bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mental health care utilisation among internally displaced persons in Ukraine: results from a nation-wide survey
Authors: Roberts B. , Makhashvili N. , Javakhishvili J. , Karachevskyy A. , Kharchenko N. , Shpiker M. , Richardson E. 
Published: July 2017

AimsThere are an estimated 1.5 million internally displaced persons (IDPs) in Ukraine because of the armed conflict in the east of the country. The aim of this paper is to examine utilisation patterns of mental health and psychosocial support (MHPSS) care among IDPs in Ukraine.MethodsA cross-sectional survey design was used. Data were collected from 2203 adult IDPs throughout Ukraine between March and May 2016. Data on mental health care utilisation were collected, along with outcomes including post-traumatic stress disorder (PTSD), depression and anxiety. Descriptive and multivariate regression analyses were used.ResultsPTSD prevalence was 32%, depression prevalence was 22%, and anxiety prevalence was 17%. Among those that likely required care (screened positive with one of the three disorders, and also self-reporting a problem) there was a large treatment gap, with 74% of respondents who likely required MHPSS care over the past 12 months not receiving it. For the 26% (N = 180) that had sought care, the most common sources of services/support were pharmacies, family or district doctor/paramedic (feldsher), neurologist at a polyclinic, internist/neurologist at a general hospital, psychologists visiting communities, and non-governmental organisations/volunteer mental health/psychosocial centres. Of the 180 respondents who did seek care, 163 could recall whether they had to pay for their care. Of these 163 respondents, 72 (44%) recalled paying for the care they received despite government care officially being free in Ukraine. The average costs they paid for care was US$107 over the previous 12 months. All 180 respondents reported having to pay for medicines and the average costs for medicines was US$109 over the previous 12 months. Among the 74% had not sought care despite likely needing it; the principal reasons for not seeking care were: thought that they would get better by using their own medications, could not afford to pay for health services or medications, no awareness of where to receive help, poor understanding by health care providers, poor quality of services, and stigma/embarrassment. The findings from multivariate regression analysis show the significant influence of a poor household economic situation on not accessing care.ConclusionsThe study highlights a high burden of mental disorders and large MHPSS treatment gap among IDPs in Ukraine. The findings support the need for a scaled-up, comprehensive and trauma-informed response to provision of MHPSS care of IDPs in Ukraine alongside broader health system strengthening.
Biography and Borderlands: Chao Sone Bouttarobol, a Champassak Royal, and Thailand, Laos and Cambodia
Authors: Baird Ian G. 
Published: July 2017

AbstractAlthough biographical and life history approaches are potentially important tools for historical geographers, biographical methodologies have rarely been used to specifically investigate borderland dynamics. In this article, I argue that biography can be useful for understanding the ways in which borders have been recognised and negotiated historically. As a case study, I examine the life of Chao Sone Bouttarobol, a member of the Champassak Royal House, who was born in 1895 and died in 1979. As his life story illustrates, the emergence of new national borders had a significant impact on Sone, although family ties and relationships allowed him to cross the national administrative borders that now exist between Thailand, Laos, and Cambodia, often with relative ease. Studying one individual makes it possible to explore the ways in which he interacted and negotiated with borders that cut across the Champassak Royal House's traditional space of influence.
Pre-synaptic TrkB in basolateral amygdala neurons mediates BDNF signaling transmission in memory extinction
Authors: Li Yuan , Wang Dongdong , Li Yang , Chu Hongxia , Zhang Lining , Hou Ming , Jiang Xingyu , Chen Zheyu , Su Bo , Sun Tao 
Published: July 2017

AbstractBrain-derived neurotrophic factor (BDNF) and its high affinity receptor, TrkB, play an essential role in memory extinction. Our previous work has shown that JIP3 (JNK interacted protein 3) mediates anterograde axonal transport of TrkB through the direct binding of its coiled-coil domain 1 (CC1) with TrkB. Here, we constructed a fluorescent CC1 and enhanced green fluorescent protein (EGFP) fused protein, CC1-EGFP, and found that CC1-EGFP could specifically interrupt TrkB anterograde axonal transport and its localization at the pre-synaptic site. Consistent with this, TrkB-mediated pre-synaptic vesicle release and retrograde axonal signaling transmission were disrupted by CC1-EGFP. Neuronal expression of CC1-EGFP in the basolateral amygdala (BLA) impaired fear memory extinction. And, it blocked BDNF in the BLA-induced enhancement of TrkB phosphorylation in the infralimbic prefrontal cortex (IL). Together, this study not only suggests that pre-synaptic TrkB in BLA neurons is necessary for memory extinction and contributes to the BDNF signaling transduction from the BLA to IL, but also provides CC1-EGFP as a novel tool to specifically regulate pre-synaptic TrkB expression in vitro and in vivo.
The cohesin complex prevents Myc-induced replication stress
Authors: Rohban Sara , Cerutti Aurora , Morelli Marco J , d'Adda di Fagagna Fabrizio , Campaner Stefano 
Published: July 2017

