HFPK 334: An unusual Supernova Remnant in the Small Magellanic Cloud

We present new Australia Telescope Compact Array (ATCA) radio-continuum and XMM-Newton/Chandra X-ray Observatory (CXO) observations of the unusual supernova remnant HFPK 334 in the Small Magellanic Cloud (SMC). The remnant follows a shell type morphology in the radio-continuum and has a size of $\sim$20~pc at the SMC distance. The X-ray morphology is similar, however, we detect a prominent point source close to the center of the SNR exhibiting a spectrum with a best fit powerlaw with a photon index of $\Gamma = 2.7 \pm 0.5$. This central point source is most likely a background object and cannot be directly associated with the remnant. The high temperature, nonequilibrium conditions in the diffuse region suggest that this gas has been recently shocked and point toward a younger SNR with an age of $\lesssim 1800$ years. With an average radio spectral index of $\alpha=-0.59\pm0.09$ we find that an equipartition magnetic field for the remnant is $\sim$90~$\mu$G, a value typical of younger SNRs in low-density environments. Also, we report detection of scattered radio polarisation across the remnant at 20~cm, with a peak fractional polarisation level of 25$\pm$5\%.Comment: 19 pages, 6-figures, submitted to A

A HIF1α Regulatory Loop Links Hypoxia and Mitochondrial Signals in Pheochromocytomas

Pheochromocytomas are neural crest–derived tumors that arise from inherited or sporadic mutations in at least six independent genes. The proteins encoded by these multiple genes regulate distinct functions. We show here a functional link between tumors with VHL mutations and those with disruption of the genes encoding for succinate dehydrogenase (SDH) subunits B (SDHB) and D (SDHD). A transcription profile of reduced oxidoreductase is detected in all three of these tumor types, together with an angiogenesis/hypoxia profile typical of VHL dysfunction. The oxidoreductase defect, not previously detected in VHL-null tumors, is explained by suppression of the SDHB protein, a component of mitochondrial complex II. The decrease in SDHB is also noted in tumors with SDHD mutations. Gain-of-function and loss-of-function analyses show that the link between hypoxia signals (via VHL) and mitochondrial signals (via SDH) is mediated by HIF1α. These findings explain the shared features of pheochromocytomas with VHL and SDH mutations and suggest an additional mechanism for increased HIF1α activity in tumors