bluuebunny/crossref_metadata_2025_split huggingface dataset:
Growth and elongation within and along the axon
Authors: Lamoureux Phillip , Heidemann Steven R. , Martzke Nathan R. , Miller Kyle E. 
Published: November 2009

AbstractMechanical tension is a particularly effective stimulus for axonal elongation, but little is known about how it leads to the formation of new axon. To better understand this process, we examined the movement of axonal branch points, beads bound to the axon, and docked mitochondria while monitoring axonal width. We found these markers moved in a pattern that suggests elongation occurs by viscoelastic stretching and volume addition along the axon. To test the coupling between “lengthening” and “growth,” we measured axonal width while forcing axons to grow and then pause by controlling the tension applied to the growth cone or to the cell body. We found axons thinned during high rates of elongation and thickened when the growth cones were stationary. These findings suggest that forces cause lengthening because they stretch the axon and that growth occurs, in a loosely coupled step, by volume addition along the axon. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2010
Prenatal stress causes dendritic atrophy of pyramidal neurons in hippocampal CA3 region by glutamate in offspring rats
Authors: Jia Ning , Yang Kun , Sun Qinru , Cai Qing , Li Hui , Cheng Daxin , Fan Xiaoli , Zhu Zhongliang 
Published: November 2009

AbstractA substantial number of human epidemiological data, as well as experimental studies, suggest that adverse maternal stress during gestation is involved in abnormal behavior, mental, and cognition disorder in offspring. To explore the effect of prenatal stress (PS) on hippocampal neurons, in this study, we observed the dendritic field of pyramidal neurons in hippocampal CA3, examined the concentration of glutamate (Glu), and detected the expression of synaptotagmin‐1 (Syt‐1) and N‐methyl‐D‐aspartate receptor 1 (NR1) in hippocampus of juvenile female offspring rats. Pregnant rats were divided into two groups: control group (CON) and PS group. Female offspring rats used were 30‐day old. The total length of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly shorter in PS than that in CON (p < 0.01). The number of branch points of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly less in PS (p < 0.01). PS offspring had a higher concentration of hippocampal Glu compared with CON (p < 0.05). PS offspring displayed increased expression of Syt‐1 and decreased NR1 in hippocampus compared with CON (p < 0.001 and p < 0.01, respectively). The expression of NR1 in different hippocampus subfields of offspring was significantly decreased in PS than that in CON (p < 0.05‐0.01). This study shows that PS increases the Glu in hippocampus and causes apical dendritic atrophy of pyramidal neurons of hippocampal CA3 in offspring rats. The decline of NR1 in hippocampus may be an adaptive response to the increased Glu. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2010
Age differences in genetic and environmental influences on weight and shape concerns
Authors: Klump Kelly L. , Burt S. Alexandra , Spanos Alexia , McGue Matt , Iacono William G. , Wade Tracey D. 
Published: November 2009

AbstractObjectivePrevious research has shown important developmental shifts ingenetic and environmental influences for disordered eating. However, little research has examined age differences for weight/shape concerns, two key components of eating disorders. The goal of this study was to investigate these age differences in preadolescent, adolescent, young adult, and mid‐adult twins.MethodParticipants included 2,618 female twins (ages of 10–41 years) from three large twin registries. Shape and weight concerns were assessed with the Eating Disorders Examination Questionnaire.ResultsGenetic influences were modest in preadolescent twins, but significant from early‐adolescence through middle adulthood. Shared environmental factors showed the opposite pattern, with the largest shared environmental contributions occurring in the youngest age group. Nonshared environmental effects remained relatively constant across age.DiscussionFindings highlight the importance of age differences in genetic and environmental influences. Possible mechanisms include gene x environment interactions and biological changes associated with key developmental stages. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2010; 43:679–688
Recurrent acute hepatic dysfunction in severe anorexia nervosa
Authors: Dowman Joanna , Arulraj Ramakrishnan , Chesner Ian 
Published: November 2009

AbstractAnorexia nervosa (AN) is an eating disorder predominantly affecting young women. Abnormal liver function tests (LFT's) resulting from AN is well‐described but to date few cases of dramatic rises in liver enzymes have been described. We report a 32‐year‐old women with severe anorexia having dramatic rise in LFT's with liver failure during extremely poor nutritional status. Acute rise in liver enzymes observed on several occasions in this patient resulted from ischaemic hepatitis secondary to liver hypoperfusion. Clinicians caring for patients with severe AN should monitor haemodynamic parameters with the knowledge that acute liver failure can be a consequence of sudden liver hypoperfusion. Therapeutic intervention comprising volume support with gradual nutritional support results in normalization of LFT's. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2010; 43:770–772
Differences in coping across stages of recovery from an eating disorder
Authors: Fitzsimmons Ellen E. , Bardone‐Cone Anna M. 
Published: November 2009

