Inauguration de la bibliothèque en open access au Centre for Information and Library de l’Université agronomique n°1 de Hanoï

Aboutissement du projet open acces lancé en mars 2005 avec le soutien de la CUD, le libre accès des collections de la Bibliothèque centrale de l’UAh a été inauguré le 11 octobre dernier. Un cap supplémentaire franchi en matière d’accès à la connaissance et à ses modes d’appropriation

Position morphologique du crâne des Lémuriens dans l'ensemble des Primates

La variation cranio-faciale de tous les Primates est décrite ici par l'analyse factorielle des mensurations prises sur 764 crânes d'individus de tous âges et des deux sexes, appartenant à toutes les familles de l'Ordre. La plupart des espèces actuelles y sont représentées, bien que l'échantillonnage soit irrégulier et assez restreint en crânes infantiles. En dépit de ces imperfections, les résultats du «tri factoriel» effectué sont bons et montrent que notre échantillon était représentatif

Primate cranium morphology through ontogenesis and phylogenesis: factorial analysis of global variation

International audienceFactorial analysis of Primate cranial morphology describes variation of the Order in postnatal growth, and shows the positions of some fossil specimens relative to present species

Morphogenèse du crâne des Primates: analyse factorielle, implications taxinomiques, place et redéfinition du genre Homo

International audienceUne analyse factorielle de crânes de Primates décrit la variation totale de l'ordre à partir de la croissance post-natale et la position de quelques spécimens fossiles par rapport à la morphologie crânienne d'espèces actuelles

Normal Aging Modulates the Neurotoxicity of Mutant Huntingtin

Aging likely plays a role in neurodegenerative disorders. In Huntington's disease (HD), a disorder caused by an abnormal expansion of a polyglutamine tract in the protein huntingtin (Htt), the role of aging is unclear. For a given tract length, the probability of disease onset increases with age. There are mainly two hypotheses that could explain adult onset in HD: Either mutant Htt progressively produces cumulative defects over time or “normal” aging renders neurons more vulnerable to mutant Htt toxicity. In the present study, we directly explored whether aging affected the toxicity of mutant Htt in vivo. We studied the impact of aging on the effects produced by overexpression of an N-terminal fragment of mutant Htt, of wild-type Htt or of a β-Galactosidase (β-Gal) reporter gene in the rat striatum. Stereotaxic injections of lentiviral vectors were performed simultaneously in young (3 week) and old (15 month) rats. Histological evaluation at different time points after infection demonstrated that the expression of mutant Htt led to pathological changes that were more severe in old rats, including an increase in the number of small Htt-containing aggregates in the neuropil, a greater loss of DARPP-32 immunoreactivity and striatal neurons as assessed by unbiased stereological counts

Over-expression of Bcl-2 does not protect cells from hypericin photo-induced mitochondrial membrane depolarization, but delays subsequent events in the apoptotic pathway

AbstractHypericin (HY) is a powerful photo-inducer of apoptosis in Jurkat cells as measured by caspase-3 activation, cell shrinkage, phosphatidylserine (PS) exposure and the appearance of hypoploid DNA. These processes are preceded by rapid Bcl-2-independent mitochondrial transmembrane depolarization and a drop in cytoplasmic pH. Pre-incubation of cells with inhibitors of the mitochondrial permeability transition pore, such as cyclosporin A or bongkrekic acid, does not protect cells from mitochondrial membrane potential (Δψm) decrease. However, monitoring of mitochondrial entrapped calcein by confocal fluorescence imaging gives clear evidence of HY photo-induced mitochondrial permeability. This should be considered as the result of a non-specific alteration of mitochondrial membrane integrity brought about by lipid peroxidation. Nevertheless, synthesis of the anti-apoptotic protein Bcl-2 appears to delay the subsequent time course of PS exposure and to reduce caspase-3 activation and the fraction of cells which become hypoploid. We interpret this partially protective effect as the consequence of a direct interaction of Bcl-2 with cytosolic cytochrome c previously released from mitochondria upon Δψm decrease and/or of Bcl-2 inhibition of the deleterious retro-effect of caspase-3 on the mitochondrial permeability transition pore and/or the mitochondrial membrane components

