Assessment of the composition and condition of animation cels made from cellulose acetate

Cellulose diacetate and cellulose triacetate cels from animated feature films in the collection of the Walt Disney Animation Research Library were tested by several analytical techniques in order to assess their composition and look for evidence of degradation. Triphenyl phosphate and a range of phthalate plasticizers were identified using pyrolysis-gas chromatography/mass spectrometry, which also showed evidence that evaporation of more volatile plasticizers may have occurred. Plasticizer content measurements by solvent extraction, found to be more accurate than volatile content data from thermogravimetric analysis, revealed there was less residual plasticizer in triacetate cels compared to diacetate cels. Gas chromatography/mass spectrometry, performed to quantify the acetyl content of cels after removal of plasticizers by solvent extraction, revealed some evidence for hydrolysis of the oldest cels, although the reduction could be related to original variations in acetate content from the polymer manufacturers. Use of Fourier-transform infrared spectroscopy to measure deacetylation of the cellulose acetate polymer based on the hydroxyl to carbonyl peak area ratio proved less satisfactory. Moreover, because the cels cannot be measured directly due to interference from plasticizers, non-invasive assessment of deacetylation using a portable instrument would be impossible. The results from this analytical survey provide an important point of reference against which long-term changes in cel composition can be monitored. © 2014 The J. Paul Getty Trust. Published by Elsevier Ltd. All rights reserved

Human MLH1 Protein Participates in Genomic Damage Checkpoint Signaling in Response to DNA Interstrand Crosslinks, while MSH2 Functions in DNA Repair

DNA interstrand crosslinks (ICLs) are among the most toxic types of damage to a cell. For this reason, many ICL-inducing agents are effective therapeutic agents. For example, cisplatin and nitrogen mustards are used for treating cancer and psoralen plus UVA (PUVA) is useful for treating psoriasis. However, repair mechanisms for ICLs in the human genome are not clearly defined. Previously, we have shown that MSH2, the common subunit of the human MutSα and MutSβ mismatch recognition complexes, plays a role in the error-free repair of psoralen ICLs. We hypothesized that MLH1, the common subunit of human MutL complexes, is also involved in the cellular response to psoralen ICLs. Surprisingly, we instead found that MLH1-deficient human cells are more resistant to psoralen ICLs, in contrast to the sensitivity to these lesions displayed by MSH2-deficient cells. Apoptosis was not as efficiently induced by psoralen ICLs in MLH1-deficient cells as in MLH1-proficient cells as determined by caspase-3/7 activity and binding of annexin V. Strikingly, CHK2 phosphorylation was undetectable in MLH1-deficient cells, and phosphorylation of CHK1 was reduced after PUVA treatment, indicating that MLH1 is involved in signaling psoralen ICL-induced checkpoint activation. Psoralen ICLs can result in mutations near the crosslinked sites; however, MLH1 function was not required for the mutagenic repair of these lesions, and so its signaling function appears to have a role in maintaining genomic stability following exposure to ICL-induced DNA damage. Distinguishing the genetic status of MMR-deficient tumors as MSH2-deficient or MLH1-deficient is thus potentially important in predicting the efficacy of treatment with psoralen and perhaps with other ICL-inducing agents

Genome-Wide Profile of Pleural Mesothelioma versus Parietal and Visceral Pleura: The Emerging Gene Portrait of the Mesothelioma Phenotype

Malignant pleural mesothelioma is considered an almost incurable tumour with increasing incidence worldwide. It usually develops in the parietal pleura, from mesothelial lining or submesothelial cells, subsequently invading the visceral pleura. Chromosomal and genomic aberrations of mesothelioma are diverse and heterogenous. Genome-wide profiling of mesothelioma versus parietal and visceral normal pleural tissue could thus reveal novel genes and pathways explaining its aggressive phenotype.Well-characterised tissue from five mesothelioma patients and normal parietal and visceral pleural samples from six non-cancer patients were profiled by Affymetrix oligoarray of 38 500 genes. The lists of differentially expressed genes tested for overrepresentation in KEGG PATHWAYS (Kyoto Encyclopedia of Genes and Genomes) and GO (gene ontology) terms revealed large differences of expression between visceral and parietal pleura, and both tissues differed from mesothelioma. Cell growth and intrinsic resistance in tumour versus parietal pleura was reflected in highly overexpressed cell cycle, mitosis, replication, DNA repair and anti-apoptosis genes. Several genes of the “salvage pathway” that recycle nucleobases were overexpressed, among them TYMS, encoding thymidylate synthase, the main target of the antifolate drug pemetrexed that is active in mesothelioma. Circadian rhythm genes were expressed in favour of tumour growth. The local invasive, non-metastatic phenotype of mesothelioma, could partly be due to overexpression of the known metastasis suppressors NME1 and NME2. Down-regulation of several tumour suppressor genes could contribute to mesothelioma progression. Genes involved in cell communication were down-regulated, indicating that mesothelioma may shield itself from the immune system. Similarly, in non-cancer parietal versus visceral pleura signal transduction, soluble transporter and adhesion genes were down-regulated. This could represent a genetical platform of the parietal pleura propensity to develop mesothelioma.Genome-wide microarray approach using complex human tissue samples revealed novel expression patterns, reflecting some important features of mesothelioma biology that should be further explored

