bluuebunny/crossref_metadata_2025_split huggingface dataset:
Molecular differences between stromal cell populations from deciduous and permanent human teeth
Authors: Kaukua Nina , Chen Mo , Guarnieri Paolo , Dahl Markus , Lim Mei Ling , Yucel-Lindberg Tülay , Sundström Erik , Adameyko Igor , Mao Jeremy J , Fried Kaj 
Published: April 2015

Abstract
Introduction
Deciduous and permanent human teeth represent an excellent model system to study aging of stromal populations. Aging is tightly connected to self-renewal and proliferation and thus, mapping potential molecular differences in these characteristics between populations constitutes an important task.

Methods
Using specifically designed microarray panels, Real-Time Quantitative Polymerase Chain Reaction (RT q-PCR), Western blot, immunohistochemistry and siRNA-mediated knock down experiments, we have detected a number of molecules that were differentially expressed in dental pulp from deciduous and permanent teeth extracted from young children and adults, respectively.

Results
Among the differentially regulated genes, high-mobility group AT-hook 2 (HMGA2), a stem cell-associated marker, stood out as a remarkable example with a robust expression in deciduous pulp cells. siRNA-mediated knock down of HMGA2 expression in cultured deciduous pulp cells caused a down-regulated expression of the pluripotency marker NANOG. This finding indicates that HMGA2 is a pulpal stem cell regulatory factor. In addition to this, we discovered that several proliferation-related genes, including CDC2A and CDK4, were up-regulated in deciduous pulp cells, while matrix genes COL1A1, fibronectin and several signaling molecules, such as VEGF, FGFr-1 and IGFr-1 were up-regulated in the pulp cells from permanent teeth.

Conclusions
Taken together, our data suggest that deciduous pulp cells are more robust in self- renewal and proliferation, whereas adult dental pulp cells are more capable of signaling and matrix synthesis.
Adipose-derived mesenchymal stromal cells modulate tendon fibroblast responses to macrophage-induced inflammation in vitro
Authors: Manning Cionne N , Martel Catherine , Sakiyama-Elbert Shelly E , Silva Matthew J , Shah Shivam , Gelberman Richard H , Thomopoulos Stavros 
Published: April 2015

Abstract
Introduction
Macrophage-driven inflammation is a key feature of the early period following tendon repair, but excessive inflammation has been associated with poor clinical outcomes. Modulation of the inflammatory environment using molecular or cellular treatments may provide a means to enhance tendon healing.

Methods
To examine the effect of pro-inflammatory cytokines secreted by macrophages on tendon fibroblasts (TF), we established in vitro models of cytokine and macrophage-induced inflammation. Gene expression, protein expression, and cell viability assays were used to examine TF responses. In an effort to reduce the negative effects of inflammatory cytokines on TFs, adipose-derived mesenchymal stromal cells (ASCs) were incorporated into the model and their ability to modulate inflammation was investigated.

Results
The inflammatory cytokine interleukin 1 beta (IL-1β) and macrophages of varying phenotypes induced up-regulation of pro-inflammatory factors and matrix degradation factors and down-regulation of factors related to extracellular matrix formation by TFs in culture. ASCs did not suppress these presumably negative effects induced by IL-1β. However, ASC co-culture with M1 (pro-inflammatory) macrophages successfully suppressed the effects of M1 macrophages on TFs by inducing a phenotypic switch from a pro-inflammatory macrophage phenotype to an anti-inflammatory macrophage phenotype, thus resulting in exposure of TFs to lower levels of pro-inflammatory cytokines (e.g., IL-1β, tumor necrosis factor alpha (TNFα)).

