Green Governance - One Solution for two problems? Climate change and economic shocks: risk perceptions and coping strategies in China, India and Bangladesh

This collection of papers is based on an international workshop held in the summer of 2009 at the University of Duisburg-Essen. It brings together different perceptions regarding China, India and Bangladesh as they face the risks and crises of climate change and economic shocks like the recent global financial crisis. The papers reflect assumptions concerning the concept of Risk Society and discuss the extent to which Sustainable Development and the rather new concepts of Green Governance, Green Economy and the New Great Deal offer avenues for transforming risk societies into risk-avoiding and riskresistant societies and states. On the basis of these concepts, the current situation in China, India and Bangladesh is described, including the coping strategies which have been implemented so far. Contents: Tobias Debiel / Thomas Heberer: Preface - - - Anja Senz / Dieter Reinhardt: Introduction: Crisis Perception and Green Governance in Comparative Perspective: Questions, Concerns and Format of the Publication - - - Karen Shire: Risks as a Research Topic - Concepts and Methods - - - Chen Yugang: Measure for Meeting Challenges of Climate Change - a Chinese Perspective - - - Yang Long: Potential Instability Caused by the Financial Crisis - Measures Taken by the Chinese State - - - Anja Senz: Green Governance and Sustainable Development in China: Two Problems - One Solution? - - - Dinoo Anna Mathew: Climate Change in India with Special Reference to Women - - - Ash Narain Roy: Coping with Climate Change and Financial Crisis - the Indian Narrative - - - Dalem Barman: Climate Change and Security: A South Asian Perspective - - - Dil Rowshan: Anthropogenic Intervention in Natural Eco-Systems and Climate Change Adaptation in Bangladesh - - - Özlem Ipiv / Dieter Reinhardt: Sustainable Green Investments and Policies in Bangladesh: Two problems - One Solution? - - - Dieter Reinhardt / Anja Senz: Conclusions: Risks, the Green New Deal, and Green Governance - Lessons from South and East Asia --green governance,risk perception,climate change,financial crises,sustainable development,green new deal,green jobs,implementation,civil society,donor policies,China,India,Bangladesh

Global Governance in the field of humanitarian assistance, UN coordination in complex emergencies since the end of the Cold War: Modes of operation and Need for Reform

