Specific and spatial labeling of choline-containing teichoic acids in Streptococcus pneumoniae by click chemistry.

Propargyl-choline was efficiently incorporated into teichoic acid (TA) polymers on the surface of Streptococcus pneumoniae. The introduction of a fluorophore by click chemistry enabled sufficient labeling of the pneumococcus, as well as its specific detection when mixed with other bacterial species. The labeling is localized at the septal site, suggesting a similar location of the TA and peptidoglycan (PG) synthetic machineries. This method is a unique opportunity to improve our understanding of the spatial location of pneumococcal TA biosynthesis.

Metal homeostasis disruption and mitochondrial dysfunction in hepatocytes exposed to sub-toxic doses of zinc oxide nanoparticles.

Increased production and use of zinc oxide nanoparticles (ZnO-NPs) in consumer products has prompted the scientific community to investigate their potential toxicity, and understand their impact on the environment and organisms. Molecular mechanisms involved in ZnO-NP toxicity are still under debate and focus essentially on high dose expositions. In our study, we chose to evaluate the effect of sub-toxic doses of ZnO-NPs on human hepatocytes (HepG2) with a focus on metal homeostasis and redox balance disruptions. We showed massive dissolution of ZnO-NPs outside the cell, transport and accumulation of zinc ions inside the cell but no evidence of nanoparticle entry, even when analysed by high resolution TEM microscopy coupled with EDX. Gene expression analysis highlighted zinc homeostasis disruptions as shown by metallothionein 1X and zinc transporter 1 and 2 (ZnT1, ZnT2) over-expression. Major oxidative stress response genes, such as superoxide dismutase 1, 2 and catalase were not induced. Phase 2 enzymes in term of antioxidant response, such as heme oxygenase 1 (HMOX1) and the regulating subunit of the glutamate-cysteine ligase (GCLM) were slightly upregulated, but these observations may be linked solely to metal homeostasis disruptions, as these actors are involved in both metal and ROS responses. Finally, we observed abnormal mitochondria morphologies and autophagy vesicles in response to ZnO-NPs, indicating a potential role of mitochondria in storing and protecting cells from zinc excess but ultimately causing cell death at higher doses.

Experimental observation of spatially localized dynamo magnetic fields.

We report the first experimental observation of a spatially localized dynamo magnetic field, a common feature of astrophysical dynamos and convective dynamo simulations. When the two propellers of the von Kármán sodium experiment are driven at frequencies that differ by 15%, the mean magnetic field's energy measured close to the slower disk is nearly 10 times larger than the one close to the faster one. This strong localization of the magnetic field when a symmetry of the forcing is broken is in good agreement with a prediction based on the interaction between a dipolar and a quadrupolar magnetic mode.

[Quantification of valvular regurgitation by the convergence zone method]. / Quantification des régurgitations valvulaires par la méthode de la zone de convergence.

The convergence zone method is currently used routinely to quantify valvular regurgitation, particularly mitral insufficiency, but also aortic and tricuspid regurgitation. It is quick to perform, requires relatively little training and remains valid in the presence of atrial fibrillation and in the association of regurgitation-stenosis. It relies on the measurement of output at the level of an isovelocity hemisphere and allows calculation of the regurgitant orifice surface (SOR) and the regurgitant volume per beat (VR). It is reserved for severe regurgitation corresponding to angiographic grade 4: SOR > 40 mm2 and VR > 60 ml for mitral insufficiency, SOR > 30 mm2 and VR > 60 ml for aortic insufficiency, and SOR > 40 mm2 and VR > 40 ml for tricuspid insufficiency.

[Use of echocardiography in mitral regurgitation for the assessment of its mechanism and etiology for the morphological analysis of the mitral valve]. / Apport de l'échocardiographie pour le bilan lésionnel des insuffisances mitrales.