AbstractObjectiveThis study examined the relation between coping skills and eating disorder recovery by comparing these skills across healthy controls, fully recovered, partially recovered, and active eating disorder cases. Full recovery was defined using physical, behavioral, and psychological components.MethodIndividuals formerly seen for an eating disorder at a Midwestern clinic were categorized as having an active eating disorder (n= 53), as partially recovered (n= 15), or as fully recovered (n= 20). The coping skills of these groups were compared to each other and to 67 healthy controls.ResultsHealthy controls and fully recovered individuals utilized similarly high levels of task‐ and avoidance‐oriented coping and similarly low levels of emotion‐oriented coping. Partially recovered individuals looked more similar to those with an active eating disorder.DiscussionResults provide support for a comprehensive definition of eating disorder recovery, of which healthy coping may be an integral component, and for the re‐evaluation of the notion of “maladaptive” coping. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2010; 43:689–693
PKC‐α controls MYD88‐dependent TLR/IL‐1R signaling and cytokine production in mouse and human dendritic cells
Authors: Langlet Christelle , Springael Cécile , Johnson Jolyn , Thomas Séverine , Flamand Véronique , Leitges Michael , Goldman Michel , Aksoy Ezra , Willems Fabienne 
Published: November 2009

AbstractConventional PKC (cPKC)‐α regulates TRIF‐dependent IFN response factor 3 (IRF3)‐mediated gene transcription, but its role in MyD88‐dependent TLR signaling remains unknown. Herein, we demonstrate that PKC‐α is induced by several MyD88‐dependent TLR/IL‐1R ligands and regulates cytokine expression in human and murine DC. First, inhibition of cPKC activity in human DC by cPKC‐specific inhibitors, Gö6976 or HBDDe, downregulated the production of classical inflammatory/immunomodulatory cytokines induced by TLR2, TLR5 or IL‐1R but not by TLR3 stimulation. Similarly, dominant negative PKC‐α repressed Pam3CSK4 induced NF‐κB‐ and AP‐1‐driven promoter activities in TLR2‐expressing human embryonic kidney 293 T cells. Dominant negative PKC‐α inhibited NF‐κB reporter activity mediated by overexpression of MyD88 but not TRIF. Unexpectedly, BM‐derived DC from PKC‐α−/− mice exhibited decreased TNF‐α and IL‐12p40 production induced by both MyD88‐ and TRIF‐dependent ligands. Furthermore, PKC‐α is coupled to TLR2 signaling proximal to MyD88 since MAPK and IκB kinase‐α/β phosphorylations and IκBα degradation were inhibited in PKC‐α−/− BM‐derived DC. Finally, co‐immunoprecipitation assays revealed that PKC‐α physically interacts with Pam3CSK4 activated TLR2 in WT but not in MyD88−/− DC. Collectively this study identifies a species‐specific role of PKC‐α as a key component that controls MyD88‐dependent cytokine gene expression in human and mouse but differentially regulates production of TRIF‐dependent cytokines.
c‐Rel phenocopies PKCθ but not Bcl‐10 in regulating CD8+ T‐cell activation versus tolerance
Authors: Deenick Elissa K. , Po Leslie , Chapatte Laurence , Murakami Kiichi , Lu Yong‐Chen , Elford Alisha R. , Saibil Samuel D. , Ruland Jürgen , Gerondakis Steve , Mak Tak W. , Ohashi Pamela S. 
Published: November 2009

