The Gardener and the Sick Garden: How Not to Address the Planet\u27s Environmental Issues

A truly workable environmental strategy would start by being grounded in better, more realistic and empirically accurate models of how nature works, how humans behave, and humankind\u27s relationship to nature. Such an environmental policy would realize that the gardener and the garden are not separate, but one. And this environmental policy would embrace two correlative legal norms: (1) we should recognize a positive right, held by both humans and their natural surroundings, to environmental conditions that may sustain human survivability\u27; and (2) we should impose an affirmative duty on humans to promote and support natural systems

Energy spectrum, density of states and optical transitions in strongly biased narrow-gap quantum wells

We study theoretically the effect of an electric field on the electron states and far-infrared optical properties in narrow-gap lead salt quantum wells. The electron states are described by a two-band Hamiltonian. An application of a strong electric field across the well allows the control of the energy gap between the two-dimensional (2D) states in a wide range. A sufficiently strong electric field transforms the narrow-gap quantum well to a nearly gapless 2D system, whose electron energy spectrum is described by linear dispersion relations \epsilon_{\sigma} (k) ~\pm (k-k_{\sigma}), where k_{\sigma} are the field-dependent 2D momenta corresponding to the minimum energy gaps for the states with spin numbers \sigma. Due to the field-induced shift of the 2D subband extrema away from k=0 the density of states has inverse-square-root divergencies at the edges. This property may result in a considerable increase of the magnitude of the optical absorption and in the efficiency of the electrooptical effect.Comment: Text 18 pages in Latex/Revtex format, 7 Postscript figure

System-based proteomic and metabonomic analysis of the Df(16)A(+/-) mouse identifies potential miR-185 targets and molecular pathway alterations

Deletions on chromosome 22q11.2 are a strong genetic risk factor for development of schizophrenia and cognitive dysfunction. We employed shotgun liquid chromatography-mass spectrometry (LC-MS) proteomic and metabonomic profiling approaches on prefrontal cortex (PFC) and hippocampal (HPC) tissue from Df(16)A(+/-) mice, a model of the 22q11.2 deletion syndrome. Proteomic results were compared with previous transcriptomic profiling studies of the same brain regions. The aim was to investigate how the combined effect of the 22q11.2 deletion and the corresponding miRNA dysregulation affects the cell biology at the systems level. The proteomic brain profiling analysis revealed PFC and HPC changes in various molecular pathways associated with chromatin remodelling and RNA transcription, indicative of an epigenetic component of the 22q11.2DS. Further, alterations in glycolysis/gluconeogenesis, mitochondrial function and lipid biosynthesis were identified. Metabonomic profiling substantiated the proteomic findings by identifying changes in 22q11.2 deletion syndrome (22q11.2DS)-related pathways, such as changes in ceramide phosphoethanolamines, sphingomyelin, carnitines, tyrosine derivates and panthothenic acid. The proteomic findings were confirmed using selected reaction monitoring mass spectrometry, validating decreased levels of several proteins encoded on 22q11.2, increased levels of the computationally predicted putative miR-185 targets UDP-N-acetylglucosamine-peptide N-acetylglucosaminyltransferase 110 kDa subunit (OGT1) and kinesin heavy chain isoform 5A and alterations in the non-miR-185 targets serine/threonine-protein phosphatase 2B catalytic subunit gamma isoform, neurofilament light chain and vesicular glutamate transporter 1. Furthermore, alterations in the proteins associated with mammalian target of rapamycin signalling were detected in the PFC and with glutamatergic signalling in the hippocampus. Based on the proteomic and metabonomic findings, we were able to develop a schematic model summarizing the most prominent molecular network findings in the Df(16)A(+/-) mouse. Interestingly, the implicated pathways can be linked to one of the most consistent and strongest proteomic candidates, (OGT1), which is a predicted miR-185 target. Our results provide novel insights into system-biological mechanisms associated with the 22q11DS, which may be linked to cognitive dysfunction and an increased risk to develop schizophrenia. Further investigation of these pathways could help to identify novel drug targets for the treatment of schizophrenia.Molecular Psychiatry advance online publication, 22 March 2016; doi:10.1038/mp.2016.27