Is the Environmental Kuznets Curve Driven by Structural Change? What Extended Time Series May Imply for Developing Countries

Until recently, it was thought that the relationship between economic growth and environmental degradation was a monotonic one, even though there was little agreement as to whether economic growth led to environmental degradation or to increasing environmental quality. At the one extreme there are those who argue that economic growth results in ever increasing use of energy and materials and expanding worker productivity and hence more environmental degeneration. At the other extreme are those who claim that the fastest road to environmental improvement is along the path of economic growth; with higher income comes increased demand for improved environmental protection measures. From this perspective, as Beckerman (1992) put it: "the surest way to improve your environment is to get rich" (quoted by Rothman 1998, pp. 178). A number of empirical studies in the early 1990s (Grossman and Krueger 1991, 1994; Shafik and Bandyopadhyay 1992; and Panayotou 1992, 1993, and 1995) found a nonmonotonic, inverted U-relationship between a number of local pollutants such as particulates and sulfur dioxide and income suggesting a changing relationship between environment and growth along the course of economic development (see Figure 1). At an early stage of development the environment deteriorates with economic growth until a certain level of per capita income is reached beyond which further increases in income result in environmental improvements. The changing income-environment relationship in the course of economic development, known as the Environmental Kuznets Curve (EKC) was attributed largely to behavioral factors: as income rises the effective demand for environmental quality (an income-elastic amenity) rises and eventually overwhelms any scale effects of economic growth on pollution. The behavioral explanation of the EKC presumes a perceived impact of pollution on health, quality of life, or welfare more generally; it is the changing valuation of these impacts as income increases that brings about the reversal of the growth-environment relationship. It is, therefore, surprising that empirical studies in the late 1990s (e.g. Schmalensee, Stoker, and Judson 1998 and Panayotou, Sachs, and Peterson 1999) found the same inverted U-relationship between a global pollutant, CO2, and economic growth. CO2 is greenhouse gas, which is not visible or in anyway perceptible, and any impact (global warming) it may have is distant, dispersed, and highly uncertain. It is, therefore, unlikely that behavioral changes (due to perceptible climate change) can explain falling CO2 emissions per capita once a certain level of per capita income is reached. A different explanation is called for

Growth inhibition of cytosolic Salmonella by caspase-1 and caspase-11 precedes host cell death

Sensing bacterial products in the cytosol of mammalian cells by NOD-like receptors leads to the activation of caspase-1 inflammasomes, and the production of the pro-inflammatory cytokines interleukin (IL)-18 and IL-1β. In addition, mouse caspase-11 (represented in humans by its orthologs, caspase-4 and caspase-5) detects cytosolic bacterial LPS directly. Activation of caspase-1 and caspase-11 initiates pyroptotic host cell death that releases potentially harmful bacteria from the nutrient-rich host cell cytosol into the extracellular environment. Here we use single cell analysis and time-lapse microscopy to identify a subpopulation of host cells, in which growth of cytosolic Salmonella Typhimurium is inhibited independently or prior to the onset of cell death. The enzymatic activities of caspase-1 and caspase-11 are required for growth inhibition in different cell types. Our results reveal that these proteases have important functions beyond the direct induction of pyroptosis and proinflammatory cytokine secretion in the control of growth and elimination of cytosolic bacteria

Balanced electron-hole transport in spin-orbit semimetal SrIrO3 heterostructures

Relating the band structure of correlated semimetals to their transport properties is a complex and often open issue. The partial occupation of numerous electron and hole bands can result in properties that are seemingly in contrast with one another, complicating the extraction of the transport coefficients of different bands. The 5d oxide SrIrO3 hosts parabolic bands of heavy holes and light electrons in gapped Dirac cones due to the interplay between electron-electron interactions and spin-orbit coupling. We present a multifold approach relying on different experimental techniques and theoretical calculations to disentangle its complex electronic properties. By combining magnetotransport and thermoelectric measurements in a field-effect geometry with first-principles calculations, we quantitatively determine the transport coefficients of different conduction channels. Despite their different dispersion relationships, electrons and holes are found to have strikingly similar transport coefficients, yielding a holelike response under field-effect and thermoelectric measurements and a linear, electronlike Hall effect up to 33 T.Comment: 5 pages, 4 figure

Rigorous Multicomponent Reactive Separations Modelling : Complete Consideration of Reaction-Diffusion Phenomena

