25 research outputs found
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
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 . 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 years.
With an average radio spectral index of we find that an
equipartition magnetic field for the remnant is 90~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 255\%.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
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A HIF1alpha 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 HIF1alpha. These findings explain the shared features of pheochromocytomas with VHL and SDH mutations and suggest an additional mechanism for increased HIF1alpha activity in tumors