bluuebunny/crossref_metadata_2025_split huggingface dataset:
Beyond reuse distance analysis
Authors: Fauzia Naznin , Elango Venmugil , Ravishankar Mahesh , Ramanujam J. , Rastello Fabrice , Rountev Atanas , Pouchet Louis-Noël , Sadayappan P. 
Published: January 2014

Emerging computer architectures will feature drastically decreased flops/byte (ratio of peak processing rate to memory bandwidth) as highlighted by recent studies on Exascale architectural trends. Further, flops are getting cheaper, while the energy cost of data movement is increasingly dominant. The understanding and characterization of data locality properties of computations is critical in order to guide efforts to enhance data locality.
Reuse distance analysis of memory address traces is a valuable tool to perform data locality characterization of programs. A single reuse distance analysis can be used to estimate the number of cache misses in a fully associative LRU cache of any size, thereby providing estimates on the minimum bandwidth requirements at different levels of the memory hierarchy to avoid being bandwidth bound. However, such an analysis only holds for the particular execution order that produced the trace. It cannot estimate potential improvement in data locality through dependence-preserving transformations that change the execution schedule of the operations in the computation.
In this article, we develop a novel dynamic analysis approach to characterize the inherent locality properties of a computation and thereby assess the potential for data locality enhancement via dependence-preserving transformations. The execution trace of a code is analyzed to extract a Computational-Directed Acyclic Graph (CDAG) of the data dependences. The CDAG is then partitioned into convex subsets, and the convex partitioning is used to reorder the operations in the execution trace to enhance data locality. The approach enables us to go beyond reuse distance analysis of a single specific order of execution of the operations of a computation in characterization of its data locality properties. It can serve a valuable role in identifying promising code regions for manual transformation, as well as assessing the effectiveness of compiler transformations for data locality enhancement. We demonstrate the effectiveness of the approach using a number of benchmarks, including case studies where the potential shown by the analysis is exploited to achieve lower data movement costs and better performance.
From RSSI to CSI
Authors: Yang Zheng , Zhou Zimu , Liu Yunhao 
Published: January 2014

The spatial features of emitted wireless signals are the basis of location distinction and determination for wireless indoor localization. Available in mainstream wireless signal measurements, the Received Signal Strength Indicator (RSSI) has been adopted in vast indoor localization systems. However, it suffers from dramatic performance degradation in complex situations due to multipath fading and temporal dynamics.
Break-through techniques resort to finer-grained wireless channel measurement than RSSI. Different from RSSI, the PHY layer power feature, channel response, is able to discriminate multipath characteristics, and thus holds the potential for the convergence of accurate and pervasive indoor localization. Channel State Information (CSI, reflecting channel response in 802.11 a/g/n) has attracted many research efforts and some pioneer works have demonstrated submeter or even centimeter-level accuracy. In this article, we survey this new trend of channel response in localization. The differences between CSI and RSSI are highlighted with respect to network layering, time resolution, frequency resolution, stability, and accessibility. Furthermore, we investigate a large body of recent works and classify them overall into three categories according to how to use CSI. For each category, we emphasize the basic principles and address future directions of research in this new and largely open area.
Sequential Gene Targeting to Make Chimeric Tumor Models with De Novo Chromosomal Abnormalities
Authors: Chambers Jennifer S. , Tanaka Tomoyuki , Brend Tim , Ali Hanif , Geisler Nicola J. , Khazin Leah , Cigudosa Juan C. , Neil Dear T. , MacLennan Kenneth , Rabbitts Terence H. 
Published: January 2014

