Effect of Backgrounding System on Steer Performance and Carcass Characteristics

The impact of 3 backgrounding systems: grazing corn residue with distillers grains supplementation at 0.86% BW/d, grazing an oats-brassica forage, or feeding a grower ration in a drylot on finishing performance and carcass characteristics were evaluated. Backgrounding phase gains were greatest for steers fed a grower ration in the drylot (3.58 lb/d), intermediate for steers grazing oats-brassica forage and then fed the grower ration for short period (2.65 lb/d), and least for steers grazing corn residue while supplemented distillers grains and then fed the grower ration for short period (2.22 lb/d). These backgrounding treatment differences did not affect ADG during the finishing period (3.73 lb/d). However, the 2 grazing treatments had greater DMI resulting in poorer F:G. Overall, these backgrounding systems did not affect carcass quality. Increased finishing phase cost for the 2 grazing treatments due to poorer F:G, can be off set by less input cost during backgrounding, but ultimately the cost effectiveness is dependent on the production resources and scenarios of each individual producer

Epistemic pluralism, epistemic relativism and ‘hinge’ epistemology

According to Paul Boghossian (2006, 73) a core tenet of epistemic relativism is what he calls epistemic pluralism, according to which (i) ‘there are many fundamentally different, genuinely alternative epistemic systems’, but (ii) ‘no facts by virtue of which one of these systems is more correct than any of the others’. Embracing the former claim is more or less uncontroversial–viz., a descriptive fact about epistemic diversity. The latter claim by contrast is very controversial. Interestingly, the Wittgenstenian ‘hinge’ epistemologist, in virtue of maintaining that rational evaluation is essentially local, will (arguably, at least) be committed to the more controversial leg of the epistemic pluralist thesis, simply in virtue of countenancing the descriptive leg. This paper does three central things. First, it is shown that this ‘relativistic’ reading of Wittgenstein’s epistemology is plausible only if the locality of rational evaluation (in conjunction with a reasonable appreciation of epistemic diversity) commits the Wittgenstenian to a further epistemic incommensurability thesis. Next, Duncan Pritchard’s (e.g., 2009; 2015) novel attempt to save the hinge epistemologist from a commitment to epistemic incommensurability is canvassed and critiqued. Finally, it is suggested how, regardless of whether Pritchard’s strategy is successful, there might be another very different way—drawing from recent work by John MacFarlane (2014)—for the hinge epistemologist to embrace epistemic pluralism while steering clear of epistemic relativism, understood in a very specific way

Teratology Primer-2nd Edition (7/9/2010)