Echocardiographic assessment of mitral regurgitation allows the diagnosis of its mechanism and cause which are major determinants in the feasibility of mitral valve repair. This assessment is based on a systematic analysis of the different structures of the mitral valve apparatus: mitral annulus (enlargement, calcification), mitral valve morphology (thickening, calcification, floppy valve, vegetations, perforation), mitral valve motion (restriction, identification of the prolapsed leaflets and scallops in patients with mitral valve prolapse or flail leaflets), subvalvular apparatus (ruptured chordae, thickening), papillary muscles, and left ventricular wall. This analysis can diagnose the mechanism of mitral regurgitation according to the Carpentier classification, and can clarify its cause: degenerative lesions (prolapse or flail leaflet with or without ruptured chordae), rheumatic lesions (thickened valves with restricted motion), endocarditis (vegetations, perforation, ruptured chordae), ischemic mitral regurgitation (restricted valve motion with inferior or posterior left ventricular wall asynergy), or functional mitral regurgitation (annular dilatation, displacement of papillary muscles with restricted leaflet motion). Transthoracic echocardiography with harmonic imaging usually allows a comprehensive assessment of functional anatomy of mitral regurgitation. Transesophageal echocardiography is indicated if transthoracic echocardiography is inadequate. It is also indicated just before surgery and as an intraoperative procedure. Real time 3D echocardiography should probably complete the evaluation of mitral regurgitation in the near future.

[Atrophic involution of juvenile xanthogranulomas]. / Involution atrophique de xanthogranulomes juvéniles.

INTRODUCTION: We report an unusual atrophic involution of juvenile xanthogranulomas. CASE REPORT: A newborn boy presented with 5 papular, nodular and necrotic lesions located on the upper part of the body. The diameter of the lesions ranged between 1 and 3 cm. Light microscopy showed an infiltrate with foamy and Touton cells. Langerhans' cell histiocytosis was eliminated because none of these cells showed reactivity for S100 protein and CD1a. At the age of 8 years, all the lesions had spontaneously regressed leaving unusual atrophic scars that had the same size as the active lesions. DISCUSSION: We compared the clinical, histological and evolution data of our patient with 251 published cases. The most significant clinical feature of juvenile xanthogranuloma is the spontaneous involution without any trace. However, hyperpigmentation, anetoderma or atrophy may occur. Atrophy is not frequent and can result from 2 mechanisms. Inflammation of the hypodermic tissue, which becomes atrophic and atrophy that may also result from collagen remodeling anomalies during the scarring process.

Acute myocardial ischemia after high-dose therapy with BEAM regimen.

We describe a case of acute myocardial ischemia following carmustine treatment during the BEAM regimen. Despite this, full completion of the autologous peripheral stem-cell transplant was possible.

[Perforation of the aorta after percutaneous closure of an atrial septal defect with an Amplatz prosthesis, presenting with acute severe hemolysis]. / Perforation de l'aorte après fermeture percutanée d'une communication interauriculaire par prothèse d'Amplatz, révélée par une hémolyse aiguë sévère.

We report a case of aortic perforation three weeks after transcatheter occlusion of an atrial septal defect (ASD) by an Amplatzer device. Revealed by acute hemolysis, this complication needed an emergency surgical operation. The fistula between the no coronary Valsalva sinus of the aorta and the left atrium was repaired. The ASD was closed by patch. This serious accident should consider a short antero-superior rim as a risk factor for aortic perforation in transcatheter closure for ASD.

[Acute coronary syndromes in patients treated with HIV protease inhibitors]. / Les inhibiteurs de la protéase du VIH favorisent-ils la survenue de syndromes coronaires aigus?

