Biomedical subjects

Bernard Royer

Publications and source records attributed to Bernard Royer.

8 recordsLinked to original sources

PubMed2006

ABCA1 single nucleotide polymorphisms on high-density lipoprotein-cholesterol and overweight: the D.E.S.I.R. study.

The adenosine triphosphate-binding cassette A1 (ABCA1) gene plays a key role in reverse cholesterol transport. Some ABCA1 gene polymorphisms have been associated with high-density lipoprotein-cholesterol (HDL-C) concentrations. The aim of this study was to assess the effect of three polymorphisms, C69T, G378C, and G1051A (R219K), on HDL-C levels and their interaction with BMI in more than 5000 French whites from the D.E.S.I.R. (Data from an Epidemiological Study on the Insulin Resistance syndrome) cohort study. The T allele of the C69T single nucleotide polymorphism (SNP) was associated with higher HDL-C levels in normal-weight men (BMI <25 kg/m(2)). The C allele of the G378C SNP was associated with lower HDL-C in overweight subjects (BMI > or =25 kg/m(2)). For the G1051A SNP, in the normal-weight group, the minor A allele was significantly associated with higher HDL-C levels. In contrast, in overweight people, the minor allele was associated with lower HDL-C levels. After accounting for multiple testing, empiric p values remained significant for the associations between G378C SNP and HDL-C in the overweight group and between G1051A SNP and HDL-C in the normal-weight group. This study suggests that ABCA1 gene polymorphisms modulate HDL-C concentrations, in interaction with BMI, and, thus, they might influence cardiovascular risk in the general population.

ATP Binding Cassette Transporter 1↗

PubMed2006

Feasibility of using intraperitoneal epinephrine and cisplatin in patients with advanced peritoneal carcinomatosis.

Intraperitoneal epinephrine above 1 mg/l concentration has been shown to enhance the intratumoral accumulation and antitumor activity of intraperitoneal cisplatin in rats with advanced peritoneal carcinomatosis. The aim of this study was to determine the tolerance of intraperitoneal epinephrine combined with intraperitoneal cisplatin in patients with advanced peritoneal carcinomatosis (17 ovarian cancers, one peritoneal mesothelioma). Intraperitoneal epinephrine (1-5 mg/l) and cisplatin (50 mg/l; 100 mg total dose) were infused in 2 l of saline solution over 2 h. The maximal tolerated concentration of intraperitoneal epinephrine was not reached at 5 mg/l. Cardiovascular symptoms were infrequent and not strictly related to the epinephrine concentration. Tumor responses were obtained in some patients with disease resistant to intravenous platinum compounds. This work demonstrates for the first time that intraperitoneal epinephrine at sufficient concentration enhances the cisplatin effect and can be safely infused into the peritoneal cavity of patients with peritoneal carcinomatosis. The greatest limitation was abdominal pain and limited intraperitoneal distribution of the peritoneal fluid in this closed-abdomen procedure.

Aged↗

PubMed2005

Serum and intraperitoneal pharmacokinetics of cisplatin within intraoperative intraperitoneal chemotherapy: influence of protein binding.

Intraperitoneal (i.p.) chemotherapy is a promising therapeutic method to improve the effectiveness of cisplatin in patients with ovarian cancer and peritoneum involvement. Intraperitoneal treatment can be intraoperatively performed just after a complete surgical resection of peritoneal tumor nodules. However, little is known regarding the pharmacokinetics of platinum during intraoperative i.p. chemotherapy (IIC). Serum and i.p. measurements of total and ultrafilterable platinum were performed to determined pharmacokinetic parameters in 11 consecutive patients who received a 2-h IIC with 50 mg/m cisplatin. Protein concentrations were determined in serum and peritoneal liquid at the same times. The cisplatin concentration required to kill OVCAR-3 human ovarian cancer cells and evaluation of cisplatin binding to proteins were determined in vitro. Platinum i.p. concentration decreased rapidly and quickly came under the cytotoxicity threshold (10 mg for 2 h). About 85% of i.p. and serum cisplatin was ultrafilterable during IIC. Platinum concentrations were closely related to protein concentrations. Due to the very low level of serum protein (almost 25 g/l), serum cisplatin binding during chemotherapy was very low (almost 25%), but increased with protein concentration recovery. These pharmacokinetic data show that a sufficient concentration to kill human ovarian cancer is not reached with a single i.p. bath containing 50 mg/m cisplatin for 2 h. A new protocol with a renewed bath and a higher cisplatin concentration is under investigation.

Aged↗

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↗

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↗