Seit dem Ende des Ost-West-Konflikts ist das Wort ‚humanitär’ zu einem Schlüsselbegriff der internationalen politischen Rhetorik und des sich entwickelnden Völkerrechts geworden. Nach der Beendigung der politischen Blockade der fünf Veto-Mächte im UN-Sicherheitsrat Ende der Achtzigerjahre, hat der Rat deutlich mehr zivil-militärische ‚humanitäre Interventionen’ als zuvor mit der Aufgabe mandatiert, Gewaltkonflikte zu beenden, einen Friedensprozess zu initiieren und zu begleiten und Menschen in diesen Krisengebieten mit humanitärer Hilfe zu unterstützen. Trotz der Zunahme von UN-Missionen waren der UN-Sicherheitsrat und andere internationale Gremien in vielen Fällen aber nicht in der Lage, systematische Verbrechen gegen die Menschlichkeit, Kriegsverbrechen und Völkermord zu verhindern und überlebende und notleidende Menschen rechtzeitig humanitär zu versorgen.“Global Governance in the field of humanitarian assistance, UN coordination in complex emergencies since the end of the Cold War: Modes of operation and Need for Reform” Serious problems facing the civil-military humanitarian ‘Operation Provide Comfort’ in Northern Iraq in 1991 and 1992 were a main reason for the decision of the UN General Assembly to establish new UN structures for the coordination of international humanitarian assistance in complex emergencies and natural disasters in December 1991. The GA assigned extensive administrative, financial and political tasks to these structures which are composed of the ‘Emergency Relief Coordinator (ERC)’, the ‘Department of Humanitarian Affairs (DHA)’, renamed as ‘Office for the Coordination of Humanitarian Affairs (OCHA)’ in 1998, the ‘Inter-Agency Standing Committee (IASC)’, and the 1998 established ‘Executive Committee for Humanitarian Assistance (ECHA)’. The main operational humanitarian organisations at the international level are UN agencies (UNHCR, UNICEF, WFP, UNDP), NGOs and the International Red Cross and Red Crescent Movement. Although the UN coordination structures have been reformed several times during the last twenty years, they are still not capable to fulfil their tasks defined by the GA. The key questions of the dissertation are: - What are the functions and instruments of humanitarian UN coordination structures in complex emergencies? - Why can they only partly fulfil their tasks even though they have been reformed several times by the GA since 1991? - What conclusions can be drawn for a reform agenda that aims to establish effective international humanitarian coordination structures in complex emergencies? To specify the modes of operation and impact of UN humanitarian coordination structures the dissertation is analysing - the power resources of donor states, private humanitarian organisations and relevant stakeholders in UN humanitarian coordination structures; - the degree of institutionalisation of UN humanitarian coordination structures; - and their scope and impact on international humanitarian assistance in complex emergencies. The power resources are measured by using the following indicators: financial resources; operational capabilities; sanctions and enforcement instruments; legal status; and discursive power/campaign capabilities. The degree of institutionalisation of UN humanitarian coordination structures is measured by the following indicators: relevance of participating stakeholders; degree of successful integration of new players; precision of formal rules and norms; binding force of these rules and norms; and the quality of sanctions and enforcement instruments, of complementary division of work, of operational implementation and of financial coordination. The scope and impact of these structures are measured by comparing humanitarian assistance which is provided inside and outside the humanitarian UN coordination structures, and by analysing the degree of instrumentalisation (politisation, securitisation and militarisation) of humanitarian assistance and UN coordination structures. As a result of these analyses it is possible to specify the governance-form of the UN coordination structures along the three modes of non-hierarchical, hierarchical and competitive governance. The data collection is based on the analysis of primary literature (resolutions of the GA and the UN Security Council, reports on ‘Strengthening of the coordination of emergency humanitarian assistance’ of the UN Secretary-General, publications of OCHA and UNHCR) and secondary resources. Four case studies are illustrating the strengths and weaknesses of different types of UN humanitarian coordination structures at the country level and the growing tendency of instrumentalisation of humanitarian assistance in ‘integrated’ UN-Missions. The ‚lead agency’-type of humanitarian coordination was used in Ex-Yugoslavia (1991-1995) and Kosovo (1999). In the African Great Lakes Region/Rwanda (1994-1998), several regional and national ‘Humanitarian UN-Coordinators’ and ‘Humanitarian Coordinators/Resident Coordinators’ were established. The fourth type of coordination is represented by the ‘Deputy Representative of the Secretary-General’, the deputy leader of an ‘integrated’ UN-Mission who also holds the HC/RC-function. This is illustrated by case studies on Sudan (2003-2011) and Afghanistan (2002-2011)

Cell adhesion and integrin binding to recombinant human fibrillin-1

AbstractFibrillin-1 is a major constituent of tissue microfibrils that occur in most connective tissues, either in close association with or independent of elastin. To test possible cell-adhesive functions of this protein, we used recombinant human fibrillin-1 polypeptides produced in a mammalian expression system in cell attachment and solid-phase integrin binding assays. Fibrillin-1 polypeptides containing the single RGD sequence located in the fourth 8-cysteine domain, mediated distinct cell adhesion of a variety of cell lines and bound to purified integrin αVβ3. Integrins αIIbβ3, α5β1, α2β1 and α1β1 did not interact with any of the recombinant fibrillin-1 peptides. Our results indicate a novel role for fibrillin-1 in cellular interactions mediated via an RGD motif that is appropriately exposed for recognition by integrin αVβ3

Roles of fibronectin isoforms in neonatal vascular development and matrix integrity

Fibronectin (FN) exists in two forms—plasma FN (pFN) and cellular FN (cFN). Although the role of FN in embryonic blood vessel development is well established, its function and the contribution of individual isoforms in early postnatal vascular development are poorly understood. Here, we employed a tamoxifen-dependent cFN inducible knockout (cFN iKO) mouse model to study the consequences of postnatal cFN deletion in smooth muscle cells (SMCs), the major cell type in the vascular wall. Deletion of cFN influences collagen deposition but does not affect life span. Unexpectedly, pFN translocated to the aortic wall in the cFN iKO and in control mice, possibly rescuing the loss of cFN. Postnatal pFN deletion did not show a histological aortic phenotype. Double knockout (dKO) mice lacking both, cFN in SMCs and pFN, resulted in postnatal lethality. These data demonstrate a safeguard role of pFN in vascular stability and the dispensability of the individual FN isoforms in postnatal vascular development. Complete absence of FNs in the dKOs resulted in a disorganized tunica media of the aortic wall. Matrix analysis revealed common and differential roles of the FN isoforms in guiding the assembly/deposition of elastogenic extracellular matrix (ECM) proteins in the aortic wall. In addition, we determined with two cell culture models that that the two FN isoforms acted similarly in supporting matrix formation with a greater contribution from cFN. Together, these data show that pFN exerts a critical role in safeguarding vascular organization and health, and that the two FN isoforms function in an overlapping as well as distinct manner to maintain postnatal vascular matrix integrity

