Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.5 (thrombin)
 33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet function tests were performed on 11 patients with myotonic dystrophy of Steinert (MD) and on 21 healthy control subjects. Using citrated platelet-rich plasma or washed platelets, MD patients had normal aggregation and secretion responses after stimulation with adrenaline, ADP, collagen, PAF, arachidonic acid and thrombin. Using intact and functional washed platelets, MD patients responded normally to adrenaline and had a similar affinity and number of alpha 2-adrenergic receptors as control patients as measured by [3H]dihydroergocryptine and [3H]yohimbine binding. In addition platelets from MD patients had normal basal and stimulated levels of cytoplasmic free Ca2+ as measured with the fluorescent Ca2+ probe quin2. Thus platelet functions, alpha 2-adrenergic receptors and cytoplasmic free Ca2+ are normal in MD.
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PMID:Platelet functions, alpha 2-adrenergic receptors and cytoplasmic free calcium are normal in the myotonic dystrophy of Steinert. 303 64

In 18 patients with myotonic dystrophy, spontaneous aggregation and platelet aggregation induced by thrombin, adenosine diphosphate and epinephrine were compared with normal aggregation patterns. In 17 of the 18 patients the results were not significantly different from normal. In 1 patient spontaneous aggregation and hypersensitive platelets were found. These results are in disagreement with earlier reports on a specific hypersensitivity to epinephrine in myotonic dystrophy. Neither the clinical data (myotonia, paresis) nor the laboratory data (creatine kinase, myoglobin, immunoglobulin G) were correlated with the platelet aggregations.
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PMID:Normal platelet aggregation in myotonic dystrophy. 629 58

We present the cloning and sequencing of the human gene for a novel G-protein coupled receptor (GPR4), from the critical myotonic dystrophy (DM) region on chromosome 19q13.3. The homologous porcine gene was isolated and sequenced as well. The genes of both species are intronless and contain an open reading frame encoding a protein of 362 amino acids. In human, two isoforms of GPR4 are expressed, differing in their 3' untranslated region due to the use of alternate polyadenylation signals and measuring approximately 2.8 and 1.8 kb, respectively. Northern blot analysis showed that GPR4 is widely expressed, with higher levels in kidney, heart, and especially lung, where it is at least fivefold greater than in other tissues. Sequence analysis suggests that GPR4 is a peptide receptor and shares strongest homologies with purinergic receptors and receptors for angiotensin II, platelet activating factor, thrombin, and bradykinin.
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PMID:Isolation of a novel G protein-coupled receptor (GPR4) localized to chromosome 19q13.3. 859 9

Hyphema (blood in the anterior chamber) can occur after blunt or lacerating trauma, after intraocular surgery, spontaneously (e.g., in conditions such as rubeosis iridis, juvenile xanthogranuloma, iris melanoma, myotonic dystrophy, keratouveitis (e.g., herpes zoster), leukemia, hemophilia, von Willebrand disease, and in association with the use of substances that alter platelet or thrombin function (e.g., ethanol, aspirin, warfarin). The purpose of this review is to consider the management of hyphemas that occur after closed globe trauma. Complications of traumatic hyphema include increased intraocular pressure, peripheral anterior synechiae, optic atrophy, corneal bloodstaining, secondary hemorrhage, and accommodative impairment. The reported incidence of secondary anterior chamber hemorrhage, that is, rebleeding, in the setting of traumatic hyphema ranges from 0% to 38%. The risk of secondary hemorrhage may be higher in African-Americans than in whites. Secondary hemorrhage is generally thought to convey a worse visual prognosis, although the outcome may depend more directly on the size of the hyphema and the severity of associated ocular injuries. Some issues involved in managing a patient with hyphema are: use of various medications (e.g., cycloplegics, systemic or topical steroids, antifibrinolytic agents, analgesics, and antiglaucoma medications); the patient's activity level; use of a patch and shield; outpatient vs. inpatient management; and medical vs. surgical management. Special considerations obtain in managing children, patients with hemoglobin S, and patients with hemophilia. It is important to identify and treat associated ocular injuries, which often accompany traumatic hyphema. We consider each of these management issues and refer to the pertinent literature in formulating the following recommendations. We advise routine use of topical cycloplegics and corticosteroids, systemic antifibrinolytic agents or corticosteroids, and a rigid shield. We recommend activity restriction (quiet ambulation) and interdiction of non-steroidal anti-inflammatory agents. If there is no concern regarding compliance (with medication use or activity restrictions), follow-up, or increased risk for complications (e.g., history of sickle cell disease, hemophilia), outpatient management can be offered. Indications for surgical intervention include the presence of corneal blood staining or dangerously increased intraocular pressure despite maximum tolerated medical therapy, among others.
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PMID:Management of traumatic hyphema. 1268 17

Diabetes is associated with a hypercoagulable state. Eighty percent of patients with diabetes mellitus die due to various thrombotic vascular complications. Disorder of coagulation and fibrynolysis is associated with diabetic retinopathy and nephropathy. Angiogenesis requires degradation of vascular basement membrane prior to migration and proliferation of endothelial cells. Various serine proteases play important role in this process. The homeostatic system is also the source of endogenous inhibitors of angiogenesis. Human serum contains various factors able to induce or suppress formation of new blood vessels. The aim of the present study was to evaluate the activity of some angiogenesis inhibitors, anti-proteases, anti-thrombin III, a1 anti-trypsin and a2 anti-plasmin in sera of patients with diabetes mellitus type 1 and 2 and non-proliferative retinopathy, and to correlate this activity to total angiogenic potential of these sera, measured by mice cutaneous test. Sera of 22 persons with DM1, aged 33-70 years, 35 persons with DM2, aged 37-79 years, and 51 healthy people, aged 22-80 years (as control group) were studied. Direct serum-induced cutaneous angiogenesis test in mice (SIA) was applied. Berichrom (ade Behring) tests and immunoturbidimetric method were used for evaluation of anti-proteases activity. Angiogenic activity of DM1 patients sera was statistically lower than this parameter in DM2 patients and in control group. Levels of anti-proteases were similar in DM1, DM2 and control group, with one exception: anti-thrombin level was lower in DM2 patients' sera than this in the control group. Analysis of correlation revealed important difference in behaviour of DM1 sera, as compared to other groups. Significant negative correlation was observed between angiogenic activity and anti-thrombin, as well as anti-trypsin level of DM1 patients' sera. On the other hand, correlation analysis performed for the sera of control group revealed significant positive correlation between their angiogenic activity and anti-thrombin level. No other correlations were found.
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PMID:[Proteinases inhibitors in sera of diabetic patients with non-proliferative retinopathy]. 1563 23