Porous dendritic copper: an electrocatalyst for highly selective CO 2 reduction to formate in water/ ionic liquid electrolyte

International audienceCopper is currently extensively studied because it provides promising electrodes for carbon dioxide electroreduction. The original combination, reported here, of a nanostructured porous dendritic Cu-based material, characterized by electron microcopy (SEM, TEM) and X-ray diffraction methods, and a water/ionic liquid mixture as the solvent, contributing to CO 2 solubilization and activation, results in a remarkably efficient (large current densities at low overpotentials), stable and selective (large faradic yields) electrocatalytic system for the conversion of CO 2 into formic acid, a product with a variety of uses. These results provide new directions for the further improvement of Cu electrodes

Millimeter-wave Evolution for 5G Cellular Networks

Triggered by the explosion of mobile traffic, 5G (5th Generation) cellular network requires evolution to increase the system rate 1000 times higher than the current systems in 10 years. Motivated by this common problem, there are several studies to integrate mm-wave access into current cellular networks as multi-band heterogeneous networks to exploit the ultra-wideband aspect of the mm-wave band. The authors of this paper have proposed comprehensive architecture of cellular networks with mm-wave access, where mm-wave small cell basestations and a conventional macro basestation are connected to Centralized-RAN (C-RAN) to effectively operate the system by enabling power efficient seamless handover as well as centralized resource control including dynamic cell structuring to match the limited coverage of mm-wave access with high traffic user locations via user-plane/control-plane splitting. In this paper, to prove the effectiveness of the proposed 5G cellular networks with mm-wave access, system level simulation is conducted by introducing an expected future traffic model, a measurement based mm-wave propagation model, and a centralized cell association algorithm by exploiting the C-RAN architecture. The numerical results show the effectiveness of the proposed network to realize 1000 times higher system rate than the current network in 10 years which is not achieved by the small cells using commonly considered 3.5 GHz band. Furthermore, the paper also gives latest status of mm-wave devices and regulations to show the feasibility of using mm-wave in the 5G systems.Comment: 17 pages, 12 figures, accepted to be published in IEICE Transactions on Communications. (Mar. 2015

Influenza aviaire dans le monde : situation au 31 janvier 2015

Une recrudescence des foyers de virus influenza aviaires hautement pathogène (IAHP) de type H5 est observée depuis novembre 2014, avec des foyers d'IHAP H5N8 et H5N1 observés en Europe, au Moyen-Orient, en Afrique et en Asie avec également des cas d'IAHP H5N2, H5N3, H5N6 et H7N9. Pour la première fois des cas d'infection par les virus H5N1, H5N2 et H5N8 ont été observés en Amérique du Nord chez des volailles domestiques et des oiseaux sauvages. Cette nouvelle vague d'IAHP H5N1 rappelle la panzootie de 2006 durant laquelle le virus s'était propagé en Europe et en Afrique suite à l'épizootie asiatique débutée en 2003. Ces nouvelles infections correspondent à l'apparition et la propagation d'une nouvelle souche d'IHAP H5N8 d'Asie vers l'Europe puis l'Amérique du Nord, qui en se recombinant avec des souches de virus faiblement pathogènes circulant localement en Amérique du Nord et en Asie a engendré de nouveaux variants d'IAHP H5N1, H5N2, H5N3. Cette souche est similaire à celle présente en Asie depuis 2010, sans cas humains déclarés. Elle s'apparente au virus IAHP H5N1 circulant toujours sous un mode endémique en Asie depuis 2003 et qui a infecté plus de 650 personnes avec un nombre probable de personnes exposées de plusieurs millions. Les risques de transmission du virus IAHP H5N8 sur de longues distances par les oiseaux sauvages ne peuvent être négligés, mais doivent être examinés de façon comparative aux autres voies d'introduction comme le commerce international de volailles. La gestion des risques liés aux virus H5 doit s'appuyer sur des études relatives aux mobilités animales et humaines et à des méthodes d'évaluation innovantes des systèmes de surveillance et de contrôle

Catalase Prevents Maternal Diabetes–Induced Perinatal Programming via the Nrf2–HO-1 Defense System

