69 research outputs found
Towards Descartes’ Scientific Method: a posteriori Evidence and the Rhetoric of Les Météores
I argue that Descartes uses his method as evidence in the Discours and Les Météores. I begin by establishing there is a single method in Descartes’ works, using his meteorology as a case study. First, I hold that the method of the Regulae is best explained by two examples: one scientific, his proof of the anaclastic curve (1626), and one metaphysical, his question of the essence and scope of human knowledge (1628). Based on this account, I suggest that the form of his early metaphysics (not its content) is similar to the method of doubt of the Meditationes. Second, I argue that Descartes’ explanation of the cause of parhelia (1629) likewise contains a formulation of this procedure. I provide a novel reading of Les Météores, where, following Descartes’ guidance in the Discours and Correspondance, I interpret his meteorology by reasoning from effects to causes, in this case, from Christoph Scheiner’s 1626 observation of parhelia to his meteorological foundation. This backwards orientation to Les Météores, I argue, reveals an instance of Descartes’ scientific method. I conclude with remarks on Descartes’ concept of evidentia, in which I explain how he incorporates a posteriori evidence and an apparent hypothetical foundation into his rationalist epistemology where he uses his method as evidence for his claims
Shared heritability and functional enrichment across six solid cancers
Correction: Nature Communications 10 (2019): art. 4386 DOI: 10.1038/s41467-019-12095-8Quantifying the genetic correlation between cancers can provide important insights into the mechanisms driving cancer etiology. Using genome-wide association study summary statistics across six cancer types based on a total of 296,215 cases and 301,319 controls of European ancestry, here we estimate the pair-wise genetic correlations between breast, colorectal, head/neck, lung, ovary and prostate cancer, and between cancers and 38 other diseases. We observed statistically significant genetic correlations between lung and head/neck cancer (r(g) = 0.57, p = 4.6 x 10(-8)), breast and ovarian cancer (r(g) = 0.24, p = 7 x 10(-5)), breast and lung cancer (r(g) = 0.18, p = 1.5 x 10(-6)) and breast and colorectal cancer (r(g) = 0.15, p = 1.1 x 10(-4)). We also found that multiple cancers are genetically correlated with non-cancer traits including smoking, psychiatric diseases and metabolic characteristics. Functional enrichment analysis revealed a significant excess contribution of conserved and regulatory regions to cancer heritability. Our comprehensive analysis of cross-cancer heritability suggests that solid tumors arising across tissues share in part a common germline genetic basis.Peer reviewe
Why Did so Many People Make so Many Ex Post Bad Decisions? The Causes of the Foreclosure Crisis
Shared heritability and functional enrichment across six solid cancers
Quantifying the genetic correlation between cancers can provide important insights into the mechanisms driving cancer etiology. Using genome-wide association study summary statistics across six cancer types based on a total of 296,215 cases and 301,319 controls of European ancestry, here we estimate the pair-wise genetic correlations between breast, colorectal, head/neck, lung, ovary and prostate cancer, and between cancers and 38 other diseases. We observed statistically significant genetic correlations between lung and head/neck cancer (r(g) = 0.57, p = 4.6 x 10(-8)), breast and ovarian cancer (r(g) = 0.24, p = 7 x 10(-5)), breast and lung cancer (r(g) = 0.18, p = 1.5 x 10(-6)) and breast and colorectal cancer (r(g) = 0.15, p = 1.1 x 10(-4)). We also found that multiple cancers are genetically correlated with non-cancer traits including smoking, psychiatric diseases and metabolic characteristics. Functional enrichment analysis revealed a significant excess contribution of conserved and regulatory regions to cancer heritability. Our comprehensive analysis of cross-cancer heritability suggests that solid tumors arising across tissues share in part a common germline genetic basis
The laboratory diagnosis of Trichomonas vaginalis
Trichomonas vaginalis, a parasitic protozoa that causes the sexually transmitted infection trichomoniasis, is the sexually transmitted infection with the largest annual incidence, exceeding 170 million cases per year. The disease can be difficult to diagnose due to its heterogeneous presentation and problems with diagnostic testing. All diagnostic tests are fraught with imperfections, but the old, reliable wet mount examination (in trained hands), and the newer InPouch method may be advantageous due to simplicity in technology and cost. The present article reviews the pros and cons of culture, antibody and nucleic acid-based technologies that may point to future diagnostic advances
New concepts in the diagnosis and pathogenesis of Trichomonas vaginalis
Trichomonas vaginalis infection is the most commonly encountered sexually transmitted disease. There is a need for more accurate and rapid laboratory diagnostic methods, leading to better control and treatment strategies. Various virulence factors such as adherence, contact-independent factors, hemolysis and acquisition of host macromolecules have been shown to play a role in the pathogenesis of this infection. Detection of the factors that are only present in the pathogenic isolates of trichomonads will lead to a better understanding of the epidemiology of this pathogen. Culture technique is highly specific compared with microscopic techniques, but it is time consuming. Immunological techniques lack proper correlation with clinical manifestations. The application of monoclonal antibodies, either singly or in a group that recognizes a common antigen, along with methods such as detection of common DNA fragment from clinical specimens, may have a promising future in the laboratory diagnosis of trichomoniasis
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