bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sociodemographic characteristics, clinical factors, and genetic polymorphisms associated with Alzheimer's disease
Authors: Bicalho Maria Aparecida Camargos , Pimenta Fausto Aloísio , Bastos‐Rodrigues Luciana , de Oliveira Hansen Érika , Neves Samara Canguçu , Melo Marina , Rosa Daniela Valadão , de Souza Renan Pedra , de Miranda Débora Marques , de Moraes Edgar Nunes , Romano‐Silva Marco Aurélio , Marco Luiz De 
Published: August 2012

ObjectiveAlzheimer's disease (AD) has a multifactorial etiology involving an interaction of genetic and environmental factors. The Apolipoprotein E ε4 (ApoE ε4) is the single most important genetic risk factor for sporadic AD. Our aim was to study the association between sociodemographic, clinical data and gene polymorphisms in patients with sporadic AD in a heterogeneous genomic Brazilian population with low educational levels.MethodsWe selected 169 sporadic AD patients and 97 controls older than 65 years and compared co‐variables between them: age, years of education, vascular risk factors, genomic ancestry, and functional polymorphisms of ApoE, BDNF, COMT, and 5‐HTTLPR. We also determined the genomic ancestry of all individuals.ResultsThe average years of education was significantly smaller in the patient's group (p = 0.003), and they had a history of depression when compared with controls (p < 0.001). The carriers of ApoE ε4 have an earlier onset of the disease (76.9 years) (p = 0.001) than ApoE ε3 (79.5 years) (p = 0.024). Patients with Met allele of Val66Met have a tendency to later onset of disease (p = 0.056). There were no differences in the genomic ancestry between groups.ConclusionLow level of education and history of depression were associated with AD. Public policies and intensive observation of old‐age patients with lifetime history of depression, especially APOE ε4 carriers, could improve the well‐being of our population. Copyright © 2012 John Wiley & Sons, Ltd.
Ultrasound‐Assisted Synthesis of 3‐(Arylamino)‐1‐ferrocenylpropan‐1‐ones
Authors: Pejović Anka , Stevanović Dragana , Damljanović Ivan , Vukićević Mirjana , Novaković Sladjana B. , Bogdanović Goran A. , Mihajilov‐Krstev Tatjana , Radulović Niko , Vukićević Rastko D. 
Published: August 2012

AbstractA successful aza‐Michael addition of arylamines to a conjugated enone, acryloylferrocene, has been achieved by ultrasonic irradiation of the mixture of these reactants and the catalyst, i.e., montmorillonite K‐10. This solvent‐free reaction, yielding ferrocene containing Mannich bases, 3‐(arylamino)‐1‐ferrocenylpropan‐1‐ones, considered as valuable precursors in organic synthesis, has been performed by using a simple ultrasonic cleaner. Among 17 synthesized β‐amino ketones, three were new ones, and these were fully characterized by spectroscopic means. X‐Ray crystallographic analysis of three of these crystalline products enabled the insight into the conformational details of these compounds. All compounds were evaluated for their antibacterial activities against six Gram‐positive and five Gram‐negative strains in a microdilution assay. The observed promising antibacterial activity (with a MIC value of 25 μg/ml (ca. 0.07 μmol/ml) as the best result for almost all tested compounds against Micrococcus flavus) seems not only to be compound but also bacterial species‐specific.
Preparation and Characterization of New C2‐ and C1‐Symmetric Nitrogen, Oxygen, Phosphorous, and Sulfur Derivatives and Analogs of TADDOL. Part II
Authors: Pichota Arkadius , Gramlich Volker , Bichsel Hans‐Ulrich , Styner Thomas , Knöpfel Thomas , Wünsch Ralf , Hintermann Tobias , Schweizer W. Bernd , Beck Albert K. , Seebach Dieter 
Published: August 2012

AbstractTADDOL (=α,α,α′,α′‐Tetraaryl‐1,3‐dioxolane‐4,5‐dimethanol) and the corresponding dichloride are converted to TADDAMINs (=(4S,5S)‐2,2,N,N′‐tetramethyl‐α,α,α′,α′‐tetraphenyl‐1,3‐dioxolan‐4,5‐dimethanamines) (Scheme 2) and ureas, 12–15, and to TADDOP derivatives with seven‐membered OPO ester rings (Schemes 3 and 4). Cl/P‐Replacement via the MichaelisArbuzov reaction (Scheme 7) on mono‐ and dichlorides, derived from TADDOL, are described. It was not possible to obtain phosphines with the P‐atom attached to the benzhydrylic C‐atom of the TADDOL skeleton (Schemes 6 and 7). The X‐ray crystal structures (Figs. 1 and 2) of ten of the more than 30 new TADDOL derivatives are discussed. Full experimental details are presented.
Plasmablastic haemato‐lymphoid neoplasm with a complex genetic signature of Burkitt lymphoma responding to bortezomib
Authors: Dasanu Constantin A. , Bauer Frank , Codreanu Ion , Padmanabhan Premkumar , Rampurwala Murtuza 
Published: August 2012

AbstractPlasmablastic lymphoma shares many morphologic features with plasmablastic plasma cell myeloma. The activation of MYC oncogene in these lymphomas may be an important pathogenetic element associated with Epstein–Barr virus infection. We describe herein an elderly man with a plasmablastic lymphoid neoplasm displaying unique morphologic, cytogenetic and clinical features. This case might offer additional insights to the complex but fascinating topic of hybrid haemato‐lymphoid neoplasms such as plasmablastic lymphoma‐myeloma. In addition, the patient responded to the treatment with bortezomib. Newer antimyeloma agents such as bortezomib have shown promise in the treatment of these neoplasms and should further be explored for their therapy. Copyright © 2012 John Wiley & Sons, Ltd.
Hepatic gene expression analysis of mice exposed to raw water from Meiliang Bay, Lake Taihu, China
Authors: Wu Bing , Liu Su , Cheng Shupei , Zhang Yan , Zhang Xuxiang 
Published: August 2012

ABSTRACTLake water is a micro‐polluted water system, and characterization of its toxicity remains difficult. Microarray‐based determination of altered gene expression might be an alterative approach. We chose raw water from Meiliang Bay, Lake Taihu, China as the target water. Male mice were exposed to the lake water for 90 days. Total hepatic RNA was applied to interrogate the Affymetrix Mouse Genome 430A 2.0 array. Gene ontology analysis, pathway analysis and gene network analysis were used to identify biological effects of differently expressed genes. The results showed that the expressions of 170 genes were altered. Nine biological processes and nine biological pathways were significantly perturbed (P ≤ 0.01), mainly linked to the regulation of cell processes, DNA repair, chromatin modification, oxidative reduction and carbohydrate metabolism. Important genes, such as Prkca, Pik3r1, Fgfr1 and Zbtb16, were identified by gene network analysis. This study provided excellent insights into early toxicological effects related to raw Lake Taihu water, and illustrated that the toxicogenomic approach might be a useful tool to evaluate potential environmental health effects of raw lake water. Copyright © 2012 John Wiley & Sons, Ltd.
Hybrid nanocomposite films for laser‐activated tissue bonding
Authors: Matteini Paolo , Ratto Fulvio , Rossi Francesca , de Angelis Marella , Cavigli Lucia , Pini Roberto 
Published: August 2012

AbstractWe report new advancements in the biomedical exploitation of plasmonic nanoparticles as an effective platform for the photothermal repair of biological tissue. Chitosan films are loaded with gold nanorods with intense optical absorption in the “therapeutic window” of deepest light penetration through the body, and then activated by near infrared laser excitation to give adhesion with adjacent connective tissues. The adhesion consists of 0.07 mm2 welds of ∼20 kPa tensile strength at the film/tissue interface, which are obtained by administration of pulses with duration in the hundreds of millisecond timescale from a diode laser at ∼130 J cm–2. We investigate the adhesive effect as a function of pulse power and duration and identify an optimal operative window to achieve effective and reproducible welds with minimal detrimental superheating. These results may prove valuable to standardize laser bonding techniques and meet current needs for new knowledge which is urged by the penetration of nanotechnology into biomedical optics. (© 2012 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Disease modification of breast cancer–induced bone remodeling by cannabinoid 2 receptor agonists
Authors: Lozano-Ondoua Alysia N , Hanlon Katherine E , Symons-Liguori Ashley M , Largent-Milnes Tally M , Havelin Josh J , Ferland Henry L , Chandramouli Anupama , Owusu-Ankomah Mabel , Nikolich-Zugich Tijana , Bloom Aaron P , Jimenez-Andrade Juan Miguel , King Tamara , Porreca Frank , Nelson Mark A , Mantyh Patrick W , Vanderah Todd W 
Published: August 2012

Abstract
Most commonly originating from breast malignancies, metastatic bone cancer causes bone destruction and severe pain. Although novel chemotherapeutic agents have increased life expectancy, patients are experiencing higher incidences of fracture, pain, and drug-induced side effects; furthermore, recent findings suggest that patients are severely undertreated for their cancer pain. Strong analgesics, namely opiates, are first-line therapy in alleviating cancer-related pain despite the severe side effects, including enhanced bone destruction with sustained administration. Bone resorption is primarily treated with bisphosphonates, which are associated with highly undesirable side effects, including nephrotoxicity and osteonecrosis of the jaw. In contrast, cannabinoid receptor 2 (CB2) receptor-specific agonists have been shown to reduce bone loss and stimulate bone formation in a model of osteoporosis. CB2 agonists produce analgesia in both inflammatory and neuropathic pain models. Notably, mixed CB1/CB2 agonists also demonstrate a reduction in ErbB2-driven breast cancer progression. Here we demonstrate for the first time that CB2 agonists reduce breast cancer–induced bone pain, bone loss, and breast cancer proliferation via cytokine/chemokine suppression. Studies used the spontaneously-occurring murine mammary cell line (66.1) implanted into the femur intramedullary space; measurements of spontaneous pain, bone loss, and cancer proliferation were made. The systemic administration of a CB2 agonist, JWH015, for 7 days significantly attenuated bone remodeling, assuaged spontaneous pain, and decreased primary tumor burden. CB2-mediated effects in vivo were reversed by concurrent treatment with a CB2 antagonist/inverse agonist but not with a CB1 antagonist/inverse agonist. In vitro, JWH015 reduced cancer cell proliferation and inflammatory mediators that have been shown to promote pain, bone loss, and proliferation. Taken together, these results suggest CB2 agonists as a novel treatment for breast cancer–induced bone pain, in which disease modifications include a reduction in bone loss, suppression of cancer growth, attenuation of severe bone pain, and increased survival without the major side effects of current therapeutic options. © 2013 American Society for Bone and Mineral Research
EPA, an omega‐3 fatty acid, induces apoptosis in human pancreatic cancer cells: Role of ROS accumulation, caspase‐8 activation, and autophagy induction
Authors: Fukui Masayuki , Kang Ki Sung , Okada Kazushi , Zhu Bao Ting 
Published: August 2012

AbstractIn a recent study, we showed that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two common omega‐3 fatty acids, can cause ROS accumulation and subsequently induce caspase‐8‐dependent apoptosis in human breast cancer cells (Kang et al. [2010], PLoS ONE 5: e10296). In this study, we showed that the pancreas has a unique ability to accumulate EPA at a level markedly higher than several other tissues analyzed. Based on this finding, we sought to further investigate the anticancer actions of EPA and its analog DHA in human pancreatic cancer cells using both in vitro and in vivo models. EPA and DHA were found to induce ROS accumulation and caspase‐8‐dependent cell death in human pancreatic cancer cells (MIA‐PaCa‐2 and Capan‐2) in vitro. Feeding animals with a diet supplemented with 5% fish oil, which contains high levels of EPA and DHA, also strongly suppresses the growth of MIA‐PaCa‐2 human pancreatic cancer xenografts in athymic nude mice, by inducing oxidative stress and cell death. In addition, we showed that EPA can concomitantly induce autophagy in these cancer cells, and the induction of autophagy diminishes its ability to induce apoptotic cell death. It is therefore suggested that combination of EPA with an autophagy inhibitor may be a useful strategy in increasing the therapeutic effectiveness in pancreatic cancer. J. Cell. Biochem. 114: 192–203, 2012. © 2012 Wiley Periodicals, Inc.
Identification of lysosomal sialidase NEU1 and plasma membrane sialidase NEU3 in human erythrocytes
Authors: D'Avila Francesca , Tringali Cristina , Papini Nadia , Anastasia Luigi , Croci Gianluigi , Massaccesi Luca , Monti Eugenio , Tettamanti Guido , Venerando Bruno 
Published: August 2012

AbstractThe sialylation level of molecules, sialoglycoproteins and gangliosides, protruding from plasma membranes regulates multiple facets of erythrocyte function, from interaction with endothelium to cell lifespan. Our results demonstrate that: (a) Both sialidases NEU1 and NEU3 are present on erythrocyte plasma membrane; (b) NEU1 is kept on the plasma membrane in absence of the protective protein/cathepsin A (PPCA); (c) NEU1 and NEU3 are retained on the plasma membrane, as peripheral proteins, associated to the external leaflet and released by alkaline treatments; (d) NEU1 and NEU3 are segregated in Triton X‐100 detergent‐resistant membrane domains (DRMs); (e) NEU3 shows activity also at neutral pH; and (f) NEU1 and NEU3 are progressively lost during erythrocyte life. Interestingly, sialidase activity released from erythrocyte membranes after an alkaline treatment preserves its functionality and recognizes sialoglycoproteins and gangliosides. On the other hand, the weak anchorage of sialidases to the plasma membrane and their loss during erythrocyte life could be a tool to preserve the cellular sialic acid content in order to avoid the early ageing of erythrocyte and processes of cell aggregation in the capillaries. J. Cell. Biochem. 114: 204–211, 2012. © 2012 Wiley Periodicals, Inc.
Mitochondrial accumulation under oxidative stress is due to defects in autophagy
Authors: Luo Cheng , Li Yan , Wang Hui , Feng Zhihui , Li Yuan , Long Jiangang , Liu Jiankang 
Published: August 2012

AbstractMitochondrial dynamics maintains normal mitochondrial function by degrading damaged mitochondria and generating newborn mitochondria. The accumulation of damaged mitochondria influences the intracellular environment by promoting mitochondrial dysfunction, and thus initiating a vicious cycle. Oxidative stress induces mitochondrial malfunction, which is involved in many cardiovascular diseases. However, the mechanism of mitochondrial accumulation in cardiac myoblasts remains unclear. We observed mitochondrial dysfunction and an increase in mitochondrial mass under the oxidative conditions produced by tert‐butyl hydroperoxide (tBHP) in cardiac myoblast H9c2 cells. However, in contrast to the increase in mitochondrial mass, mitochondrial DNA (mtDNA) decreased, suggesting that enhanced mitochondrial biogenesis may be not the primary cause of the mitochondrial accumulation. Therefore, we investigated changes in a number of proteins involved in autophagy. Beclin1, Atg12–Atg5 conjugate, Atg7 contents decreased but LC3‐II accumulated in tBHP‐treated H9c2 cells. Moreover, the capacity for acid hydrolysis decreased in H9c2 cells. We also demonstrated a decrease in DJ‐1 protein under the oxidative conditions that deregulate mitochondrial dynamics. These results reveal that autophagy became defective under oxidative stress. We therefore suggest that defects in autophagy mediate mitochondrial accumulation under these conditions. J. Cell. Biochem. 114: 212–219, 2012. © 2012 Wiley Periodicals, Inc.
Macrophages modulate the viability and growth of human mesenchymal stem cells
Authors: Freytes Donald O. , Kang Jung W. , Marcos‐Campos Ivan , Vunjak‐Novakovic Gordana 
Published: August 2012

AbstractFollowing myocardial infarction, tissue repair is mediated by the recruitment of monocytes and their subsequent differentiation into macrophages. Recent findings have revealed the dynamic changes in the presence of polarized macrophages with pro‐inflammatory (M1) and anti‐inflammatory (M2) properties during the early (acute) and late (chronic) stages of cardiac ischemia. Mesenchymal stem cells (MSCs) delivered into the injured myocardium as reparative cells are subjected to the effects of polarized macrophages and the inflammatory milieu. The present study investigated how cytokines and polarized macrophages associated with pro‐inflammatory (M1) and anti‐inflammatory (M2) responses affect the survival of MSCs. Human MSCs were studied using an in vitro platform with individual and combined M1 and M2 cytokines: IL‐1β, IL‐6, TNF‐α, and IFN‐γ (for M1), and IL‐10, TGF‐β1, TGF‐β3, and VEGF (for M2). In addition, polarization molecules (M1: LPS and IFN‐γ; M2: IL‐4 and IL‐13) and common chemokines (SDF‐1 and MCP‐1) found during inflammation were also studied. Indirect and direct co‐cultures were conducted using M1 and M2 polarized human THP‐1 monocytes. M2 macrophages and their associated cytokines supported the growth of hMSCs, while M1 macrophages and their associated cytokines inhibited the growth of hMSCs in vitro under certain conditions. These data imply that an anti‐inflammatory (M2) environment is more accommodating to the therapeutic hMSCs than a pro‐inflammatory (M1) environment at specific concentrations. J. Cell. Biochem. 114: 220–229, 2012. © 2012 Wiley Periodicals, Inc.
Altered mitochondrial functioning induced by preoperative fasting may underlie protection against renal ischemia/reperfusion injury
Authors: Verweij Mariëlle , Sluiter Wim , van den Engel Sandra , Jansen Eugène , IJzermans Jan N.M. , de Bruin Ron W.F. 
Published: August 2012