Abstract
The discovery of chromosomal translocations in leukemia/lymphoma and sarcomas presaged a widespread discovery in epithelial tumors. With the advent of new-generation whole-genome sequencing, many consistent chromosomal abnormalities have been described together with putative driver and passenger mutations. The multiple genetic changes required in mouse models to assess the interrelationship of abnormalities and other mutations are severe limitations. Here, we show that sequential gene targeting of embryonic stem cells can be used to yield progenitor cells to generate chimeric offspring carrying all the genetic changes needed for cell-specific cancer. Illustrating the technology, we show that MLL–ENL fusion is sufficient for lethal leukocytosis and proof of genome integrity comes from germline transmission of the sequentially targeted alleles. This accelerated technology leads to a reduction in mouse numbers (contributing significantly to the 3Rs), allows fluorescence tagging of cancer-initiating cells, and provides a flexible platform for interrogating the interaction of chromosomal abnormalities with mutations. Cancer Res; 74(5); 1588–97. ©2014 AACR.
GRHL1Acts as Tumor Suppressor in Neuroblastoma and Is Negatively Regulated by MYCN and HDAC3
Authors: Fabian Johannes , Lodrini Marco , Oehme Ina , Schier Marie C. , Thole Theresa M. , Hielscher Thomas , Kopp-Schneider Annette , Opitz Lennart , Capper David , von Deimling Andreas , Wiegand Inga , Milde Till , Mahlknecht Ulrich , Westermann Frank , Popanda Odilia , Roels Frederik , Hero Barbara , Berthold Frank , Fischer Matthias , Kulozik Andreas E. , Witt Olaf , Deubzer Hedwig E. 
Published: January 2014

AbstractNeuroblastoma is an embryonic solid tumor of neural crest origin and accounts for 11% of all cancer-related deaths in children. Novel therapeutic strategies are therefore urgently required. MYCN oncogene amplification, which occurs in 20% of neuroblastomas, is a hallmark of high risk. Here, we aimed to exploit molecular mechanisms that can be pharmacologically addressed with epigenetically modifying drugs, such as histone deacetylase (HDAC) inhibitors. Grainyhead-like 1 (GRHL1), a gene critical for Drosophila neural development, belonged to the genes most strongly responding to HDAC inhibitor treatment of neuroblastoma cells in a genome-wide screen. An increase in the histone H4 pan-acetylation associated with its promoter preceded transcriptional activation. Physically adjacent, HDAC3 and MYCN colocalized to the GRHL1 promoter and repressed its transcription. High-level GRHL1 expression in primary neuroblastomas correlated on transcriptional and translational levels with favorable patient survival and established clinical and molecular markers for favorable tumor biology, including lack of MYCN amplification. Enforced GRHL1 expression in MYCN-amplified neuroblastoma cells with low endogenous GRHL1 levels abrogated anchorage-independent colony formation, inhibited proliferation, and retarded xenograft growth in mice. GRHL1 knockdown in MYCN single-copy cells with high endogenous GRHL1 levels promoted colony formation. GRHL1 regulated 170 genes genome-wide, and most were involved in pathways regulated during neuroblastomagenesis, including nervous system development, proliferation, cell–cell adhesion, cell spreading, and cellular differentiation. In summary, the data presented here indicate a significant role of HDAC3 in the MYCN-mediated repression of GRHL1 and suggest drugs that block HDAC3 activity and suppress MYCN expression as promising candidates for novel treatment strategies of high-risk neuroblastoma. Cancer Res; 74(9); 2604–16. ©2014 AACR.
LEF1 and B9L Shield β-Catenin from Inactivation by Axin, Desensitizing Colorectal Cancer Cells to Tankyrase Inhibitors
Authors: de la Roche Marc , Ibrahim Ashraf E.K. , Mieszczanek Juliusz , Bienz Mariann 
Published: January 2014

Abstract
Hyperactive β-catenin drives colorectal cancer, yet inhibiting its activity remains a formidable challenge. Interest is mounting in tankyrase inhibitors (TNKSi), which destabilize β-catenin through stabilizing Axin. Here, we confirm that TNKSi inhibit Wnt-induced transcription, similarly to carnosate, which reduces the transcriptional activity of β-catenin by blocking its binding to BCL9, and attenuates intestinal tumors in ApcMin mice. By contrast, β-catenin's activity is unresponsive to TNKSi in colorectal cancer cells and in cells after prolonged Wnt stimulation. This TNKSi insensitivity is conferred by β-catenin's association with LEF1 and BCL9-2/B9L, which accumulate during Wnt stimulation, thereby providing a feed-forward loop that converts transient into chronic β-catenin signaling. This limits the therapeutic value of TNKSi in colorectal carcinomas, most of which express high LEF1 levels. Our study provides proof-of-concept that the successful inhibition of oncogenic β-catenin in colorectal cancer requires the targeting of its interaction with LEF1 and/or BCL9/B9L, as exemplified by carnosate. Cancer Res; 74(5); 1495–505. ©2014 AACR.
CBP-Mediated FOXO-1 Acetylation Inhibits Pancreatic Tumor Growth by Targeting SirT
Authors: Pramanik Kartick C. , Fofaria Neel M. , Gupta Parul , Srivastava Sanjay K. 
Published: January 2014

