bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ordinary people do not ignore base rates
Authors: Laming Donald 
Published: October 2007

AbstractHuman responses to probabilities can be studied through gambling and through experiments presenting biased sequences of stimuli. In both cases, participants are sensitive to base rates. They adjust automatically to changes in base rate; such adjustment is incompatible with conformity to Bayes' Theorem. ”Base-rate neglect” is therefore specific to the exercises in mental arithmetic reviewed in the target article.
The versatility and generality of nested set operations
Authors: Patterson Richard 
Published: October 2007

AbstractThe target article makes an impressive case that nested set operations (NS) facilitate probability computations by helping make clear the relevant natural frequency partitions; however, NS can also contribute to common errors. That NS constitute a general reasoning process is supported by their role in deductive, modal, causal, and other reasoning. That NS are solely a rule-based process is problematic.
Base-rate respect: From statistical formats to cognitive structures
Authors: Barbey Aron K. , Sloman Steven A. 
Published: October 2007

AbstractThe commentaries indicate a general agreement that one source of reduction of base-rate neglect involves making structural relations among relevant sets transparent. There is much less agreement, however, that this entails dual systems of reasoning. In this response, we make the case for our perspective on dual systems. We compare and contrast our view to the natural frequency hypothesis as formulated in the commentaries.
The costs of mental time travel
Authors: Brüne Martin , Brüne-Cohrs Ute 
Published: October 2007

AbstractA species like ours, whose life critically depends on the ability to foresee, plan, and shape future events, is vulnerable to dysfunction if any one facet contributing to what Suddendorf & Corballis (S&C) call “mental time travel” (MTT) is affected by disease. Although the authors mention brain pathology as a potential cause of disturbed MTT, they fail to explore psychopathological syndromes as a source to better understand the significance of MTT for normal functioning and adaptive behaviour.
A unique role for the hippocampus in recollecting the past and remembering the future
Authors: Carr Valerie A. , Viskontas Indre V. 
Published: October 2007

AbstractSuddendorf & Corballis (S&C) argue that episodic memory is the most flexible and recently evolved memory system, and point to the reorganization of prefrontal cortex throughout human evolution as the neuroanatomical substrate. Their approach, however, fails to address the unique role that the hippocampus, a primitive brain region, plays in creating and recalling episodic memories, as well as future event construction.
Mental time travel in the rat: Dissociation of recall and familiarity
Authors: Eacott Madeline J. , Easton Alexander 
Published: October 2007

AbstractWe examine and reject the claim that the past-directed aspect of mental time travel (episodic memory) is unique to humans. Recent work in our laboratory with rats has demonstrated behaviours that resemble “remember, know” judgements about past occasions. Similar to human episodic memory, we can also demonstrate a dissociation in the neural basis of recollection and familiarity in nonhumans.
Mental time travel sickness and a Bayesian remedy
Authors: Hegdé Jay 
Published: October 2007

AbstractMental time travel is a principled, but a narrow and computationally limiting, implementation of foresight. Future events can be predicted with sufficient specificity without having to have episodic memory of specific past events. Bayesian estimation theory provides a framework by which one can make predictions about specific future events by combining information about various generic patterns in the past experience.
Past and future, human and nonhuman, semantic/procedural and episodic
Authors: Hurford James R. , Flaherty Molly , Argyropoulos Giorgis 
Published: October 2007

AbstractThe overlap of representations of past and future is not a completely new idea. Suddendorf & Corballis (S&C) usefully discuss the problems of testing the existence of such representations. Our taxonomy of memory differs from theirs, emphasizing the late evolutionary emergence of notions of time in memory.
Characterization of cholera outbreak isolates from Namibia, December 2006 to February 2007
Authors: SMITH A. M. , KEDDY K. H. , De WEE L. 
Published: October 2007

