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Biomedical subjects

Z Kadri

Publications and source records attributed to Z Kadri.

9 recordsLinked to original sources
PubMed2006

Bypassing the emergency room reduces delays and mortality in ST elevation myocardial infarction: the USIC 2000 registry.

OBJECTIVE: To study the impact on outcomes of direct admission versus emergency room (ER) admission in patients with ST-segment elevation myocardial infarction (STEMI) DESIGN: Nationwide observational registry of STEMI patients SETTING: 369 intensive care units in France. INTERVENTIONS: Patients were categorised on the basis of the initial management pathway (direct transfer to the coronary care unit or catheterisation laboratory versus transfer via the ER). MAIN OUTCOME MEASURES: Delays between symptom onset, admission and reperfusion therapy. Mortality at five days and one year. RESULTS: Of 1204 patients enrolled, 66.9% were admitted direct and 33.1% via the ER. Bypassing the ER was associated with more frequent use of reperfusion (61.7% v 53.1%; p = 0.001) and shorter delays between symptom onset and admission (244 (interquartile range 158) v 292 (172) min; p < 0.001), thrombolysis (204 (150) v 258 (240) min; p < 0.01), hospital thrombolysis (228 (156) v 256 (227) min, p = 0.22), and primary percutaneous coronary intervention (294 (246) v 402 (312) min; p < 0.005). Five day mortality rates were lower in patients who bypassed the ER (4.9% v 8.6%; p = 0.01), regardless of the use and type of reperfusion therapy. After adjusting for the simplified Thrombolysis in Myocardial Infarction (TIMI) risk score, admission via the ER was an independent predictor of five day mortality (odds ratio 1.67, 95% confidence interval 1.01 to 2.75). CONCLUSIONS: In this observational analysis, bypassing the ER was associated with more frequent and earlier use of reperfusion therapy, and with an apparent survival benefit compared with admission via the ER.

Aged↗
PubMed2005

Major impact of admission glycaemia on 30 day and one year mortality in non-diabetic patients admitted for myocardial infarction: results from the nationwide French USIC 2000 study.

OBJECTIVE: To analyse the short and long term prognostic significance of admission glycaemia in a large registry of non-diabetic patients with acute myocardial infarction. METHODS: Assessment of short and long term prognostic significance of admission blood glucose in a consecutive population of 1604 non-diabetic patients admitted to intensive care units in France in November 2000 for a recent (<or= 48 hours) myocardial infarction. RESULTS: In-hospital mortality, compared with that of patients with admission glycaemia below the median value of 6.88 mmol/l (3.7%), rose gradually with each of the three upper sextiles of glycaemia: 6.5%, 12.5% and 15.2%. Conversely, one year survival decreased from 92.5% to 88%, 83% and 75% (p < 0.001). Admission glycaemia remained an independent predictor of in-hospital and one year mortality after multivariate analyses accounting for potential confounders. Increased admission glycaemia also was a predictor of poor outcome in all clinical subsets studied: patients without heart failure on admission, younger and older patients, patients with or without reperfusion therapy, and patients with or without ST segment elevation. CONCLUSION: In non-diabetic patients, raised admission blood glucose is a strong and independent predictor of both in-hospital and long term mortality.

Blood Glucose↗
PubMed2005

[Admission and fasting blood glucose are important prognostic markers in acute coronary syndromes].

This paper reviews current evidence on the role of admission and fasting glycaemia as prognostic markers in patients with acute coronary syndromes. Though both parameters are correlated, they give different prognostic information and are related to both in-hospital complications, including death, and long-term outcomes. As hyperglycemia at the acute stage of myocardial infarction is an independent predictor of untoward cardiovascular events, blood glucose measurements should become routine in all patients presenting with acute coronary syndromes.

Angina, Unstable↗
PubMed2005

[Management of patients admitted for acute myocardial infarction in France from 1995 to 2000: time to admission dependent improvement in outcome].