We investigated whether overexpression of catalase (CAT) in renal proximal tubular cells (RPTCs) could prevent the programming of hypertension and kidney disease in the offspring of dams with maternal diabetes. Male offspring of nondiabetic and diabetic dams from two transgenic (Tg) lines (Hoxb7-green fluorescent protein [GFP]-Tg [controls] and Hoxb7/CAT-GFP-Tg, which overexpress CAT in RPTCs) were studied from the prenatal period into adulthood. Nephrogenesis, systolic blood pressure, renal hyperfiltration, kidney injury, and reactive oxygen species (ROS) generation were assessed. Gene expression of transforming growth factor-β1 (TGF-β1), nuclear factor erythroid 2p45–related factor-2 (Nrf2), and heme oxygenase-1 (HO-1) was tested in both in vitro and in vivo studies. Renal dysmorphogenesis was observed in offspring of Hoxb7-GFP-Tg dams with severe maternal diabetes; the affected male offspring displayed higher renal ROS generation and developed hypertension and renal hyperfiltration as well as renal injury with heightened TGF-β1 expression in adulthood. These changes were ameliorated in male offspring of diabetic Hoxb7/CAT-GFP-Tg dams via the Nrf2–HO-1 defense system. CAT promoted Nrf2 nuclear translocation and HO-1 gene expression, seen in both in vitro and in vivo studies. In conclusion, CAT overexpression in the RPTCs ameliorated maternal diabetes–induced perinatal programming, mediated, at least in part, by triggering the Nrf2–HO-1 defense system

Deregulated lipid sensing by intestinal CD36 in diet-induced hyperinsulinemic obese mouse model

The metabolic syndrome (MetS) greatly increases risk of cardiovascular disease and diabetes and is generally associated with abnormally elevated postprandial triglyceride levels. We evaluated intestinal synthesis of triglyceride-rich lipoproteins (TRL) in a mouse model of the MetS obtained by feeding a palm oil-rich high fat diet (HFD). By contrast to control mice, MetS mice secreted two populations of TRL. If the smaller size population represented 44% of total particles in the beginning of intestinal lipid absorption in MetS mice, it accounted for only 17% after 4 h due to the secretion of larger size TRL. The MetS mice displayed accentuated postprandial hypertriglyceridemia up to 3 h due to a defective TRL clearance. These alterations reflected a delay in lipid induction of genes for key proteins of TRL formation (MTP, L-FABP) and blood clearance (ApoC2). These abnormalities associated with blunted lipid sensing by CD36, which is normally required to optimize jejunal formation of large TRL. In MetS mice CD36 was not downregulated by lipid in contrast to control mice. Treatment of controls with the proteosomal inhibitor MG132, which prevented CD36 downregulation, resulted in blunted lipid-induction of MTP, L-FABP and ApoC2 gene expression, as in MetS mice. Absence of CD36 sensing was due to the hyperinsulinemia in MetS mice. Acute insulin treatment of controls before lipid administration abolished CD36 downregulation, lipid-induction of TRL genes and reduced postprandial triglycerides (TG), while streptozotocin-treatment of MetS mice restored lipid-induced CD36 degradation and TG secretion. In vitro, insulin treatment abolished CD36-mediated up-regulation of MTP in Caco-2 cells. In conclusion, HFD treatment impairs TRL formation in early stage of lipid absorption via insulin-mediated inhibition of CD36 lipid sensing. This impairment results in production of smaller TRL that are cleared slowly from the circulation, which might contribute to the reported association of CD36 variants with MetS risk

Coma in fatal adult human malaria is not caused by cerebral oedema

BACKGROUND: The role of brain oedema in the pathophysiology of cerebral malaria is controversial. Coma associated with severe Plasmodium falciparum malaria is multifactorial, but associated with histological evidence of parasitized erythrocyte sequestration and resultant microvascular congestion in cerebral vessels. To determine whether these changes cause breakdown of the blood-brain barrier and resultant perivascular or parenchymal cerebral oedema, histology, immunohistochemistry and image analysis were used to define the prevalence of histological patterns of oedema and the expression of specific molecular pathways involved in water balance in the brain in adults with fatal falciparum malaria. METHODS: The brains of 20 adult Vietnamese patients who died of severe malaria were examined for evidence of disrupted vascular integrity. Immunohistochemistry and image analysis was performed on brainstem sections for activation of the vascular endothelial growth factor (VEGF) receptor 2 and expression of the aquaporin 4 (AQP4) water channel protein. Fibrinogen immunostaining was assessed as evidence of blood-brain barrier leakage and perivascular oedema formation. Correlations were performed with clinical, biochemical and neuropathological parameters of severe malaria infection. RESULTS: The presence of oedema, plasma protein leakage and evidence of VEGF signalling were heterogeneous in fatal falciparum malaria and did not correlate with pre-mortem coma. Differences in vascular integrity were observed between brain regions with the greatest prevalence of disruption in the brainstem, compared to the cortex or midbrain. There was a statistically non-significant trend towards higher AQP4 staining in the brainstem of cases that presented with coma (P = .02). CONCLUSIONS: Histological evidence of cerebral oedema or immunohistochemical evidence of localised loss of vascular integrity did not correlate with the occurrence of pre-mortem coma in adults with fatal falciparum malaria. Enhanced expression of AQP4 water channels in the brainstem may, therefore, reflect a mix of both neuropathological or attempted neuroprotective responses to oedema formation