cometadata/datacite-rtg-text-other-reclassification-records huggingface dataset:
C-C Chemokine Receptor 5 on Pulmonary Fibrocytes Facilitates Migration and Promotes Metastasis via Matrix Metalloproteinase 9
Creators: name: Ting, Jenny P.-Y.
name: Wu, Qing Ping
name: Bergstralh, Daniel T.
name: van Deventer, Hendrik W.
name: Davis, Beckley K.
name: Serody, Jonathan S.
name: O'Connor, Brian P.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2008

description: Previously, our group has used a B16-F10 melanoma model to show that C-C chemokine receptor 5 (CCR5) knockout (CCR5−/−) mice form fewer pulmonary metastases than wild-type mice. This advantage can be eliminated by injecting CCR5−/− mice with wild-type pulmonary mesenchymal cells before tumor injection. In this article, we present the mechanisms underlying this finding. First, we demonstrate that wild-type mesenchymal cells migrate to CCL4 more efficiently in vitro than CCR5−/− cells. Wild-type mesenchymal cells were also 3.6 (1.85 to 5.85) times more efficient than CCR5−/− cells at migrating into the lung after intravenous injection (P < 0.01). The injection of wild-type but not CCR5−/− mesenchymal cells led to a 7.0 ± 1.6 (P < 0.05)-fold induction of matrix metalloproteinase 9 (MMP9) in the host lung. Neither wild-type nor CCR5−/− cells caused significant increases in MMP2, MMP3, or MMP8. Inhibition of the gelatinase activity of MMP9 decreased the number of metastases and restored the advantage that CCR5−/− mice have over wild-type mice. Further analysis showed that the CCR5+ mesenchymal cells expressed CD45+ and CD13+ but did not express α-smooth muscle actin. This phenotype is characteristic of a subset of mesenchymal cells called fibrocytes. Together, these data suggest a novel role for CCR5 in the migration of pulmonary fibrocytes and the promotion of metastasis.
Quantifizierte Bewertung urbaner kultureller Begrünungsleistungen im Bahnhof (Q3B)
Creators: name: Kalla, Matthias
Publisher: name: Zenodo
Year: 2023

description: Die Präsentation beinhaltet die Vorstellung eines Promotionsvorhabens mit dem Thema: Quantifizierte Bewertung von urbanen kulturellen Begrünungsleistungen im Bahnhof (Q3B)
Local subgraph structure can cause localization in continuous-time quantum walk
Creators: name: Ide, Yusuke
Publisher: name: arXiv
Year: 2014
Subjects: subject: Quantum Physics (quant-ph)
subject: Combinatorics (math.CO)
subject: FOS: Physical sciences
subject: FOS: Mathematics

description: In this paper, we consider continuous-time quantum walks (CTQWs) on finite graphs determined by the Laplacian matrices. By introducing fully interconnected graph decomposition of given graphs, we show a decomposition method for the Laplacian matrices. Using the decomposition method, we show several conditions for graph structure which return probability of CTQW tends to 1 while the number of vertices tends to infinity.
description: 8 pages, Accepted for publication in Yokohama Mathematical Journal
The relationships between parent psychological distress, distress intolerance, and family accommodation in the context of child anxiety: a narrative review and empirical study
Creators: name: Wang, Jinjin
Publisher: name: Macquarie University
Year: 2022
Subjects: Other education not elsewhere classified

description: Anxiety disorders are the most common psychiatric mental problems of childhood. Research shows that psychopathology in parents is associated with the development, maintenance, and exacerbation of childhood anxiety disorders. Similarly, as a nascent focus of research in child anxiety, increasing studies identify family accommodation to be linked to increased anxiety symptoms in children. To date, literature has largely focused on the associations of parent psychopathology and family accommodation with child anxiety separately, with minimal empirical investigation into how these two important constructs are related. This thesis aimed to extend current knowledge about the relationships between parent psychopathology, such as psychological distress and distress intolerance, and family accommodation in the context of child anxiety. A narrative review of parent distress and distress intolerance research identified that parents who have difficulty tolerating distress, especially distress elicited by children’s distress, are more likely to be associated with dysfunctional parenting discipline and poorer emotional outcomes in children. To explore the relationships between parent distress, distress intolerance, and family accommodation, an online study was undertaken with parents of clinically anxious and non-anxious children according to the DSM-V diagnostic criteria for an anxiety disorder. Parents were split into high and low distress groups. Results found that parents with higher distress levels were more likely to have children who met criteria for an anxiety disorder, more severe child anxiety symptoms, and engaged in greater frequency of accommodation behaviour compared to parents with lower distress levels. Parent intolerance of child distress significantly predicted accommodation frequency assessed via a clinician-administered tool, while parent intolerance of general distress did not. Results are discussed with respect to previous research and limitations are noted. Additional research is required to examine the differential impacts general distress intolerance and child-specific distress intolerance have on family accommodation.
Molecular Characterization of Human Breast Tumor Vascular Cells
Creators: name: Klauber-DeMore, Nancy
name: Fan, Cheng
name: Gabrielli, Franco
name: Hu, Zhiyuan
name: Perou, Charles M.
name: Livasy, Chad A.
name: Moore, Dominic T.
name: Ketelsen, David
name: Reynolds, Evangeline
name: Patterson, Cam
name: Tanner, Catherine
name: Bhati, Rajendra
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2008

