bluuebunny/crossref_metadata_2025_split huggingface dataset:
The use of small instant loans among young adults – a gateway to a consumer insolvency?
Authors: Autio Minna , Wilska Terhi‐Anna , Kaartinen Risto , Lähteenmaa Jaana 
Published: June 2009

AbstractThe aim of this paper is to study 18‐ to 29‐year‐old Finnish consumers' use of instant small loans (i.e. SMS loan) and other consumer credit services that have increased notably in the past few years. We examine what kind of expenditures instant credit is used for and focus also on young consumers' financial situation and their perceptions of themselves as money handlers. The research method is quantitative, and data are derived from an open online survey (n = 1610). Our results reveal that consumer credit is used by young people in all income brackets and employment positions. However, there is a clear connection between certain life‐course stages (young, single parent), financial positions (low income), employment situations (marginal) and the propensity to take instant loans and consumer credit. The young people who take an instant loan once are likely to do it again. Typical purposes of use included buying alcohol, cigarettes and partying. For some consumers, the use of small loans is part of controlled and economical use of money. However, particularly in the low‐income brackets, it is also common to buy food and to repay credit or interest. Young people, who use instant loans recognize flaws in their money management and see themselves as ‘wasteful’ consumers more often than those who do not use instant loans. On the basis of this empirical study, it is unquestioned that young people's consumer education needs to be strengthened. In Finland, this need has already been recognized in both consumer policy and teacher education.
Focal liver necrosis appears early after partial hepatectomy and is dependent on T cells and antigen delivery from the gut
Authors: Rudich Noam , Zamir Gideon , Pappo Orit , Shlomai Zipora , Faroja Muhamad , Weiss Ido D. , Wald Hanna , Galun Eithan , Peled Amnon , Wald Ori 
Published: June 2009

AbstractIntroduction: Progressive liver failure may develop following removal of a large part of the liver or transplantation of a small for size liver graft. The pathophysiology of this clinical syndrome is only partially understood.Methods: We assessed liver damage and hepatocyte 5‐bromo‐2′‐deoxyuridine (BrdU) incorporation following partial hepatectomy (PH) in C57BL/6, BALB/C and immune‐deficient mice. Hepatic lymphocyte subpopulations were characterized. Lipopolysaccharide (LPS) treatment and bowel decontamination determined the role of gut antigens.Results: Discrete, round necrotic lesions were observed as early as 2 h following 70%, but not 30% PH. In immune competent mice the extent of hepatocyte necrosis inversely correlated with BrdU incorporation. T, natural killer and natural killer T cells were recruited to the liver early after PH; however, only T‐cell depletion abrogated hepatic necrosis. Hepatic injury was significantly reduced in non‐obese diabetic/severe combined immunodeficient mice undergoing PH, while BrdU incorporation was not affected. Liver injury was augmented by LPS injection and reduced by gut decontamination.Conclusions: A distinct pattern of early focal hepatic necrosis is observed following extensive PH in mice. T cells infiltrating the liver immediately after PH and gut‐derived antigens are indispensable for the observed liver necrosis and may thus provide therapeutic targets to ameliorate liver damage following PH.
Langerhans cells are critical in the development of atopic dermatitis‐like inflammation and symptoms in mice
Authors: Elentner Andreas , Finke Daniela , Schmuth Matthias , Chappaz Stéphane , Ebner Susanne , Malissen Bernard , Kissenpfennig Adrien , Romani Nikolaus , Dubrac Sandrine 
Published: June 2009

AbstractGenetic or vitamin D3‐induced overexpression of thymic stromal lymphopoietin (TSLP) by keratinocytes results in an atopic dermatitis (AD)‐like inflammatory phenotype in mice echoing the discovery of high TSLP expression in epidermis from AD patients. Although skin dendritic cells (DC) are suspected to be involved in AD, direct evidence of a pathogenetic role for skin DC in TSLP‐induced skin inflammation has not yet been demonstrated. In a mouse model of AD, i.e. mice treated with the low‐calcemic vitamin D3 analogue, MC903, we show that epidermal Langerhans cells (LC)‐depleted mice treated with MC903 do neither develop AD‐like inflammation nor increased serum IgE as compared to vitamin D3 analogue‐treated control mice. Accordingly, we show that, in mice treated with MC903 or in K14‐TSLP transgenic mice, expression of maturation markers by LC is increased whereas maturation of dermal DC is not altered. Moreover, only LC are responsible for the polarization of naïve CD4+ T cells to a Th2 phenotype, i.e. decrease in interferon‐γ and increase in interleukin (IL)‐13 production by CD4+ T cells. This effect of LC on T‐lymphocytes does not require OX40‐L/CD134 and is mediated by a concomitant down‐regulation of IL‐12 and CD70. Although it was previously stated that TSLP up‐regulates the production of thymus and activation‐regulated chemokine (TARC)/chemokine (C‐C motif) ligand 17 (CCL17) and macrophage‐derived chemokine (MDC)/CCL22 by human LC in vitro, our work shows that production of these Th2‐ cell attracting chemokines is increased only in keratinocytes in response to TSLP overexpression. These results demonstrate that LC are required for the development of AD in mouse models of AD involving epidermal TSLP overexpression.
Methylglyoxal modulates immune responses: relevance to diabetes
Authors: Price Claire L. , Hassi Hafid O. S. Al , English Nicholas R. , Blakemore Alexandra I. F. , Stagg Andrew J. , Knight Stella C. 
Published: June 2009