AbstractThe cohesin complex is mutated in cancer and in a number of rare syndromes collectively known as Cohesinopathies. In the latter case, cohesin deficiencies have been linked to transcriptional alterations affecting Myc and its target genes. Here, we set out to understand to what extent the role of cohesins in controlling cell cycle is dependent on Myc expression and activity. Inactivation of the cohesin complex by silencing the RAD21 subunit led to cell cycle arrest due to both transcriptional impairment of Myc target genes and alterations of replication forks, which were fewer and preferentially unidirectional. Ectopic activation of Myc in RAD21 depleted cells rescued Myc-dependent transcription and promoted S-phase entry but failed to sustain S-phase progression due to a strong replicative stress response, which was associated to a robust DNA damage response, DNA damage checkpoint activation and synthetic lethality. Thus, the cohesin complex is dispensable for Myc-dependent transcription but essential to prevent Myc-induced replicative stress. This suggests the presence of a feed-forward regulatory loop where cohesins by regulating Myc level control S-phase entry and prevent replicative stress.
Knockout of MARCH2 inhibits the growth of HCT116 colon cancer cells by inducing endoplasmic reticulum stress
Authors: Xia Dan , Ji Wanli , Xu Chentong , Lin Xin , Wang Xiaokun , Xia Yan , Lv Ping , Song Quansheng , Ma Dalong , Chen Yingyu 
Published: July 2017

AbstractMembrane-associated RING-CH protein 2 (MARCH2), a member of the MARCH family, functions in vesicle trafficking and autophagy regulation. In this study, we established MARCH2 knockout HCT116 cell lines using CRISPR/Cas9-mediated genome editing to evaluate the role of MARCH2 in colon cancer in vitro and in vivo. Knockout of MARCH2 suppressed cell proliferation, and promoted autophagy, apoptosis and G2/M phase cell cycle arrest. These effects were associated with activation of endoplasmic reticulum (ER) stress. In addition, loss of MARCH2 sensitized HCT116 cells to the chemotherapy drugs etoposide and cisplatin. Moreover, we analyzed the clinical significance of MARCH2 in human colon carcinoma (n=100). High MARCH2 expression was significantly associated with advanced clinicopathological features and poorer overall survival in colon carcinoma. MARCH2 expression correlated negatively with expression of the unfolded protein response molecule p-PERK in colon cancer. Collectively, these data reveal a relationship between MARCH2, ER stress and colon cancer, and indicates MARCH2 may have an important role in the development and progression of colon cancer.
Bayesian association scan reveals loci associated with human lifespan and linked biomarkers
Authors: McDaid Aaron F. , Joshi Peter K. , Porcu Eleonora , Komljenovic Andrea , Li Hao , Sorrentino Vincenzo , Litovchenko Maria , Bevers Roel P. J. , Rüeger Sina , Reymond Alexandre , Bochud Murielle , Deplancke Bart , Williams Robert W. , Robinson-Rechavi Marc , Paccaud Fred , Rousson Valentin , Auwerx Johan , Wilson James F. , Kutalik Zoltán 
Published: July 2017

AbstractThe enormous variation in human lifespan is in part due to a myriad of sequence variants, only a few of which have been revealed to date. Since many life-shortening events are related to diseases, we developed a Mendelian randomization-based method combining 58 disease-related GWA studies to derive longevity priors for all HapMap SNPs. A Bayesian association scan, informed by these priors, for parental age of death in the UK Biobank study (n=116,279) revealed 16 independent SNPs with significant Bayes factor at a 5% false discovery rate (FDR). Eleven of them replicate (5% FDR) in five independent longevity studies combined; all but three are depleted of the life-shortening alleles in older Biobank participants. Further analysis revealed that brain expression levels of nearby genes (RBM6, SULT1A1andCHRNA5) might be causally implicated in longevity. Gene expression and caloric restriction experiments in model organisms confirm the conserved role forRBM6andSULT1A1in modulating lifespan.
Thermally stable single atom Pt/m-Al2O3 for selective hydrogenation and CO oxidation
Authors: Zhang Zailei , Zhu Yihan , Asakura Hiroyuki , Zhang Bin , Zhang Jiaguang , Zhou Maoxiang , Han Yu , Tanaka Tsunehiro , Wang Aiqin , Zhang Tao , Yan Ning 
Published: July 2017