INTRODUCTION: Cardiovascular complications occurring in patients infected by the human immunodeficient virus (HIV) have considerably changed since the appearance, in April 1996, of highly active antiretroviral tri-therapy (HAART), associating reverse transcriptase and protease HIV-1 inhibitors. The spectacular efficacy of anti-proteases has led to the almost complete disappearance of these opportunistic complications. However, in May 1998, acute coronary accidents were reported in the literature, thus questioning the possible responsibility of antiprotease treatment in the occurrence of accelerated atheroma. METHOD: We report a series of 8 seropositive patients in whom an acute coronary event had occurred between February 1997 and February 1999. RESULTS: The patients were young and all exhibited cardiovascular risk factors (smoking, dyslipidemia) and were treated with HIV-1 protease inhibitors. Six patients presented myocardial infarction, one patient unstable angina and one patient effort angina. COMMENTS: A rise in triglycerides was observed principally on ingestion of ritonavir and a rise in cholesterol and LDL-cholesterol with all the antiprotease agents. Glucose intolerance was observed with indinavir. The occurrence of acute coronary events appeared to be related to antiprotease treatment (at the origin of metabolic disorders, endothelial dysfunction...), although it was impossible to say whether the antiprotease agents were responsible for the early atheroma or whether they simply contributed to the event. The coronary lesions were characterized by their number (single artery) and their topography (proximal or median). Nelfinavir may carry less cardiovascular risks than the other antiproteases. Mean term prognosis was relatively good, after therapeutic adjustment (change in antiprotease, strategic measures against cardiovascular risk factors, introduction of anti-anginal treatment...). CONCLUSION: Larger and longer studies would help to specify the role of antiproteases in the occurrence of early coronary events. Rigorous monitoring (lipid and glucose measurements, tests to search for myocardial infarction,..) together with the development of new antiretroviral molecules would reduce the number of coronary events in this type of patient.

Severe intermittent intraprosthetic regurgitation after mitral valve replacement with subvalvular preservation.

Preservation of the subvalvular apparatus during mitral valve replacement preserves left ventricular function and improves long-term survival. Complications of subvalvular preservation include left ventricular outflow tract obstruction and prosthesis impingement. We report a case of severe intermittent intraprosthetic mitral regurgitation detected by transesophageal echocardiography after mitral valve replacement by a bileaflet mechanical prosthesis with subvalvular preservation. Intravalvular prosthetic valve regurgitation was caused by remnants of the subvalvular apparatus, which were shown at reoperation to interfere with prosthetic leaflet motion and which were excised. Postoperative transesophageal echocardiography showed neither abnormal mitral regurgitation nor residual mass. The use of intraoperative transesophageal echocardiography could enable the detection of this rare complication.

[Dynamic left ventricular obstruction associated with a pheochromocytoma reversible after tumor ablation]. / Obstruction dynamique intraventriculaire gauche associée à un phéochromocytome et réversible après son exérèse.

The association of dynamic left ventricular outflow tract obstruction and pheochromocytoma is rare with only about fifteen previously reported cases in the literature. The association may be the result of chronic increased catecholamine secretion which induces intra-ventricular obstruction in a hypertrophied ventricle due to hypertension. The authors report a new case in which the intraventricular gradient on Doppler echocardiography was particularly high at 120 mmHg. The gradient totally regressed after removal of the pheochromocytoma. The finding of a systolic murmur in a patient with pheochromocytoma should lead to the prescription of Doppler echocardiography and diagnosis of left ventricular tract obstruction must lead to the association of betablocker and alphablocker therapy before surgery. The removal of the pheochromocytoma is usually followed by the complete regression of left intraventricular obstruction, as in this case.

[Cardiac side effects of anti-HIV agents]. / Complications cardiaques des médicaments au cours de l'infection par le VIH.

Both nature and prognosis of cardiac complications occurring in patients infected by the Human Immunodeficiency Virus-1 (HIV-1) have changed considerably since the introduction of highly acive and anti-retroviral triple therapy ("HART"). Opportunist cardiac infections have thus been displaced and side effects of drugs now occupy the primary aetiological role. Torsades de pointe may be exceptionally triggered by anti-infectious agents such as pentacarinat or trimethoprime-sulfamethoxazole, as are those induced by the association of ketoconazole and terfenadine or cisapride, the dangers of which are well known and the prevention more effective, especially with the association with HIV antiproteases which inhibit the cytochrome P450. The diagnosis of iatrogenic myocardial dysfunction is more difficult, except when it occurs acutely as with phosphonoformate (Foscarnet), or interleukine-2. Progressive cardiomyopathy caused by -interferon and dideoxynucleosides (zidovudine, didanosine and zalcitabine), reversible on withdrawal of the drug responsible in half the cases, should be distinguished from those due to the HIV itself (therapeutic relay) or to another associated cause (alcohol, coronary artery disease). The coronary complications of diseases treated by antiproteases usually occur in smokers whose cholesterol and triglyceride levels are rapidly increased with HAART. In a series of 9 patients (amongst 700 treated with the antiproteases), after the acute phase of myocardial infarction during which the interventional approach is often preferred, the medium-term prognosis is relatively good, on condition that the patients correct the hyperlipidaemia and give up smoking.

