bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Political Impact of Displacement: Wartime IDPs, Religiosity, and Post-War Politics in Bosnia
Authors: Zic Borjan 
Published: June 2017

Abstract
Following armed conflict, why do some members of ethno-religious groups vote for political parties that use religious appeals while others do not? I argue that internal displacement shapes the relationship between conflict and post-war political outcomes. Specifically, individuals who become internally displaced during armed conflict will use their religious faith to cope with the trauma of displacement, thereby strengthening their religiosity. This heightened religiosity then leads them to prefer religiously oriented parties after conflict. Analyzing survey data from Bosnian Muslims, I show that internally displaced respondents were more likely to vote for the religious nationalist Party of Democratic Action nearly a decade after conflict. Employing matching analysis, I then verify that these internally displaced persons became more religious than other respondents compared to before the war. My findings therefore provide evidence that trauma and religiosity combine to shape post-war voting behavior for members of ethno-religious groups.
The NF-κB1 is a key regulator of acute but not chronic renal injury
Authors: Fearn Amy , Situmorang Gerhard R , Fox Christopher , Oakley Fiona , Howarth Rachel , Wilson Caroline L , Kiosia Agklinta , Robson Michael G , Mann Derek A , Moles Anna , Sheerin Neil S 
Published: June 2017

AbstractThe NF-κB family of transcription factors is important for many cellular functions, in particular initiation and propagation of inflammatory and immune responses. However, recent data has suggested that different subunits of the NF-κB family can suppress the inflammatory response. NF-κB1, from the locus nfκb1, can inhibit transcription, acting as a brake to the recognised pro-inflammatory activity of other NF-κB subunits. We tested the function of NF-κB1 in an acute (nephrotoxic serum (NTS) nephritis) and a chronic (unilateral ureteric obstruction (UUO)) model of renal injury using NF-κB1 (nfκb1−/−) knockout mice. Deficiency in NF-κB1 increased the severity of glomerular injury in NTS-induced nephritis and was associated with greater proteinuria and persistent pro-inflammatory gene expression. Induction of disease in bone marrow chimeric mice demonstrated that the absence of NF-κB1 in either bone marrow or glomerular cells increased the severity of injury. Early after UUO (day 3) there was more severe histological injury in the nfκb1−/− mice but by day 10, disease severity was equivalent in wild type and nfκb1−/− mice. In conclusion, NF-κB1 modifies acute inflammatory renal injury but does not influence chronic fibrotic injury.
Concomitant epigenetic targeting of LSD1 and HDAC synergistically induces mitochondrial apoptosis in rhabdomyosarcoma cells
Authors: Haydn Tinka , Metzger Eric , Schuele Roland , Fulda Simone 
Published: June 2017

AbstractThe lysine-specific demethylase 1 (LSD1) is overexpressed in several cancers including rhabdomyosarcoma (RMS). However, little is yet known about whether or not LSD1 may serve as therapeutic target in RMS. We therefore investigated the potential of LSD1 inhibitors alone or in combination with other epigenetic modifiers such as histone deacetylase (HDAC) inhibitors. Here, we identify a synergistic interaction of LSD1 inhibitors (i.e., GSK690, Ex917) and HDAC inhibitors (i.e., JNJ-26481585, SAHA) to induce cell death in RMS cells. By comparison, LSD1 inhibitors as single agents exhibit little cytotoxicity against RMS cells. Mechanistically, GSK690 acts in concert with JNJ-26481585 to upregulate mRNA levels of the proapoptotic BH3-only proteins BMF, PUMA, BIM and NOXA. This increase in mRNA levels is accompanied by a corresponding upregulation of BMF, PUMA, BIM and NOXA protein levels. Importantly, individual knockdown of either BMF, BIM or NOXA significantly reduces GSK690/JNJ-26481585-mediated cell death. Similarly, genetic silencing of BAK significantly rescues cell death upon GSK690/JNJ-26481585 cotreatment. Also, overexpression of antiapoptotic BCL-2 or MCL-1 significantly protects RMS cells from GSK690/JNJ-26481585-induced cell death. Furthermore, GSK690 acts in concert with JNJ-26481585 to increase activation of caspase-9 and -3. Consistently, addition of the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD.fmk) significantly reduces GSK690/JNJ-26481585-mediated cell death. In conclusion, concomitant LSD1 and HDAC inhibition synergistically induces cell death in RMS cells by shifting the ratio of pro- and antiapoptotic BCL-2 proteins in favor of apoptosis, thereby engaging the intrinsic apoptotic pathway. This indicates that combined treatment with LSD1 and HDAC inhibitors is a promising new therapeutic approach in RMS.
Connective tissue growth factor promotes temozolomide resistance in glioblastoma through TGF-β1-dependent activation of Smad/ERK signaling
Authors: Zeng Huijun , Yang Zhao , Xu Ningbo , Liu Boyang , Fu Zhao , Lian Changlin , Guo Hongbo 
Published: June 2017

AbstractLimited benefits and clinical utility of temozolomide (TMZ) for glioblastoma (GB) are frequently compromised by the development of acquired drug resistance. Overcoming TMZ resistance and uncovering the underlying mechanisms are challenges faced during GB chemotherapy. In this study, we reported that connective tissue growth factor (CTGF) was associated with GB chemoresistance and significantly upregulated in TMZ-treated GB cells. CTGF knockdown promoted TMZ-induced cell apoptosis and enhanced chemosensitivity, whereas its overexpression markedly conferred TMZ resistance in vitro and in vivo. Moreover, CTGF promoted TMZ resistance through stem-like properties acquisition and CD44 interference reversed the CTGF-induced TMZ resistance. Mechanistically, further investigation revealed that the TMZ-induced CTGF upregulation was tissue growth factor (TGF-β) dependent, and regulated by TGF-β1 activation through Smad and ERK1/2 signaling. Together, our results suggest a pivotal role of CTGF-mediated TMZ resistance through TGF-β1-dependent activation of Smad/ERK signaling pathways. These data provide us insights for identifying potential targets that are beneficial for overcoming TMZ resistance in GB.
Cdc20 directs proteasome-mediated degradation of the tumor suppressor SMAR1 in higher grades of cancer through the anaphase promoting complex
Authors: Paul Debasish , Ghorai Suvankar , Dinesh U S , Shetty Praveenkumar , Chattopadhyay Samit , Santra Manas Kumar 
Published: June 2017

AbstractThe Tumor suppressor SMAR1 (scaffold matrix attachment region binding protein 1) has a crucial role in maintaining genomic stability, cell cycle progression and apoptosis.Our previous finding showed that it is highly suppressed in higher grade of cancer. However, the underlying mechanism of this suppression was not well understood. In this study, we show that SMAR1 expression levels are controlled at the proteasomal level by five RING finger E3 ubiquitin ligases including, Cdc20, a substrate receptor of ubiquitin ligase APC/C complex. We found that Cdc20 binds and promotes proteasomal degradation of SMAR1 in a D-box motif dependent manner. Further, our results demonstrated that Cdc20 promotes proteasomal degradation of SMAR1 through K48-linked specific polyubiquitylation, and that short hairpin RNA mediated inactivation of Cdc20 leads to significant stabilization of SMAR1. These findings suggest that Cdc20 is responsible for maintaining the cellular levels of SMAR1. However, since Cdc20 fails to target SMAR1 upon exposure to genotoxic stresses, SMAR1 helps to maintain genomic stability under these conditions through its DNA damage repair activity. Interestingly, Cdc20-mediated degradation of SMAR1 promotes cell migration and invasion.The reciprocal relationship of the duo is evident in breast cancer cell lines as well as in patient samples, suggesting that Cdc20 functions as an important negative regulator of SMAR1 in higher grades of cancer. Our study reveals for the first time, the molecular mechanism associated with lower levels of expression of the important tumor suppressor SMAR1 in higher grades of breast cancer.
BST2 confers cisplatin resistance via NF-κB signaling in nasopharyngeal cancer
Authors: Kuang Chun-mei , Fu Xiang , Hua Yi-jun , Shuai Wen-di , Ye Zhi-hua , Li Yingchang , Peng Qi-hua , Li Yi-zhuo , Chen Shuai , Qian Chao-nan , Huang Wenlin , Liu Ran-yi 
Published: June 2017

