bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Question of Control? Examining the Role of Control Conditions in Experimental Psychopathology using the Example of Cognitive Bias Modification Research
Authors: Blackwell Simon E. , Woud Marcella L. , MacLeod Colin 
Published: October 2017

AbstractWhile control conditions are vitally important in research, selecting the optimal control condition can be challenging. Problems are likely to arise when the choice of control condition is not tightly guided by the specific question that a given study aims to address. Such problems have become increasingly apparent in experimental psychopathology research investigating the experimental modification of cognitive biases, particularly as the focus of this research has shifted from theoretical questions concerning mechanistic aspects of the association between cognitive bias and emotional vulnerability, to questions that instead concern the clinical efficacy of ‘cognitive bias modification’ (CBM) procedures. We discuss the kinds of control conditions that have typically been employed in CBM research, illustrating how difficulties can arise when changes in the types of research questions asked are not accompanied by changes in the control conditions employed. Crucially, claims made on the basis of comparing active and control conditions within CBM studies should be restricted to those conclusions allowed by the specific control condition employed. CBM studies aiming to establish clinical utility are likely to require quite different control conditions from CBM studies aiming to illuminate mechanisms. Further, conclusions concerning the clinical utility of CBM interventions cannot necessarily be drawn from studies in which the control condition has been chosen to answer questions concerning mechanisms. Appreciating the need to appropriately alter control conditions in the transition from basic mechanisms-focussed investigations to applied clinical research could greatly facilitate the translational process.
Positive Technologies for Understanding and Promoting Positive Emotions
Authors: Baños Rosa María , Carrillo Alba , Etchemendy Ernestina , Botella Cristina 
Published: October 2017

AbstractInformation and Communication Technologies (ICTs) have become increasingly present in our lives, and their use has spread considerably. This paper presents a review of the way ICTs can help practitioners and researchers to study, promote, and train positive emotions. It is framed within the field of Positive Technologies: the applied scientific approach to the study of the use of technology to improve the quality of personal experience, with the goal of increasing wellbeing. First, the article presents an introduction to the topic of technologies and positive emotions. Then, it describes how ICTs can aid in monitoring, assessing, promoting, modifying, and training positive emotions. Finally, implications and future directions of the role of Positive Technologies in positive emotions are discussed. The authors conclude that, in the near future, Positive Technologies and the field of positive emotions will interact synergistically, producing an exponential growth in the understanding and promotion of positive emotions.
Confirmatory Factor Analysis of the Coalitional Mate Retention	Inventory (CMRI) and Evidence for Two Superordinate Domains
Authors: Barbaro Nicole , Sela Yael , Lopes Guilherme S. , Shackelford Todd K. 
Published: October 2017

Abstract. The Coalitional Mate Retention Inventory (CMRI; Pham, Barbaro, Mogilski, & Shackelford, 2015 ) assesses the frequency with which individuals solicit allies to assist with mate retention efforts. The current study subjected the CMRI to confirmatory factor analyses (CFAs). A model comparison approach was employed using data from a large community sample of participants currently in a heterosexual romantic relationship ( n = 1,003, 54% male). The seven-factor structure of the CMRI demonstrates good model fit and provides significantly better fit than an alternative single-factor structure. The results also demonstrate that the seven tactics of the CMRI are subsumed by two superordinate domains of Benefit-Provisioning and Cost-Inflicting coalitional mate retention. Correlational analyses with the superordinate domains of coalitional mate retention are presented and highlight their predictive utility. We recommend the continued use of the CMRI in psychological research.
Inhibition of Caspase-8 does not protect from alcohol-induced liver apoptosis but alleviates alcoholic hepatic steatosis in mice
Authors: Hao Fengjie , Cubero Francisco Javier , Ramadori Pierluigi , Liao Lijun , Haas Ute , Lambertz Daniela , Sonntag Roland , Bangen Jörg- Martin , Gassler Nikolaus , Hoss Mareike , Streetz Konrad L , Reissing Johanna , Zimmermann Henning W , Trautwein Christian , Liedtke Christian , Nevzorova Yulia A 
Published: October 2017