description: A detailed understanding of the assortment of genes that are expressed in breast tumor vessels is needed to facilitate the development of novel, molecularly targeted anti-angiogenic agents for breast cancer therapies. Rapid immunohistochemistry using factor VIII-related antibodies was performed on sections of frozen human luminal-A breast tumors (n = 5) and normal breast (n = 5), followed by laser capture microdissection of vascular cells. RNA was extracted and amplified, and fluorescently labeled cDNA was synthesized and hybridized to 44,000-element long-oligonucleotide DNA microarrays. Statistical analysis of microarray was used to compare differences in gene expression between tumor and normal vascular cells, and Expression Analysis Systematic Explorer was used to determine enrichment of gene ontology categories. Protein expression of select genes was confirmed using immunohistochemistry. Of the 1176 genes that were differentially expressed between tumor and normal vascular cells, 55 had a greater than fourfold increase in expression level. The extracellular matrix gene ontology category was increased while the ribosome gene ontology category was decreased. Fibroblast activation protein, secreted frizzled-related protein 2, Janus kinase 3, and neutral sphingomyelinase 2 proteins localized to breast tumor endothelium as assessed by immunohistochemistry, showing significantly greater staining compared with normal tissue. These tumor endothelial marker proteins also exhibited increased expression in breast tumor vessels compared with that in normal tissues. Therefore, these genetic markers may serve as potential targets for the development of angiogenesis inhibitors.
Chloride Intracellular Channel Protein-4 Functions in Angiogenesis by Supporting Acidification of Vacuoles Along the Intracellular Tubulogenic Pathway
Creators: name: Gordon, Nicarter
name: Ulmasov, Barbara
name: Edwards, John C.
name: Bruno, Jonathan
name: Hartnett, M. Elizabeth
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2009

description: Endothelial cells form capillary tubes through the process of intracellular tubulogenesis. Chloride intracellular channel (CLIC) family proteins have been previously implicated in intracellular tubulogenesis, but their specific role has not been defined. In this study, we show that disruption of the Clic4 gene in mice results in defective angiogenesis in vivo as reflected in a Matrigel plug angiogenesis assay. An angiogenesis defect is also apparent in the retina, both in the decreased spontaneous development of retinal vasculature of unstressed mice and in the dramatically decreased angiogenic response of retinal vessels to an oxygen toxicity challenge. We found that endothelial cells derived from Clic4−/− mice demonstrated impaired tubulogenesis in three-dimensional fibrin gels compared with cells derived from wild-type mice. Furthermore, we found that tubulogenesis of wild-type cells in culture was inhibited by both an inhibitor of CLICs and an inhibitor of the vacuolar proton ATPase. Finally, we showed that vacuoles along the endothelial tubulogenesis pathway are acidic in wild-type cells, and that vacuolar acidification is impaired in Clic4−/− cells while lysosomal acidification is intact. We conclude that CLIC4 plays a critical role in angiogenesis by supporting acidification of vacuoles along the cell-hollowing tubulogenic pathway.
title: Triphenyl Tetrazolium Chloride Ringtest
Creators: name: Karrer, Gerhard
name: Kazinczi, Gabriella
name: Sölter, Ulrike
name: Starfinger, Uwe
name: Verschwele, Arnd
name: Basky, Zsuzsa
name: Lener, Felicia
name: Waldhäuser, Nina
name: Kerepesi, Ildikó
name: Pál-Fám, Ferenc
name: Máté, Sándor
name: Mathiassen, Solvejg K.
name: Kudsk, Per
name: Leskovšek, Robert
name: Van Valkenburg, Johan
Publisher: name: Julius Kühn-Institut
Year: 2016

description: Julius-Kühn-Archiv, Nr. 455 (2016): HALT Ambrosia - final project report and general publication of project findings
Disruption of Tissue-Specific Fucosyltransferase VII, an Enzyme Necessary for Selectin Ligand Synthesis, Suppresses Atherosclerosis in Mice
Creators: name: Counselman, Jessica
name: Bulgrien, Joshua
name: Boisvert, William A.
name: Homeister, Jonathon W.
name: Gitlin, Jonathan M.
name: Lowe, John B.
name: Curtiss, Linda K.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2009

description: A hallmark feature of atherosclerosis is that circulating mononuclear cells adhere to the endothelium and migrate into the subendothelial space. This adhesion is mediated by molecules such as selectins that are expressed on the surfaces of both leukocytes and endothelial cells. In this study, we have determined the role of tissue-specific fucosyltransferase VII (FucT-VII), an enzyme necessary for selectin ligand synthesis, in the development of atherosclerosis. We adopted a scheme of transplanting either FucT-VII−/−GFP+ bone marrow into lethally irradiated low-density lipoprotein receptor low density lipoprotein receptor mice or FucT-VII+/+ GFP+ bone marrow into FucT-VII−/−, low density lipoprotein receptor double-mutant mice to evaluate the roles of E- and P-selectin ligands versus L-selectin ligands, respectively, in diet-induced atherosclerosis. GFP was used to track the transplanted cells. Our results indicate that, compared with controls, selective disruption of E- and P-selectin ligand synthesis resulted in a significant reduction in atherosclerosis. Selective disruption of L-selectin ligand production did not reduce atherosclerosis as robustly as disruption of E- and P-selectin ligands. In both groups, however, there was a significant reduction in the accumulation of macrophages in the lesion. These studies indicate that selectin ligands, particularly those for E- and P-selectins, play an important role in the pathogenesis of atherosclerosis by regulating macrophage accumulation in atherosclerotic lesions.
Rapid Myeloid Cell Transcriptional and Proteomic Responses to Periodontopathogenic Porphyromonas gingivalis
Creators: name: Rangel, Zoila G.
name: Nares, Salvador
name: Moutsopoulos, Niki M.
name: Angelov, Nikola
name: Wahl, Sharon M.
name: Sinha, Neha
name: Munson, Peter J.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2009

