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Under the fold:

Rebels? No, Simply Scientists:

The problem of creativity is common to the arts and sciences. What distinguishes geniuses from ordinary mortals? In the arts, from Mozart to van Gogh, creativity has frequently been associated with the artist’s opposition to the society of their time. A good artist is a rebel. Paradoxically, whereas science might appear as a progressive rational construction of new knowledge, the same relation has been postulated between rebellion and scientific creativity. There are many historical accounts of how scientists who made decisive breakthroughs saw their ideas rejected, and became “rebels.”

A Molecular Link between Albinism and Visual Deficits:

Following a long tradition of demonizing those who look different, a surprising number of Hollywood movies cast serial killers, mass murderers, and assassins as albinos who invariably wind up meeting a gruesome end for their menacing ways. The cold-blooded sharpshooter portrayal is especially ludicrous, points out dermatologist Vail Reese (on http://www.skinema.com), given that vision problems routinely arise with this rare genetic condition.

Tolerance to Self: Which Cells Kill:

The mammalian immune system is tightly controlled to be activated by infectious agents but not by self. The ability to respond to the universe of potential antigens is mediated by a repertoire of T and B lymphocytes with an extraordinary range of specificities. The diversity of T and B lymphocyte antigen receptors is generated by completely random rearrangement of gene segments. Thus, this diverse repertoire must be purged of autoreactive specificities–a process known as negative selection. T cell tolerance is established in the thymus, an organ uniquely specialized to support the development of T cells and regulate their self-tolerance. In a recent paper published in PLoS Biology [1], Ahn and colleagues delve into a longstanding question about the process of negative selection: which cells in the thymus induce tolerance to self to prevent autoimmunity?

Animal Models of Inflammatory Bowel Disease at the Dawn of the New Genetics Era:

Crohn disease (CD) and ulcerative colitis (UC) are chronic inflammatory intestinal diseases with multifactorial etiologies. CD and UC are distinguished both by the location and by the nature of the inflammation. CD displays a transmural discontinuous inflammation, often with granulomas, in any part of the digestive system (most often ileum and/or colon). UC is almost exclusively restricted to the colon with a continuous superficial mucosal and submucosal inflammation. Both CD and UC can be further subphenotyped, suggesting that there is heterogeneity within each disorder. Despite many clinical and pathological features that distinguish CD and UC, the collective term inflammatory bowel disease (IBD) is often used for the two diseases. Clustering of IBD in families without specificity for a given form of IBD supports the notion of common genetic factors in the etiologies of the two conditions. In addition, higher concordance rates in monozygotic twins than dizygotic twins, particularly in CD, points to the importance of genes [1]. Recent advances in genetics have proven that both CD and UC are truly polygenic, but there are also strong environmental influences on IBD. This notion is first and foremost supported by the rapid increase in incidence of IBD during the past 50 years.

Birth Size and the Pathogenesis of Breast Cancer:

In a major undertaking reported in this issue of PLoS Medicine, a collaborative group co-ordinated by Isobel dos Santos Silva provide all but conclusive evidence that birth size is a predictor of breast cancer risk in adult life [1]. The researchers compiled and reanalysed individual participant data from 32 studies, comprising 22,058 cases of breast cancer. On the basis of reliable data retrieved from birth records, they found that an increase of birth weight by 500 grams was associated with a statistically significant 6% increase in breast cancer risk; whereas, controlling for birth weight, an increase of birth length by two centimetres was associated with a 9% increase in this risk. The relative size of the effects is small, but the individual studies driving the conclusion were of sound epidemiological design (cohort or nested case-control) and relied on objectively documented birth size parameters, allowing little room for selection or information bias. Now that the question of whether birth size is associated with breast cancer risk appears to be settled, a number of additional questions need to be addressed.

Making Sense of Non-Financial Competing Interests:

Imagine you’re a peer reviewer who’s received a request to referee a paper. The paper reports the results of a study using cell lines derived from an aborted fetus as a diagnostic tool in identifying certain viral infections. You are also a member of a religious organization morally opposed to fetal cell research. In your review, you raise questions about the study’s validity and methodology that might undermine the paper’s chance of publication.

Imagine you’re an editor and you receive a paper from the scientist who supervised your postdoctoral fellowship. It’s been a couple of years since you left his lab, but he has supported your career and you have warm feelings toward him; plus you still join your former lab mates occasionally at their monthly pub night. You select sympathetic reviewers and you fight hard for the paper at the editorial meeting.

These two scenarios reflect true ones; and each provides an example of how a personal interest might conflict with your responsibility to ensure the integrity of the publication process. Are such non-financial competing interests of less concern than commercial interests in the publication of research? Not if they disrupt honest reporting, fair review, and transparent publication.