Adamtsl2 deletion results in bronchial fibrillin microfibril accumulation and bronchial epithelial dysplasia: A novel mouse model providing insights on geleophysic dysplasia

Mutations in the secreted glycoprotein ADAMTSL2 cause recessive geleophysic dysplasia (GD) in humans and Musladin–Lueke syndrome (MLS) in dogs. GD is a severe, often lethal, condition presenting with short stature, brachydactyly, stiff skin, joint contractures, tracheal-bronchial stenosis and cardiac valve anomalies, whereas MLS is non-lethal and characterized by short stature and severe skin fibrosis. Although most mutations in fibrillin-1 (FBN1) cause Marfan syndrome (MFS), a microfibril disorder leading to transforming growth factor-β (TGFβ) dysregulation, domain-specific FBN1 mutations result in dominant GD. ADAMTSL2 has been previously shown to bind FBN1 and latent TGFβ-binding protein-1 (LTBP1). Here, we investigated mice with targeted Adamtsl2 inactivation as a new model for GD (Adamtsl2−/− mice). An intragenic lacZ reporter in these mice showed that ADAMTSL2 was produced exclusively by bronchial smooth muscle cells during embryonic lung development. Adamtsl2−/− mice, which died at birth, had severe bronchial epithelial dysplasia with abnormal glycogen-rich inclusions in bronchial epithelium resembling the cellular anomalies described previously in GD. An increase in microfibrils in the bronchial wall was associated with increased FBN2 and microfibril-associated glycoprotein-1 (MAGP1) staining, whereas LTBP1 staining was increased in bronchial epithelium. ADAMTSL2 was shown to bind directly to FBN2 with an affinity comparable to FBN1. The observed extracellular matrix (ECM) alterations were associated with increased bronchial epithelial TGFβ signaling at 17.5 days of gestation; however, treatment with TGFβ-neutralizing antibody did not correct the epithelial dysplasia. These investigations reveal a new function of ADAMTSL2 in modulating microfibril formation, and a previously unsuspected association with FBN2. Our studies suggest that the bronchial epithelial dysplasia accompanying microfibril dysregulation in Adamtsl2−/− mice cannot be reversed by TGFβ neutralization, and thus might be mediated by other mechanisms

A New Type of Thermoalkalophilic Hydrolase of Paucimonas lemoignei with High Specificity for Amorphous Polyesters of Short Chain-length Hydroxyalkanoic Acids

A novel type of hydrolase was purified from culture fluid of Paucimonas (formerly Pseudomonas) lemoignei. Biochemical characterization revealed an unusual substrate specificity of the purified enzyme for amorphous poly((R)-3-hydroxyalkanoates) (PHA) such as native granules of natural poly((R)-3-hydroxybutyrate) (PHB) or poly((R)-3-hydroxyvalerate) (PHV), artificial cholate-coated granules of natural PHB or PHV, atactic poly((R,S)-3-hydroxybutyrate), and oligomers of (R)-3-hydroxybutyrate (3HB) with six or more 3HB units. The enzyme has the unique property to recognize the physical state of the polymeric substrate by discrimination between amorphous PHA (good substrate) and denatured, partially crystalline PHA (no substrate). The pentamers of 3HB or 3HV were identified as the main products of enzymatic hydrolysis of native PHB or PHV, respectively. No activity was found with any denatured PHA, oligomers of (R)-3HB with five or less 3HB units, poly(6-hydroxyhexanoate), substrates of lipases such as tributyrin or triolein, substrates for amidases/nitrilases, DNA, RNA, casein, N-alpha-benzoyl-l-arginine-4-nitranilide, or starch. The purified enzyme (M(r) 36,209) was remarkably stable and active at high temperature (60 degrees C), high pH (up to 12.0), low ionic strength (distilled water), and in solvents (e.g. n-propyl alcohol). The depolymerase contained no essential SH groups or essential disulfide bridges and was insensitive to high concentrations of ionic (SDS) and nonionic (Triton and Tween) detergents. Characterization of the cloned structural gene (phaZ7) and the DNA-deduced amino acid sequence revealed no homologies to any PHB depolymerase or any other sequence of data banks except for a short sequence related to the active site serine of serine hydrolases. A classification of the enzyme into a new family (family 9) of carboxyesterases (Arpigny, J. L., and Jaeger, K.-E. (1999) Biochem. J. 343, 177-183) is suggested

