bluuebunny/crossref_metadata_2025_split huggingface dataset:
How Santa Claus Became a Slave Driver: The Work of Print Culture in a Nineteenth-Century Musical Controversy
Authors: SHADLE DOUGLAS W. 
Published: December 2014

AbstractThe transnational character of the literate musical community in the United States created an environment in which language barriers, ideological biases, and other potential sources of misunderstanding caused print items to change shape quickly as they were transferred from one reader to the next. The aesthetic controversy between William Henry Fry and Richard Storrs Willis surrounding the 1853 premiere of Fry'sSanta Claus: Christmas Symphonyprovides a rich case in point. The controversy at times seemed to draw from a parallel debate in Europe, often called “The War of the Romantics,” which concerned the future of symphonic composition and music's capacity for representation. At others, the controversy seemed to diverge from its European counterpart as central concepts were articulated in new intellectual contexts. The vagaries of print culture help explain these discrepancies. This article outlines the central arguments of the debate, situates them within their transatlantic contexts, and examines how print culture played a significant role in the controversy's unfolding as early as 1839, fifteen years before it took place. More broadly, it constructs a new framework for examining the function and meaning of nineteenth-century music periodicals by illustrating how an antislavery newspaper became an unlikely voice in a debate over program music.
The Fugs, the Lower East Side, and the Slum Aesthetic in 1960s Rock
Authors: BURKE PATRICK 
Published: December 2014

AbstractDuring the mid-to-late 1960s, impoverished urban districts throughout the United States witnessed an influx of white middle-class youth who attempted to remake society and themselves against a backdrop of inner-city grit and decay. This article focuses on the Lower East Side of Manhattan to explore the significance of slumming in the creation and reception of 1960s rock. Lower East Side rock musicians drew little overt influence from their neighborhood's longstanding ethnic communities, which included eastern Europeans, Puerto Ricans, and African Americans. Rather, these musicians were fascinated with the concept of the “slum” itself as a more abstract signifier of authenticity, adventure, and nonconformity. I propose that a “slum aesthetic” emphasizing dirt, obscenity, and willful amateurism, exemplified by local band the Fugs, was crucial to the Lower East Side rock scene. Examining this “slum aesthetic” helps paint a more nuanced picture of both the political significance of rock and the connections between popular music and urban life. As the Lower East Side's musicians sought both radical social change and a large audience, they represented their neighborhood in ways that combined thoughtful engagement with broad caricature, a contradiction that inspired both musical creativity and social tension.
Enhancing mammary differentiation by overcoming lineage-specific epigenetic modification and signature gene expression of fibroblast-derived iPSCs
Authors: Li Y , Hong N , Zhang A , Chen W , Wang R-H , Xu X-L , Deng C-X 
Published: December 2014

AbstractRecent studies have shown that induced pluripotent stem cells (iPSCs) retain a memory of their origin and exhibit biased differentiation potential. This finding reveals a severe limitation in the application of iPSCs to cell-based therapy because it means that certain cell types are not available for reprogramming for patients. Here we show that the iPSC differentiation process is accompanied by profound gene expression and epigenetic modifications that reflect cells’ origins. Under typical conditions for mammary differentiation, iPSCs reprogrammed from tail-tip fibroblasts (TF-iPSCs) activated a fibroblast-specific signature that was not compatible with mammary differentiation. Strikingly, under optimized conditions, including coculture with iPSCs derived from the mammary epithelium or in the presence of pregnancy hormones, the fibroblast-specific signature of TF-iPSCs obtained during differentiation was erased and cells displayed a mammary-specific signature with a markedly enhanced ability for mammary differentiation. These findings provide new insights into the precise control of differentiation conditions that may have applications in personalized cell-based therapy.
Analysis of gene expression array in TSC2-deficient AML cells reveals IRF7 as a pivotal factor in the Rheb/mTOR pathway
Authors: Makovski V , Jacob-Hirsch J , Gefen-Dor C , Shai B , Ehrlich M , Rechavi G , Kloog Y 
Published: December 2014

