bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neuroimaging Support for Discrete Neural Correlates of Basic Emotions: A Voxel-based Meta-analysis
Authors: Vytal Katherine , Hamann Stephan 
Published: November 2009

AbstractWhat is the basic structure of emotional experience and how is it represented in the human brain? One highly influential theory, discrete basic emotions, proposes a limited set of basic emotions such as happiness and fear, which are characterized by unique physiological and neural profiles. Although many studies using diverse methods have linked particular brain structures with specific basic emotions, evidence from individual neuroimaging studies and from neuroimaging meta-analyses has been inconclusive regarding whether basic emotions are associated with both consistent and discriminable regional brain activations. We revisited this question, using activation likelihood estimation (ALE), which allows spatially sensitive, voxelwise statistical comparison of results from multiple studies. In addition, we examined substantially more studies than previous meta-analyses. The ALE meta-analysis yielded results consistent with basic emotion theory. Each of the emotions examined (fear, anger, disgust, sadness, and happiness) was characterized by consistent neural correlates across studies, as defined by reliable correlations with regional brain activations. In addition, the activation patterns associated with each emotion were discrete (discriminable from the other emotions in pairwise contrasts) and overlapped substantially with structure–function correspondences identified using other approaches, providing converging evidence that discrete basic emotions have consistent and discriminable neural correlates. Complementing prior studies that have demonstrated neural correlates for the affective dimensions of arousal and valence, the current meta-analysis results indicate that the key elements of basic emotion views are reflected in neural correlates identified by neuroimaging studies.
Functional Dissociations within the Ventral Object Processing Pathway: Cognitive Modules or a Hierarchical Continuum?
Authors: Cowell Rosemary A. , Bussey Timothy J. , Saksida Lisa M. 
Published: November 2009

Abstract
We examined the organization and function of the ventral object processing pathway. The prevailing theoretical approach in this field holds that the ventral object processing stream has a modular organization, in which visual perception is carried out in posterior regions and visual memory is carried out, independently, in the anterior temporal lobe. In contrast, recent work has argued against this modular framework, favoring instead a continuous, hierarchical account of cognitive processing in these regions. We join the latter group and illustrate our view with simulations from a computational model that extends the perceptual-mnemonic feature-conjunction model of visual discrimination proposed by Bussey and Saksida [Bussey, T. J., & Saksida, L. M. The organization of visual object representations: A connectionist model of effects of lesions in perirhinal cortex. European Journal of Neuroscience, 15, 355–364, 2002]. We use the extended model to revisit early data from Iwai and Mishkin [Iwai, E., & Mishkin, M. Two visual foci in the temporal lobe of monkeys. In N. Yoshii & N. Buchwald (Eds.), Neurophysiological basis of learning and behavior (pp. 1–11). Japan: Osaka University Press, 1968]; this seminal study was interpreted as evidence for the modularity of visual perception and visual memory. The model accounts for a double dissociation in monkeys' visual discrimination performance following lesions to different regions of the ventral visual stream. This double dissociation is frequently cited as evidence for separate systems for perception and memory. However, the model provides a parsimonious, mechanistic, single-system account of the double dissociation data. We propose that the effects of lesions in ventral visual stream on visual discrimination are due to compromised representations within a hierarchical representational continuum rather than impairment in a specific type of learning, memory, or perception. We argue that consideration of the nature of stimulus representations and their processing in cortex is a more fruitful approach than attempting to map cognition onto functional modules.
Minds Made for Sharing: Initiating Joint Attention Recruits Reward-related Neurocircuitry
Authors: Schilbach Leonhard , Wilms Marcus , Eickhoff Simon B. , Romanzetti Sandro , Tepest Ralf , Bente Gary , Shah N. Jon , Fink Gereon R. , Vogeley Kai 
Published: November 2009