AbstractIncreased methylglyoxal (MG) concentrations and formation of advanced glycation end‐products (AGEs) are major pathways of glycaemic damage in diabetes, leading to vascular and neuronal complications. Diabetes patients also suffer increased susceptibility to many common infections, the underlying causes of which remain elusive. We hypothesized that immune glycation damage may account for this increased susceptibility. We previously showed that the reaction mixture (RM) for MG glycation of peptide blocks up regulation of CD83 in myeloid cells and inhibits primary stimulation of T cells. Here, we continue to investigate immune glycation damage, assessing surface and intracellular cytokine protein expression by flow cytometry, T‐cell proliferation using a carboxyfluorescein succinimidyl ester assay, and mRNA levels by RT‐PCR. We show that the immunomodulatory component of this RM was MG itself, with MG alone causing equivalent block of CD83 and loss of primary stimulation. Block of CD83 expression could be reversed by MG scavenger N‐acetyl cysteine. Further, MG within RM inhibited stimulated production of interleukin (IL)‐10 protein from myeloid cells plus interferon (IFN)‐γ and tumour necrosis factor (TNF)‐α from T cells. Loss of IL‐10 and IFN‐γ was confirmed by RT‐PCR analysis of mRNA, while TNF‐α message was raised. Loss of TNF‐α protein was also shown by ELISA of culture supernatants. In addition, MG reduced major histocompatibility complex (MHC) class I expression on the surface of myeloid cells and increased their propensity to apoptose. We conclude that MG is a potent suppressor of myeloid and T‐cell immune function and may be a major player in diabetes‐associated susceptibility to infection.
A clinically relevant model of osteoinduction: a process requiring calcium phosphate and BMP/Wnt signalling
Authors: Eyckmans J. , Roberts S. J. , Schrooten J. , Luyten F. P. 
Published: June 2009

AbstractIn this study, we investigated a clinically relevant model of in vivo ectopic bone formation utilizing human periosteum derived cells (HPDCs) seeded in a Collagraft™ carrier and explored the mechanisms by which this process is driven. Bone formation occurred after eight weeks when a minimum of one million HPDCs was loaded on Collagraft™ carriers and implanted subcutaneously in NMRI nu/nu mice. De novo bone matrix, mainly secreted by the HPDCs, was found juxta‐proximal of the calcium phosphate (CaP) granules suggesting that CaP may have triggered the ‘osteoinductive program’. Indeed, removal of the CaP granules by ethylenediaminetetraacetic acid decalcification prior to cell seeding and implantation resulted in loss of bone formation. In addition, inhibition of endogenous bone morphogenetic protein and Wnt signalling by overexpression of the secreted antagonists Noggin and Frzb, respectively, also abrogated osteoinduction. Proliferation of the engrafted HPDCs was strongly reduced in the decalcified scaffolds or when seeded with adenovirus‐Noggin/Frzb transduced HPDCs indicating that cell division of the engrafted HPDCs is required for the direct bone formation cascade. These data suggest that this model of bone formation is similar to that observed during physiological intramembranous bone development and may be of importance when investigating tissue engineering strategies.
Spermidine is indispensable in differentiation of 3T3‐L1 fibroblasts to adipocytes
Authors: Vuohelainen Susanna , Pirinen Eija , Cerrada‐Gimenez Marc , Keinänen Tuomo A. , Uimari Anne , Pietilä Marko , Khomutov Alex R. , Jänne Juhani , Alhonen Leena 
Published: June 2009

