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:2.7.10.2 (focal adhesion kinase)
44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The periodic influx of large numbers of people into resort areas substantially increases the use of emergency medical services. This investigation assesses the effects of such a threefold increase in the summer population of the Cape Cod area upon the accuracy of emergency medical technicians' diagnoses and treatments. The technicians' diagnoses for ambulance patients were evaluated against those given by the emergency room physicians during the months of August 1975 and February 1976. The distribution of conditions was similar for both months and the observed frequency of correct diagnoses for common conditions was more than 90% in both months. The overdiagnosis rate of 25% to 50% for common conditions and the correct treatment rate for suspected myocardial infarction of 65% did not vary significantly between summer and winter. Thus, a large influx in population does not seem to affect adversely EMT diagnosis rates. Although misdiagnoses were uncommon, a failure to follow through with a correct treatment for patients with suspected myocardial infarctions, thus indicating the need for better quality control on EMT performance.
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PMID:An assessment of emergency medical technicians' performance as related to seasonal population influx. 72 57

In this case report of a patient presenting with an acute inferior wall myocardial infarction, the infarct conduit was a saphenous vein graft. Extraction atherectomy using the TEC successfully reestablished patency and reversed the patient's clinical symptoms. Extraction atherectomy is a feasible procedure during acute coronary events and deserves further investigation.
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PMID:Extraction atherectomy during myocardial infarction in a patient with prior coronary artery bypass surgery. 160 99

Columbus, Ohio added prehospital coronary care to its Emergency Medical Services System (EMS) in 1969. The EMS System, which is citizen activated and tax supported (+5 per citizen per year), currently sees 32,000 patients a year in a city with a population of 650,000. Ninety-six per cent of the population is aware of the system. Over two thirds of patients with ischemic sudden death or myocardial infarction are seen by advanced life support paramedic (EMT-P) units. The EMT-Ps operate by protocol without telemetry and carry all standard resuscitative drugs and devices. Serial evaluations have shown that within the limits of the protocol, the EMT-Ps perform as effectively as physicians in diagnosis and care of acute cardiovascular emergencies, including endotracheal intubation. One third of ischemic cardiac arrest patients in whom resuscitation is possible (60% of such patients seen) are discharged from the hospital alive (14.2/100,000 lives saved per year). Lives are also saved by treatment of other life-threatening prehospital complications. In Columbus, the estimated annual mortality from ischemic heart disease is only 19%. The EMS System contributes significantly to this low figure.
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PMID:The role of paramedics in resuscitation of patients with prehospital cardiac arrest from coronary artery disease. 651 10

Coronary perforation is a rare, but potentially catastrophic, complication of percutaneous coronary intervention. A retrospective review of the Cardiology Quality Assurance Database was performed for all percutaneous coronary interventions (n = 8,932) at William Beaumont Hospital from October 1988 to December 1992. Coronary artery perforation was reported in 35 patients (0.4%), including after percutaneous transluminal coronary angioplasty (PTCA, 11/7,905, 0.14%), transluminal extraction coronary atherectomy (TEC, 6/420, 1.3%), directional coronary atherectomy (DCA, 1/249, 0.25%), and excimer laser coronary angioplasty (ELCA, 5/242, 2%); and none after high-speed mechanical rotational atherectomy with the Rotablator (MRA, 0/116, 0%). Perforations were classified by coronary angiography as free perforations (n = 10), contained perforations (n = 17), or other types of perforation (n = 8). Although perforation was apparent in 32 (91%) of 35 angiograms, delayed cardiac tamponade occurred in 3 patients (9%), despite the absence of angiographic evidence for perforation at the time of the procedure. Causes of perforation were the guidewire in 7 (20%), an interventional device in 26 (74%), and indeterminate in 2 (6%). Complex B2 or C lesions accounted for 83% of perforations. Final treatment included conservative therapy (reversal of anticoagulation and/or PTCA) in 22 (63%) and surgical intervention (with or without bypass surgery) in 13 (37%). Serious clinical complications included cardiac tamponade in 6 (17%), blood transfusion in 12 (34%), myocardial infarction in 9 (26%), and death in 3 (9%).
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PMID:Perforations after percutaneous coronary interventions: clinical, angiographic, and therapeutic observations. 1128 14

Recently occluded saphenous vein grafts (SVG) contain abundant thrombus. Distal embolization and myocardial infarction often occur when recanalization of such SVG is attempted. In 80 patients with occluded SVG, we employed transcatheter devices to lyse, compress or extract thrombus. Primary treatment for these SVG was performed in the following manner; PTCA 29, intragraft urokinase 12, TEC atherectomy 39. Following urokinase or atherectomy, adjunctive PTCA was performed to diminish the residual stenosis. All patients had class III or IV angina. Clinically, SVG occlusions were 3 days to 3 months old. TIMI flow was grade 0, and occlusion length was greater than 6 cm for all SVG. Each strategy resulted in a similar procedure success rate. However, when used as a primary treatment, TEC may be associated with lower rates of distal embolization and myocardial infarction.
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PMID:PTCA, thrombolysis or atherectomy: rational treatment of recently occluded saphenous vein grafts. 871 2