AbstractMutations in tuberous sclerosis (TSC) genes cause the genetic disorder TSC, as well as other neoplasms, including lymphangioleiomyomatosis (LAM) and angiomyolipomas (AMLs). AMLs are benign renal tumors occur both in sporadic LAM and in TSC. As they carry the same mutations, AML cell lines serve as a model for TSC and LAM. Rheb/mammalian target of rapamycin complex 1 (mTORC1) pathway is chronically activated in TSC-deficient cells, and this activation can be diminished using the appropriate inhibitors. Rapamycin (sirolimus) is a known specific inhibitor of mTORC1, whereas S-trans,trans-farnesylthiosalicylic acid (FTS; salirasib) has been shown to inhibit Rheb. To examine the effect of the Rheb/mTOR inhibition pathway, we used human TSC2-deficient AML cells, derived from a LAM patient. FTS indeed inhibited Rheb in these cells and attenuated their proliferation. After comparative treatments with FTS or rapamycin or by re-expression of TSC2, we carried out a gene array analysis. This yielded a substantial number of commonly altered genes, many of which we identified as downstream targets of the interferon (IFN) regulatory factor 7 (IRF7) transcription factor, a central activator of the IFN type 1 immune response. Furthermore, nuclear localization of IRF7 was impaired by each of the three treatments. Interestingly, the phenomena seen on FTS or rapamycin treatment were selective for TSC2-deficient cells. Moreover, knockdown of IRF7 by siRNA mimicked the decrease in number of the abovementioned genes and also inhibited AML cell proliferation. Altogether, these findings support FTS as a potential treatment for TSC and its related pathologies and IRF7 as a novel target for treatment.
DNA methylation and differential gene regulation in photoreceptor cell death
Authors: Farinelli P , Perera A , Arango-Gonzalez B , Trifunovic D , Wagner M , Carell T , Biel M , Zrenner E , Michalakis S , Paquet-Durand F , Ekström P A R 
Published: December 2014

AbstractRetinitis pigmentosa (RP) defines a group of inherited degenerative retinal diseases causing progressive loss of photoreceptors. To this day, RP is still untreatable and rational treatment development will require a thorough understanding of the underlying cell death mechanisms. Methylation of the DNA base cytosine by DNA methyltransferases (DNMTs) is an important epigenetic factor regulating gene expression, cell differentiation, cell death, and survival. Previous studies suggested an involvement of epigenetic mechanisms in RP, and in this study, increased cytosine methylation was detected in dying photoreceptors in the rd1, rd2, P23H, and S334ter rodent models for RP. Ultrastructural analysis of photoreceptor nuclear morphology in the rd1 mouse model for RP revealed a severely altered chromatin structure during retinal degeneration that coincided with an increased expression of the DNMT isozyme DNMT3a. To identify disease-specific differentially methylated DNA regions (DMRs) on a genomic level, we immunoprecipitated methylated DNA fragments and subsequently analyzed them with a targeted microarray. Genome-wide comparison of DMRs between rd1 and wild-type retina revealed hypermethylation of genes involved in cell death and survival as well as cell morphology and nervous system development. When correlating DMRs with gene expression data, we found that hypermethylation occurred alongside transcriptional repression. Consistently, motif analysis showed that binding sites of several important transcription factors for retinal physiology were hypermethylated in the mutant model, which also correlated with transcriptional silencing of their respective target genes. Finally, inhibition of DNMTs in rd1 organotypic retinal explants using decitabine resulted in a substantial reduction of photoreceptor cell death, suggesting inhibition of DNA methylation as a potential novel treatment in RP.
Cellular and Kaposi’s sarcoma-associated herpes virus microRNAs in sepsis and surgical trauma
Authors: Tudor S , Giza D E , Lin H Y , Fabris L , Yoshiaki K , D'Abundo L , Toale K M , Shimizu M , Ferracin M , Challagundla K B , Angelica Cortez M , Fuentes-Mattei E , Tulbure D , Gonzalez C , Henderson J , Row M , Rice T W , Ivan C , Negrini M , Fabbri M , Morris J S , Yeung S-C J , Vasilescu C , Calin G A 
Published: December 2014