Conclusions
These findings suggest that IL-1β and M1 macrophages are detrimental to tendon healing and that ASC-mediated modulation of the post-operative inflammatory response may be beneficial for tendon healing.
RETRACTED ARTICLE: Activation of Wnt/β-catenin signalling promotes mesenchymal stem cells to repair injured alveolar epithelium induced by lipopolysaccharide in mice
Authors: Cai Shi-xia , Liu Ai-ran , Chen Song , He Hong-li , Chen Qi-hong , Xu Jing-yuan , Pan Chun , Yang Yi , Guo Feng-mei , Huang Ying-zi , Liu Ling , Qiu Hai-bo 
Published: April 2015

Abstract
Introduction
Mesenchymal stem cells (MSCs) have potential for re-epithelization and recovery in acute respiratory distress syndrome (ARDS). In a previous in vitro study, the results showed that the canonical Wnt/β-catenin pathway promoted the differentiation of MSCs into type II alveolar epithelial cells, conferred resistance to oxidative stress, and promoted their migration, suggesting that the Wnt/β-catenin pathway might be one of the key mechanisms underling the therapeutic effect of mouse MSCs in ARDS.

Methods
Mouse MSCs stable transfected with β-catenin or green fluorescent protein control were transplanted intratracheally into the ARDS mice induced by lipopolysaccharide. Lung tissue injury and repair assessment were examined using haematoxylin and eosin staining, lung injury scoring, Masson’s trichrome staining and fibrosis scoring. Homing and differentiation of mouse MSCs were assayed by labelling and tracing MSCs using NIR815 dye, immunofluorescent staining, and Western immunoblot analysis. The inflammation and permeability were evaluated by detecting the cytokine and protein measurements in bronchoalveolar lavage fluid using enzyme-linked immunosorbent assay.

Results
In this study, β-catenin-overexpressing MSC engraftment led to more significant effects than the GFP controls, including the retention of the MSCs in the lung, differentiation into type II alveolar epithelial cells, improvement in alveolar epithelial permeability, and the pathologic impairment of the lung tissue.

Conclusion
These results suggest that the activation of canonical Wnt/β-catenin pathway by mouse MSCs by overexpressing β-catenin could further improve the protection of mouse MSCs against epithelial impair and the therapeutic effects of mouse MSCs in ARDS mice.
Influence of vascular endothelial growth factor stimulation and serum deprivation on gene activation patterns of human adipose tissue-derived stromal cells
Authors: Tratwal Josefine , Mathiasen Anders Bruun , Juhl Morten , Brorsen Sonja Kim , Kastrup Jens , Ekblond Annette 
Published: April 2015

Abstract
Introduction
Stimulation of mesenchymal stromal cells and adipose tissue-derived stromal cells (ASCs) with vascular endothelial growth factor (VEGF) has been used in multiple animal studies and clinical trials for regenerative purposes. VEGF stimulation is believed to promote angiogenesis and VEGF stimulation is usually performed under serum deprivation. Potential regenerative molecular mechanisms are numerous and the role of contributing factors is uncertain. The aim of the current study was to investigate the effect of in vitro serum deprivation and VEGF stimulation on gene expression patterns of ASCs.

Methods
Gene expressions of ASCs cultured in complete medium, ASCs cultured in serum-deprived medium and ASCs stimulated with VEGF in serum-deprived medium were compared. ASC characteristics according to criteria set by the International Society of Cellular Therapy were confirmed by flow cytometry. Microarray gene expressions were obtained using the Affymetrix HT HG-U133+ GeneChip®. Gene set enrichment analysis was performed using the Kyoto Encyclopedia of Genes and Genomes and gene ontology terms. Transcription of selected genes of interest was confirmed by quantitative PCR.

Results
Compared to ASCs in complete medium, 190 and 108 genes were significantly altered by serum deprivation and serum deprivation combined with VEGF, respectively. No significant differences in gene expression patterns between serum-deprived ASCs and serum-deprived ASCs combined with VEGF stimulation were found. Genes most prominently and significantly upregulated by both conditions were growth factors (IGF1, BMP6, PDGFD, FGF9), adhesion molecule CLSTN2, extracellular matrix-related proteins such as matricellular proteins SMOC2, SPON1 and ADAMTS12, and inhibitors of proliferation (JAG1). The most significantly downregulated genes included matrix metalloproteinases (MMP3, MMP1), and proliferation markers (CDKN3) and GREM2 (a BMP6 antagonist).

