Interferometric weak value deflections: quantum and classical treatments

We derive the weak value deflection given in a paper by Dixon et al. (Phys. Rev. Lett. 102, 173601 (2009)) both quantum mechanically and classically. This paper is meant to cover some of the mathematical details omitted in that paper owing to space constraints

The factors influencing car use in a cycle-friendly city: the case of Cambridge.

Encouraging people out of their cars and into other modes of transport, which has major advantages for health, the environment and urban development, has proved difficult. Greater understanding of the influences that lead people to use the car, particularly for shorter journeys, may help to achieve this. This paper examines the predictors of car use compared with the bicycle to explore how it may be possible to persuade more people to use the bicycle instead of the car. Multivariable logistic regression was used to examine the socio-demographic, transport and health-related correlates of mode choice for work, shopping and leisure trips in Cambridge, a city with high levels of cycling by UK standards. The key findings are that commuting distance and free workplace parking were strongly associated with use of the car for work trips, and car availability and lower levels of education were associated with car use for leisure, shopping and short-distanced commuting trips. The case of Cambridge shows that more policies could be adopted, particularly a reduction in free car parking, to increase cycling and reduce the use of the car, especially over short distances

Characterization of endogenous players in Fibroblast Growth Factor‐regulated functions of hypothalamic tanycytes and energy‐balance nuclei

The mammalian hypothalamus regulates key homeostatic and neuroendocrine functions ranging from circadian rhythm and energy‐balance to growth and reproductive cycles via the hypothalamo‐pituitary and hypothalamo‐thyroid axes. In addition to its neurons, tanycytes are taking centre stage in the short and long term augmentation and integration of diverse hypothalamic functions, but the genetic regulators and mediators of their involvement are poorly understood. Exogenous interventions have implicated Fibroblast growth factor (FGF) signalling, but the focal point of FGF action and any role for putative endogenous players also remains elusive. We carried out a comprehensive high‐resolution screen of FGF signalling pathway mediators and modifiers using a combination of in situ hybridization, immunolabelling and transgenic reporter mice, to map their spatial distribution in the adult hypothalamus. Our findings suggest that beta tanycytes are the likely focal point of exogenous and endogenous FGF action in the third ventricular wall, utilising FGF‐receptors (FGFRs) ‐1 and ‐2 IIIc isoforms, but not FGFR3. Key IIIc‐activating endogenous ligands include FGFs 1, 2, 9 and 18, which are expressed by a subset of ependymal and parenchymal cells. In the parenchymal compartment, FGFRs 1‐3 show divergent patterns, with FGFR1 predominant in neuronal nuclei and FGFR3 expression being associated with glial cell function. Intracrine FGFs are also present, suggestive of multiple modes of FGF function. Our findings provide a testable framework for understanding the complex role of FGFs in regulating the metabolic endocrine and neurogenic functions of hypothalamus in vivo

Antimalarial activity of the anticancer histone deacetylase inhibitor SB939

Histone deacetylase (HDAC) enzymes posttranslationally modify lysines on histone and nonhistone proteins and play crucial roles in epigenetic regulation and other important cellular processes. HDAC inhibitors (e.g., suberoylanilide hydroxamic acid [SAHA; also known as vorinostat]) are used clinically to treat some cancers and are under investigation for use against many other diseases. Development of new HDAC inhibitors for noncancer indications has the potential to be accelerated by piggy-backing onto cancer studies, as several HDAC inhibitors have undergone or are undergoing clinical trials. One such compound, SB939, is a new orally active hydroxamate-based HDAC inhibitor with an improved pharmacokinetic profile compared to that of SAHA. In this study, the in vitro and in vivo antiplasmodial activities of SB939 were investigated. SB939 was found to be a potent inhibitor of the growth of Plasmodium falciparum asexual-stage parasites in vitro (50% inhibitory concentration [IC50], 100 to 200 nM), causing hyperacetylation of parasite histone and nonhistone proteins. In combination with the aspartic protease inhibitor lopinavir, SB939 displayed additive activity. SB939 also potently inhibited the in vitro growth of exoerythrocytic-stage Plasmodium parasites in liver cells (IC50, similar to 150 nM), suggesting that inhibitor targeting to multiple malaria parasite life cycle stages may be possible. In an experimental in vivo murine model of cerebral malaria, orally administered SB939 significantly inhibited P. berghei ANKA parasite growth, preventing development of cerebral malaria-like symptoms. These results identify SB939 as a potent new antimalarial HDAC inhibitor and underscore the potential of investigating next-generation anticancer HDAC inhibitors as prospective new drug leads for treatment of malaria

NASA Response to 2015 M7.8 Nepal Earthquake

No abstract availabl

Innovative Analyses Support a Role for DNA Damage and an Aberrant Cell Cycle in Myelodysplastic Syndrome Pathogenesis

We used flow cytometry to analyze the cell cycle, DNA damage, and apoptosis in hematopoietic subsets in MDS marrow. Subsets were assigned using CD45, side scatter, CD34, and CD71. Cell cycle fractions were analyzed using DRAQ 5 (DNA content) and MPM-2 (mitoses). DNA damage was assessed using p-H2A.X, and apoptosis using Annexin V. Compared to controls, MDS patients demonstrated no increased mitoses in erythroid, myeloid, or CD34+ cells. Myeloid progenitors demonstrated increased G2 cells, which with no increased mitoses suggested delayed passage through G2. Myeloid progenitors demonstrated increased p-H2A.X, consistent with DNA damage causing this delay. Annexin V reactivity was equivalent in MDS and controls. Results for each parameter varied among hematopoietic compartments, demonstrating the need to analyze compartments separately. Our results suggest that peripheral cytopenias in MDS are due to delayed cell cycle passage of marrow progenitors and that this delayed passage and leukemic progression derive from excessive DNA damage