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PubMed1996

Chronic inflammatory demyelinating polyneuropathy in dogs and cats.

Over the past several years, we have accumulated data on a spontaneous demyelinating peripheral neuropathy that is not well identified in domestic animals. This disorder occurs in dogs and cats of either sex and does not appear breed-related. Onset of signs is usually insidious and the course is typically chronic, sometimes relapsing, and often slowly progressive. Mature animals of any age may be affected. Clinical signs include tetraparesis, sometimes progressing to tetraplegia, stumbling gait, and hyporeflexia. Motor nerve conduction velocities are decreased. Pathologically, changes in teased single fibers from peripheral nerves are dominated by multifocal paranodal demyelination. Scattered, thinly myelinated fibers are seen on semithin sections. Ultrastructural studies reveal macrophages within myelinated fibers stripping the myelin sheaths, naked and remyelinating axons, and focal/multifocal endoneurial mononuclear cells. Indirect immunofluorescence revealed positive IgG staining in peripheral nerve myelin sheaths from two dogs. The course of the disease, clinical signs, electrophysiology, and pathology have similarities to chronic inflammatory demyelinating polyneuropathy in people.

Age Factors↗
PubMed2002

DNA gene fusion vaccines against cancer.

The ability of DNA vaccination to induce effective immune responses has been shown in a range of preclinical disease models. However, the potency of DNA vaccines must be further improved for their use in patients. DNA fusion vaccine strategies, whereby target antigens are genetically linked to immuno-enhancing molecules, are currently being explored. The ease of DNA manipulation has allowed incorporation of a wide variety of molecules able to promote antigen uptake, processing and presentation by professional antigen-presenting cells, to provide critical CD4 T-cell help and to activate more effective immune effector pathways. These strategies are particularly important for cancer vaccines to increase their immunogenicity and to overcome tolerance.

Animals↗
PubMed1991

Attenuation of intra-operative surgical stress response has no influence on post-operative degranulation of polymorphonuclear granulocytes.

Degranulation of polymorphonuclear (PMN) granulocytes, complement activation, and the endocrine metabolic response to hysterectomy were compared in two groups of patients receiving either general anaesthesia (GA group) or combined epidural analgesia and general anaesthesia (GAE group). The B-leucocyte and the cortisol responses were attenuated in the GAE group. There was no sign of complement activation. The post-operative rise in elastase-alpha-1-proteinase levels 4 h post-operatively on the first, second and third post-operative days was similar in the two groups. Plasma lactoferrin values were significantly elevated 4 h post-operatively and reached pre-operative values on Day 1 in both groups. Attenuation of the surgical stress response during uncomplicated hysterectomy did not influence the post-operative increase in proteinase activity. Mediators generated at the site of surgical trauma may account for the PMN degranulation observed after major surgery.

Adult↗
PubMed1989

[Pemphigus herpetiformis--the value of simple diagnostic measures].

Herpetiform pemphigus is a rare variety of pemphigus vulgaris. Although the final diagnosis requires thorough clinical, histological and immunological investigations, there are simple examinations which may be carried out at once (such as assessment of blister stability, negative Nikolski's sign, predominance of eosinophils, spongiotic and non-acantholytic epidermal cells in the Tzanck smear). These ad hoc findings may help the practising dermatologist to tell herpetiform pemphigus from other blistering diseases. We discuss and evaluate the various diagnostic procedures regarding herpetiform pemphigus.

Aged↗
PubMedDate not supplied

The effect of physical training on patients with rheumatoid arthritis: changes in disease activity, muscle strength and aerobic capacity. A clinically controlled minimized cross-over study.

For decades, physical training of rheumatoid arthritis (RA)-patients has been controversial, especially for patients with active disease. The aim of this study was to investigate whether RA-patients could receive graduated training without increasing the activity of the disease. In a controlled cross-over study the effect of graduated progressive training has been evaluated in 18 RA-patients with moderately active disease. The training was performed twice weekly with aerobic conditioning and strength exercises progressing to strenuous exercises over an 8-week period. The design was a crossover project with two groups obtained by minimisation. After training the patients had significantly fewer swollen joints than before. Training of the muscles acting over the swollen joints resulted in more than a 35% decrease in the number of swollen joints. The hemoglobin level increased significantly after the training period. The erythrocyte sedimentation rate, the complement factor C3d, and the number of sore joints remained unchanged. A decrease in the need for medicine was non-significant. From this study it appears that RA-patients with some activity are trainable without aggravating the disease, even in the chronically swollen joints. The rheumatoid arthritis activity decreased with fewer swollen joints and higher hemoglobin level after training.