AbstractHepatic apoptosis is involved in the progression of alcoholic liver disease (ALD). Caspase-8, the apical initiator in death receptor-mediated apoptosis, has been implicated in acute liver injury and in non-alcoholic steatohepatitis. However, the relevance of Caspase-8 in the pathogenesis of ALD remains unclear. In the present study, we investigated the impact of Caspase-8 in human and murine alcohol-induced apoptosis and in ALD. We investigated human samples from ALD patients, primary mouse hepatocytes, and hepatocyte-specific Caspase-8 knockout (Casp8Δhepa) mice in acute and chronic models of ethanol (EtOH) administration. Caspase-8 activation was detected in liver biopsies from ALD patients, as well as in livers of wild-type (WT) mice after chronic ethanol feeding for 8 weeks using the Lieber-DeCarli model. Lack of Caspase-8 expression in Casp8Δhepa animals failed to prevent alcohol-induced liver damage and apoptosis. Instead, inhibition of Caspase-8 shifted the ethanol-induced death signals towards pronounced activation of the intrinsic, mitochondria-dependent apoptosis pathway in Casp8Δhepa livers involving enhanced release of cytochrome c, stronger Caspase-9 activation and specific morphological changes of mitochondria. In vitro and in vivo intervention using a pan-caspase inhibitor markedly attenuated alcohol-induced hepatocyte damage in a Caspase-8-independent manner. Surprisingly, EtOH-fed Casp8Δhepa mice displayed significantly attenuated steatosis and reduced hepatic triglyceride and free fatty acids content. Caspase-8 is dispensable for alcohol-induced apoptosis, but plays an unexpected role for alcohol-dependent fat metabolism. We provide evidence that simultaneous inhibition of extrinsic and intrinsic apoptosis signaling using pan-caspase inhibitors in vivo might be an optimal approach to treat alcohol-induced liver injury.
Glucocorticoid mediates prenatal caffeine exposure-induced endochondral ossification retardation and its molecular mechanism in female fetal rats
Authors: Shangguan Yangfan , Jiang Hongqiang , Pan Zhengqi , Xiao Hao , Tan Yang , Tie Kai , Qin Jun , Deng Yu , Chen Liaobin , Wang Hui 
Published: October 2017

AbstractOur previous studies discovered that prenatal caffeine exposure (PCE) could induce intrauterine growth retardation (IUGR) and long-bone dysplasia in offspring rats, accompanied by maternal glucocorticoid over-exposure. This study is to explore whether intrauterine high glucocorticoid level can cause endochondral ossification retardation and clarify its molecular mechanism in PCE fetal rats. Pregnant Wistar rats were intragastrically administered 30 and 120 mg/kg day of caffeine during gestational days (GDs) 9–20, then collected fetal serum and femurs at GD20. In vitro, primary chondrocytes were treated with corticosterone (0–1250 nM), caffeine (0–100 μM), mitogen-inducible gene 6 (Mig-6) siRNA and epidermal growth factor receptor (EGFR) siRNA, respectively, or together. Results showed that the hypertrophic chondrocytes zone (HZ) of PCE fetal femur was widened. Meanwhile, the expression levels of chondrocytes terminal differentiation genes in the HZ were decreased, and the chondrocytes apoptosis rate in the HZ was decreased too. Furthermore, PCE upregulated Mig-6 and suppressed EGFR expression in the HZ. In vitro, a high-concentration corticosterone (1250 nM) upregulated Mig-6 expression, inhibit EGFR/c-Jun N-terminal kinase (JNK) signaling pathway and terminal differentiation genes expression in chondrocytes and reduced cell apoptosis, and these above alterations could be partly reversed step-by-step after Mig-6 and EGFR knockdown. However, caffeine concentration dependently increased chondrocyte apoptosis without significant changes in the expression of terminal differentiation genes. Collectively, PCE caused endochondral ossification retardation in the female fetal rats, and its main mechanism was associated with glucocorticoid (rather than caffeine)-mediated chondrocyte terminal differentiation suppression by the upregulation of Mig-6 and then inhibition of EGFR/JNK pathway-mediated chondrocyte apoptosis.
Calreticulin promotes EGF-induced EMT in pancreatic cancer cells via Integrin/EGFR-ERK/MAPK signaling pathway
Authors: Sheng Weiwei , Chen Chuanping , Dong Ming , Wang Guosen , Zhou Jianping , Song He , Li Yang , Zhang Jian , Ding Shuangning 
Published: October 2017

