Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On healthy individuals fibrin(ogen) split products cannot be demonstrated in the blood. Catabolic products of fibrin and fibrinogen appear in the blood in case of general fibrinolysis, consumption coagulopathy with secondary fibrinolysis as well as local fibrin films with secondary fibrinolysis. The regular routine determination of fibrin(ogen) split products in serum or urine may indicate starting complications of many diseases. The appearance of these split products in case of renal affections indicates acute and active processes on the kidneys themselves; fibrin films appear in case of acute and chronic glomerulonephritis, casting-off crises on renal transplants, EPH gestosis, renal phlebothrombosis, hemolytic-uremic syndrom and occasionally urinary tract infections. The demonstration of fibrin(ogen) split products in serum or urine allows the following conclusions: a) acute and active process on the kidneys themselves; b) HMWS in urine indicate a fibrin film in the kidneys; c) an immediate beginning of an anticoagulation therapy; d) good possibilities to judge the therapeutic effect and by this the further progress of disease.
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PMID:[Fibrin (ogen) Split products of nephropathies]. 23 43

Blood viscosity studies were carried out at regular intervals in 51 patients with normal pregnancy and in 27 patients with high risk pregnancy, i.e. with EPH-gestosis and placental insufficiency. During gestation the relative blood viscosity is significantly increased compared to 15 normal non-pregnant women. At a corrected hematocrit of 45% we found a direct correlation to plasma fibrinogen and to the blood sedimentation rate. Although the whole blood viscosity does not indicate any change in normal pregnant women, there is, however, a viscosity increase in the last trimester of high risk pregnancies. Additionally a mathematical model of the oxygen diffusion in the placental cotyledo demonstrates rapid decrease of the oxygen partial pressure in the maternal intervillous channel if the microcirculation of the "Placenton" is impaired.
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PMID:[Changes in the blood rheology and their influence on the oxygen diffusion in normal and pathological pregnancies (author's transl)]. 57 82

EPH gestosis and placental insufficiency sui generis are cause of fetal hazards. Clinical symptomatology and anamnesis indicate different tests to detect pathological conditions for the fetus. HPL, HCG, urinary estriol, measuring the placental flow-rate, ultrasonic diagnosis as all other usual examinations during pregnancy were carried out. In EPH gestosis a reduction of all placental functions was found like as for thrombocytes and fibrinogen. Placental insufficiency showed an even greater reduction of placental function, only thrombocytes and fibrinogen remained constant. Weight and length of the newborn were according the pathological placental function reduced. Morphology of the placenta could proof the results of the previous done tests.
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PMID:[Optimal monitoring in EPH gestosis and idiopathic placentar insufficiency (author's transl)]. 118 12

SK-HEP-1 is an immortal, human cell line derived from the ascitic fluid of a patient with adenocarcinoma of the liver. We have determined that these cells are of endothelial origin. Despite the location of the tumor from which SK HEP-1 was derived, the cell line does not have properties of hepatocytes. Northern blot analysis of total cellular RNA shows no messenger RNA for the hepatic-specific proteins albumin, alpha-fibrinogen, or gamma-fibrinogen. Endothelial characteristics are seen by transmission electron microscopy. These features include numerous pinocytotic vesicles, electron dense granules consistent with Weibel-Palade bodies, and abundant intermediate filaments, identified immunocytochemically as vimentin. Cultures grown on plastic dishes grow in bundles of polygonal to spindle-shaped cells. Proteins characteristic for endothelial cells are identified by immunocytochemistry. Addition of basement membrane material (Matrigel) or type I collagen to the cultures induces these cells to organize into a tubular network.
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PMID:SK HEP-1: a human cell line of endothelial origin. 137 4