SUMMARYWe report on the first recorded outbreak of cholera in Namibia. From December 2006 to February 2007, more than 250 cases of cholera were reported from the Omusati and Kunene provinces of Namibia. However, only nine bacterial isolates were obtainable for analysis. Isolates were all identified as Vibrio cholerae O1 serotype Inaba biotype El Tor. All isolates were susceptible to ampicillin, augmentin, chloramphenicol, nalidixic acid, ciprofloxacin, tetracycline, kanamycin, imipenem, ceftriaxone and ceftazidime; and they all showed resistance to trimethoprim, sulfamethoxazole and streptomycin. Pulsed-field gel electrophoresis analysis of bacteria incorporating either SfiI or NotI digestion revealed an identical fingerprint pattern for all isolates. These data together with results indicating identical antimicrobial susceptibility profiles for all isolates determined that the outbreak was caused by a single strain of V. cholerae.
Correlation of a 140-year global time signature in cancer mortality birth cohorts with galactic cosmic ray variation
Authors: Juckett David A. 
Published: October 2007

AbstractAn understanding of the cosmic ray modulation of life processes is critical to space exploration, evolution and current medical science. Previous evidence has implicated a role for cosmic rays in US female cancer, involving a possible cross-generational foetal effect. This study explores the global nature of that effect by examining cancer time variations for population cohorts in five countries on three continents. Age–period–cohort analysis was used to separate cohort-related effects from period-related effects, generating time signatures for comparisons among both male and female populations in the United States (US), United Kingdom (UK), Australia (AU), Canada (CA) and New Zealand (NZ). The available cancer mortality data spanned most of the 20th century for US, UK and AU, with shorter periods for CA and NZ. The longest cohort series spanned 1825 to 1965 and exhibited two peaks of higher mortality likelihood approximately 75 years apart in all countries and in both sexes. The constancy of this oscillation on three continents and both hemispheres suggests the presence of a global environmental effect. To explore a possible source for this effect, the birth cohort oscillation is shown to correlate with the variations in background cosmic radiation one generation prior to the birth cohorts. This confirms an earlier study correlating human breast cancer mortality and galactic cosmic rays. A corroborating correlation is also noted between the latitude dependences of cancer incidence in 42 countries and the intensity of background cosmic rays. The role of germ cells as a possible target of this radiation is discussed, emphasizing the amplification that must occur to make this weak radiation relevant to human health. Germ cell timing for this effect has profound implications for evolution, long-distance space travel and the colonization of planets with high background radiation.
Behavioral effects of employer-sponsored retirement plans
Authors: NYCE STEVEN A. 
Published: October 2007

AbstractMany organizations have either already terminated their defined benefit (DB) plans or are thinking about it, in order to offload the financial and regulatory risks these programs pose. But plan sponsors should think carefully about how their decision might affect their workers' commitment and productivity – and ultimately their organization's success.To answer those and other retirement questions, Watson Wyatt set out to learn how DB and defined contribution (DC) plans affect employees' workforce behavior and decisions. Watson Wyatt's Retirement Attitude Survey (WWRAS) found that, while most workers value both types of plans very highly, workers with DB plans generally appreciate their retirement programs significantly more than those with only a DC plan. This was particularly the case for those with a hybrid pension plan. This analysis found that retirement plan generosity and effective communication strongly affect a plan's perceived value to employees. This has important implications for plan sponsors, since greater plan appreciation is strongly linked to employee commitment. In fact, we found that workers covered by a defined benefit plan express a very strong commitment to their current employer, while DC plan coverage has no effect on employee commitment. This is partly owing to a selection effect, whereby firms with DB plans tend to attract more committed workers. However, even after controlling for the selection effect, DB plans exert an independent effect on the likelihood that employees will stay with their employer.
Endogenous pro‐resolving and anti‐inflammatory lipid mediators: a new pharmacologic genus
Authors: Serhan C N , Chiang N 
Published: October 2007

Complete resolution of an acute inflammatory response and its return to homeostasis are essential for healthy tissues. Here, we overview ongoing efforts to characterize cellular and molecular mechanisms that govern the resolution of self‐limited inflammation. Systematic temporal analyses of evolving inflammatory exudates using mediator lipidomics‐informatics, proteomics, and cellular trafficking with murine resolving exudates demonstrate novel endogenous pathways of local‐acting mediators that share both anti‐inflammatory and pro‐resolving properties. In murine systems, resolving‐exudate leukocytes switch their phenotype to actively generate new families of mediators from major omega‐3 fatty acids EPA and DHA termed resolvins and protectins. Recent advances on their biosynthesis and actions are reviewed with a focus on the E‐series resolvins (RvE1, RvE2), D series resolvins (RvD1, RvD2) and the protectins including neuroprotectin D1/protectin D1 (NPD1/PD1) as well as their aspirin‐triggered epimeric forms. Members of each new family demonstrate potent stereo‐specific actions, joining the lipoxins as endogenous local signals that govern resolution and endogenous anti‐inflammation mechanisms. In addition to their origins and roles in resolution biology in the immune system, recent findings indicate that these new mediator families also display potent protective actions in lung, kidney, and eye as well as enhance microbial clearance. Thus, these endogenous agonists of resolution pathways constitute a novel genus of chemical mediators that possess pro‐resolving, anti‐inflammatory, and antifibrotic as well as host‐directed antimicrobial actions. These may be useful in the design of new therapeutics and treatments for diseases with the underlying trait of uncontrolled inflammation and redox organ stress.British Journal of Pharmacology (2008) 153, S200–S215; doi:10.1038/sj.bjp.0707489; published online 29 October 2007
A day in the life of a G protein‐coupled receptor: the contribution to function of G protein‐coupled receptor dimerization
Authors: Milligan G 
Published: October 2007

G protein‐coupled receptors are one of the most actively studied families of proteins. However, despite the ubiquity of protein dimerization and oligomerization as a structural and functional motif in biology, until the last decade they were generally considered as monomeric, non‐interacting polypeptides. For the metabotropic glutamate‐like group of G protein‐coupled receptors, it is now firmly established that they exist and function as dimers or, potentially, even within higher‐order structures. Despite some evidence continuing to support the view that rhodopsin‐like G protein‐coupled receptors are predominantly monomers, many recent studies are consistent with the dimerization/oligomerization of such receptors. Key roles suggested for dimerization of G protein‐coupled receptors include control of protein maturation and cell surface delivery and providing the correct framework for interactions with both hetero‐trimeric G proteins and arrestins to allow signal generation and its termination. As G protein‐coupled receptors are the most targeted group of proteins for the development of therapeutic small molecule medicines, recent indications that hetero‐dimerization between co‐expressed G protein‐coupled receptors may be a common process offers the potential for the development of more selective and tissue restricted medicines. However, many of the key experiments have, so far, been limited to model cell systems. Priorities for the future include the generation of tools and reagents able to identify unequivocally potential G protein‐coupled receptor hetero‐dimers in native tissues and detailed analyses of the influence of hetero‐dimerization on receptor function and pharmacology.British Journal of Pharmacology (2008) 153, S216–S229; doi:10.1038/sj.bjp.0707490; published online 29 October 2007
Antagonism of thromboxane receptors by diclofenac and lumiracoxib
Authors: Selg E , Buccellati C , Andersson M , Rovati G E , Ezinga M , Sala A , Larsson A‐K , Ambrosio E , Låstbom L , Capra V , Dahlén B , Ryrfeldt Å , Folco G C , Dahlén S‐E 
Published: October 2007

Background and purpose:Non‐steroidal anti‐inflammatory drugs (NSAIDs) are analgesic and anti‐inflammatory by virtue of inhibition of the cyclooxygenase (COX) reaction that initiates biosynthesis of prostaglandins. Findings in a pulmonary pharmacology project gave rise to the hypothesis that certain members of the NSAID class might also be antagonists of the thromboxane (TP) receptor.Experimental approach:Functional responses due to activation of the TP receptor were studied in isolated airway and vascular smooth muscle preparations from guinea pigs and rats as well as in human platelets. Receptor binding and activation of the TP receptor was studied in HEK293 cells.Key results:Diclofenac concentration‐dependently and selectively inhibited the contraction responses to TP receptor agonists such as prostaglandin D2and U‐46619 in the tested smooth muscle preparations and the aggregation of human platelets. The competitive antagonism of the TP receptor was confirmed by binding studies and at the level of signal transduction. The selective COX‐2 inhibitor lumiracoxib shared this activity profile, whereas a number of standard NSAIDs and other selective COX‐2 inhibitors did not.Conclusions and implications:Diclofenac and lumiracoxib, in addition to being COX unselective and highly COX‐2 selective inhibitors, respectively, displayed a previously unknown pharmacological activity, namely TP receptor antagonism. Development of COX‐2 selective inhibitors with dual activity as potent TP antagonists may lead to coxibs with improved cardiovascular safety, as the TP receptor mediates cardiovascular effects of thromboxane A2and isoprostanes.British Journal of Pharmacology(2007)152, 1185–1195; doi:10.1038/sj.bjp.0707518; published online 29 October 2007
Beneficial effects of C36, a novel breaker of advanced glycation endproducts cross‐links, on the cardiovascular system of diabetic rats
Authors: Cheng G , Wang L‐L , Long L , Liu H‐Y , Cui H , Qu W‐S , Li S 
Published: October 2007

