Motor antagonism exposed by spatial segregation and timing of neurogenesis

Walking is a key motor behaviour of limbed animals, executed by contraction of functionally antagonistic muscle groups during swing and stance phases. Nevertheless, neuronal circuits regulating the activation of antagonistic extensor-flexor muscles remain poorly understood. Here we use monosynaptically restricted trans-synaptic viruses to elucidate premotor anatomical substrates for extensor-flexor control in mice. We observe a medio-lateral spatial segregation between extensor and flexor premotor interneurons in the dorsal spinal cord. These premotor interneuron populations are derived from common progenitor domains, but segregate by timing of neurogenesis. We find that proprioceptive sensory feedback from the periphery is targeted to medial extensor premotor populations and is required for extensor-specific connectivity profiles during development. Our findings provide evidence for a discriminating anatomical basis of antagonistic circuits at the level of premotor interneurons, and point to synaptic input and developmental ontogeny as key factors in the establishment of circuits regulating motor behavioural dichotomy.     

Voltammetric detection of nanomolar levels of hypoxanthine in the presence of copper (II) at glassy carbon electrode

Nanomolar levels of the hypoxanthine in NaOH electrolyte cantaining copper (II) can be determined by anodic stripping voltammetry at a glassy carbon electrode. In the present article hypoxanthine-Cu⁺ is shown to be adsorbed on the electrode surface in the presence of an excess of copper(II). After accumulation period, hypoxanthine-Cu⁺ was stripped from the electrode surface and the anodic current coming near to the oxidation of Cu(I) to Cu(II) was measured. A linear calibration curve in the range of 5 nmol/L-1.5 mmol/L hypoxanthine, with a detection limit of 0.5 nmol/L hypoxanthine were obtained. Supported by State Key Laboratories of Transducer Technology, Chinese Academy of Sciences Hu Shengshui: born in 1946, Associate professor     

Palmitate-induced skeletal muscle insulin resistance does not require NF-κB activation

Palmitate activates the NF-κB pathway, and induces accumulation of lipid metabolites and insulin resistance in skeletal muscle cells. Little information is available whether and how these processes are causally related. Therefore, the objectives were to investigate whether intra-cellular lipid metabolites are involved in FA-induced NF-κB activation and/or insulin resistance in skeletal muscle and to investigate whether FA-induced insulin resistance and NF-κB activation are causally related. Inhibiting DGAT or CPT-1 by using, respectively, amidepsine or etomoxir increased DAG accumulation and sensitized myotubes to palmitate-induced insulin resistance. While co-incubation of palmitate with etomoxir increased NF-κB transactivation, co-incubation with amidepsine did not, indicating that DAG accumulation is associated with insulin resistance but not with NF-κB activation. Furthermore, pharmacological or genetic inhibition of the NF-κB pathway could not prevent palmitate-induced insulin resistance. In conclusion, we have demonstrated that activation of the NF-κB pathway is not required for palmitate-induced insulin resistance in skeletal muscle cells.     

On the existence of intermediate compounds between hemoglobin (wholly ferrous) and methemoglobin (wholly ferric)

Zusammenfassung Experimentelle Befunde vonDarling undRoughton wurden mathematisch mittels der stöchiometrischen Gleichung analysiert. Entgegen der Meinung jener Versuche sind der vorgenannten Gleichung nach in einer Lösung von Hämoglobin plus Methämoglobin (durch Ferrizyanid) nur Moleküle anwesend, deren vier Eisenatome alle in dem Ferro- bzw. in dem Ferrizustand sind.     

Antibiotico attivo sui bacilli del tifo

Résumé Les cultures d'unPenicillium, probablement identique àP. expansum, fournissent des filtrats dont l'action antibiotique sur le Bacille d'Eberth a été étudiée. La substance active, concentrée par extractions successives, a été purifiée par des procédés chromatographiques. Par ses propriétés, cette substance diffère des antibiotiques déjà connus: son action est remarquablement sélective et sa haute toxicité ne laisse pas espérer d'application thérapeutique.     

非线性及自适应控制：使用者的工具和方法

本书总结了为期四年的欧洲“非线性及自适应控制”研究项目的主要成果。该项目由多所世界顶尖研究机构的参与。     

Bacterial RNA and small antiviral compounds activate caspase-1 through cryopyrin/Nalp3

Missense mutations in the CIAS1 gene cause three autoinflammatory disorders: familial cold autoinflammatory syndrome, Muckle-Wells syndrome and neonatal-onset multiple-system inflammatory disease. Cryopyrin (also called Nalp3), the product of CIAS1, is a member of the NOD-LRR protein family that has been linked to the activation of intracellular host defence signalling pathways. Cryopyrin forms a multi-protein complex termed 'the inflammasome', which contains the apoptosis-associated speck-like protein (ASC) and caspase-1, and promotes caspase-1 activation and processing of pro-interleukin (IL)-1beta (ref. 4). Here we show the effect of cryopyrin deficiency on inflammasome function and immune responses. Cryopyrin and ASC are essential for caspase-1 activation and IL-1beta and IL-18 production in response to bacterial RNA and the imidazoquinoline compounds R837 and R848. In contrast, secretion of tumour-necrosis factor-alpha and IL-6, as well as activation of NF-kappaB and mitogen-activated protein kinases (MAPKs) were unaffected by cryopyrin deficiency. Furthermore, we show that Toll-like receptors and cryopyrin control the secretion of IL-1beta and IL-18 through different intracellular pathways. These results reveal a critical role for cryopyrin in host defence through bacterial RNA-mediated activation of caspase-1, and provide insights regarding the pathogenesis of autoinflammatory syndromes.     

Space geodesy: subsidence and flooding in New Orleans

It has long been recognized that New Orleans is subsiding and is therefore susceptible to catastrophic flooding. Here we present a new subsidence map for the city, generated from space-based synthetic-aperture radar measurements, which reveals that parts of New Orleans underwent rapid subsidence in the three years before Hurricane Katrina struck in August 2005. One such area is next to the Mississippi River-Gulf Outlet (MRGO) canal, where levees failed during the peak storm surge: the map indicates that this weakness could be explained by subsidence of a metre or more since their construction.