A Framework to Evaluate the SDG Contribution of Fluvial Nature-Based Solutions

Nature-based solutions (NBSs) are measures reflecting the ‘cooperation with nature’ approach: mitigating fluvial flood risk while being cost-effective, resource-efficient, and providing numerous environmental, social, and economic benefits. Since 2015, the United Nations (UN) 2030 Agenda has provided UN member states with goals, targets, and indicators to facilitate an integrated approach focusing on economic, environmental, and social improvements simultaneously. The aim of this study is to evaluate the contribution of fluvial NBSs to the UN 2030 Agenda, using all its components: Sustainable Development Goals (SDGs), targets, and indicators. We propose a four-step framework with inputs from the UN 2030 Agenda, scientific literature, and case studies. The framework provides a set of fluvial flooding indicators that are linked to SDG indicators of the UN 2030 Agenda. Finally, the fluvial flooding indicators are tested by applying them to a case study, the Eddleston Water Project, aiming to examine its contribution to the UN 2030 Agenda. This reveals that the Eddleston Water Project contributes to 9 SDGs and 33 SDG targets from environmental, economic, societal, policy, and technical perspectives. Our framework aims to enhance the systematic considerations of the SDG indicators, adjust their notion to the system of interest, and thereby enhance the link between the sustainability performance of NBSs and the UN 2030 AgendaRivers, Ports, Waterways and Dredging Engineerin

The role of supply chain collaboration in disruption recovery : a logistics services perspective

Purpose of the study: Supply chains are faced with various disruptions which impact the performance of the focal firm and its network partners, such as third-party logistics providers (3PLs). Successful supply chain collaboration (SCC) can improve supply chain performance and provide greater synergistic advantages to network partners than could be achieved when working independently. SCC has been addressed extensively in the literature, but the specific role of SCC in supply chain disruption (SCD) recovery is unclear. This study aimed to explore how South African 3PLs and their clients collaborate during SCD recovery and the enablers of and barriers to such SCC. DESIGN/METHODOLOGY/APPROACH : This study employed a generic qualitative research design. Data were collected from ten 3PLs and ten client firms through semi-structured interviews with senior managers. FINDINGS : The study identified four distinct roles of SCC during disruption recovery: facilitating, contributing, interconnecting and retaining. Furthermore, 3PLs and clients identified communication, IT, risk mitigation, and risk response tools and techniques for SCC during SCD recovery. In addition, the findings also reveal a range of intra- and inter-firm enablers and barriers to SCC during disruption recovery. RECOMMENDATIONS/VALUE : This study builds on the current literature by exploring SCC in SCD recovery within an emerging market setting, and SCC between 3PLs and their clients in an SCD recovery context. MANAGERIAL IMPLICATIONS : Having a deeper understanding of the role of SCC in SCD recovery, the tools and techniques for SCC in SCD recovery and what drives and prevents SCC in SCD recovery, practitioners can fully realise the benefits associated with successful SCC in SCD recovery.https://www.jcman.co.za/#/homeam2023Business Managemen

Workshop Diversified strip- and inter-cropping systems: what can we gain in modern organic farming?

The main questions at the workshop are: What can strip- and inter-cropped vegetable and arable systems look like in space, time and genetic material - to increase biodiversity and biocontrol - to increase soil nutrient use efficiency - when managed with new agronomic technology, e.g. robots and sensors to support the development of strip- and inter-cropping on medium and larger-scale farms? What are experiences, challenges and barriers in practice and what can we learn from researchers

Human severe sepsis cytokine mixture increases β2-integrin-dependent polymorphonuclear leukocyte adhesion to cerebral microvascular endothelial cells in vitro.