Background and purpose:Advanced glycation endproducts (AGE) have been implicated in the pathogenesis of diabetic complications, including diabetic cardiovascular dysfunctions. 3‐benzyloxycarbonylmethyl‐4‐methyl‐thiazol‐3‐ium bromide (C36), a novel AGE breaker, was investigated for its beneficial effects on the cardiovascular system of diabetic rats.Experimental approach:The in vitro breaking abilities of C36 on AGE cross‐links formed in vitro and in vivo were assessed. After 4 weeks' treatment with C36, cardiovascular and left ventricular functions in diabetic (streptozotocin–induced) rats were evaluated by haemodynamic studies. Effects of C36 on AGE accumulation, collagen distribution, and fibrosis‐associated gene expression were also investigated by biochemical and morphological methods and reverse transcription‐PCR, respectively.Key results:In vitro, C36 released bovine serum albumin (BSA) from preformed AGE‐BSA‐collagen complexes and decreased the IgG cross‐linked to red blood cell surface (RBC‐IgG). In vivo, C36 treatment of diabetic rats resulted in a significant increase in left ventricular systolic pressure and the maximal rate of left ventricular pressure rise and pressure fall, induction in cardiac output and systemic arterial compliance, decrease of total peripheral resistance, reduction of diabetes‐induced RBC‐IgG content, increase of myocardial and tail tendon collagen solubility, and normalization of collagen type III/I ratio in diabetic rats. In addition, C36 treatment attenuated mRNA levels of diabetes‐induced genes, including receptors for AGE, transforming growth factor β1, connective tissue growth factor, and collagen III.Conclusions and implications:C36 was an effective breaker of AGE cross‐links and had beneficial effects on the cardiovascular system of diabetic rats.British Journal of Pharmacology (2007) 152, 1196–1206; doi:10.1038/sj.bjp.0707533; published online 29 October 2007
Anti‐angiogenic properties of a sulindac analogue
Authors: Pyriochou A , Tsigkos S , Vassilakopoulos T , Cottin T , Zhou Z , Gourzoulidou E , Roussos C , Waldmann H , Giannis A , Papapetropoulos A 
Published: October 2007

Background and purpose:Angiopoietins (Ang) are crucial for new blood vessel formation and exert their effects by acting on the Tie2 receptor. We have recently described a sulindac analogue 2‐((1E,Z)‐1‐benzylidene‐5‐bromo‐2‐methyl‐1H‐inden‐3‐yl)acetic acid; termed C‐18 from now onwards) that inhibits Tie2 receptor activity in kinase assays in vitro. Here, we have assessed the ability of C‐18 to inhibit angiogenesis‐related properties of endothelial cells and tested its selectivity for the Tie2 receptor.Experimental approach:For in vitro experiments human umbilical vein endothelial cells (HUVEC) were used. Proliferation was measured using the MTT assay; migration assays were performed in a modified Boyden chamber and tube‐like structure formation was determined on matrigel. The effects of C‐18 in vivo were evaluated in the chicken chorioallantoic membrane (CAM).Key results:Pre‐treatment of HUVEC with C‐18 blocked Ang‐1‐stimulated migration, but also abolished vascular endothelial cell growth factor (VEGF)‐ and fibroblast growth factor 2‐induced responses. Incubation with C‐18 inhibited serum‐induced proliferation in a concentration‐dependent manner; C‐18 was, however, without effect on Ang‐1‐induced survival. In addition, we observed that C‐18 did not inhibit ligand‐induced receptor phosphorylation of Tie2 or VEGFR2. On the other hand, C‐18 blocked activation of members of the mitogen‐activated protein kinase family and of the Ser/Thr kinase Akt induced by both VEGF and Ang‐1. Furthermore, incubation of CAMs with C‐18 led to a dose‐dependent inhibition of vascular length.Conclusions and implications:C‐18 did not act as a Tie2 inhibitor, as originally thought, but rather inhibited growth factor‐stimulated signalling pathways that regulate endothelial cell migration and potently reduces neovascularization in vivo.British Journal of Pharmacology (2007) 152, 1207–1214; doi:10.1038/sj.bjp.0707534; published online 29 October 2007
Coexistence of hERG current block and disruption of protein trafficking in ketoconazole‐induced long QT syndrome
Authors: Takemasa H , Nagatomo T , Abe H , Kawakami K , Igarashi T , Tsurugi T , Kabashima N , Tamura M , Okazaki M , Delisle B P , January C T , Otsuji Y 
Published: October 2007