description: Long-lived monocytes, macrophages, and dendritic cells (DCs) are Toll-like receptor-expressing, antigen-presenting cells derived from a common myeloid lineage that play key roles in innate and adaptive immune responses. Based on immunohistochemical and molecular analyses of inflamed tissues from patients with chronic destructive periodontal disease, these cells, found in the inflammatory infiltrate, may drive the progressive periodontal pathogenesis. To investigate early transcriptional signatures and subsequent proteomic responses to the periodontal pathogen, Porphyromonas gingivalis, donor-matched human blood monocytes, differentiated DCs, and macrophages were exposed to P. gingivalis lipopolysaccharide (LPS) and gene expression levels were measured by oligonucleotide microarrays. In addition to striking differences in constitutive transcriptional profiles between these myeloid populations, we identify a P. gingivalis LPS-inducible convergent, transcriptional core response of more than 400 annotated genes/ESTs among these populations, reflected by a shared, but quantitatively distinct, proteomic response. Nonetheless, clear differences emerged between the monocytes, DCs, and macrophages. The finding that long-lived myeloid inflammatory cells, particularly DCs, rapidly and aggressively respond to P. gingivalis LPS by generating chemokines, proteases, and cytokines capable of driving T-helper cell lineage polarization without evidence of corresponding immunosuppressive pathways highlights their prominent role in host defense and progressive tissue pathogenesis. The shared, unique, and/or complementary transcriptional and proteomic profiles may frame the context of the host response to P. gingivalis, contributing to the destructive nature of periodontal inflammation.
Assessing the Association Between Nutritional Status, Caries, and Gingivitis in Schoolchildren: A Cross-Sectional Study
Creators: name: Barbosa, Mariane C. F.
name: Reis, Caio L. B.
name: Lopes, Célia M. C. F.
name: Madalena, Isabela R.
name: Küchler, Erika C.
name: Baratto-Filho, Flares
name: Storrer, Carmen L. M.
name: Lima, Daniela C.
name: Oliveira, Daniela S. B.
Publisher: name: Universität Regensburg
Year: 2021
Subjects: subject: caries, gingivitis, nutritional status, obesity, children
subject: 610 Medizin

description: Objective. To evaluate if nutritional status is associated with caries and gingivitis in Brazilian schoolchildren. Material and methods. Children of both genders, age ranging from 8 to 11 years old, were included in this study. Caries was diagnosed using ICDAS (International System for Detection and Assessment of Carious Lesions) and gingivitis was diagnosed using the Community Periodontal Index. The nutritional status of each child was defined by BMI Z-score calculation. Data on oral health behavior and dietary habit were collected through parent’s questionnaires. Parametric analyzes were performed to compare the groups. The established alpha was 5%. Results. The sample consisted of 353 schoolchildren: 16 underweight children, 247 eutrophic children, 64 overweight children, and 26 were obese children. Overweight, Obese and Overweight + Obese children presented less cavitated caries lesion than Eutrophic children (P < .05). Gingivitis was not associated with nutritional status (P > .05). Conclusion. Caries was associated with overweight and obesity in Brazilian schoolchildren.
Symmetry effects on spin switching of adatoms
Creators: name: Hübner, Christoph
name: Baxevanis, Benjamin
name: Khajetoorians, Alexander Ako
name: Pfannkuche, Daniela
Publisher: name: arXiv
Year: 2014
Subjects: subject: Mesoscale and Nanoscale Physics (cond-mat.mes-hall)
subject: FOS: Physical sciences