AbstractElucidating the signaling events that promote T‐cell tolerance versus activation provides important insights for manipulating immunity in vivo. Previous studies have suggested that the absence of PKCθ results in the induction of anergy and that the balance between the induction of the transcription factors NFAT, AP1 and NF‐κB plays a key role in determining whether T‐cell anergy or activation is induced. Here, we examine whether Bcl‐10 and specific family members of NF‐κB act downstream of PKCθ to alter CD8+ T‐cell activation and/or anergy. We showed that T cells from mice deficient in c‐Rel but not NF‐κB1 (p50) have increased susceptibility to the induction of anergy, similar to T cells from PKCθ‐deficient mice. Surprisingly T cells from Bcl‐10‐deficient mice showed a strikingly different phenotype to the PKCθ‐deficient T cells, with a severe block in TCR‐mediated activation. Furthermore, we have also shown that survival signals downstream of NF‐κB, are uncoupled from signals that mediate T‐cell anergy. These results suggest that c‐Rel plays a critical role downstream of PKCθ in controlling CD8+ T‐cell anergy induction.
Human rhinoviruses induce IL‐35‐producing Treg via induction of B7‐H1 (CD274) and sialoadhesin (CD169) on DC
Authors: Seyerl Maria , Kirchberger Stefanie , Majdic Otto , Seipelt Joachim , Jindra Christoph , Schrauf Catharina , Stöckl Johannes 
Published: November 2009

AbstractIL‐35 is a heterodimer of EBV‐induced gene 3 and of the p35 subunit of IL‐12, and recently identified as an inhibitory cytokine produced by natural Treg in mice, but not in humans. Here we demonstrate that DC activated by human rhinoviruses (R‐DC) induce IL‐35 production and release, as well as a suppressor function in CD4+ and CD8+ T cells derived from human peripheral blood but not in naïve T cells from cord blood. The induction of IL‐35‐producing T cells by R‐DC was FOXP3‐independent, but blocking of B7‐H1 (CD274) and sialoadhesin (CD169) on R‐DC with mAb against both receptors prevented the induction of IL‐35. Thus, the combinatorial signal delivered by R‐DC to T cells via B7‐H1 and sialoadhesin is crucial for the induction of human IL‐35+ Treg. These results demonstrate a novel pathway and its components for the induction of immune‐inhibitory T cells.
The role of sex hormones in the development of Th2 immunity in a gender‐biased model of Trichuris muris infection
Authors: Hepworth Matthew R. , Hardman Matthew J. , Grencis Richard K. 
Published: November 2009

AbstractTrichuris muris infection is an ideal model for defining T‐cell‐driven immunity, and also provides essential insights that may impact on potential helminth therapies currently in development. Conflicting host variables determine the efficiency of such treatments and we have identified host‐derived sex steroid hormones as key factors in the development of immunity. The female‐associated hormone 17‐β estradiol (E2) significantly enhanced the generation of a Th2 response in vitro; however, this stimulatory effect was found to be dispensable for the generation of immunity to Trichuris in the gender‐biased IL‐4KO mouse model. In contrast, the male‐associated hormone dihydrotestosterone significantly inhibited the T‐cell stimulatory capacity of DC and directly suppressed the immune response of male IL‐4KO mice, with worm expulsion restored following castration. This finding was associated with dramatically reduced IL‐18 mRNA expression suggesting androgens may act via this cytokine to suppress Th2 immunity to Trichuris. This study has critical implications for the development and efficacy of potential helminth therapeutics and identifies host gender – specifically sex hormones – as important factors in the development of Th2 immunity in susceptible and immunocompromised mice.
Apoptotic lymphocytes treated with IgG from Trypanosoma cruzi infection increase TNF‐α secretion and reduce parasite replication in macrophages
Authors: Montalvão Fabricio , Almeida Geisy M. , Silva Elisabeth M. , Borges Valeria M. , Vasconcellos Rita , Takiya Christina M. , Lopes Marcela F. , Nunes Marise P. , DosReis George A. 
Published: November 2009

AbstractPhagocytic removal of apoptotic lymphocytes exacerbates replication of Trypanosoma cruzi in macrophages. We investigated the presence of Ab against apoptotic lymphocytes in T. cruzi infection and the role of these Ab in parasite replication. Both control and chagasic serum contained IgG Ab that opsonized apoptotic lymphocytes. Treatment of apoptotic lymphocytes with purified IgG from chagasic, but not control serum, reduced T. cruzi replication in macrophages. The protective effect of chagasic IgG depended on Fcγ receptors, as demonstrated by the requirement for the intact Fc portion of IgG, and the effect could be abrogated by treating macrophages with an anti‐CD16/CD32 Fab fragment. Chagasic IgG displayed increased reactivity against a subset of apoptotic cell Ag, as measured by flow cytometry and immunoblot analyses. Apoptotic lymphocytes treated with chagasic IgG, but not control IgG, increased production of TNF‐α, while decreasing production of TGF‐β1 by infected macrophages. Increased control of parasite replication required TNF‐α production. Previous immunization with apoptotic cells or injection of apoptotic cells opsonized with chagasic IgG reduced parasitemia in infected mice. These results indicate that Ab raised against apoptotic cells could play a protective role in control of T. cruzi replication by macrophages.
IL‐33 receptor (T1/ST2) signalling is necessary to prevent the development of encephalitis in mice infected with Toxoplasma gondii
Authors: Jones Leigh A. , Roberts Fiona , Nickdel Mohammad B. , Brombacher Frank , McKenzie Andrew N. J. , Henriquez Fiona L. , Alexander James , Roberts Craig W. 
Published: November 2009