AbstractWe reported previously that the robust protection against renal ischemia/reperfusion (I/R) injury in mice by fasting was largely initiated before the induction of renal I/R. In addition, we found that preoperative fasting downregulated the gene expression levels of complexes I, IV, and V of the mitochondrial oxidative phosphorylation (OXPHOS) system, while it did not change those of complexes II and III. Hence, we now investigated the effect of 3 days of fasting on the functioning of renal mitochondria in order to better understand our previous findings. Fasting did not affect mitochondrial density. Surprisingly, fasting significantly increased the protein expression of complex II of the mitochondrial OXPHOS system by 19%. Complex II‐driven state 3 respiratory activity was significantly reduced by fasting (46%), which could be partially attributed to the significant decrease in the enzyme activity of complex II (16%). Fasting significantly inhibited Ca2+‐dependent mitochondrial permeability transition pore opening that is directly linked to protection against renal I/R injury. The inhibition of the mitochondrial permeability transition pore did not involve the expression of the voltage‐dependent anion channel by fasting. In conclusion, 3 days of fasting clearly induces the inhibition of complex II‐driven mitochondrial respiration state 3 in part by decreasing the amount of functional complex II, and inhibits mitochondrial permeability transition pore opening. This might be a relevant sequence of events that could contribute to the protection of the kidney against I/R injury. J. Cell. Biochem. 114: 230–237, 2012. © 2012 Wiley Periodicals, Inc.
Effectiveness and Feasibility of a Cognitive‐Behavioral Group Intervention for Body Image Disturbance in Women With Eating Disorders
Authors: Bhatnagar Kelly A.C. , Wisniewski Lucene , Solomon Mindy , Heinberg Leslie 
Published: August 2012

ObjectiveThe present study investigated the effectiveness and feasibility of a cognitive‐behavioral group intervention for the treatment of body image disturbance in women with eating disorders.MethodThe study used a multiple‐baseline design and enrolled 38 participants with a range of eating disorders. The intervention targeted attitudinal and behavioral components of body image disturbance using psychoeducation, self‐monitoring, systematic desensitization, and cognitive restructuring. Primary outcomes included multidimensional body image assessment (effectiveness) and treatment adherence and satisfaction (feasibility).ResultsParticipants undergoing manualized group treatment reported significantly less body image disturbance than participants randomized to a waitlist control condition. However, differences disappeared after both groups had been through intervention. Participants also reported less depression and eating disorder pathology from baseline to posttreatment, however this difference was not considered statistically significant. Feasibility outcomes suggest the intervention was well received and highly acceptable to participants.ConclusionsFindings emphasize the importance of adding an evidence‐based body image component to standard eating disorder treatment. ©2012 Wiley Periodicals, Inc. J. Clin. Psychol. 00:1‐13, 2012.
Cardiac imaging techniques for physicians: Late enhancement
Authors: Kellman Peter , Arai Andrew E. 
Published: August 2012

AbstractLate enhancement imaging is used to diagnose and characterize a wide range of ischemic and nonischemic cardiomyopathies, and its use has become ubiquitous in the cardiac MR exam. As the use of late enhancement imaging has matured and the span of applications has widened, the demands on image quality have grown. The characterization of subendocardial MI now includes the accurate quantification of scar size, shape, and characterization of borders which have been shown to have prognostic significance. More diverse patterns of late enhancement including patchy, mid‐wall, subepicardial, or diffuse enhancement are of interest in diagnosing nonischemic cardiomyopathies. As clinicians are examining late enhancement images for more subtle indication of fibrosis, the demand for lower artifacts has increased. A range of new techniques have emerged to improve the speed and quality of late enhancement imaging including: methods for acquisition during free breathing, and fat water separated imaging for characterizing fibrofatty infiltration and reduction of artifacts related to the presence of fat. Methods for quantification of T1 and extracellular volume fraction are emerging to tackle the issue of discriminating globally diffuse fibrosis from normal healthy tissue which is challenging using conventional late enhancement methods. The aim of this review will be to describe the current state of the art and to provide a guide to various clinical protocols that are commonly used. J. Magn. Reson. Imaging 2012;36:529–542. Published 2012 Wiley Periodicals, Inc.
Minimally invasive surgery for gastric cancer
Authors: Bamboat Zubin M. , Strong Vivian E. 
Published: August 2012

AbstractApplication of minimally invasive techniques to gastric cancer in the West has been curbed by concerns of feasibility and oncologic adequacy. Growing evidence supports improved short‐term and equivalent oncologic outcomes in selected patients undergoing laparoscopic surgery for early‐stage disease. Laparoscopic resection for advanced gastric cancer remains controversial due to few reliable studies on long‐term outcomes. We focus on important studies from Asia and highlight the Western experience with laparoscopic and robotic surgery for gastric carcinoma. J. Surg. Oncol. 2013;107:271–276. © 2012 Wiley Periodicals, Inc.