description: Highly symmetric magnetic environments have been suggested to stabilize the magnetic information stored in magnetic adatoms on a surface. Utilized as memory devices such systems are subjected to electron tunneling and external magnetic fields. We analyze theoretically how such perturbations affect the switching probability of a single quantum spin for two characteristic symmetries encountered in recent experiments and suggest a third one that exhibits robust protection against surface induced spin flips. Further we illuminate how the switching of an adatom spin exhibits characteristic behavior with respect to low energy excitations from which the symmetry of the system can be inferred.
Adiponectin Lowers Glucose Production by Increasing SOGA
Creators: name: Zeisel, Steven H.
name: Combs, Terry P.
name: Mayer-Davis, Elizabeth
name: Rusyn, Ivan
name: Alderman, J. McKee
name: Asmar, Melissa M.
name: Tisch, Roland
name: Busby, Walker H.
name: Garland, Alaina L.
name: Bodnar, Wanda M.
name: Swenberg, James A.
name: Cowerd, Rachael B.
name: Alderman, Elizabeth A.
name: Medoff, Benjamin D.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: Adiponectin is a hormone that lowers glucose production by increasing liver insulin sensitivity. Insulin blocks the generation of biochemical intermediates for glucose production by inhibiting autophagy. However, autophagy is stimulated by an essential mediator of adiponectin action, AMPK. This deadlock led to our hypothesis that adiponectin inhibits autophagy through a novel mediator. Mass spectrometry revealed a novel protein that we call suppressor of glucose by autophagy (SOGA) in adiponectin-treated hepatoma cells. Adiponectin increased SOGA in hepatocytes, and siRNA knockdown of SOGA blocked adiponectin inhibition of glucose production. Furthermore, knockdown of SOGA increased late autophagosome and lysosome staining and the secretion of valine, an amino acid that cannot be synthesized or metabolized by liver cells, suggesting that SOGA inhibits autophagy. SOGA decreased in response to AICAR, an activator of AMPK, and LY294002, an inhibitor of the insulin signaling intermediate, PI3K. AICAR reduction of SOGA was blocked by adiponectin; however, adiponectin did not increase SOGA during PI3K inhibition, suggesting that adiponectin increases SOGA through the insulin signaling pathway. SOGA contains an internal signal peptide that enables the secretion of a circulating fragment of SOGA, providing a surrogate marker for intracellular SOGA levels. Circulating SOGA increased in parallel with adiponectin and insulin activity in both humans and mice. These results suggest that adiponectin-mediated increases in SOGA contribute to the inhibition of glucose production.
Suppressor of Cytokine Signaling-2 Gene Disruption Promotes ApcMin/+ Tumorigenesis and Activator Protein-1 Activation
Creators: name: Newton, Victoria A.
name: Lund, P. Kay
name: Ramocki, Nicole M.
name: Simmons, James G.
name: Scull, Brooks P.
name: McNaughton, Kirk
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: Epigenetic in vitro and in vivo studies suggest that suppressor of cytokine signaling-2 (SOCS2) may normally limit tumorigenesis in the intestine; however, this theory has not been directly tested. We hypothesized that SOCS2 deficiency promotes spontaneous intestinal tumorigenesis in ApcMin/+ mice. Therefore, we quantified tumor number, size, and load in the small intestine and colon using SOCS2+/+/ApcMin/+, SOCS2+/−/ApcMin/+, and SOCS2−/−/ApcMin/+ mice and assayed hematocrit as an indirect marker of disease severity. Biochemical and histological assays were used to assess mechanisms. Heterozygous and homozygous disruption of SOCS2 alleles promoted 166 and 441% increases in tumor load in the small intestine, respectively, accelerated development of colon tumors, and caused severe anemia. SOCS2 deletion promoted significant increases in intestinal insulin-like growth factor-I mRNA but did not affect plasma insulin-like growth factor-I. Western blots and immunohistochemical analysis demonstrated that tumor and nontumor intestinal tissue of SOCS2−/−/ApcMin/+ mice had increased serine 727 phosphorylation of signal transducer and activator of transcription 3 compared with SOCS2+/+/ApcMin/+ mice. Moreover, electromobility shift assays showed that SOCS2 deletion did not alter signal transducer and activator of transcription 3 DNA binding. However, tumors and small intestine from SOCS2−/−/ApcMin/+ showed dramatic increases in activator protein-1 (AP-1) DNA binding, and SOCS2 overexpression in vitro reduced levels of AP-1. These studies indicate that SOCS2 deletion promotes the spontaneous development of intestinal tumors driven by mutations in the adenomatous polyposis coli/β-catenin pathway and activates AP-1. Therefore, reduced expression or epigenetic silencing of SOCS2 may serve as a useful biomarker for colorectal cancer risk.
Quantized electromagnetic response of three-dimensional chiral topological insulators
Creators: name: Wang, Sheng-Tao
name: Deng, Dong-Ling
name: Moore, Joel E.
name: Sun, Kai
name: Duan, Lu-Ming
Publisher: name: arXiv
Year: 2014
Subjects: subject: Mesoscale and Nanoscale Physics (cond-mat.mes-hall)
subject: Strongly Correlated Electrons (cond-mat.str-el)
subject: FOS: Physical sciences

description: Protected by the chiral symmetry, three dimensional chiral topological insulators are characterized by an integer-valued topological invariant. How this invariant could emerge in physical observables is an important question. Here we show that the magneto-electric polarization can identify the integer-valued invariant if we gap the system without coating a quantum Hall layer on the surface. The quantized response is demonstrated to be robust against weak perturbations. We also study the topological properties by adiabatically coupling two nontrivial phases, and find that gapless states appear and are localized at the boundary region. Finally, an experimental scheme is proposed to realize the Hamiltonian and measure the quantized response with ultracold atoms in optical lattices.
description: 8 pages, 6 figures, 2 Appendices
Infinitesimal CR automorphisms and stability groups of infinite type models in $\mathbb C^2$
Creators: name: Hayashimoto, Atsushi
name: Van Thu, Ninh
Publisher: name: arXiv
Year: 2014
Subjects: subject: Complex Variables (math.CV)
subject: FOS: Mathematics
subject: 32M05

description: The purpose of this paper is to give explicit descriptions for stability groups of real rigid hypersurfaces of infinite type in $\mathbb C^2$. The decompositions of infinitesimal CR automorphisms are also given.
description: 20 pages
WNT5A Expression in Ameloblastoma and Its Roles in Regulating Enamel Epithelium Tumorigenic Behaviors
Creators: name: Wright, J. Timothy
name: Sukarawan, Waleerat
name: Suggs, Cynthia
name: Long, Kimberly
name: Simmons, Darrin
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2010

