cometadata/datacite-rtg-text-other-reclassification-records huggingface dataset:
Neumann boundary controllability of the Korteweg-de Vries equation on a bounded domain
Creators: name: Caicedo, Miguel
name: Capistrano-Filho, Roberto de A.
name: Zhang, Bingyu
Publisher: name: arXiv
Year: 2015
Subjects: subject: Analysis of PDEs (math.AP)
subject: Optimization and Control (math.OC)
subject: FOS: Mathematics

description: In this paper we study boundary controllability of the Korteweg-de Vries (KdV) equation posed on a finite domain $(0,L)$ with the Neumann boundary conditions: u_t+u_x+uu_x+u_{xxx}=0 in (0,L)x(0,T), u_{xx}(0,t)=0, u_x(L,t)=h(t), u_{xx}(L,t)=0 in (0,T), u(x,0)=u_0(x) in (0,L). We show that the associated linearized system u_t+(1+β)u_x+u_{xxx}=0 in (0,L)x(0,T), u_{xx}(0,t)=0, u_x(L,t)=h(t), u_{xx}(L,t)=0 in (0,T), u(x,0)=u_0(x) in (0,L) is exactly controllable if and only if the length $L$ of the spatial domain $(0,L)$ does not equal to $-1$ or does not belong to set R_β:={\frac{2π}{\sqrt{3(1+β)}}\sqrt{k^{2}+kl+l^{2}}:k,l\in\mathbb{N}^{\ast}}\cup{\frac{kπ}{\sqrt{1+β}}:k\in\mathbb{N}^{\ast}} and the nonlinear system is locally exactly controllable around a constant steady state $β$ if the associated linear system is exactly controllable.
description: arXiv admin note: text overlap with arXiv:1401.6833 by other authors
title: Structural and diffusion neuroimaging for prediction of antidepressant response using machine learning
Creators: name: Ali, Farzana
Publisher: name: European Congress of Radiology
Year: 2022
Subjects: subject: Artificial Intelligence
subject: Computer applications
subject: Neuroradiology brain
subject: Image manipulation / Reconstruction
subject: MR
subject: MR-Diffusion/Perfusion
subject: Computer Applications-General
subject: Decision analysis
subject: Experimental investigations
subject: Biological effects
subject: Outcomes

description: Purpose Methods and materials Results Conclusion Personal information and conflict of interest References
description: Purpose: Our purpose is to develop a predictive model using Machine Learning ( ML ) with pretreatment brain Magnetic Resonance Imaging ( MRI ) data, by predicting remission (absence of depression) following antidepressant treatment, that can assist...
title: Progressive supranuclear palsy (PSP): a kind of Parkinsonism with funny brain MRI features
Creators: name: Mendoza Ferradas, Francisco
Publisher: name: European Congress of Radiology
Year: 2022
Subjects: subject: Anatomy
subject: CNS
subject: Neuroradiology brain
subject: CT
subject: MR
subject: Nuclear medicine conventional
subject: Education
subject: Dementia

description: Learning objectives Background Findings and procedure details Conclusion Personal information and conflict of interest References
description: Learning objectives: *To describe brain MRI funny features in PSP: from “Hummingbird” to “Mickey mouse”. *To provide different planimetric measurements that help distinguish PSP from other parkinsonian syndromes (PD, MSA). *To analyze new image modalities,...
Causal Dynamical Triangulations in the Spincube Model of Quantum Gravity
Creators: name: Vojinovic, Marko
Publisher: name: arXiv
Year: 2015
Subjects: subject: General Relativity and Quantum Cosmology (gr-qc)
subject: High Energy Physics - Theory (hep-th)
subject: FOS: Physical sciences

description: We study the implications of the simplicity constraint in the spincube model of quantum gravity. By relating the edge-lengths to the integer areas of triangles, the simplicity constraint imposes very strong restrictions between them, ultimately leading to a requirement that all 4-simplices in the triangulation must be almost mutually identical. As a surprising and unexpected consequence of this property, one can obtain the CDT state sum as a special case of the spincube state sum. This relationship brings new insight into the long-standing problem of the relationship between the spinfoam approach and the CDT approach to quantum gravity. In particular, it turns out that the spincube model contains properties of both approaches, providing a single unifying framework for their analysis and comparison. In addition, the spincube state sum also contains some other special cases, very similar but not equivalent to the CDT state sum.
description: v4: published version; 18 pages
Fibroblast Growth Factor Receptor Signaling Dramatically Accelerates Tumorigenesis and Enhances Oncoprotein Translation in the Mouse Mammary Tumor Virus-Wnt-1 Mouse Model of Breast Cancer
Creators: name: Zhang, Yiqun
name: Perou, Charles M.
name: Rosen, Jeffrey M.
name: York, Brian
name: Hilsenbeck, Susan
name: Creighton, Chad J.
name: Welm, Bryan
name: Pond, Adam C.
name: Lloyd, Richard E.
name: Schwertfeger, Kathryn L.
name: Herschkowitz, Jason I.
name: Cardiff, Robert D.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: Fibroblast growth factor (FGF) cooperates with the Wnt/β-catenin pathway to promote mammary tumorigenesis. To investigate the mechanisms involved in FGF/Wnt cooperation, we genetically engineered a model of inducible FGF receptor (iFGFR) signaling in the context of the well-established mouse mammary tumor virus–Wnt-1 transgenic mouse. In the bigenic mice, iFGFR1 activation dramatically enhanced mammary tumorigenesis. Expression microarray analysis did not show transcriptional enhancement of Wnt/β-catenin target genes but instead showed a translational gene signature that also correlated with elevated FGFR1 and FGFR2 in human breast cancer data sets. Additionally, iFGFR1 activation enhanced recruitment of RNA to polysomes, resulting in a marked increase in protein expression of several different Wnt/β-catenin target genes. FGF pathway activation stimulated extracellular signal-regulated kinase and the phosphorylation of key translation regulators both in vivo in the mouse model and in vitro in a human breast cancer cell line. Our results suggest that cooperation of the FGF and Wnt pathways in mammary tumorigenesis is based on the activation of protein translational pathways that result in, but are not limited to, increased expression of Wnt/β-catenin target genes (at the level of protein translation). Further, they reveal protein translation initiation factors as potential therapeutic targets for human breast cancers with alterations in FGF signaling.
Approximate Message Passing Algorithm with Universal Denoising and Gaussian Mixture Learning
Creators: name: Ma, Yanting
name: Zhu, Junan
name: Baron, Dror
Publisher: name: arXiv
Year: 2015
Subjects: subject: Information Theory (cs.IT)
subject: FOS: Computer and information sciences

