Evolution or revolution: where next for impact assessment?

Impact assessment (IA) has become one of the most prevalent environmental policy instruments today. Its introduction under the National Environmental Policy Act (US) in 1969 was revolutionary. Perhaps it is not surprising, then, that such a widely used tool has received its share of criticism, including that it fails to meet some of its fundamental goals. Over the last fifty years, IA has broadened in scope and application and embraced new techniques. It has followed evolved, but has not changed fundamentally.

We believe that IA must continue to change to meet the societal and environmental challenges of the 21^st century. But will it be enough for IA to progress through incremental change (evolution), or is a complete overhaul of impact assessment (revolution) needed? We provide some ideas as to what ‘evolution’ and ‘revolution’ may look like, but rather then offering a definitive way forward now, we invite stakeholders to present their thoughts and suggestions at the IAIA19 Annual Conference in Brisbane, which carries the same theme as the title of this article.     

GPC study of ethylene-propylene copolymers combined with viscometry and IR spectroscopy

Summary By combining GPC fractionation with IR spectroscopy of ethylene-propylene copolymer (EP) samples, it has been shown that copolymer composition of EP's used in this study does not dep-end on molecular weight. Thus, contrary to earlier investigations by others, molecular weight distributions (MWD) and averages of EP's have been determined by using only experimental data such as GPC traces, universal calibration curve of GPC, and intrinsic viscosities. A comparative study has been carried out by using the MV method (called median value method) and the method of Ogawa and Inaba (OI method) for determination of MWD's and molecular weight averages of EP's. Application of the MV method results in lower molecular weight averages than the use of the equations proposed by Ogawa and Inaba for calculation of Mark-Houwing constants of EP's. However, polydispersities were found to be the same in both methods. The MV method also yields composition depending reliable pairs of Mark-Houwink constants, a and K, for EP's in 1,2,4-trichloro-benzene at 135 °C.     

Fine structure of hepatocytes during the etiology of several common pathologies

Hepatocytes respond to injury by a few basic pathological reactions that are reflected in cell death, different types of degeneration, regeneration, or tumorous transformation. At the ultrastructural level, alterations of cell organelles can be observed in different combinations as a result of the injury, depending on the etiological agent(s) or pathological conditions developed. Nuclear bodies, dilation and fragmentation of rough endoplasmic reticulum (rer), swelling of mitochondria, and an increased number of lysosomes occur during acute viral hepatitis. The core and surface components of the hepatitis B virus can be localized in the liver cells in chronic hepatitis and in carriers. Close contact of hepatocytic and lymphocytic cell membranes were observed in chronic active hepatitis. Hepatocytes surrounded by an increased amount of collagen fibers are characteristic of cirrhosis. Loosely arranged, fine fibrils or condensed forms of Mallory bodies are pathognomic for alcoholic injury. A wide spectrum of alterations are noted after drug treatment: the proliferation of smooth endoplasmic reticulum (ser) as an adaptive phenomenon, focal or complete necrosis of the cell, inflammation, and the like. The fine structural analysis of hepatocytic inclusions in storage diseases has a differential diagnostic value. The storage of copper and other elements can be measured by x-ray microanalysis. The study of the hepatocytic differentiation in liver tumors is highly important in establishing the diagnosis and in proving the hepatocytic origin of the tumor.     

Functional Comparison of Blood-Derived Human Neural Progenitor Cells

Induced pluripotent stem cell (iPSC)-derived neural progenitor cells (NPCs) are promising tools to model complex neurological or psychiatric diseases, including schizophrenia. Multiple studies have compared patient-derived and healthy control NPCs derived from iPSCs in order to investigate cellular phenotypes of this disease, although the establishment, stabilization, and directed differentiation of iPSC lines are rather expensive and time-demanding. However, interrupted reprogramming by omitting the stabilization of iPSCs may allow for the generation of a plastic stage of the cells and thus provide a shortcut to derive NPSCs directly from tissue samples. Here, we demonstrate a method to generate shortcut NPCs (sNPCs) from blood mononuclear cells and present a detailed comparison of these sNPCs with NPCs obtained from the same blood samples through stable iPSC clones and a subsequent neural differentiation (classical NPCs—cNPCs). Peripheral blood cells were obtained from a schizophrenia patient and his two healthy parents (a case–parent trio), while a further umbilical cord blood sample was obtained from the cord of a healthy new-born. The expression of stage-specific markers in sNPCs and cNPCs were compared both at the protein and RNA levels. We also performed functional tests to investigate Wnt and glutamate signaling and the oxidative stress, as these pathways have been suggested to play important roles in the pathophysiology of schizophrenia. We found similar responses in the two types of NPCs, suggesting that the shortcut procedure provides sNPCs, allowing an efficient screening of disease-related phenotypes.     