AbstractT1/ST2 is an immunoregulatory protein of the IL‐1 receptor family that has recently been reported as being a component of the IL‐33 receptor. IL‐33 is a newly described cytokine known to amplify the Th2 response and reduce production of Th1 cytokines. The function of T1/ST2 during Toxoplasma gondii infection is as yet undescribed. Given the requirement of a balanced type 1/type 2 response for effective control of parasite number and immunopathology, it is likely that T1/ST2 may play a part in aiding this process. Accordingly, we have shown that T1/ST2 mRNA transcripts are upregulated in the brains of mice infected with T. gondii and that mice deficient in T1/ST2 demonstrated increased susceptibility to infection with T. gondii that correlated with increased pathology and greater parasite burden in the brains. Real‐time PCR analysis of cerebral cytokine levels revealed increased mRNA levels of iNOS, IFN‐γ and TNF‐α in infected T1/ST2−/− mice. These effects were independent of changes in IL‐10 production. This study provides the first evidence of a specific role for IL‐33 receptor signalling in the brain as well as highlighting the requirement of this mechanism in limiting infection with an intracellular parasite.
IL‐7 is superior to IL‐2 for ex vivo expansion of tumour‐specific CD4+ T cells
Authors: Caserta Stefano , Alessi Patrizia , Basso Veronica , Mondino Anna 
Published: November 2009

AbstractIt is well established that tumours hinder both natural and vaccine‐induced tumour‐specific CD4+ T‐cell responses. Adoptive T‐cell therapy has the potential to circumvent functional tolerance and enhance anti‐tumour protective responses. While protocols suitable for the expansion of cytotoxic CD8+ T cells are currently available, data on tumour‐specific CD4+ T cells remain scarce. We report here that CD4+ T cells sensitized to tumour‐associated Ag in vivo, proliferate in vitro in response to IL‐7 without the need for exogenous Ag stimulation and accumulate several folds while preserving a memory‐like phenotype. Both cell proliferation and survival accounts for the outgrowth of tumour‐sensitized T cells among other memory and naive lymphocytes following exposure to IL‐7. Also IL‐2, previously used to expand anti‐tumour CTL, promotes tumour‐specific CD4+ T‐cell accumulation. However, IL‐7 is superior to IL‐2 at preserving lymphocyte viability, in vitro and in vivo, maintaining those properties, that are required by helper CD4+ T cells to confer therapeutic efficacy upon transplantation in tumour‐bearing hosts. Together our data support a unique role for IL‐7 in retrieving memory‐like CD4+ T cells suitable for adoptive T‐cell therapy.
Specific CD8+ T‐lymphocytes control dissemination of measles virus
Authors: de Vries Rory D. , Yüksel Selma , Osterhaus Albert D. M. E. , de Swart Rik L. 
Published: November 2009

AbstractMeasles continues to be an important cause of childhood mortality in developing countries. Measles virus (MV) is lymphotropic and infects high percentages of B‐ and T‐lymphocytes in lymphoid tissues. Cellular immunity is considered crucial for viral clearance; however, MV‐specific T‐lymphocytes generated during primary infection also constitute a potential target for MV infection. We therefore aimed to identify T‐lymphocyte subsets that can clear MV infection without becoming infected. To this end, we infected human EBV transformed B‐lymphoblastic cell lines (B‐LCL) with a recombinant MV strain expressing enhanced GFP, and co‐cultured these with non‐infected B‐LCL resulting in rapid viral spread. MV‐specific CD8+ T‐cell clones efficiently suppressed MV dissemination in autologous and HLA‐matched, but not in HLA‐mismatched B‐LCL. In contrast, CD4+ T‐cell clones could not control MV dissemination but became a target for MV infection themselves. Furthermore, PBMC collected 6–9 months after acute measles and stimulated with autologous MV‐infected B‐LCL also efficiently suppressed MV dissemination; this was mediated by the fraction containing CD8+ T‐lymphocytes. In conclusion, we have developed a powerful tool to study cellular immunity against measles, and demonstrate that control of MV dissemination is mediated by virus‐specific CD8+ rather than by CD4+ T‐lymphocytes.
Experimental cerebral malaria progresses independently of the Nlrp3 inflammasome
Authors: Reimer Thornik , Shaw Michael H. , Franchi Luigi , Coban Cevayir , Ishii Ken J. , Akira Shizuo , Horii Toshihiro , Rodriguez Ana , Núñez Gabriel 
Published: November 2009