description: We study compressed sensing (CS) signal reconstruction problems where an input signal is measured via matrix multiplication under additive white Gaussian noise. Our signals are assumed to be stationary and ergodic, but the input statistics are unknown; the goal is to provide reconstruction algorithms that are universal to the input statistics. We present a novel algorithmic framework that combines: (i) the approximate message passing (AMP) CS reconstruction framework, which solves the matrix channel recovery problem by iterative scalar channel denoising; (ii) a universal denoising scheme based on context quantization, which partitions the stationary ergodic signal denoising into independent and identically distributed (i.i.d.) subsequence denoising; and (iii) a density estimation approach that approximates the probability distribution of an i.i.d. sequence by fitting a Gaussian mixture (GM) model. In addition to the algorithmic framework, we provide three contributions: (i) numerical results showing that state evolution holds for non-separable Bayesian sliding-window denoisers; (ii) an i.i.d. denoiser based on a modified GM learning algorithm; and (iii) a universal denoiser that does not need information about the range where the input takes values from or require the input signal to be bounded. We provide two implementations of our universal CS recovery algorithm with one being faster and the other being more accurate. The two implementations compare favorably with existing universal reconstruction algorithms in terms of both reconstruction quality and runtime.
description: To appear in IEEE Transaction on Signal Processing
Max-cut and extendability of matchings in distance-regular graphs
Creators: name: Cioabă, Sebastian M.
name: Koolen, Jack H.
name: Li, Weiqiang
Publisher: name: arXiv
Year: 2015
Subjects: subject: Combinatorics (math.CO)
subject: Discrete Mathematics (cs.DM)
subject: FOS: Mathematics
subject: FOS: Computer and information sciences

