bluuebunny/crossref_metadata_2025_split huggingface dataset:
Association between dietary patterns and chronic kidney disease in a middle-aged Chinese population
Authors: Xu Shan-Shan , Hua Jun , Huang Yi-Qian , Shu Long 
Published: October 2019

AbstractObjective:To explore the relationship between dietary patterns and risk of chronic kidney disease (CKD) in Chinese adults aged 45–59 years.Design:Dietary data were collected using a semi-quantitative FFQ. Factor analysis was used to identify the major dietary patterns. Logistic regression models were applied to clarify the association between dietary patterns and the risk of CKD.Setting:The present study population was a part of the population-based Nutrition and Health Study performed in the city of Hangzhou, Zhejiang Province, eastern China.Participants:A total of 2437 eligible participants (45–59 years) were enrolled in the present cross-sectional study from June 2015 to December 2016.Results:Three major dietary patterns were identified: ‘traditional southern Chinese’, ‘Western’ and ‘grains–vegetables’ patterns, collectively accounting for 25·6 % of variance in the diet. After adjustment for potential confounders, participants in the highest quartile of the Western pattern had greater odds for CKD (OR = 1·83, 95 % CI 1·21, 2·81; P < 0·05) than those in the lowest quartile. Compared with the lowest quartile of the grains–vegetables pattern, the highest quartile had lower odds for CKD (OR = 0·84, 95 % CI 0·77, 0·93; P < 0·05). In addition, there was no significant association between the traditional southern Chinese pattern and risk of CKD (P > 0·05).Conclusions:Our results suggest that the Western pattern is associated with an increased risk, whereas the grains–vegetables pattern is associated with a reduced risk for CKD. These findings can guide dietary interventions for the prevention of CKD in a middle-aged Chinese population.
Identification of promising resistance sources against sheath blight from the annual wild species of riceOryza nivara(SharmaetShastry)
Authors: Aggarwal S. K. , Neelam K. , Jain Jyoti , Kaur Rupinder , Pannu P. P. S. , Lenka S. K. , Lore J. S. , Singh Kuldeep 
Published: October 2019

AbstractSheath blight caused by soil borne necrotrophic fungusRhizoctonia solani[teleomorph-Thanatephorus cucumeris(Frank) Donk.] is a major disease of rice. The disease is increasing over the year in India and cause up to 69% yield loss under favourable conditions. A total of 67 accessions ofOryza nivarawere screened to identify resistance against sheath blight during 2015. Out of these, 16 accessions were found moderately resistant (MR) which were further evaluated during the year 2016 and 2017. After three years of screening, 12 of them were found to have a consistent moderate resistant reaction whereas four of theO. nivaraaccessions namely, IRGC81941, IRGC102463C, CR100097 and CR100110A have shown moderately susceptible to susceptible reaction against sheath blight. A correlation study revealed that different disease variables measured were significantly (P< 0.05) correlated. All the genotypes and genotype × environment interaction had a significant (P< 0.001) effect on all the disease variables. Cluster analysis showed that all the accessions were clustered into four groups which showed resistant, MR, moderately susceptible and susceptible reactions. Among all theO. nivaraaccessions IRGC81941A showed the maximum potential against sheath blight due to a least relative lesion height of 22.80%. None of the accession had complete resistance to the disease. The identified promising accessions such as IRGC81835, IRGC81941A, CR100008 and CR100111B can be utilized in a sheath blight resistance breeding program.
Guerrillas, Peasants, and Communists:Agrarian Reform in Cuba's 1958 Liberated Territories
Authors: Kozameh Sara 
Published: October 2019

AbstractIn October of 1958, amidst the guerrilla war to topple Fulgencio Batista, Fidel Castro's Rebel Army passed an Agrarian Reform Law that would serve as an embryo for the Cuban Revolution's 1959 land reform. Relying on rare documents from the insurgency, this paper reanimates the debate over the role of peasants during the war, arguing that peasants not only helped shape the movement to topple Batista, but that their mobilization led to the articulation of important guerrilla agrarian policies—including land reform. As the liberated territories became a laboratory in which rebels experimented with how to run a state, peasants took part in civil projects, simultaneously bestowing legitimacy on the movement and harnessing its organizational apparatus for the achievement of the peasants’ own goals. In highlighting the political subjectivity of Cuban peasants, this paper also gives new insight into everyday life during the rebel insurgency.
ROCK1 induces dopaminergic nerve cell apoptosis via the activation of Drp1-mediated aberrant mitochondrial fission in Parkinson’s disease
Authors: Zhang Qian , Hu Changpeng , Huang Jingbin , Liu Wuyi , Lai Wenjing , Leng Faning , Tang Qin , Liu Yali , Wang Qing , Zhou Min , Sheng Fangfang , Li Guobing , Zhang Rong 
Published: October 2019