AbstractOur previous study showed that Calreticulin (CRT) promoted the development of pancreatic cancer (PC) through ERK/MAPK pathway. We next investigate whether CRT promotes EGF-induced epithelial–mesenchymal transition (EMT) in PC via Integrin/EGFR-ERK/MAPK signaling, which has not been reported yet to our knowledge. EGF simultaneously induced EMT and activated Integrin/EGFR–ERK/MAPK signaling pathway in 3 PC cells. However, CRT silencing significantly inhibited EGF function, including inhibiting EGF-induced EMT-like cell morphology, EGF-enhanced cell invasion and migration, and EGF induced the decrease of E-cadherin, ZO-1, and β-catenin and the increase of the key proteins in Integrin/EGFR-ERK/MAPK signaling (pEGFR-tyr1173, Fibronectin, Integrinβ1, c-Myc and pERK). Conversely, CRT overexpression rescued the change of EMT-related proteins induced by EGF in CRT silencing PC cells. Additionally, CRT was co-stained with pEGFR1173 (with EGF), Fibronectin and Integrinβ1 by IF under confocal microscopy and was co-immunoprecipitated with Fibronectin, Integrinβ1 and c-Myc in both PC cells, all of which indicating a close interaction of CRT with Integrin/EGFR–ERK/MAPK signaling pathway in PC. In vivo, CRT silencing inhibited subcutaneous tumor growth and liver metastasis of pancreatic tumor. A positive relationship of CRT with Fibronectin, Integrinβ1, c-Myc and pERK and a negative association of CRT with E-cad was also observed in vivo and clinical samples. Meanwhile, overexpression of the above proteins was closely associated with multiple aggressive clinicopathological characteristics and the poor prognosis of PC patients. CRT promotes EGF-induced EMT in PC cells via Integrin/EGFR-ERK/MAPK signaling pathway, which would be a promising therapy target for PC.
CITED2 affects leukemic cell survival by interfering with p53 activation
Authors: Mattes Katharina , Berger Gerbrig , Geugien Marjan , Vellenga Edo , Schepers Hein 
Published: October 2017

AbstractCITED2 (CBP/p300-interacting-transactivator-with-an-ED-rich-tail 2) is a regulator of the acetyltransferase CBP/p300 and elevated CITED2 levels are shown in a number of acute myeloid leukemia (AML). To study the in vivo role of CITED2 in AML maintenance, AML cells were transduced with a lentiviral construct for RNAi-mediated knockdown of CITED2. Mice transplanted with CITED2-knockdown AML cells (n=4) had a significantly longer survival compared to mice transplanted with control AML cells (P<0.02). In vitro, the reduction of CITED2 resulted in increased p53-mediated apoptosis and CDKN1A expression, whereas BCL2 levels were reduced. The activation of p53 upon CITED2 knockdown is not a direct consequence of increased CBP/p300-activity towards p53, since no increased formation of CBP/p300/p53 complexes was demonstrated and inhibition of CBP/p300-activity could not rescue the phenotype of CITED2-deficient cells. Instead, loss of CITED2 had an inhibitory effect on the AKT-signaling pathway, which was indicated by decreased levels of phosphorylated AKT and altered expression of the AKT-pathway regulators PHLDA3 and SOX4. Notably, simultaneous upregulation of BCL2 or downregulation of the p53-target gene PHLDA3 rescued the apoptotic phenotype in CITED2-knockdown cells. Furthermore, knockdown of CITED2 led to a decreased interaction of p53 with its inhibitor MDM2, which results in increased amounts of total p53 protein. In summary, our data indicate that CITED2 functions in pathways regulating p53 activity and therefore represents an interesting target for AML therapy, since de novo AML cases are characterized by an inactivation of the p53 pathway or deregulation of apoptosis-related genes.
PLOD2 regulated by transcription factor FOXA1 promotes metastasis in NSCLC
Authors: Du Hongzhi , Chen Yulong , Hou Xiaoying , Huang Yue , Wei Xiaohui , Yu Xiaowen , Feng Shuyun , Wu Yao , Zhan Meixiao , Shi Xin , Lin Sensen , Lu Ligong , Yuan Shengtao , Sun Li 
Published: October 2017