description: Let $G$ be a distance-regular graph of order $v$ and size $e$. In this paper, we show that the max-cut in $G$ is at most $e(1-1/g)$, where $g$ is the odd girth of $G$. This result implies that the independence number of $G$ is at most $\frac{v}{2}(1-1/g)$. We use this fact to also study the extendability of matchings in distance-regular graphs. A graph $G$ of even order $v$ is called $t$-extendable if it contains a perfect matching, $t
description: 18 pages, accepted to European Journal of Combinatorics
K-ras Mutation Targeted to Gastric Tissue Progenitor Cells Results in Chronic Inflammation, an Altered Microenvironment, and Progression to Intraepithelial Neoplasia
Creators: name: Ericksen, Russell E.
name: Wang, Sophie S.W.
name: Wang, Timothy C.
name: Okumura, Tomoyuki
name: Rogers, Arlin B.
name: Betz, Kelly S.
name: Takaishi, Shigeo
name: Fox, James G.
name: Shibata, Wataru
name: Dubeykovskiy, Zinaida
name: Rustgi, Anil K.
name: Muthupalani, Sureshkuma
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: Chronic infectious diseases, such as Helicobacter pylori, can promote cancer in a large part through induction of chronic inflammation. Oncogenic K-Ras mutation in epithelial cells activates inflammatory pathways, which could compensate for a lack of infectious stimulus. Gastric histopathology and putative progenitor markers (Dcamkl1, Keratin 19) in Keratin 19-K-Ras-V12 (K19-kras) transgenic mice were assessed at 3, 6, 12 and 18 months of age, in comparison with Helicobacter felis (H. felis)-infected wild-type littermates. Inflammation was evaluated by RT-PCR of pro-inflammatory cytokines, and K19-kras mice were transplanted with GFP-labeled bone marrow. Both H. felis infection and kras mutation induced upregulation of pro-inflammatory cytokines, expansion of Dcamkl1+ cells, and progression to oxyntic atrophy, metaplasia, hyperplasia and high-grade dysplasia. K19-kras transgenic mice uniquely displayed mucous metaplasia as early as 3 months, and progressed to high-grade dysplasia and invasive intramucosal carcinoma by 20 months. In bone marrow transplanted K19-kras mice that progressed to dysplasia, a large proportion of stromal cells were GFP+ and bone marrow-derived, but only rare GFP+ epithelial cells were observed. GFP+ BMDCs included leukocytes and CD45− stromal cells that expressed vimentin or αSMA and were often found surrounding clusters of Dcamkl1+ cells at the base of gastric glands. In conclusions, the expression of mutant Kras in K19+ gastric epithelial cells can induce chronic inflammation and promote the development of dysplasia.
Reexpression of hSNF5 in Malignant Rhabdoid Tumor Cell Lines Causes Cell Cycle Arrest through a p21CIP1/WAF1-Dependent Mechanism
Creators: name: Knudsen, Erik S.
name: Weissman, Bernard E.
name: Kuwahara, Yasumichi
name: Charboneau, Aubri
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: Loss of hSNF5 function is usually observed in malignant rhabdoid tumor (MRT), a highly aggressive pediatric neoplasm. Previous studies have shown that reexpression of hSNF5 in MRT cell lines causes G1 cell cycle arrest with p16INK4A, p21CIP1/WAF1 and cyclin D1 playing key roles in MRT cell growth control. However, we have shown that reexpression of hSNF5 induced cell cycle arrest in the absence of p16INK4A expression. These results indicate that the mechanism of hSNF5-induced cell cycle arrest is context dependent. Here, we investigated the relationship between p21CIP1/WAF1 and hSNF5 in the regulation of growth using several MRT cell lines. We found that G1 cell cycle arrest occurred concomitant with an increase in p21CIP1/WAF1 mRNA and protein levels and preceeded p16INK4A mRNA and protein up-regulation. Chromatin immunoprecipitation data confirmed that hSNF5 appeared at both p21CIP1/WAF1 and p16INK4A promoters after reexpression. We further showed that p21CIP1/WAF1 induction showed both p53 dependent and independent mechanisms. We also demonstrated that reduction of p21CIP1/WAF1 expression by RNAi significantly inhibited hSNF5-induced G1 arrest. Our results demonstrate that both p21CIP1/WAF1 and p16INK4A are targets for hSNF5, and that p21CIP1/WAF1 up-regulation during hSNF5-induced G1 arrest precedes p16INK4A up-regulation. These findings indicate that SNF5 mediates a temporally controlled program of CDK inhibition to restrict aberrant proliferation in MRT cells.
Requirement of the NF- B Subunit p65/RelA for K-Ras-Induced Lung Tumorigenesis
Creators: name: Baldwin, Albert S.
name: Ebbs, Aaron
name: Levantini, Elena
name: Bassères, Daniela S.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: K-Ras-induced lung cancer is a very common disease, for which there are currently no effective therapies. Because therapy directly targeting the activity of oncogenic Ras has been unsuccessful, a different approach for novel therapy design is to identify critical Ras downstream oncogenic targets. Given that oncogenic Ras proteins activate the transcription factor NF-κB, and the importance of NF-κB in oncogenesis, we hypothesized that NF-κB would be an important K-Ras target in lung cancer. To address this hypothesis, we generated an NF-κB-EGFP reporter mouse model of K-Ras-induced lung cancer and determined that K-Ras activates NF-κB in lung tumors in situ. Furthermore, a mouse model was generated where activation of oncogenic K-Ras in lung cells was coupled with inactivation of the NF-κB subunit p65/RelA. In this model, deletion of p65/RelA reduces the number of K-Ras-induced lung tumors both in the presence and absence of the tumor suppressor p53. Lung tumors with loss of p65/RelA have higher numbers of apoptotic cells, reduced spread and lower grade. Using lung cell lines expressing oncogenic K-Ras, we show that NF-κB is activated in these cells in a K-Ras-dependent manner and that NF-κB activation by K-Ras requires IKKβ kinase activity. Taken together, these results demonstrate the importance of the NF-κB subunit p65/RelA in K-Ras induced lung transformation and identify IKKβ as a potential therapeutic target for K-Ras-induced lung cancer.
Magnetoresistive detection of perpendicular switching in a magnetic insulator
Creators: name: Damerio, Silvia
name: Sunil, Achintya
name: Mehraeen, M.
name: Zhang, Steven S. -L.
name: Avci, Can O.
Publisher: name: arXiv
Year: 2023
Subjects: subject: Mesoscale and Nanoscale Physics (cond-mat.mes-hall)
subject: FOS: Physical sciences