Abstract
Dopamine deficiency is mainly caused by apoptosis of dopaminergic nerve cells in the substantia nigra of the midbrain and the striatum and is an important pathologic basis of Parkinson’s disease (PD). Recent research has shown that dynamin-related protein 1 (Drp1)-mediated aberrant mitochondrial fission plays a crucial role in dopaminergic nerve cell apoptosis. However, the upstream regulatory mechanism remains unclear. Our study showed that Drp1 knockdown inhibited aberrant mitochondrial fission and apoptosis. Importantly, we found that ROCK1 was activated in an MPP+-induced PD cell model and that ROCK1 knockdown and the specific ROCK1 activation inhibitor Y-27632 blocked Drp1-mediated aberrant mitochondrial fission and apoptosis of dopaminergic nerve cells by suppressing Drp1 dephosphorylation/activation. Our in vivo study confirmed that Y-27632 significantly improved symptoms in a PD mouse model by inhibiting Drp1-mediated aberrant mitochondrial fission and apoptosis. Collectively, our findings suggest an important molecular mechanism of PD pathogenesis involving ROCK1-regulated dopaminergic nerve cell apoptosis via the activation of Drp1-induced aberrant mitochondrial fission.
The contrary intracellular and extracellular functions of PEDF in HCC development
Authors: Li Cen , Huang Zhijian , Zhu Liuqing , Yu Xianhuan , Gao Tianxiao , Feng Juan , Hong Honghai , Yin Haofan , Zhou Ti , Qi Weiwei , Yang Zhonghan , Liu Chao , Yang Xia , Gao Guoquan 
Published: October 2019

AbstractPigment epithelium-derived factor (PEDF), a classic angiogenic inhibitor, has been reported to function as a tumor suppression protein and to downregulate in many types of solid tumors. However, the expression level of PEDF and its role in hepatocellular carcinoma (HCC) are contradictory. The present study investigates the expression and different activities of secreted and intracellular PEDF during HCC development, as well as the underlying mechanism of PEDF on HCC lipid disorders. We found that PEDF had no association with patients’ prognosis, although PEDF was highly expressed and inhibited angiogenesis in HCC tumor tissues. The animal experiments indicated that full-length PEDF exhibited equalizing effects on tumor growth activation and tumor angiogenesis inhibition in the late stage of HCC progression. Importantly, the pro-tumor activity was mediated by the intracellular PEDF, which causes accumulation of free fatty acids (FFAs) in vivo and in vitro. Based on the correlation analysis of PEDF and lipid metabolic indexes in human HCC tissues, we demonstrated that the intracellular PEDF led to the accumulation of FFA and eventually promoted HCC cell growth by inhibiting the activation of AMPK via ubiquitin–proteasome-mediated degradation, which causes increased de novo fatty acid synthesis and decreased FFA oxidation. Our findings revealed why elevated PEDF did not improve the patients’ prognosis as the offsetting intracellular and extracellular activities. This study will lead to a comprehensive understanding of the diverse role of PEDF in HCC and provide a new selective strategy by supplement of extracellular PEDF and downregulation of intracellular PEDF for the prevention and treatment of liver cancer.
Verteporfin-induced lysosomal compartment dysregulation potentiates the effect of sorafenib in hepatocellular carcinoma
Authors: Gavini Jacopo , Dommann Noëlle , Jakob Manuel O. , Keogh Adrian , Bouchez Laure C. , Karkampouna Sofia , Julio Marianna Kruithof-de , Medova Michaela , Zimmer Yitzhak , Schläfli Anna M. , Tschan Mario P. , Candinas Daniel , Stroka Deborah , Banz Vanessa 
Published: October 2019