AbstractIn multiple types of tumors, fibrotic collagen is regarded as the 'highway' for cancer cell migration, which is mainly modified by lysyl hydroxylase 2 (PLOD2). The previous findings have demonstrated that the expression of PLOD2 was regulated by multiple factors, including HIF-1α, TGF-β and microRNA-26a/b. Although PLOD2 was confirmed to be related to poor prognosis in lung adenocarcinoma, the regulatory mechanism and function of PLOD2 in human lung adenocarcinoma is poorly understood. On the other hand, upregulation or hyperactivation of epidermal growth factor receptor is considered as a prognostic marker in many cancers, especially in non-small-cell lung cancer (NSCLC). In this study, we found that PLOD2 was elevated in NSCLC specimens and positively links to NSCLC poor prognosis. Gain- and loss-of-function studies and orthotopic implantation metastasis model pinpointed that PLOD2 promotes NSCLC metastasis directly by enhancing migration and indirectly by inducing collagen reorganization. In addition, we revealed that PLOD2 was regulated by PI3K/AKT-FOXA1 axis. The transcription factor FOXA1 directly bound to the PLOD2 promoter, and turned on PLOD2 transcription. In summary, our findings revealed a regulatory mechanism of NSCLC metastasis through EGFR-PI3K/AKT-FOXA1-PLOD2 pathway, and provided PLOD2 as a therapeutic target for NSCLC treatment.
The non-invasive serum biomarker soluble Axl accurately detects advanced liver fibrosis and cirrhosis
Authors: Staufer Katharina , Dengler Mirko , Huber Heidemarie , Marculescu Rodrig , Stauber Rudolf , Lackner Carolin , Dienes Hans-Peter , Kivaranovic Danijel , Schachner Christian , Zeitlinger Markus , Wulkersdorfer Beatrix , Rauch Peter , Prager Gerhard , Trauner Michael , Mikulits Wolfgang 
Published: October 2017

