Macroscopic effects of the spectral structure in turbulent flows

Two aspects of turbulent flows have been the subject of extensive, split research efforts: macroscopic properties, such as the frictional drag experienced by a flow past a wall, and the turbulent spectrum. The turbulent spectrum may be said to represent the fabric of a turbulent state; in practice it is a power law of exponent \alpha (the "spectral exponent") that gives the revolving velocity of a turbulent fluctuation (or "eddy") of size s as a function of s. The link, if any, between macroscopic properties and the turbulent spectrum remains missing. Might it be found by contrasting the frictional drag in flows with differing types of spectra? Here we perform unprecedented measurements of the frictional drag in soap-film flows, where the spectral exponent \alpha = 3 and compare the results with the frictional drag in pipe flows, where the spectral exponent \alpha = 5/3. For moderate values of the Reynolds number Re (a measure of the strength of the turbulence), we find that in soap-film flows the frictional drag scales as Re^{-1/2}, whereas in pipe flows the frictional drag scales as Re^{-1/4} . Each of these scalings may be predicted from the attendant value of \alpha by using a new theory, in which the frictional drag is explicitly linked to the turbulent spectrum. Our work indicates that in turbulence, as in continuous phase transitions, macroscopic properties are governed by the spectral structure of the fluctuations.Comment: 6 pages, 3 figure

Somatic coding mutations in human induced pluripotent stem cells

Defined transcription factors can induce epigenetic reprogramming of adult mammalian cells into induced pluripotent stem cells. Although DNA factors are integrated during some reprogramming methods, it is unknown whether the genome remains unchanged at the single nucleotide level. Here we show that 22 human induced pluripotent stem (hiPS) cell lines reprogrammed using five different methods each contained an average of five protein-coding point mutations in the regions sampled (an estimated six protein coding point mutations per exome). The majority of these mutations were non-synonymous, nonsense, or splice variants, and were enriched in genes mutated or having causative effects in cancers. At least half of these reprogramming-associated mutations pre-existed in fibroblast progenitors at low frequencies, while the rest were newly occurring during or after reprogramming. Thus, hiPS cells acquire genetic modifications in addition to epigenetic modifications. Extensive genetic screening should become a standard procedure to ensure hiPS safety before clinical use

Unruhe und Ungewissheit – Stem Cells and Risks

“Die Unruhe und Ungewissheit sind unser Theil”, writes Goethe in a letter to the German novelist Sophie von la Roche in 1774. But is it the incalculable and indeterminate that cause disquiet, or is it our bustling pursuit of knowledge that makes us uncertain? Contemporary psychologists have taught us a great deal about the way we perceive risks and about the way affects and emotions influence our behaviour. Their research has shown that, as decision makers, as risk-assessors, and as risk-controllers, we are short-sighted, one-eyed and prone to serious errors of refraction. Who would have guessed that? We generate too few, and too narrow, hypotheses. We gather information, or evidence, in favour of our guesses that is too narrow, readily available, and skewed in favour of preferred beliefs. Once we have a pet hypothesis, we look for confirmatory evidence, neglecting countervailing evidence. We are simply not rational—not in the way our theories of rationality (logic, probability and decision-making) assume, at any rate. This is an alarming fact, considering the serious risk assessment and risk management tasks that lie ahead of us. This fact of irrationality (the phrase “fact of irrationality” seems fair, since the claim is supported by a vast amount of empirical evidence) should not just bring about unrest; it should make us think—think at least twice about our state of knowledge, in particular when the task is to make a serious risk-assessment in a convoluted situation [1]. We must not go gentle into that uncertainty. In this paper we will focus on a particular type of risk: the risk of unknown and uncertain long-term effects. The problem here is one of not knowing what will happen, and when we know it will, when; and of not being acquainted with the consequences, and therefore being unable to value the unfamiliar. Doing this our centre of attention will be human embryonic stem cells and induced pluripotent stem cells. Adult stem cells are not as interesting – they do not bear the same type of risks and moral difficulties. The paper urges risk analysts to take a Socratic approach to their discipline

MiR-23 similar to 27 similar to 24-mediated control of humoral immunity reveals a TOX-driven regulatory circuit in follicular helper T cell differentiation

Follicular helper T (TFH) cells are essential for generating protective humoral immunity. To date, microRNAs (miRNAs) have emerged as important players in regulating TFH cell biology. Here, we show that loss of miR-23~27~24 clusters in T cells resulted in elevated TFH cell frequencies upon different immune challenges, whereas overexpression of this miRNA family led to reduced TFH cell responses. Mechanistically, miR-23~27~24 clusters coordinately control TFH cells through targeting a network of genes that are crucial for TFH cell biology. Among them, thymocyte selection-associated HMG-box protein (TOX) was identified as a central transcription regulator in TFH cell development. TOX is highly up-regulated in both mouse and human TFH cells in a BCL6-dependent manner. In turn, TOX promotes the expression of multiple molecules that play critical roles in TFH cell differentiation and function. Collectively, our results establish a key miRNA regulon that maintains optimal TFH cell responses for resultant humoral immunity