AbstractLysosomal sequestration of anti-cancer compounds reduces drug availability at intracellular target sites, thereby limiting drug-sensitivity and inducing chemoresistance. For hepatocellular carcinoma (HCC), sorafenib (SF) is the first line systemic treatment, as well as a simultaneous activator of autophagy-induced drug resistance. The purpose of this study is to elucidate how combination therapy with the FDA-approved photosensitizer verteporfin (VP) can potentiate the antitumor effect of SF, overcoming its acquired resistance mechanisms. HCC cell lines and patient-derived in vitro and in vivo preclinical models were used to identify the molecular mechanism of action of VP alone and in combination with SF. We demonstrate that SF is lysosomotropic and increases the total number of lysosomes in HCC cells and patient-derived xenograft model. Contrary to the effect on lysosomal stability by SF, VP is not only sequestered in lysosomes, but induces lysosomal pH alkalinization, lysosomal membrane permeabilization (LMP) and tumor-selective proteotoxicity. In combination, VP-induced LMP potentiates the antitumor effect of SF, further decreasing tumor proliferation and progression in HCC cell lines and patient-derived samples in vitro and in vivo. Our data suggest that combination of lysosome-targeting compounds, such as VP, in combination with already approved chemotherapeutic agents could open a new avenue to overcome chemo-insensitivity caused by passive lysosomal sequestration of anti-cancer drugs in the context of HCC.
Modeling and observation of mid-infrared nonlocality in effective epsilon-near-zero ultranarrow coaxial apertures
Authors: Yoo Daehan , Vidal-Codina Ferran , Ciracì Cristian , Nguyen Ngoc-Cuong , Smith David R. , Peraire Jaime , Oh Sang-Hyun 
Published: October 2019

AbstractWith advances in nanofabrication techniques, extreme-scale nanophotonic devices with critical gap dimensions of just 1–2 nm have been realized. Plasmons in such ultranarrow gaps can exhibit nonlocal response, which was previously shown to limit the field enhancement and cause optical properties to deviate from the local description. Using atomic layer lithography, we create mid-infrared-resonant coaxial apertures with gap sizes as small as 1 nm and observe strong evidence of nonlocality, including spectral shifts and boosted transmittance of the cutoff epsilon-near-zero mode. Experiments are supported by full-wave 3-D nonlocal simulations performed with the hybridizable discontinuous Galerkin method. This numerical method captures atomic-scale variations of the electromagnetic fields while efficiently handling extreme-scale size mismatch. Combining atomic-layer-based fabrication techniques with fast and accurate numerical simulations provides practical routes to design and fabricate highly-efficient large-area mid-infrared sensors, antennas, and metasurfaces.
A tunable dual-input system for on-demand dynamic gene expression regulation
Authors: Pedone Elisa , Postiglione Lorena , Aulicino Francesco , Rocca Dan L. , Montes-Olivas Sandra , Khazim Mahmoud , di Bernardo Diego , Pia Cosma Maria , Marucci Lucia 
Published: October 2019

AbstractCellular systems have evolved numerous mechanisms to adapt to environmental stimuli, underpinned by dynamic patterns of gene expression. In addition to gene transcription regulation, modulation of protein levels, dynamics and localization are essential checkpoints governing cell functions. The introduction of inducible promoters has allowed gene expression control using orthogonal molecules, facilitating its rapid and reversible manipulation to study gene function. However, differing protein stabilities hinder the generation of protein temporal profiles seen in vivo. Here, we improve the Tet-On system integrating conditional destabilising elements at the post-translational level and permitting simultaneous control of gene expression and protein stability. We show, in mammalian cells, that adding protein stability control allows faster response times, fully tunable and enhanced dynamic range, and improved in silico feedback control of gene expression. Finally, we highlight the effectiveness of our dual-input system to modulate levels of signalling pathway components in mouse Embryonic Stem Cells.
Reduced mu opioid receptor availability in schizophrenia revealed with [11C]-carfentanil positron emission tomographic Imaging
Authors: Ashok Abhishekh H. , Myers Jim , Reis Marques Tiago , Rabiner Eugenii A. , Howes Oliver D. 
Published: October 2019

AbstractNegative symptoms, such as amotivation and anhedonia, are a major cause of functional impairment in schizophrenia. There are currently no licensed treatments for negative symptoms, highlighting the need to understand the molecular mechanisms underlying them. Mu-opioid receptors (MOR) in the striatum play a key role in hedonic processing and reward function and are reduced post-mortem in schizophrenia. However, it is unknown if mu-opioid receptor availability is altered in-vivo or related to negative symptoms in schizophrenia. Using [11 C]-carfentanil positron emission tomography (PET) scans in 19 schizophrenia patients and 20 age-matched healthy controls, here we show a significantly lower MOR availability in patients with schizophrenia in the striatum (Cohen’s d = 0.7), and the hedonic network. In addition, we report a marked global increase in inter-regional covariance of MOR availability in schizophrenia, largely due to increased cortical-subcortical covariance.
Insulin-producing organoids engineered from islet and amniotic epithelial cells to treat diabetes
Authors: Lebreton Fanny , Lavallard Vanessa , Bellofatto Kevin , Bonnet Romain , Wassmer Charles H. , Perez Lisa , Kalandadze Vakhtang , Follenzi Antonia , Boulvain Michel , Kerr-Conte Julie , Goodman David J. , Bosco Domenico , Berney Thierry , Berishvili Ekaterine 
Published: October 2019

AbstractMaintaining long-term euglycemia after intraportal islet transplantation is hampered by the considerable islet loss in the peri-transplant period attributed to inflammation, ischemia and poor angiogenesis. Here, we show that viable and functional islet organoids can be successfully generated from dissociated islet cells (ICs) and human amniotic epithelial cells (hAECs). Incorporation of hAECs into islet organoids markedly enhances engraftment, viability and graft function in a mouse type 1 diabetes model. Our results demonstrate that the integration of hAECs into islet cell organoids has great potential in the development of cell-based therapies for type 1 diabetes. Engineering of functional mini-organs using this strategy will allow the exploration of more favorable implantation sites, and can be expanded to unlimited (stem-cell-derived or xenogeneic) sources of insulin-producing cells.
Interplay between the human gut microbiome and host metabolism
Authors: Visconti Alessia , Le Roy Caroline I. , Rosa Fabio , Rossi Niccolò , Martin Tiphaine C. , Mohney Robert P. , Li Weizhong , de Rinaldis Emanuele , Bell Jordana T. , Venter J. Craig , Nelson Karen E. , Spector Tim D. , Falchi Mario 
Published: October 2019

AbstractThe human gut is inhabited by a complex and metabolically active microbial ecosystem. While many studies focused on the effect of individual microbial taxa on human health, their overall metabolic potential has been under-explored. Using whole-metagenome shotgun sequencing data in 1,004 twins, we first observed that unrelated subjects share, on average, almost double the number of metabolic pathways (82%) than species (43%). Then, using 673 blood and 713 faecal metabolites, we found metabolic pathways to be associated with 34% of blood and 95% of faecal metabolites, with over 18,000 significant associations, while species showed less than 3,000 associations. Finally, we estimated that the microbiome was involved in a dialogue between 71% of faecal, and 15% of blood, metabolites. This study underlines the importance of studying the microbial metabolic potential rather than focusing purely on taxonomy to find therapeutic and diagnostic targets, and provides a unique resource describing the interplay between the microbiome and the systemic and faecal metabolic environments.
Directing isomerization reactions of cumulenes with electric fields
Authors: Zang Yaping , Zou Qi , Fu Tianren , Ng Fay , Fowler Brandon , Yang Jingjing , Li Hexing , Steigerwald Michael L. , Nuckolls Colin , Venkataraman Latha 
Published: October 2019

AbstractElectric fields have been proposed as having a distinct ability to catalyze chemical reactions through the stabilization of polar or ionic intermediate transition states. Although field-assisted catalysis is being researched, the ability to catalyze reactions in solution using electric fields remains elusive and the understanding of mechanisms of such catalysis is sparse. Here we show that an electric field can catalyze the cis-to-trans isomerization of [3]cumulene derivatives in solution, in a scanning tunneling microscope. We further show that the external electric field can alter the thermodynamics inhibiting the trans-to-cis reverse reaction, endowing the selectivity toward trans isomer. Using density functional theory-based calculations, we find that the applied electric field promotes a zwitterionic resonance form, which ensures a lower energy transition state for the isomerization reaction. The field also stabilizes the trans form, relative to the cis, dictating the cis/trans thermodynamics, driving the equilibrium product exclusively toward the trans.
Single-particle electroluminescence of CsPbBr3 perovskite nanocrystals reveals particle-selective recombination and blinking as key efficiency factors
Authors: Sharma Dharmendar Kumar , Hirata Shuzo , Vacha Martin 
Published: October 2019

