Does change in positive affect mediate and/or moderate the impact of symptom distress on psychological adjustment after cancer diagnosis? A prospective analysis

Physical symptom distress is one of the commonest correlates of psychological adjustment in cancer patients. Positive affect (PA) can be a dynamic resource for patients to cope with the cancer-related physical demands. The present study examined whether differential patterns of change in PA were associated with anxiety and depressed mood, and whether PA modified the association between change in symptom distress and psychological distress in 215 Chinese people newly diagnosed with colorectal cancer (CRC). Participants completed measures of physical symptoms, PA, and anxiety and depression at diagnosis and again at 3-month follow-up. Multivariate analyses of covariance revealed that at follow-up, people reporting higher anxiety and depressed mood demonstrated loss in PA, whereas those reporting lower depressed mood demonstrated a gain in PA. Structural equation modelling revealed that change in PA significantly mediated and moderated the associations between increased symptom distress and anxiety and depressed mood. We conclude that in line with Hobfoll's conservation of resources theory, continuous physical symptom distress depletes PA of newly diagnosed cancer patients, resulting in higher levels of anxiety and depressed mood. Effectiveness of symptom management intervention could be enhanced by preserving or enhancing PA in patients. © 2010 Taylor & Francis.postprin

The Role of Implant Position on Longâ Term Success

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141259/1/cap0187.pd

Extended Functionality in Verifiable Searchable Encryption

Abstract. When outsourcing the storage of sensitive data to an (un-trusted) remote server, a data owner may choose to encrypt the data beforehand to preserve confidentiality. However, it is then difficult to efficiently retrieve specific portions of the data as the server is unable to identify the relevant information. Searchable encryption has been well studied as a solution to this problem, allowing data owners and other au-thorised users to generate search queries which the server may execute over the encrypted data to identify relevant data portions. However, many current schemes lack two important properties: verifia-bility of search results, and expressive queries. We introduce Extended Verifiable Searchable Encryption (eVSE) that permits a user to verify that search results are correct and complete. We also permit verifiabl

The marginally stable Bethe lattice spin glass revisited

Bethe lattice spins glasses are supposed to be marginally stable, i.e. their equilibrium probability distribution changes discontinuously when we add an external perturbation. So far the problem of a spin glass on a Bethe lattice has been studied only using an approximation where marginally stability is not present, which is wrong in the spin glass phase. Because of some technical difficulties, attempts at deriving a marginally stable solution have been confined to some perturbative regimes, high connectivity lattices or temperature close to the critical temperature. Using the cavity method, we propose a general non-perturbative approach to the Bethe lattice spin glass problem using approximations that should be hopeful consistent with marginal stability.Comment: 23 pages Revised version, hopefully clearer that the first one: six pages longe

A fresh look at the evolution and diversification of photochemical reaction centers

In this review, I reexamine the origin and diversification of photochemical reaction centers based on the known phylogenetic relations of the core subunits, and with the aid of sequence and structural alignments. I show, for example, that the protein folds at the C-terminus of the D1 and D2 subunits of Photosystem II, which are essential for the coordination of the water-oxidizing complex, were already in place in the most ancestral Type II reaction center subunit. I then evaluate the evolution of reaction centers in the context of the rise and expansion of the different groups of bacteria based on recent large-scale phylogenetic analyses. I find that the Heliobacteriaceae family of Firmicutes appears to be the earliest branching of the known groups of phototrophic bacteria; however, the origin of photochemical reaction centers and chlorophyll synthesis cannot be placed in this group. Moreover, it becomes evident that the Acidobacteria and the Proteobacteria shared a more recent common phototrophic ancestor, and this is also likely for the Chloroflexi and the Cyanobacteria. Finally, I argue that the discrepancies among the phylogenies of the reaction center proteins, chlorophyll synthesis enzymes, and the species tree of bacteria are best explained if both types of photochemical reaction centers evolved before the diversification of the known phyla of phototrophic bacteria. The primordial phototrophic ancestor must have had both Type I and Type II reaction centers

Observation of a ppb mass threshoud enhancement in \psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p}) decay

The decay channel $\psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p})$ is studied using a sample of $1.06\times 10^8$ $\psi^\prime$ events collected by the BESIII experiment at BEPCII. A strong enhancement at threshold is observed in the $p\bar{p}$ invariant mass spectrum. The enhancement can be fit with an $S$-wave Breit-Wigner resonance function with a resulting peak mass of $M=1861^{+6}_{-13} {\rm (stat)}^{+7}_{-26} {\rm (syst)} {\rm MeV/}c^2$ and a narrow width that is $\Gamma<38 {\rm MeV/}c^2$ at the 90% confidence level. These results are consistent with published BESII results. These mass and width values do not match with those of any known meson resonance.Comment: 5 pages, 3 figures, submitted to Chinese Physics

Phosphorylation of a splice variant of collapsin response mediator protein 2 in the nucleus of tumour cells links cyclin dependent kinase-5 to oncogenesis

Background Cyclin-dependent protein kinase-5 (CDK5) is an unusual member of the CDK family as it is not cell cycle regulated. However many of its substrates have roles in cell growth and oncogenesis, raising the possibility that CDK5 modulation could have therapeutic benefit. In order to establish whether changes in CDK5 activity are associated with oncogenesis one could quantify phosphorylation of CDK5 targets in disease tissue in comparison to appropriate controls. However the identity of physiological and pathophysiological CDK5 substrates remains the subject of debate, making the choice of CDK5 activity biomarkers difficult. Methods Here we use in vitro and in cell phosphorylation assays to identify novel features of CDK5 target sequence determinants that confer enhanced CDK5 selectivity, providing means to select substrate biomarkers of CDK5 activity with more confidence. We then characterize tools for the best CDK5 substrate we identified to monitor its phosphorylation in human tissue and use these to interrogate human tumour arrays. Results The close proximity of Arg/Lys amino acids and a proline two residues N-terminal to the phosphorylated residue both improve recognition of the substrate by CDK5. In contrast the presence of a proline two residues C-terminal to the target residue dramatically reduces phosphorylation rate. Serine-522 of Collapsin Response Mediator-2 (CRMP2) is a validated CDK5 substrate with many of these structural criteria. We generate and characterise phosphospecific antibodies to Ser522 and show that phosphorylation appears in human tumours (lung, breast, and lymphoma) in stark contrast to surrounding non-neoplastic tissue. In lung cancer the anti-phospho-Ser522 signal is positive in squamous cell carcinoma more frequently than adenocarcinoma. Finally we demonstrate that it is a specific and unusual splice variant of CRMP2 (CRMP2A) that is phosphorylated in tumour cells. Conclusions For the first time this data associates altered CDK5 substrate phosphorylation with oncogenesis in some but not all tumour types, implicating altered CDK5 activity in aspects of pathogenesis. These data identify a novel oncogenic mechanism where CDK5 activation induces CRMP2A phosphorylation in the nuclei of tumour cells