Conclusion
The decisive factor for the observed change in ASC gene expression proves to be serum starvation rather than VEGF stimulation. Changes in expression of growth factors, matricellular proteins and matrix metalloproteinases in concert, diverge from direct pro-angiogenic paracrine mechanisms as a primary consequence of the used protocol. In vitro serum starvation (with or without VEGF present) appears to favour cardioprotection, extracellular matrix remodelling and blood vessel maturation relevant for the late maturation phase in infarct healing.
Myoblast-conditioned media improve regeneration and revascularization of ischemic muscles in diabetic mice
Authors: Kozakowska Magdalena , Kotlinowski Jerzy , Grochot-Przeczek Anna , Ciesla Maciej , Pilecki Bartosz , Derlacz Rafal , Dulak Jozef , Jozkowicz Alicja 
Published: April 2015

Abstract
Introduction
Diabetes is associated with reduced expression of heme oxygenase-1 (HO-1), a heme-degrading enzyme with cytoprotective and proangiogenic properties. In myoblasts and muscle satellite cells HO-1 improves survival, proliferation and production of proangiogenic growth factors. Induction of HO-1 in injured tissues facilitates neovascularization, the process impaired in diabetes. We aimed to examine whether conditioned media from the HO-1 overexpressing myoblast cell line can improve a blood-flow recovery in ischemic muscles of diabetic mice.

Methods
Analysis of myogenic markers was performed at the mRNA level in primary muscle satellite cells, isolated by a pre-plate technique from diabetic db/db and normoglycemic wild-type mice, and then cultured under growth or differentiation conditions. Hind limb ischemia was performed by femoral artery ligation in db/db mice and blood recovery was monitored by laser Doppler measurements. Mice were treated with a single intramuscular injection of conditioned media harvested from wild-type C2C12 myoblast cell line, C2C12 cells stably transduced with HO-1 cDNA, or with unconditioned media.

Results
Expression of HO-1 was lower in muscle satellite cells isolated from muscles of diabetic db/db mice when compared to their wild-type counterparts, what was accompanied by increased levels of Myf5 or CXCR4, and decreased Mef2 or Pax7. Such cells also displayed diminished differentiation potential when cultured in vitro, as shown by less effective formation of myotubes and reduced expression of myogenic markers (myogenic differentiation antigen - myoD, myogenin and myosin). Blood flow recovery after induction of severe hind limb ischemia was delayed in db/db mice compared to that in normoglycemic individuals. To improve muscle regeneration after ischemia, conditioned media collected from differentiating C2C12 cells (control and HO-1 overexpressing) were injected into hind limbs of diabetic mice. Analysis of blood flow revealed that media from HO-1 overexpressing cells accelerated blood-flow recovery, while immunohistochemical staining assessment of vessel density in injected muscle confirmed increased angiogenesis. The effect might be mediated by stromal-cell derived factor-1α proangiogenic factor, as its secretion is elevated in HO-1 overexpressing cells.

Conclusions
In conclusion, paracrine stimulation of angiogenesis in ischemic skeletal muscle using conditioned media may be a safe approach exploiting protective and proangiogenic properties of HO-1 in diabetes.
Mouse aorta-derived mesenchymal progenitor cells contribute to and enhance the immune response of macrophage cells under inflammatory conditions
Authors: Evans Jodi F , Salvador Veronica , George Sheela , Trevino-Gutierrez Cristina , Nunez Catherine 
Published: April 2015

Abstract
Introduction
Mesenchymal progenitor cells interact with immune cells and modulate inflammatory responses. The cellular characteristics required for this modulation are under fervent investigation. Upon interaction with macrophage cells, they can contribute to or suppress an inflammatory response. Current studies have focused on mesenchymal progenitors derived from bone marrow, adipose, and placenta. However, the arterial wall contains many mesenchymal progenitor cells, which during vascular disease progression have the potential to interact with macrophage cells. To examine the consequence of vascular-tissue progenitor cell-macrophage cell interactions in an inflammatory environment, we used a recently established mesenchymal progenitor cell line derived from the mouse aorta.

Methods
Mouse bone marrow-derived macrophage (MΦ) cells and mouse aorta-derived mesenchymal progenitor (mAo) cells were cultured alone or co-cultured directly and indirectly. Cells were treated with oxidized low-density lipoprotein (ox-LDL) or exposed to the inflammatory mediators lipopolysaccharide (LPS) and interferon-gamma (IFNγ) or both. A Toll-like receptor-4 (TLR4)-deficient macrophage cell line was used to determine the role of the mAo cells. To monitor inflammation, nitric oxide (NO), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNFα) secretions were measured.