AbstractSingle-atom metal catalysts offer a promising way to utilize precious noble metal elements more effectively, provided that they are catalytically active and sufficiently stable. Herein, we report a synthetic strategy for Pt single-atom catalysts with outstanding stability in several reactions under demanding conditions. The Pt atoms are firmly anchored in the internal surface of mesoporous Al2O3, likely stabilized by coordinatively unsaturated pentahedral Al3+ centres. The catalyst keeps its structural integrity and excellent performance for the selective hydrogenation of 1,3-butadiene after exposure to a reductive atmosphere at 200 °C for 24 h. Compared to commercial Pt nanoparticle catalyst on Al2O3 and control samples, this system exhibits significantly enhanced stability and performance for n-hexane hydro-reforming at 550 °C for 48 h, although agglomeration of Pt single-atoms into clusters is observed after reaction. In CO oxidation, the Pt single-atom identity was fully maintained after 60 cycles between 100 and 400 °C over a one-month period.
Increased mitochondrial fusion allows the survival of older animals in diverse C. elegans longevity pathways
Authors: Chaudhari Snehal N. , Kipreos Edward T. 
Published: July 2017

AbstractMitochondria are dynamic organelles that undergo fusion and fission events. Mitochondrial dynamics are required for mitochondrial viability and for responses to changes in bioenergetic status. Here we describe an insulin-signaling and SCFLIN-23-regulated pathway that controls mitochondrial fusion in Caenorhabditis elegans by repressing the expression of the mitochondrial proteases SPG-7 and PPGN-1. This pathway is required for mitochondrial fusion in response to physical exertion, and for the associated extension in lifespan. We show that diverse longevity pathways exhibit increased levels of elongated mitochondria. The increased mitochondrial fusion is essential for longevity in the diverse longevity pathways, as inhibiting mitochondrial fusion reduces their lifespans to wild-type levels. Our results suggest that increased mitochondrial fusion is not a major driver of longevity, but rather is essential to allow the survival of older animals beyond their normal lifespan in diverse longevity pathways.
Loss of succinyl-CoA synthase ADP-forming β subunit disrupts mtDNA stability and mitochondrial dynamics in neurons
Authors: Zhao Yujun , Tian Jing , Sui Shaomei , Yuan Xiaodong , Chen Hao , Qu Chuanqiang , Du Yifeng , Guo Lan , Du Heng 
Published: July 2017

AbstractSuccinyl Coenzyme A synthetase (SCS) is a key mitochondrial enzyme. Defected SCS ADP-forming β subunit (SCS A-β) is linked to lethal infantile Leigh or leigh-like syndrome. However, the impacts of SCS A-β deficiency on mitochondria specifically in neurons have not yet been comprehensively investigated. Here, by down-regulating the expression levels of SCS A-β in cultured mouse neurons, we have found that SCS A-β deficiency induces severe mitochondrial dysfunction including lowered oxidative phosphorylation (OXPHOS) efficiency, increased mitochondrial superoxide production, and mtDNA depletion as well as aberrations of mitochondrial fusion and fission proteins, which eventually leads to neuronal stress. Our data also suggest that the deregulation of mitochondrial nucleoside diphosphate kinase (NDPK) together with defects in mitochondrial transcription factors including mitochondrial DNA pol γ and Twinkle contribute to SCS A-β deficiency-mediated mtDNA instability. Furthermore, we have found that SCS A-β deficiency has detrimental influence on neuronal mitochondrial dynamics. Put together, the results have furnished our knowledge on the pathogenesis of SCS A-β deficiency-related mitochondrial diseases and revealed the vital role of SCS A-β in maintaining neuronal mitochondrial quality control and neuronal physiology.
Intercellular Genetic Interaction Between Irf6 and Twist1 during Craniofacial Development
Authors: Fakhouri Walid D. , Metwalli Kareem , Naji Ali , Bakhiet Sarah , Quispe-Salcedo Angela , Nitschke Larissa , Kousa Youssef A. , Schutte Brian C. 
Published: July 2017