Background and purpose:Many drugs associated with acquired long QT syndrome (LQTS) directly block humanether‐a‐go‐go‐related gene (hERG) K+channels. Recently, disrupted trafficking of the hERG channel protein was proposed as a new mechanism underlying LQTS, but whether this defect coexists with the hERG current block remains unclear. This study investigated how ketoconazole, a direct hERG current inhibitor, affects the trafficking of hERG channel protein.Experimental approach:Wild‐type hERG andSCN5A/hNav1.5 Na+channels or the Y652A and F656C mutated forms of the hERG were stably expressed in HEK293 cells. The K+and Na+currents were recorded in these cells by using the whole‐cell patch‐clamp technique (23°C). Protein trafficking of the hERG was evaluated by Western blot analysis and flow cytometry.Key results:Ketoconazole directly blocked the hERG channel current and reduced the amount of hERG channel protein trafficked to the cell surface in a concentration‐dependent manner. Current density of the hERG channels but not of the hNav1.5 channels was reduced after 48 h of incubation with ketoconazole, with preservation of the acute direct effect on hERG current. Mutations in drug‐binding sites (F656C or Y652A) of the hERG channel significantly attenuated the hERG current blockade by ketoconazole, but did not affect the disruption of trafficking.Conclusions and implications:Our findings indicate that ketoconazole might cause acquired LQTS via a direct inhibition of current through the hERG channel and by disrupting hERG protein trafficking within therapeutic concentrations. These findings should be considered when evaluating new drugs.British Journal of Pharmacology(2008)153, 439–447; doi:10.1038/sj.bjp.0707537; published online 29 October 2007
Curcumin inhibits connective tissue growth factor gene expression in activated hepatic stellate cellsin vitroby blocking NF‐κB and ERK signalling
Authors: Chen A , Zheng S 
Published: October 2007

Background and purpose:Gene expression of connective tissue growth factor (CTGF) is induced in activated hepatic stellate cells (HSC), the major effectors in hepatic fibrosis, and production of extracellular matrix (ECM) is consequently increased. We previously reported that curcumin, the yellow pigment in curry, suppressedctgfexpression, leading to decreased production of ECM by HSC. The purpose of this study is to evaluate signal transduction pathways involved in the curcumin suppression ofctgfexpression in HSC.Experimental approaches:Transient transfection assays were performed to evaluate effects of activation of signalling pathways on thectgfpromoter activity. Real‐time PCR and Western blotting analyses were conducted to determine expression of genes.Results:Suppression ofctgfexpression by curcumin was dose‐dependently reversed by lipopolysaccharide (LPS), an NF‐κB activator. LPS increased the abundance of CTGF and type I collagen in HSCin vitro. Activation of NF‐κB by dominant active IκB kinase (IKK), or inhibition of NF‐κB by dominant negative IκBα, caused the stimulation, or suppression of thectgfpromoter activity, respectively. Curcumin suppressed gene expression of Toll‐like receptor‐4, leading to the inhibition of NF‐κB. On the other hand, interruption of ERK signalling by inhibitors or dominant negative ERK, like curcumin, reduced NF‐κB activity and inctgfexpression. In contrast, the stimulation of ERK signalling by constitutively active ERK prevented the inhibitory effects of curcumin.Conclusions and implications:These results demonstrate that the interruption of NF‐κB and ERK signalling by curcumin results in the suppression ofctgfexpression in activated HSCin vitro.British Journal of Pharmacology(2008)153, 557–567; doi:10.1038/sj.bjp.0707542; published online 29 October 2007