AbstractImpaired adipogenesis has been shown to predispose to disturbed adipocyte function and development of metabolic abnormalities. Previous studies indicate that polyamines are essential in the adipogenesis in 3T3‐L1 fibroblasts. However, the specific roles of individual polyamines during adipogenesis have remained ambiguous as the natural polyamines are readily interconvertible inside the cells. Here, we have defined the roles of spermidine and spermine in adipogenesis of 3T3‐L1 cells by using (S’)‐ and (R’)‐ isomers of α‐methylspermidine and (S,S’)‐, (R,S)‐ and (R,R’)‐diastereomers of α,ω‐bismethylspermine. Polyamine depletion caused by α‐difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase, prevented adipocyte differentiation by suppressing the expression of its key regulators, peroxisome proliferator‐activated receptor γ and CCAAT/enhancer binding protein α. Adipogenesis was restored by supplementation of methylspermidine isomers but not of bismethylspermine diastereomers. Although both spermidine analogues supported adipocyte differentiation only (S)‐methylspermidine was able to fully support cell growth after extended treatment with α‐DFMO. The distinction between the spermidine analogues in maintaining growth was found to be in their different capability to maintain functional hypusine synthesis. However, the differential ability of spermidine analogues to support hypusine synthesis did not correlate with their ability to support differentiation. Our results show that spermidine, but not spermine, is essential for adipogenesis and that the requirement of spermidine for adipogenesis is not strictly associated with hypusine modification. The involvement of polyamines in the regulation of adipogenesis may offer a potential application for the treatment of dysfunctional adipocytes in patients with obesity and metabolic syndrome.
Cognitive impairment in the Tg6590 transgenic rat model of Alzheimer’s disease
Authors: Kloskowska Ewa , Pham Therese M. , Nilsson Tatjana , Zhu Shunwei , Öberg Johanna , Codita Alina , Pedersen Lars Ø. , Pedersen Jan T. , Malkiewicz Katarzyna , Winblad Bengt , Folkesson Ronnie , Benedikz Eirikur 
Published: June 2009

AbstractRecently, interest in the rat as an animal model of Alzheimer’s disease (AD) has been growing. We have previously described the Tg6590 transgenic rat line expressing the amyloid precursor protein containing the Swedish AD mutation (K670M/N671L) that shows early stages of Aβ deposition, predominantly in cerebrovascular blood vessels, after 15 months of age. Here we show that by the age of 9 months, that is long before the appearance of Aβ deposits, the Tg6590 rats exhibit deficits in the Morris water maze spatial navigation task and altered spontaneous behaviour in the open‐field test. The levels of soluble Aβ were elevated both in the hippocampus and cortex of transgenic animals. Magnetic resonance imaging showed no major changes in the brains of transgenic animals, although they tended to have enlarged lateral ventricles when compared to control animals. The Tg6590 transgenic rat line should prove a suitable model of early AD for advanced studies including serial cerebrospinal fluid sampling, electrophysiology, neuroimaging or complex behavioural testing.
Leukocyte – endothelial interactions in inflammation
Authors: Langer Harald F. , Chavakis Triantafyllos 
Published: June 2009

Abstract

Introduction
Adhesion molecules
Leukocyte margination, capture and cell rolling
Activation and adhesion of leukocytes
Transmigration
Endogenous inhibitors of leukocyte adhesion
Platelet–leukocyte crosstalk
Conclusions

At sites of inflammation, infection or vascular injury local proinflammatory or pathogen‐derived stimuli render the luminal vascular endothelial surface attractive for leukocytes. This innate immunity response consists of a well‐defined and regulated multi‐step cascade involving consecutive steps of adhesive interactions between the leukocytes and the endothelium. During the initial contact with the activated endothelium leukocytes roll along the endothelium via a loose bond which is mediated by selectins. Subsequently, leukocytes are activated by chemokines presented on the luminal endothelial surface, which results in the activation of leukocyte integrins and the firm leukocyte arrest on the endothelium. After their firm adhesion, leukocytes make use of two transmigration processes to pass the endothelial barrier, the transcellular route through the endothelial cell body or the paracellular route through the endothelial junctions. In addition, further circulating cells, such as platelets arrive early at sites of inflammation contributing to both coagulation and to the immune response in parts by facilitating leukocyte–endothelial interactions. Platelets have thereby been implicated in several inflammatory pathologies. This review summarizes the major mechanisms and molecules involved in leukocyte–endothelial and leukocyte‐platelet interactions in inflammation.
Reciprocal regulation of transcription factors and PLC isozyme gene expression in adult cardiomyocytes
Authors: Singal Tushi , Dhalla Naranjan S. , Tappia Paramjit S. 
Published: June 2009

