Analysis of Rwandan Economic Performance Before and After the 1994 Genocide

This article analyses economic performance of Rwanda between 1973 and 2011. The economic history of Rwanda during this period can be divided into three periods i.e. pre-genocide period (1973-1989), inter-genocide period (1990-1994) and post—genocide period(1995-2011). Real GDP (constant 2000 US$) was used as the dependent variable and as a proxy for economic performance. The explanatory variables used were all expressed as percentages of GDP. They included Domestic Investment (DI), Foreign Direct Investment (FDI), Domestic Savings (DS) and Trade (TR).Chow test based on data for the entire period (1973-2011) rejected the null hypothesis of no structural change/break. After exclusion of observations for the conflict and genocide period, the Chow test  corroborated by the Wald test further showed strong presence of structural break for the pre and post genocide periods. The apparent existence of structural change for the two regimes suggests that the disequilibrium impact of genocide on the Rwandan economy was transitory. This could be explained by the interventions and policies initiated by post genocide leadership to develop, pacify and unite the people of Rwanda. Although structural change was established for the pre and post genocide periods, the change did not emanate from the shift in the intercept, but rather from slope vectors. This means the unobserved qualitative characteristics of the two regimes were similar but that the policies which led to changes in theexplanatory variables impacted differently on performance in the two regimes. Incidentally, it was found out that the bulk of the difference in the models across the two regimes was explained mainly by changes in the intercept, DI and FDI.Keywords: Economic performance, structural change/break, pooled model, fixed effects model, separate regressions, subset of coefficients

Dynamic Relationship Between Gross Domestic Product and Domestic Investments in Rwanda

This study uses a VAR model to analyse the dynamic relationship between gross domestic product (GDP) and domestic investment (DI) in Rwanda for the period 1970 to 2011. Several selection lag criteria chose a maximum lag of one and a bivariate VAR(1) model specification in levels was adopted. Unit root tests show that both GDP and DI series are nonstationary in levels but stationary in first differences, implying that both are integrated of order one I(1). Tests of cointegration established that GDP and DI are CI(1,1), suggesting there is a long-run equilibrium relationship between the two series. The error correction model indicates that DI adjusts to GDP with a lag whereby 0.2 percent of the discrepancy between long-term and short-term DI is corrected within the year. Granger causality tests show that there is unidirectional causality where GDP causes DI. The bivariate VAR (1) was unstable when estimated at levels, but was stable in first differences. Finally it was found out that GDP almost perfectly predicts DI in the estimated VAR (1) model. The forecasted value of DI in 2011 was 22.6%of GDP while the actual value was 22.7% of GDP. The small discrepancy may be attributed to the appropriate policy measures the Rwandan government and the private sector federation have thus far taken to facilitate investors in their businesses.Keywords: Gross Domestic Product (GDP); Domestic Investment (DI); Granger Causality; Cointegration; Vector Autoregression (VAR) and Vector Error Correction Model (VECM

High-resolution bathymetries and shorelines for the Great Lakes of the White Nile basin

This article is licensed under a Creative Commons Attribution 4.0 International License.HRBS-GLWNB 2020 presents the first open-source and high-resolution bathymetry, shoreline, and water level data for Lakes Victoria, Albert, Edward, and George in East Africa. For each Lake, these data have three primary products collected for this project. The bathymetric datasets were created from approximately 18 million acoustic soundings. Over 8,200 km of shorelines are delineated across the three lakes from high-resolution satellite systems and uncrewed aerial vehicles. Finally, these data are tied together by creating lake surface elevation models collected from GPS and altimeter measures. The data repository includes additional derived products, including surface areas, water volumes, shoreline lengths, lake elevation levels, and geodetic information. These data can be used to make allocation decisions regarding the freshwater resources within Africa, manage food resources on which many tens of millions of people rely, and help preserve the region’s endemic biodiversity. Finally, as these data are tied to globally consistent geodetic models, they can be used in future global and regional climate change models.ECU Open Access Publishing Support Fun

A CYP26B1 Polymorphism Enhances Retinoic Acid Catabolism and May Aggravate Atherosclerosis

All-trans retinoic acid, controlled by cytochrome P450, family 26 (CYP26) enzymes, potentially has beneficial effects in atherosclerosis treatment. This study investigates CYP26 subfamily B, polypeptide 1 (CYP26B1) in atherosclerosis and the effects of a genetic polymorphism in CYP26B1 on retinoid catabolism. We found that CYP26B1 mRNA was induced by retinoic acid in human atherosclerotic arteries, and CYP26B1 and the macrophage marker CD68 were colocalized in human atherosclerotic lesions. In mice, Cyp26B1 mRNA was higher in atherosclerotic arteries than in normal arteries. Databases were queried for nonsynonymous CYP26B1 single nucleotide polymorphisms (SNPs) and rs2241057 selected for further studies. Constructs of the CYP26B1 variants were created and used for production of purified proteins and transfection of macrophagelike cells. The minor variant catabolized retinoic acid with significantly higher efficiency, indicating that rs2241057 is functional and suggesting reduced retinoid availability in tissues with the minor variant. rs2241057 was investigated in a Stockholm Coronary Atherosclerosis Risk Factor (SCARF) subgroup. The minor allele was associated with slightly larger lesions, as determined by angiography. In summary, this study identifies the first CYP26B1 polymorphism that alters CYP26B1 capacity to metabolize retinoic acid. CYP26B1 was expressed in macrophage-rich areas of human atherosclerotic lesions, induced by retinoic acid and increased in murine atherosclerosis. Taken together, the results indicate that CYP26B1 capacity is genetically regulated and suggest that local CYP26B1 activity may influence atherosclerosis