description: Spintronics offers promising routes for efficient memory, logic, and computing technologies. The central challenge in spintronics is electrically manipulating and detecting magnetic states in devices. The electrical control of magnetization via spin-orbit torques is effective in both conducting and insulating magnetic layers. However, the electrical readout of magnetization in the latter is inherently difficult, limiting its use in practical applications. Here, we demonstrate magnetoresistive detection of perpendicular magnetization reversal in an electrically insulating ferrimagnet, terbium iron garnet (TbIG). To do so, we use TbIG|Cu|TbCo, where TbCo is a conducting ferrimagnet and serves as the reference layer, and Cu is a nonmagnetic spacer. Current injection through Cu|TbCo allows us to detect the magnetization reversal of TbIG with a simple resistance readout during an external magnetic field sweep. By examining the effect of measurement temperature, TbCo composition, and Cu thickness on the sign and amplitude of the magnetoresistance, we conclude that the spin-dependent electron scattering at the TbIG|Cu interface is the underlying cause. Technologically-feasible magnetoresistive detection of perpendicular switching in a ferrimagnetic garnet is a breakthrough, as it opens broad avenues for novel insulating spintronic devices and concepts.
Similar Nucleotide Excision Repair Capacity in Melanocytes and Melanoma Cells
Creators: name: Smith-Roe, Stephanie L.
name: Gaddameedhi, Shobhan
name: Sancar, Aziz
name: Shields, Janiel M.
name: Reardon, Joyce T.
name: Kaufmann, William K.
name: Kemp, Michael G.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: Sunlight UV exposure produces DNA photoproducts in skin that are repaired solely by nucleotide excision repair in humans. A significant fraction of melanomas are thought to result from UV-induced DNA damage that escapes repair, however, little evidence is available regarding the functional capacity of normal human melanocytes, malignant melanoma cells and metastatic melanoma cells to repair UV-induced photoproducts in DNA. In this study, we measured nucleotide excision repair in both normal melanocytes and a panel of melanoma cell lines. Our results show that in 11 of 12 melanoma cell lines tested, UV photoproduct repair occurred as efficiently as in primary melanocytes. Importantly, repair capacity was not affected by mutation in the N-Ras or B-Raf oncogenes, nor was a difference observed between a highly metastatic melanoma cell line (A375SM) or its parental line (A375P). Lastly, we found that while p53 status contributed to photoproduct removal efficiency its role did not appear to be mediated by enhanced expression or activity of DNA binding protein DDB2. We concluded that melanoma cells retain capacity for nucleotide excision repair, the loss of which probably does not commonly contribute to melanoma progression.
The Inflammasome Component Nlrp3 Impairs Antitumor Vaccine by Enhancing the Accumulation of Tumor-Associated Myeloid-Derived Suppressor Cells
Creators: name: Wu, Qing Ping
name: Serody, Jonathan S.
name: Van Deventer, Hendrik W.
name: Ting, Jenny P.Y.
name: Brickey, W. June
name: McElvania-Tekippe, Erin
name: Woodford, Rita Marie T.
name: Burgents, Joseph E.
name: Allen, Irving C.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: The inflammasome is a proteolysis complex that generates the active forms of the pro-inflammatory cytokines IL-1β and IL-18. Inflammasome activtation is mediated by NLR proteins that respond to microbial and nonmicrobial stimuli. Among NLRs, NLRP3 senses the widest array of stimuli and enhances adaptive immunity. However, its role in antitumor immunity is unknown. Therefore, we evaluated the function of the NLRP3 inflammasome in the immune response using dendritic cell vaccination against the poorly immunogenic melanoma cell line B16-F10. Vaccination of Nlrp3−/− mice led to a relative 4-fold improvement in survival relative to control animals. Immunity depended upon CD8+ T cells and exhibited immune specificity and memory. Increased vaccine efficacy in Nlrp3−/− hosts did not reflect differences in dendritic cells but rather differences in myeloid-derived suppressor cells (MDSCs). Although Nlrp3 was expressed in MDSCs, the absence of Nlrp3 did not alter either their functional capacity to inhibit T cells or their presence in peripheral lymphoid tissues. Instead, the absence of Nlrp3 caused a 5-fold reduction in the number of tumor-associated MDSCs found in host mice. Adoptive transfer experiments also showed that Nlrp3−/− MDSCs were less efficient in reaching the tumor site. Depleting MDSCs with an anti-Gr-1 antibody increased the survival of tumor-bearing wild-type mice but not Nlrp3−/− mice. We concluded that Nlrp3 was critical for accumulation of MDSCs in tumors and for inhibition of antitumor T cell immunity after dendritic cell vaccination. Our findings establish an unexpected role for Nlrp3 in impeding antitumor immune responses, suggesting novel approaches to improve the response to antitumor vaccines by limiting Nlrp3 signaling.
Tumor Antigen Acrosin Binding Protein Normalizes Mitotic Spindle Function to Promote Cancer Cell Proliferation
Creators: name: Larson, Brittany
name: Schorge, John O.
name: Purinton, Scott C.
name: Whitehurst, Angelique W.
name: Swanik, Jackie T.
name: Xie, Yang
name: Girard, Luc
name: Cappell, Kathryn M.
name: White, Michael A.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: Cancer cells manage to divide in the context of gross chromosomal abnormalities. These abnormalities can promote bypass of normal restraints on cell proliferation, but at a cost of mitotic vulnerabilities that can be attacked by chemotherapy. Determining how cancer cells balance these issues may permit chemotherapeutic sensitivity to be leveraged more efficiently. From a pan-genomic siRNA screen for modifiers of chemoresponsiveness, we identified the tumor antigen ACRBP/OY-TES-1 as a specifier of paclitaxel resistance. ACRBP expression is normally restricted to the testes but detected in a wide variety of cancers, including most ovarian cancers. We found that ACRBP is both necessary and sufficient for paclitaxel resistance in ovarian cancer cell lines and ovarian tumor explants. Moreover, high ACRBP expression correlated with reduced survival time and faster relapse among ovarian cancer patients. We identified the mitotic spindle protein NuMA as an ACRBP-interacting protein that could account for the effects of ACRBP on paclitaxel sensitivity. In cancer cells, ACRBP restricted a NuMA-dependent abrogation of mitotic spindle assembly that is otherwise pathologic. As a consequence, ACRBP depletion resulted in mitotic errors and reduced proliferative fitness that could be rescued by NuMA co-depletion. We propose that the co-dependent relationship of ACRBP and NuMA in cancer cells reflects their passage through a selection bottleneck during tumor evolution, one which requires the acquisition of traits which normalize mitotic perturbations that originally drove the plasticity of a pre-neoplastic genome. The molecular definition of such traits as defined by the ACRBP-NuMA complex may represent conceptually ideal intervention targets, based on the wide therapeutic windows they may offer.
Understanding Time Value of Money: A Supplement for Introductory Finance
Creators: name: Golubeva, Evgenia
Publisher: name: University of Illinois at Chicago
Year: 2020
Subjects: subject: 150201 Finance
subject: FOS: Economics and business

description: This item is a supplementary text for the introductory finance course and is recommended for an instructor who would like to reinforce the delivery of Time Value of Money.
New OB star candidates in the Carina Arm around Westerlund 2 from VPHAS+
Creators: name: Mohr-Smith, M.
name: Drew, J. E.
name: Barentsen, G.
name: Wright, N. J.
name: Napiwotzki, R.
name: Corradi, R. L. M.
name: Eislöffel, J.
name: Groot, P.
name: Kalari, V.
name: Parker, Q. A.
name: Raddi, R.
name: Sale, S. E.
name: Unruh, Y. C.
name: Vink, J. S.
name: Wesson, R.
Publisher: name: arXiv
Year: 2015
Subjects: subject: Solar and Stellar Astrophysics (astro-ph.SR)
subject: FOS: Physical sciences

