Letter to Editor

A rare case of myxedema with cardiac tamponad

The SAMI Galaxy Survey: The cluster redshift survey, target selection and cluster properties

We describe the selection of galaxies targeted in eight low redshift clusters (APMCC0917, A168, A4038, EDCC442, A3880, A2399, A119 and A85; $0.029 < z < 0.058$) as part of the Sydney-AAO Multi-Object integral field Spectrograph Galaxy Survey (SAMI-GS). We have conducted a redshift survey of these clusters using the AAOmega multi-object spectrograph on the 3.9m Anglo-Australian Telescope. The redshift survey is used to determine cluster membership and to characterise the dynamical properties of the clusters. In combination with existing data, the survey resulted in 21,257 reliable redshift measurements and 2899 confirmed cluster member galaxies. Our redshift catalogue has a high spectroscopic completeness ($\sim 94\%$) for $r_{\rm petro} \leq 19.4$ and clustercentric distances $R< 2\rm{R}_{200}$. We use the confirmed cluster member positions and redshifts to determine cluster velocity dispersion, $\rm{R}_{200}$, virial and caustic masses, as well as cluster structure. The clusters have virial masses $14.25 \leq {\rm log }({\rm M}_{200}/\rm{M}_{\odot}) \leq 15.19$. The cluster sample exhibits a range of dynamical states, from relatively relaxed-appearing systems, to clusters with strong indications of merger-related substructure. Aperture- and PSF-matched photometry are derived from SDSS and VST/ATLAS imaging and used to estimate stellar masses. These estimates, in combination with the redshifts, are used to define the input target catalogue for the cluster portion of the SAMI-GS. The primary SAMI-GS cluster targets have $R< \rm{R}_{200}$, velocities $|v_{\rm pec}| < 3.5\sigma_{200}$ and stellar masses $9.5 \leq {\rm log(M}^*_{approx}/\rm{M}_{\odot}) \leq 12$. Finally, we give an update on the SAMI-GS progress for the cluster regions

The emerging problem of bacterial resistance in cancer patients; proceedings of a workshop held by MASCC “Neutropenia, Infection and Myelosuppression” Study Group during the MASCC annual meeting held in Berlin on 27–29 June 2013

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Chronic Diseases in North-West Tanzania and Southern Uganda. Public Perceptions of Terminologies, Aetiologies, Symptoms and Preferred Management

Research outputs produced to support a quantitative population survey, quantitative health facility survey, focus groups and in-depth interviews performed by the projec

Complement C1q Activates Tumor Suppressor WWOX to Induce Apoptosis in Prostate Cancer Cells

BACKGROUND:Tissue exudates contain low levels of serum complement proteins, and their regulatory effects on prostate cancer progression are largely unknown. We examined specific serum complement components in coordinating the activation of tumor suppressors p53 and WWOX (also named FOR or WOX1) and kinases ERK, JNK1 and STAT3 in human prostate DU145 cells. METHODOLOGY/PRINCIPAL FINDINGS:DU145 cells were cultured overnight in 1% normal human serum, or in human serum depleted of an indicated complement protein. Under complement C1q- or C6-free conditions, WOX1 and ERK were mainly present in the cytoplasm without phosphorylation, whereas phosphorylated JNK1 was greatly accumulated in the nuclei. Exogenous C1q rapidly restored the WOX1 activation (with Tyr33 phosphorylation) in less than 2 hr. Without serum complement C9, p53 became activated, and hyaluronan (HA) reversed the effect. Under C6-free conditions, HA induced activation of STAT3, an enhancer of metastasis. Notably, exogenous C1q significantly induced apoptosis of WOX1-overexpressing DU145 cells, but not vehicle-expressing cells. A dominant negative and Y33R mutant of WOX1 blocked the apoptotic effect. C1q did not enhance p53-mediated apoptosis. By total internal reflection fluorescence (TIRF) microscopy, it was determined that C1q destabilized adherence of WOX1-expressing DU145 cells by partial detaching and inducing formation of clustered microvilli for focal adhesion particularly in between cells. These cells then underwent shrinkage, membrane blebbing and death. Remarkably, as determined by immunostaining, benign prostatic hyperplasia and prostate cancer were shown to have a significantly reduced expression of tissue C1q, compared to age-matched normal prostate tissues. CONCLUSIONS/SIGNIFICANCE:We conclude that complement C1q may induce apoptosis of prostate cancer cells by activating WOX1 and destabilizing cell adhesion. Downregulation of C1q enhances prostate hyperplasia and cancerous formation due to failure of WOX1 activation