Abstract
The ability and motivation to share attention is a unique aspect of human cognition. Despite its significance, the neural basis remains elusive. To investigate the neural correlates of joint attention, we developed a novel, interactive research paradigm in which participants' gaze behavior—as measured by an eye tracking device—was used to contingently control the gaze of a computer-animated character. Instructed that the character on screen was controlled by a real person outside the scanner, 21 participants interacted with the virtual other while undergoing fMRI. Experimental variations focused on leading versus following the gaze of the character when fixating one of three objects also shown on the screen. In concordance with our hypotheses, results demonstrate, firstly, that following someone else's gaze to engage in joint attention resulted in activation of anterior portion of medial prefrontal cortex (MPFC) known to be involved in the supramodal coordination of perceptual and cognitive processes. Secondly, directing someone else's gaze toward an object activated the ventral striatum which—in light of ratings obtained from participants—appears to underlie the hedonic aspects of sharing attention. The data, therefore, support the idea that other-initiated joint attention relies upon recruitment of MPFC previously related to the “meeting of minds.” In contrast, self-initiated joint attention leads to a differential increase of neural activity in reward-related brain areas, which might contribute to the uniquely human motivation to engage in the sharing of experiences.
N400-like Potentials and Reaction Times Index Semantic Relations between Highly Repeated Individual Words
Authors: Renoult Louis , Debruille J. Bruno 
Published: November 2009

AbstractThe N400 ERP is an electrophysiological index of semantic processing. Its amplitude varies with the semantic category of words, their concreteness, or whether their meaning matches that of a preceding context. The results of a number of studies suggest that these effects could be markedly reduced or suppressed for stimuli that are repeated. Nevertheless, we have recently shown that significant effects of semantic matching and category could be obtained on N400-like potentials elicited by massively repeated target words in a prime–target semantic categorization task. If such effects could be obtained when primes also are repeated, it would then be possible to study the semantic associations between individual words. The present study thus aimed to test this hypothesis while (1) controlling for a potential contribution of physical matching to the processing of repeated targets and (2) testing if the N400-like effects obtained in these conditions are modulated by task instruction, as are classic N400 effects. Two category words were used as primes and two exemplars as targets. In one block of trials, subjects had to respond according to the semantic relation between prime and target (semantic instruction) and, in another block, they had to report changes in letter case (physical instruction). Results showed that the amplitude of the N400-like ERP obtained was modulated by semantic matching and category but not by letter case. The effect of semantic matching was observed only in the semantic instruction block. Interestingly, the effect of category was not modulated by task instruction. An independent component analysis showed that the component that made the greatest contribution to the effect of semantic matching in the time window of the N400-like potential had a scalp distribution similar to that reported for the N400 and was best fit as a bilateral generator in the superior temporal gyrus. The use of repetition could thus allow, at least in explicit semantic tasks, a drastic simplification of N400 protocols. Highly repeated individual words could be used to study semantic relations between individual concepts.
Classic Balint Group Work and the Thinking of W.R. Bion: How Balint Work Increases the Ability to Think One’s Own Thoughts
Authors: Rüth Ulrich 
Published: November 2009

Some of W.R. Bion’s specific ideas can further the understanding of the classic Balint group technique. The group leader supports a ‘container-contained’ process, preventing the group from attacking or criticizing the presenter. ‘Projective identification’ helps the group to understand what has been presented. Meaningless impressions, feelings, emotions, and simple facts are transferred to the group, such as still unthinkable bizarre ‘beta-elements’ to be transformed by the ‘alpha-function’ to the now thinkable ‘alpha-elements’. Abstaining from the group process, the presenter is protected from re-projections of feelings and emotions. The Balint group technique makes sense to promote the ‘digestion’ of bizarre beta-element-like aspects into alpha-elements, enabling the presenter to ‘think his or her own thoughts’ instead of projected one, giving the chance to change into a response model instead of a reacting one. ‘Mental growth’ occurs when feelings and thoughts can be tolerated at a higher level.
The Use of Substitutes—Continuity and the Group-as-a-Whole
Authors: Nielsen Jan , Luggin Randi , Thygesen Bente , Aagaard Søren 
Published: November 2009

This article is based on experiences in two group analytic therapy groups during periods where substitutes were used in the absence of the regular therapists. The article’s aim is—by means of examples—to illustrate and discuss how this was experienced by group members, substitutes and therapists. Considering the group-as-a-whole as the primary therapeutic medium, the article will illustrate how the groups used their substitutes and their regular therapists, how they experienced their roles and functions as well as their symbolic significance. The group-as-a-whole is also considered as the carrier of continuity, i.e. the self-sustaining power of the group and the limits of this is illustrated and discussed in connection with planned versus unplanned substitute periods, showing the importance of preparation when the therapist has to be away and a substitute is used.
Congenital erythropoietic porphyria: a novel uroporphyrinogen III synthase branchpoint mutation reveals underlying wild-type alternatively spliced transcripts
Authors: Bishop David F. , Schneider-Yin Xiaoye , Clavero Sonia , Yoo Han-Wook , Minder Elisabeth I. , Desnick Robert J. 
Published: November 2009