Results
Mesenchymal progenitor cells isolated from aorta and cloned by high proliferative capacity (mAo) can differentiate into multiple mesenchymal lineages and are positive for several commonly used mouse mesenchymal stem cell markers (that is, CD29, CD44, CD105, CD106, and Sca-1) but are negative for CD73 and ecto-5′-nucleotidase. In co-culture with MΦ cells, they increase MΦ oxidized-LDL uptake by 52.2%. In an inflammatory environment, they synergistically and additively contribute to local production of both NO and IL-6. After exposure to ox-LDL, the inflammatory response of MΦ cells to LPS and LPS/IFNγ is muted. However, when lipid-laden MΦ cells are co-cultured with mAo cell progenitors, the muted response is recovered and the contribution by the mAo cell progenitor is dependent upon cell contact.

Conclusions
The resident mesenchymal progenitor cell is a potential contributor to vascular inflammation when in contact with inflamed and lipid-laden MΦ cells. This interaction represents an additional target in vascular disease treatment. The potential for resident cells to contribute to the local immune response should be considered when designing therapeutics targeting inflammatory vascular disease.
A survey on security attacks and countermeasures with primary user detection in cognitive radio networks
Authors: Marinho José , Granjal Jorge , Monteiro Edmundo 
Published: April 2015

AbstractCurrently, there are several ongoing efforts for the definition of new regulation policies, paradigms, and technologies aiming a more efficient usage of the radio spectrum. In this context, cognitive radio (CR) emerges as one of the most promising players by enabling the dynamic access to vacant frequency bands on a non-interference basis. However, the intrinsic characteristic of CR opens new ways for attackers, namely in the context of the effective detection of incumbent or primary users (PUs), the most fundamental and challenging requirement for the successful operation of CR networks. In this article, we provide a global and integrated vision of the main threats affecting CR environments in the context of the detection of primary users, with a particular focus on spectrum sensing data falsification and primary user emulation attacks. We also address solutions and research challenges still required to address such threats. Our discussion aims at being complete and self-contained, while also targeting readers with no specific background on this important topic of CR environments. It is, as far as our knowledge goes, the first work providing a global and clear vision of security threats and countermeasures in the context of primary user detection in CR.
Gene expression in the liver of female, but not male mice treated with rapamycin resembles changes observed under dietary restriction
Authors: Yu Zhen , Sunchu Bharath , Fok Wilson C , Alshaikh Nahla , Pérez Viviana I 
Published: April 2015

Abstract
It is well known that in mice the extension in lifespan by rapamycin is sexually dimorphic, in that it has a larger effect in females than males. In a previous study we showed that in male C57BL6 mice, rapamycin had less profound effects in both gene expression and liver metabolites when compared to dietary restriction (DR), but no data was available in females. Because recent studies showed that rapamycin increases longevity in a dose dependent manner and at every dose tested the effect remains larger in females than in males, we hypothesized that rapamycin should have a stronger effect on gene expression in females, and this effect could be dose dependent. To test this hypothesis, we measured the changes in liver gene expression induced by rapamycin (14 ppm) with a focus on several genes involved in pathways known to play a role in aging and that are altered by DR. To investigate whether any effects are dose dependent, we also analyzed females treated with two additional doses of rapamycin (22 and 42 ppm). We observed striking differences between male and female in gene expression at 14 ppm, where females have a larger response to rapamycin than males, and the effects of rapamycin in females resemble what we observed under DR. However, these effects were generally not dose dependent. These data support the notion that female mice respond better to rapamycin, and at least with the set of genes studied here, the effect of rapamycin in females resemble the effect of DR.
Depression and anxiety in expectant and new fathers: longitudinal findings in Australian men
Authors: Leach Liana S. , Mackinnon Andrew , Poyser Carmel , Fairweather-Schmidt A. Kate 
Published: April 2015

