Characterising small solutions in delay differential equations through numerical approximations

This paper discusses how the existence of small solutions for delay differential equations can be predicted from the behaviour of the spectrum of the finite dimensional approximations.Manchester Centre for Computational Mathematic

Données épidémiologiques dans le monde et traitements disponibles du VHB

Date du colloque&nbsp;: 09/2008</p

The Formation, Structure, and Stability of a Shear Layer in a Fluid with Temperature-Dependent Viscosity

The presence of viscosity normally has a stabilizing effect on the flow of a fluid. However, experiments show that the flow of a fluid might form shear bands or shear layers, narrow bands in which the velocity of the fluid changes sharply. In general, adiabatic shear layers are observed not only in fluids but also in thermo-plastic materials subject to shear at a high-strain rate and in combustion. Therefore there is widespread interest in modeling the formation of shear layers. In this paper we investigate the basic system of conservation laws for a one-dimensional flow with temperature-dependent viscosity using a combination of analytical and numerical tools. We present results to substantiate the claim that the formation of shear layers is due to teh fact that viscosity decreases sufficiently quickly as temperature increases and analyze the structure and stability properties of the layers

Traitement des hépatites B, C, D

Les hépatites virales sont un problème majeur de santé publique au niveau international. Environ 2 milliards de sujets dans le monde ont été en contact avec le VHB, soit qu\u27ils aient une infection, soit qu\u27ils aient éliminé partiellement le virus [1]. Quatre cents millions d\u27individus sont porteurs chroniques d\u27une infection par le virus de l\u27hépatite B (VHB) et parmi ceux-ci, environ à 15 millions sont co-infectés par un virus satellite du virus de l\u27hépatite B appelé le virus de l\u27hépatite Delta (VHD).Dans le monde, près de 200 millions de sujets sont également infectés par le virus de l\u27hépatite C [2]. Les chiffres concernant la mortalité et la morbidité globale de ces infections sont partiellement connus. L\u27OMS estime qu\u27environ 2 millions de décès par an sont dus aux infections par les virus des hépatites C (http://www.who.int/fr/). On sait également que les patients porteurs d\u27une infection chronique ont un risque majeur d\u27évoluer vers la cirrhose du foie et le carcinome hépato-cellulaire (le risque serait de 200 par rapport à un sujet non infecté [3, 4] ). Dans les pays développés, les hépatites B et C sont également responsables d\u27une grande partie des transplantations hépatiques [1] . L\u27objectif de cette revue est de faire le point sur le traitement des hépatites B, C et Delta en envisageant les schémas thérapeutiques les plus adaptés à l\u27Afrique. Nous aborderons d\u27abord le traitement des hépatites B, le traitement des co-infections B-Delta, le traitement des hépatites B chez les patients VIH puis le traitement des hépatites C et celui des hépatites C chez les patients vivant avec le VIH

The potential for reassortment between Oropouche and Schmallenberg Orthobunyaviruses

A number of viruses within the Peribunyaviridae family are naturally occurring reassortants, a common phenomenon for segmented viruses. Using a minigenome-reporter and virus-like particle (VLP) production assay, we have accessed the potential of Oropouche virus (OROV), Schmallenberg virus (SBV), and other orthobunyaviruses within the Simbu serogroup to reassort. We found that the untranslated region (UTR) in the medium segment is a potential contributing factor for reassortment by the tested viruses. We demonstrate that for promoter activity to occur it was essential that the viral RNA polymerase (L) and nucleocapsid (N) proteins were from the same virus, reinforcing the hypothesis that the large and small segments that encode these proteins segregate together during genome reassortment. Our results indicate that, given the right epidemiological setting, reassortment between SBV and OROV would potentially be feasible and could contribute to the emergence of a new Simbu virus

Маркерные иммунофенотипические признаки бластов при т-клеточном остром лимфобластном лейкозе у детей

Острые лимфобластные лейкозы (ОЛЛ) Т-клеточного происхождения у детей составляют около 12% среди всех ОЛЛ. Они отличаются чрезвычайно тяжелым клиническим течением и неблагоприятным прогнозом. По морфоцитохимическим признакам невозможно разграничить Т-клеточные ОЛЛ от В-клеточных, поэтому важным является определение иммунофенотипа бластных клеток. У 168 детей с ОЛЛ в возрасте от 1 года до 14 лет проведено иммунофенотипирование бластных клеток; Т-ОЛЛ выявлен у 23 больных. Выявлены особенности фенотипа бластных клеток при T-I, T-II и T-III подвариантах ОЛЛ у детей.T-lineage acute lymphoblastic leukaemias (ALL) represent approximately 12% of all ALL in children. They feature unfavorable prognosis and extraordinarily hard clinical course. T-cell ALL cannot be differentiated from B-cell ALL by morphocytochemical features; therefore, it is crucial to define the immunophenotype of blast cells. Immunophenotyping of blast cells in 168 children with ALL aged from 1 to 14 was carried out. In 23 patients T-ALL was revealed. Peculiarities of the immunophenotype of blast cells in T-I, T-II, and T-III subgroups of ALL were established in children