description: O and early B stars are at the apex of galactic ecology, but in the Milky Way, only a minority of them may yet have been identified. We present the results of a pilot study to select and parametrise OB star candidates in the Southern Galactic plane, down to a limiting magnitude of $g=20$. A 2 square-degree field capturing the Carina Arm around the young massive star cluster, Westerlund 2, is examined. The confirmed OB stars in this cluster are used to validate our identification method, based on selection from the $(u-g, g-r)$ diagram for the region. Our Markov Chain Monte Carlo fitting method combines VPHAS+ $u, g, r, i$ with published $J, H, K$ photometry in order to derive posterior probability distributions of the stellar parameters $\log(\rm T_{\rm eff})$ and distance modulus, together with the reddening parameters $A_0$ and $R_V$. The stellar parameters are sufficient to confirm OB status while the reddening parameters are determined to a precision of $σ(A_0)\sim0.09$ and $σ(R_V)\sim0.08$. There are 489 objects that fit well as new OB candidates, earlier than $\sim$B2. This total includes 74 probable massive O stars, 5 likely blue supergiants and 32 reddened subdwarfs. This increases the number of previously known and candidate OB stars in the region by nearly a factor of 10. Most of the new objects are likely to be at distances between 3 and 6 kpc. We have confirmed the results of previous studies that, at these longer distances, these sight lines require non-standard reddening laws with $3.5
description: 21 Pages, 17 Figures, 8 Tables. Accepted for publication in MNRAS
Activation and Involvement of Ral GTPases in Colorectal Cancer
Creators: name: Samuel, Jonathan C.
name: Yeh, Jen Jen
name: Routh, Elizabeth D.
name: Martin, Timothy D.
name: Der, Channing J.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: Current approaches to block KRAS oncogene function focus on inhibition of K-Ras downstream effector signaling. We evaluated the anti-tumor activity of selumetinib (AZD6244, ARRY-142886), a potent and selective MEK1/2 inhibitor, on a panel of colorectal carcinoma (CRC) cells and found no inhibition of KRAS mutant CRC cell anchorage-independent growth. While AKT activity was elevated in KRAS mutant cells, and PI3K inhibition did impair the growth of MEK inhibitor-insensitive CRC cell lines, concurrent treatment with selumetinib did not provide additional anti-tumor activity. Therefore, we speculated that inhibition of the Ral guanine exchange factor (RalGEF) effector pathway may be a more effective approach for blocking CRC growth. RalGEFs are activators of the related RalA and RalB small GTPases and we found activation of both in CRC cell lines and patient tumors. Interfering RNA stable suppression of RalA expression reduced CRC tumor cell anchorage-independent growth, but surprisingly, stable suppression of RalB greatly enhanced soft agar colony size and formation frequency. Despite their opposing activities, both RalA and RalB regulation of anchorage-independent growth required interaction with RalBP1/RLIP76 and components of the exocyst complex. Interestingly, RalA interaction with the Exo84 but not Sec5 exocyst component was necessary for supporting anchorage-independent growth, whereas RalB interaction with Sec5 but not Exo84 was necessary for inhibition of anchorage-independent growth. We suggest that anti-RalA-selective therapies may provide an effective approach for KRAS mutant CRC.
Activation of the Androgen Receptor by Intratumoral Bioconversion of Androstanediol to Dihydrotestosterone in Prostate Cancer
Creators: name: Kennerley, Brian J.
name: Bai, Suxia
name: Wilson, Elizabeth M.
name: Mohler, James L.
name: Titus, Mark A.
name: Lih, Fred B.
name: Tomer, Kenneth B.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: The androgen receptor (AR) mediates the growth of benign and malignant prostate in response to dihydrotestosterone (DHT). In patients undergoing androgen deprivation therapy for prostate cancer, AR drives prostate cancer growth despite low circulating levels of testicular androgen and normal levels of adrenal androgen. In this report we demonstrate the extent of AR transactivation in the presence of 5α-androstane-3α,17β-diol (androstanediol) in prostate-derived cell lines parallels the bioconversion of androstanediol to DHT. AR transactivation in the presence of androstanediol in prostate cancer cell lines correlated mainly with mRNA and protein levels of 17β-hydroxysteroid dehydrogenase 6 (17β-HSD6), one of several enzymes required for the interconversion of androstanediol to DHT and the inactive metabolite, androsterone. Levels of retinol dehydrogenase 5, and dehydrogenase/reductase short-chain dehydrogenase/reductase family member 9, which also convert androstanediol to DHT, were lower than 17β-HSD6 in prostate-derived cell lines, and higher in the castration-recurrent human prostate cancer xenograft. Measurements of tissue androstanediol using mass spectrometry demonstrated androstanediol metabolism to DHT and androsterone. Administration of androstanediol dipropionate to castration-recurrent CWR22R tumor bearing athymic castrated male mice produced a 28-fold increase in intratumoral DHT levels. AR transactivation in prostate cancer cells in the presence of androstanediol resulted from the cell-specific conversion of androstanediol to DHT, and androstanediol increased LAPC-4 cell growth. The ability to convert androstanediol to DHT provides a mechanism for optimal utilization of androgen precursors and catabolites for DHT synthesis.
(401772) James Stirling
Creators: name: Professions, Victorian
Publisher: name: University of Oxford
Year: 2022
Subjects: subject: 220201 Business and Labour History
subject: FOS: Philosophy, ethics and religion
subject: History
subject: 140203 Economic History
subject: FOS: Economics and business

