Bell inequalities for entangled kaons and their unitary time evolution

We investigate Bell inequalities for neutral kaon systems from Phi resonance decay to test local realism versus quantum mechanics. We emphasize the unitary time evolution of the states, that means we also include all decay product states, in contrast to other authors. Only this guarantees the use of the complete Hilbert space. We develop a general formalism for Bell inequalities including both arbitrary "quasi spin" states and different times; finally we analyze Wigner-type inequalities. They contain an additional term, a correction function h, as compared to the spin 1/2 or photon case, which changes considerably the possibility of quantum mechanics to violate the Bell inequality. Examples for special "quasi spin" states are given, especially those which are sensitive to the CP parameters epsilon and epsilon'.Comment: REVTeX, 22 page

The Charge Form Factor of the Neutron at Low Momentum Transfer from the 2H⃗(e⃗,e′n)p^{2}\vec{\rm H}(\vec{\rm e},{\rm e}'{\rm n}){\rm p} Reaction

We report new measurements of the neutron charge form factor at low momentum transfer using quasielastic electrodisintegration of the deuteron. Longitudinally polarized electrons at an energy of 850 MeV were scattered from an isotopically pure, highly polarized deuterium gas target. The scattered electrons and coincident neutrons were measured by the Bates Large Acceptance Spectrometer Toroid (BLAST) detector. The neutron form factor ratio $G^{n}_{E}/G^{n}_{M}$ was extracted from the beam-target vector asymmetry $A_{ed}^{V}$ at four-momentum transfers $Q^{2}=0.14$, 0.20, 0.29 and 0.42 (GeV/c)$^{2}$.Comment: 5 pages, 3 figures, submitted to Phys. Rev. Let

Measurement of the proton electric to magnetic form factor ratio from \vec ^1H(\vec e, e'p)

We report the first precision measurement of the proton electric to magnetic form factor ratio from spin-dependent elastic scattering of longitudinally polarized electrons from a polarized hydrogen internal gas target. The measurement was performed at the MIT-Bates South Hall Ring over a range of four-momentum transfer squared $Q^2$ from 0.15 to 0.65 (GeV/c)$^2$. Significantly improved results on the proton electric and magnetic form factors are obtained in combination with previous cross-section data on elastic electron-proton scattering in the same $Q^2$ region.Comment: 4 pages, 2 figures, submitted to PR

Tobacco smoking and somatic mutations in human bronchial epithelium

Tobacco smoking causes lung cancer, a process that is driven by more than 60 carcinogens in cigarette smoke that directly damage and mutate DNA. The profound effects of tobacco on the genome of lung cancer cells are well-documented, but equivalent data for normal bronchial cells are lacking. Here we sequenced whole genomes of 632 colonies derived from single bronchial epithelial cells across 16 subjects. Tobacco smoking was the major influence on mutational burden, typically adding from 1,000 to 10,000 mutations per cell; massively increasing the variance both within and between subjects; and generating several distinct mutational signatures of substitutions and of insertions and deletions. A population of cells in individuals with a history of smoking had mutational burdens that were equivalent to those expected for people who had never smoked: these cells had less damage from tobacco-specific mutational processes, were fourfold more frequent in ex-smokers than current smokers and had considerably longer telomeres than their more-mutated counterparts. Driver mutations increased in frequency with age, affecting 4–14% of cells in middle-aged subjects who had never smoked. In current smokers, at least 25% of cells carried driver mutations and 0–6% of cells had two or even three drivers. Thus, tobacco smoking increases mutational burden, cell-to-cell heterogeneity and driver mutations, but quitting promotes replenishment of the bronchial epithelium from mitotically quiescent cells that have avoided tobacco mutagenesis

APOBEC mutagenesis is a common process in normal human small intestine

APOBEC mutational signatures SBS2 and SBS13 are common in many human cancer types. However, there is an incomplete understanding of its stimulus, when it occurs in the progression from normal to cancer cell and the APOBEC enzymes responsible. Here we whole-genome sequenced 342 microdissected normal epithelial crypts from the small intestines of 39 individuals and found that SBS2/SBS13 mutations were present in 17% of crypts, more frequent than most other normal tissues. Crypts with SBS2/SBS13 often had immediate crypt neighbors without SBS2/SBS13, suggesting that the underlying cause of SBS2/SBS13 is cell-intrinsic. APOBEC mutagenesis occurred in an episodic manner throughout the human lifespan, including in young children. APOBEC1 mRNA levels were very high in the small intestine epithelium, but low in the large intestine epithelium and other tissues. The results suggest that the high levels of SBS2/SBS13 in the small intestine are collateral damage from APOBEC1 fulfilling its physiological function of editing APOB mRNA. Whole-genome sequencing of healthy human epithelial crypts from the small intestines of 39 individuals highlights APOBEC enzymes as a common contributor to the overall mutational burden in this tissue.Peer reviewe

