PubMed Health⌕ Search

Biomedical subjects

A Cristea

Publications and source records attributed to A Cristea.

At least 19 recordsLinked to original sources
PubMed1995

Clinical evaluation of antineutrophil cytoplasmic autoantibodies in ANCA-associated diseases.

Antineutrophil cytoplasmic autoantibodies have been performed in 110 patients referred to the laboratory as a presumptive systemic vasculitis, idiopathic crescentic glomerulonephritis, inflammatory bowel disease or SLE with vascular manifestation. 25 patients were found to be positive with c-, or p-ANCA patterns in indirect immunofluorescent test. We describe several cases in which histological confirmation is not available, an early consideration of a positive ANCA test may offer a reliable diagnosis and effective therapeutic handling, while the cases when the test was not considered, the occurence of relapse was inevitable.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1994

Homozygous or compound heterozygous qualitative antithrombin III deficiency.

A male patient of 24 years who had experienced thrombotic episodes since the age of 15 displayed an unusually low antithrombin III (AT III) activity measured as heparin cofactor (13% of the normal), while a similarly decreased value (16% of normal) was found in a 26 year old brother who had suffered from thrombotic events since the age of 12 years. AT III heparin cofactor activities were close to 50% of normal in the father, mother, another brother and a sister, none of whom had experienced thrombotic episodes. Since all available members of the family, including the patient, displayed near normal AT III antigen levels (73-85%) normal total progressive antithrombin activities (92-110%) as assessed by the thrombin agarose diffusion technique and normal total progressive anti-Xa activities, the propositus and his brother could be considered to be homozygotes or compound heterozygotes for a qualitative familial AT III deficiency probably caused by an abnormality of the heparin binding site. Molecular techniques would be required to elucidate the precise mutation giving rise to the deficiency.

Adolescent↗
PubMed1988

Implications of endogenous opioids in the informational aggression syndrome.

Starting from the observation that the informational aggression syndrome (IAS) in animals resembles the opioid abstinence syndrome, the authors studied the implications of endogenous opioids in experimentally induced IAS. They induced an IAS in rats, by means of specific sound signals and examined the animals' behaviour by a test used in the study of the opioid abstinence syndrome, as well as their reaction to noxious stimuli by means of thermal stimulation. The results show the implications of endogenous opioids in the IAS. During the first stage, a larger amount of endogenous opioids is secreted; specific symptoms of the opioid abstinence syndrome develop during the second stage. These symptoms can be prevented with clonidine, that has been used in the treatment of the exogenous opioid abstinence syndrome.

Aggression↗
PubMed1986

Immunoelectron-microscopic localization of the terminal C5b-9 complement complex in human atherosclerotic fibrous plaque.

The assembly of the terminal C5b-9 complement complex is a prime mechanism of complement-induced membrane damage followed by inflammatory response mediation and subsequent extensive tissue damage. In the assembly process the terminal complement components expose neoantigenic determinants which can be recognized by specific antibodies. Using such a specific antibody, affinity-purified rabbit IgG and by means of immunoelectron microscopy, the C5b-9 neoantigens were localized on the structures of the human fibrous plaque from 3 iliac and 3 femoral arteries obtained at surgery. The immunoelectron-dense deposits were localized on the cell debris, enmeshed in the connective tissue matrix, consisting of irregular particles that frequently had the shape and size of intracellular organelles or vesicles with concentric osmiophilic lamellae. No deposits could be found on the intact cells, on the connective tissue matrix or on cholesterol and lipid deposits. The presence of C5b-9 neoantigens deposits in the fibrous plaques frequently associated with other immune-related proteins indicates that complement activation has occurred in situ and could be related to the chronic progression of the atherosclerotic lesion.

Aged↗
PubMed1986

Characterization of circulating immune complexes in heart disease.