This paper reports in vivo protein adsorption onto polymers, including Biomer, PEO grafted Biomer (B-PEO-4K), heparin immobilized Biomer with PEO spacers (B-PEO-4K-HEP), and HEMA-Styrene block copolymer (H-S). Vascular grafts (6 mm ID, 7 cm in length) were fabricated with Biomer, coated on their luminal surfaces with test polymers, and implanted into the abdominal aorta of dogs. After 3 weeks-1 month, the grafts were retrieved and processed for TEM and SEM. TEM measured the thickness of adsorbed protein layers stained with a OsO4 solution, and the distribution pattern of adsorbed proteins (albumin, IgG and fibrinogen) using the immunoperoxidase technique. Retrieved grafts of Biomer and B-PEO-4K showed mural thrombi along the graft length, while thrombus formation on B-PEO-4K-HEP and H-S grafts was limited to the anastomotic sites. SEM pictures of B-PEO-4-HEP and H-S surfaces demonstrated clear morphology, with minimal platelet adhesion and activation, and microthrombi. Biomer and B-PEO-4K demonstrated a thick proteinaceous layer (1000-2000 A), whereas B-PEO-4K-HEP and H-S showed what can be described as a monolayer protein thickness (200-300 A). B-PEO-4K-HEP and H-S showed a monolayer-like adsorbed protein pattern, with high concentrations of albumin and IgG, and less fibrinogen, while Biomer and B-PEO-4K showed multilayered patterns with relatively high concentrations of fibrinogen, and less albumin. These results suggest that the surface properties of polymer may control protein adsorption pattern, and the composition of adsorbed protein is essential to in vivo long-term blood compatibility.
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PMID:In vivo protein adsorption onto polymers: a transmission electron microscopic study. 268 16

The coexistence of arterial hypertension and disturbances of haemostasis in pregnant women with EPH-gestosis allow to expect a role of fibrinolysis and kinin-forming systems in pathomechanism of this syndrome. For these reasons blood plasma of 34 patients with EPH-gestosis, 23 patients with normal pregnancy and 19 nonpregnant women was investigated. All pregnant women were in third trimester of pregnancy. The following parameters were investigated: kinin-forming system compounds (kininogens and prokininogenases - biological methods), fibrinolytic activity (plasma euglobulin fibrinolysis time), total plasma protein and fibrinogen concentration, protease inhibitors - antithrombin III, C1-esterase inhibitor, alpha 2-antiplasmin, alpha 1-protease inhibitor and alpha 2-macroglobulin (by electroimmunodiffusion). Furthermore hematocrit was measured. In pregnant women with EPH-gestosis significant increase of high molecular weight kininogen concentration was found (p less than 0.02), decreased fibrinolytic activity (p less than 0.01) and (except alpha 2-antiplasmin) decreased concentration of protease inhibitors (p less than 0.005 - p less than 0.01) were observed. Further statistical analysis demonstrated positive correlation between the concentrations of kininogens and prokallikrein-prokininogenases and between low molecular weight kininogen and plasma euglobulin fibrinolysis time. On the other hand negative correlation between concentrations of those proenzymes and severity of gestosis was observed. The above described phenomena indicate on significance of disturbances of proteolytic enzyme activation in pathogenesis of EPH-gestosis.
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PMID:[Plasma kininogenesis and fibrinolysis in the pathogenesis of EPH gestosis]. 321 8

Immunofluorescent findings are revealing EPH-gestosis as an immunological disease similar to graft rejection. Deposits of immunoglobulins, complement, and fibrinogen/fibrin are localized in the glomerular capillaries, mesangium of the kidney and in the decidual arteries resembling findings in transplanted organs with signs of rejection. Fibrinoid changes of the villous stroma are found in greater amounts in placentae after gestosis revealing a more lively humoral reaction of the immune system. By mixed lymphocyte culture a cellular hyperreactivity of the mother against her fetus can be demonstrated. In conclusion, gestosis is a disease of humoral and cellular hyperreactivity finally resulting in the well-known peripheral symptoms edema, hypertension, and proteinuria. Early diagnosis followed by an effective therapy is desirable in preventing these secondary effects.
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PMID:[Immunological concepts of the etiology of EPH-gestosis]. 644 14

