Fast reconstruction of hyperspectral radiative transfer simulations by using small spectral subsets: application to the oxygen A band

Hyperspectral radiative transfer simulations are a versatile tool in remote sensing but can pose a major computational burden. We describe a simple method to construct hyperspectral simulation results by using only a small spectral subsample of the simulated wavelength range, thus leading to major speedups in such simulations. This is achieved by computing principal components for a small number of representative hyperspectral spectra and then deriving a reconstruction matrix for a specific spectral subset of channels to compute the hyperspectral data. The method is applied and discussed in detail using the example of top-of-atmosphere radiances in the oxygen A band, leading to speedups in the range of one to two orders of magnitude when compared to radiative transfer simulations at full spectral resolution

Potential of the TROPOspheric Monitoring Instrument (TROPOMI) onboard the Sentinel-5 Precursor for the monitoring of terrestrial chlorophyll fluorescence

Global monitoring of sun-induced chlorophyll fluorescence (SIF) is improving our knowledge about the photosynthetic functioning of terrestrial ecosystems. The feasibility of SIF retrievals from spaceborne atmospheric spectrometers has been demonstrated by a number of studies in the last years. In this work, we investigate the potential of the upcoming TROPOspheric Monitoring Instrument (TROPOMI) onboard the Sentinel-5 Precursor satellite mission for SIF retrieval. TROPOMI will sample the 675–775 nm spectral window with a spectral resolution of 0.5 nm and a pixel size of 7 km × 7 km. We use an extensive set of simulated TROPOMI data in order to assess the uncertainty of single SIF retrievals and subsequent spatio-temporal composites. Our results illustrate the enormous improvement in SIF monitoring achievable with TROPOMI with respect to comparable spectrometers currently in-flight, such as the Global Ozone Monitoring Experiment-2 (GOME-2) instrument. We find that TROPOMI can reduce global uncertainties in SIF mapping by more than a factor of 2 with respect to GOME-2, which comes together with an approximately 5-fold improvement in spatial sampling. Finally, we discuss the potential of TROPOMI to map other important vegetation parameters at a global scale with moderate spatial resolution and short revisit time. Those include leaf photosynthetic pigments and proxies for canopy structure, which will complement SIF retrievals for a self-contained description of vegetation condition and functioning

Potential of the TROPOspheric Monitoring Instrument (TROPOMI) onboard the Sentinel-5 Precursor for the monitoring of terrestrial chlorophyll fluorescence

Global monitoring of sun-induced chlorophyll fluorescence (SIF) is improving our knowledge about the photosynthetic functioning of terrestrial ecosystems. The feasibility of SIF retrievals from spaceborne atmospheric spectrometers has been demonstrated by a number of studies in the last years. In this work, we investigate the potential of the upcoming TROPOspheric Monitoring Instrument (TROPOMI) onboard the Sentinel-5 Precursor satellite mission for SIF retrieval. TROPOMI will sample the 675–775 nm spectral window with a spectral resolution of 0.5 nm and a pixel size of 7 km × 7 km. We use an extensive set of simulated TROPOMI data in order to assess the uncertainty of single SIF retrievals and subsequent spatio-temporal composites. Our results illustrate the enormous improvement in SIF monitoring achievable with TROPOMI with respect to comparable spectrometers currently in-flight, such as the Global Ozone Monitoring Experiment-2 (GOME-2) instrument. We find that TROPOMI can reduce global uncertainties in SIF mapping by more than a factor of 2 with respect to GOME-2, which comes together with an approximately 5-fold improvement in spatial sampling. Finally, we discuss the potential of TROPOMI to map other important vegetation parameters at a global scale with moderate spatial resolution and short revisit time. Those include leaf photosynthetic pigments and proxies for canopy structure, which will complement SIF retrievals for a self-contained description of vegetation condition and functioning

Space-based remote imaging spectroscopy of the Aliso Canyon CH_4 superemitter

The Aliso Canyon gas storage facility near Porter Ranch, California, produced a large accidental CH_4 release from October 2015 to February 2016. The Hyperion imaging spectrometer on board the EO-1 satellite successfully detected this event, achieving the first orbital attribution of CH_4 to a single anthropogenic superemitter. Hyperion measured shortwave infrared signatures of CH_4 near 2.3 μm at 0.01 μm spectral resolution and 30 m spatial resolution. It detected the plume on three overpasses, mapping its magnitude and morphology. These orbital observations were consistent with measurements by airborne instruments. We evaluate Hyperion instrument performance, draw implications for future orbital instruments, and extrapolate the potential for a global survey of CH_4 superemitters

A p53-independent role for the MDM2 antagonist Nutlin-3 in DNA damage response initiation.

