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Siamak Davani

Publications and source records attributed to Siamak Davani.

9 recordsLinked to original sources
PubMed2005

Can stem cells mend a broken heart?

Myocardial infarction is the leading cause of heart failure in developed countries. The therapeutic measures of today are usually not sufficient to prevent left ventricular remodelling as they fall short of actual replacement of necrotic cardiac myocytes. However, current insights into stem cell plasticity have opened up new perspectives for regenerating the infarcted heart. Recently, a wide range of stem/progenitor cell types have been used for cardiac cell therapy (CCT), including embryonic or foetal stem cells, myoblasts, and bone marrow stem cells. To date, the choice of stem cells has yet to be optimised. This review details recent experimental data and discusses the clinical potential of the various stem cell sources for CCT.

Animals↗
PubMed2004

Comparison of fluorescence polarization immunoassay and high-performance liquid chromatography methods for assay of teicoplanin: can correlation be improved?

Teicoplanin is a glycopeptide indicated in serious infections due to Staphylococcus aureus and requires monitoring and dose adjustment based on measurement of trough concentration. Measurement of teicoplanin can be carried out by the fluorescence polarization immunoassay (FPIA) method or by high-performance liquid chromatography (HPLC) methods. We aimed to compare HPLC method using the sum of the peaks of A2-2, A2-3, A2-4 and A2-5 with FPIA method. Thirty-six serum samples obtained over a 6-month period from patients treated by teicoplanin were first analyzed by a HPLC method by determining both the A2-2 peak and the sum of areas of A2-2 to A2-5 and were then stored at -20 degrees C for FPIA assay. Correlation between FPIA and HPLC A2-2 methods was as: HPLC(A2-2) = 0.694FPIA - 0.892 with r(2) = 0.93. A paired t-test revealed significant differences between the results (P < 0.001). To improve the FPIA and HPLC correlation, we performed a linear regression between FPIA and the sum of A2-2, A2-3, A2-4 and A2-5 obtained in the HPLC method: HPLC(A2-2 to A2-5) = 0.953FPIA - 0.915 with r(2) = 0.96. A paired t-test did not show any significant difference between the results of the two methods (P = 0.94). These results show a better correlation between FPIA and HPLC when the sum of A2-2 to A2-5 was used for calculations. In conclusion, HPLC(A2-2 to A2-5) must be preferred to HPLC(A2-2) for the assay of teicoplanin, even if the HPLC(A2-2 to A2-5) runtime is higher than in the HPLC(A2-2) method.

Anti-Bacterial Agents↗
PubMed2003

Mesenchymal progenitor cells differentiate into an endothelial phenotype, enhance vascular density, and improve heart function in a rat cellular cardiomyoplasty model.

BACKGROUND: Cellular cardiomyoplasty is a promising approach to improve postinfarcted cardiac function. The differentiation pathways of engrafted mesenchymal progenitor cells (MPCs) and their effects on the left ventricular function in a rat myocardial infarct heart model were analyzed. METHODS AND RESULTS: A ligation model of left coronary artery of Lewis rats was used. MPCs were isolated by bone marrow cell adherence. Seven days after ligation, MPCs labeled with 4',6-diamidino-2'-phenylindole were injected into the infarcted myocardium (n=8). Culture medium was injected in the infarcted myocardium of control animals (n=8). Thirty days after implantation, immunofluorescence studies revealed some engrafted cells expressing a smooth muscle phenotype (alpha SM actin+), as similarly observed in culture. Other engrafted cells lost their smooth muscle phenotype and acquired an endothelial phenotype (CD31+). Furthermore, vessel density was augmented in the MPC group in comparison with the control group. After 30 days, echocardiography showed an improvement on left ventricular performance in the MPCs compared with the control group. CONCLUSIONS: In vivo administration of syngenic MPCs into a rat model of myocardial infarcted heart was safety demonstrated. Some engrafted cells appeared to differentiate into endothelial cells and loss their smooth muscle phenotype. MPC engraftment might to contribute to the improvement on the cardiac function in such a setting.

Animals↗
PubMed2003

A neutropenia suggesting an interaction between valacyclovir and mycophenolate mofetil.

Mycophenolate mofetil (MMF) is a drug which decreases the frequency of renal transplantation rejection. However, cytomegalovirus infections are a common feature of this treatment leading the physicians to prescribe antiviral prophylactic drugs like valacyclovir. During this association, neutropenia occur and the cause of this adverse effect is difficult to define. This report presents a case of neutropenia in a woman treated with MMF and valacyclovir. As the duration of the valacyclovir treatment exactly corresponds to the neutropenia duration, and the mycophenolate trough levels increased with the neutrophil count, the responsibility of this neutropenia was ascribed to valacyclovir. However, an examination of the literature for cases of neutropenia led to the suspicion of an interaction between MMF and valacyclovir. Mycophenolate may increase intracellular concentrations of valacyclovir up to haematotoxic levels. This mechanism may explain the interaction and further research is needed to confirm this interaction.