Circulating immune complexes (CIC) were characterized for the content in IgG, IgA, IgM, C3 and C4 in patients with heart disease. The levels of IgG, IgM and C4 in PEG-precipitates of patients' sera were significantly higher than those found in controls, and the precipitation profile was similar to that of rheumatoid arthritis patients. Differences were observed in the composition of CIC: IgM was highest in association with myocarditis, and C3 predominated in cases of valvular disease. Complex-bound C4 was significantly higher in patients with myocardial infarction which developed pericarditis either early or late in the evolution of the disorder. Antimyocardial antibodies could be detected in sera and in corresponding PEG-precipitates. The bulk of the data suggests that CIC might play a pathogenetic role in various heart diseases.

Adult↗
PubMed1986

Immunohistochemical detection of the terminal C5b-9 complement complex in children with glomerular diseases.

Kidney biopsies were obtained in 28 children with glomerular diseases and studied using indirect immunofluorescence and immunoperoxidase for IgG, IgA, IgM, C1q, C3c, C4, fibrinogen and the neoantigens of the terminal C5b-9 complement complex. C5b-9 deposits were detected in glomeruli of 14, in tubules of eight and in vessels of 12 cases. Patients with C5b-9 deposits fared worse than those without such deposits, even with the same histopathological type of glomerulonephritis. The C5b-9 complex suggests an in situ complement activation.

Adolescent↗
PubMed1985

Clinical studies on plasma fibronectin and factor XIII; with special reference to hyperlipoproteinemia.

When compared to age-matched normal weight normolipidemic control subjects, plasma factor XIII, plasma fibronectin and serum cholinesterase levels were found to be markedly decreased in patients with decompensated cirrhosis of the liver, not significantly changed in hyperlipoproteinemia type IIa (heterozygous subjects) and increased in hypertriglyceridemic subjects (type IIb and IV) as well as in hyperlipidemic nephrotic patients. A possible accelerated hepatic synthesis of certain plasma proteins including factor XIII and fibronectin in patients with the nephrotic syndrome as well as in endogenous hypertriglyceridemia is envisaged. It is also considered that mural thrombi, richer in factor XIII and fibronectin, would be more resistant to fibrinolysis and more readily attached to subendothelial structures.

Adult↗
PubMed1985

Immunohistochemical localization of the terminal C5b-9 complement complex in human aortic fibrous plaque.

The terminal C5b-9 complex of the complement system was localized in 26 aortic, 3 iliac and 4 femoral human fibrous plaques using indirect immunofluorescence and immunoperoxidase. IgG, IgA, IgM, Clq, C3c, C4, C9 and fibrinogen were investigated simultaneously. All the fibrous plaques presented C5b-9 deposits appearing like thin threads in the fibrous cap and masses and spots in the amorphous areas. The extent and intensity were in agreement with the size of the fibrous plaques. The intimal thickenings presented less intense deposits which were absent in atherosclerosis-free samples. The C5b-9 deposits were frequently associated with immunoglobulins and complement components in the same areas. Whereas the demonstration of complement components reflected only a nonspecific trapping, the presence of assembled C5b-9 in the damaged tissues is more indicative of the involvement of complement activation in the tissue injury. The absence of C5b-9 in the atherosclerosis-free intima and its presence at lower intensity in the intimal thickenings than in the fibrous plaques suggest a pathogenic involvement in the chronic progression of the atherosclerotic lesion.

Adult↗
PubMed1985

Immunoglobulins and complement components in human aortic atherosclerotic intima.

Concentration and preferential retention of immunoglobulins and complement components were studied in comparison with other plasma proteins in 42 human aortae with atherosclerosis. Saline and acid extracted IgG, IgA, IgM, C1q, C3c, C4, C9, C3A, C-reactive protein, alpha 1-antitrypsin, alpha 2-macroglobulin, albumin, transferrin and fibrinogen were quantitatively determined using the radial immunodiffusion. The fibrous plaques and their adjacent areas contained higher levels of each protein than intima with only fatty streaks. No significant differences were found between the fibrous plaques and their adjacent areas presenting intimal thickenings. Saline eluted IgG and IgA were significantly higher in the fibrous plaque intima than in intimal samples with fatty streaks and were the only proteins detected in the acid eluates. The complement components were present in all saline eluates, while C-reactive protein was found in 23 samples. Crossed immunoelectrophoretic studies showed the activation of saline C3 and C4. In 8 cases serum levels of the studied proteins were compared with their concentration in saline eluates obtained from intima and media. The immunoglobulins and complement components presented higher intima/serum and lower media/intima retention ratios than the other studied proteins suggesting their preferential retention in the intima. The presence of immune related proteins in the atherosclerotic intima and their preferential retention might be explained not only by an altered permeability but also in relation to their function.

