Genetic Variation of MtDNA Cytochrome Oxidase Subunit I (COI) in Local Swamp Buffaloes in Indonesia

The objective of this research was to identify genetic variation of mitochondria DNA especially in cytochrome oxidase subunit I (COI) among population of Indonesian buffaloes. Samples of swamp buffaloes were collected from Aceh (n= 3), North Sumatra (n= 3), Riau (n= 3), Banten (n= 3), Central Java (n= 3), West Nusa Tenggara (n= 3) and South Sulawesi (n= 3), and riverine buffalo from North Sumatra (n= 1) out of group for comparison. Sequence of COI was analyzed using MEGA 5.10 software with neighbor-joining method kimura 2-parameter model to reconstruct phylogeny tree. The result showed that three haplotypes for swamp buffalo and one haplotype for riverine buffalo in Indonesia resulted from 41 polymorphic sites. This finding showed that the COI gene could be considered as a marker to distinguish among swamp buffaloes in Indonesia

Utilizing linkage disequilibrium information from Indian genome variation database for mapping mutations: SCA₁₂ case study

Stratification in heterogeneous populations poses an enormous challenge in linkage disequilibrium (LD) based identification of causal loci using surrogate markers. In this study, we demonstrate the enormous potential of endogamous Indian populations for mapping mutations in candidate genes using minimal SNPs, mainly due to larger regions of LD. We show this by a case study of the PPP2R2B gene (∼400 kb) that harbours a CAG repeat, expansion of which has been implicated in spinocerebellar ataxia type 12 (SCA12). Using LD information derived from Indian Genome Variation database (IGVdb) on populations which share similar ethnic and linguistic backgrounds as the SCA12 study population, we could map the causal loci using a minimal set of three SNPs, without the generation of additional basal data from the ethnically matched population. We could also demonstrate transferability of tagSNPs from a related HapMap population for mapping the mutation

Regional variation in livelihood strategies in Malawi

Livelihood strategies are identified at the household level as a function of assets held, using survey data. Only endowments that are likely to be predetermined are included in the empirical analysis. As expected, land, household size, age and primary education turn out to be important determinants of livelihood strategies. It appears that the relatively equal land-distribution among small-holders in Malawi still allows some wealthier households, and force others, to do non-farm activities. This, in turn, may lead to small-scale development within villages. Furthermore, investment in primary education, taking into account the low initial level of education in Malawi, is probably a good investment for rural development. And, we find it promising that younger people are able to find non-farm livelihoods. It also turns out to be significant regional variation in livelihood strategies, with more diversification in the Southern region, and with regional variation in the role of ethnic and religious identity as determinants of livelihood strategies. It appears that lack of agricultural opportunities in the south imply that households do, maybe more low-status, salaried work and household businesses in this region. For some households this may still be a way out of poverty. The policy implications for the poorer Southern region are not obvious. But, to the extent feasible, the farmers may learn from the more productive farmers in the Central region, where there is more emphasize on cash-crop production.Livelihoods Non-farm employment Multinomial-logit Malawi

Invariant Variation Problems

The problems in variation here concerned are such as to admit a continuous group (in Lie's sense); the conclusions that emerge from the corresponding differential equations find their most general expression in the theorems formulated in Section 1 and proved in following sections. Concerning these differential equations that arise from problems of variation, far more precise statements can be made than about arbitrary differential equations admitting of a group, which are the subject of Lie's researches. What is to follow, therefore, represents a combination of the methods of the formal calculus of variations with those of Lie's group theory. For special groups and problems in variation, this combination of methods is not new; I may cite Hamel and Herglotz for special finite groups, Lorentz and his pupils (for instance Fokker), Weyl and Klein for special infinite groups. Especially Klein's second Note and the present developments have been mutually influenced by each other, in which regard I may refer to the concluding remarks of Klein's Note.Comment: M. A. Tavel's English translation of Noether's Theorems (1918), reproduced by Frank Y. Wang. Thanks to Lloyd Kannenberg for corrigend

Variational causal claims in epidemiology

The paper examines definitions of ‘cause’ in the epidemiological literature. Those definitions all describe causes as factors that make a difference to the distribution of disease or to individual health status. In the philosophical jargon, causes in epidemiology are difference-makers. Two claims are defended. First, it is argued that those definitions underpin an epistemology and a methodology that hinge upon the notion of variation, contra the dominant Humean paradigm according to which we infer causality from regularity. Second, despite the fact that causes be defined in terms of ‘difference-making’, this cannot fixes the causal metaphysics. Causality in epidemiology ought to be interpreted according to the epistemic theory. In this approach relations are deemed causal depending on the evidence and on the available methods. Indeed, evidence to establish causal claims requires difference-making considerations; furthermore, those definitions of cause reflect the ‘variational’ epistemology and methodology of epidemiology