Abstract
Splicing mutations account for approximately 10% of lesions causing genetic diseases, but few branchpoint sequence (BPS) lesions have been reported. In 3 families with autosomal recessive congenital erythropoietic porphyria (CEP) resulting from uroporphyrinogen III synthase (URO-synthase) deficiency, sequencing the promoter, all 10 exons and the intron/exon boundaries did not detect a mutation. Northern analyses of lymphoblast mRNAs from 2 patients and reverse-transcribed polymerase chain reaction (RT-PCR) of lymphoblast mRNAs from all 3 patients revealed multiple longer transcripts involving intron 9 and low levels of wild-type message. Sequencing intron 9 RT-PCR products and genomic DNA in each case revealed homozygosity for a novel BPS mutation (c.661-31T→G) and alternatively spliced transcripts containing 81, 246, 358, and 523 nucleotides from intron 9. RT-PCR revealed aberrant transcripts in both wild-type and CEP lymphoblasts, whereas BPS mutation reduced the wild-type transcript and enzyme activity in CEP lymphoblasts to approximately 10% and 15% of normal, respectively. Although the +81-nucleotide alternative transcript was in-frame, it only contributed approximately 0.2% of the lymphoblast URO-synthase activity. Thus, the BPS mutation markedly reduced the wild-type transcript and enzyme activity, thereby causing the disease. This is the first BPS mutation in the last intron, presumably accounting for the observed 100% intron retention without exon skipping.
Interleukin-24 inhibits the plasma cell differentiation program in human germinal center B cells
Authors: Maarof Ghyath , Bouchet-Delbos Laurence , Gary-Gouy Hélène , Durand-Gasselin Ingrid , Krzysiek Roman , Dalloul Ali 
Published: November 2009

Abstract
Complex molecular mechanisms control B-cell fate to become a memory or a plasma cell. Interleukin-24 (IL-24) is a class II family cytokine of poorly understood immune function that regulates the cell cycle. We previously observed that IL-24 is strongly expressed in leukemic memory-type B cells. Here we show that IL-24 is also expressed in human follicular B cells; it is more abundant in CD27+ memory B cells and CD5-expressing B cells, whereas it is low to undetectable in centroblasts and plasma cells. Addition of IL-24 to B cells, cultured in conditions shown to promote plasma cell differentiation, strongly inhibited plasma cell generation and immunoglobulin G (IgG) production. By contrast, IL-24 siRNA increased terminal differentiation of B cells into plasma cells. IL-24 is optimally induced by BCR triggering and CD40 engagement; IL-24 increased CD40-induced B-cell proliferation and modulated the transcription of key factors involved in plasma cell differentiation. It also inhibited activation-induced tyrosine phosphorylation of signal transducer and activator of transcription-3 (STAT-3), and inhibited the transcription of IL-10. Taken together, our results indicate that IL-24 is a novel cytokine involved in T-dependent antigen (Ag)–driven B-cell differentiation and suggest its physiologic role in favoring germinal center B-cell maturation in memory B cells at the expense of plasma cells.
High-mobility group protein HMGB2 regulates human erythroid differentiation through trans-activation of GFI1B transcription
Authors: Laurent Benoît , Randrianarison-Huetz Voahangy , Maréchal Vincent , Mayeux Patrick , Dusanter-Fourt Isabella , Duménil Dominique 
Published: November 2009

Abstract
Gfi-1B is a transcriptional repressor that is crucial for erythroid differentiation: inactivation of the GFI1B gene in mice leads to embryonic death due to failure to produce differentiated red cells. Accordingly, GFI1B expression is tightly regulated during erythropoiesis, but the mechanisms involved in such regulation remain partially understood. We here identify HMGB2, a high-mobility group HMG protein, as a key regulator of GFI1B transcription. HMGB2 binds to the GFI1B promoter in vivo and up-regulates its trans-activation most likely by enhancing the binding of Oct-1 and, to a lesser extent, of GATA-1 and NF-Y to the GFI1B promoter. HMGB2 expression increases during erythroid differentiation concomitantly to the increase of GfI1B transcription. Importantly, knockdown of HMGB2 in immature hematopoietic progenitor cells leads to decreased Gfi-1B expression and impairs their erythroid differentiation. We propose that HMGB2 potentiates GATA-1–dependent transcription of GFI1B by Oct-1 and thereby controls erythroid differentiation.
KSHV-induced notch components render endothelial and mural cell characteristics and cell survival
Authors: Liu Ren , Li Xiuqing , Tulpule Anil , Zhou Yue , Scehnet Jeffrey S. , Zhang Shaobing , Lee Jong-Soo , Chaudhary Preet M. , Jung Jae , Gill Parkash S. 
Published: November 2009