There have been many studies concerning the hemodynamics and physiological mechanisms in ischemic heart disease, little is known about molecular mechanisms during myocardial ischemia in in vivo study. As the signal transduction pathway responsible for myocardial hypertrophy and apoptosis, janus kinase (JAK) and signal transducers and activators of transcription (STAT) are suggested to play an important role. However, whether in vivo activation of JAK-STAT pathway occurs during myocardial ischemia is still unknown. The purpose of this study was to determine whether myocardial JAK or STAT is activated in ischemic heart, and to evaluate the angiotensin blockade on the pathway. Myocardial infarction was produced by ligation of the coronary artery in Wistar rats. After myocardial ischemia, we analysed both activated levels and total amounts of JAK1, JAK2, STAT1 and STAT3 by Western blot analyses at 0, 5, 15, 30, 60, 120 and 240 min. Compared with JAK activities at 0 min, JAK1 activities were significantly increased at 60 and 120 min (3.0- and 3.7-fold, respectively, P<0.01). JAK2 and STAT1 activities of ischemic myocardium were unchanged through the time course. STAT3 activities were increased at 5 min (3.3-fold, P<0.01) and markedly enhanced at 30, 60 and 120 min (4.6-, 7.7- and 8.7-fold, respectively, P<0.01). Pretreatment with imidapril (ACE inhibitor) and candesartan cilexitil (AT1 receptor antagonist) significantly prevented the increase in the phosphorylation of JAK1 at 120 min and STAT3 at 30 and 120 min. Sis-inducing factor (SIF) DNA complex was supershifted by specific anti-STAT3 antibody, indicating that increased SIF complex at least contained activated STAT3 proteins in ischemic myocardium. Imidapril and candesartan cilexitil inhibited the activation of SIF DNA binding at 1 day after coronary ligation. In conclusion, we showed that JAK1 and STAT3 were activated by ischemia from the basal activities in in vivo rat myocardial ischemia model. Imidapril and candesartan cilexitil prevented the increase in phosphorylated JAK1 and STAT3, thereby suggesting that angiotensin II, especially angiotensin II type I receptor, partially mediates activation of myocardial JAK-STAT pathway in acute myocardial ischemia.
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PMID:Myocardial ischemia activates the JAK-STAT pathway through angiotensin II signaling in in vivo myocardium of rats. 1116 35

In this study we compared several parameters characterizing differences in the lipoprotein profile between members of families with a positive or negative family history of coronary artery disease (CAD). In addition to regular parameters such as the body mass index (BMI), total plasma cholesterol (TC), low density (LDL-C) and high density (HDL-C) cholesterol and triglycerides (TG) we estimated the fractional esterification rate of cholesterol in apoB lipoprotein-depleted plasma (FER(HDL)) which reflects HDL and LDL particle size distribution. A prevalence of smaller particles for the atherogenic profile of plasma lipoproteins is typical. Log (TG/HDL-C) as a newly established atherogenic index of plasma (AIP) was calculated and correlated with other parameters. The cohort in the study consisted of 29 young (< 54 years old) male survivors of myocardial infarction (MI), their spouses and at least one offspring (MI group; n=116). The control group consisted of 29 apparently healthy men with no family history of premature CAD in three generations, their spouses and at least one offspring (control group; n=124). MI families had significantly higher BMI than the controls, with the exception of spouses. Plasma TC did not significantly differ between MI and the controls. MI spouses had significantly higher TG. Higher LDL-C had MI survivors only, while lower HDL-C had both MI survivors and their spouses compared to the controls. FER(HDL) was significantly higher in all the MI subgroups (probands 25.85+/-1.22, spouses 21.55+/-2.05, their daughters 16.93+/-1.18 and sons 19.05+/-1.33 %/h) compared to their respective controls (men 20.80+/-1.52, spouses 14.70+/-0.98, daughters 13.23+/-0.74, sons 15.7+/-0.76 %/h, p<0.01 to p<0.05). Log(TG/HDL-C) ranged from negative values in control subjects to positive values in MI probands. High correlation between FER(HDL) and Log (TG/HDL-C) (r=0.80, p<0.0001) confirmed close interactions among TG, HDL-C and cholesterol esterification rate. The finding of significantly higher values of FER(HDL) and Log (TG/HDL-C) indicate higher incidence of atherogenic lipoprotein phenotype in members of MI families. The possibility that, in addition to genetic factors, a shared environment likely contributes to the familial aggregation of CAD risk factors is supported by a significant correlation of the FER(HDL) values within spousal pairs (control pairs: r=0.51 p<0.01, MI pairs: r=0.41 p<0.05).
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PMID:Atherogenic lipoprotein profile in families with and without history of early myocardial infarction. 1130 Feb 20