AbstractInterferon Regulatory Factor 6 (IRF6) and TWIST1 are transcription factors necessary for craniofacial development. Human genetic studies showed that mutations in IRF6 lead to cleft lip and palate and mandibular abnormalities. In the mouse, we found that loss of Irf6 causes craniosynostosis and mandibular hypoplasia. Similarly, mutations in TWIST1 cause craniosynostosis, mandibular hypoplasia and cleft palate. Based on this phenotypic overlap, we asked if Irf6 and Twist1 interact genetically during craniofacial formation. While single heterozygous mice are normal, double heterozygous embryos (Irf6+/−
; Twist1+/−
) can have severe mandibular hypoplasia that leads to agnathia and cleft palate at birth. Analysis of spatiotemporal expression showed that Irf6 and Twist1 are found in different cell types. Consistent with the intercellular interaction, we found reduced expression of Endothelin1 (EDN1) in mandible and transcription factors that are critical for mandibular patterning including DLX5, DLX6 and HAND2, were also reduced in mesenchymal cells. Treatment of mandibular explants with exogenous EDN1 peptides partially rescued abnormalities in Meckel’s cartilage. In addition, partial rescue was observed when double heterozygous embryos also carried a null allele of p53. Considering that variants in IRF6 and TWIST1 contribute to human craniofacial defects, this gene-gene interaction may have implications on craniofacial disorders.
High-Coverage Whole-Exome Sequencing Identifies Candidate Genes for Suicide in Victims with Major Depressive Disorder
Authors: Tombácz Dóra , Maróti Zoltán , Kalmár Tibor , Csabai Zsolt , Balázs Zsolt , Takahashi Shinichi , Palkovits Miklós , Snyder Michael , Boldogkői Zsolt 
Published: July 2017

AbstractWe carried out whole-exome ultra-high throughput sequencing in brain samples of suicide victims who had suffered from major depressive disorder and control subjects who had died from other causes. This study aimed to reveal the selective accumulation of rare variants in the coding and the UTR sequences within the genes of suicide victims. We also analysed the potential effect of STR and CNV variations, as well as the infection of the brain with neurovirulent viruses in this behavioural disorder. As a result, we have identified several candidate genes, among others three calcium channel genes that may potentially contribute to completed suicide. We also explored the potential implication of the TGF-β signalling pathway in the pathogenesis of suicidal behaviour. To our best knowledge, this is the first study that uses whole-exome sequencing for the investigation of suicide.
Synergistic Strategy for Multicolor Two-photon Microscopy: Application to the Analysis of Germinal Center Reactions In Vivo
Authors: Rakhymzhan Asylkhan , Leben Ruth , Zimmermann Hanna , Günther Robert , Mex Peggy , Reismann David , Ulbricht Carolin , Acs Andreas , Brandt Alexander U. , Lindquist Randall L. , Winkler Thomas H. , Hauser Anja E. , Niesner Raluca A. 
Published: July 2017

AbstractSimultaneous detection of multiple cellular and molecular players in their native environment, one of the keys to a full understanding of immune processes, remains challenging for in vivo microscopy. Here, we present a synergistic strategy for spectrally multiplexed in vivo imaging composed of (i) triple two-photon excitation using spatiotemporal synchronization of two femtosecond lasers, (ii) a broad set of fluorophores with emission ranging from blue to near infrared, (iii) an effective spectral unmixing algorithm. Using our approach, we simultaneously excite and detect seven fluorophores expressed in distinct cellular and tissue compartments, plus second harmonics generation from collagen fibers in lymph nodes. This enables us to visualize the dynamic interplay of all the central cellular players during germinal center reactions. While current in vivo imaging typically enables recording the dynamics of 4 tissue components at a time, our strategy allows a more comprehensive analysis of cellular dynamics involving 8 single-labeled compartments. It enables to investigate the orchestration of multiple cellular subsets determining tissue function, thus, opening the way for a mechanistic understanding of complex pathophysiologic processes in vivo. In the future, the design of transgenic mice combining a larger spectrum of fluorescent proteins will reveal the full potential of our method.
Changes in the soil organic carbon balance on China’s cropland during the last two decades of the 20th century
Authors: Zhang F. , Wang Z. , Glidden S. , Wu Y. P. , Tang L. , Liu Q. Y. , Li C. S. , Frolking S. 
Published: July 2017

AbstractAgro-ecosystems play an important role in regulating global changes caused by greenhouse gas emissions. Restoration of soil organic carbon (SOC) in agricultural soils can not only improve soil quality but also influence climate change and agronomic productivity. With about half of its land area under agricultural use, China exhibits vast potential for carbon (C) sequestration that needs to be researched. Chinese cropland has experienced SOC change over the past century. The study of SOC dynamics under different bioclimatic conditions and cropping systems can help us to better understand this historical change, current status, the impacts of bioclimatic conditions on SOC and future trends. We used a simulation based on historical statistical data to analyze the C balance of Chinese croplands during the 1980s and 1990s, taking into account soil, climate and agricultural management. Nationwide, 77.6% of the national arable land is considered to be in good condition. Appropriate farm management practices should be adopted to improve the poor C balance of the remaining 22.4% of cropland to promote C sequestration.
Effect of Niacin on Inflammation and Angiogenesis in a Murine Model of Ulcerative Colitis
Authors: Salem Hesham Aly , Wadie Walaa 
Published: July 2017

AbstractButyrate and niacin are produced by gut microbiota, however butyrate has received most attention for its effects on colonic health. The present study aimed at exploring the effect of niacin on experimental colitis as well as throwing some light on the ability of niacin to modulate angiogenesis which plays a crucial role of in the pathogenesis of inflammatory bowel disease. Rats were given niacin for 2 weeks. On day 8, colitis was induced by intrarectal administration of iodoacetamide. Rats were sacrificed on day 15 and colonic damage was assessed macroscopically and histologically. Colonic myeloperoxidase (MPO), tumour necrosis factor (TNF)-α, interleukin (IL)-10, vascular endothelial growth factor (VEGF), angiostatin and endostatin levels were determined. Niacin attenuated the severity of colitis as demonstrated by a decrease in weight loss, colonic wet weight and MPO activity. Iodoacetamide-induced rise in the colonic levels of TNF-α, VEGF, angiostatin and endostatin was reversed by niacin. Moreover, niacin normalized IL-10 level in colon. Mepenzolate bromide, a GPR109A receptor blocker, abolished the beneficial effects of niacin on body weight, colon wet weight as well as colonic levels of MPO and VEGF. Therefore, niacin was effective against iodoacetamide-induced colitis through ameliorating pathologic angiogenesis and inflammatory changes in a GPR109A-dependent manner.
Increased EphA4-ephexin1 signaling in the medial prefrontal cortex plays a role in depression-like phenotype
Authors: Zhang Ji-chun , Yao Wei , Qu Youge , Nakamura Mayumi , Dong Chao , Yang Chun , Ren Qian , Ma Min , Han Mei , Shirayama Yukihiko , Hayashi-Takagi Akiko , Hashimoto Kenji 
Published: July 2017

AbstractAccumulating evidence suggests a role of the ephrin receptor EphA4 and the downstream protein ephexin1 in synaptic plasticity, which is implicated in depression. We examined whether EphA4–ephexin1 signaling plays a role in the pathophysiology of depression, and the antidepressant-like effect of EphA4 inhibitor rhynchophylline. We found increased ratios of p-EphA4/EphA4 and p-ephexin1/ephexin1 in the prefrontal cortex (PFC) and hippocampus but not in the nucleus accumbens (NAc), of susceptible mice after social defeat stress. Furthermore, the p-EphA4/EphA4 ratio was higher in the parietal cortex of depressed patients compared with controls. Systemic administration of rhynchophylline, produced a rapid antidepressant-like effect in a social defeat stress model by inhibiting EphA4–ephexin1 signaling and activating brain-derived neurotrophic factor-TrkB signaling in the PFC and hippocampus. Pretreatment with rhynchophylline before each social defeat stress could prevent the onset of the depression-like phenotype after repeated social defeat stress. Overexpression of EphA4 in the medial PFC owing to infection with an EphA4 adeno-associated virus caused the depression-like phenotype 3 weeks later and rhynchophylline had a rapid antidepressant-like effect in these mice. These findings suggest that increased EphA4–ephexin1 signaling in the PFC plays a role in the pathophysiology of depression.