Climate and southern Africa's water-energy-food nexus

In southern Africa, the connections between climate and the water-energy-food nexus are strong. Physical and socioeconomic exposure to climate is high in many areas and in crucial economic sectors. Spatial interdependence is also high, driven for example, by the regional extent of many climate anomalies and river basins and aquifers that span national boundaries. There is now strong evidence of the effects of individual climate anomalies, but associations between national rainfall and Gross Domestic Product and crop production remain relatively weak. The majority of climate models project decreases in annual precipitation for southern Africa, typically by as much as 20% by the 2080s. Impact models suggest these changes would propagate into reduced water availability and crop yields. Recognition of spatial and sectoral interdependencies should inform policies, institutions and investments for enhancing water, energy and food security. Three key political and economic instruments could be strengthened for this purpose; the Southern African Development Community, the Southern African Power Pool, and trade of agricultural products amounting to significant transfers of embedded water

Biological Case Against Downlisting the Whooping Crane and for Improving Implementation under the Endangered Species Act

The Whooping Crane (Grus americana; WHCR) is a large, long-lived bird endemic to North America. The remnant population migrates between Aransas National Wildlife Refuge, USA, and Wood Buffalo National Park, Canada (AWBP), and has recovered from a nadir of 15-16 birds in 1941 to ~540 birds in 2022. Two ongoing reintroduction efforts in Louisiana and the Eastern Flyway together total ~150 birds. Evidence indicates the U.S. Fish and Wildlife Service (USFWS) is strongly considering downlisting the species from an endangered to a threatened status under the Endangered Species Act (ESA). We examined the current status of the WHCR through the lens of ESA threat factors, the USFWS’s Species Status Assessment (SSA) framework, and other avian downlisting actions to determine if the action is biologically warranted. Our research indicates that WHCRs are facing an intensification of most threat drivers across populations and important ranges. The AWBP is still relatively small compared to other crane species and most birds of conservation concern. To date, only one avian species has been downlisted from an endangered status with an estimated population of \u3c3,000 individuals. Representation in terms of WHCRs historic genetic, geographic, and life history variation remains limited. Also, the lack of spatial connectivity among populations, reliance of the reintroduced populations on supplementation, and continued habitat loss suggest that WHCR populations may not be resilient to large stochastic disturbances. Given that reintroduced populations are not self-sustaining, neither supplies true redundancy for the AWBP. Proposed downlisting before recovery plan population criteria have been met is objectively unwarranted 3 and reflects USFWS inconsistency across ESA actions. Only by incorporating basic quantitative criteria and added oversight into ESA listing decisions can we avoid an action as misguided as downlisting the Whooping Crane without consideration of its recovery plan criteria or ostensibly its population ecology

All-In-One: Advanced preparation of Human Parenchymal and Non-Parenchymal Liver Cells

BACKGROUND & AIMS: Liver cells are key players in innate immunity. Thus, studying primary isolated liver cells is necessary for determining their role in liver physiology and pathophysiology. In particular, the quantity and quality of isolated cells are crucial to their function. Our aim was to isolate a large quantity of high-quality human parenchymal and non-parenchymal cells from a single liver specimen. METHODS: Hepatocytes, Kupffer cells, liver sinusoidal endothelial cells, and stellate cells were isolated from liver tissues by collagenase perfusion in combination with low-speed centrifugation, density gradient centrifugation, and magnetic-activated cell sorting. The purity and functionality of cultured cell populations were controlled by determining their morphology, discriminative cell marker expression, and functional activity. RESULTS: Cell preparation yielded the following cell counts per gram of liver tissue: 2.0+/-0.4x107 hepatocytes, 1.8+/-0.5x106 Kupffer cells, 4.3+/-1.9x105 liver sinusoidal endothelial cells, and 3.2+/-0.5x105 stellate cells. Hepatocytes were identified by albumin (95.5+/-1.7%) and exhibited time-dependent activity of cytochrome P450 enzymes. Kupffer cells expressed CD68 (94.5+/-1.2%) and exhibited phagocytic activity, as determined with 1mum latex beads. Endothelial cells were CD146+ (97.8+/-1.1%) and exhibited efficient uptake of acetylated low-density lipoprotein. Hepatic stellate cells were identified by the expression of alpha-smooth muscle actin (97.1+/-1.5%). These cells further exhibited retinol (vitamin A)-mediated autofluorescence. CONCLUSIONS: Our isolation procedure for primary parenchymal and non-parenchymal liver cells resulted in cell populations of high purity and quality, with retained physiological functionality in vitro. Thus, this system may provide a valuable tool for determining liver function and disease

Pathways and hidden benefits of healthcare spending growth in the U.S.

After a brief reprieve, healthcare spending in the United States is expected to once again rise rapidly, continuing the trend of the past half-century. To inform the debate about whether policymakers should take action to contain high and rising medical care costs, we use panel data on all 50 states for the period 1993 to 2009 to estimate a healthcare spending model. Our framework, which includes a structural spending equation and a health production function, identifies the pathways through which medical technology and income affect healthcare costs and the potential health benefits they produce. We find evidence that medical technology and income are important factors fueling rising healthcare costs in the United States. However, our results also indicate they generate large health benefits in the form of lower mortality that may outweigh the costs and increase social economic welfare

New evidence on factors affecting the level and growth of U.S. health care spending

The dual problems of high and rising medical care expenditures and substantial differences in spending across geographic regions have long plagued the US health care system. We provide new evidence to explain why some states and regions of the country spend much more on medical care than others, and why health care spending for the nation as a whole has been growing rapidly over the last several decades. To do this, we estimate a health care spending panel data model using annual data on all 50 states for the period 1993–2009. Our model includes a number of socio-economic, health care provider, lifestyle and environmental variables that past studies indicate may affect the level or growth of aggregate health care spending. We exploit the time effect component of our model to obtain an upper-bound estimate of the effect of advances in medical technology. Our findings indicate that the most important factors influencing the level of spending are availability of providers, income, excessive alcohol consumption, Medicaid coverage, HMO health plans and the proportion of the population elderly and African-American. The principal drivers of growth have been the continual introduction of new medical technologies, and the growth of providers and income

Vitamin D ameliorates stress ligand expression elicited by free fatty acids in the hepatic stellate cell line LX-2

PubMedID: 21948571Background/aims: Hepatic stellate cells play an important role as the major source of fibrillar and non-fibrillar matrix proteins in the process of liver fibrosis. Natural killer cells have an anti-fibrotic effect through the killing of activated hepatic stellate cells. Major histocompatibility complex class I-related molecules, MICA and MICB, function as ligands for the NKG2D receptor and play an important role in hepatic stellate cells susceptibility to natural killer cells during hepatic inflammation. The aim of this study was therefore to investigate the effect of vitamin D 2 and free fatty acids on stress ligands and pro-fibrotic activity in LX-2 cells and human primary hepatic stellate cells. Methods: LX-2 cells and primary human hepatic stellate cells were treated with vitamin D 2 (10 -6 M) and free fatty acids at different concentrations (0.25 mM, 0.5 mM, and 1 mM) for 24 hours, and expressions of the stress ligands MICA/B as well as of transforming growth factor-ß, ?-smooth muscle actin and collagen 1? were assessed by quantitative real time-polymerase chain reaction. Results: Treatment of cells with 0.5 mM and 1 mM free fatty acids induced ?-smooth muscle actin and transforming growth factor-ß expression in LX-2 cells. Moreover, 1 mM free fatty acids resulted in increased expression of MICA. Surprisingly, collagen 1? expression was reduced after addition of free fatty acids. MICA/B expression in primary hepatic stellate cells was not affected by free fatty acids treatment. Vitamin D 2 treatment significantly downregulated the free fatty acids-induced expression of transforming growth factor-ß and ?-smooth muscle actin in LX-2 cells. Further, in hepatic stellate cells, a significant decrease in MICA/B mRNA with vitamin D 2, independent of free fatty acids treatment, was detectable. Conclusions: These results indicate that vitamin D2 may reduce inflammatory and pro-fibrogenic activity of stellate cells in vitro

Expression of apoptosis- and vitamin D pathway-related genes in hepatocellular carcinoma

PubMedID: 23635474Background/Aims: Hepatocellular carcinoma (HCC) is the sixth most common malignancy worldwide and therapeutic options are scarce. As they might represent future targets for cancer therapy, the expression of apoptosis-related genes in HCC is of particular interest. In this pilot study, we further examined apoptosis-related genes in human HCC and also focused on vitamin D signaling as this might be a regulator of HCC cell apoptosis. Methods: We employed tumor tissue and serum samples from 62 HCC patients as well as 62 healthy controls for these studies. Tissue and serum specimens were analyzed by quantitative RT-PCR, immunohistochemistry and ELISA. Results: In HCC patients the apoptosis marker M30 was found to be elevated and several pro-apoptotic (TRAIL, FasL and FasR) as well as anti-apoptotic genes (Mcl-1 and Bcl-2) were simultaneously upregulated in tumor tissue and especially tumor-surrounding tissue as compared to healthy control livers. Moreover, vitamin D serum levels were decreased in HCC patients whereas vitamin D receptor mRNA expression was increased in tumor tissue and tumor-surrounding tissue as compared to healthy livers. Conclusions: In human HCC, M30 serum levels are elevated indicating an increased cell turnover. Modulation of the vitamin D pathway might be a supportive, pro-apoptotic HCC therapy. Copyright © 2013 S. Karger AG, Basel