AbstractCerebral malaria is the most severe complication of Plasmodium falciparum infection in humans and the pathogenesis is still unclear. Using the P. berghei ANKA infection model of mice, we investigated a potential involvement of Nlrp3 and the inflammasome in the pathogenesis of cerebral malaria. Nlrp3 mRNA expression was upregulated in brain endothelial cells after exposure to P. berghei ANKA. Although β‐hematin, a synthetic compound of the parasites heme polymer hemozoin, induced the release of IL‐1β in macrophages through Nlrp3, we did not obtain evidence for a role of IL‐1β in vivo. Nlrp3 knock‐out mice displayed a delayed onset of cerebral malaria; however, mice deficient in caspase‐1, the adaptor protein ASC or the IL‐1 receptor succumbed as WT mice. These results indicate that the role of Nlrp3 in experimental cerebral malaria is independent of the inflammasome and the IL‐1 receptor pathway.
The Extension of the Solid‐Angle Concept to Bidentate Ligands
Authors: Niksch Tobias , Görls Helmar , Weigand Wolfgang 
Published: November 2009

AbstractIn search of an applicable parameter to express the steric requirement of bidentate ligands, the generalised equivalent cone angle Θ–b is established. It is designed in the style of the solid‐angle concept for monodentate ligands, utilising crystal structure data. Its reliability is tested with bidentate phosphanes coordinated to a central platinum atom. Therefore, a detailed evaluation of the Cambridge Database for platinum complexes with bridging phosphanes is performed. Herein, we present the results of the analysis of more than 900 molecular structures and over 280 different bidentate phosphanes. We intend to establish diselenolatoplatinum(II) complexes as model compounds for the fast prediction of Θ–b instead of calculating a multiplicity of molecular structures that is often not available. The complexes reported in Part 1 of this publication turn out to be rather acceptable for rough estimates of the generalised equivalent cone angle. On the other hand, the compounds are used to demonstrate the practicability of the concept, which is easily extended to other bidentate ligands, as is shown for the 2,2‐bis(hydroxymethyl)‐1,3‐diselenolato moiety. In conclusion, the generalised equivalent cone angle Θ–b proves to be a feasible parameter for the steric demand of bidentate ligands.
Formation of Unusual Trinuclear Assemblies: Scope and Mechanism of Zn(salphen)‐Templated Activation of Pyridine‐Alcohol Substrates (Eur. J. Inorg. Chem. 35/2009)
Authors: Martínez Belmonte Marta , Escudero‐Adán Eduardo C. , Benet‐Buchholz Jordi , Kleij Arjan W. 
Published: November 2009

AbstractThe cover picture shows a schematic view of the templated process that is mediated by Zn(salphen) complexes in the presence of pyridine‐alcohol ligands. The products of the templated reactions are unusual trinuclear Zn3 assemblies that comprise a central, nonsymmetrical Zn complex of which the anionic O‐donor atoms coordinate to two Zn(salphen) units. Full details on the stability and structural features of a small library of these supramolecular systems are discussed in the article by A. W. Kleij et al. on p. 5307 ff.
Indirect influence and divergent thinking as a function of member status and task structure in small groups
Authors: Goodman Jeffrey A. , Alexander Michele G. , Chizhik Alexander W. , Chizhik Estella W. , Eidelman Scott 
Published: November 2009

AbstractA laboratory experiment examined the effect of confederate status and task structure on group members' use of the confederate's problem solving strategies (private/indirect influence) and divergent thinking. Twenty‐eight three‐member, all‐female groups, with an experimental confederate acting as one of the group members, solved an open‐structured or closed‐structured logic problem. The confederate, randomly assigned to be higher‐, lower‐, or of undesignated‐status, presented a scripted but unique solution to the group while solving the task. Lower‐status confederates and open‐structured tasks, relative to higher‐status confederates and closed‐structured tasks, had more private, indirect influence on group members and caused more divergent thinking. We discuss the implications of these findings for group dynamics and social influence literatures. Copyright © 2009 John Wiley & Sons, Ltd.