The AdS 3 × S 3 × S 3 × S 1 worldsheet S matrix

We investigate type IIB strings on AdS 3 × S 3 × S 3 × S 1 with mixed Ramond–Ramond and Neveu–Schwarz–Neveu–Schwarz flux. By suitably gauge-fixing the closed string Green–Schwarz action of this theory, we derive the off-shell symmetry algebra and its representations. We use these to determine the non-perturbative worldsheet S matrix of fundamental excitations in the theory. The analysis involves both massive and massless modes in complete generality. The S matrix we find involves a number of phase factors, which in turn satisfy crossing equations that we also determine. We comment on the nature of the heaviest modes of the theory, but leave their identification either as composites or bound-states to a future investigation

On the dressing factors, Bethe equations and Yangian symmetry of strings on AdS3 × S3 × T4

Integrability is believed to underlie the AdS3/CFT2 correspondence with sixteen supercharges. We elucidate the role of massless modes within this integrable framework. Firstly, we find the dressing factors that enter the massless and mixed-mass worldsheet S matrix. Secondly, we derive a set of all-loop Bethe Equations for the closed strings, determine their symmetries and weak-coupling limit. Thirdly, we investigate the underlying Yangian symmetry in the massless sector and show that it fits into the general framework of Yangian integrability. In addition, we compare our S matrix in the near-relativistic limit with recent perturbative worldsheet calculations of Sundin and Wulff

Targeting cancer metabolism: a therapeutic window opens

Genetic events in cancer activate signalling pathways that alter cell metabolism. Clinical evidence has linked cell metabolism with cancer outcomes. Together, these observations have raised interest in targeting metabolic enzymes for cancer therapy, but they have also raised concerns that these therapies would have unacceptable effects on normal cells. However, some of the first cancer therapies that were developed target the specific metabolic needs of cancer cells and remain effective agents in the clinic today. Research into how changes in cell metabolism promote tumour growth has accelerated in recent years. This has refocused efforts to target metabolic dependencies of cancer cells as a selective anticancer strategy.Burroughs Wellcome FundSmith Family FoundationStarr Cancer ConsortiumDamon Runyon Cancer Research FoundationNational Institutes of Health (U.S.

A rise in NAD precursor nicotinamide mononucleotide (NMN) after injury promotes axon degeneration.

NAD metabolism regulates diverse biological processes, including ageing, circadian rhythm and axon survival. Axons depend on the activity of the central enzyme in NAD biosynthesis, nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2), for their maintenance and degenerate rapidly when this activity is lost. However, whether axon survival is regulated by the supply of NAD or by another action of this enzyme remains unclear. Here we show that the nucleotide precursor of NAD, nicotinamide mononucleotide (NMN), accumulates after nerve injury and promotes axon degeneration. Inhibitors of NMN-synthesising enzyme NAMPT confer robust morphological and functional protection of injured axons and synapses despite lowering NAD. Exogenous NMN abolishes this protection, suggesting that NMN accumulation within axons after NMNAT2 degradation could promote degeneration. Ectopic expression of NMN deamidase, a bacterial NMN-scavenging enzyme, prolongs survival of injured axons, providing genetic evidence to support such a mechanism. NMN rises prior to degeneration and both the NAMPT inhibitor FK866 and the axon protective protein Wld(S) prevent this rise. These data indicate that the mechanism by which NMNAT and the related Wld(S) protein promote axon survival is by limiting NMN accumulation. They indicate a novel physiological function for NMN in mammals and reveal an unexpected link between new strategies for cancer chemotherapy and the treatment of axonopathies

Depth-dependent photodegradation of marine dissolved organic matter.

Marine dissolved organic matter (DOM) in surface and deep waters of the eastern Atlantic Ocean and Sargasso Sea was analyzed by excitation emission matrix (EEM) fluorescence spectroscopy and parallel factor analysis (PARAFAC). Photo-degradation with semi-continuous monitoring of EEMs and absorbance spectra was used to measure the photo-degradation kinetics and changes of the PARAFAC components in a depth profile of DOM at the Bermuda Atlantic Time Series (BATS) station in the Sargasso Sea. A five component model was fit to the EEMs, which included traditional terrestrial-like, marine-like, and protein-like components. Terrestrial-like components showed the expected high photo-reactivity, but surprisingly, the traditional marine-like peak showed slight photo-production in surface waters, which may account for its prevalence in marine systems. Surface waters were depleted in photo-labile components while protein-like fluorescent components were enriched, consistent with previous studies. Ultra-high resolution mass spectrometry detected unique aliphatic compounds in the surface waters at the BATS site, which may be photo-produced or photo-stable. Principle component and canonical analysis showed strong correlations between relative contributions of unsaturated/aromatic molecular formulas and depth, with aliphatic compounds more prevalent in surface waters and aromatic compounds in deep waters. Strong correlations were seen between these aromatic compounds and humic-like fluorescent components. The rapid photo-degradation of the deep-sea fluorescent DOM in addition to the surface water relative depletion of aromatic compounds suggests that deep-sea fluorescent DOM may be too photochemically labile to survive during overturning circulation