bluuebunny/crossref_metadata_2025_split huggingface dataset:
Remodeling pharmaceutical care in Sub‐Saharan Africa (SSA) amidst human resources challenges and the HIV/AIDS pandemic
Authors: King Rosalyn C. , Fomundam Henry N. 
Published: April 2009

AbstractPharmaceutical care, meant to complement a proper drug supply system, is a key component of a robust health care system and is the direct, responsible provision of medication‐related care designed to achieve definite outcomes that improve a patient's quality of life. Beyond simply dispensing medicine, pharmaceutical care promotes adherence to therapeutic regimens and addresses problems such as overdosage, sub‐therapeutic dosage, adverse drug reactions, medication errors, and untreated indications. The dearth of health care workers trained in pharmaceutical care coupled with inadequate access to medications creates multiple disease management challenges in Sub‐Saharan Africa (SSA), which has 25% of the world's disease burden but only 1.3% of the world's health workforce. To prevent and treat HIV/AIDS, TB, malaria, and other maladies, the need is urgent to train and integrate the contributions of current workers who handle medications for major and minor health problems, especially those in licensed pharmacies and drug shops. On the aggregate in SSA, pharmaceutical care is in a nascent stage in most countries but needs to grow as a discipline as well as be tailored to specific country needs. The SSA solution lies in establishing health care system components where cadres of workers engage in pharmaceutical care practices, as well as store and distribute medications. Curriculum changes in pre‐service education, more continuing education for the health workforce in place, and training pharmacists to supervise a lower cadre of assistants and others are among the elements in a pharmaceutical care paradigm shift which is the focus of this article. Copyright © 2009 John Wiley & Sons, Ltd.
Effects of the CYP2D6*10 alleles and co‐medication with CYP2D6‐dependent drugs on risperidone metabolism in patients with schizophrenia
Authors: Yagihashi Tatsuhiko , Mizuno Masafumi , Chino Bun , Sato Yuji , Sakuma Kei , Takebayashi Toru , Takao Takahashi , Kosaki Kenjiro 
Published: April 2009

AbstractObjectiveRisperidone is converted to 9‐hydroxyrisperidone by CYP2D6. Two parameters were used to examine the influences of CYP2D6 polymorphism and of co‐medication on risperidone metabolism: the risperidone:9‐hydroxyrisperidone concentration ratio (R:9‐OHR ratio) and the sum of the risperidone and 9‐hydroxyrisperidone concentrations divided by the dose (C:D ratio). We evaluated the effect of the CYP2D6*10 allele, which is a prevalent mutant allele among East Asians.MethodsGenotyping using the P450 microarray system was performed for 89 Japanese patients with schizophrenia receiving risperidone. The patients with CYP2D6*1/*1, *1/*2, or *2/*2 were classified as Group 1, those with one CYP2D6*10 allele (CYP2D6*1/*10 or *2/*10) were classified as Group 2, and those with two CYP2D6*10 alleles were classified as Group 3. The R:9‐OHR and C:D ratios were analyzed using two‐way ANOVAs with the CYP2D6 genotype and co‐medication with CYP2D6‐dependent drugs as independent variables.ResultsBoth the “genotype” and the “co‐medication” factors had significant impacts on the R:9‐OHR ratio (p = 0.011,p < 0.001). The “genotype” factor also had a significant impact on the C:D ratio (p = 0.032). However, the “co‐medication” factor did not have a significant impact on the C:D ratio (p = 0.129).ConclusionsThe CYP2D6*10 polymorphism and the presence of co‐medication exerted significant influences on the pharmacokinetics of risperidone. Copyright © 2009 John Wiley & Sons, Ltd.
Undifferentiated nasopharyngeal carcinoma from a nonendemic area: Protective role of HLA allele products presenting conserved EBV epitopes
Authors: Pasini Elisa , Caggiari Laura , Maso Luigino Dal , Martorelli Debora , Guidoboni Massimo , Vaccher Emanuela , Barzan Luigi , Franchin Giovanni , Gloghini Annunziata , De Re Valli , Sacchi Nicoletta , Serraino Diego , Carbone Antonino , Rosato Antonio , Dolcetti Riccardo 
Published: April 2009

AbstractThe role of genetic factors involved in the development of undifferentiated nasopharyngeal carcinoma (UNPC) in nonendemic areas has been poorly investigated. High‐resolution human leukocyte antigen (HLA) class I genotyping carried out in 82 Italian UNPC patients and 286 bone marrow donors born in the same province showed that A*0201, B*1801, and B*3501, known to efficiently present Epstein‐Barr virus (EBV)‐derived epitopes, were significantly under‐represented in UNPC patients. Moreover, the A*0201/B*1801 haplotype was significantly less frequent in UNPC cases, with a 90% reduced risk (odds ratio [OR] 0.1, 95% confidence interval [CI] = 0.0–0.5) to develop UNPC, suggesting an additive effect. Notably, all 5 BARF1 epitopes and 7 of the 8 LMP‐2 epitopes known to bind A*0201 showed a fully conserved sequence in all the 31 Italian EBV isolates investigated. The 4 amino acid changes affecting the 436–447 LMP‐2 epitope do not reduce, but rather increase in two cases, the predicted ability of “variant” epitopes to bind the HLA‐A*0201 allele, as shown by immunoinformatic analysis. Moreover, a significantly increased risk for UNPC was associated with A*2601 (OR 2.4, 95% CI = 1.1–4.9) and B*4101 (OR 9.2, 95% CI = 2.5–34.3). These findings indicate that Italian UNPC patients have a distinct HLA‐A and ‐B genotypic profile and suggest that the decreased risk for UNPC conferred by definite HLA class I molecules is probably related to their ability to efficiently present LMP‐2 and BARF1 epitopes that are highly conserved in EBV isolates from this geographic region. These results have practical implications for the immunotherapy of UNPC. © 2009 UICC
Methylation‐associated silencing of SFRP1 with an 8p11‐12 amplification inhibits canonical and non‐canonical WNT pathways in breast cancers
Authors: Yang Zeng‐Quan , Liu Gang , Bollig‐Fischer Aliccia , Haddad Ramsi , Tarca Adi L. , Ethier Stephen P. 
Published: April 2009

AbstractRecently, we analysed the 8p11‐12 genomic region for copy number and gene expression changes in a panel of human breast cancer cell lines and primary specimens. We found that SFRP1 (Secreted frizzled related protein 1) is frequently under expressed even in breast tumours with copy number increases in this genomic region. SFRP1 encodes a WNT signalling antagonist, and plays a role in the development of multiple solid tumour types. In this study, we analysed methylation‐associated silencing of the SFRP1 gene in breast cancer cells with the 8p11‐12 amplicon, and investigated the tumour suppressor properties of SFRP1 in breast cancer cells. SFRP1 expression was markedly reduced in both the breast cancer cell lines and primary tumour specimens relative to normal primary human mammary epithelial cells even when SFRP1 is amplified. Suppression of SFRP1 expression in breast cancer cells with an SFRP1 gene amplification is associated with SFRP1 promoter methylation. Furthermore, restoration of SFRP1 expression suppressed the growth of breast cancer cells in monolayer, and inhibited anchorage independent growth. We also examined the relationship between the silencing of SFRP1 gene and WNT signalling in breast cancer. Ectopic SFRP1 expression in breast cancer cells suppressed both canonical and non‐canonical WNT signalling pathways, and SFRP1 expression was negatively associated with the expression of a subset of WNT responsive genes including RET and MSX2. Thus, down‐regulation of SFRP1 can be triggered by epigenetic and/or genetic events and may contribute to the tumourigenesis of human breast cancer through both canonical and non‐canonical WNT signalling pathways. © 2009 UICC
What are the effects of fiscal policy shocks?
Authors: Mountford Andrew , Uhlig Harald 
Published: April 2009

AbstractWe propose and apply a new approach for analyzing the effects of fiscal policy using vector autoregressions. Specifically, we use sign restrictions to identify a government revenue shock as well as a government spending shock, while controlling for a generic business cycle shock and a monetary policy shock. We explicitly allow for the possibility of announcement effects, i.e., that a current fiscal policy shock changes fiscal policy variables in the future, but not at present. We construct the impulse responses to three linear combinations of these fiscal shocks, corresponding to the three scenarios of deficit‐spending, deficit‐financed tax cuts and a balanced budget spending expansion. We apply the method to US quarterly data from 1955 to 2000. We find that deficit‐financed tax cuts work best among these three scenarios to improve GDP, with a maximal present value multiplier of five dollars of total additional GDP per each dollar of the total cut in government revenue 5 years after the shock. Copyright © 2009 John Wiley & Sons, Ltd.
Economic transition and growth
Authors: Phillips Peter C. B. , Sul Donggyu 
Published: April 2009

AbstractSome extensions of neoclassical growth models are discussed that allow for cross‐section heterogeneity among economies and evolution in rates of technological progress over time. The models offer a spectrum of transitional behavior among economies that includes convergence to a common steady‐state path as well as various forms of transitional divergence and convergence. Mechanisms for modeling such transitions, measuring them econometrically, assessing group behavior and selecting subgroups are developed in the paper. Some econometric issues with the commonly used augmented Solow regressions are pointed out, including problems of endogeneity and omitted variable bias which arise under conditions of transitional heterogeneity. Alternative regression methods for analyzing economic transition are given which lead to a new test of the convergence hypothesis and a new procedure for detecting club convergence clusters. Transition curves for individual economies and subgroups of economies are estimated in a series of empirical applications of the methods to regional US data, OECD data and Penn World Table data. Copyright © 2009 John Wiley & Sons, Ltd.
Uthethane dimethacrylate: A molecule that may cause confusion in dental research
Authors: Polydorou Olga , König Armin , Hellwig Elmar , Kümmerer Klaus 
Published: April 2009

AbstractIn recent years, the elution of monomers from dental materials has been a cause for public concern. Urethane dimethacrylate, commonly abbreviated to UDMA, is one of the monomers that are most often tested with regard to elution from and cytotoxicity of resin‐based materials. Although each chemical name represents the chemical type, chemical structure, and molecular weight of a molecule, it does not seem to be the same with UDMA. In the present paper, the different forms of UDMA are presented. These include those used by dental manufacturers to produce composite materials and the different types of urethane dimethacrylate used in studies concerning the elution of monomers from composite materials. High‐performance liquid chromatography (HPLC) is usually used to detect the eluted monomers, but it does not appear to be adequate in determining the different forms of UDMA. The combination of HPLC with mass spectrometry is shown to be able to specifically identify the compounds eluted in addition to those compounds used as standards in the various studies. The fact that the same name is given to different molecules causes confusion about the results of studies testing the elusion of monomers from composite materials and their possible toxicity. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2009
In vitro adherence of oral streptococci to zirconia core and veneering glass‐ceramics
Authors: Rosentritt Martin , Behr Michael , Bürgers Ralf , Feilzer Albert J. , Hahnel Sebastian 
Published: April 2009

AbstractPlaque formation on dental ceramics may cause gingival inflammation and secondary caries. This in vitro study compared the susceptibility of various dental ceramics to adhere oral streptococci, and verified the influence of substratum surface roughness and surface hydrophobicity. Three zirconia ceramic materials and three veneering glass‐ceramics were investigated. Fifteen test specimens were prepared for each material, polished, and surface roughness and hydrophobicity were determined. After incubation with artificial saliva (2 h, 37°C) for pellicle formation, specimens were incubated with suspensions of Streptococcus gordonii DSMZ 6777, Streptococcus mutans DSMZ 20523, Streptococcus oralis DSMZ 20627, or Streptococcus sanguinis DSMZ 20068, respectively, for 2.5 h at 37°C. Adherent bacteria were quantified using a fluorescence dye for viable cell quantification (Alamar Blue/Resazurin). Statistical analysis was performed using one‐ and two‐way ANOVA and the Tukey‐Kramer multiple comparison test for post hoc analysis (α < 0.05). Surface roughness and surface hydrophobicity differed significantly among the various ceramics; protein coating hydrophilized the surfaces, and led to a homogenization of the surface hydrophobicity of the various ceramics. Before protein coating, almost similar relative fluorescence intensities indicating similar adhesion of streptococci were found for the various ceramics; more distinct differences were observed after protein coating. Correlations between surface parameters and streptococcal adhesion were poor. Within the limitations of these experiments, the findings of this in vitro study indicate only little differences between zirconia and glass ceramic with regard to streptococcal adhesion. Judging from these results, it is unlikely that exposed zirconia surfaces yield more plaque than glass ceramic surfaces in vivo. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2009
Grape seed proanthocyanidins protect cardiomyocytes from ischemia and reperfusion injury via Akt‐NOS signaling
Authors: Shao Zuo‐Hui , Wojcik Kimberly R. , Dossumbekova Anar , Hsu Chinwang , Mehendale Sangeeta R. , Li Chang‐Qing , Qin Yimin , Sharp Willard W. , Chang Wei‐Tien , Hamann Kimm J. , Yuan Chun‐Su , Hoek Terry L. Vanden 
Published: April 2009

AbstractIschemia/reperfusion (I/R) injury in cardiomyocytes is related to excess reactive oxygen species (ROS) generation and can be modulated by nitric oxide (NO). We have previously shown that grape seed proanthocyanidin extract (GSPE), a naturally occurring antioxidant, decreased ROS and may potentially stimulate NO production. In this study, we investigated whether GSPE administration at reperfusion was associated with cardioprotection and enhanced NO production in a cardiomyocyte I/R model. GSPE attenuated I/R‐induced cell death [18.0 ± 1.8% (GSPE, 50 µg/ml) vs. 42.3 ± 3.0% (I/R control), P < 0.001], restored contractility (6/6 vs. 0/6, respectively), and increased NO release. The NO synthase (NOS) inhibitor Nω‐nitro‐L‐arginine methyl ester (L‐NAME, 200 µM) significantly reduced GSPE‐induced NO release and its associated cardioprotection [32.7 ± 2.7% (GSPE + L‐NAME) vs. 18.0 ± 1.8% (GSPE alone), P < 0.01]. To determine whether GSPE induced NO production was mediated by the Akt‐eNOS pathway, we utilized the Akt inhibitor API‐2. API‐2 (10 µM) abrogated GSPE‐induced protection [44.3% ± 2.2% (GSPE + API‐2) vs. 27.0% ± 4.3% (GSPE alone), P < 0.01], attenuated the enhanced phosphorylation of Akt at Ser473 in GSPE‐treated cells and attenuated GSPE‐induced NO increases. Simultaneously blocking NOS activation (L‐NAME) and Akt (API‐2) resulted in decreased NO levels similar to using each inhibitor independently. These data suggest that in the context of GSPE stimulation, Akt may help activate eNOS, leading to protective levels of NO. GSPE offers an alternative approach to therapeutic cardioprotection against I/R injury and may offer unique opportunities to improve cardiovascular health by enhancing NO production and increasing Akt‐eNOS signaling. J. Cell. Biochem. 107: 697–705, 2009. © 2009 Wiley‐Liss, Inc.
Schizotypy, depression, and anxiety in physical and social anhedonia
Authors: Rey Gwladys , Jouvent Roland , Dubal Stéphanie 
Published: April 2009

AbstractSocial anhedonia is a more promising indicator of vulnerability to schizophrenia than physical anhedonia, both as assessed by Chapman scales. More broadly, the populations identified by these scales would have a propensity to different psychiatric disorders. This cross‐sectional study examined the respective profiles of schizotypy, anxiety, and depression in French students with physical and social anhedonia, using psychometric and interview‐based measures. Compared to controls (n=46), subjects with social anhedonia (n=19) reported higher schizotypal scores for interpersonal, paranoid, disorganization, and cognitive/perceptual dimensions, whereas subjects with physical anhedonia (n=35) had more extensive interpersonal deficits and paranoia. Both groups had more depressive and anxiety symptoms than controls, in particular subjects with social anhedonia. © 2009 Wiley Periodicals, Inc. J Clin Psychol 65:1 –14, 2009.
Eating disorder behaviors and depression: a minimal relationship beyond social comparison, self‐esteem, and body dissatisfaction
Authors: Green Melinda A. , Scott Norman A. , Cross Susan E. , Liao Kelly Yu‐Hsin , Hallengren Jada J. , Davids Christopher M. , Carter Lindsey P. , Kugler David W. , Read Katherine E. , Jepson Amanda J. 
Published: April 2009

AbstractExisting literature fails to comprehensively identify factors contributing to the comorbid relationship between eating disorder (ED) behaviors and unipolar depression. Maladaptive social comparison, body dissatisfaction, and low self‐esteem are disruptive psychological patterns common to both constructs. It is unclear whether a unique relationship exists between depression and eating disorder behaviors beyond the effects exerted by this negative cognitive triad. The purpose of the present study is to examine whether a unique relationship exists between depression and ED behaviors after controlling for maladaptive social comparison, body dissatisfaction, and low self‐esteem. We predict minimal unique variance in ED behaviors will be explained by depression after controlling for this negative cognitive triad. © 2009 Wiley Periodicals, Inc. J Clin Psychol 65:1–11, 2009.
Mindfulness and experiential avoidance as predictors and outcomes of the narrative emotional disclosure task
Authors: Moore Susan D. , Brody Leslie R. , Dierberger Amy E. 
Published: April 2009

AbstractThis randomized study examined whether narrative emotional disclosure improves mindfulness, experiential avoidance, and mental health, and how baseline levels of and changes in mindfulness and experiential avoidance relate to mental health. Participants (N=233) wrote repeated traumatic (experimental condition) or unemotional daily events narratives (control condition). Regression analyses showed neither condition nor gender effects on mental health or experiential avoidance at a 1‐month follow‐up, although the control condition significantly increased in one component of mindfulness. Decreased experiential avoidance (across conditions) and increased mindfulness (in the experimental condition) significantly predicted improved mental health. Narrative disclosure thus did not improve outcomes measured here. However, increasing mindfulness when writing narratives with traumatic content, and decreasing experiential avoidance regardless of writing content, was associated with improved mental health. © 2009 Wiley Periodicals, Inc. J Clin Psychol 65: 1–18, 2009.
Amyloid‐β up‐regulates complement factor B in retinal pigment epithelial cells through cytokines released from recruited macrophages/microglia: Another mechanism of complement activation in age‐related macular degeneration
Authors: Wang Jiying , Ohno‐Matsui Kyoko , Yoshida Takeshi , Shimada Noriaki , Ichinose Shizuko , Sato Tetsuji , Mochizuki Manabu , Morita Ikuo 
Published: April 2009

AbstractOne of the earliest signs of age‐related macular degeneration (AMD) is the formation of drusen which are extracellular deposits beneath the retinal pigmented epithelium (RPE). To investigate the relationship between drusen and AMD, we focused on amyloid β (Aβ), a major component of drusen and also of senile plaques in the brain of Alzheimer's patients. We previously reported that Aβ was accumulated in drusen‐like structure in senescent neprilysin gene‐disrupted mice. The purpose of this study was to investigate the influence of Aβ on factor B, the main activator of the complement alternative pathway. The results showed that Aβ did not directly modulate factor B expression in RPE cells, but increased the production of monocyte chemoattractant protein‐1 (MCP‐1). Aβ also increased the production of IL‐1β and TNF‐α in macrophages/microglia, and exposure of RPE cells to IL‐1β and TNF‐α significantly up‐regulated factor B. Co‐cultures of RPE cells and macrophages/microglia in the presence of Aβ significantly increased the expression of factor B in RPE. These findings indicate that cytokines produced by macrophages/microglia that were recruited by MCP‐1 produced in RPE cells stimulated by Aβ up‐regulate factor B in RPE cells. Thus, a combined mechanism exists for Aβ‐induced for the activation of the complement alternative pathway in the subretinal space; cytokine‐induced up‐regulation of activator factor B and dysfunction of the inhibitor factor I by direct binding to Aβ as suggested in our earlier study. J. Cell. Physiol. 220: 119–128, 2009. © 2009 Wiley‐Liss, Inc.
Retinoid‐responsive transcriptional changes in epidermal keratinocytes
Authors: Lee Ding‐Dar , Stojadinovic Olivera , Krzyzanowska Agata , Vouthounis Constantinos , Blumenberg Miroslav , Tomic‐Canic Marjana 
Published: April 2009

AbstractRetinoids (RA) have been used as therapeutic agents for numerous skin diseases, from psoriasis to acne and wrinkles. While RA is known to inhibit keratinocyte differentiation, the molecular effects of RA in epidermis have not been comprehensively defined. To identify the transcriptional targets of RA in primary human epidermal keratinocytes, we compared the transcriptional profiles of cells grown in the presence or absence of all‐trans retinoic acid for 1, 4, 24, 48, and 72 h, using large DNA microarrays. As expected, RA suppresses the protein markers of cornification; however the genes responsible for biosynthesis of epidermal lipids, long‐chain fatty acids, cholesterol, and sphingolipids, are also suppressed. Importantly, the pathways of RA synthesis, esterification and metabolism are activated by RA; therefore, RA regulates its own bioavailability. Unexpectedly, RA regulates many genes associated with the cell cycle and programmed cell death. This led us to reveal novel effects of RA on keratinocyte proliferation and apoptosis. The response to RA is very fast: 315 genes were regulated already after 1 h. More than one‐third of RA‐regulated genes function in signal transduction and regulation of transcription. Using in silico analysis, we identified a set of over‐represented transcription factor binding sites in the RA‐regulated genes. Many psoriasis‐related genes are regulated by RA, some induced, others suppressed. These results comprehensively document the transcriptional changes caused by RA in keratinocytes, add new insights into the molecular mechanism influenced by RA in the epidermis and demonstrate the hypothesis‐generating power of DNA microarray analysis. J. Cell. Physiol. 220: 427–439, 2009. © 2009 Wiley‐Liss, Inc.