Observation of Two New Excited Ξb0 States Decaying to Λb0 K-π+

Two narrow resonant states are observed in the Λb0K-π+ mass spectrum using a data sample of proton-proton collisions at a center-of-mass energy of 13 TeV, collected by the LHCb experiment and corresponding to an integrated luminosity of 6 fb-1. The minimal quark content of the Λb0K-π+ system indicates that these are excited Ξb0 baryons. The masses of the Ξb(6327)0 and Ξb(6333)0 states are m[Ξb(6327)0]=6327.28-0.21+0.23±0.12±0.24 and m[Ξb(6333)0]=6332.69-0.18+0.17±0.03±0.22 MeV, respectively, with a mass splitting of Δm=5.41-0.27+0.26±0.12 MeV, where the uncertainties are statistical, systematic, and due to the Λb0 mass measurement. The measured natural widths of these states are consistent with zero, with upper limits of Γ[Ξb(6327)0]<2.20(2.56) and Γ[Ξb(6333)0]<1.60(1.92) MeV at a 90% (95%) credibility level. The significance of the two-peak hypothesis is larger than nine (five) Gaussian standard deviations compared to the no-peak (one-peak) hypothesis. The masses, widths, and resonant structure of the new states are in good agreement with the expectations for a doublet of 1D Ξb0 resonances

Angular Analysis of the B+ -> K*(+)mu(+) mu(-) Decay

We present an angular analysis of the B + → K * + ( → K 0 S π + ) μ + μ − decay using 9     fb − 1 of p p collision data collected with the LHCb experiment. For the first time, the full set of C P -averaged angular observables is measured in intervals of the dimuon invariant mass squared. Local deviations from standard model predictions are observed, similar to those in previous LHCb analyses of the isospin-partner B 0 → K * 0 μ + μ − decay. The global tension is dependent on which effective couplings are considered and on the choice of theory nuisance parameters

Precise determination of the B-s(0)-B-s(-0) oscillation frequency

Mesons comprising a beauty quark and a strange quark can oscillate between particle (B0s) and antiparticle (B0s) flavour eigenstates, with a frequency given by the mass difference between heavy and light mass eigenstates, deltams. Here we present ameasurement of deltams using B0s2DsPi decays produced in proton-proton collisions collected with the LHCb detector at the Large Hadron Collider. The oscillation frequency is found to be deltams = 17.7683 +- 0.0051 +- 0.0032 ps-1, where the first uncertainty is statistical and the second systematic. This measurement improves upon the current deltams precision by a factor of two. We combine this result with previous LHCb measurements to determine deltams = 17.7656 +- 0.0057 ps-1, which is the legacy measurement of the original LHCb detector.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2021-005.html (LHCb public pages

Study of the ψ2(3823)ψ_2(3823) and χc1(3872)χ_{c1}(3872) states in B+→(Jψπ+π−)K+B^+ \rightarrow \left( Jψπ^+π^-\right)K^+ decays

The decays $B^+\rightarrow J/\psi \pi^+ \pi^- K^+$ are studied using a data set corresponding to an integrated luminosity of 9fb$^{-1}$ collected with the LHCb detector in proton-proton collisions between 2011 and 2018. Precise measurements of the ratios of branching fractions with the intermediate $\psi_2(3823)$, $\chi_{c1}(3872)$ and $\psi(2S)$ states are reported. The decay of $B^+\rightarrow \psi_2(3823)K^+$ with $\psi_2(3823)\rightarrow J\psi\pi^+\pi^-$ is observed for the first time with a significance of 5.1 standard deviations. The mass differences between the $\psi_2(3823)$, $\chi_{c1}(3872)$ and $\psi(2S)$ states are measured to be $$\begin{array}{rcl} m_{\chi_{c1(3872)}} - m_{\psi_2(3823)} &= & 47.50 \pm 0.53 \pm 0.13\,\mathrm{MeV/}c^2\,, \\ m_{\psi_2(3823)} - m_{\psi(2S)} &= & 137.98 \pm 0.53 \pm 0.14\,\mathrm{MeV/}c^2\,, \\ m_{\chi_{c1}(3872)} - m_{\psi(2S)} &= & 185.49 \pm 0.06 \pm 0.03\,\mathrm{MeV/}c^2\,, \end{array}$$ resulting in the most precise determination of the $\chi_{c1}(3782)$ mass. The width of the $\psi_2(3823)$ state is found to be below 5.2MeV at 90\% confidence level. The Breit-Wigner width of the $\chi_{c1}(3872)$ state is measured to be $$\Gamma^{\mathrm{BW}}_{\chi_{c1}(3872)} = 0.96^{+0.19}_{-0.18}\pm0.21 \mathrm{MeV},$$ which is inconsistent with zero by 5.5 standard deviations

Search for the doubly heavy baryons Omega(0)(bc) and Xi(0)(bc) decaying to Lambda(+)(c)pi(-) and Xi(+)(c)pi-

Abstract available from publisher's website