description: This three-year research project began in January 2014 and investigated whether, during the Victorian period, the professions formed a distinct self-sustaining social group with its own mores and values. The project looked at 16,000 individuals drawn from census data for Alnwick, Brighton, Bristol, Dundee, Greenock, Leeds, Merthyr Tydfil, Morpeth, and Winchester. The research project was funded by the UK Economic & Social Research Council and was based at the Universities of Oxford and Northumbria.
title: Cerebral Venous Thrombosis
Creators: name: Lois Bermejo, Alicia Margarita
Publisher: name: European Congress of Radiology
Year: 2022
Subjects: subject: CNS
subject: CT
subject: CT-Angiography
subject: MR-Angiography
subject: Imaging sequences
subject: Normal variants
subject: Embolism / Thrombosis

description: Learning objectives Background Findings and procedure details Conclusion Personal information and conflict of interest References
description: Learning objectives: Cerebral venous thrombosis (CVT) is an uncommon pathology that requires high grade of clinical and radiologic suspicion not to be underdiagnosed. Our purpose is to describe its clinical presentation, cerebral venous anatomy, imaging techniques,...
$x-y$ duality in Topological Recursion for exponential variables via Quantum Dilogarithm
Creators: name: Hock, Alexander
Publisher: name: arXiv
Year: 2023
Subjects: subject: Mathematical Physics (math-ph)
subject: High Energy Physics - Theory (hep-th)
subject: Algebraic Geometry (math.AG)
subject: Exactly Solvable and Integrable Systems (nlin.SI)
subject: FOS: Physical sciences
subject: FOS: Mathematics
subject: 05A15, 14N10, 14H70, 30F30

description: For a given spectral curve, the theory of topological recursion generates two different families $ω_{g,n}$ and $ω_{g,n}^\vee$ of multi-differentials, which are for algebraic spectral curves related via the universal $x-y$ duality formula. We propose a formalism to extend the validity of the $x-y$ duality formula of topological recursion from algebraic curves to spectral curves with exponential variables of the form $e^x=F(e^y)$ or $e^x=F(y)e^{a y}$ with $F$ rational and $a$ some complex number, which was in principle already observed in \cite{Dunin-Barkowski:2017zsd,Bychkov:2020yzy}. From topological recursion perspective the family $ω_{g,n}^\vee$ would be trivial for these curves. However, we propose changing the $n=1$ sector of $ω_{g,n}^\vee$ via a version of the Faddeev's quantum dilogarithm which will lead to the correct two families $ω_{g,n}$ and $ω_{g,n}^\vee$ related by the same $x-y$ duality formula as for algebraic curves. As a consequence, the $x-y$ symplectic transformation formula extends further to important examples governed by topological recursion including, for instance, the topological vertex curve which computes Gromov-Witten invariants of $\mathbb{C}^3$, equivalently triple Hodge integrals on the moduli space of complex curves, orbifold Hurwitz numbers, or stationary Gromov-Witten invariants of $\mathbb{P}^1$. The proposed formalism is related to the issue topological recursion encounters for specific choices of framings for the topological vertex curve.
description: 30 pages, 3 figures
(401773) Helen Kirkwood
Creators: name: Professions, Victorian
Publisher: name: University of Oxford
Year: 2022
Subjects: subject: 220201 Business and Labour History
subject: FOS: Philosophy, ethics and religion
subject: History
subject: 140203 Economic History
subject: FOS: Economics and business

description: This three-year research project began in January 2014 and investigated whether, during the Victorian period, the professions formed a distinct self-sustaining social group with its own mores and values. The project looked at 16,000 individuals drawn from census data for Alnwick, Brighton, Bristol, Dundee, Greenock, Leeds, Merthyr Tydfil, Morpeth, and Winchester. The research project was funded by the UK Economic & Social Research Council and was based at the Universities of Oxford and Northumbria.
Finite element approximations for second order stochastic differential equation driven by fractional Brownian motion
Creators: name: Cao, Yanzhao
name: Hong, Jialin
name: Liu, Zhihui
Publisher: name: arXiv
Year: 2015
Subjects: subject: Numerical Analysis (math.NA)
subject: FOS: Mathematics
subject: Primary 60H35, Secondary 60H15, 60G05

description: We consider finite element approximations for a one dimensional second order stochastic differential equation of boundary value type driven by a fractional Brownian motion with Hurst index $H\le 1/2$. We make use of a sequence of approximate solutions with the fractional noise replaced by its piecewise con- stant approximations to construct the finite element approximations for the equation. The error estimate of the approximations is derived through rigorous convergence analysis.
description: To appear in IMA Journal of Numerical Analysis; the time-dependent case such as stochastic heat equation and stochastic wave equation driven by fractional Brownian sheet with temporal Hurst index $1/2$ and spatial Hurst index $H\le 1/2$ has been considered by arXiv:1601.02085 for spatially Galerkin approximations and a forthcoming paper for fully discrete approximations
title: Imaging of pediatric presacral masses: a practical approach
Creators: name: Jadib, Abdelhamid
Publisher: name: European Congress of Radiology
Year: 2022
Subjects: subject: Paediatric
subject: Pelvis
subject: CT
subject: MR
subject: Ultrasound
subject: Diagnostic procedure
subject: Cancer
subject: Congenital
subject: Neoplasia