Loss of the thyroid hormone-binding protein Crym renders striatal neurons more vulnerable to mutant huntingtin in Huntington's disease

The mechanisms underlying preferential atrophy of the striatum in Huntington's disease (HD) are unknown. One hypothesis is that a set of gene products preferentially expressed in the striatum could determine the particular vulnerability of this brain region to mutant huntingtin (mHtt). Here, we studied the striatal protein µ-crystallin (Crym). Crym is the NADPH-dependent p38 cytosolic T3-binding protein (p38CTBP), a key regulator of thyroid hormone (TH) T3 (3,5,3′-triiodo-l-thyronine) transportation. It has been also recently identified as the enzyme that reduces the sulfur-containing cyclic ketimines, which are potential neurotransmitters. Here, we confirm the preferential expression of the Crym protein in the rodent and macaque striatum. Crym expression was found to be higher in the macaque caudate than in the putamen. Expression of Crym was reduced in the BACHD and Knock-in 140CAG mouse models of HD before onset of striatal atrophy. We show that overexpression of Crym in striatal medium-size spiny neurons using a lentiviral-based strategy in mice is neuroprotective against the neurotoxicity of an N-terminal fragment of mHtt in vivo. Thus, reduction of Crym expression in HD could render striatal neurons more susceptible to mHtt suggesting that Crym may be a key determinant of the vulnerability of the striatum. In addition our work points to Crym as a potential molecular link between striatal degeneration and the THs deregulation reported in HD patient

Envisioning the future: creating sustainable, healthy and resilient BioCities

Numerous challenges – from population increase to climate change – threaten the sustainable development of cities and call for a fundamental change of urban development and green-blue resource management. Urban forests are vital in this transition, as they provide various ecosystem services and allow to re-shape and re-think cities. Based on a Europe-wide community effort with diverse experts centered around urban forests and urban greening, we propose five key research fields to generate the knowledge required to unlock fundamental changes in urban development and green-blue resource management: circular bioeconomy, climate resilience, governance, social and human environment, and biodiversity. To support the design of greener, cooler, more inclusive and resilient cities, all these research fields require inter- and transdisciplinary collaboration, engaging stakeholders in transforming urban engagement and functioning. We summarise main inter-, trans- und multidisciplinary research paths for each field and the cross-cutting knowledge areas that can help to address the challenges many cities face (e.g., modelling and assessment of the urban microclimate). For transforming cities further knowledge is needed on e.g., urban innovation, transition, participation, and more. Finally, we address how the identified research gaps can be implemented (e.g., international coordinated research effort, interdisciplinary networks)

Jet-Powered Molecular Hydrogen Emission from Radio Galaxies

H2 pure-rotational emission lines are detected from warm (100-1500 K) molecular gas in 17/55 (31% of) radio galaxies at redshift z<0.22 observed with the Spitzer IR Spectrograph. The summed H2 0-0 S(0)-S(3) line luminosities are L(H2)=7E38-2E42 erg/s, yielding warm H2 masses up to 2E10 Msun. These radio galaxies, of both FR radio morphological types, help to firmly establish the new class of radio-selected molecular hydrogen emission galaxies (radio MOHEGs). MOHEGs have extremely large H2 to 7.7 micron PAH emission ratios: L(H2)/L(PAH7.7) = 0.04-4, up to a factor 300 greater than the median value for normal star-forming galaxies. In spite of large H2 masses, MOHEGs appear to be inefficient at forming stars, perhaps because the molecular gas is kinematically unsettled and turbulent. Low-luminosity mid-IR continuum emission together with low-ionization emission line spectra indicate low-luminosity AGNs in all but 3 radio MOHEGs. The AGN X-ray emission measured with Chandra is not luminous enough to power the H2 emission from MOHEGs. Nearly all radio MOHEGs belong to clusters or close pairs, including 4 cool core clusters (Perseus, Hydra, A 2052, and A 2199). We suggest that the H2 in radio MOHEGs is delivered in galaxy collisions or cooling flows, then heated by radio jet feedback in the form of kinetic energy dissipation by shocks or cosmic rays.Comment: ApJ in press, 40 pages, 18 figures, 14 table