This paper gives the first step of the development of a rigorous multicomponent reactive separation model. Such a model is highly essential to further the optimization of acid gases removal plants (CO2 capture, gas treating, etc.) in terms of size and energy consumption, since chemical solvents are conventionally used.Firstly, two main modelling approaches are presented: the equilibrium-based and the rate-based approaches. Secondly, an extended rate-based model with rigorous modelling methodology for diffusion-reaction phenomena is proposed. The film theory and the generalized Maxwell-Stefan equations are used in order to characterize multicomponent interactions. The complete chain of chemical reactions is taken into account. The reactions can be kinetically controlled or at chemical equilibrium, and they are considered for both liquid film and liquid bulk. Thirdly, the method of numerical resolution is described. Coupling the generalized Maxwell-Stefan equations with chemical equilibrium equations leads to a highly non-linear Differential-Algebraic Equations system known as DAE index 3. The set of equations is discretized with finite-differences as its integration by Gear method is complex. The resulting algebraic system is resolved by the Newton- Raphson method. Finally, the present model and the associated methods of numerical resolution are validated for the example of esterification of methanol. This archetype non-electrolytic system permits an interesting analysis of reaction impact on mass transfer, especially near the phase interface. The numerical resolution of the model by Newton-Raphson method gives good results in terms of calculation time and convergence. The simulations show that the impact of reactions at chemical equilibrium and that of kinetically controlled reactions with high kinetics on mass transfer is relatively similar. Moreover, the Fick’s law is less adapted for multicomponent mixtures where some abnormalities such as counter-diffusion take place

The helicase HAGE prevents interferon-a-induced PML expression in ABCB5+ malignant melanoma-initiating cells by promoting the expression of SOCS1

The tumour suppressor PML (promyelocytic leukaemia protein) regulates several cellular pathways involving cell growth, apoptosis, differentiation and senescence. PML also has an important role in the regulation of stem cell proliferation and differentiation. Here, we show the involvement of the helicase HAGE in the transcriptional repression of PML expression in ABCB5 + malignant melanoma-initiating cells (ABCB5 + MMICs), a population of cancer stem cells which are responsible for melanoma growth, progression and resistance to drug-based therapy. HAGE prevents PML gene expression by inhibiting the activation of the JAK-STAT (janus kinase-signal transducers and activators of transcription) pathway in a mechanism which implicates the suppressor of cytokine signalling 1 (SOCS1). Knockdown of HAGE led to a significant decrease in SOCS1 protein expression, activation of the JAK-STAT signalling cascade and a consequent increase of PML expression. To confirm that the reduction in SOCS1 expression was dependent on the HAGE helicase activity, we showed that SOCS1, effectively silenced by small interfering RNA, could be rescued by re-introduction of HAGE into cells lacking HAGE. Furthermore, we provide a mechanism by which HAGE promotes SOCS1 mRNA unwinding and protein expression in vitro

Bi-allelic GAD1 variants cause a neonatal onset syndromic developmental and epileptic encephalopathy.

Developmental and epileptic encephalopathies are a heterogeneous group of early-onset epilepsy syndromes dramatically impairing neurodevelopment. Modern genomic technologies have revealed a number of monogenic origins and opened the door to therapeutic hopes. Here we describe a new syndromic developmental and epileptic encephalopathy caused by bi-allelic loss-of-function variants in GAD1, as presented by 11 patients from six independent consanguineous families. Seizure onset occurred in the first 2 months of life in all patients. All 10 patients, from whom early disease history was available, presented with seizure onset in the first month of life, mainly consisting of epileptic spasms or myoclonic seizures. Early EEG showed suppression-burst or pattern of burst attenuation or hypsarrhythmia if only recorded in the post-neonatal period. Eight patients had joint contractures and/or pes equinovarus. Seven patients presented a cleft palate and two also had an omphalocele, reproducing the phenotype of the knockout Gad1-/- mouse model. Four patients died before 4 years of age. GAD1 encodes the glutamate decarboxylase enzyme GAD67, a critical actor of the γ-aminobutyric acid (GABA) metabolism as it catalyses the decarboxylation of glutamic acid to form GABA. Our findings evoke a novel syndrome related to GAD67 deficiency, characterized by the unique association of developmental and epileptic encephalopathies, cleft palate, joint contractures and/or omphalocele