AbstractSoluble Axl (sAxl) was recently shown to be strongly released into the blood during liver fibrogenesis and hepatocellular carcinoma suggesting sAxl as a biomarker of liver diseases. In this study we are the first to evaluate sAxl in human serum in comparison to Enhanced Liver Fibrosis (ELF) test and transient elastography (TE; Fibroscan) for its value to detect significant (F≥2), advanced fibrosis (F≥3), and cirrhosis (F4) in different liver disease etiologies and healthy controls. To properly determine the diagnostic accuracy of sAxl, a test cohort as well as a validation cohort was employed using liver biopsy as a reference method. Most notably, sAxl was confirmed to be an accurate biomarker of liver fibrosis and cirrhosis. Its accuracy was increased, if total serum albumin was added to build a sAxl/albumin ratio. Thereby an AUC of 0.763, 0.776, 0.826, and 0.832 was achieved corresponding to histological fibrosis stages F≥2, F≥3, F4 with liver biopsy as a reference method, and cirrhosis according to imaging techniques, respectively. With a cut-off of 1.29, a sensitivity, specificity, PPV, and NPV of 78.5%, 80.1%, 44%, 94.9% for the detection of cirrhosis was achieved. In comparison, ELF test and TE showed an AUC of 0.910, and 0.934, respectively, for the detection of cirrhosis. However, performance of TE was not possible in 14.4% of patients and both, ELF™ test and TE bear the disadvantage of high costs. In conclusion, the sAxl/albumin ratio is suggested as an accurate biomarker of liver fibrosis and cirrhosis. Due to its easy applicability and low costs it is suitable as screening parameter for significant to advanced liver fibrosis and cirrhosis, especially if TE is not available or not applicable.
Requirement for CCNB1 in mouse spermatogenesis
Authors: Tang Ji-Xin , Li Jian , Cheng Jin-Mei , Hu Bian , Sun Tie-Cheng , Li Xiao-Yu , Batool Aalia , Wang Zhi-Peng , Wang Xiu-Xia , Deng Shou-Long , Zhang Yan , Chen Su-Ren , Huang Xingxu , Liu Yi-Xun 
Published: October 2017

AbstractSpermatogenesis, which involves mitosis and meiosis of male germ cells, is a highly complicated and coordinately ordered process. Cyclin B1 (CCNB1), an important regulator in cell cycle machinery, is proved essential for mouse embryonic development. However, the role of CCNB1 in mammalian spermatogenesis remains unclear. Here we tested the requirement for CCNB1 using conditional knockout mice lacking CCNB1 in male germ cells. We found that ablation of CCNB1 in gonocytes and spermatogonia led to mouse sterile caused by the male germ cells’ depletion. Gonocyte and spermatogonia without CCNB1 is unable to proliferate normally and apoptosis increased. Moreover, CCNB1 ablation in spermatogonia may promote their differentiation by downregulating Lin28a and upregulating let-7 miRNA. However, ablation of CCNB1 in premeiotic male germ cells did not have an effect on meiosis of spermatocytes and male fertility, suggesting that CCNB1 may be dispensable for meiosis of spermatocytes. Collectively, these results indicate that CCNB1 is critically required for the proliferation of gonocytes and spermatogonia but may be redundant in meiosis of spermatocytes in mouse spermatogenesis.
SIRT3 protects hepatocytes from oxidative injury by enhancing ROS scavenging and mitochondrial integrity
Authors: Liu Jingxin , Li Dan , Zhang Tian , Tong Qiang , Ye Richard Dequan , Lin Ligen 
Published: October 2017

AbstractEvidences of oxidative stress and mitochondrial dysfunction have been recognized in most of clinical and experimental liver diseases. SIRT3, a member of NAD+-dependent deacetylases, is mainly localized in mitochondria. So far, the role of SIRT3 in protecting hepatocytes against oxidative stress remains elusive. Herein, we found SIRT3 protein expression is decreased in tert-butyl hydroperoxide (t-BHP)-treated AML12 cells in vitro and primary hepatocytes from CCl4-injured mice in vivo. To further verify the role of SIRT3 in protecting hepatocytes from t-BHP-induced injury, SIRT3 overexpressed AML12 cell line and primary hepatocytes were generated. SIRT3 overexpressed hepatocytes showed improved cell viability upon t-BHP challenge, with less intracellular reactive oxygen species (ROS) accumulation. SIRT3 overexpression reduced superoxide dismutase 2 acetylation level and stimulated nuclear factor erythroid 2-related factor 2 nuclear translocation to enhance anti-oxidative capacity. Moreover, SIRT3 deacetylated peroxisome proliferator-activated receptor γ coactivator 1α to promote mitochondrial biogenesis, and 8-oxoguanine DNA glycosylase 1 to orchestrate DNA repair, resulting in improved mitochondrial function. Through deacetylating Ku70, SIRT3 also abated mitochondrial translocation of dynamin-related protein 1, to attenuate mitochondrial fragmentation in t-BHP-injured hepatocytes. These results suggested that SIRT3 protected hepatocytes against oxidative stress by enhancing ROS scavenging and maintaining mitochondrial integrity.
Carbon dioxide capture and conversion by an acid-base resistant metal-organic framework
Authors: Liang Linfeng , Liu Caiping , Jiang Feilong , Chen Qihui , Zhang Linjie , Xue Hui , Jiang Hai-Long , Qian Jinjie , Yuan Daqiang , Hong Maochun 
Published: October 2017