Abstract
Here, we investigated the potential mechanism of capsaicin-mediated apoptosis in pancreatic cancer cells. Capsaicin treatment phosphorylated c-jun-NH2-kinase (JNK); forkhead box transcription factor, class O (FOXO1); and BIM in BxPC-3, AsPC-1, and L3.6PL cells. The expression of BIM increased in response to capsaicin treatment. Capsaicin treatment caused cleavage of caspase-3 and PARP, indicating apoptosis. Antioxidants tiron and PEG-catalase blocked capsaicin-mediated JNK/FOXO/BIM activation and protected the cells from apoptosis. Furthermore, capsaicin treatment caused a steady increase in the nuclear expression of FOXO-1, leading to increased DNA binding. Capsaicin-mediated expression of BIM was found to be directly dependent on the acetylation of FOXO-1. The expression of CREB-binding protein (CBP) was increased, whereas SirT-1 was reduced by capsaicin treatment. Using acetylation mimic or defective mutants, our result demonstrated that phosphorylation of FOXO-1 was mediated through acetylation by capsaicin treatment. JNK inhibitor attenuated the phosphorylation of FOXO-1, activation of BIM, and abrogated capsaicin-induced apoptosis. Moreover, silencing FOXO1 by siRNA blocked capsaicin-mediated activation of BIM and apoptosis, whereas overexpression of FOXO-1 augmented its effects. Silencing Bim drastically reduced capsaicin-mediated cleavage of caspase-3 and PARP, indicating the role of BIM in apoptosis. Oral administration of 5 mg/kg capsaicin substantially suppressed the growth of BxPC-3 tumor xenografts in athymic nude mice. Tumors from capsaicin-treated mice showed an increase in the phosphorylation of JNK, FOXO-1, BIM, and levels of CBP, cleavage of caspase-3, PARP, and decreased SirT-1 expression. Taken together, our results suggest that capsaicin activated JNK and FOXO-1, leading to the acetylation of FOXO-1 through CBP and SirT-1. Acetylated FOXO1 induced apoptosis in pancreatic cancer cells through BIM activation. Mol Cancer Ther; 13(3); 687–98. ©2014 AACR.
Reoxygenation‐Derived Toxic Reactive Oxygen/Nitrogen Species Modulate the Contribution of Bone Marrow Progenitor Cells to Remodeling After Myocardial Infarction
Authors: Moldovan Nicanor I. , Anghelina Mirela , Varadharaj Saradhadevi , Butt Omer I. , Wang Tiangshen , Yang Fuchun , Moldovan Leni , Zweier Jay L. 
Published: January 2014

Background

The core region of a myocardial infarction is notoriously unsupportive of cardiomyocyte survival. However, there has been less investigation of the potentially beneficial spontaneous recruitment of endogenous bone marrow progenitor cells (
BMPC
s) within infarcted areas. In the current study we examined the role of tissue oxygenation and derived toxic species in the control of
BMPC
engraftment during postinfarction heart remodeling.

Methods and Results

For assessment of cellular origin, local oxygenation, redox status, and fate of cells in the infarcted region, myocardial infarction in mice with or without LacZ
+
bone marrow transplantation was induced by coronary ligation. Sham‐operated mice served as controls. After 1 week, LacZ
+
BMPC
‐derived cells were found inhomogeneously distributed into the infarct zone, with a lower density at its core. Electron paramagnetic resonance (EPR) oximetry showed that
pO
2
in the infarct recovered starting on day 2 post–myocardial infarction, concomitant with wall thinning and erythrocytes percolating through muscle microruptures. Paralleling this reoxygenation, increased generation of reactive oxygen/nitrogen species was detected at the infarct core. This process delineated a zone of diminished
BMPC
engraftment, and at 1 week infiltrating cells displayed immunoreactive 3‐nitrotyrosine and apoptosis. In vivo treatment with a superoxide dismutase mimetic significantly reduced reactive oxygen species formation and amplified
BMPC
accumulation. This treatment also salvaged wall thickness by 43% and left ventricular ejection fraction by 27%, with significantly increased animal survival.

