Peritoneal exudate, with mononucleated cells, during normal pregnancy in different species]

A peritoneal cell rich fluid, containing mononucleated leukocytes, macrophages, monocytes, mast cells and lymphocytes, was observed during normal pregnancy in animals belonging to various species. These cells might be concerned in a homograft-like, mother-foetus, relationship.     

High constitutive activity of native H3 receptors regulates histamine neurons in brain

Some G-protein-coupled receptors display 'constitutive activity', that is, spontaneous activity in the absence of agonist. This means that a proportion of the receptor population spontaneously undergoes an allosteric transition, leading to a conformation that can bind G proteins. The process has been shown to occur with recombinant receptors expressed at high density, and/or mutated, but also non-mutated recombinant receptors expressed at physiological concentrations. Transgenic mice that express a constitutively active mutant of the beta2-adrenergic receptor display cardiac anomalies; and spontaneous receptor mutations leading to constitutive activity are at the origin of some human diseases. Nevertheless, this process has not previously been found to occur in animals expressing normal levels of receptor. Here we show that two isoforms of the recombinant rat H3 receptor display high constitutive activity. Using drugs that abrogate this activity ('inverse agonists') and a drug that opposes both agonists and inverse agonists ('neutral antagonist'), we show that constitutive activity of native H3 receptors is present in rodent brain and that it controls histaminergic neuron activity in vivo. Inverse agonists may therefore find therapeutic applications, even in the case of diseases involving non-mutated receptors expressed at normal levels.     

Transport and Anderson localization in disordered two-dimensional photonic lattices

One of the most interesting phenomena in solid-state physics is Anderson localization, which predicts that an electron may become immobile when placed in a disordered lattice. The origin of localization is interference between multiple scatterings of the electron by random defects in the potential, altering the eigenmodes from being extended (Bloch waves) to exponentially localized. As a result, the material is transformed from a conductor to an insulator. Anderson's work dates back to 1958, yet strong localization has never been observed in atomic crystals, because localization occurs only if the potential (the periodic lattice and the fluctuations superimposed on it) is time-independent. However, in atomic crystals important deviations from the Anderson model always occur, because of thermally excited phonons and electron-electron interactions. Realizing that Anderson localization is a wave phenomenon relying on interference, these concepts were extended to optics. Indeed, both weak and strong localization effects were experimentally demonstrated, traditionally by studying the transmission properties of randomly distributed optical scatterers (typically suspensions or powders of dielectric materials). However, in these studies the potential was fully random, rather than being 'frozen' fluctuations on a periodic potential, as the Anderson model assumes. Here we report the experimental observation of Anderson localization in a perturbed periodic potential: the transverse localization of light caused by random fluctuations on a two-dimensional photonic lattice. We demonstrate how ballistic transport becomes diffusive in the presence of disorder, and that crossover to Anderson localization occurs at a higher level of disorder. Finally, we study how nonlinearities affect Anderson localization. As Anderson localization is a universal phenomenon, the ideas presented here could also be implemented in other systems (for example, matter waves), thereby making it feasible to explore experimentally long-sought fundamental concepts, and bringing up a variety of intriguing questions related to the interplay between disorder and nonlinearity.     

Effects of elevation on spring phenological sensitivity to temperature in Tibetan Plateau grasslands

Vegetation phenology is an important indicator of climate change impacts on the seasonal dynamics of the biosphere. However, little is known about the influence of elevation on spring phenological sensitivity to temperature in an alpine ecosystem. Based on remotely sensed land surface phenology and temperature data from 2001 to 2010, this study investigated the rate of spring phenological change of the Tibetan Plateau （TP） grasslands in response to interannual temperature variations at different elevations. Results suggest that spring phenology in the TP grasslands exhibits a stronger response to changes in temperature at higher elevations than at lower ones. In particular, spring phenology advanced by 1-2 days in response to a 1 ℃ increase in May average temperature at elevations from 3,000 to 3,500 m, while the rate was up to 8-9 days/℃ at 5,000-5,500 m. Analysis using accumulated growing degree days （AGDD） from January 1 through May 31 showed the same general trend with increased elevation associated with increased sensitivity （as measured by phenological change per unit of AGDD change）. Such temperature sensitivity gradients in the TP grasslands could be partly explained by the growth efficiency hypothesis which suggests that vegetation adapted to colder climates likely requires less heat energy for the onset of growing season and vice versa in warmer climates. Furthermore, accumulated growing degree days from January 1 to the greenup date were found to decrease with increasing elevations, which provided evidence to support the applicability of the growth efficiency hypothesis in an alpine grassland ecosystem.     

A recurrent 15q13.3 microdeletion syndrome associated with mental retardation and seizures

We report a recurrent microdeletion syndrome causing mental retardation, epilepsy and variable facial and digital dysmorphisms. We describe nine affected individuals, including six probands: two with de novo deletions, two who inherited the deletion from an affected parent and two with unknown inheritance. The proximal breakpoint of the largest deletion is contiguous with breakpoint 3 (BP3) of the Prader-Willi and Angelman syndrome region, extending 3.95 Mb distally to BP5. A smaller 1.5-Mb deletion has a proximal breakpoint within the larger deletion (BP4) and shares the same distal BP5. This recurrent 1.5-Mb deletion contains six genes, including a candidate gene for epilepsy (CHRNA7) that is probably responsible for the observed seizure phenotype. The BP4-BP5 region undergoes frequent inversion, suggesting a possible link between this inversion polymorphism and recurrent deletion. The frequency of these microdeletions in mental retardation cases is approximately 0.3% (6/2,082 tested), a prevalence comparable to that of Williams, Angelman and Prader-Willi syndromes.     

Ambra1 regulates autophagy and development of the nervous system

Autophagy is a self-degradative process involved both in basal turnover of cellular components and in response to nutrient starvation or organelle damage in a wide range of eukaryotes. During autophagy, portions of the cytoplasm are sequestered by double-membraned vesicles called autophagosomes, and are degraded after fusion with lysosomes for subsequent recycling. In vertebrates, this process acts as a pro-survival or pro-death mechanism in different physiological and pathological conditions, such as neurodegeneration and cancer; however, the roles of autophagy during embryonic development are still largely uncharacterized. Beclin1 (Becn1; coiled-coil, myosin-like BCL2-interacting protein) is a principal regulator in autophagosome formation, and its deficiency results in early embryonic lethality. Here we show that Ambra1 (activating molecule in Beclin1-regulated autophagy), a large, previously unknown protein bearing a WD40 domain at its amino terminus, regulates autophagy and has a crucial role in embryogenesis. We found that Ambra1 is a positive regulator of the Becn1-dependent programme of autophagy, as revealed by its overexpression and by RNA interference experiments in vitro. Notably, Ambra1 functional deficiency in mouse embryos leads to severe neural tube defects associated with autophagy impairment, accumulation of ubiquitinated proteins, unbalanced cell proliferation and excessive apoptotic cell death. In addition to identifying a new and essential element regulating the autophagy programme, our results provide in vivo evidence supporting the existence of a complex interplay between autophagy, cell growth and cell death required for neural development in mammals.