when a combination of WBC and alpha-2 globulin level was used as variables. A simple discriminant formula which we calculated was considered to be of practical use for the differentiation of the two clinical entities.
The relationship between the renal pathologic activity of systemic lupus erythematosus (SLE) and serum lactate dehydrogenase (LDH) was examined in 28 patients with active SLE involving only the kidney. Serum levels of total LDH, LDH1, and LDH2 were significantly higher in the patients with diffuse proliferative lupus nephritis (World Health Organization class IV) than in those with milder renal disease (classes I through III and V). Total LDH levels showed good correlations with the activity index and the total pathologic score of the renal pathologic scoring system, and with the glomerular hypercellularity and overall deposits. The elevated level of LDH was mainly due to elevated levels of its isozymes LDH1 and LDH2. These results suggest that the elevation of serum LDH levels in patients with SLE reflects the renal pathologic changes due to lupus nephritis.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
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A girl had frequent ureteric infections from the age of three years onwards, passed 2.8-dihydroxyadenine ureteric stones and was in renal failure. At six years of age she was without symptoms, but even during this stage characteristic round crystals of 2,8-dihydroxyadenine were found in the urinary sediment. Activity of adenine-phosphoribosyltransferase (A-PRTase) in red blood cells was markedly diminished to 4.5% of normal values. Crystal excretion was inhibited by allopurinol. These findings suggest that it may be possible to detect cases of considerable A-PRTase deficiency and thus prevent the development of stones and renal insufficiency.