AbstractOnce a patient is in septic shock, survival rates drop by 7.6% for every hour of delay in antibiotic therapy. Biomarkers based on the molecular mechanism of sepsis are important for timely diagnosis and triage. Here, we study the potential roles of a panel of cellular and viral miRNAs as sepsis biomarkers. We performed genome-wide microRNA (miRNA) expression profiling in leukocytes from septic patients and nonseptic controls, combined with quantitative RT-PCR in plasmas from two cohorts of septic patients, two cohorts of nonseptic surgical patients and healthy volunteers. Enzyme-linked immunosorbent assay, miRNA transfection and chromatin immunoprecipitation were used to study the effects of Kaposi sarcoma herpes virus (KSHV) miRNAs on interleukin's secretion. Differences related to sepsis etiology were noted for plasma levels of 10 cellular and 2 KSHV miRNAs (miR-K-10b and miR-K-12-12*) between septic and nonseptic patients. All the sepsis groups had high KSHV miRNAs levels compared with controls; Afro-American patients had higher levels of KSHV-miR-K12-12* than non-Afro-American patients. Both KSHV miRNAs were increased on postoperative day 1, but returned to baseline on day 7; they acted as direct agonists of Toll-like receptor 8 (TLR8), which might explain the increased secretion of the IL-6 and IL-10. Cellular and KSHV miRNAs are differentially expressed in sepsis and early postsurgical patients and may be exploited for diagnostic and therapeutic purposes. Increased miR-K-10b and miR-K12-12* are functionally involved in sepsis as agonists of TLR8, forming a positive feedback that may lead to cytokine dysregulation.
A novel biomarker Linc00974 interacting with KRT19 promotes proliferation and metastasis in hepatocellular carcinoma
Authors: Tang J , Zhuo H , Zhang X , Jiang R , Ji J , Deng L , Qian X , Zhang F , Sun B 
Published: December 2014

AbstractLocation-associated long noncoding RNA (lncRNA) was reported to interact with target protein via a cis-regulatory process especially for the Flank10kb class lncRNA. Based on this theory, we aimed to explore the regulatory mechanisms of Linc00974 and KRT19 (an lncRNA beyond the Flank10kb class with protein) when we first confirmed the aberrant expression in hepatocellular carcinoma in a previous study. Knockdown of Linc00974 resulted in an inhibition of cell proliferation and invasion with an activation of apoptosis and cell cycle arrest in vitro, which was also validated by a subcutaneous and tail vein/intraperitoneal injection xenotransplantation model in vivo. We further investigated the interaction pattern of Linc00974 and KRT19. MiR-642 was identified, by acting as the competing endogenous RNA in regulating Linc00974 and KRT19. Linc00974 was increased owing to an abnormal hypomethylation promoter, which induced the upregulation of KRT19 via ceRNA interaction, resulting in the activation of the Notch and TGF-β pathways as detected by cDNA microarray. We also discovered Linc00974F-1 stably expressed in the plasma. By the combined analysis of Linc00974F-1 with CYFRA21-1, we found that these joint indicators predicted growth and metastasis of tumor in HCC patients. In conclusion, the combination of Linc00974 and KRT19 may be novel indices for clinical diagnosis of tumor growth and metastasis in HCC, while Linc00974 may become a potential therapeutic target for the prevention of HCC progression.
Koschei the immortal and anti-aging drugs
Authors: Blagosklonny M V 
Published: December 2014

AbstractIn Slavic folklore, Koschei the Immortal was bony, thin and lean. Was his condition caused by severe calorie restriction (CR)? CR deactivates the target of rapamycin pathway and slows down aging. But the life-extending effect of severe CR is limited by starvation. What if Koschei’s anti-aging formula included rapamycin? And was rapamycin (or another rapalog) combined with commonly available drugs such as metformin, aspirin, propranolol, angiotensin II receptor blockers and angiotensin-converting enzyme inhibitors.
Sudden motility reversal indicates sensing of magnetic field gradients in Magnetospirillum magneticum AMB-1 strain
Authors: González Lina M , Ruder Warren C , Mitchell Aaron P , Messner William C , LeDuc Philip R 
Published: December 2014

Abstract
Many motile unicellular organisms have evolved specialized behaviors for detecting and responding to environmental cues such as chemical gradients (chemotaxis) and oxygen gradients (aerotaxis). Magnetotaxis is found in magnetotactic bacteria and it is defined as the passive alignment of these cells to the geomagnetic field along with active swimming. Herein we show that Magnetospirillum magneticum (AMB-1) show a unique set of responses that indicates they sense and respond not only to the direction of magnetic fields by aligning and swimming, but also to changes in the magnetic field or magnetic field gradients. We present data showing that AMB-1 cells exhibit sudden motility reversals when we impose them to local magnetic field gradients. Our system employs permalloy (Ni80Fe20) islands to curve and diverge the magnetic field lines emanating from our custom-designed Helmholtz coils in the vicinity of the islands (creating a drop in the field across the islands). The three distinct movements we have observed as they approach the permalloy islands are: unidirectional, single reverse and double reverse. Our findings indicate that these reverse movements occur in response to magnetic field gradients. In addition, using a permanent magnet we found further evidence that supports this claim. Motile AMB-1 cells swim away from the north and south poles of a permanent magnet when the magnet is positioned less than ∼30 mm from the droplet of cells. All together, these results indicate previously unknown response capabilities arising from the magnetic sensing systems of AMB-1 cells. These responses could enable them to cope with magnetic disturbances that could in turn potentially inhibit their efficient search for nutrients.
Niches of two polysaccharide-degrading Polaribacter isolates from the North Sea during a spring diatom bloom
Authors: Xing Peng , Hahnke Richard L , Unfried Frank , Markert Stephanie , Huang Sixing , Barbeyron Tristan , Harder Jens , Becher Dörte , Schweder Thomas , Glöckner Frank Oliver , Amann Rudolf I , Teeling Hanno 
Published: December 2014