BACKGROUND: The mammalian DNA-damage response (DDR) has evolved to protect genome stability and maximize cell survival following DNA-damage. One of the key regulators of the DDR is p53, itself tightly regulated by MDM2. Following double-strand DNA breaks (DSBs), mediators including ATM are recruited to the site of DNA-damage. Subsequent phosphorylation of p53 by ATM and ATM-induced CHK2 results in p53 stabilization, ultimately intensifying transcription of p53-responsive genes involved in DNA repair, cell-cycle checkpoint control and apoptosis. METHODS: In the current study, we investigated the stabilization and activation of p53 and associated DDR proteins in response to treatment of human colorectal cancer cells (HCT116p53+/+) with the MDM2 antagonist, Nutlin-3. RESULTS: Using immunoblotting, Nutlin-3 was observed to stabilize p53, and activate p53 target proteins. Unexpectedly, Nutlin-3 also mediated phosphorylation of p53 at key DNA-damage-specific serine residues (Ser15, 20 and 37). Furthermore, Nutlin-3 induced activation of CHK2 and ATM - proteins required for DNA-damage-dependent phosphorylation and activation of p53, and the phosphorylation of BRCA1 and H2AX - proteins known to be activated specifically in response to DNA damage. Indeed, using immunofluorescent labeling, Nutlin-3 was seen to induce formation of γH2AX foci, an early hallmark of the DDR. Moreover, Nutlin-3 induced phosphorylation of key DDR proteins, initiated cell cycle arrest and led to formation of γH2AX foci in cells lacking p53, whilst γH2AX foci were also noted in MDM2-deficient cells. CONCLUSION: To our knowledge, this is the first solid evidence showing a secondary role for Nutlin-3 as a DDR triggering agent, independent of p53 status, and unrelated to its role as an MDM2 antagonist

The Grizzly, December 8, 1978

Campus Entertainment Limited?: Activities Discussed By Task Force • Pi Omega Delta Becomes a Reality; Register Now for Evening Courses; Meistersingers In Televised Concert; Holiday Baskets Distributed By APO • Community And Civilization To Offer Interesting Approach • Bears Crack Garnets • Liberal Education In Our Times • Be Cool Or Bolt • From Beads and Bennies to Bedsheets and Budweiser • Letters to the Editor: Guyana Attitudes - Sig Rho Responds • Touring: Leave The Crowds On The Mountain • le Club Francais s\u27Amuse • The Year In Music • V-Ball Set To Spike Foes • Martha Franklin: For The Love Of Ursinus • Sports Profile: Clayton Ebling • Flying High Downs Slappers • Two No Shows Leave Mermaids Dry • Aquamen Splash To Win • Women Hoopers Drop Twohttps://digitalcommons.ursinus.edu/grizzlynews/1009/thumbnail.jp

Modelling mutational landscapes of human cancers in vitro

Experimental models that recapitulate mutational landscapes of human cancers are needed to decipher the rapidly expanding data on human somatic mutations. We demonstrate that mutation patterns in immortalised cell lines derived from primary murine embryonic fibroblasts (MEFs) exposed in vitro to carcinogens recapitulate key features of mutational signatures observed in human cancers. In experiments with several cancer-causing agents we obtained high genome-wide concordance between human tumour mutation data and in vitro data with respect to predominant substitution types, strand bias and sequence context. Moreover, we found signature mutations in well-studied human cancer driver genes. To explore endogenous mutagenesis, we used MEFs ectopically expressing activation-induced cytidine deaminase (AID) and observed an excess of AID signature mutations in immortalised cell lines compared to their non-transgenic counterparts. MEF immortalisation is thus a simple and powerful strategy for modelling cancer mutation landscapes that facilitates the interpretation of human tumour genome-wide sequencing data

p53 mutations in human cutaneous melanoma correlate with sun exposure but are not always involved in melanomagenesis

In melanoma, the relationship between sun exposure and the origin of mutations in either the N-ras oncogene or the p53 tumour-suppressor gene is not as clear as in other types of skin cancer. We have previously shown that mutations in the N-ras gene occur more frequently in melanomas originating from sun-exposed body sites, indicating that these mutations are UV induced. To investigate whether sun exposure also affects p53 in melanoma, we analysed 81 melanoma specimens for mutations in the p53 gene. The mutation frequency is higher than thus far reported: 17 specimens (21%) harbour one or more p53 mutations. Strikingly, 17 out of 22 mutations in p53 are of the C:G to T:A or CC:GG to TT:AA transitional type, strongly suggesting an aetiology involving UV exposure. Interestingly, the p53 mutation frequency in metastases was much lower than in primary tumours. In the case of metastases, a role for sun exposure was indicated by the finding that the mutations are present exclusively in skin metastases and not in internal metastases. Together with a relatively frequent occurrence of silent third-base pair mutations in primary melanomas, this indicates that the p53 mutations, at least in these tumours, have not contributed to melanomagenesis and may have originated after establishment of the primary tumour. 1999 Cancer Research Campaig