Conclusions

BMPC
engraftment in the infarct inversely mirrored the distribution of reactive oxygen/nitrogen species. Antioxidant treatment resulted in increased numbers of engrafted
BMPC
s, provided functional protection to the heart, and decreased the incidence of myocardial rupture and death.
The meaning of dignity in nursing home care as seen by relatives
Authors: Rehnsfeldt Arne , Lindwall Lillemor , Lohne Vibeke , Lillestø Britt , Slettebø Åshild , Heggestad Anne Kari T , Aasgaard Trygve , Råholm Maj-Britt , Caspari Synnøve , Høy Bente , Sæteren Berit , Nåden Dagfinn 
Published: January 2014

Background: As part of an ongoing Scandinavian project on the dignity of care for older people, this study is based on ‘clinical caring science’ as a scientific discipline. Clinical caring science examines how ground concepts, axioms and theories are expressed in different clinical contexts. Central notions are caring culture, dignity, at-home-ness, the little extra, non-caring cultures versus caring cultures and ethical context – and climate. Aim and assumptions: This study investigates the individual variations of caring cultures in relation to dignity and how it is expressed in caring acts and ethical contexts. Three assumptions are formulated: (1) the caring culture of nursing homes influences whether dignified care is provided, (2) an ethos that is reflected on and appropriated by the caregiver mirrors itself in ethical caring acts and as artful caring in an ethical context and (3) caring culture is assumed to be a more ontological or universal concept than, for example, an ethical context or ethical person-to-person acts. Research design: The methodological approach is hermeneutic. The data consist of 28 interviews with relatives of older persons from Norway, Denmark and Sweden. Ethical considerations: The principles of voluntariness, confidentiality and anonymity were respected during the whole research process. Findings: Three patterns were revealed: dignity as at-home-ness, dignity as the little extra and non-dignifying ethical context. Discussion: Caring communion, invitation, at-home-ness and ‘the little extra’ are expressions of ethical contexts and caring acts in a caring culture. A non-caring culture may not consider the dignity of its residents and may be represented by routinized care that values organizational efficiency and instrumentalism rather than an individual’s dignity and self-worth. Conclusion: An ethos must be integrated in both the organization and in the individual caregiver in order to be expressed in caring acts and in an ethical context that supports these caring acts.
Skill development in the transition to a ‘green economy’: A ‘varieties of capitalism’ analysis
Authors: Stroud Dean , Fairbrother Peter , Evans Claire , Blake Joanne 
Published: January 2014

AbstractMany traditional regions are being transformed as industries restructure. Paradoxically, the global economic downturn offers opportunities to innovate on policies to regenerate areas experiencing deindustrialisation, with one emerging focus being the development of ‘green skills’ to facilitate the transition of these places to ‘green economies’. In this article, we explore similar policy objectives (i.e. regeneration activity based (in part) on green economy transitions) across three deindustrialising/deindustrialised regions – Appalachia (United States), Ruhr (Germany) and the Valleys (South Wales) – to provide an account of the ways in which different regions with similar industrial pasts diverge in their approach to moving towards greener futures. Our argument is that the emphasis in such transitions should be the creation of ‘decent’ jobs, with new economic activity and employment initiatives embracing a ‘high road’ (i.e. high skill/high pay/high quality) trajectory. Utilising a ‘varieties of capitalism’ analysis, we contend that an effective, socially inclusive and ‘high road’ transition is more likely to emerge within co-ordinated market economy contexts, for example, Germany, than within the liberal market economy contexts of, for example, the United States and United Kingdom. In identifying the critical success factors leading to ‘high road’ green economy, the implications for any such transition within the liberal market economy context of Australia are highlighted.
Human urinary bladder regeneration through tissue engineering – An analysis of 131 clinical cases
Authors: Pokrywczynska Marta , Adamowicz Jan , Sharma Arun K , Drewa Tomasz 
Published: January 2014

