The Right and Wrong of Growing Old: Assessing the Argument from Evolution

One argument which is frequently levelled against the enhancement of human biology is that we do not understand the evolved function of our bodies well enough to meddle in our biology without producing unintended and potentially catastrophic effects. In particular, this argument is levelled against attempts to slow or eliminate the processes of human ageing, or ‘senescence’, which cause us to grow decrepit before we die. In this article, I claim that even if this argument could usefully be applied against attempts to enhance other human traits, it cannot be valid in the case of attempts to enhance the various processes that constitute senescence. I begin by reviewing the biology of ageing to show how it consists of a number of unrelated traits. Then, following the arguments of a number of evolutionary biologists, I explain that every one of these traits is a product of evolutionary ‘neglect’ rather than ‘intent’. Finally, I consider the strongest version of the argument against enhancing senescence, which acknowledges these facts about the evolution of ageing but insists that we have nevertheless have prudential reasons to avoid enhancement wherever there is some uncertainty about the genetics or evolutionary function of a trait. I provide two reasons for rejecting this version of the argument as well, even in the case of human senescence, where such uncertainty is currently significant

The Ethical Placebo

Introduction Are placebos indeed deceptive? Is deception necessary in placebo prescription? Is placebo deception unethical? Placebo deception as a special case A limitation Other limitations on placebo deception What to do when pushed Conclusion

The relationship between adverse childhood experiences, coping using sex, and adult sexual coercion in non-incarcerated, community-based females

Adverse childhood experiences have been associated with negative outcomes in adulthood, including sexual offending. Using a cross-sectional design, we investigated whether self-reported adverse childhood experiences related to the perpetration of coercive sexual acts among 250 females recruited from the community. Furthermore, we examined whether sexualised coping mediated any potential relationship between childhood experiences and sexual coercion. A Spearman’s rank order correlation revealed no relationship between adverse childhood experiences and sexual coercion. However, adverse childhood experiences were significantly correlated with sexualised coping, which in turn was correlated with sexual coercion. Additionally, there was a significant but small indirect effect of adverse childhood experiences on sexual coercion through sexualised coping. Findings may help researchers to better understand the causal relationship between childhood experiences, sexual coping, and sexual coercion in females

Beyond Prejudice as Simple Antipathy: Hostile and Benevolent Sexism Across Cultures

The authors argue that complementary hostile and benevolent componen:s of sexism exist ac ro.ss cultures. Male dominance creates hostile sexism (HS). but men's dependence on women fosters benevolent sexism (BS)-subjectively positive attitudes that put women on a pedestal but reinforce their subordination. Research with 15,000 men and women in 19 nations showed that (a) HS and BS are coherenl constructs th at correlate positively across nations, but (b) HS predicts the ascription of negative and BS the ascription of positive traits to women, (c) relative to men, women are more likely to reject HS than BS. especially when overall levels of sexism in a culture are high, and (d) national averages on BS and HS predict gender inequal ity across nations. These results challenge prevailing notions of prejudice as an antipathy in that BS (an affectionate, patronizing ideology) reflects inequality and is a cross-culturally pervasive complement to HS

Considering the Definition of Addiction

The definition of addiction is explored. Elements of addiction derived from a literature search that uncovered 52 studies include: (a) engagement in the behavior to achieve appetitive effects, (b) preoccupation with the behavior, (c) temporary satiation, (d) loss of control, and (e) suffering negative consequences. Differences from compulsions are suggested. While there is some debate on what is intended by the elements of addictive behavior, we conclude that these five constituents provide a reasonable understanding of what is intended by the concept. Conceptual challenges for future research are mentioned

A human embryonic kidney 293T cell line mutated at the Golgi -mannosidase II locus

Disruption of Golgi -mannosidase II activity can result in type II congenital dyserythropoietic anemia and can induce lupus-like autoimmunity in mice. Here, we isolate a mutant human embryonic kidney (HEK) 293T cell line, called Lec36, that displays sensitivity to ricin that lies between the parental HEK 293T cells, whose secreted and membrane-expressed proteins are dominated by complex-type glycosylation, and 293S Lec1 cells, which only produce oligomannose-type N-linked glycans. The stem cell marker, 19A, was transiently expressed in the HEK 293T Lec36 cells, and in parental HEK 293T cells with and without the potent Golgi -mannosidase II inhibitor, swainsonine. Negative-ion nano-electrospray ionization mass spectra of the 19A N-linked glycans from HEK 293T Lec36 and swainsonine-treated HEK 293T cells were qualitatively indistinguishable and, as shown by collision-induced dissociation spectra, dominated by hybrid-type glycosylation. Nucleotide sequencing revealed mutations in each allele of MAN2A1, the gene encoding Golgi -mannosidase II: a point mutation in one allele mapping to the active site and an in-frame deletion of twelve-nucleotides in the other. Expression of wild-type but not the mutant MAN2A1 alleles in Lec36 cells restored processing of the 19A reporter glycoprotein to complex-type glycosylation. The Lec36 cell line will be useful for expressing therapeutic glycoproteins with hybrid-type glycans and provides a sensitive host for detecting mutations in human MAN2A1 causing type II congenital dyserythropoietic anemia