AbstractBy employing a pharmacological approach, we have shown that phospholipase C (PLC) activity is involved in the regulation of gene expression of transcription factors such as c‐Fos and c‐Jun in cardiomyocytes in response to norepinephrine (NE). However, there is no information available regarding the identity of specific PLC isozymes involved in the regulation of c‐Fos and c‐Jun or on the involvement of these transcription factors in PLC isozyme gene expression in adult cardiomyocytes. In this study, transfection of cardiomyocytes with PLC isozyme specific siRNA was found to prevent the NE‐mediated increases in the corresponding PLC isozyme gene expression, protein content and activity. Unlike PLC γ1gene, silencing of PLC β1, β3and δ1genes with si RNA prevented the increases in c‐Fos and c‐Jun gene expression in response to NE. On the other hand, transfection with c‐Jun si RNA suppressed the NE‐induced increase in c‐Jun as well as PLC β1, β3and δ1gene expression, but had no effect on PLC γ1gene expression. Although transfection of cardiomyocytes with c‐Fos si RNA prevented NE‐induced expression of c‐Fos, PLC β1and PLC β3genes, it did not affect the increases in PLC δ1and PLC γ1gene expression. Silencing of either c‐Fos or c‐Jun also depressed the NE‐mediated increases in PLC β1, β3and γ1protein content and activity in an isozyme specific manner. Furthermore, silencing of all PLC isozymes as well as of c‐Fos and c‐Jun resulted in prevention of the NE‐mediated increase in atrial natriuretic factor gene expression. These findings, by employing gene silencing techniques, demonstrate that there occurs a reciprocal regulation of transcription factors and specific PLC isozyme gene expression in cardiomyocytes.
Development of enteric neuron diversity
Authors: Hao Marlene M. , Young Heather M. 
Published: June 2009

Abstract

Neuronal diversity in the adult enteric nervous system (ENS)
Developmental appearance and birthdating of enteric neuron subtypes and glial cells
Morphological development of enteric neurons
Axon guidance in the developing ENS
Development of connectivity
Mechanisms controlling enteric neuronal differentiation and the generation of neuron diversity
Development of enteric glia
Development of neurons and neuronal subtypes in the human ENS and clinical relevance
Conclusions

The mature enteric nervous system (ENS) is composed of many different neuron subtypes and enteric glia, which all arise from the neural crest. How this diversity is generated from neural crest‐derived cells is a central question in neurogastroenterology, as defects in these processes are likely to underlie some paediatric motility disorders. Here we review the developmental appearance (the earliest age at which expression of specific markers can be localized) and birthdates (the age at which precursors exit the cell cycle) of different enteric neuron subtypes, and their projections to some targets. We then focus on what is known about the mechanisms underlying the generation of enteric neuron diversity and axon pathfinding. Finally, we review the development of the ENS in humans and the etiologies of a number of paediatric motility disorders.
Anti‐proliferative effect of rhein, an anthraquinone isolated from Cassia species, on Caco‐2 human adenocarcinoma cells
Authors: Aviello Gabriella , Rowland Ian , Gill Christopher I. , Acquaviva Angela Maria , Capasso Francesco , McCann Mark , Capasso Raffaele , Izzo Angelo A. , Borrelli Francesca 
Published: June 2009

AbstractIn recent years, the use of anthraquinone laxatives, in particular senna, has been associated with damage to the intestinal epithelial layer and an increased risk of developing colorectal cancer. In this study, we evaluated the cytotoxicity of rhein, the active metabolite of senna, on human colon adenocarcinoma cells (Caco‐2) and its effect on cell proliferation. Cytotoxicity studies were performed using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT), neutral red (NR) and trans‐epithelial electrical resistance (TEER) assays whereas 3H‐thymidine incorporation and Western blot analysis were used to evaluate the effect of rhein on cell proliferation. Moreover, for genoprotection studies Comet assay and oxidative biomarkers measurement (malondialdehyde and reactive oxygen species) were used. Rhein (0.1–10 μg/ml) had no significant cytotoxic effect on proliferating and differentiated Caco‐2 cells. Rhein (0.1 and 1 μg/ml) significantly reduced cell proliferation as well as mitogen‐activated protein (MAP) kinase activation; by contrast, at high concentration (10 μg/ml) rhein significantly increased cell proliferation and extracellular‐signal‐related kinase (ERK) phosphorylation. Moreover, rhein (0.1–10 μg/ml): (i) did not adversely affect the integrity of tight junctions and hence epithelial barrier function; (ii) did not induce DNA damage, rather it was able to reduce H2O2‐induced DNA damage and (iii) significantly inhibited the increase in malondialdehyde and reactive oxygen species (ROS) levels induced by H2O2/Fe2+. Rhein was devoid of cytotoxic and genotoxic effects in colon adenocarcinoma cells. Moreover, at concentrations present in the colon after a human therapeutic dosage of senna, rhein inhibited cell proliferation via a mechanism that seems to involve directly the MAP kinase pathway. Finally, rhein prevents the DNA damage probably via an anti‐oxidant mechanism.
Spheroid‐forming subpopulation of breast cancer cells demonstrates vasculogenic mimicry via hsa‐miR‐299–5p regulated de novo expression of osteopontin
Authors: Shevde Lalita A. , Metge Brandon J. , Mitra Aparna , Xi Yaguang , Ju Jingfang , King Judy A. , Samant Rajeev S. 
Published: June 2009