Replacement of urinary bladder tissue with functional equivalents remains one of the most challenging problems of reconstructive urology over the last several decades. The gold standard treatment for urinary diversion after radical cystectomy is the ileal conduit or neobladder; however, this technique is associated with numerous complications including electrolyte imbalances, mucus production, and the potential for malignant transformation. Tissue engineering techniques provide the impetus to construct functional bladder substitutes de novo. Within this review, we have thoroughly perused the literature utilizing PubMed in order to identify clinical studies involving bladder reconstruction utilizing tissue engineering methodologies. The idea of urinary bladder regeneration through tissue engineering dates back to the 1950s. Many natural and synthetic biomaterials such as plastic mold, gelatin sponge, Japanese paper, preserved dog bladder, lyophilized human dura, bovine pericardium, small intestinal submucosa, bladder acellular matrix, or composite of collagen and polyglycolic acid were used for urinary bladder regeneration with a wide range of outcomes. Recent progress in the tissue engineering field suggest that in vitro engineered bladder wall substitutes may have expanded clinical applicability in near future but preclinical investigations on large animal models with defective bladders are necessary to optimize the methods of bladder reconstruction by tissue engineering in humans.
The F-BAR protein PSTPIP1 controls extracellular matrix degradation and filopodia formation in macrophages
Authors: Starnes Taylor W. , Bennin David A. , Bing Xinyu , Eickhoff Jens C. , Grahf Daniel C. , Bellak Jason M. , Seroogy Christine M. , Ferguson Polly J. , Huttenlocher Anna 
Published: January 2014

Key PointsPSTPIP1 regulates the transition from podosomes to filopodia in macrophages by modulating WASP activity. The novel PSTPIP1-R405C mutant induces filopodia formation, increases matrix degradation, and is associated with severe pyoderma gangrenosum.
Generalized "Equation missing" -expansive mappings and related fixed-point theorems
Authors: Karapınar Erdal , Shahi Priya , Kaur Jatinderdeep , Bhatia Satvinder Singh 
Published: January 2014

Abstract
In this paper, we introduce a new class of expansive mappings called generalized

(
ξ
,
α
)

-expansive mappings and investigate the existence of a fixed point for the mappings in this class. We conclude that several fixed-point theorems can be considered as a consequence of main results. Moreover, some examples are given to illustrate the usability of the obtained results.

MSC:46T99, 54H25, 47H10, 54E50.
Transcriptome profiling of granulosa cells of bovine ovarian follicles during growth from small to large antral sizes
Authors: Hatzirodos Nicholas , Irving-Rodgers Helen F , Hummitzsch Katja , Harland Margaret L , Morris Stephanie E , Rodgers Raymond J 
Published: January 2014

AbstractBackgroundAt later stages of folliculogenesis, the mammalian ovarian follicle contains layers of epithelial granulosa cells surrounding an antral cavity. During follicle development granulosa cells replicate, secrete hormones and support the growth of the oocyte. In cattle, the follicle needs to grow > 10 mm in diameter to allow an oocyte to ovulate, following which the granulosa cells cease dividing and differentiate into the specialised cells of the corpus luteum. To better understand the molecular basis of follicular growth and granulosa cell maturation, we undertook transcriptome profiling of granulosa cells from small (< 5 mm; n = 10) and large (> 10 mm, n = 4) healthy bovine follicles using Affymetrix microarrays (24,128 probe sets).ResultsPrincipal component analysis for the first two components and hierarchical clustering showed clustering into two groups, small and large, with the former being more heterogeneous. Size-frequency distributions of the coefficient of variation of the signal intensities of each probe set also revealed that small follicles were more heterogeneous than the large. IPA and GO enrichment analyses revealed that processes of axonal guidance, immune signalling and cell rearrangement were most affected in large follicles. The most important networks were associated with: (A) Notch,SLIT/ROBOandPI3Ksignalling, and (B)ITGB5and extracellular matrix signalling through extracellular signal related kinases (ERKs). Upstream regulator genes which were predicted to be active in large follicles includedSTATandXBP1.By comparison, developmental processes such as those stimulated byKIT,IHHandMESTwere most active in small follicles.MGEA5was identified as an upstream regulator in small follicles. It encodes an enzyme that modifies the activity of many target proteins, including those involved in energy sensing, by removal of N-acetylglucosamine from serine and threonine residues.ConclusionsOur data suggest that as follicles enlarge more genes and/or pathways are activated than are inactivated, and gene expression becomes more uniform. These findings could be interpreted that either the cells in large follicles are more uniform in their gene expression, or that follicles are more uniform or a combination of both and that additional factors, such as LH, are additionally controlling the granulosa cells.