EFFECT OF pH ON THE GROWTH AND CHARACTERIZATION OF GLYCINE SODIUM CHLORIDE (GSC) SINGLE CRYSTAL

ABSTRACT Single crystals of semi-organic non-linear optical Glycine Sodium Chloride (GSC) have been successfully grown from three different pH (1.1, 6.0, and 10.8

Remarks on the Formulation of Quantum Mechanics on Noncommutative Phase Spaces

We consider the probabilistic description of nonrelativistic, spinless one-particle classical mechanics, and immerse the particle in a deformed noncommutative phase space in which position coordinates do not commute among themselves and also with canonically conjugate momenta. With a postulated normalized distribution function in the quantum domain, the square of the Dirac delta density distribution in the classical case is properly realised in noncommutative phase space and it serves as the quantum condition. With only these inputs, we pull out the entire formalisms of noncommutative quantum mechanics in phase space and in Hilbert space, and elegantly establish the link between classical and quantum formalisms and between Hilbert space and phase space formalisms of noncommutative quantum mechanics. Also, we show that the distribution function in this case possesses 'twisted' Galilean symmetry.Comment: 25 pages, JHEP3 style; minor changes; Published in JHE

On Structural Parameterizations of the Bounded-Degree Vertex Deletion Problem

We study the parameterized complexity of the Bounded-Degree Vertex Deletion problem (BDD), where the aim is to find a maximum induced subgraph whose maximum degree is below a given degree bound. Our focus lies on parameters that measure the structural properties of the input instance. We first show that the problem is W[1]-hard parameterized by a wide range of fairly restrictive structural parameters such as the feedback vertex set number, pathwidth, treedepth, and even the size of a minimum vertex deletion set into graphs of pathwidth and treedepth at most three. We thereby resolve an open question stated in Betzler, Bredereck, Niedermeier and Uhlmann (2012) concerning the complexity of BDD parameterized by the feedback vertex set number. On the positive side, we obtain fixed-parameter algorithms for the problem with respect to the decompositional parameter treecut width and a novel problem-specific parameter called the core fracture number

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Metabolic adaptation drives arsenic trioxide resistance in acute promyelocytic leukemia.

Acquired genetic mutations can confer resistance to arsenic trioxide (ATO) in the treatment of acute promyelocytic leukemia (APL). However, such resistance-conferring mutations are rare and do not explain most disease recurrence seen in the clinic. We have generated stable ATO-resistant promyelocytic cell lines that are also less sensitive to ATRA and the combination of ATO and ATRA compared to the sensitive cell line. Characterization of these in-house generated resistant cell lines showed significant differences in immunophenotype, drug transporter expression, anti-apoptotic protein dependence, and PML-RARA mutation. Gene expression profiling revealed prominent dysregulation of the cellular metabolic pathways in these ATO resistant APL cell lines. Glycolytic inhibition by 2-DG was sufficient and comparable to the standard of care (ATO) in targeting the sensitive APL cell line. 2-DG was also effective in the in vivo transplantable APL mouse model; however, it did not affect the ATO resistant cell lines. In contrast, the resistant cell lines were significantly affected by compounds targeting the mitochondrial respiration when combined with ATO, irrespective of the ATO resistance-conferring genetic mutations or the pattern of their anti-apoptotic protein dependency. Our data demonstrate that the addition of mitocans in combination with ATO can overcome ATO resistance. We further show that this combination has the potential in the treatment of non-M3 AML and relapsed APL. The translation of this approach in the clinic needs to be explored further

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin