bluuebunny/crossref_metadata_2025_split huggingface dataset:
Translating Key Competences into the School Curriculum: lessons from the Polish experience
Authors: Dąbrowski Mirosław , Wiśniewski Jerzy 
Published: August 2011

Over the last 20 years, Poland has gone through a major transition process in which the challenges for education in terms of new approaches to learning and teaching have been compounded by broader changes such as the democratisation of structures and processes and the major economic and social changes. This article is a case study that examines the early stages of significant shifts in the learning and teaching process, the stepped approach that was taken and the different international influences. It was decided to focus on the top‐down, policy level actions in order to trace how influences have shaped current policy on outcomes‐based approaches and key competences, which are increasingly implemented in schools today.The Polish education and training system has been through a complex series of reforms, many simultaneously. The introduction of outcome‐based approaches and key competences is part of much broader reforms that have affected mindsets and attitudes by having addressed the structure of the system (e.g. the length of compulsory education), school governance, the roles of principals and teachers, teacher training, etc. Parents' expectations have evolved and students are growing up in a much more connected environment with Internet and social networks and an exponential development of access to ICT and the need for digital competences and a range of key competences for lifelong learning and work (Gordon et al., 2009). Although change has taken place at all levels and in all sub‐sectors of the system, this article focuses on general education in primary and secondary schools.
Self‐assessed consequences of unemployment on individual wellbeing and family relationships: A study of unemployed women and men in Finland
Authors: Weckström Sirpa 
Published: August 2011

Weckström S. Self‐assessed consequences of unemployment on individual wellbeing and family relationships: a study of unemployed women and men in FinlandThe present study investigated how family situation and gender affect the experience of unemployment. The sample consisted of 494 Finnish women and 387 Finnish men who had been registered as unemployed for at least 3 months. The main method used in the study was analysis of covariance. Women assessed the consequences of unemployment on their individual wellbeing and on the parent–child relationship less negatively than men, but there was no corresponding gender difference concerning spousal relationship. Lone mothers experienced the change in individual wellbeing slightly more negatively than women in other family situations; this difference was in part related to financial strain. Financial strain and non‐financial work motivation predicted negative changes in individual wellbeing and in spousal relationship for both genders. Parent–child relationships were, however, independent from these variables. The way family relationships were affected was connected to changes in individual wellbeing.
Securing the Majority: Living through Uncertainty in Jakarta
Authors: SIMONE ABDOUMALIQ , RAO VYJAYANTHI 
Published: August 2011

AbstractDrawing on research in Jakarta, this article reconsiders the importance of heterogeneous economic practices in the remaking of central‐city districts in ways that provide ongoing platforms of residence and operation for residents from wide‐ranging walks of life. The emphasis on good governance and rights‐based discourses have sometimes occluded the operations of urban real economies that, even if waning in the face of the proliferation of mega‐developments, constitute the critical capacity of the majority of urban residents' efforts to secure a viable place in the city.RésuméÀ partir de recherches menées à Jakarta, cet article réexamine l'importance des pratiques économiques hétérogènes en matière de remaniement des quartiers centraux selon des modalités qui offrent des bases de résidence et d'activité permanentes à des résidents venus d'horizons très divers. L'accent mis sur les discours prônant une gouvernance efficiente et le respect des droits a parfois bloqué les opérations des économies réelles urbaines qui, bien qu'en déclin face à la prolifération des méga‐aménagements, constituent la capacité cruciale dans le cadre des efforts de la majorité des résidents urbains pour se procurer un lieu viable dans la ville.
Extracellular matrix molecules implicated in hypertrophic and keloid scarring
Authors: Sidgwick G.P. , Bayat A. 
Published: August 2011

AbstractTissue regeneration repairs the fabric of the skin to maintain homeostasis after injury. The expression and proliferation of extracellular matrix (ECM) molecules in the dermis, mediated by a range of growth factors and cytokines, is a fundamental element of wound repair. Previous work focused on how these complex molecular mechanisms relate to the formation of raised dermal scars, including keloid and hypertrophic scars, characterized by excessive deposition of ECM molecules. However, the mechanisms in the wound repair pathway which lead to the differential expression and organization of ECM molecules observed in different types of scar tissue are not fully understood. To summarize what is known about the expression and composition of ECM molecules in abnormal scarring, an extensive search of the literature was conducted, focusing on keywords connected to skin scarring, hypertrophic scars and keloid disease. The transcription and translation of collagen I and III, fibronectin, laminin, periostin and tenascin are all increased in raised dermal scar tissue. However, hyaluronic acid, dermatopontin and decorin are decreased, and the expression and localisation of fibrillin and elastin fibres in the dermis are altered compared with normal skin and scars. Recent whole genome profiling and proteomic studies have led to the identification of regulatory elements with different expression profiles in hypertrophic and keloid tissue. If the mechanisms of raised dermal scar formation are to be elucidated and effective therapeutic treatments developed, an integrated approach to research is required, focussing on the interactions between ECM molecules, regulatory elements and pathways.
Osteopontin expression in plasma of melanoma patients and in melanocytic tumours
Authors: Maier T. , Laubender R.P. , Sturm R.A. , Klingenstein A. , Korting H.C. , Ruzicka T. , Berking C. 
Published: August 2011

AbstractBackground  While the serological tumour marker S100 is well established for the detection of metastatic melanoma, the extracellular matrix protein osteopontin (OPN) seems to be a promising novel marker for invasive melanoma.Objectives  We analysed the potential of OPN as a serological tumour marker for metastatic melanoma and evaluated its combination with S100 and lactate dehydrogenase (LDH) levels to increase the reliability of these biomarkers for the detection of metastatic disease.Methods  We examined OPN in the peripheral blood of 110 melanoma patients using enzyme‐linked immunosorbent assay and combined it with S100 and LDH levels. In addition, the protein expression of OPN was analysed in tissue sections of melanocytic nevi and melanomas of different progression stages by immunohistochemistry.Results  The independent comparison of S100 and OPN levels in metastatic vs. non‐metastatic patients revealed a P‐value <0.001 respectively. The predictiveness of OPN, S100 and LDH was 0.85, 0.89 and 0.69 as measured by the area under the receiver operating curve (AUC) respectively, while the combination of the two biomarkers OPN and S100 showed an AUC of 0.97. The optimal cut‐off of the combination of OPN and S100 yielded a specificity of 85.9% and a sensitivity of 95.5%.By immunohistochemistry, OPN protein expression was detected in 29% (7/24) of melanocytic nevi, 67% (30/45) of primary melanomas and 39% (7/18) of metastatic melanomas.Conclusions  Together, OPN seems to be a promising novel biomarker for the detection of metastatic disease in melanoma patients, showing elevated plasma levels in metastatic disease and increased protein expression in melanocytic lesions. The combination of OPN with the well‐established tumour marker S100 might increase the prediction of metastases.
The fatty acid oxidation product 15‐A3t‐Isoprostane is a potent inhibitor of NFκB transcription and macrophage transformation
Authors: Brooks Joshua D. , Musiek Erik S. , Koestner Tyler R. , Stankowski Jeannette N. , Howard Jocelyn R. , Brunoldi Enrico M. , Porta Alessio , Zanoni Giuseppe , Vidari Giovanni , Morrow Jason D. , Milne Ginger L. , McLaughlin BethAnn 
Published: August 2011

J. Neurochem. (2011) 119, 604–616.AbstractFatty acids such as eicosapentaenoic acid (EPA) have been shown to be beneficial for neurological function and human health. It is widely thought that oxidation products of EPA are responsible for biological activity, although the specific EPA peroxidation product(s) which exert these responses have not yet been identified. In this work we provide the first evidence that the synthesized representative cyclopentenone IsoP, 15‐A3t‐IsoP, serves as a potent inhibitor of lipopolysaccharide‐stimulated macrophage activation. The anti‐inflammatory activities of 15‐A3t‐IsoP were observed in response not only to lipopolysaccharide, but also to tumor necrosis factor alpha and IL‐1b stimulation. Subsequently, this response blocked the ability of these compounds to stimulate nuclear factor kappa b (NFκB) activation and production of proinflammatory cytokines. The bioactivity of 15‐A3t‐IsoP was shown to be dependent upon an unsaturated carbonyl residue which transiently adducts to free thiols. Site directed mutagenesis of the redox sensitive C179 site of the Ikappa kinase beta subunit, blocked the biological activity of 15‐A3t‐IsoP and NFκB activation. The vasoprotective potential of 15‐A3t‐IsoP was underscored by the ability of this compound to block oxidized lipid accumulation, a critical step in foam cell transformation and atherosclerotic plaque formation. Taken together, these are the first data identifying the biological activity of a specific product of EPA peroxidation, which is formed in abundance in vivo. The clear mechanism linking 15‐A3t‐IsoP to redox control of NFκB transcription, and the compound’s ability to block foam cell transformation suggest that 15‐A3t‐IsoP provides a unique and potent tool to provide vaso‐ and cytoprotection under conditions of oxidative stress.
Altered ERK/MAPK signaling in the hippocampus of the mrsk2_KO mouse model of Coffin‐Lowry syndrome
Authors: Schneider Anne , Mehmood Tahir , Pannetier Solange , Hanauer André 
Published: August 2011

J. Neurochem. (2011) 119, 447–459.AbstractCoffin–Lowry syndrome is a syndromic form of mental retardation caused by mutations of the Rps6ka3 gene encoding ribosomal s6 kinase (RSK)2. RSK2 belongs to a family containing four members in mammals: RSK1–4. RSKs are serine/threonine kinases and cytosolic substrates of extracellular signal‐regulated kinase (ERK) in the Ras/MAPK signaling pathway. RSK2 is highly expressed in the hippocampus, and mrsk2_KO mice display spatial learning and memory impairment. In the present study, we provide evidence of abnormally increased phosphorylation of ERK1/2 in the hippocampus of mrsk2_KO mice. Further studies based on cultured hippocampal neurons revealed that glutamate activates ERK1/2 and RSKs, and confirmed a stronger activation of ERK1/2 in mrsk2_KO neurons than in WT cells. We, thus, provide further evidence that RSK2 exerts a feedback inhibitory effect on the ERK1/2 pathway. We also observed a transient sequestration of P‐ERK1/2 in the cytoplasm upon glutamate stimulation. In addition, the transcription factors cAMP response element binding and Ets LiKe gene1 show over‐activation in RSK2‐deficient neurons. Finally, c‐Fos, Zif268 and Arc were significantly over‐expressed in mrsk2_KO neurons upon glutamate stimulation. Importantly, the increased phosphorylation of other RSK family members observed in mutant neurons was unable to compensate for RSK2 deficiency. This aberrant ERK1/2 signaling can influence various neuronal functions, and thus play a significant role in cognitive dysfunction in mrsk2_KO mice and in the Coffin‐Lowry syndrome.
The effects of chronic treatment with mood stabilizers on the rat hippocampal post‐synaptic density proteome
Authors: Nanavati Dhaval , Austin Daniel R. , Catapano Lisa A. , Luckenbaugh David A. , Dosemeci Ayse , Manji Husseini K. , Chen Guang , Markey Sanford P. 
Published: August 2011

J. Neurochem. (2011) 119, 617–629.AbstractBipolar disorder is a devastating illness that is marked by recurrent episodes of mania and depression. There is growing evidence that the disease is correlated with disruptions in synaptic plasticity cascades involved in cognition and mood regulation. Alleviating the symptoms of bipolar disorder involves chronic treatment with mood stabilizers like lithium or valproate. These two structurally dissimilar drugs are known to alter prominent signaling cascades in the hippocampus, but their effects on the post‐synaptic density complex remain undefined. In this work, we utilized mass spectrometry for quantitative profiling of the rat hippocampal post‐synaptic proteome to investigate the effects of chronic mood stabilizer treatment. Our data show that in response to chronic treatment of mood stabilizers there were not gross qualitative changes but rather subtle quantitative perturbations in post‐synaptic density proteome linked to several key signaling pathways. Our data specifically support the changes in actin dynamics on valproate treatment. Using label‐free quantification methods, we report that lithium and valproate significantly altered the abundance of 21 and 43 proteins, respectively. Seven proteins were affected similarly by both lithium and valproate: Ank3, glutamate receptor 3, dynein heavy chain 1, and four isoforms of the 14‐3‐3 family. Immunoblotting the same samples confirmed the changes in Ank3 and glutamate receptor 3 abundance. Our findings support the hypotheses that BPD is a synaptic disorder and that mood stabilizers modulate the protein signaling complex in the hippocampal post‐synaptic density.
Ovariectomy in grasshoppers increases somatic storage, but proportional allocation of ingested nutrients to somatic tissues is unchanged
Authors: Judd Evan T. , Wessels Frank J. , Drewry Michelle D. , Grove Matthew , Wright Katharine , Hahn Daniel A. , Hatle John D. 
Published: August 2011