INTRODUCTION: Sepsis-associated encephalopathy (SAE) is a state of acute brain dysfunction in response to a systemic infection. We propose that systemic inflammation during sepsis causes increased adhesion of leukocytes to the brain microvasculature, resulting in blood-brain barrier dysfunction. Thus, our objectives were to measure inflammatory analytes in plasma of severe sepsis patients to create an experimental cytokine mixture (CM), and to use this CM to investigate the activation and interactions of polymorphonuclear leukocytes (PMN) and human cerebrovascular endothelial cells (hCMEC/D3) in vitro. METHODS: The concentrations of 41 inflammatory analytes were quantified in plasma obtained from 20 severe sepsis patients and 20 age- and sex-matched healthy controls employing an antibody microarray. Two CMs were prepared to mimic severe sepsis (SSCM) and control (CCM), and these CMs were then used for PMN and hCMEC/D3 stimulation in vitro. PMN adhesion to hCMEC/D3 was assessed under conditions of flow (shear stress 0.7 dyn/cm(2)). RESULTS: Eight inflammatory analytes elevated in plasma obtained from severe sepsis patients were used to prepare SSCM and CCM. Stimulation of PMN with SSCM led to a marked increase in PMN adhesion to hCMEC/D3, as compared to CCM. PMN adhesion was abolished with neutralizing antibodies to either β2 (CD18), αL/β2 (CD11α/CD18; LFA-1) or αM/β2 (CD11β/CD18; Mac-1) integrins. In addition, immune-neutralization of the endothelial (hCMEC/D3) cell adhesion molecule, ICAM-1 (CD54) also suppressed PMN adhesion. CONCLUSIONS: Human SSCM up-regulates PMN pro-adhesive phenotype and promotes PMN adhesion to cerebrovascular endothelial cells through a β2-integrin-ICAM-1-dependent mechanism. PMN adhesion to the brain microvasculature may contribute to SAE

Human severe sepsis cytokine mixture increases beta 2-integrin-dependent polymorphonuclear leukocyte adhesion to cerebral microvascular endothelial cells in vitro

Introduction: Sepsis-associated encephalopathy (SAE) is a state of acute brain dysfunction in response to a systemic infection. We propose that systemic inflammation during sepsis causes increased adhesion of leukocytes to the brain microvasculature, resulting in blood-brain barrier dysfunction. Thus, our objectives were to measure inflammatory analytes in plasma of severe sepsis patients to create an experimental cytokine mixture (CM), and to use this CM to investigate the activation and interactions of polymorphonuclear leukocytes (PMN) and human cerebrovascular endothelial cells (hCMEC/D3) in vitro. Methods: The concentrations of 41 inflammatory analytes were quantified in plasma obtained from 20 severe sepsis patients and 20 age- and sex-matched healthy controls employing an antibody microarray. Two CMs were prepared to mimic severe sepsis (SSCM) and control (CCM), and these CMs were then used for PMN and hCMEC/D3 stimulation in vitro. PMN adhesion to hCMEC/D3 was assessed under conditions of flow (shear stress 0.7 dyn/cm(2)). Results: Eight inflammatory analytes elevated in plasma obtained from severe sepsis patients were used to prepare SSCM and CCM. Stimulation of PMN with SSCM led to a marked increase in PMN adhesion to hCMEC/D3, as compared to CCM. PMN adhesion was abolished with neutralizing antibodies to either beta 2 (CD18), alpha(L)/beta(2) (CD11 alpha/CD18; LFA-1) or alpha(M)/beta(2) (CD11 beta/CD18; Mac-1) integrins. In addition, immune-neutralization of the endothelial (hCMEC/D3) cell adhesion molecule, ICAM-1 (CD54) also suppressed PMN adhesion. Conclusions: Human SSCM up-regulates PMN pro-adhesive phenotype and promotes PMN adhesion to cerebrovascular endothelial cells through a beta 2-integrin-ICAM-1-dependent mechanism. PMN adhesion to the brain microvasculature may contribute to SAE

A Gene Co-Expression Network in Whole Blood of Schizophrenia Patients Is Independent of Antipsychotic-Use and Enriched for Brain-Expressed Genes

Despite large-scale genome-wide association studies (GWAS), the underlying genes for schizophrenia are largely unknown. Additional approaches are therefore required to identify the genetic background of this disorder. Here we report findings from a large gene expression study in peripheral blood of schizophrenia patients and controls. We applied a systems biology approach to genome-wide expression data from whole blood of 92 medicated and 29 antipsychotic-free schizophrenia patients and 118 healthy controls. We show that gene expression profiling in whole blood can identify twelve large gene co-expression modules associated with schizophrenia. Several of these disease related modules are likely to reflect expression changes due to antipsychotic medication. However, two of the disease modules could be replicated in an independent second data set involving antipsychotic-free patients and controls. One of these robustly defined disease modules is significantly enriched with brain-expressed genes and with genetic variants that were implicated in a GWAS study, which could imply a causal role in schizophrenia etiology. The most highly connected intramodular hub gene in this module (ABCF1), is located in, and regulated by the major histocompatibility (MHC) complex, which is intriguing in light of the fact that common allelic variants from the MHC region have been implicated in schizophrenia. This suggests that the MHC increases schizophrenia susceptibility via altered gene expression of regulatory genes in this network