description: Odontogenic tumors originate from the remains of migrating enamel epithelium after the completion of normal tooth genesis. These enamel epithelium remnants exhibit the ability to recapitulate the events that occur during tooth formation. Several lines of evidence suggest that aberrance in the signaling pathways similar to the ones that are used during tooth development, including the WNT pathway, might be the cause of odontogenic tumorigenesis and maintenance. In this study we demonstrated that WNT5A expression was intense in both the epithelial component of ameloblastomas, the most common epithelial odontogenic tumor, and in this tumor's likely precursor cell, the enamel epithelium located at the cervical loop of normal developing human tooth buds. Additionally, when WNT5A was overexpressed in enamel epithelium cells (LS-8), the clones expressing high levels of WNT5A (S) exhibited characteristics of tumorigenic cells, including growth factor independence, loss of anchorage dependence, loss of contact inhibition, and tumor formation in immunocompromised mice. Moreover, overexpression of WNT5A drastically increased LS-8 cell migration and actin reorganization when compared with controls. Suppression of endogenous WNT5A in LS-8 cells (AS) greatly impaired their migration and AS cells failed to form significant actin reorganization and membrane protrusion was rarely seen. Taken together, our data indicate that WNT5A signaling is important in modulating tumorigenic behaviors of enamel epithelium cells in ameloblastomas.
PRISM: Recovery of the primordial spectrum from Planck data
Creators: name: Lanusse, F.
name: Paykari, P.
name: Starck, J. -L.
name: Sureau, F.
name: Bobin, J.
name: Rassat, A.
Publisher: name: arXiv
Year: 2014
Subjects: subject: Cosmology and Nongalactic Astrophysics (astro-ph.CO)
subject: FOS: Physical sciences

description: The primordial power spectrum describes the initial perturbations that seeded the large-scale structure we observe today. It provides an indirect probe of inflation or other structure-formation mechanisms. In this letter, we recover the primordial power spectrum from the Planck PR1 dataset, using our recently published algorithm PRISM. PRISM is a sparsity-based inversion method, that aims at recovering features in the primordial power spectrum from the empirical power spectrum of the cosmic microwave background (CMB). This ill-posed inverse problem is regularised using a sparsity prior on features in the primordial power spectrum in a wavelet dictionary. Although this non-parametric method does not assume a strong prior on the shape of the primordial power spectrum, it is able to recover both its general shape and localised features. As a results, this approach presents a reliable way of detecting deviations from the currently favoured scale-invariant spectrum. We applied PRISM to 100 simulated Planck data to investigate its performance on Planck-like data. We also tested the algorithm's ability to recover a small localised feature at $k \sim 0.125$ Mpc$^{-1}$, which caused a large dip at $\ell \sim 1800$ in the angular power spectrum. We then applied PRISM to the Planck PR1 power spectrum to recover the primordial power spectrum. We find no significant departures from the fiducial Planck PR1 near scale-invariant primordial power spectrum with $A_s=2.215\times10^{-9}$ and $n_s = 0.9624$.
description: 4 pages, 2 figures, Accepted in A&A; Updated to match the final accepted version
Electronic Structure of (Organic-)Inorganic Metal Halide Perovskites: The Dilemma of Choosing the Right Functional
Creators: name: Vona, Cecilia
name: Nabok, Dmitrii
name: Draxl, Claudia
Publisher: name: Humboldt-Universität zu Berlin
Year: 2021
Subjects: subject: hybrid functionals
subject: organic–inorganic metal halide perovskites
subject: one-shot GW
subject: spin-orbit coupling
subject: 530 Physik

description: Organic–inorganic metal halide perovskites (HaPs) are intensively studied for their light-harvesting properties. Owing to the interplay between strong electron–electron interaction and spin-orbit coupling (SOC), their quantitative theoretical description is still a challenge as evidenced by the wide variety of results available in literature. Here, various methodologies for computing their electronic structure are evaluated, also accounting for SOC. More specific, the approach as well as variants of the hybrid functionals PBE0 and HSE are at the center of the investigations. For both functionals, methods to determine the mixing parameter α are explored, and for HSE, the impact of the screening-parameter ω is investigated. An extensive investigation of PbI2, a precursor of many HaPs, leads to the conclusion that hybrid functionals with α tuned by the density-based mixing method are most suitable for obtaining band gaps comparable to
A Mouse Model of Chikungunya Virus–Induced Musculoskeletal Inflammatory Disease: Evidence of Arthritis, Tenosynovitis, Myositis, and Persistence
Creators: name: Gunn, Bronwyn M.
name: Lotstein, Alina R.
name: Heise, Mark T.
name: Morrison, Thomas E.
name: Whitmore, Alan C.
name: Montgomery, Stephanie A.
name: Elmore, Susan A.
name: Oko, Lauren
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: Chikungunya virus (CHIKV), an emerging mosquito-borne Alphavirus, causes debilitating rheumatic disease in humans that can last for weeks to months. Starting in 2004, a CHIKV outbreak in the Indian Ocean region affected millions of people, and infected travelers introduced CHIKV to new regions. The pathogenesis of CHIKV is poorly understood, and no approved vaccines or specific therapies exist. A major challenge to the study of CHIKV disease is the lack of a small animal model that recapitulates the major outcomes of human infection. In this study, the pathogenesis of CHIKV in C57BL/6J mice was investigated using biological and molecular clones of CHIKV isolated from human serum (CHIKV SL15649). After 14-day-old mice were inoculated with CHIKV SL15649 in the footpad, they displayed reduced weight gain and swelling of the inoculated limb. Histologic analysis of hind limb sections revealed severe necrotizing myositis, mixed inflammatory cell arthritis, chronic active tenosynovitis, and multifocal vasculitis. Interestingly, these disease signs and viral RNA persisted in musculoskeletal tissues for at least 3 weeks after inoculation. This work demonstrates the development of a mouse model of CHIKV infection with clinical manifestations and histopathologic findings that are consistent with the disease signs of CHIKV-infected humans, providing a useful tool for studying viral and host factors that drive CHIKV pathogenesis and for evaluating potential therapeutics against this emerging viral disease.
Characterization of a photon counting EMCCD for space-based high contrast imaging spectroscopy of extrasolar planets
Creators: name: Wilkins, Ashlee N.
name: McElwain, Michael W.
name: Norton, Timothy J.
name: Rauscher, Bernard J.
name: Rothe, Johannes F.
name: Malatesta, Michael
name: Hilton, George M.
name: Bubeck, James R.
name: Grady, Carol A.
name: Lindler, Don J.
Publisher: name: arXiv
Year: 2014
Subjects: subject: Instrumentation and Methods for Astrophysics (astro-ph.IM)
subject: FOS: Physical sciences