description: Learning objectives Background Findings and procedure details Conclusion Personal information and conflict of interest References
description: Learning objectives: Review the clinical manifestations and the epidemiology of pediatric presacral masses. Recognize the imaging features of pediatric presacral masses. Develop imaging algorithms for the evaluation of pediatric presacral...
Cytoplasmic CUL9/PARC Ubiquitin Ligase Is a Tumor Suppressor and Promotes p53-Dependent Apoptosis
Creators: name: Xiong, Yue
name: Pei, Xin Hai
name: Smith, Matthew D.
name: Jin, Ran
name: Li, Zhijun
name: Bai, Feng
name: Whitewolf, Gabrielle
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: A wide range of cell stresses, including DNA damage, signal to p53 through post-translational modification of p53. The cytoplasmic functions of p53 are emerging as an important constituent of p53’s role in tumor suppression. Here we report that deletion of the Cul9 (formerly Parc) gene, which encodes an E3 ubiquitin ligase that binds to p53 and localizes in the cytoplasm, resulted in spontaneous tumor development, accelerated Eμ-Myc-induced lymphomagenesis and rendered mice susceptible to carcinogenesis. Cul9-p53 double mutant mice exhibited indistinguishable tumor phenotypes as p53 single mutant mice, indicating that the function of Cul9 in tumor suppression is largely mediated by p53. Deletion of Cul9 had no significant effect on cell cycle progression, but attenuated DNA damage-induced apoptosis. Ectopic expression of wild-type CUL9, but not a point mutant CUL9 deficient in p53 binding, promotes apoptosis. These results demonstrate CUL9 as a potential p53 activating E3 ligase in the cytoplasm.
Mechanical Stiffness Grades Metastatic Potential in Patient Tumor Cells and in Cancer Cell Lines
Creators: name: Tim O'Brien, E.
name: Berchuck, Andrew
name: Blobe, Gerard C.
name: Swaminathan, Vinay
name: Mythreye, Karthikeyan
name: Superfine, Richard
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: Cancer cells are defined by their ability to invade through the basement membrane, a critical step during metastasis. While increased secretion of proteases, which facilitates degradation of the basement membrane, and alterations in the cytoskeletal architecture of cancer cells have been previously studied, the contribution of the mechanical properties of cells in invasion is unclear. Here we apply a magnetic tweezer system to establish that stiffness of patient tumor cells and cancer cell lines inversely correlates with migration and invasion through three-dimensional basement membranes, a correlation known as a power law. We found that cancer cells with the highest migratory and invasive potential are five times less stiff than cells with the lowest migration and invasion potential. Moreover, decreasing cell stiffness by pharmacological inhibition of myosin II increases invasiveness, while increasing cell stiffness by restoring expression of the metastasis suppressor TβRIII/betaglycan decreases invasiveness. These findings are the first demonstration of the power law relation between the stiffness and the invasiveness of cancer cells and show that mechanical phenotypes can be used to grade the metastatic potential of cell populations with the potential for single cell grading. The measurement of a mechanical phenotype, taking minutes rather than hours needed for invasion assays, is promising as a quantitative diagnostic method and as a discovery tool for therapeutics. By demonstrating that altering stiffness predictably alters invasiveness, our results indicate that pathways regulating these mechanical phenotypes are novel targets for molecular therapy of cancer.
p53 Binds to and Is Required for the Repression of Arf Tumor Suppressor by HDAC and Polycomb
Creators: name: Pei, Xin Hai
name: Xiong, Yue
name: Smith, Matthew D.
name: Kotake, Yojiro
name: Zeng, Yaxue
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: The expression of tumor suppressor Arf is tightly repressed during normal cell growth at a young age, and is activated by oncogenic insults and during aging, resulting in p53 activation and cell cycle arrest to prevent hyperproliferation. The mechanisms of both transcriptional repression and activation of Arf are not understood. We show that p53 binds to and represses Arf expression and that this repression requires the function of both histone deacetylase (HDAC) and polycomb group (PcG) proteins. Inactivation of p53 leads to increased Arf transcription in both mouse embryonic fibroblasts (MEFs) cultured in vitro and in tissues and organs of p53 null mice. Activation of endogenous p53 enhances Arf repression, and reintroduction of p53 back into p53 null MEFs restores Arf repression. Both DNA binding and trans-activation activities of p53 are required for Arf repression. We show that p53 is required for both HDAC and PcG to repress Arf expression. Bindings of both HDAC and PcG to Arf are disrupted by inactivation of p53 and can be restored in p53 null MEFs by the reintroduction of wild-type, but not mutant, p53. These results indicate that p53 recruits both HDAC and PcG to Arf locus to repress its expression, and this repression constitutes a second feedback loop in p53 regulation.
Efficient Cooper Pair Splitting Without Interactions
Creators: name: Tikhonov, E. S.
name: Khrapai, V. S.
Publisher: name: arXiv
Year: 2023
Subjects: subject: Mesoscale and Nanoscale Physics (cond-mat.mes-hall)
subject: Superconductivity (cond-mat.supr-con)
subject: FOS: Physical sciences

