Based on sub-arcsecond Atacama Large Millimeter/submillimeter Array (ALMA) and Submillimeter Array (SMA) 1.3 mm continuum images of the massive protocluster NGC 6334I obtained in 2015 and 2008, we find that the dust emission from MM1 has increased by a factor of 4.0±0.3 during the intervening years, and undergone a significant change in morphology. The continuum emission from the other cluster members (MM2, MM4 and the UCHII region MM3=NGC 6334F) has remained constant. Long term single-dish maser monitoring at HartRAO finds that multiple maser species toward NGC 6334I flared beginning in early 2015, a few months before our ALMA observation, and some persist in that state. New ALMA images obtained in 2016 July-August at 1.1 and 0.87 mm confirm the changes with respect to SMA 0.87 mm images from 2008, and indicate that the (sub)millimeter flaring has continued for at least a year. The excess continuum emission, centered on the hypercompact HII region MM1B, is extended and elongated (1.6 ′′ × 1.0 ′′ ≈ 2100 × 1300 au) with multiple peaks, suggestive of general heating of the surrounding subcomponents of MM1, some of which may trace clumps in a fragmented disk rather than separate protostars. In either case, these remarkable increases in maser and dust emission provide direct observational evidence of a sudden accretion event in the growth of a massive protostar yielding a sustained luminosity surge by a factor of 70 ± 20, analogous to the largest events in simulations by Meyer et al. (2017). This target provides an excellent opportunity to assess the impact of such a rare event on a protocluster over many years.
Cranial irradiation is a standard therapy for primary and metastatic brain tumors. A major drawback of radiotherapy (RT), however, is long-term cognitive loss that affects quality of life. Radiation-induced oxidative stress in normal brain tissue is thought to contribute to cognitive decline. We evaluated the effectiveness of a novel mimic of superoxide dismutase enzyme (SOD), MnTnBuOE-2-PyP5+ (Mn(III) meso-tetrakis(N-n-butoxyethylpyridinium-2-yl)porphyrin), to provide long-term neuroprotection following 8 Gy of whole brain irradiation. Long-term RT damage can only be assessed by brain imaging and neurocognitive studies. C57BL/6J mice were treated with MnTnBuOE-2-PyP5+ before and after RT and evaluated three months later. At this time point, drug concentration in the brain was 25 nmol/L. Mice treated with MnTnBuOE-2-PyP5+/RT exhibited MRI evidence for myelin preservation in the corpus callosum compared with saline/RT treatment. Corpus callosum histology demonstrated a significant loss of axons in the saline/RT group that was rescued in the MnTnBuOE-2-PyP5+/RT group. In addition, the saline/RT groups exhibited deficits in motor proficiency as assessed by the rotorod test and running wheel tests. These deficits were ameliorated in groups treated with MnTnBuOE-2-PyP5+/RT. Our data demonstrate that MnTnBuOE-2-PyP5+ is neuroprotective for oxidative stress damage caused by radiation exposure. In addition, glioblastoma cells were not protected by MnTnBuOE-2-PyP5+ combination with radiation in vitro. Likewise, the combination of MnTnBuOE-2-PyP5+ with radiation inhibited tumor growth more than RT alone in flank tumors. In summary, MnTnBuOE-2-PyP5+ has dual activity as a neuroprotector and a tumor radiosensitizer. Thus, it is an attractive candidate for adjuvant therapy with RT in future studies with patients with brain cancer.
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