Les mutants précore et du promoteur basal du core du virus de l’hépatite B

Le virus de l’hépatite B (VHB) est le seul virus à ADN qui possède une étape de reverse transcription au cours de son cycle de réplication. L’absence d’activité 3’-5’ exonucléasique de la fonction reversetranscriptase de l’ADN polymérase du virus génère une accumulation de mutations sur l’ensemble du génome viral. Ainsi, chez un même individu vont coexister des populations virales sauvages et mutées qui pourront évoluer tout au long de l’histoire naturelle de l’infection. La variabilité génétique du VHB s’observe dans toutes les régions du génome viral. La mutation la plus fréquemment décrite dans la région précore (PC) du VHB est la mutation G1896A qui induit la formation d’un codon stop dans l’ARN précore et abolit la synthèse de l’antigène HBe. Dans la région du promoteur basal du core (PBC), la double mutation (A1762T-G1764A) est associée à une baisse de la synthèse de l’antigène HBe. L’impact des mutants PC et du PBC dans l’histoire naturelle de l’hépatite B et dans la sévérité des lésions hépatiques n’est pas clairement établi

Actualités sur les co-infections VIH–VHC

Objectives To evaluate the incidence of HIV–HCV co-infections and analyse the outcome in co-infected patients. Epidemiology. Effects of antivirals The prevalence of the co-infection by the HCV thus varies from 10 to 14% on subjects who have sexual behaviors at risk at 80 or 90% on users of drug IV. Numerous studies showed that the infection by the HIV made worse the natural history of the infection by the HCV [J Acquir Immune Defic Syndr 6 1993 602–610; J Hepatol 28 1998 945–950]. On the other hand, the studies which endeavoured to appreciate the effect of the antiretroviral therapeutics on the natural history of the chronic hepatitis C, on the co-infected patients, are more discussed. In cohorts of big size, it was demonstrated that the hepatic mortality increased with the exposure to antiretrovirals. However, the duration of the antiretroviral treatment also reports the more important survival of the patients, which distorts credibly the figures. The effect of the infection by the HCV on the progress of the disease with HIV is more discussed. The patients infected by the HIV, in any case, have to benefit from the research for a co-infection by the viruses of hepatitis B and C (HBV and HCV). This screening must be renewed every year, in particular on the drug addicts patients or presenting behaviors at risk. Viral replication The research of a viral replication, must be implemented for any confirmed positive HCV serology. The research of the HCV RNA needs ultrasensitive techniques of molecular biology which allow a qualitative detection andor a quantification of the viral genome (viral load). The techniques of last generation of real-time PCR combine both approaches (detection and quantification). The viral load HCV is not correlated to the degree of hepatic disease and does not predict the severity of the hepatic disease, contrary to the correlation demonstrated in the infection by the HIV. On the other hand, it can be a predictive factor in the response to the treatment. The pretherapeutic check-up also includes a determination of the viral genotype because a strong involvement in the response to the treatment was clearly demonstrated. Hepatic fibrosis The hepatic fibrosis must be estimated on patients having a chronic hepatitis because it conditions the prognosis and the treatment of the hepatitis. The anatomopathological study after hepatic biopsy (DHB) remains the reference method. Recently, the development of non invasive methods of measure of the hepatic fibrosis improved the care of hepatitis C, notably the blood tests (fibrotest BioPredictive Paris, fibrometer BLS Angers) and physical measures as the impulsional elastometry (Fibroscan® Echosens) which substitutes more and more in practice to the draining hepatic biopsy. Treatment Numerous studies now validated the treatment associating interferon pegilated and ribavirine as the reference treatment on the co-infected patients HIV/HCV. This treatment involves a high virological response going from 14 to 36% in the patients infected by a genotype 1 and 2 and from 43 to 73% in the patients infected by a genotype 2 or 3. The duration of the treatment is 48 weeks. As well as usual virological factors on the mono-infected patients (genotype, viral load), the rate of CD4 is one of the best predictive factors with a good response. Many hopes go towards the new molecules in development (inhibitors of protease), inhibitors of polymerase), with promising results on the mono-infected patients. However, the toxicity of these molecules is not very well known at the moment in the co-infected patients. It is thus necessary to perform trials in this group of patient, by watching very carefully the toxicity of the therapeutic associations