description: For the three-terminal NSN device with single-mode normal terminals and without Coulomb blockade, we propose the interpretation of charge transfer process which allows us to consistently characterize the device operation as that of a Cooper pair splitter in terms of scattering matrix elements as well as in terms of measurable quantities. The obtained explicit expression for the splitting probability notably contains the two-particle interference term not available from conductance measurements. We show that splitting doesn't necessarily rely on single-particle crossed Andreev reflection amplitude thus allowing for the unit efficiency at zero energy. Our results imply that the current cross-correlator generally doesn't provide definite measure of splitting.
description: 9 pages + 14 pages Supplemental Material
Replication and Functional Genomic Analyses of the Breast Cancer Susceptibility Locus at 6q25.1 Generalize Its Importance in Women of Chinese, Japanese, and European Ancestry
Creators: name: Chan, Kelvin Y.K.
name: Le Marchand, Loic
name: Fair, Alecia Malin
name: Wu, Pei Ei
name: Qu, Shimian
name: Garcia-Closas, Montserrat
name: Wen, Wanqing
name: Xiang, Yong Bing
name: Shen, Chen Yang
name: Cui, Yong
name: Signorello, Lisa B.
name: Hu, Zhibin
name: Haiman, Christopher A.
name: Zheng, Hong
name: Santella, Regina M.
name: Shieh, Ya Lan
name: Cai, Qiuyin
name: Titus-Ernstoff, Linda
name: Chen, Kexin
name: Zhang, Lina
name: Long, Jirong
name: Gammon, Marilie D.
name: Huang, Bo
name: Chan, Sum Yin
name: Shen, Hongbing
name: Henderson, Brian E.
name: Gao, Yu Tang
name: Khoo, Ui Soon
name: Wang, Furu
name: Trentham-Dietz, Amy
name: Iwata, Hiroji
name: Egan, Kathleen M.
name: Deming, Sandra L.
name: Shu, Xiao Ou
name: Tajima, Kazuo
name: Newcomb, Polly A.
name: Lu, Wei
name: Iwasaki, Motoki
name: Kasuga, Yoshio
name: Matsuo, Keitaro
name: Li, Chun
name: Li, Guoliang
name: Blot, William J.
name: Tsugane, Shoichiro
name: Zheng, Wei
name: Shrubsole, Martha J.
name: Shi, Jiajun
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: We evaluated the generalizability of a single nucleotide polymorphism (SNP), rs2046210 (A/G allele), associated with breast cancer risk that was initially identified at 6q25.1 in a genome-wide association study conducted among Chinese women. In a pooled analysis of over 31,000 women of East-Asian, European, and African ancestry, we found a positive association for rs2046210 and breast cancer risk in Chinese women [ORs (95%CI)=1.30(1.22–1.38) and 1.64(1.50–1.80) for the AG and AA genotypes, respectively, P for trend = 1.54 × 10−30], Japanese women [ORs (95%CI)=1.31(1.13–1.52) and 1.37(1.06–1.76), P for trend = 2.51 × 10−4], and European-ancestry American women [ORs (95%CI)=1.07(0.99–1.16) and 1.18(1.04–1.34), P for trend = 0.0069]. No association with this SNP, however, was observed in African American women [ORs (95%CI)=0.81(0.63–1.06) and 0.85(0.65–1.11) for the AG and AA genotypes, respectively, P for trend = 0.4027). In vitro functional genomic studies identified a putative functional variant, rs6913578. This SNP is 1,440 bp downstream of rs2046210 and is in high LD with rs2046210 in Chinese (r2=0.91) and European-ancestry (r2=0.83) populations, but not in Africans (r2=0.57). SNP rs6913578 was found to be associated with breast cancer risk in Chinese and European-ancestry American women. After adjusting for rs2046210, the association of rs6913578 with breast cancer risk in African Americans approached borderline significance. Results from this large consortium study confirmed the association of rs2046210 with breast cancer risk among women of Chinese, Japanese, and European ancestry. This association may be explained in part by a putatively functional variant (rs6913578) identified in the region.
title: An updated roadmap of MRI lesions during West Nile Encephalitis: from the common to the ultra-rare
Creators: name: Giangregorio, Antonio
Publisher: name: European Congress of Radiology
Year: 2022
Subjects: subject: Neuroradiology brain
subject: MR
subject: Education
subject: Acute
subject: Infection
subject: Ischaemia / Infarction

description: Learning objectives Background Findings and procedure details Conclusion Personal information and conflict of interest References
description: Learning objectives: The aim of this study is to depict usual, unusual and exceptional MR findings in patients with West-Nile-meningoencephalitis and to correlate MR findings with patient...
The Nuclear Guanine Nucleotide Exchange Factors Ect2 and Net1 Regulate RhoB-Mediated Cell Death after DNA Damage
Creators: name: Srougi, Melissa C.
name: Burridge, Keith
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: Commonly used antitumor treatments, including radiation and chemotherapy, function by damaging the DNA of rapidly proliferating cells. However, resistance to these agents is a predominant clinical problem. A member of the Rho family of small GTPases, RhoB has been shown to be integral in mediating cell death after ionizing radiation (IR) or other DNA damaging agents in Ras-transformed cell lines. In addition, RhoB protein expression increases after genotoxic stress, and loss of RhoB expression causes radio- and chemotherapeutic resistance. However, the signaling pathways that govern RhoB-induced cell death after DNA damage remain enigmatic. Here, we show that RhoB activity increases in human breast and cervical cancer cell lines after treatment with DNA damaging agents. Furthermore, RhoB activity is necessary for DNA damage-induced cell death, as the stable loss of RhoB protein expression using shRNA partially protects cells and prevents the phosphorylation of c-Jun N-terminal kinases (JNKs) and the induction of the pro-apoptotic protein Bim after IR. The increase in RhoB activity after genotoxic stress is associated with increased activity of the nuclear guanine nucleotide exchange factors (GEFs), Ect2 and Net1, but not the cytoplasmic GEFs p115 RhoGEF or Vav2. Importantly, loss of Ect2 and Net1 via siRNA-mediated protein knock-down inhibited IR-induced increases in RhoB activity, reduced apoptotic signaling events, and protected cells from IR-induced cell death. Collectively, these data suggest a mechanism involving the nuclear GEFs Ect2 and Net1 for activating RhoB after genotoxic stress, thereby facilitating cell death after treatment with DNA damaging agents.