[Transesophageal echocardiography before electric cardioversion for supraventricular arrhythmia]. / Echocardiographie transoesophagienne avant cardioversion électrique pour trouble du rythme supra-ventriculaire.

OBJECTIVES: The aim of this prospective study was to assess the risks of electrical shock cardio-version in the treatment of supraventricular rhythm disorders when administered under effective-dose but short duration anticoagulation in patients with no intracavitary thrombus detectable by transesophageal echocardiography. PATIENTS AND METHODS: One hundred nineteen patients, mean age 66 years, with permanent arrhythmia due to atrial fibrillation (n = 102), atrial flutter (n = 16) or atrial tachycardia (n = 1) and taking no long-term anticoagulant therapy were treated by electrical shock cardioversion. The patients were given heparin at an effective dose 72 hours prior to cardioversion. A transthoracic and a transesophageal echocardiography were performed less than 24 hours prior to cardioversion. RESULTS: Twenty-one thrombi were evidenced in 16 patients (14.6%) including 18 in the left auricle, 1 in the left atrium and 2 in the right atrium. A spontaneous contrast was visualized in 38 patients (32%). Cardioversion was performed in 103 patients without thrombus and later in 9 of the 16 patients with thrombus after absorption under anticoagulant therapy as evidenced on the control transesophageal echocardiography. A sinus rhythm was obtained in 82% of the cases. All patients were given anti-vitamin K anticoagulants for one month. There were no clinical manifestation of ischemic vascular events during cardioversion nor during the one-month follow-up. CONCLUSION: Early use of electrical shock cardioversion in patients with supraventricular rhythm disorders can be proposed without long-term anticoagulation therapy if the absence of thrombi is demonstrated by transesophageal echocardiography and short-term heparin is given followed by oral anticoagulants for at least 4 weeks. A large-scale randomized prospective study comparing the conventional strategy with the protocol used in this study would be required to definitively validate this approach and determine its possible advantages.

[Calculation of the regurgitation fraction in mitral insufficiency by Doppler echocardiography using a study of the zone of flow convergence]. / Calcul de la fraction de régurgitation des insuffisances mitrales en échocardiographie Doppler par étude de la zone de convergence.

The aim of this study was to propose a new method for calculating the regurgitation fraction of mitral insufficiency by the proximal isovelocity surface area (PISA) method and to compare it with the value of the catheter regurgitation fraction. Thirty-five patients (21 men and 14 women) aged 59 +/- 13 years with isolated mitral insufficiency were studied. Analysis of the proximal isovelocity surface area enabled calculation of an instantaneous maximum regurgitant flow, surface of the regurgitant orifice and the regurgitant volume. The regurgitant fraction was calculated by dividing the regurgitant volume by the sum of the regurgitant volume and aortic stroke volume measured by Doppler echocardiography. These parameters were compared with the corresponding catheter data and the angiographic grade of mitral insufficiency. The echocardiographic and catheter studies were performed within 1.7 +/- 1.2 days. There was a statistically significant correlation between the instantaneous maximum regurgitant flow calculated by the PISA method and the catheter regurgitant flow (r = 0.88; p = 0.0001); between the regurgitant volume calculated by the PISA method and the catheter regurgitant volume (r = 0.85; p = 0.0001) and the regurgitation fraction calculated by the PISA method and the catheter regurgitant fraction (r = 0.82; p = 0.0001). A regurgitant fraction by the PISA method of > 45% corresponded to severe mitral regurgitation (> or = angiographic grade 3 and/or a catheter regurgitant fraction > or = 50%) with a sensitivity of 88% and a specificity of 100%. The PISA method should form part or routine quantification of mitral insufficiency.