AbstractHalide perovskites nanocrystals (NCs) are being explored as promising materials for optoelectronic applications, such as light-emitting devices or lasers. However, electroluminescence devices prepared from such NCs have long suffered from low efficiency and there has been no systematic study on the nanoscale origin of the poor efficiencies. Here, we use single-particle spectroscopy to compare electroluminescence and photoluminescence on the level of individual NCs of the perovskite CsPbBr3. The NCs form aggregates in a conducting matrix used as an emission layer in an electroluminescence device. In electroluminescence, only a small fraction of the NCs within the aggregate is emitting as a result of efficient charge migration, accumulation and selective recombination on larger NCs, leading to pronounced blinking and decreased efficiency. Under the condition of comparable excitation rates in both electroluminescence and photoluminescence, the intrinsic quantum yield in electroluminescence is on average 0.36 of that in photoluminescence.
Multicomponent fluctuation spectrum at the quantum critical point in CeCu6−xAgx
Authors: Poudel Lekh , Lawrence Jon M. , Wu Liusuo S. , Ehlers Georg , Qiu Yiming , May Andrew F. , Ronning Filip , Lumsden Mark D. , Mandrus David , Christianson Andrew D. 
Published: October 2019

AbstractQuantum critical points (QCPs) are widely accepted as a source of a diverse set of collective quantum phases of matter. The basic nature of a QCP is manifested in the critical fluctuation spectrum which in turn is determined by the adjacent phases and associated order parameters. Here we show that the critical fluctuation spectrum of CeCu5.8Ag0.2 can not be explained by fluctuations associated with a single wave vector. Interestingly, when the critical fluctuations at wave vectors corresponding to the incommensurate antiferromagnetic order adjacent to the QCP are separated they are found to be three dimensional and to obey the scaling behavior expected for long wavelength fluctuations near an itinerant antiferromagnetic QCP. Without this separation, E/T scaling with a fractional exponent is observed. Together these results demonstrate that a multicomponent fluctuation spectrum is a previously unexplored route to obtaining E/T scaling at a QCP.
Solution structure of the autophagy-related protein LC3C reveals a polyproline II motif on a mobile tether with phosphorylation site
Authors: Krichel Carsten , Möckel Christina , Schillinger Oliver , Huesgen Pitter F. , Sticht Heinrich , Strodel Birgit , Weiergräber Oliver H. , Willbold Dieter , Neudecker Philipp 
Published: October 2019

Abstract(Macro-)autophagy is a compartmental degradation pathway conserved from yeast to mammals. The yeast protein Atg8 mediates membrane tethering/hemifusion and cargo recruitment and is essential for autophagy. The human MAP1LC3/GABARAP family proteins show high sequence identity with Atg8, but MAP1LC3C is distinguished by a conspicuous amino-terminal extension with unknown functional significance. We have determined the high-resolution three-dimensional structure and measured the backbone dynamics of MAP1LC3C by NMR spectroscopy. From Ser18 to Ala120, MAP1LC3C forms an α-helix followed by the ubiquitin-like tertiary fold with two hydrophobic binding pockets used by MAP1LC3/GABARAP proteins to recognize targets presenting LC3-interacting regions (LIRs). Unlike other MAP1LC3/GABARAP proteins, the amino-terminal region of MAP1LC3C does not form a stable helix α1 but a “sticky arm” consisting of a polyproline II motif on a flexible linker. Ser18 at the interface between this linker and the structural core can be phosphorylated in vitro by protein kinase A, which causes additional conformational heterogeneity as monitored by NMR spectroscopy and molecular dynamics simulations, including changes in the LIR-binding interface. Based on these results we propose that the amino-terminal polyproline II motif mediates specific interactions with the microtubule cytoskeleton and that Ser18 phosphorylation modulates the interplay of MAP1LC3C with its various target proteins.