AbstractKaposi sarcoma–associated herpesvirus (KSHV) infection is essential to the development of Kaposi sarcoma (KS). Notch signaling is also known to play a pivotal role in KS cell survival and lytic phase entrance of KSHV. In the current study, we sought to determine whether KSHV regulates Notch components. KSHV-infected lymphatic endothelial cells showed induction of receptors Notch3 and Notch4, Notch ligands Dll4 and Jagged1, and activated Notch receptors in contrast to uninfected lymphatic endothelial cells. In addition, KSHV induced the expression of endothelial precursor cell marker (CD133) and mural cell markers (calponin, desmin, and smooth muscle alpha actin), suggesting dedifferentiation and trans-differentiation. Overexpression of latency proteins (LANA, vFLIP) and lytic phase proteins (RTA, vGPCR, viral interleukin-6) further supported the direct regulatory capacity of KSHV viral proteins to induce Notch receptors (Notch2, Notch3), ligands (Dll1, Dll4, Jagged1), downstream targets (Hey, Hes), and endothelial precursor CD133. Targeting Notch pathway with γ-secretase inhibitor and a decoy protein in the form of soluble Dll4 inhibited growth of KSHV-transformed endothelial cell line. Soluble Dll4 was also highly active in vivo against KS tumor xenograft. It inhibited tumor cell growth, induced tumor cell death, and reduced vessel perfusion. Soluble Dll4 is thus a candidate for clinical investigation.
Rho GTPases in hematopoiesis and hemopathies
Authors: Mulloy James C. , Cancelas Jose A. , Filippi Marie-Dominique , Kalfa Theodosia A. , Guo Fukun , Zheng Yi 
Published: November 2009

AbstractRho family GTPases are intracellular signaling proteins regulating multiple pathways involved in cell actomyosin organization, adhesion, and proliferation. Our knowledge of their cellular functions comes mostly from previous biochemical studies that used mutant overexpression approaches in various clonal cell lines. Recent progress in understanding Rho GTPase functions in blood cell development and regulation by gene targeting of individual Rho GTPases in mice has allowed a genetic understanding of their physiologic roles in hematopoietic progenitors and mature lineages. In particular, mouse gene–targeting studies have provided convincing evidence that individual members of the Rho GTPase family are essential regulators of cell type–specific functions and stimuli-specific pathways in regulating hematopoietic stem cell interaction with bone marrow niche, erythropoiesis, and red blood cell actin dynamics, phagocyte migration and killing, and T- and B-cell maturation. In addition, deregulation of Rho GTPase family members has been associated with multiple human hematologic diseases such as neutrophil dysfunction, leukemia, and Fanconi anemia, raising the possibility that Rho GTPases and downstream signaling pathways are of therapeutic value. In this review we discuss recent genetic studies of Rho GTPases in hematopoiesis and several blood lineages and the implications of Rho GTPase signaling in hematologic malignancies, immune pathology. and anemia.
Expression of terminal α2-6–linked sialic acid on von Willebrand factor specifically enhances proteolysis by ADAMTS13
Authors: McGrath Rachel T. , McKinnon Thomas A. J. , Byrne Barry , O'Kennedy Richard , Terraube Virginie , McRae Emily , Preston Roger J. S. , Laffan Mike A. , O'Donnell James S. 
Published: November 2009