description: We present the progress of characterization of a low-noise, photon counting Electron Multiplying Charged Coupled Device (EMCCD) operating in optical wavelengths and demonstrate possible solutions to the problems of Clock-Induced Charge (CIC) and other trapped charge through sub-bandgap illumination. Such a detector will be vital to the feasibility of future space-based direct imaging and spectroscopy missions for exoplanet characterization, and is scheduled to fly on-board the AFTA-WFIRST mission. The 512$\times$512 EMCCD is an e2v detector housed and clocked by a Nüvü Cameras controller. Through a multiplication gain register, this detector produces as many as 5000 electrons for a single, incident-photon-induced photoelectron produced in the detector, enabling single photon counting operation with read noise and dark current orders of magnitude below that of standard CCDs. With the extremely high contrasts (Earth-to-Sun flux ratio is $\sim$ 10$^{-10}$) and extremely faint targets (an Earth analog would measure 28$^{th}$ - 30$^{th}$ magnitude or fainter), a photon-counting EMCCD is absolutely necessary to measure the signatures of habitability on an Earth-like exoplanet within the timescale of a mission's lifetime, and we discuss the concept of operations for an EMCCD making such measurements.
description: 12 pages, 6 figures, presented at SPIE Astronomical Telescopes + Instrumentation 2014, conference 9154 (High Energy, Optical, and Infrared Detectors for Astronomy VI), submitted to SPIE Astronomical Telescopes + Instrumentation Proceedings (Paper 9154-6) [Replacement to update contact e-mail]
Insulin Resistance and Metabolic Hepatocarcinogenesis with Parent-of-Origin Effects in A×B Mice
Creators: name: Hartwell, Hadley J.
name: Fecteau, Michelle
name: Rogers, Arlin B.
name: Hines, Ian N.
name: Fox, James G.
name: Hashway, Sara
name: Feng, Yan
name: Connolly, Jessica
name: Theve, Elizabeth J.
name: Hall, Gregory A.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: Insulin resistance is a defining feature of metabolic syndrome and type 2 diabetes mellitus but also may occur independently of these conditions. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of these disorders, increases the risk of hepatocellular carcinoma (HCC). However, mechanisms linking hyperinsulinemia to NAFLD and HCC require clarification. We describe a novel model of primary insulin resistance and HCC with strong parent-of-origin effects. Male AB6F1 (A/JCr dam × C57BL/6 sire) but not B6AF1 (B6 dam × A/J sire) mice developed spontaneous insulin resistance, NAFLD, and HCC without obesity or diabetes. A survey of mitochondrial, imprinted, and sex-linked traits revealed modest associations with X-linked genes. However, a diet-induced obesity study, including B6.A chromosome substitution–strain (consomic) mice, showed no segregation by sex chromosome. Thus, parent-of-origin effects were specified within the autosomal genome. Next, we interrogated mechanisms of insulin-associated hepatocarcinogenesis. Steatotic hepatocytes exhibited adipogenic transition characterized by vacuolar metaplasia and up-regulation of vimentin, adipsin, fatty acid translocase (CD36), peroxisome proliferator–activated receptor-γ, and related products. This profile was largely recapitulated in insulin-supplemented primary mouse hepatocyte cultures. Importantly, pyruvate kinase M2, a fetal anabolic enzyme implicated in the Warburg effect, was activated by insulin in vivo and in vitro. Thus, our study reveals parent-of-origin effects in heritable insulin resistance, implicating adipogenic transition with acquired anabolic metabolism in the progression from NAFLD to HCC.
Mu Opioid Signaling Protects Against Acute Murine Intestinal Injury in a Manner Involving Stat3 Signaling
Creators: name: Uronis, Joshua M.
name: Jobin, Christian
name: Goldsmith, Jason R.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: Opiates have long been used as analgesics to relieve pain associated with various medical conditions. Here, we evaluated the effect and mechanism of mu opioid signaling on the intestinal wound healing response and assessed downstream pathways known to be protective against intestinal injury. Mice (C57BL/6) were exposed to 3% dextran sodium sulfate (DSS) for 7 days or 4% DSS for 5 days followed by 7 days of water. The mu opioid receptor (MOR)-specific agonist [D-Arg2,Lys4]dermorphin-(1,4)-amide (DALDA) and the antagonist cyprodime were injected s.c. daily for in vivo studies or used for in vitro analysis. We found that MOR activation attenuated DSS-induced histologic and gross intestinal injury and weight loss; diminished Ifng, Tnf, and Il6 mRNA expression; and promoted intestinal healing during recovery. DALDA also enhanced colonocyte proliferation (Ki-67 staining) by 350%. MOR activation increased Stat3 phosphorylation in both DALDA-treated mice and the CMT-93 cell line. Importantly, DALDA-induced colonocyte migration was completely ablated by shStat3 knockdown. Together, this work shows that MOR activation protects against and enhances recovery from DSS-induced intestinal injury. This is associated with an increase in Stat3 activation. Furthermore, Stat3 is required for DALDA-induced colonocyte migration. Consequently, manipulation of MOR signaling may represent a novel means to promote mucosal healing and to maintain intestinal homeostasis after intestinal injury.
NF-κB Inhibition Protects against Tumor-Induced Cardiac Atrophy in Vivo
Creators: name: Li, Lugi
name: Gore, Mitchell
name: Patterson, Cam
name: Yin, Xiaoying
name: Asher, Scott
name: Wysong, Ashley
name: Rodriguez, Jessica E.
name: Baldwin, Al
name: Shadfar, Scott
name: Couch, Marion
name: Willis, Monte S.
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: Cancer cachexia is a severe wasting syndrome characterized by the progressive loss of lean body mass and systemic inflammation. It occurs in approximately 80% of patients with advanced malignancy and is the cause of 20% to 30% of all cancer-related deaths. The mechanism by which striated muscle loss occurs is the tumor release of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α. These cytokines interact with their cognate receptors on muscle cells to enhance NF-κB signaling, which then mediates muscle loss and significant cardiac dysfunction. Genetic inhibition of NF-κB signaling has demonstrated its predominant role in skeletal muscle loss. Therefore, we tested two novel drugs designed to specifically inhibit NF-κB by targeting the IκB kinase (IKK) complex: Compound A and NEMO binding domain (NBD) peptide. Using an established mouse model of cancer cachexia (C26 adenocarcinoma), we determined how these drugs affected the development of tumor-induced cardiac atrophy and function. Echocardiographic and histological analysis revealed that both Compound A and NBD inhibit cardiac NF-κB activity and prevent the development of tumor-induced systolic dysfunction and atrophy. This protection was independent of any effects of the tumor itself (Compound A) or tumor-secreted cytokines (NBD). This study identifies for the first time, to our knowledge, that drugs targeting the IKK complex are cardioprotective against cancer cachexia–induced cardiac atrophy and systolic dysfunction, suggesting therapies that may help reduce cardiac-associated morbidities found in patients with advanced malignancies.
The mathematical physical equations satisfied by retarded and advanced Green's functions
Creators: name: Wang, Huai-Yu
Publisher: name: arXiv
Year: 2022
Subjects: subject: Quantum Physics (quant-ph)
subject: FOS: Physical sciences

