Biomedical subjects
Publications and source records attributed to P Rossmann.
A clinical-morphological study in 134 recipients of first renal allografts (15 related and 119 non-related) was performed with the aim to establish prognosis of different types of rejection nephropathy. Following order of prognosis (from the worst to the best) was found: necrotic lesion, early vascular lesion, late vascular lesion, late interstitial lesion. Several factors of importance were discussed.
Thirty-one patients with chronic mesangial-proliferative glomerulonephritis, histologically and clinically active, confirmed on biopsy, were included in a randomized therapeutic experiment. Of the total, 15 were treated by a combined prednisone, azathioprine, cyclophosphamide, Heparoid Spofa forte ling., Heparin retard Spofa and dipyridamole therapy. The control group comprised 16 untreated patients. One year later, a similar progression of glomerulonephritis was seen in both groups. Both treated and control patients exhibited a slight, but significant, decrease in proteinuria and a slow fall in the glomerular filtration rate. Despite a short period of follow-up, we succeeded to demonstrate, convincingly enough, that combined cyclophosphamide, azathioprine, prednisone, Heparoid ling., Heparin retard Spofa and dipyridamole therapy should not be indicated in chronic mesangial-proliferative glomerulonephritis.
The third component of the pig complement system (C3) was isolated in hemolytically active form and characterized. The C3 component is a beta-globulin with the molecular weight of 191,000 and is composed of 2 non-identical polypeptide chains of Mr 112,000 and 74,000. The isolated C3 can be used for the detection of the C3b receptor on the membranes of heterologous peritoneal macrophages.
In two patients with glomerulonephritis (GN) IgG and C 3 were visualized in ultrastructure by means of HRP-conjugated antisera. The first patient had an acute postinfectious extra-intracapillary GN lasting for about two months with granular fluorescence of anti-IgG, -C 3, and -C 1q. Electron microscopy revealed widespread endothelial defects, a well-pronounced polymorphonuclear stasis, and typical perimembranous "humps". These deposits reacted with HRP-anti-C 3 but the ultrastructural proof of IgG was negative. A weak and sporadic reaction of both these conjugates was seen in the swollen mesangial matrix while intraluminal plugs of coagulated plasma and extracapillary exudates yielded a dense coarse reaction product. In the second patient (allograft, three years after transplantation) the membranous and proliferative probably recurrent GN with nephrotic syndrome showed massive perimembranous deposits in the late involution stage. Granular fluorescence of the main Ig classes and of C 3 was sporadic or absent. In the ultrastructural immunoenzyme assay, too, the residues of deposits failed to react with HRP-anti-IgG or -C 3 and the mesangial matrix harboured only sporadic foci of faint positivity; however, dense product was again seen in capillary plasmatic "microthrombi". The discrepancy between immunofluorescence microscopy and immunoenzyme histochemistry, noted also by others in experimental glomerulopathies, may reflect the instability and dynamic properties of immune deposits with an early loss of antibody reactivity and a more protracted though not persistent local activation of complement. In light microscopy, fluorescent granules may correspond not only to the sites of immune deposition but also to accidental intracapillary plasma precipitates.
Rabbit anti-swine-glomerular-immunoglobulin (AG Ig) was administered in utero to 14 pig foetuses 40-103 d post-conception. In nine foetuses AG Ig was injected into the umbilical vein and 60 min later kidneys and other organs were collected. In five others, AG Ig was injected via the intact uterine wall, and the tissues were examined after further 11 or 35 d of uninterrupted pregnancy. No signs of glomerular inflammation were found by light microscopy. In electron microscopy, especially in younger foetuses, focal endothelial defects and subendothelial granular "deposits" were seen in deep glomeruli, but they appeared also in control foetuses of corresponding age. Immunofluorescence microscopy showed a strong diffuse linear positivity of the swine-anti-rabbit-Ig conjugate in the capillary loops of deep juxtamedullary glomeruli irrespective of foetal age and dose of antigen injected. Immature glomeruli and S-bodies yielded a poor to negative staining. Proof of swine Ig was negative in all kidneys as well as the test for rabbit and swine Ig in various other organs. Traces of rabbit Ig were only detected in disseminated platelet aggregates of myocardium in the early post-injection period. Ultrastructural enzyme-antibody assay visualized AG Ig throughout all three layers of glomerular capillary basement membrane, and in the early period signs of transendothelial passage and escape of unbound rabbit Ig molecules were evident. The mesangial matrix, cell membranes, and extraglomerular basement membranes remained all negative. As follows, xenogeneic antiglomerular antibodies specifically react with target structures even at the end of the first third of intrauterine life, afflicted being only the deep mature polyanion-coated glomeruli. The foetal immune system is incapable of an adequate autologous antibody response, and we have failed to find even an early glomerular lesion comparable with the postnatal anti-basement-membrane glomerulonephritis.
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C3b receptors were visualized on the cell membranes of stimulated mouse peritoneal macrophages (Mø) by the incubation with cross-reacting swine C3 with proof of this latter by FITC- or HRP-conjugated rabbit anti-swine-C3 antibody. The FITC-conjugate produced a granular and spotty fluorescence. In ultrastructure, the HRP-conjugate revealed minute dense areas of reaction product, whose modest numbers were seen in both aldehyde-prefixed and non-prefixed cell samples.
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A retrospective study in 20 seronegative and 61 seropositive (complement fixation) first cadaver donor graft recipients brought evidence that in cytomegaly, not the infection alone, but curtailment of azathioprine shortly after transplantation (or summation of both) may result in rejection and impaired graft survival. Preliminary data (accumulation of 125I-labelled fibrinogen in two and morphology of the graft in two other patients) showed that depression of graft function in cytomegaly is not necessarily due to rejection.
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Thymosin 5 was traced in calf and mouse thymuses by fluorochrome-labelled rabbit anti-calf thymosin. The presence of thymosin 5 or its individual components was found 1. in groups of cortical epithelial cells in calf thymuses and in single cortical epithelial cells in mouse thymuses. 2. In some marginal (blastema) cells of the thymus cortex of calves and 14-day-old mice. 3. In perivascular epithelial cells of the calf thymus. 4. In occasional medullary epithelial cells of the calf and mouse thymus. In all cases there was a marked alternation of entirely negative and positive cell-containing thymic lobuli. In 4 of 13 cases comparatively strong positivity was found in tightyly arranged epithelial cells in an individual acinus in the dysgenetic thymus of nude mice, the positive cases being concentrated among the youngest mice studied.
Antiserum against partially purified calf thymosin (5) was used for the localisation of this complex material in human thymus for comparison with calf thymi. Antithymosine IgG produced with human thymosin 5 by comparative immunoelectrophoresis one line identical with one of the lines of calf thymosin 5. Immunofluorescent evidence suggests the presence of the material in question, which also contains a biologically active principle, mainly in the epithelial cells of the thymus cortex. The contents of the traced material, however, fluctuates substantially between individual thymic lobules.
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During gold therapy a patient with rheumatoid arthritis developed nephrotic syndrome, and a patient with juvenile chronic arthritis proteinuria. Electron microscopic examination of bioptic specimens of the kidneys revealed in both instances membranous glomerulonephritis with typical epimembranous deposits and intracellular gold inclusions. Immunofluorescent examination performed only in the second patient revealed that the deposits in the wall of the glomerular capillaries contain IgG which suggests an immunocomplex mechanism of the development of the renal disease, induced very probably by chrysotherapy.