Foreword: What is Teratology? “What a piece of work is an embryo!” as Hamlet might have said. “In form and moving how express and admirable! In complexity how infinite!” It starts as a single cell, which by repeated divisions gives rise to many genetically identical cells. These cells receive signals from their surroundings and from one another as to where they are in this ball of cells —front or back, right or left, headwards or tailwards, and what they are destined to become. Each cell commits itself to being one of many types; the cells migrate, combine into tissues, or get out of the way by dying at predetermined times and places. The tissues signal one another to take their own pathways; they bend, twist, and form organs. An organism emerges. This wondrous transformation from single celled simplicity to myriad-celled complexity is programmed by genes that, in the greatest mystery of all, are turned on and off at specified times and places to coordinate the process. It is a wonder that this marvelously emergent operation, where there are so many opportunities for mistakes, ever produces a well-formed and functional organism. And sometimes it doesn’t. Mistakes occur. Defective genes may disturb development in ways that lead to death or to malformations. Extrinsic factors may do the same. “Teratogenic” refers to factors that cause malformations, whether they be genes or environmental agents. The word comes from the Greek “teras,” for “monster,” a term applied in ancient times to babies with severe malformations, which were considered portents or, in the Latin, “monstra.” Malformations can happen in many ways. For example, when the neural plate rolls up to form the neural tube, it may not close completely, resulting in a neural tube defect—anencephaly if the opening is in the head region, or spina bifida if it is lower down. The embryonic processes that form the face may fail to fuse, resulting in a cleft lip. Later, the shelves that will form the palate may fail to move from the vertical to the horizontal, where they should meet in the midline and fuse, resulting in a cleft palate. Or they may meet, but fail to fuse, with the same result. The forebrain may fail to induce the overlying tissue to form the eye, so there is no eye (anophthalmia). The tissues between the toes may fail to break down as they should, and the toes remain webbed. Experimental teratology flourished in the 19th century, and embryologists knew well that the development of bird and frog embryos could be deranged by environmental “insults,” such as lack of oxygen (hypoxia). But the mammalian uterus was thought to be an impregnable barrier that would protect the embryo from such threats. By exclusion, mammalian malformations must be genetic, it was thought. In the early 1940s, several events changed this view. In Australia an astute ophthalmologist, Norman Gregg, established a connection between maternal rubella (German measles) and the triad of cataracts, heart malformations, and deafness. In Cincinnati Josef Warkany, an Austrian pediatrician showed that depriving female rats of vitamin B (riboflavin) could cause malformations in their offspring— one of the early experimental demonstrations of a teratogen. Warkany was trying to produce congenital cretinism by putting the rats on an iodine deficient diet. The diet did indeed cause malformations, but not because of the iodine deficiency; depleting the diet of iodine had also depleted it of riboflavin! Several other teratogens were found in experimental animals, including nitrogen mustard (an anti cancer drug), trypan blue (a dye), and hypoxia (lack of oxygen). The pendulum was swinging back; it seemed that malformations were not genetically, but environmentally caused. In Montreal, in the early 1950s, Clarke Fraser’s group wanted to bring genetics back into the picture. They had found that treating pregnant mice with cortisone caused cleft palate in the offspring, and showed that the frequency was high in some strains and low in others. The only difference was in the genes. So began “teratogenetics,” the study of how genes influence the embryo’s susceptibility to teratogens. The McGill group went on to develop the idea that an embryo’s genetically determined, normal, pattern of development could influence its susceptibility to a teratogen— the multifactorial threshold concept. For instance, an embryo must move its palate shelves from vertical to horizontal before a certain critical point or they will not meet and fuse. A teratogen that causes cleft palate by delaying shelf movement beyond this point is more likely to do so in an embryo whose genes normally move its shelves late. As studies of the basis for abnormal development progressed, patterns began to appear, and the principles of teratology were developed. These stated, in summary, that the probability of a malformation being produced by a teratogen depends on the dose of the agent, the stage at which the embryo is exposed, and the genotype of the embryo and mother. The number of mammalian teratogens grew, and those who worked with them began to meet from time to time, to talk about what they were finding, leading, in 1960, to the formation of the Teratology Society. There were, of course, concerns about whether these experimental teratogens would be a threat to human embryos, but it was thought, by me at least, that they were all “sledgehammer blows,” that would be teratogenic in people only at doses far above those to which human embryos would be exposed. So not to worry, or so we thought. Then came thalidomide, a totally unexpected catastrophe. The discovery that ordinary doses of this supposedly “harmless” sleeping pill and anti-nauseant could cause severe malformations in human babies galvanized this new field of teratology. Scientists who had been quietly working in their laboratories suddenly found themselves spending much of their time in conferences and workshops, sitting on advisory committees, acting as consultants for pharmaceutical companies, regulatory agencies, and lawyers, as well as redesigning their research plans. The field of teratology and developmental toxicology expanded rapidly. The following pages will show how far we have come, and how many important questions still remain to be answered. A lot of effort has gone into developing ways to predict how much of a hazard a particular experimental teratogen would be to the human embryo (chapters 9–19). It was recognized that animal studies might not prove a drug was “safe” for the human embryo (in spite of great pressure from legislators and the public to do so), since species can vary in their responses to teratogenic exposures. A number of human teratogens have been identified, and some, suspected of teratogenicity, have been exonerated—at least of a detectable risk (chapters 21–32). Regulations for testing drugs before market release have greatly improved (chapter 14). Other chapters deal with how much such things as population studies (chapter 11), post-marketing surveillance (chapter 13), and systems biology (chapter 16) add to our understanding. And, in a major advance, the maternal role of folate in preventing neural tube defects and other birth defects is being exploited (chapter 32). Encouraging women to take folic acid supplements and adding folate to flour have produced dramatic falls in the frequency of neural tube defects in many parts of the world. Progress has been made not only in the use of animal studies to predict human risks, but also to illumine how, and under what circumstances, teratogens act to produce malformations (chapters 2–8). These studies have contributed greatly to our knowledge of abnormal and also normal development. Now we are beginning to see exactly when and where the genes turn on and off in the embryo, to appreciate how they guide development and to gain exciting new insights into how genes and teratogens interact. The prospects for progress in the war on birth defects were never brighter. F. Clarke Fraser McGill University (Emeritus) Montreal, Quebec, Canad

Influence of the Temperature and the Genotype of the HSP90AA1 Gene over Sperm Chromatin Stability in Manchega Rams