We report the identification of ligands for Tyro 3 (alternatively called Sky, rse, brt, or tif) and Axl (alternatively, Ark or UFO), members of a previously orphan family of receptor-like tyrosine kinases. These ligands correspond to protein S, a protease regulator that is a potent anticoagulant, and Gas6, a protein related to protein S but lacking any known function. Our results are reminiscent of recent findings that the procoagulant thrombin, a protease that drives clot formation by cleaving fibrinogen to form fibrin, also binds and activates intracellular signaling via a G protein-coupled cell surface receptor. Proteases and protease regulators that also activate specific cell surface receptors may serve to integrate coagulation with associated cellular responses required for tissue repair and growth, as well as to coordinate protease cascades and associated cellular responses in other systems, such as those involved in growth and remodeling of the nervous system.
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PMID:The anticoagulation factor protein S and its relative, Gas6, are ligands for the Tyro 3/Axl family of receptor tyrosine kinases. 786 73

Delayed hypersensitivity (DH) is a T cell-mediated form of immune response characterized by a predominantly perivascular, mononuclear cell infiltrate. The venules in DH reactions are hyperpermeable to plasma proteins, leading to extravasation of plasma fibrinogen and its extravascular clotting to form a fibrin gel that promotes induration and angiogenesis. The mechanisms responsible for microvascular hyperpermeability in DH are unknown. Recently, a cytokine named vascular permeability factor (VPF, also known as vascular endothelial growth factor or VEGF) has been implicated in the chronic vascular hyperpermeability and angiogenesis of solid and ascites tumors, healing wounds, rheumatoid arthritis, and psoriasis. These findings suggested that VPF/VEGF might also have a role in the pathogenesis of DH. Two model systems were studied: allergic contact dermatitis to poison ivy in human volunteers and classical tuberculin hypersensitivity in rats. In both, in situ hybridization revealed that the mRNAs encoding VPF/VEGF were strikingly overexpressed in keratinocytes of the epidermis; scattered mononuclear cells infiltrating the dermis also overexpressed VPF/VEGF mRNA, to a greater extent in rat tuberculin than in human contact reactions. In contact reactions, mRNAs for two VPF/VEGF vascular endothelial cell receptors, flt-1 and KDR, were also strikingly overexpressed. Abundant fibrin deposition in both models confirmed that dermal microvessels were indeed hyperpermeable to plasma fibrinogen. These results implicate VPF/VEGF as a potentially important mediator in the pathogenesis of cell-mediated immunity and provide further evidence that products of epithelial cells may regulate the inflammatory response.
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PMID:Overexpression of vascular permeability factor (VPF/VEGF) and its endothelial cell receptors in delayed hypersensitivity skin reactions. 787 50

Two study designs were conceived to evaluate the rheological significance of hypertriglyceridaemia. We first investigated the course of serum- (SV) and plasma viscosity (PV) and erythrocyte aggregation in serum (SEA) and plasma (PEA) of healthy normolipidaemic individuals over 4 h after a fatty rich meal, in native material and after removal of triglyceride rich lipoproteins by centrifugation. Secondly, blood from patients with untreated hypertriglyceridaemia was investigated under fasting conditions. PEA and SEA increased in parallel with postprandial triglycerides (+135 mg dl-1), but the effect on PEA was more pronounced (+0.8 abs% increase; 2 h after the meal) as compared to SEA (+0.4 abs% increase). PV and SV increased in parallel to the same extent (+0.05 mPas). In the triglyceride poor infranatant no significant changes occurred. In fasting plasma PEA and PV were significantly lower (1.1 abs% and PV 0.04 mPas respectively) in infranatant than in native plasma, while only small differences in triglyceride (mostly VLDL) were observed. This phenomenon was barely detectable in serum samples. We conclude that triglyceride rich lipoproteins have a profound influence on haemorheological parameters, and that fibrinogen in particular, potentiates the effect of large fasting VLDL on plasma viscosity and erythrocyte aggregation.
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PMID:Investigations into the haemorheological significance of postprandial and fasting hypertriglyceridaemia. 835 33


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