The in-hospital management and short- and long-term outcomes was assessed in 2 registries of consecutive patients admitted for acute myocardial infarction, 5 years apart, in France. The 2000 cohort was younger and with a less frequent history of cardiac diseases, but was more often diabetic and with anterior infarcts. Time to admission was actually longer in 2000 than in 1995 (median 5.25 hours vs 4.00 hours). Overall, reperfusion therapy was used in 43% of the patients in both registries. However, the use of reperfusion therapy increased from 1995 to 2000 in patients admitted within 6 hours of symptom onset (64 vs 58%), with an increasing use of primary angioplasty (from 12 to 30%). Five-day mortality significantly improved from 7.7 to 6.1% (p < 0.03) and one-year survival was also less in the most recent period (85 vs 81%, p < 0.01). Multivariate analyses showed that the period of inclusion (2000 vs 1995) was an independent predictor of both short- and long-term mortality in patients admitted within 6 hours of symptom onset. Thus, in the real world setting, a continued decline in one-year mortality was observed in patients admitted to intensive care units for recent acute myocardial infarction, especially for patients admitted early. This goes along with a shift in reperfusion therapy towards a broader use of primary angioplasty, and with an increased use of the early prescription of recognised secondary prevention medications.

Age Factors↗
PubMed2000

Involvement of the p38 mitogen-activated protein kinase pathway in tissue inhibitor of metalloproteinases-1-induced erythroid differentiation.

We examined the role of the mitogen-activated protein (MAP) kinase pathway in tissue inhibitor of metalloproteinases-1 (TIMP-1)-mediated cellular effects in a human erythroleukemic cell line UT-7. We show that TIMP-1 induced both UT-7 cell erythroid differentiation and proliferation and tyrosine phosphorylation of many intracellular proteins. Using a panel of phosphospecific antibodies, we also demonstrate that phosphorylation of the p38 and c-Jun N-terminal kinases is increased by TIMP-1 whereas phosphorylation of extracellular signal-regulated kinase 1/2 is not induced. Moreover, inhibition of the p38 activity by SB203580 significantly reduces erythroid differentiation induced by TIMP-1, suggesting that the p38 MAP kinase pathway is involved in TIMP-1-induced erythroid differentiation.

Cell Differentiation↗
PubMed2000

Erythropoietin induction of tissue inhibitors of metalloproteinase-1 expression and secretion is mediated by mitogen-activated protein kinase and phosphatidylinositol 3-kinase pathways.

In the present study, we demonstrate that erythropoietin (Epo) induces the expression and the release of tissue inhibitors of metalloproteinase-1 (TIMP-1) in a time- and dose-dependent manner in Epo-dependent cell line UT-7 cells and in normal human erythroid progenitor cells from cord blood (CD36+) and required de novo protein synthesis. TIMP-1 was not expressed in the absence of Epo. Inhibition of the mitogen-activated protein kinase pathway by the specific inhibitors PD98059 and U0126 and of phosphatidylinositol 3-kinase by LY294002, strongly inhibited Epo-induced TIMP-1 expression and secretion. In the absence of Epo, both latent and active forms of matrix metalloproteinase-9 (MMP-9) were secreted into media. Upon Epo stimulation, MMP-9 and pro-MMP-9 secretion was inhibited in a dose-dependent manner parallel to TIMP-1 induction. The addition of PD98059, U0126, and LY294002 in the presence of Epo restored MMP-9 production in UT-7 and CD36+ cells. Our findings strongly suggest an inversely coordinated regulation of the TIMP-1 gene and MMP-9 production by Epo via mitogen-activated protein kinase and phosphatidylinositol 3-kinase pathways.

Butadienes↗
PubMed1999

Erythropoietin induces glycosylphosphatidylinositol hydrolysis. Possible involvement of phospholipase c-gamma(2).

We showed that erythropoietin induced rapid glycosylphosphatidylinositol (GPI) hydrolysis and tyrosine phosphorylation of phospholipase C (PLC)-gamma(2) in FDC-P1 cells transfected with the wild-type erythropoietin-receptor. Erythropoietin-induced tyrosine phosphorylation of PLC-gamma(2) was time- and dose-dependent. By using FDC-P1 cells transfected with an erythropoietin receptor devoid of tyrosine residues, we showed that both effects required the tyrosine residues of intracellular domain on the erythropoietin receptor. Erythropoietin-activated PLC-gamma(2) hydrolyzed purified [(3)H]GPI indicating that GPI hydrolysis and PLC-gamma(2) activation under erythropoietin stimulation were correlated. Results obtained on FDC-P1 cells transfected with erythropoietin receptor mutated on tyrosine residues suggest that tyrosines 343, 401, 464, and/or 479 are involved in erythropoietin-induced GPI hydrolysis and tyrosine phosphorylation of PLC-gamma(2), whereas tyrosines 429 and/or 431 seem to be involved in an inhibition of both effects. Thus, our results suggest that erythropoietin regulates GPI hydrolysis via tyrosine phosphorylation of its receptor and PLC-gamma(2) activation.

Animals↗