description: In mathematical physics, time-dependent Green's functions (GFs) are the solutions of differential equations of the first and second time derivatives. Habitually, the time-dependent GFs are Fourier transformed into the frequency space. Then, analytical continuation of the frequency is extended to below or above the real axis. After inverse Fourier transformation, retarded and advanced GFs can be obtained, and there may be arbitrariness in such analytical continuation. In the present work, we establish the differential equations from which the retarded and advanced GFs are rigorously solved. The key point is that the derivative of the time step function is the Dirac delta function plus an infinitely small quantity, where the latter is not negligible because it embodies the meaning of time delay or time advance. The retarded and advanced GFs defined in this paper are the same as the one-body GFs defined with the help of the creation and destruction operators in many-body theory. There is no way to define the causal GF in mathematical physics, and the reason is given. This work puts the initial conditions into differential equations, thereby paving a way for solving the problem of why there are motions that are irreversible in time.
description: 28 pages
Post-Natal Knockdown of Fukutin-Related Protein Expression in Muscle by Long-Term RNA Interference Induces Dystrophic Pathology
Creators: name: Li, Juan
name: Xiao, Bin
name: Zheng, Hui
name: Ma, Hsin-I.
name: Wang, Chi-Hsien
name: Keramaris-Vrantsis, Elizabeth
name: Tang, Ru-Hang
name: Xiao, Xiao
name: Lu, Qilong
name: Jiang, Jiangang
name: Lu, Peijuan
name: Chan, Yiumo Michael
name: Qiao, Chunping
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: Limb-girdle muscular dystrophy 2I (LGMD2I) is caused by mutations in the fukutin-related protein (FKRP) gene. Unlike its severe allelic forms, LGMD2I usually involves slower onset and milder course without defects in the central nervous system. The lack of viable animal models that closely recapitulate LGMD2I clinical phenotypes led us to use RNA interference technology to knock down FKRP expression via postnatal gene delivery so as to circumvent embryonic lethality. Specifically, an adeno-associated viral vector was used to deliver short hairpin (shRNA) genes to healthy ICR mice. Adeno-associated viral vectors expressing a single shRNA or two different shRNAs were injected one time into the hind limb muscles. We showed that FKRP expression at 10 months postinjection was reduced by about 50% with a single shRNA and by 75% with the dual shRNA cassette. Dual-cassette injection also reduced a-dystroglycan glycosylation and its affinity to laminin by up to 70% and induced α-dystrophic pathology, including fibrosis and central nucleation, in more than 50% of the myofibers at 10 months after injection. These results suggest that the reduction of approximately or more than 75% of the normal level of FKRP expression induces chronic dystrophic phenotypes in skeletal muscles. Furthermore, the restoration of about 25% of the normal FKRP level could be sufficient for LGMD2I therapy to correct the genetic deficiency effectively and prevent dystrophic pathology.
Reconciling Planck cluster counts and cosmology? Chandra/XMM instrumental calibration and hydrostatic mass bias
Creators: name: Israel, Holger
name: Schellenberger, Gerrit
name: Nevalainen, Jukka
name: Massey, Richard
name: Reiprich, Thomas
Publisher: name: arXiv
Year: 2014
Subjects: subject: Cosmology and Nongalactic Astrophysics (astro-ph.CO)
subject: FOS: Physical sciences