Slc2a10 knock-out mice deficient in ascorbic acid synthesis recapitulate aspects of arterial tortuosity syndrome and display mitochondrial respiration defects

Arterial tortuosity syndrome (ATS) is a recessively inherited connective tissue disorder, mainly characterized by tortuosity and aneurysm formation of the major arteries. ATS is caused by loss-of-function mutations in SLC2A10, encoding the facilitative glucose transporter GLUT10. Former studies implicated GLUT10 in the transport of dehydroascorbic acid, the oxidized form of ascorbic acid (AA). Mouse models carrying homozygous Slc2a10 missense mutations did not recapitulate the human phenotype. Since mice, in contrast to humans, are able to intracellularly synthesize AA, we generated a novel ATS mouse model, deficient for Slc2a10 as well as Gulo, which encodes for L-gulonolactone oxidase, an enzyme catalyzing the final step in AA biosynthesis in mouse. Gulo;Slc2a10 double knock-out mice showed mild phenotypic anomalies, which were absent in single knock-out controls. While Gulo;Slc2a10 double knock-out mice did not fully phenocopy human ATS, histological and immunocytochemical analysis revealed compromised extracellular matrix formation. Transforming growth factor beta signaling remained unaltered, while mitochondrial function was compromised in smooth muscle cells derived from Gulo;Slc2a10 double knock-out mice. Altogether, our data add evidence that ATS is an ascorbate compartmentalization disorder, but additional factors underlying the observed phenotype in humans remain to be determined

Zum Gedenken an Otto Graf, universeller Bauforscher in Stuttgart. Abschiedsvorlesung von Prof. Dr.-Ing. H. W. Reinhardt

Inhalt: Reinhardt, H.-W.: Otto Graf, Rückschau im Licht von heute (Abschiedsvorlesung am 4. Juli 2006), S. 7 - 41; Gehlen, Christoph: Rede des Direktors der Materialprüfungsanstalt Universität Stuttgart (MPA-Stuttgart / Otto-Graf-Institut (FMPA)) zur Verabschiedung von Herrn Prof. Dr.-Ing. H.-W. Reinhardt am 4. Juli 2006, S. 43 - 55; Thielen, Gerd: Kurze Ansprache des stv. Sprechers des Deutschen Ausschusses für Stahlbeton (DAfStb), S. 57 - 59; Eligehausen, Rolf: Ansprache des stv. Geschäftsführenden Institutsdirektors, S. 61 - 67; Fritsch, Dieter: Grußwort des Rektors der Universität Stuttgart aus Anlass der Abschiedsvorlesung von Herrn Prof. Dr.-Ing. Hans-Wolf Reinhardt, S. 69 - 75; Lebenslauf Hans-Wolf Reinhardt, S. 76; Lebenslauf Otto Graf, S. 77; Aus der Presse, S. 78; Die Autoren, S. 7

Absence of autoantibodies against correctly folded recombinant fibrillin-1 protein in systemic sclerosis patients

Autoantibodies against short recombinant fragments of fibrillin-1 produced in bacterial expression systems have been found in tight-skin mouse, systemic sclerosis, mixed connective tissue disease, and primary pulmonary hypertension syndrome. In patients with scleroderma, the frequency of anti-fibrillin-1 antibodies was 42% in Caucasians. Until now it has been unclear whether this immune response has a primary function in disease pathogenesis or is a secondary phenomenon. In the present study we analyzed the frequency of autoantibodies against two overlapping recombinant polypeptides spanning the N-terminal and C-terminal halves of human fibrillin-1, which were produced in human embryonic kidney (HEK-293) cells. Correct three-dimensional structures of the recombinant fibrillin-1 polypeptides were shown by electron microscopy and immunoreactivity with antibodies. Screening of fibrillin-1 antibodies was performed in 41 sera from systemic sclerosis patients and in 44 healthy controls with a Caucasian background. Microtiter plates were coated with the recombinant polypeptides of fibrillin-1 and incubated with 1:100 diluted sera. Positive binding was defined as being more than 2 SD above the mean of the control group. ELISAs showed that none of the sera of patients with systemic sclerosis contained autoantibodies against the N-terminal or C-terminal recombinant fibrillin-1 polypeptide. The data show the absence of autoantibodies against recombinant fibrillin-1 protein in Caucasian systemic sclerosis patients. Because the correct three-dimensional folding of the recombinant proteins has been substantiated by several independent methods, we conclude that autoantibodies against correctly folded fibrillin are not a primary phenomenon in the pathogenesis of systemic sclerosis