Acyclovir↗
PubMed2003

Role of beta 1- and beta 2-adrenoceptor subtypes in preconditioning against myocardial dysfunction after ischemia and reperfusion.

Using an isolated nonworking rat heart model, this study investigated the role of beta-adrenergic preconditioning (beta-PC) to attenuate myocardial dysfunction after an ischemia/reperfusion injury. After a 20-min stabilization period, the noradrenaline depleted hearts were perfused for 5 min with isoproterenol (ISO) before 40-min global ischemia (I) followed by 30-min reperfusion (R). ISO 0.02 microM provided significant protection versus unconditioned in vivo reserpinized IR control, causing a decrease of creatine kinase (CK) release (mIU/min/g wet weight) on reperfusion in coronary effluent, a preservation of the mean coronary flow (MCF) and preservation of left ventricular function assessed by the rate-pressure product (RPP). These beneficial effects were similar to those of ischemic preconditioning (I-PC) in both nonreserpinized and reserpinized rats. Propranolol (1 microM) and atenolol (10 microM) completely suppressed the ISO preconditioning. In contrast, ICI 118551 (2 microM) a highly selective beta -blocker, did not blunt the salutary effects of ISO on CK release and MCF preservation. These results indicate that ISO pretreatment provides a significant cardioprotection against prolonged ischemic myocardial injury. Although endogenous catecholamines are not necessary for I-PC in isolated rat hearts, cardioprotection provided by beta-adrenergic stimulation is quite similar to I-PC. This significant cardioprotection is mediated less by beta -adrenoceptor than by beta -adrenoceptor activation, which seems to play a crucial role in the beta-PC mechanism.

Adrenergic Agonists↗
PubMed2002

Ischaemic preconditioning and mast cell histamine release: microdialysis of isolated rat hearts.

The aim of this study was to investigate the feasibility of intramyocardium kinetics of histamine release by microdialysis in the isolated rat heart and ascertain if the inhibition of histamine release is implicated in the antiarrhythmic effect of preconditioning. A 30 min normothermic global ischaemia model followed by 30 min reperfusion was carried out in the control group (n= 9). In the preconditioning group (n= 8) there was a 5 min global ischaemia followed by 10 min of reperfusion. A mast cell stabilizing group received the disodium cromoglycate ( 10 micro M, n= 10). The last group received a mast cell degranulator, compound 48/80 (1micro g ml (-1), n= 10). In the control group, the histamine release during reperfusion was significantly different from the basal concentration ( 18.4 +/- 6.5 vs 1.9 +/- 0.5 nM, P< 0.05) and was associated with a maximal period of severe arrhythmias. The ischaemic preconditioning modified the histamine release kinetics with an early mast cell degranulation ( 9.7 +/- 1.5 nM) and a significant decrease in the total period of severe arrhythmias in comparison with the control group ( P< 0.05). In the disodium cromoglycate group, the histamine release during reperfusion decreased ( 3.1 +/- 0.7 nM) and was associated with a maximal period of severe arrhythmias. In the C48/80 group, the increase in the histamine released during reperfusion ( 21.2 +/- 5.0 nM) was associated with a maximal period of severe arrhythmias. These results showed firstly the feasibility of kinetic histamine release in myocardium interstitial fluid on the isolated rat heart and secondly that the inhibition of histamine release did not play a direct role in the antiarrhythmic effect of preconditioning.

Animals↗
PubMed2002

Acitretin-associated thrombotic stroke.

OBJECTIVE: To report a case of thrombotic stroke. The etiology was difficult to identify, but was finally ascribed to psoriatic treatment with acitretin. CASE SUMMARY: Treatment with acitretin was prescribed for a 52-year-old white woman for long-standing psoriasis. Thirty-four days later, she developed nausea, vomiting, vertigo, and headaches, followed by left lateropulsion, which impeded standing and lying. Both neurologic examination and magnetic nuclear imaging indicated a rectangular infarct in the vermis cerebelli and a small bulbar infarct. Time-of-flight magnetic resonance angiography confirmed the presence of a thrombus at the beginning of the left vertebral artery. After heparin-based treatment and physiotherapy, the evolution was favorable. DISCUSSION: Etiology identification of the stroke included cardiogenic pathology and coagulopathy, but acitretin treatment was considered the likeliest explanation. On review of the literature, this seems to be the first case of a thrombotic event associated with acitretin. CONCLUSIONS: Acitretin should be considered as a possible cause of thrombotic stroke; this possibility should be kept in mind when patients taking acitretin develop an unexplained thrombotic event.

Acitretin↗