The goal of this study was to determine the role of the Janus tyrosine kinase (JAK)-signal transducers and activators of transcription (STAT) pathway in the late phase of ischemic preconditioning (PC). A total of 230 mice were used. At 5 min after ischemic PC (induced with six cycles of 4-min coronary occlusion/4-min reperfusion), immunoprecipitation with anti-phosphotyrosine (anti-pTyr) antibodies followed by immunoblotting with anti-JAK antibodies revealed increased tyrosine phosphorylation of JAK1 (+257 +/- 53%) and JAK2 (+238 +/- 35%), indicating rapid activation of these two kinases. Similar results were obtained by immunoblotting with anti-pTyr-JAK1 and anti-pTyr-JAK2 antibodies. Western analysis with anti-pTyr-STAT antibodies demonstrated a marked increase in nuclear pTyr-STAT1 (+301 +/- 61%) and pTyr-STAT3 (+253 +/- 60%) 30 min after ischemic PC, which was associated with redistribution of STAT1 and STAT3 from the cytosolic to the nuclear fraction and with an increase in STAT1 and STAT3 gamma-IFN activation site DNA-binding activity (+606 +/- 64%), indicating activation of STAT1 and STAT3. No nuclear translocation or tyrosine phosphorylation of STAT2, STAT4, STAT5A, STAT5B, or STAT6 was observed. Pretreatment with the JAK inhibitor AG-490 20 min before the six occlusion/reperfusion cycles blocked the enhanced tyrosine phosphorylation of JAK1 and JAK2 and the increased tyrosine phosphorylation, nuclear translocation, and enhanced DNA-binding activity of STAT1 and STAT3. The same dose of AG-490 abrogated the protection against myocardial infarction and the concomitant up-regulation of inducible NO synthase (iNOS) protein and activity observed 24 h after ischemic PC. Taken together, these results demonstrate that ischemic PC induces isoform-selective activation of JAK1, JAK2, STAT1, and STAT3, and that ablation of this response impedes the up-regulation of iNOS and the concurrent acquisition of ischemic tolerance. This study demonstrates that the JAK-STAT pathway plays an essential role in the development of late PC. The results reveal a signaling mechanism that underlies the transcriptional up-regulation of the cardiac iNOS gene and the adaptation of the heart to ischemic stress.
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PMID:An essential role of the JAK-STAT pathway in ischemic preconditioning. 1148 71

Platelet aggregation and subsequent thrombosis are the major cause of ischemic diseases such as heart attack and stroke. ADP, acting via G protein-coupled receptors (GPCRs), is an important signal in thrombus formation and involves activation of phosphoinositide 3-kinases (PI3K). When platelets from mice lacking the G protein-activated PI3Kgamma isoform were stimulated with ADP, aggregation was impaired. Collagen or thrombin, however, evoked a normal response. ADP stimulation of PI3Kgamma-deficient platelets resulted in decreased PKB/Akt phosphorylation and alpha(IIb)beta(3) fibrinogen receptor activation. These effects did not influence bleeding time but protected PI3Kgamma-null mice from death caused by ADP-induced platelet-dependent thromboembolic vascular occlusion. This result demonstrates an unsuspected, well-defined role for PI3Kgamma downstream of ADP and suggests that pharmacological targeting of PI3Kgamma has a potential use as antithrombotic therapy.
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PMID:Resistance to thromboembolism in PI3Kgamma-deficient mice. 1151 14

Prior to initiation of the ARG-911 and ARG-915 clinical trials, there was no optimal replacement for heparin anticoagulation in patients with heparin-induced thrombocytopenia (HIT) type II. These prospective, historical controlled studies were designed to determine the usefulness of argatroban, a direct thrombin inhibitor (DTI) that is not immunogenic and does not interact with heparin antibody, in answering this clinical need. Clinical outcomes (37-day period) for 568 argatroban-treated and 193 control patients demonstrated significantly reduced risks of the primary efficacy composite endpoint (all-cause death, all-cause amputation, new thrombosis) and the secondary endpoints (death due to thrombosis, new thrombosis) with argatroban. Argatroban patients also experienced a more rapid recovery of platelet count. Bleeding events were similar among both groups. It was concluded that argatroban anticoagulation, compared with historical controls, improves clinical outcomes without increasing bleeding risk in patients having HIT with or without thrombosis. Argatroban has since been approved in the US for both prophylaxis and treatment of thrombosis in patients with HIT. Argatroban has been used in percutaneous coronary interventions in patients with and without HIT, for peripheral vascular procedures in both large and small vessels in HIT patients, and as an adjunct to thrombolytic therapy for the treatment of AMI. Treatment success rates and the same or less bleeding was demonstrated with argatroban compared to heparin controls. These pilot studies suggest that argatroban will provide reliable anticoagulation during interventional procedures. A consistent safety profile of argatroban has been demonstrated in all studies to date. The main attributes of argatroban are its rapid onset of action, fast reversibility of its anticoagulant effect, inhibition of clot-bound thrombin, easily monitored by the aPTT and ACT and no dosage adjustment in renal-impaired individuals. These properties make argatroban a predictable and useful anticoagulant for HIT and non-HIT patients.
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PMID:Argatroban in HIT type II and acute coronary syndrome. 1281 Oct 12


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