Abstract
Members of the flavobacterial genus Polaribacter thrive in response to North Sea spring phytoplankton blooms. We analyzed two respective Polaribacter species by whole genome sequencing, comparative genomics, substrate tests and proteomics. Both can degrade algal polysaccharides but occupy distinct niches. The liquid culture isolate Polaribacter sp. strain Hel1_33_49 has a 3.0-Mbp genome with an overall peptidase:CAZyme ratio of 1.37, four putative polysaccharide utilization loci (PULs) and features proteorhodopsin, whereas the agar plate isolate Polaribacter sp. strain Hel1_85 has a 3.9-Mbp genome with an even peptidase:CAZyme ratio, eight PULs, a mannitol dehydrogenase for decomposing algal mannitol-capped polysaccharides but no proteorhodopsin. Unlike other sequenced Polaribacter species, both isolates have larger sulfatase-rich PULs, supporting earlier assumptions that Polaribacter take part in the decomposition of sulfated polysaccharides. Both strains grow on algal laminarin and the sulfated polysaccharide chondroitin sulfate. For strain Hel1_33_49, we identified by proteomics (i) a laminarin-induced PUL, (ii) chondroitin sulfate-induced CAZymes and (iii) a chondroitin-induced operon that likely enables chondroitin sulfate recognition. These and other data suggest that strain Hel1_33_49 is a planktonic flavobacterium feeding on proteins and a small subset of algal polysaccharides, while the more versatile strain Hel1_85 can decompose a broader spectrum of polysaccharides and likely associates with algae.
Intestinal epithelial MyD88 is a sensor switching host metabolism towards obesity according to nutritional status
Authors: Everard Amandine , Geurts Lucie , Caesar Robert , Van Hul Matthias , Matamoros Sébastien , Duparc Thibaut , Denis Raphael G. P. , Cochez Perrine , Pierard Florian , Castel Julien , Bindels Laure B. , Plovier Hubert , Robine Sylvie , Muccioli Giulio G. , Renauld Jean-Christophe , Dumoutier Laure , Delzenne Nathalie M. , Luquet Serge , Bäckhed Fredrik , Cani Patrice D. 
Published: December 2014

AbstractObesity is associated with a cluster of metabolic disorders, low-grade inflammation and altered gut microbiota. Whether host metabolism is controlled by intestinal innate immune system and the gut microbiota is unknown. Here we report that inducible intestinal epithelial cell-specific deletion of MyD88 partially protects against diet-induced obesity, diabetes and inflammation. This is associated with increased energy expenditure, an improved glucose homeostasis, reduced hepatic steatosis, fat mass and inflammation. Protection is transferred following gut microbiota transplantation to germ-free recipients. We also demonstrate that intestinal epithelial MyD88 deletion increases anti-inflammatory endocannabinoids, restores antimicrobial peptides production and increases intestinal regulatory T cells during diet-induced obesity. Targeting MyD88 after the onset of obesity reduces fat mass and inflammation. Our work thus identifies intestinal epithelial MyD88 as a sensor changing host metabolism according to the nutritional status and we show that targeting intestinal epithelial MyD88 constitutes a putative therapeutic target for obesity and related disorders.
Anomalous critical fields in quantum critical superconductors
Authors: Putzke C. , Walmsley P. , Fletcher J. D. , Malone L. , Vignolles D. , Proust C. , Badoux S. , See P. , Beere H. E. , Ritchie D. A. , Kasahara S. , Mizukami Y. , Shibauchi T. , Matsuda Y. , Carrington A. 
Published: December 2014