Adult↗
PubMed1985

Localization of the terminal C5b-9 complement complex in the human aortic atherosclerotic wall.

The terminal C5b-9 complement complex was investigated in 15 aortic, 2 femoral fibrous plaques and 5 fatty streaks aortic intimae using indirect immunofluorescence and immunoperoxidase. All the fibrous plaques presented C5b-9 deposit-like threads in the fibrous cap and masses in the amorphous areas of the plaque. The deposits were frequently associated with other immune-related proteins such as: IgG, IgA, IgM, Clq, C3c and C4 which were simultaneously investigated. Fatty streaks intimae presented no C5b-9 and complement component deposits. Whereas the demonstration of the complement components could merely reflect a non-specific trapping, the presence of assembled C5b-9 in the damaged tissue is more indicative of the involvement of complement activation in the progression of atherosclerotic lesions.

Adult↗
PubMed1983

Comparative behaviour of the components of the factor VIII complex in acute myocardial infarction.

The three components of the factor VIII complex: VIII coagulant (VIII:C), VIII related antigen (VIII R:Ag) and the VIII related von Willebrand factor (VIII R:WF) were studied in patients with acute myocardial infarction (AMI). Using a carefully standardized technique for the determination of VIII R:WF, a significantly higher R:WF level was found in 32 patients compared to 19 control subjects, confirming our previous results. However VIII R:AG was increased to an even greater extent, resulting in a VIII R:Ag/VIII R:WF ratio of 1.58 +/- 0.084 in patients, compared to 1.21 +/- 0.045 in controls. A similar increase of the VIII R:AG/VIII:C ratio was noted in the 13 patients in whom VIII:C was investigated. In 7 patients with severe AMI who could be investigated twice the plasma levels of both VIII R:Ag and VIII R:WF were found to be lower a week after the acute event than during the first 48 hours. However the VIII R:Ag/VIII R:WF ratio was not significantly reduced after 7 days. Acute phase reaction and endothelial injury resulting in release of multimers which are less polymerised are probably involved in the above changes.

Adult↗
PubMed1982

Increased level of the complement C3 protein in endogenous hypertriglyceridemia.

When compared to values obtained in normalweight, normolipidemic control subjects, the level of complement C3 protein and total complement activity (CH50) were found to be obviously decreased in patients with decompensated cirrhosis of the liver and slightly but significantly increased in subjects with type IIb and type IV hyperlipoproteinemia. C3 protein level was positively correlated with the concentration of serum cholesterol, the logarithm of serum triglyceride concentration, serum pseudocholinesterase and total complement activity. There were no significant differences concerning C3 protein level between hyperlipidemic subjects with clinical atherosclerosis and those without documented vascular disease. It is suggested that accelerated lipoprotein turnover occurring in many subjects with type IIb and type IV hyperlipoproteinemia might enhance the synthesis of several liver produced plasma enzymes and proteins including the C3 protein of the complement system.

Adult↗
PubMed1981

Increased plasma antithrombin III level in hyperlipidemic subjects.

When compared to values obtained in healthy normolipidemic normal weight control subjects, the plasma antithrombin III level determined by immunological, clotting and thrombin-agarose diffusion techniques was found to be obviously decreased in patients with decompensated cirrhosis of the liver and slightly but significantly increased in hyperlipidemic and especially in hypertriglyceridemic subjects. Plasma antithrombin III was positively correlated with serum cholesterol level, the logarithm of serum triglyceride concentration and serum pseudocholinesterase activity. A weaker correlation between plasma fibrinogen and antithrombin III was noted in the investigated clinical material. It is suggested that the accelerated fatty acid and lipoprotein turnover occurring in many subjects with type IIb and type IV hyperlipoproteinemia might be accompanied by an enhanced hepatic protein synthesis involving various liver secretion enzymes and clotting factors as well as antithrombin III.

Adult↗