Projecting prevalence by stage of care for prostate cancer and estimating future health service needs: protocol for a modelling study

Introduction Current strategies for the management of prostate cancer are inadequate in Australia. We will, in this study, estimate current service needs and project the future needs for prostate cancer patients in Australia. Methods and analysis First, we will project the future prevalence of prostate cancer for 2010-2018 using data for 1972-2008 from the New South Wales (NSW) Central Cancer Registry. These projections, based on modelled incidence and survival estimates, will be estimated using PIAMOD (Prevalence, Incidence, Analysis MODel) software. Then the total prevalence will be decomposed into five stages of care: initial care, continued monitoring, recurrence, last year of life and long-term survivor. Finally, data from the NSW Prostate Cancer Care and Outcomes Study, including data on patterns of treatment and associated quality of life, will be used to estimate the type and amount of services that will be needed by prostate cancer patients in each stage of care. In addition, Central Cancer Registry episode data will be used to estimate transition rates from localised or locally advanced prostate cancer to metastatic disease. Medicare and Pharmaceutical Benefits data, linked with Prostate Cancer Care and Outcomes Study data, will be used to complement the Cancer Registry episode data. The methods developed will be applied Australia-wide to obtain national estimates of the future prevalence of prostate cancer for different stages of clinical care. Ethics and dissemination This study was approved by the NSW Population and Health Services Research Ethics Committee. Results of the study will be disseminated widely to different interest groups and organisations through a report, conference presentations and peer-reviewed articles.This work is supported by the Prostate Cancer Foundation of Australia (grant number: PCFA – YI 0410). Both David Smith and Xue Qin Yu are supported by an Australian NHMRC Training Fellowship (Ref 1016598, 550002). Mark Clements is supported by an Australian NHMRC Career Development Award (Ref 471491)

Conduction mechanisms of epitaxial EuTiO3 thin films

To investigate leakage current density versus electric field characteristics, epitaxial EuTiO3 thin films were deposited on (001) SrTiO3 substrates by pulsed laser deposition and were post-annealed in a reducing atmosphere. This investigation found that conduction mechanisms are strongly related to temperature and voltage polarity. It was determined that from 50 to 150 K the dominant conduction mechanism was a space-charge-limited current under both negative and positive biases. From 200 to 300 K, the conduction mechanism shows Schottky emission and Fowler-Nordheim tunneling behaviors for the negative and positive biases, respectively. This work demonstrates that Eu3+ is one source of leakage current in EuTiO3 thin films.Comment: 17 pages,4 figures, conferenc

The Fornax Spectroscopic Survey I. Survey Strategy and Preliminary Results on the Redshift Distribution of a Complete Sample of Stars and Galaxies

The Fornax Spectroscopic Survey will use the Two degree Field spectrograph (2dF) of the Anglo-Australian Telescope to obtain spectra for a complete sample of all 14000 objects with 16.5<=Bj<=19.7 in a 12 square degree area centred on the Fornax Cluster. By selecting all objects---both stars and galaxies---independent of morphology, we cover a much larger range of surface brightness and scale size than previous surveys. In this paper we present results from the first 2dF field. Redshift distributions and velocity structures are shown for all observed objects in the direction of Fornax, including Galactic stars, galaxies in and around the Fornax Cluster, and for the background galaxy population. The velocity data for the stars show the contributions from the different Galactic components, plus a small tail to high velocities. We find no galaxies in the foreground to the cluster in our 2dF field. The Fornax Cluster is clearly defined kinematically. The mean velocity from the 26 cluster members having reliable redshifts is 1560+/-80 km/s. They show a velocity dispersion of 380+/-50 km/s. Large-scale structure can be traced behind the cluster to a redshift beyond z=0.3. Background compact galaxies and low surface brightness galaxies are found to follow the general galaxy distribution.Comment: LaTeX format; uses aa.cls (included). Accepted for publication in Astronomy and Astrophysic

Methods for preventing and treating cancer using N-thiolated β-lactam compounds and analogs thereof

The subject invention concerns N-thiolated β-lactam compounds of formula A, wherein R1 is a hydrocarbon group having 1–8 carbon atoms; R3 is an organothio group; and R4 is alkyl, alkenyl, alkynyl, aryl, heteroaryl, cycloalkyl, heterocycloalkyl, cycloalkenyl, or heterocycloalkenyl, and analogs and pharmaceutically acceptable salts, esters and amides thereof. The subject invention also concerns methods for inducing tumor cell death or inhibiting tumor cell proliferation, and methods for inducing DNA damage, inhibiting DNA replication, activating p38 MAP kinase, or activating caspase cascade activation, or releasing cytochrome C from mitochondria into the cytoplasm in a tumor cell. Methods for treating cancer using N-thiolated β-lactam compounds, as well as pharmaceutical compositions comprising the same are further disclosed

Deletion within the Src homology domain 3 of Bruton's tyrosine kinase resulting in X-linked agammaglobulinemia (XLA).

The gene responsible for X-linked agammaglobulinemia (XLA) has been recently identified to code for a cytoplasmic tyrosine kinase (Bruton's agammaglobulinemia tyrosine kinase, BTK), required for normal B cell development. BTK, like many other cytoplasmic tyrosine kinases, contains Src homology domains (SH2 and SH3), and catalytic kinase domain. SH3 domains are important for the targeting of signaling molecules to specific subcellular locations. We have identified a family with XLA whose affected members have a point mutation (g--&gt;a) at the 5' splice site of intron 8, resulting in the skipping of coding exon 8 and loss of 21 amino acids forming the COOH-terminal portion of the BTK SH3 domain. The study of three generations within this kinship, using restriction fragment length polymorphism and DNA analysis, allowed identification of the mutant X chromosome responsible for XLA and the carrier status in this family. BTK mRNA was present in normal amounts in Epstein-Barr virus-induced B lymphoblastoid cell lines established from affected family members. Although the SH3 deletion did not alter BTK protein stability and kinase activity of the truncated BTK protein was normal, the affected patients nevertheless have a severe B cell defect characteristic for XLA. The mutant protein was modeled using the normal BTK SH3 domain. The deletion results in loss of two COOH-terminal beta strands containing several residues critical for the formation of the putative SH3 ligand-binding pocket. We predict that, as a result, one or more crucial SH3 binding proteins fail to interact with BTK, interrupting the cytoplasmic signal transduction process required for B cell differentiation