The present study addresses the effect of heat stress on males' reproduction ability. For that, we have evaluated the sperm DNA fragmentation (DFI) by SCSA of ejaculates incubated at 37°C during 0, 24 and 48 hours after its collection, as a way to mimic the temperature circumstances to which spermatozoa will be subject to in the ewe uterus. The effects of temperature and temperature-humidity index (THI) from day 60 prior collection to the date of semen collection on DFI were examined. To better understand the causes determining the sensitivity of spermatozoa to heat, this study was conducted in 60 males with alternative genotypes for the SNP G/C−660 of the HSP90AA1 promoter, which encode for the Hsp90α protein. The Hsp90α protein predominates in the brain and testis, and its role in spermatogenesis has been described in several species. Ridge regression analyses showed that days 29 to 35 and 7 to 14 before sperm collection (bsc) were the most critical regarding the effect of heat stress over DFI values. Mixed model analyses revealed that DFI increases over a threshold of 30°C for maximum temperature and 22 for THI at days 29 to 35 and 7 to 14 bsc only in animals carrying the GG−660 genotype. The period 29–35 bsc coincide with the meiosis I process for which the effect of the Hsp90α has been described in mice. The period 7–14 bsc may correspond with later stages of the meiosis II and early stages of epididymal maturation in which the replacement of histones by protamines occurs. Because of GG−660 genotype has been associated to lower levels of HSP90AA1 expression, suboptimal amounts of HSP90AA1 mRNA in GG−660 animals under heat stress conditions make spermatozoa DNA more susceptible to be fragmented. Thus, selecting against the GG−660 genotype could decrease the DNA fragmentation and spermatozoa thermal susceptibility in the heat season, and its putative subsequent fertility gainsPublishe

X-ray Polarization Observations of BL Lacertae

Blazars are a class of jet-dominated active galactic nuclei with a typical double-humped spectral energy distribution. It is of common consensus the Synchrotron emission to be responsible for the low frequency peak, while the origin of the high frequency hump is still debated. The analysis of X-rays and their polarization can provide a valuable tool to understand the physical mechanisms responsible for the origin of high-energy emission of blazars. We report the first observations of BL Lacertae performed with the Imaging X-ray Polarimetry Explorer ({IXPE}), from which an upper limit to the polarization degree $\Pi_X<$12.6\% was found in the 2-8 keV band. We contemporaneously measured the polarization in radio, infrared, and optical wavelengths. Our multiwavelength polarization analysis disfavors a significant contribution of proton synchrotron radiation to the X-ray emission at these epochs. Instead, it supports a leptonic origin for the X-ray emission in BL Lac.Comment: 17 pages, 5 figures, accepted for publication in ApJ

Rethinking Epistemic Relativism

‘Relativism’ is often treated as a dirty word in philosophy. Showing that a view entails relativism is almost always considered tantamount to showing that it is nonsensical. However, relativistic theories are not entirely unappealing – they have features which might be tempting if they weren’t thought to be outweighed by problematic consequences. In this paper I argue that it’s possible to secure the intuitively appealing features of at least one kind of relativism – epistemic relativism – without having to accept any problematic consequences. I do this by defending what I call 'stratified relativism'

A Consistent Relativism&apos;,

Relativism is one of the most tenacious theories about truth, with a pedigree as old as philosophy itself. Nearly as ancient is the chief criticism of relativism, namely the charge that the theory is self-refuting. This paper develops a logic of relativism that (1) illuminates the classic self-refutation charge and shows how to escape it; (2) makes rigorous the ideas of truth as relative and truth as absolute, and shows the relations between them; (3) develops an intensional logic for relativism; (4) provides a framework in which relativists can consistently promote ethical, mathematical, scientific, religious, and political truths (among others) as being relative; (5) argues that the notion of incommensurability is far less troubling than is commonly thought; and &quot;We all know that cultural relativism is inconsistent.&quot; (Putnam 1983, p. 236) I Relativism is one of the most tenacious theories about truth, with a pedigree as old as philosophy itself. Nearly as ancient is the chief criticism of relativism, namely the charge that the theory is self-refuting. 1 This paper will develop a logic of relativism that will (1) illuminate the self-refutation charge and show how to escape it; (2) make rigorous the ideas of truth as relative and truth as absolute, and show the relations between them; (3) develop an intensional logic for relativism; (4) provide a framework in 1 Opponents of relativism are legion. Recent worthies who subscribe to the self-refutation thesis include Putnam (1981, pp. 119-24; see also the epigraph); Margolis (1991, pp. 9-13; the kind of relativism Margolis considers &quot;logically incoherent&quot; and I show is not is what he calls &quot;relationalism&quot;); Harris (1992, pp