AbstractConcurrent/adjuvant cisplatin-based chemoradiotherapy is regarded as the standard of treatment for locoregionally advanced nasopharyngeal carcinoma (NPC). However, patients who do not respond to cisplatin suffer, rather than benefit, from chemotherapy treatment. The goal of this study was to identify molecules involved in cisplatin resistance and to clarify their molecular mechanisms, which would help in the discovery of potential therapeutic targets and in developing a personalized and precise treatment approach for NPC patients. We previously generated a cisplatin-sensitive NPC cell line, S16, from CNE2 cells and found that eIF3a, ASNS and MMP19 are upregulated in S16 cells, which contributes to their cisplatin sensitivity. In this study, we found that BST2 is downregulated in cisplatin-sensitive S16 cells compared with CNE2 cells. Knockdown of BST2 in NPC cells sensitized their response to cisplatin and promoted cisplatin-induced apoptosis, whereas exogenous overexpression of BST2 increased their cisplatin resistance and inhibited cisplatin-induced apoptosis. Further investigation demonstrated that BST2-mediated cisplatin resistance depended on the activation of the NF-κB signaling pathway and consequent upregulation of anti-apoptotic genes, such as Bcl-XL and livin. Moreover, an analysis of clinical data revealed that a high BST2 level might serve as an independent indicator of poor prognosis in patients with locally advanced NPC treated with platinum-based chemoradiotherapy. These findings suggest that BST2 likely mediates platinum resistance in NPC, offering guidance for personalized and precise treatment strategies for patients with NPC.
VHL deficiency augments anthracycline sensitivity of clear cell renal cell carcinomas by down-regulating ALDH2
Authors: Gao Yao-Hui , Wu Zhao-Xia , Xie Li-Qi , Li Cai-Xia , Mao Yu-Qin , Duan Yan-Tao , Han Bing , Han San-Feng , Yu Yun , Lu Hao-Jie , Yang Peng-Yuan , Xu Tian-Rui , Xia Jing-Lin , Chen Guo-Qiang , Wang Li-Shun 
Published: June 2017

AbstractThe von Hippel-Lindau (VHL) is deficient in ∼70% of clear-cell renal cell carcinomas (ccRCC), which contributes to the carcinogenesis and drug resistance of ccRCC. Here we show that VHL-deficient ccRCC cells present enhanced cytotoxicity of anthracyclines in a hypoxia-inducible factor-independent manner. By subtractive proteomic analysis coupling with RNAi or overexpression verification, aldehyde dehydrogenase 2 (ALDH2) is found to be transcriptionally regulated by VHL and contributes to enhanced anthracyclines cytotoxicity in ccRCC cells. Furthermore, VHL regulates ALDH2 expression by directly binding the promoter of −130 bp to −160 bp to activate the transcription of hepatocyte nuclear factor 4 alpha (HNF-4α). In addition, a positive correlation is found among the protein expressions of VHL, HNF-4α and ALDH2 in ccRCC samples. These findings will deepen our understanding of VHL function and shed light on precise treatment for ccRCC patients.
Platelet releasates promote the proliferation of hepatocellular carcinoma cells by suppressing the expression of KLF6
Authors: He Ao-Di , Xie Wen , Song Wei , Ma Yuan-Yuan , Liu Gang , Liang Ming-Lu , Da Xing-Wen , Yao Guang-Qiang , Zhang Bi-xiang , Gao Cun-Ji , Xiang Ji-zhou , Ming Zhang-Yin 
Published: June 2017

AbstractPlatelets in the primary tumor microenvironment play crucial roles in the regulation of tumor progression, but the mechanisms underlying are poorly understood. Here, we report that platelet releasates exerted a proliferative effect on hepatocellular carcinoma (HCC) cells both in vitro and in vivo. This effect depended on a reduction of KLF6 expression in HCC cells. After incubation with either platelets or platelet granule contents, SMMC.7721 and HepG2 cells exhibited significant increases in proliferation and decreases in apoptosis. However, no effect was observed when incubating cancer cells with resuspended activated platelet pellet which exhausted of releasates. Platelet releasates also increased the population of HCC cells in the S and G2/M phases of the cell cycle and reduced the cell population in the G0/G1 phase. Moreover, knocking down KLF6 expression significantly diminished the platelet-mediated enhancement of HCC growth. In addition, blocking TGF-β signaling with the TGF-β receptor inhibitor SB431542 counteracted the effect of platelets on KLF6 expression and proliferation of HCC cells. Based on these findings, we conclude that platelet releasates, especially TGF-β, promote the proliferation of SMMC.7721 and HepG2 cells by decreasing expression of KLF6. This discovery identifies a potential new therapeutic target for the prevention and treatment of hepatocellular carcinoma.
Transient cell assembly networks encode stable spatial memories
Authors: Babichev Andrey , Dabaghian Yuri 
Published: June 2017