Entanglement, Bell Inequalities and Decoherence in Particle Physics

We demonstrate the relevance of entanglement, Bell inequalities and decoherence in particle physics. In particular, we study in detail the features of the ``strange'' $K^0 \bar K^0$ system as an example of entangled meson--antimeson systems. The analogies and differences to entangled spin--1/2 or photon systems are worked, the effects of a unitary time evolution of the meson system is demonstrated explicitly. After an introduction we present several types of Bell inequalities and show a remarkable connection to CP violation. We investigate the stability of entangled quantum systems pursuing the question how possible decoherence might arise due to the interaction of the system with its ``environment''. The decoherence is strikingly connected to the entanglement loss of common entanglement measures. Finally, some outlook of the field is presented.Comment: Lectures given at Quantum Coherence in Matter: from Quarks to Solids, 42. Internationale Universit\"atswochen f\"ur Theoretische Physik, Schladming, Austria, Feb. 28 -- March 6, 2004, submitted to Lecture Notes in Physics, Springer Verlag, 45 page

Notch signaling during human T cell development

Notch signaling is critical during multiple stages of T cell development in both mouse and human. Evidence has emerged in recent years that this pathway might regulate T-lineage differentiation differently between both species. Here, we review our current understanding of how Notch signaling is activated and used during human T cell development. First, we set the stage by describing the developmental steps that make up human T cell development before describing the expression profiles of Notch receptors, ligands, and target genes during this process. To delineate stage-specific roles for Notch signaling during human T cell development, we subsequently try to interpret the functional Notch studies that have been performed in light of these expression profiles and compare this to its suggested role in the mouse

Targetable NOTCH1 rearrangements in reninoma

Reninomas are exceedingly rare renin-secreting kidney tumours that derive from juxtaglomerular cells, specialised smooth muscle cells that reside at the vascular inlet of glomeruli. They are the central component of the juxtaglomerular apparatus which controls systemic blood pressure through the secretion of renin. We assess somatic changes in reninoma and find structural variants that generate canonical activating rearrangements of, NOTCH1 whilst removing its negative regulator, NRARP. Accordingly, in single reninoma nuclei we observe excessive renin and NOTCH1 signalling mRNAs, with a concomitant non-excess of NRARP expression. Re-analysis of previously published reninoma bulk transcriptomes further corroborates our observation of dysregulated Notch pathway signalling in reninoma. Our findings reveal NOTCH1 rearrangements in reninoma, therapeutically targetable through existing NOTCH1 inhibitors, and indicate that unscheduled Notch signalling may be a disease-defining feature of reninoma

An extended window of opportunity for G-CSF treatment in cerebral ischemia

BACKGROUND: Granulocyte-colony stimulating factor (G-CSF) is known as a powerful regulator of white blood cell proliferation and differentiation in mammals. We, and others, have shown that G-CSF is effective in treating cerebral ischemia in rodents, both relating to infarct size as well as functional recovery. G-CSF and its receptor are expressed by neurons, and G-CSF regulates apoptosis and neurogenesis, providing a rational basis for its beneficial short- and long-term actions in ischemia. In addition, G-CSF may contribute to re-endothelialisation and arteriogenesis in the vasculature of the ischemic penumbra. In addition to these trophic effects, G-CSF is a potent neuroprotective factor reliably reducing infarct size in different stroke models. RESULTS: Here, we have further delayed treatment and studied effects of G-CSF on infarct volume in the middle cerebral artery occlusion (MCAO) model and functional outcome in the cortical photothrombotic model. In the MCAO model, we applied a single dose of 60 μg/kg bodyweight G-CSF in rats 4 h after onset of ischemia. Infarct volume was determined 24 h after onset of ischemia. In the rat photothrombotic model, we applied 10 μg/kg bodyweight G-CSF daily for a period of 10 days starting either 24 or 72 h after induction of ischemia. G-CSF both decreased acute infarct volume in the MCAO model, and improved recovery in the photothrombotic model at delayed timepoints. CONCLUSION: These data further strengthen G-CSF's profile as a unique candidate stroke drug, and provide an experimental basis for application of G-CSF in the post-stroke recovery phase