BackgroundDespite growing interest in men's perinatal mental health, we still know little about whether becoming a new father is associated with increases in psychological distress.AimsTo use prospective longitudinal data to investigate whether becoming a first-time expectant (partner pregnant) and/or new father (child <1 year) is associated with increases in depression and anxiety.MethodMen were aged 20–24 years at baseline (n= 1162). Levels of depression and anxiety were measured at four time points over 12 years. Over this time, 88 men were expectant fathers, 108 men were new fathers and 626 men remained non-fathers.ResultsLongitudinal mixed models showed no significant increase in depression or anxiety as a function of expectant or new fatherhood, as compared with pre-fatherhood levels.ConclusionsOur findings suggest that, generally, expectant and new fathers are not at greater risk of depression or anxiety. Future epidemiological research should continue to identify men who are most (and least) at risk to focus resources and assistance most effectively.
Case Report: A case of neurogenic bladder in the setting of Behçet's disease after an initial diagnosis of multiple sclerosis
Authors: Pastuszak Alexander W , Boone Timothy B. 
Published: April 2015

Behçet’s disease (BD) is an autoimmune vasculitis with an unclear etiology presenting with a classic triad of symptoms including oral and genital ulcers as well as iridocyclitis. A subset of BD patients exhibit neurological symptoms including psychiatric disturbances, balance problems, and voiding dysfunction, and the symptoms of BD can mimic other neurological diseases, including multiple sclerosis (MS). Differentiating between potential diagnoses is challenging due to the lack of specific tests for these disorders and the overlap between clinical symptoms and radiological findings. We describe the case of a 52 year old woman initially diagnosed with and treated for MS. From the urologic standpoint, she was treated for neurogenic detrusor overactivity with detrusor-sphincter-dyssynergia utilizing ileocecal augmentation cystoplasty with a continent stoma for intermittent catheterization. The patient was later diagnosed with BD in light of additional clinical findings.
The Impact of Budget Constraints on Flexible vs. Dedicated Technology Choice
Authors: Boyabatlı Onur , Leng Tiecheng , Toktay L. Beril 
Published: April 2015

This paper studies the flexible versus dedicated technology choice and capacity investment decisions of a multiproduct firm under demand uncertainty in the presence of budget constraints. The firm operates under a capital budget for financing the capacity investment, and an operating budget, which is uncertain in the capacity investment stage, for financing the production. We investigate how the tightening of the capital budget and a lower financial flexibility in the production stage (the likelihood of having a sufficient operating budget) shape the optimal technology choice. We find that the dominant regime is one where dedicated technology should be adopted for a larger investment cost range, and thus, is the best response to the tighter capital budget, whereas flexible technology is the best response to lower financial flexibility. We identify the key roles that the capacity intensity (the ratio of unit capacity cost to total unit capacity and production cost) of each technology and the pooling value of operating budget with dedicated technology, which brings this technology closer to flexible technology in terms of the resource network’s flexibility, play in a budget-constrained environment. Managerially, our results underline that in the presence of financial constraints, firms should manage technology adoption together with plant location, which shapes capacity intensity, or product portfolio, which shapes financial flexibility. This paper was accepted by Serguei Netessine, operations management.
Contemporary meanings and experiences of television in the digital age
Authors: Urresti Xabier Landabidea , Loos Eugène 
Published: April 2015

Abstract
Television was an everyday reality for millions of people at the beginning of the twenty-first century, and arguably remains one of the most important features of media-related leisure. It provides a fertile conceptual and empirical starting point for the exploration of the everyday leisure experiences of media audiences. In this article, contemporary meanings and experiences of television are examined on three dimensions, namely the practices of (watching) television, television and the understanding of everydayness, and the experience of television itself. The emerging meanings and experiences of TV in the digital age are contrasted with the continuities and momentum of more traditional forms of watching and understanding television. Differences were found among the four different age groups (younger adults, middle-aged adults, older adults and elderly) studied, as were important similarities among people belonging to the same age group. The notion and experience of television are being transformed in the digital age, and televisual leisure opportunities appear inserted both in a transforming media ecosystem and in the everyday life of people. The article argues that it is in the contested, negotiated and complex domains of leisure experience and generational belonging that we should continue to explore the notion(s) of television by using new epistemological approaches. This will help us to understand not only its contemporary but also its future status.