SummaryReduced reproduction increases storage and extends lifespan in several animal species. The disposable soma hypothesis suggests this life extension occurs by shifting allocation of ingested nutrients from reproduction to the soma. A great deal of circumstantial evidence supports this hypothesis, but no direct tracking of nutrients has been performed in animals that are long‐lived because of direct reduction in reproduction. Here, we use the stable isotopes to track carbon and nitrogen from ingestion to somatic organs in long‐lived, ovariectomized grasshoppers. Three estimates of somatic storage (viz., quantity of hemolymph storage proteins, amount of femur muscle carbohydrates, and size of the fat body) all doubled upon ovariectomy. In stark contrast, ovariectomy did not increase the proportion of these tissues that were made from recently ingested foods. In other words, the physiology underlying relative allocation to these somatic tissues was not affected by ovariectomy. Thus, at the level of whole tissue storage, these results are consistent with a trade‐off between reproduction and longevity. In contrast, our stable isotope data are inconsistent with the prediction that enhanced storage in ovariectomized females results from a physiological shift in allocation of ingested nutrients.
The H3K27 demethylase UTX‐1 regulates C. elegans lifespan in a germline‐independent, insulin‐dependent manner
Authors: Maures Travis J. , Greer Eric L. , Hauswirth Anna G. , Brunet Anne 
Published: August 2011

SummaryAging is accompanied by alterations in epigenetic marks that control chromatin states, including histone acetylation and methylation. Enzymes that reversibly affect histone marks associated with active chromatin have recently been found to regulate aging in Caenorhabditis elegans. However, relatively little is known about the importance for aging of histone marks associated with repressed chromatin. Here, we use a targeted RNAi screen in C. elegans to identify four histone demethylases that significantly regulate worm lifespan, UTX‐1, RBR‐2, LSD‐1, and T26A5.5. Interestingly, UTX‐1 belongs to a conserved family of histone demethylases specific for lysine 27 of histone H3 (H3K27me3), a mark associated with repressed chromatin. Both utx‐1 knockdown and heterozygous mutation of utx‐1 extend lifespan and increase the global levels of the H3K27me3 mark in worms. The H3K27me3 mark significantly drops in somatic cells during the normal aging process. UTX‐1 regulates lifespan independently of the presence of the germline, but in a manner that depends on the insulin‐FoxO signaling pathway. These findings identify the H3K27me3 histone demethylase UTX‐1 as a novel regulator of worm lifespan in somatic cells.
Expression, assembly and function of novel C‐terminal truncated variants of the mouse P2X7 receptor: re‐evaluation of P2X7 knockouts
Authors: Masin Marianela , Young Christopher , Lim KoiNi , Barnes Sara J , Xu Xing Jian , Marschall Viola , Brutkowski Wojciech , Mooney Elizabeth R , Gorecki Dariusz C , Murrell‐Lagnado Ruth 
Published: August 2011

BACKGROUND AND PURPOSE Splice variants of P2X7 receptor transcripts contribute to the diversity of receptor‐mediated responses. Here, we investigated expression and function of C‐terminal truncated (ΔC) variants of the mP2X7 receptor, which are predicted to escape inactivation in one strain of P2X7−/− mice (Pfizer KO).EXPERIMENTAL APPROACH Expression in wild‐type (WT) and Pfizer KO tissue was investigated by reverse transcription (RT)‐PCR and Western blot analysis. ΔC variants were also cloned and expressed in HEK293 cells to investigate their assembly, trafficking and function.KEY RESULTS RT‐PCR indicates expression of a ΔC splice variant in brain, salivary gland (SG) and spleen from WT and Pfizer KO mice. An additional ΔC hybrid transcript, containing sequences of P2X7 upstream of exon 12, part of exon 13 followed in‐frame by the sequence of the vector used to disrupt the P2X7 gene, was also identified in the KO mice. By blue native (BN) PAGE analysis and the use of cross linking reagents followed by SDS‐PAGE, P2X7 trimers, dimers and monomers were detected in the spleen and SG of Pfizer KO mice. The molecular mass was reduced compared with P2X7 in WT mice tissue, consistent with a ΔC variant. When expressed in HEK293 cells the ΔC variants were inefficiently trafficked to the cell surface and agonist‐evoked whole cell currents were small. Co‐expressed with P2X7A, the ΔC splice variant acted in a dominant negative fashion to inhibit function.CONCLUSIONS AND IMPLICATIONS Pfizer KO mice are not null for P2X7 receptor expression but express ΔC variants with reduced function.
Chronic blockade of cannabinoid CB2 receptors induces anxiolytic‐like actions associated with alterations in GABAA receptors
Authors: García‐Gutiérrez María S , García‐Bueno Borja , Zoppi Silvia , Leza Juan C , Manzanares Jorge 
Published: August 2011