AbstractConsidering the rapid increase of CO2 emission, especially from power plants, there is a constant need for materials which can effectively eliminate post-combustion CO2 (the main component: CO2/N2 = 15/85). Here, we show the design and synthesis of a Cu(II) metal-organic framework (FJI-H14) with a high density of active sites, which displays unusual acid and base stability and high volumetric uptake (171 cm3 cm−3) of CO2 under ambient conditions (298 K, 1 atm), making it a potential adsorbing agent for post-combustion CO2. Moreover, CO2 from simulated post-combustion flue gas can be smoothly converted into corresponding cyclic carbonates by the FJI-H14 catalyst. Such high CO2 adsorption capacity and moderate catalytic activity may result from the synergistic effect of multiple active sites.
E-cadherin integrates mechanotransduction and EGFR signaling to control junctional tissue polarization and tight junction positioning
Authors: Rübsam Matthias , Mertz Aaron F. , Kubo Akiharu , Marg Susanna , Jüngst Christian , Goranci-Buzhala Gladiola , Schauss Astrid C. , Horsley Valerie , Dufresne Eric R. , Moser Markus , Ziegler Wolfgang , Amagai Masayuki , Wickström Sara A. , Niessen Carien M. 
Published: October 2017

AbstractGeneration of a barrier in multi-layered epithelia like the epidermis requires restricted positioning of functional tight junctions (TJ) to the most suprabasal viable layer. This positioning necessitates tissue-level polarization of junctions and the cytoskeleton through unknown mechanisms. Using quantitative whole-mount imaging, genetic ablation, and traction force microscopy and atomic force microscopy, we find that ubiquitously localized E-cadherin coordinates tissue polarization of tension-bearing adherens junction (AJ) and F-actin organization to allow formation of an apical TJ network only in the uppermost viable layer. Molecularly, E-cadherin localizes and tunes EGFR activity and junctional tension to inhibit premature TJ complex formation in lower layers while promoting increased tension and TJ stability in the granular layer 2. In conclusion, our data identify an E-cadherin-dependent mechanical circuit that integrates adhesion, contractile forces and biochemical signaling to drive the polarized organization of junctional tension necessary to build an in vivo epithelial barrier.
Developmental increases in white matter network controllability support a growing diversity of brain dynamics
Authors: Tang Evelyn , Giusti Chad , Baum Graham L. , Gu Shi , Pollock Eli , Kahn Ari E. , Roalf David R. , Moore Tyler M. , Ruparel Kosha , Gur Ruben C. , Gur Raquel E. , Satterthwaite Theodore D. , Bassett Danielle S. 
Published: October 2017

AbstractAs the human brain develops, it increasingly supports coordinated control of neural activity. The mechanism by which white matter evolves to support this coordination is not well understood. Here we use a network representation of diffusion imaging data from 882 youth ages 8–22 to show that white matter connectivity becomes increasingly optimized for a diverse range of predicted dynamics in development. Notably, stable controllers in subcortical areas are negatively related to cognitive performance. Investigating structural mechanisms supporting these changes, we simulate network evolution with a set of growth rules. We find that all brain networks are structured in a manner highly optimized for network control, with distinct control mechanisms predicted in child vs. older youth. We demonstrate that our results cannot be explained by changes in network modularity. This work reveals a possible mechanism of human brain development that preferentially optimizes dynamic network control over static network architecture.