Land acquisition, investment, and development in the Lao coffee sector: Successes and failures

Despite the increasing acknowledgment of scholars and practitioners that many large-scale agricultural land acquisitions in developing countries fail or never materialize, empirical evidence about how and why they fail to date is still scarce. Too often, land deals are portrayed as straightforward investments and their success is taken for granted. Looking at the coffee sector in Laos, the authors of this article explore dimensions of the land grab debate that have not yet been sufficiently examined. Coffee concessionaires in southern Laos often fail to use all of the land granted them and fail to produce high yields on the land they do use. Thus, the authors challenge the often-assumed superiority and effectiveness of large-scale versus small-scale production, specifically the argument that they modernize agricultural production and optimize land use. They argue that examining failed investments is as important as studying successful ones for understanding the implications of the land grabbing phenomenon for social, economic, and environmental outcomes. Knowledge about the scale of “failed land deals” provides important motivation for national governments to close the gap between intentions and actual outcomes. This article engages with the current debate on quality of investment and challenges the approach of employing land concessions as a vehicle for economic development in the Lao coffee sector and in other sectors and countries.

Prolonged inflammation following critical illness may impair long-term survival: a hypothesis with potential therapeutic implications

Despite successful intensive care a substantial portion of critically ill patients dies after discharge from the intensive care unit or hospital. Observational studies investigating long-term survival of critically ill patients reported that most deaths occur during the first months or year after discharge. Only limited data on the causes of impaired quality of life and post-intensive care unit deaths exist in the current literature. In this manuscript we hypothesize that the acute inflammatory response which characteristically accompanies critical illness is ensued by a prolonged imbalance or activation of the immune system. Such a chronic low-grade inflammatory response to critical illness may be sub-clinical and persist for a variable period of time after discharge from the intensive care unit and hospital. Chronic inflammation is a well-recognized risk factor for long-term morbidity and mortality, particularly from cardiovascular causes, and may thus partly contribute to the impaired quality of life as well as increased morbidity and mortality following intensive care unit and hospital discharge of critically ill patients. Assuming that critical illness is indeed followed by a prolonged inflammatory response, important implications for treatment would arise. An interesting and potentially beneficial therapy could be the administration of immune-modulating drugs during the time after intensive care unit or hospital discharge until chronic inflammation has subsided. Statins are well-investigated and effective drugs to attenuate chronic inflammation and could potentially also improve long-term outcome of critically ill patients after intensive care unit or hospital discharge. Future studies evaluating the course of inflammation during and after critical illness as well as its response to statin therapy are required.

Critical roles for Rac GTPases in T-cell migration to and within lymph nodes

Naive T cells continuously recirculate between secondary lymphoid tissue via the blood and lymphatic systems, a process that maximizes the chances of an encounter between a T cell and its cognate antigen. This recirculation depends on signals from chemokine receptors, integrins, and the sphingosine-1-phosphate receptor. The authors of previous studies in other cell types have shown that Rac GTPases transduce signals leading to cell migration and adhesion; however, their roles in T cells are unknown. By using both 3-dimensional intravital and in vitro approaches, we show that Rac1- and Rac2-deficient T cells have multiple defects in this recirculation process. Rac-deficient T cells home very inefficiently to lymph nodes and the white pulp of the spleen, show reduced interstitial migration within lymph node parenchyma, and are defective in egress from lymph nodes. These mutant T cells show defective chemokine-induced chemotaxis, chemokinesis, and adhesion to integrin ligands. They have reduced lateral motility on endothelial cells and transmigrate in-efficiently. These multiple defects stem from critical roles for Rac1 and Rac2 in transducing chemokine and sphingosine-1-phosphate receptor 1 signals leading to motility and adhesion.