Heme, heme oxygenase and ferritin in vascular endothelial cell injury

Iron-derived reactive oxygen species are implicated in the pathogenesis of numerous vascular disorders including atherosclerosis, microangiopathic hemolytic anemia, vasculitis, and reperfusion injury. One abundant source of redox active iron is heme, which is inherently dangerous when released from intracellular heme proteins. The present review concerns the involvement of heme in vascular endothelial cell damage and the strategies used by endothelium to minimize such damage. Exposure of endothelium to heme greatly potentiates cell killing mediated by polymorphonuclear leukocytes and other sources of reactive oxygen. Free heme also promotes the conversion of low-density lipoprotein (LDL) into cytotoxic oxidized products. Only because of its abundance, hemoglobin probably represents the most important potential source of heme within the vascular endothelium; hemoglobin in plasma, when oxidized, transfers heme to endothelium and LDL, thereby enhancing cellular susceptibility to oxidant-mediated injury. As a defense against such toxicity, upon exposure to heme or hemoglobin, endothelial cells up-regulate heme oxygenase-1 and ferritin. Heme oxygenase-1 is a heme-degrading enzyme that opens the porphyrin ring, producing biliverdin, carbon monoxide, and the most dangerous product - free redox active iron. The latter can be effectively controlled by ferritin via sequestration and ferroxidase activity. Ferritin serves as a protective gene by virtue of antioxidant, antiapoptotic, and antiproliferative actions. These homeostatic adjustments have been shown effective in the protection of endothelium against the damaging effects of exogenous heme and oxidants. The central importance of this protective system was recently highlighted by a child diagnosed with heme oxygenase-1 deficiency, who exhibited extensive endothelial damage.     

How strategic environmental assessment can inform lenders about potential environmental risks

In this paper, we explore the potential for strategic environmental assessment (SEA) to be a useful tool for banks to manage environmental risks and inform lending decisions. SEA is an environmental assessment tool that was developed to assist strategic-level decision-makers, such as policy-makers, planners, government authorities and environmental practitioners in improving developmental outcomes, aiming to facilitate the transition to sustainable development. We propose that SEA may also be a valuable tool for banks because it has the capacity to provide information about environmental risks at a time when it can be used as an input to bank lending decisions, which can assist banks in making lending decisions with better environmental outcomes. For these reasons, we argue that in some circumstances, and particularly for project finance transactions, SEA may be a more useful environmental assessment tool for lenders than environmental impact assessment, which many banks are currently relying on to help assess and mitigate environmental risks. Furthermore, we suggest that the use of SEA by banks would contribute to the sustainability goals of SEA.     

Conserved and Distinct Elements of Phagocytosis in Human and C. elegans

Endocytosis provides the cellular nutrition and homeostasis of organisms, but pathogens often take advantage of this entry point to infect host cells. This is counteracted by phagocytosis that plays a key role in the protection against invading microbes both during the initial engulfment of pathogens and in the clearance of infected cells. Phagocytic cells balance two vital functions: preventing the accumulation of cell corpses to avoid pathological inflammation and autoimmunity, whilst maintaining host defence. In this review, we compare elements of phagocytosis in mammals and the nematode Caenorhabditis elegans. Initial recognition of infection requires different mechanisms. In mammals, pattern recognition receptors bind pathogens directly, whereas activation of the innate immune response in the nematode rather relies on the detection of cellular damage. In contrast, molecules involved in efferocytosis—the engulfment and elimination of dying cells and cell debris—are highly conserved between the two species. Therefore, C. elegans is a powerful model to research mechanisms of the phagocytic machinery. Finally, we show that both mammalian and worm studies help to understand how the two phagocytic functions are interconnected: emerging data suggest the activation of innate immunity as a consequence of defective apoptotic cell clearance.     

Amplification line of 119 μm wavelength of methanol molecules at the presence of He buffer gas

The gain line shape of wevelength 119 um of the methanol molecule is measured at different He buffer gas pressure. The amplitude of the gain decreases and the linewidth increases with the increase of the buffer gas pressure. The rate of the increase of the width is 3MHz/torr.