AbstractOne of the mysteries of memory is that it can last despite changes in the underlying synaptic architecture. How can we, for example, maintain an internal spatial map of an environment over months or years when the underlying network is full of transient connections? In the following, we propose a computational model for describing the emergence of the hippocampal cognitive map in a network of transient place cell assemblies and demonstrate, using methods of algebraic topology, how such a network can maintain spatial memory over time.
Experimental evidence for reciprocity in allogrooming among wild-type Norway rats
Authors: Schweinfurth Manon K. , Stieger Binia , Taborsky Michael 
Published: June 2017

AbstractIf individuals help more those who have previously helped them, stable cooperation may ensue through alternation of roles between donors and recipients. Allogrooming, which is costly to donors and beneficial to recipients, is often exchanged between social partners. Arguably, allogrooming and allopreening are the most frequently exchanged social services and have been used as a standard model of reciprocal cooperation. However, evidence for the application of reciprocity rules among social partners allogrooming each other hitherto is merely correlational. Here, we tested whether female Norway rats (Rattus norvegicus) apply the decision rule characterising direct reciprocity: help someone who has helped you before, by experimentally manipulating both the need for allogrooming and the behavioural response. Furthermore, we checked whether trading of grooming services is influenced by the rank of the social partner. We show that rats groom social partners reciprocally and prefer to do so up the hierarchy, i.e. they groom dominant partners more often than subordinates, while reciprocating with both. This provides experimental evidence that animals render a costly social service by applying reciprocity decision rules when showing a natural hygienic behaviour. The fact that allogrooming is more readily shown up the hierarchy may suggest an appeasing function.
A note on the stationary distribution of stochastic SEIR epidemic model with saturated incidence rate
Authors: Han Qixing , Chen Liang , Jiang Daqing 
Published: June 2017

AbstractThe stochastic SEIR infectious diseases model with saturated incidence rate is studied in this paper. By constructing appropriate Lyapunov functions, we show that there is a stationary distribution for the system and the ergodicity holds provided $${R}_{0}^{s}$$

R

0

s

> 1. In particular, we improve the results obtained by previous studies greatly, condition in our Theorem is more concise and elegant.
Bounds for coherence of quantum superpositions in high dimension
Authors: Yue Qiu-Ling , Gao Fei , Wen Qiao-Yan , Zhang Wei-Wei 
Published: June 2017

AbstractQuantum coherence plays a major role in the promotion for quantum information processing and designing quantum technology. Since coherence is rooted in superposition principle, it is vital to understand the coherence change with respect to superpositions. Here we study the bounds for coherence of quantum superpositions in high dimension. We consider three most frequently used measures of coherence, i.e. the relative entropy of coherence, l1 norm of coherence and robustness of coherence. For a quantum state (an arbitrary dimension) and its arbitrary decomposition, we give the upper and lower bounds for coherence of the superposition state in terms of the coherence of the states being superposed.
Identification and expression analysis of chemosensory receptor genes in an aphid endoparasitoid Aphidius gifuensis
Authors: Kang Zhi-Wei , Tian Hong-Gang , Liu Fang-Hua , Liu Xiang , Jing Xiang-Feng , Liu Tong-Xian 
Published: June 2017

AbstractOlfaction and gustation play critical roles during the host-location search process of insects. Several chemosensory receptor genes are thought to be involved in providing specificity to the olfactory sensory neuron responses. The aphid endoparasitoid, Aphidius gifuensis, has been used as a biological control agent against a variety of aphid species; this parasitoid is able to detect its target host(s) effectively during the parasitic process. To understand the mechanism of host detection in A. gifuensis, we assembled specific antennal transcriptomes of each sex through next generation sequencing technology to identify the major chemosensory receptor genes. Using a bioinformatics screen, we identified 100 olfactory receptors candidates (62 odorant receptors, 15 gustatory receptors, and 23 ionotropic receptors) from the sex-specific antennal transcriptome. In addition, combining with the demonstrated functions of chemosensory genes in other insects, the sex-, tissue-, and host-specific expression profile of chemosensory genes potentially revealed the candidate physiological functions. The identification and expression profile of chemosensory receptor genes in A. gifuensis provide valuable information for understanding and investigating the intraspecific or interspecific chemical communications in the solitary parasitic wasps.
Mycobacterial heat shock protein 65 mediated metabolic shift in decidualization of human endometrial stromal cells
Authors: Subramani Elavarasan , Rameshbabu Arun Prabhu , Jothiramajayam Manivannan , Subramanian Bhuvaneshwaran , Chakravorty Debangana , Bose Gunja , Joshi Mamata , Ray Chaitali Datta , Lodh Indrani , Chattopadhyay Ratna , Saha Sudipto , Mukherjee Anita , Dhara Santanu , Chakravarty Baidyanath , Chaudhury Koel 
Published: June 2017