Adult↗
PubMedDate not supplied

Prekallikrein activation in the adult respiratory distress syndrome.

Prekallikrein is the zymogen form of plasma kallikrein, a proteolytic enzyme of the contact system of blood coagulation, fibrinolysis and kinin formation. To assess whether prekallikrein was activated in the adult respiratory distress syndrome (ARDS), we examined plasma samples from 12 critically ill patients including five individuals with ARDS. Using the ratio between functional prekallikrein and prekallikrein-kallikrein antigen as an index for prekallikrein activation, we found that prekallikrein was extensively activated in patients with ARDS, while this was significantly less in the case of critically ill patients without ARDS. Following activation of prekallikrein in plasma, kallikrein reacts with its substrates and with protease inhibitors, among which the alpha 2-glycoprotein C1-inhibitor. Thus, we examined whether C1-inhibitor of critically ill individuals was modified in a way suggesting that it had reacted with kallikrein. Such a modification was found in the five patients with ARDS, while it was not detectable in the seven patients without ARDS. This observation further confirmed the activation of prekallikrein in patients with ARDS. We suggest that plasma kallikrein-mediated reactions, which include bradykinin release and neutrophil activation, may contribute to the pathogenesis of ARDS.

Adolescent↗
PubMed1983

Heterogeneity in electrophoretic mobility of C3-derived molecules expressing D but not C-epitopes following in vivo activation of the complement system.

Four different populations of C3-derived molecules expressing D but not C epitopes were identified following in vivo activation of the complement system. The four molecular forms, differing in electrophoretic migration velocity, were assigned the nos. 1, 2, 3 and 4 after decreasing electrophoretic mobility. Analysis of the time-dependent changes in the relative concentration of the different molecular forms demonstrated an increase in the plasma concentration of population 4 and a decrease of populations 2 and 3, whereas form 1 remained rather constant after acute activation of the complement system.

Animals↗
PubMed1984

[Immunologic findings in juvenile Mediterranean kala-azar].

The course of immunological parameters in a 2 year old patient with mediterranean kala-azar is reported. Plasma-fibronectin was reduced to 33% of the normal value at the time of diagnosis. When the clinical symptoms of the disease were most severe, a marked activation of complement without demonstrable circulating immune complexes was observed. Therapy with sodium-stibogluconate lead to improvement of the child's condition, normalization of complement reaction and fibronectin levels, and detection of circulating immune complexes. The activity of the disease seems to be well indicated by the level of C-reactive protein and the complement cleavage product C3 d. Incubation of living Leishmania donovani with normal human serum leads to activation of complement in vitro.

Antibodies↗
PubMed1983

Abnormal leucocyte locomotion induced by haemodialysis membranes. A clue to dialysis leucopenia.

In a study on polymorphonuclear leucocyte (PMN) chemotaxis and random locomotion carried out on 16 patients undergoing haemodialysis and on the same functions in normal PMN which were separated from plasma and subjected to laboratory haemodialysis, it was shown that random PMN locomotion is reduced and that there is a concomitant fall in the leucocyte count in haemodialyzed patients. The laboratory haemodialysis demonstrated that serum factors were not responsible for the PMN dysfunction, which lasted for the entire period of the procedure. The changes were observed only when cellulose membranes were used, and not when haemodialysis was performed with polyacrilonitrile membranes. The reduction in random PMN locomotion may be involved in the genesis of dialysis leucopenia, as well as in the increased susceptibility of uremic patients to infections.

Cell Movement↗
PubMed1993

The third component of complement: new functions for an old friend.

The present review has evaluated four biologic processes in which the participation of C3 as a primary mediator deserves more extensive investigation. These novel functions of C3 derive in part from the biochemistry ascribable to a thiolester-containing protein and are underscored by its remarkably high concentration in plasma and widespread presence in tissues. Such physiologic characteristics argue that we have only begun to understand the functions of this most versatile complement protein. The availability of full-length cDNA and the ability to manipulate the C3 gene in tissue culture or embryonic stem cells should help to illuminate the pluripotent nature of this fascinating protein.