BACKGROUND AND PURPOSE The aim of this study was to explore the effects of CB2 receptor agonist and antagonist in the regulation of anxiety‐like behaviours.EXPERIMENTAL APPROACHES Effects of acute and chronic treatment with the CB2 receptor agonist JWH133 and CB2 receptor antagonist AM630 were evaluated in the light‐dark box (LDB) and elevated plus maze (EPM) tests in Swiss ICR mice. CB2 receptor, GABAAα2 and GABAAγ2 gene and protein expression in the cortex and amygdala of mice chronically treated with JWH133 or AM630 were examined by RT‐PCR and Western blot. Effects of chronic AM630 treatment were evaluated in spontaneously anxious DBA/2 mice in LDB.KEY RESULTS Acute JWH133 treatment failed to produce any effect. Acute AM630 treatment increased anxiety and was blocked by pre‐treatment with JWH133. Chronic JWH133 treatment increased anxiety‐like behaviour whereas chronic AM630 treatment was anxiolytic in LDB and EPM tests. Chronic AM630 treatment increased gene and reduced protein expression of CB2 receptors, GABAAα2 and GABAAγ2 in cortex and amygdala. Chronic JWH133 treatment resulted in opposite gene and protein alterations. In addition, chronic AM630 administration decreased the anxiety of DBA/2 mice in the LDB test.CONCLUSIONS AND IMPLICATIONS The opposing behavioural and molecular changes observed after chronic treatment with AM630 or JWH133 support the key role of CB2 receptors in the regulation of anxiety. Indeed, the efficacy of AM630 in reducing the anxiety of the spontaneously anxious DBA/2 strain of mice strengthens the potential of the CB2 receptor as a new target in the treatment of anxiety‐related disorders.
Long‐term treatment with ivabradine in post‐myocardial infarcted rats counteracts f‐channel overexpression
Authors: Suffredini S , Stillitano F , Comini L , Bouly M , Brogioni S , Ceconi C , Ferrari R , Mugelli A , Cerbai E 
Published: August 2011

BACKGROUND AND PURPOSE Recent clinical data suggest beneficial effects of ivabradine, a specific heart rate (HR)‐lowering drug, in heart failure patients. However, the mechanisms responsible for these effects have not been completely clarified. Thus, we investigated functional/molecular changes in If, the specific target of ivabradine, in the failing atrial and ventricular myocytes where this current is up‐regulated as a consequence of maladaptive remodelling.EXPERIMENTAL APPROACH We investigated the effects of ivabradine (IVA; 10 mg·kg−1·day−1 for 90 days) on electrophysiological remodelling in left atrial (LA), left ventricular (LV) and right ventricular (RV) myocytes from post‐mycardial infarcted (MI) rats, with sham‐operated (sham or sham + IVA) rats as controls. If current was measured by patch‐clamp; hyperpolarization‐activated cyclic nucleotide‐gated (HCN) channel isoforms and microRNA (miRNA‐1 and miR‐133) expression were evaluated by reverse transcription quantitative PCR.KEY RESULTS Maximal specific conductance of If was increased in MI, versus sham, in LV (P < 0.01) and LA myocytes (P < 0.05). Ivabradine reduced HR in both MI and sham rats (P < 0.05). In MI + IVA, If overexpression was attenuated and HCN4 transcription reduced by 66% and 54% in LV and RV tissue, respectively, versus MI rats (all P < 0.05). miR‐1 and miR‐133, which modulate post‐transcriptional expression of HCN2 and HCN4 genes, were significantly increased in myocytes from MI + IVA.CONCLUSION AND IMPLICATION The beneficial effects of ivabradine may be due to the reversal of electrophysiological cardiac remodelling in post‐MI rats by reduction of functional overexpression of HCN channels. This is attributable to transcriptional and post‐transcriptional mechanisms.