AbstractThe growth of cancer cells as multicellular spheroids has frequently been reported to mimic the in vivo tumour architecture and physiology and has been utilized to study antitumour drugs. In order to determine the distinctive characteristics of the spheroid‐derived cells compared to the corresponding monolayer‐derived cells, we enriched multicellular spheroid‐forming subpopulations of cells from three human breast cancer cell lines (MCF7, MCF10AT and MCF10DCIS.com). These spheroid‐derived cells were injected into female athymic nude mice to assess their tumorigenic potential and were profiled for their characteristic miRNA signature. We discovered that the spheroid‐derived cells expressed increased levels of osteopontin (OPN), an oncogenic protein that has been clinically correlated with increased tumour burden and adverse prognosis in patients with breast cancer metastasis. Our studies further show that increased OPN levels are brought about in part, by decreased levels of hsa‐mir‐299–5p in the spheroid‐forming population from all three cell lines. Moreover, the spheroid‐forming cells can organize into vascular structures in response to nutritional limitation; these structures recapitulate a vascular phenotype by the expression of endothelial markers CD31, Angiopoeitin‐1 and Endoglin. In this study, we have validated that hsa‐mir‐299–5p targets OPN; de novo expression of OPN in turn plays a critical role in enhancing proliferation, tumorigenicity and the ability to display vasculogenic mimicry of the spheroid‐forming cells.
Multiple clustered dermatofibroma with overlying sebaceous hyperplasia
Authors: Rognstad Øyvind Bakken , Haas Norbert , Sterry Wolfram , Astner Susanne 
Published: June 2009

SummaryMultiple clustered dermatofibroma is a very rare clinical variant of the dermatofibroma, and sebaceous differentiation overlying dermatofibromas is also unusual. We report the first case of a multiple clustered dermatofibroma with overlying sebaceous hyperplasia.
Modulation of wound contracture α‐smooth muscle actin and multispecific vitronectin receptor integrin αvβ3 in the rabbit's experimental model
Authors: El Kahi Cynthia G , Atiyeh Bishara S , Abdallah Hajj Hussein Inaya , Jurjus Rosalyne , Dibo Saad A , Jurjus Alice , Jurjus Abdo 
Published: June 2009

ABSTRACTThe myofibroblast, a major component of granulation tissue, is a key cell during wound healing, tissue repair and connective tissue remodelling. Persistence of myofibroblasts within a fibrotic lesion leads to excessive scarring impairing function and aesthetics. Various wound‐healing cytokines can be modulated by topical application of active agents to promote optimal wound healing and improve scar quality. Thus, the myofibroblast may represent an important target for wound‐healing modulation to improve the evolution of conditions such as hypertrophic scars. The purpose of this work is to study the modulation of myofibroblasts and integrin αvβ3 in a full thickness wound performed on rabbits treated with different topical agents using: (1) saline, (2) Tegaderm occlusive dressing (3) silver sulfadiazine and (4) moist exposed burn ointment (MEBO). The reepithelialisation was 4 days faster in the MEBO group compared with the other therapies with less oedema formation, delayed contraction, less inflammatory cells and the lowest transepidermal water loss (TEWL) resulting in a soft scar. Although α‐smooth muscle actin (α‐SMA) was the highest around day 12 in the MEBO group, wound contraction and myofibroblast's activity were the least for the same period probably because of a downregulation of the integrin αvβ3. It seems that the effect of MEBO could be more pronounced on force transmission rather then on force generation. Greater insight into the pathology of scars may translate into non surgical treatments in the future and further work in myofibroblast biology will eventually result in efficient pharmacological tools, improving the evolution of healing and scar formation.