description: The mass of galaxy clusters can be inferred from the temperature of their X-ray emitting gas, $T_{\mathrm{X}}$. Their masses may be underestimated if it is assumed that the gas is in hydrostatic equilibrium, by an amount $b^{\mathrm{hyd}}\sim(20\pm10)$ % suggested by simulations. We have previously found consistency between a sample of observed \textit{Chandra} X-ray masses and independent weak lensing measurements. Unfortunately, uncertainties in the instrumental calibration of {\em Chandra} and {\em XMM-Newton} observatories mean that they measure different temperatures for the same gas. In this paper, we translate that relative instrumental bias into mass bias, and infer that \textit{XMM-Newton} masses of $\sim 10^{14}\,\mbox{M}_{\odot}$ ($> 5\cdot 10^{14} \mbox{M}_{\odot}$) clusters are unbiased ($\sim 35$ % lower) compared to WL masses. For massive clusters, \textit{Chandra}'s calibration may thus be more accurate. The opposite appears to be true at the low mass end. We observe the mass bias to increase with cluster mass, but presence of Eddington bias precludes firm conclusions at this stage. Nevertheless, the systematic \textit{Chandra} -- \textit{XMM-Newton} difference is important because {\em Planck}'s detections of massive clusters via the Sunyaev-Zeldovich (SZ) effect are calibrated via {\em XMM-Newton} observations. The number of detected SZ clusters are inconsistent with {\em Planck}'s cosmological measurements of the primary Cosmic Microwave Background (CMB). Given the \textit{Planck} cluster masses, if an (unlikely) uncorrected $\sim 20$ % calibration bias existed, this tension would be eased, but not resolved.
description: 8 pages, 4 figures
Protease-Activated Receptor 1 and Hematopoietic Cell Tissue Factor Are Required for Hepatic Steatosis in Mice Fed a Western Diet
Creators: name: Li, Guodong
name: Tawfik, Ossama
name: Guo, Grace L.
name: Luyendyk, James P.
name: Kassel, Karen M.
name: Mackman, Nigel
name: Rockwell, Cheryl E.
name: Sullivan, Bradley P.
name: Owens, A. Phillip
name: Wang, Ruipeng
Publisher: name: The University of North Carolina at Chapel Hill University Libraries
Year: 2011

description: Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of obesity and metabolic syndrome and contributes to increased risk of cardiovascular disease and liver-related morbidity and mortality. Indeed, obese patients with metabolic syndrome generate greater amounts of thrombin, an indication of coagulation cascade activation. However, the role of the coagulation cascade in Western diet–induced NAFLD has not been investigated. Using an established mouse model of Western diet–induced NAFLD, we tested whether the thrombin receptor protease-activated receptor 1 (PAR-1) and hematopoietic cell–derived tissue factor (TF) contribute to hepatic steatosis. In association with hepatic steatosis, plasma thrombin-antithrombin levels and hepatic fibrin deposition increased significantly in C57Bl/6J mice fed a Western diet for 3 months. PAR-1 deficiency reduced hepatic inflammation, particularly monocyte chemoattractant protein-1 expression and macrophage accumulation. In addition, PAR-1 deficiency was associated with reduced steatosis in mice fed a Western diet, including reduced liver triglyceride accumulation and CD36 expression. Similar to PAR-1 deficiency, hematopoietic cell TF deficiency was associated with reduced inflammation and reduced steatosis in livers of low-density lipoprotein receptor–deficient mice fed a Western diet. Moreover, hematopoietic cell TF deficiency reduced hepatic fibrin deposition. These studies indicate that PAR-1 and hematopoietic cell TF are required for liver inflammation and steatosis in mice fed a Western diet.
$L$-band Spectra of Young Brown Dwarfs
Creators: name: Beiler, Samuel
name: Allers, Katelyn
name: Cushing, Michael
name: Faherty, Jacqueline
name: Marley, Mark
name: Skemer, Andrew
Publisher: name: arXiv
Year: 2022
Subjects: subject: Solar and Stellar Astrophysics (astro-ph.SR)
subject: Earth and Planetary Astrophysics (astro-ph.EP)
subject: FOS: Physical sciences

description: We present a $L$-band (2.98--3.96$μ$m) spectroscopic study of 8 young L dwarfs with spectral types ranging from L2 to L7. Our spectra ($λ/{Δλ}\approx$ 250 to 600) were collected using the Gemini Near-InfraRed Spectrograph. We first examine the young $L$-band spectral sequence, most notably analyzing the evolution of the $Q$-branch of methane absorption feature at 3.3 $μ$m. We find the $Q$-branch feature first appears between L3 and L6, as previously seen in older field dwarfs. Secondly, we analyze how well various atmospheric models reproduce the $L$-band and published near-IR (0.7--2.5 $μ$m) spectra of our objects by fitting five different grids of model spectra to the data. Best-fit parameters for the combined near-IR and $L$-band data are compared to best-fit parameters for just the near-IR data, isolating the impact that the addition of the $L$-band has on the results. This addition notably causes a $\sim$100 K drop in the best-fit effective temperature. Also, when clouds and a vertical mixing rate ($K_{\mathrm{zz}}$) are included in the models, thick clouds and higher $K_{\mathrm{zz}}$ values are preferred. Five of our objects also have previously published effective temperatures and surface gravities derived using evolutionary models, age estimates, and bolometric luminosities. Comparing model spectra matching these parameters to our spectra, we find disequilibrium chemistry and clouds are needed to match these published effective temperatures. Three of these objects are members of AB Dor, allowing us to show the temperature dependence of the $Q$-branch of methane.
description: 26 pages, 19 figures, Accepted for publication in MNRAS