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  • Svetlana Alexievich’s Voices from Chernobyl
  • As for fiction, I’m still puzzling over why Colm Tóibín’s Nora Webster (Pen­guin) failed to win a major literary prize in 2015. Judges just not up to it, I suppose.
  • Helen Ellis’s American Housewife

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  • found myself rereading Edward St Aubyn’s extraordinary Patrick Melrose novels
  • The Second Half (Weidenfeld & Nicolson), written with Roddy Doyle. Honest
  • For Christmas, I would like all of Philip Kerr’s Berlin Noir novels

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  • Introduction

    The changes of immune system during short- or long-duration of spaceflights include altered leukocyte distribution, altered serum cytokine level, reduced functions of natural killer (NK) cell, granulocyte, and monocyte, reduced leukocyte proliferation following activation, decreased delayed-type hypersensitivity to recall antigens, and latent viral reactivation [1-24]. Physiological and psychological stresses, microgravity, vibration exposure, disrupted circadian rhythms, impaired nutrition, and radiation were thought to contribute to the deregulation in immunity [24]

  • the head-down bed rest (HDBR) of -6° is determined to be the best by NASA, representing the most practical model for examining multi-system responses to microgravity in humans during spaceflight [14]. Using this model, various immnue alterations have been reported. Some of them mimic the changes found in astronauts [14,25-30], such as a gradual decrease in the number of IFN-γ-producing T cells and Cytomegalovirus- and Epstein-Barr virus-specific T cells. However, many such studies focused on the percentages of immune cell populations, cytokines in the serum, proliferation and cytotoxicities of T and NK cell

  • The fatigue in MS is not correlated with the extent of the CNS lesions but may be associated with where lesions are found. The association of lesions in the prefrontal, temporal and hypothalamic regions of the brain with fatigue suggests that damage to these regions causes fatigue.
    • Motor region – Lesions in the motor region are associated with quick fatigability in MS during physical exercises.
  • They proposed that the fatigue in MS probably results from a broad breakdown of a master subcortico-cortical network in the brain that governs alertness, energy production, etc. This suggests that different regions of the brain that keep us alert are simply not communicating well with each other.


    This hypothesis suggests that the thalamus may play a key role as it controls the activation of the cerebral cortex. Both fatigue and thalamic atrophy occur early in MS.

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  • The fatigue was a post-exertional, multidimensional, fluctuating phenomenon with varying  degrees of severity and several distinct characteristics and was accompanied by concomitant  symptoms. Fatigue was perceived to be an all-pervasive complex experience that substantially  reduced the ability to function personally or professionally. A range of trigger mechanisms  evoked or worsened the fatigue, but the affected were not always aware of what triggered  it. There was an excessive increase in fatigue in response to even minor activities.  An increase in fatigue resulted in the exacerbation of other concomitant symptoms.  The term fatigue does not capture the participants’ experiences, which are accompanied  by a considerable symptom burden that contributes to the illness experience and the  severe disability.

  • we followed the complete Norwegian population as of October 1, 2009, through national registries of vaccination, communicable diseases, primary health, and specialist health care until December 31, 2012. Hazard ratios (HRs) of CFS/ME, as diagnosed in the specialist health care services (diagnostic code G93.3 in the International Classification of Diseases, Version 10), after influenza infection and/or vaccination were estimated using Cox proportional-hazards regression.

    The incidence rate of CFS/ME was 2.08 per 100,000 person-months at risk. The adjusted HR of CFS/ME after pandemic vaccination was 0.97 (95% confidence interval [CI]: 0.91-1.04), while it was 2.04 (95% CI: 1.78-2.33) after being diagnosed with influenza infection during the peak pandemic period.


    Pandemic influenza A (H1N1) infection was associated with a more than two-fold increased risk of CFS/ME. We found no indication of increased risk of CFS/ME after vaccination. Our findings are consistent with a model whereby symptomatic infection, rather than antigenic stimulation may trigger CFS/ME.

  • We used quantitative magnetization transfer (qMT) imaging, a magnetic resonance imaging technique that enables quantification of changes in brain macromolecular density, together with experimentally induced inflammation to investigate effects of systemic inflammatory challenge on human brain microstructure.
  • The qMT data demonstrated that inflammation induced a rapid change in brain microstructure, reflected in increased magnetization exchange from free (water) to macromolecular-bound protons, within a discrete region of insular cortex implicated in representing internal physiologic states including inflammation. The functional significance of this change in insular microstructure was demonstrated by correlation with inflammation-induced fatigue and fluorodeoxyglucose positron emission tomography imaging, which revealed increased resting glucose metabolism within this region following the same inflammatory challenge.
  • Conclusions

    Together these observations highlight a novel structural biomarker of the central physiologic and behavioral effects of mild systemic inflammation