AbstractSuccessful implantation is dependent on the appropriate decidualization of endometrial stromal cells for the establishment of pregnancy in women. Mycobacterial heat shock protein 65 (HSP65) is involved in pathogenesis of the genital tuberculosis (GTB), one of the common causes of infertility in emerging countries. Though implantation failure appears to be the major cause, understanding the status of decidualizaiton process in women diagnosed with GTB has not been thoroughly addressed. We, therefore, explored the effect of HSP65 protein on the endometrial cell metabolism duringin vitrodecidualization. In order to identify the cellular metabolism of decidual cells with and without HSP65 treatment, proton NMR based characterization of metabolites extracted from cells and culture media were performed. In presence of HSP65, significant reduction in the decidual phenotype of endometrial stromal cells and prolactin expression is suggestive of impairment in decidualization. The intracellular and extracellular metabolic changes in HSP65 treated endometrial stromal cells produced a distinct pattern, reflecting the interaction between the protein and cellular metabolism. HSP65 mediated dysregulation in cellular metabolism is associated with poor decidualization. Besides enriching the present knowledge on metabolic changes underlying stromal cells decidualization, these findings assist in identifying potential molecular causes for decidualization failure in GTB women.
Mesoscopic Multimodal Imaging Provides New Insight to Tumor Tissue Evaluation: An Example of Macrophage Imaging of Hepatic Tumor using Organosilica Nanoparticles
Authors: Nakamura Michihiro , Hayashi Koichiro , Kubo Hitoshi , Harada Masafumi , Izumi Keisuke , Tsuruo Yoshihiro , Yogo Toshinobu 
Published: June 2017

AbstractMultimodal imaging using novel multifunctional nanoparticles provides new approach to biomedical field. Thiol-organosilica nanoparticles containing iron oxide magnetic nanoparticles (MNPs) and rhodamine B (thiol OS-MNP/Rho) were applied to multimodal imaging of hepatic tumor of Long−Evans Cinnamon (LEC) rat. The magnetic resonance imaging (MRI) of LEC rats revealed tumors in the liver clearly and semi-quantitatively due to a labeling of macrophages in liver. The fluorescent imaging (FI) showed abnormal fluorescent patterns of the liver at the mesoscopic level that was between macroscopic and microscopic level. We performed correlation analysis between optical imaging including FI and MRI. We found that the labeled macrophages located specific area in the tumor tissue and influenced the tumor size on MRI. In addition histological observation showed the labeled macrophages related specific tissue in the pathological region. We demonstrated a new approach to evaluate tumor tissue at the macroscopic and microscopic level as well as mesoscopic level using multimodal imaging.
Linking the rotation of a rigid body to the Schrödinger equation: The quantum tennis racket effect and beyond
Authors: Damme L. Van , Leiner D. , Mardešić P. , Glaser S. J. , Sugny D. 
Published: June 2017

AbstractThe design of efficient and robust pulse sequences is a fundamental requirement in quantum control. Numerical methods can be used for this purpose, but with relatively little insight into the control mechanism. Here, we show that the free rotation of a classical rigid body plays a fundamental role in the control of two-level quantum systems by means of external electromagnetic pulses. For a state to state transfer, we derive a family of control fields depending upon two free parameters, which allow us to adjust the efficiency, the time and the robustness of the control process. As an illustrative example, we consider the quantum analog of the tennis racket effect, which is a geometric property of any classical rigid body. This effect is demonstrated experimentally for the control of a spin 1/2 particle by using techniques of Nuclear Magnetic Resonance. We also show that the dynamics of a rigid body can be used to implement one-qubit quantum gates. In particular, non-adiabatic geometric quantum phase gates can be realized based on the Montgomery phase of a rigid body. The robustness issue of the gates is discussed.