Abstractvon Willebrand factor (VWF) multimeric composition is regulated in plasma by ADAMTS13. VWF deglycosylation enhances proteolysis by ADAMTS13. In this study, the role of terminal sialic acid residues on VWF glycans in mediating proteolysis by ADAMTS13 was investigated. Quantification and distribution of VWF sialylation was examined by sequential digestion and high-performance liquid chromatography analysis. Total sialic acid expression on VWF was 167nmol/mg, of which the majority (80.1%) was present on N-linked glycan chains. Enzymatic desialylation of VWF by α2-3,6,8,9 neuraminidase (Neu-VWF) markedly impaired ADAMTS13-mediated VWF proteolysis. Neu-VWF collagen binding activity was reduced to 50% (± 14%) by ADAMTS13, compared with 11% (± 7%) for untreated VWF. Despite this, Neu-VWF exhibited increased susceptibility to other proteases, including trypsin, chymotrypsin, and cathepsin B. VWF expressing different blood groups exhibit altered ADAMTS13 proteolysis rates (O ≥ B > A ≥ AB). However, ABO blood group regulation of ADAMTS13 proteolysis was ablated on VWF desialylation, as both Neu-O-VWF and Neu-AB-VWF were cleaved by ADAMTS13 at identical rates. These novel data show that sialic acid protects VWF against proteolysis by serine and cysteine proteases but specifically enhances susceptibility to ADAMTS13 proteolysis. Quantitative variation in VWF sialylation therefore represents a key determinant of VWF multimeric composition and, as such, may be of pathophysiologic significance.
Attenuation by dextromethorphan on the higher liability to morphine-induced reward, caused by prenatal exposure of morphine in rat offspring
Authors: Wu Ling-Yi , Chen Jain-Fang , Tao Pao-Luh , Huang Eagle Yi-Kung 
Published: November 2009

AbstractCo-administration of dextromethorphan (DM) with morphine during pregnancy and throughout lactation has been found to reduce morphine physical dependence and tolerance in rat offspring. No evidence was presented, however, for the effect of DM co-administered with morphine during pregnancy on morphine-induced reward and behavioral sensitization (possibly related to the potential to induce morphine addiction) in morphine-exposed offspring. Conditioned place preference and locomotor activity tests revealed that the p60 male offspring of chronic morphine-treated female rats were more vulnerable to morphine-induced reward and behavioral sensitization. The administration of a low dose of morphine (1 mg/kg, i.p.) in these male offspring also increased the dopamine and serotonin turnover rates in the nucleus accumbens, which implied that they were more sensitive to morphine. Co-administration of DM with morphine in the dams prevented this adverse effect of morphine in the offspring rats. Thus, DM may possibly have a great potential in the prevention of higher vulnerability to psychological dependence of morphine in the offspring of morphine-addicted mothers.
Colorectal cancer cell-derived microvesicles are enriched in cell cycle-related mRNAs that promote proliferation of endothelial cells
Authors: Hong Bok Sil , Cho Ji-Hoon , Kim Hyunjung , Choi Eun-Jeong , Rho Sangchul , Kim Jongmin , Kim Ji Hyun , Choi Dong-Sic , Kim Yoon-Keun , Hwang Daehee , Gho Yong Song 
Published: November 2009

Abstract

Background
Various cancer cells, including those of colorectal cancer (CRC), release microvesicles (exosomes) into surrounding tissues and peripheral circulation. These microvesicles can mediate communication between cells and affect various tumor-related processes in their target cells.

Results
We present potential roles of CRC cell-derived microvesicles in tumor progression via a global comparative microvesicular and cellular transcriptomic analysis of human SW480 CRC cells. We first identified 11,327 microvesicular mRNAs involved in tumorigenesis-related processes that reflect the physiology of donor CRC cells. We then found 241 mRNAs enriched in the microvesicles above donor cell levels, of which 27 were involved in cell cycle-related processes. Network analysis revealed that most of the cell cycle-related microvesicle-enriched mRNAs were associated with M-phase activities. The integration of two mRNA datasets showed that these M-phase-related mRNAs were differentially regulated across CRC patients, suggesting their potential roles in tumor progression. Finally, we experimentally verified the network-driven hypothesis by showing a significant increase in proliferation of endothelial cells treated with the microvesicles.

Conclusion
Our study demonstrates that CRC cell-derived microvesicles are enriched in cell cycle-related mRNAs that promote proliferation of endothelial cells, suggesting that microvesicles of cancer cells can be involved in tumor growth and metastasis by facilitating angiogenesis-related processes. This information will help elucidate the pathophysiological functions of tumor-derived microvesicles, and aid in the development of cancer diagnostics, including colorectal cancer.