Amino Acid Sequence↗
PubMed1987

Identification of a spontaneously shed fragment of B cell complement receptor type two (CR2) containing the C3d-binding site.

CR2 is a 140-kilodalton glycoprotein expressed on B lymphocytes which binds to both C3d and Epstein-Barr virus (EBV). The present study identified a 72-kilodalton C3d-binding protein (gp72) in the spent culture media of Raji B lymphoblastoid cells as a spontaneously shed fragment of the 140-kilodalton CR2 molecule. Both polyclonal and monoclonal antibodies (AB) were used in several assay systems to detect antigenic determinants shared between the gp72 fragment and CR2. Rabbit antibodies to either intact CR2 or gp72 blocked C3d receptor activity, and this inhibitory activity was removed by absorption of anti-CR2 with purified gp72.OKB7, a monoclonal anti-CR2 AB that blocks both C3d and EBV binding to CR2, reacted specifically with both CR2 and gp72, whereas both anti-B2 and HB-5 monoclonal anti-CR2 AB, that block neither of these receptor sites, were unreactive with gp72. The data suggested that the gp72 fragment was not present as such in intact cells, but rather was a product of cells generated by proteolysis of CR2. Thus, intrinsically labeled gp72 was isolated from Raji cell media by affinity chromatography on OKB7-Sepharose, but only intact CR2 was isolated from the Raji cell fraction solubilized in the presence of protease inhibitors. Several lines of evidence suggested that gp72 was not a second type of C3d receptor that was distinct from CR2. First, Raji cells expressed nearly identical amounts of OKB7 and HB-5 epitopes when analyzed by flow cytometry or radioimmune assay, excluding the possibility that B cells expressed OKB7 antigens in both CR2 and a distinct HB-5-negative C3d receptor. Second, all Raji cell surface C3d receptor activity was associated with HB-5-reactive CR2 molecules. We conclude that gp72 represents a spontaneously shed proteolytic fragment of CR2 that contains the C3d-binding site and the closely associated OKB7 epitope.

B-Lymphocytes↗
PubMed2001

Kinetic analysis of the interactions of complement receptor 2 (CR2, CD21) with its ligands C3d, iC3b, and the EBV glycoprotein gp350/220.

The molecular mechanisms involved in the interaction of complement receptor 2 (CR2) with its natural ligands iC3b and C3d are still not well understood. In addition, studies regarding the binding site(s) of the receptor on C3 as well as the affinities of the C3 fragments for CR2 have produced contradictory results. In the present study, we have used surface plasmon resonance technology to study the interaction of CR2 with its ligands C3d, iC3b, and the EBV surface glycoprotein gp350/220. We measured the kinetics of binding of the receptor to its ligands, examined the influence of ionic contacts on these interactions, and assessed whether immobilized and soluble iC3b bound with similar kinetics to CR2. Our results indicate that 1) gp350 binding to CR2 follows a simple 1:1 interaction, whereas that of the C3 fragments is more complex and involves more than one intramolecular component; 2) kinetic differences exist between the binding of C3d and iC3b to CR2, which may be due to an additional binding site found on the C3c region of iC3b; and 3) iC3b binds to CR2 with different kinetics, depending on whether the iC3b is in solution or immobilized on the surface. These findings suggest that binding of CR2 to iC3b and C3d is more complex than previously thought.

Alanine↗
PubMed1987

Immune complexes and complement activation following rupture of intracranial saccular aneurysms.

Circulating immune complexes (CIC) and complement activation (plasma C3d levels) were monitored during a 2-week period in patients with ruptured cerebral aneurysms and also in patients with cerebral hematoma unrelated to saccular aneurysms. Thirteen of 18 aneurysm patients were found to have CIC on admission as compared to three of 21 healthy blood donors (p less than 0.001). The presence of CIC in aneurysm patients was associated with a poor prognosis. Eight of nine patients who developed angiographic vasospasm had CIC on admission compared with one of four without vasospasm. Patients with vasospasm showed a twofold increase in plasma C3d levels at the time when the spasm occurred, whereas no significant changes in the C3d concentration could be demonstrated in aneurysm patients without spasm or in patients with hematoma unrelated to aneurysm rupture. These findings suggest that immunological processes involving complement-activating immune complexes are involved in the pathogenesis of cerebral vasospasm following rupture of saccular aneurysms.

Adult↗