AbstractFluctuations around an antiferromagnetic quantum critical point (QCP) are believed to lead to unconventional superconductivity and in some cases to high-temperature superconductivity. However, the exact mechanism by which this occurs remains poorly understood. The iron-pnictide superconductor BaFe2(As1−xPx)2 is perhaps the clearest example to date of a high-temperature quantum critical superconductor, and so it is a particularly suitable system to study how the quantum critical fluctuations affect the superconducting state. Here we show that the proximity of the QCP yields unexpected anomalies in the superconducting critical fields. We find that both the lower and upper critical fields do not follow the behaviour, predicted by conventional theory, resulting from the observed mass enhancement near the QCP. Our results imply that the energy of superconducting vortices is enhanced, possibly due to a microscopic mixing of antiferromagnetism and superconductivity, suggesting that a highly unusual vortex state is realized in quantum critical superconductors.
Inositol Polyphosphate-5-Phosphatase F (INPP5F) inhibits STAT3 activity and suppresses gliomas tumorigenicity
Authors: Kim Hong Sug , Li Aiguo , Ahn Susie , Song Hua , Zhang Wei 
Published: December 2014

AbstractGlioblastoma (GBM), the most common type of primary malignant brain tumors harboring a subpopulation of stem-like cells (GSCs), is a fast-growing and often fatal tumor. Signal Transducer and Activator of Transcription 3 (STAT3) is one of the major signaling pathways in GSCs maintenance but the molecular mechanisms underlying STAT3 deregulation in GSCs are poorly defined. Here, we demonstrate that Inositol Polyphosphate-5-Phosphatase F (INPP5F), one of the polyphosphoinositide phosphatases, is differentially expressed in GSCs from glioma patients and is identified as an inhibitor of STAT3 signaling via interaction with STAT3 and inhibition of its phosphorylation. Constitutively expressed INPP5F showed to suppress self-renewal and proliferation potentials of glioblastoma cells and reduced tumorigenicity of glioblastoma. In addition, loss of INPP5F gene in gliomas is significantly correlated with lower overall patient survivals. These findings suggest that INPP5F is a potential tumor suppressor in gliomas via inhibition of STAT3 pathway and that deregulation of INPP5F may lead to contribution to gliomagenesis.
Systematic analysis of the in situ crosstalk of tyrosine modifications reveals no additional natural selection on multiply modified residues
Authors: Pan Zhicheng , Liu Zexian , Cheng Han , Wang Yongbo , Gao Tianshun , Ullah Shahid , Ren Jian , Xue Yu 
Published: December 2014

AbstractRecent studies have indicated that different post-translational modifications (PTMs) synergistically orchestrate specific biological processes by crosstalks. However, the preference of the crosstalk among different PTMs and the evolutionary constraint on the PTM crosstalk need further dissections. In this study, the in situ crosstalk at the same positions among three tyrosine PTMs including sulfation, nitration and phosphorylation were systematically analyzed. The experimentally identified sulfation, nitration and phosphorylation sites were collected and integrated with reliable predictions to perform large-scale analyses of in situ crosstalks. From the results, we observed that the in situ crosstalk between sulfation and nitration is significantly under-represented, whereas both sulfation and nitration prefer to co-occupy with phosphorylation at same tyrosines. Further analyses suggested that sulfation and nitration preferentially co-occur with phosphorylation at specific positions in proteins and participate in distinct biological processes and functions. More interestingly, the long-term evolutionary analysis indicated that multi-PTM targeting tyrosines didn't show any higher conservation than singly modified ones. Also, the analysis of human genetic variations demonstrated that there is no additional functional constraint on inherited disease, cancer or rare mutations of multiply modified tyrosines. Taken together, our systematic analyses provided a better understanding of the in situ crosstalk among PTMs.
Getting a Head in the Renaissance: Mementos of Lost Love in Boccaccio and Beyond*
Authors: Ruggiero Guido 
Published: December 2014

AbstractThis essay offers a historian’s reading of Boccaccio’s tale of Lisabetta da Messina (4:5), rethinking it in terms of fourteenth-century ways of understandingvirtùand identity. In analyzing the tale in the context of theDecameron,while reading it against archival material from the period, the deeper context of its discussion of love suggests a reading that makes the tale central to the tragic stories of the fourth day and highlights a lesson about the dangers of passion that make it fit powerfully as the day’s central tale. In the end, love offers many things in theDecameron,but Boccaccio’sbrigataof storytellers and his readers could appreciate a danger more difficult to see today — that the powerful passions associated with lost love and mourning without the support of the groups that surrounded and sustained one’s sense of identity also threatened in the most profound way the negation of self: death.