  • This morning we saw an example of this when a prominent study just published in PNAS drew some flack on Twitter. Small N, no replication, big story.  Personally I saw it as just another day at the office -- just another unremarkable exemplar of the low empirical standards we set for ourselves in cognitive neuroscience. I realise that sounds harsh but that's just how I feel about it. We need to set higher standards, and step one is being publicly honest about our reactions to published work.
  • Our field is peppered with small studies pumped out by petty fiefdoms, each vying for a coveted spot in high impact journals so we can have careers and get tenure and maybe make a few discoveries along the way. It would be disingenous to say that I'm any different. I've got my own fiefdom, just like the rest. It's no less petty; I am no better than anyone else.
  • Some folks get upset at the direct nature of post publication peer review. They might know the scientists involved; they might think they're careful; they might like them. And they might think such criticism is an attack on the integrity of the researchers -- that robust post-publication-peer-review, pointing out probable bias or low reproducibility, is tantamount to an accusation of misconduct. 
     This is false because questionable practices aren't the same as fraud and bias isn't the same as misconduct. Much, if not most, research bias happens unconsciously. It can and does distort our results despite our best efforts because we're humans rather than robots

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  • Observational epidemiological studies are prone to confounding, reverse causation and various biases and have generated findings  that have proved to be unreliable indicators of the causal effects of modifiable exposures on disease outcomes. Mendelian  randomization (MR) is a method that utilizes genetic variants that are robustly associated with such modifiable exposures  to generate more reliable evidence regarding which interventions should produce health benefits.

  • The epigenome may also harbour useful information about life-time exposures (measured or unmeasured) irrespective  of their influence on health or disease, creating the potential for a person-specific biosocial archive. Furthermore, such  data may prove of use in providing identifying information, providing the possibility of a future forensic epigenome
  • Epigenetics encompasses different mechanisms of gene expression regulation, the most commonly discussed ones being DNA methylation,  histone modifications and non-coding RNAs
  • Both blood and oral epithelium are tissues with a rapid turnover of cells and therefore are dependent on adult stem cells  (ASCs) for their maintenance, or tissue homeostasis as this has been termed,96 involving both tissue repair following injury and physiological tissue renewal.97 Briefly, ASCs are a cell sub-type that promotes tissue renewal by replenishing more differentiated cells (Figure 2).98,99 There are many differences between ASCs and more differentiated cells within the same tissue, including both gene expression98–100 and cellular environment.98,101

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  • Total samples with donor genotype

  • Science
  • analysis of RNA sequencing data from 1641 samples across  43 tissues from 175 individuals, generated as part of the pilot phase of the Genotype-Tissue Expression (GTEx) project.

  • MR analyses found that each genetically determined one-standard-deviation decrease in log-transformed 25OHD level conferred a 2.0-fold increase in the odds of MS (95% CI: 1.7–2.5; p = 7.7 × 10−12; I2 = 63%, 95% CI: 0%–88%).
  • A genetically lowered 25OHD level is strongly associated with increased susceptibility to MS. Whether vitamin D sufficiency can delay, or prevent, MS onset merits further investigation in long-term randomized controlled trials.

  • Panmixia (or panmixis) means random mating.[1][2]


    A panmictic population is one where all individuals are potential partners. This assumes that there are no mating restrictions, neither genetic nor behavioural, upon the population, and that therefore all recombination is possible. The Wahlund effect assumes that the overall population is panmictic.[3]


    In genetics, random mating involves the mating of individuals regardless of any physical, genetic, or social preference. In other words, the mating between two organisms is not influenced by any environmental, hereditary, or social interaction. Hence, potential mates have an equal chance of being selected

  • Random mating is a factor assumed in the Hardy-Weinberg principle and is distinct from lack of natural selection: in viability selection for instance, selection occurs before mating.

  • first described by Gray and Wheatley (1991) as a method for obtaining unbiased estimates of the effects of a putative causal variable without conducting a traditional randomised trial. These authors also coined the term Mendelian randomization. The design has a powerful control for reverse causation and confounding which otherwise bedevil epidemiological studies. [1
  • The reason for such spurious findings in observational epidemiology is most likely to be confounding by social, behavioural or physiological factors which are difficult to control for and particularly difficult to measure accurately. Moreover, many findings cannot be replicated by RCTs for ethical reasons.
  • The different genotypes possible from the same mating have been beautifully randomised by the meiotic process. A more perfect control of conditions is scarcely possible, than that of different genotypes appearing in the same litter." --R.A. Fisher[2]

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  • Hirsch suggested that, for physicists, a value for h of about 12 might be typical for advancement to tenure (associate professor) at major research universities. A value of about 18 could mean a full professorship, 15–20 could mean a fellowship in the American Physical Society, and 45 or higher could mean membership in the United States National Academy of Sciences.[13]
  • Among 36 new inductees in the National Academy of Sciences in biological and biomedical sciences in 2005, the median h-index was 57.[3]
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