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2,767 results on '"R. Jia"'

1. A 28-time-point cropland area change dataset in Northeast China from 1000 to 2020

Author

R. Jia, X. Fang, Y. Yang, M. Yokozawa, and Y. Ye

Subjects
Environmental sciences, GE1-350, Geology, QE1-996.5
Abstract

Based on historical documents, population data, published results, remote sensing data products, statistical data, and survey data, this study reconstructed the cropland area and the spatial pattern changes at 28 time points from 1000 to 2020 in Northeast China. The period from 1000 to 1600 corresponds to historical provincial-level administrative districts, while the period from 1700 to 2020 corresponds to modern county-level administrative districts. The main findings are as follows: (1) the cropland in Northeast China exhibited phase changes of expansion–reduction–expansion over the past millennium. (2) The cropland area in Northeast China increased from 0.55×104 km2 in 1000 to 37.90×104 km2 in 2020, and the average cropland fraction increased from 0.37 % to 26.27 %; (3) from 1000 to 1200, the cropland area exhibited an increasing trend, which peaked in 1200. The scope of land reclamation was comparable to modern times, but the overall cropland fraction remained low. The cropland area significantly decreased between 1300 and 1600, with the main land reclamation area being reduced southward into Liaoning province. From 1700 to 1850, the cropland area increased slowly and the agricultural reclamation gradually expanded northward. After 1850, there was almost exponential growth, with the cropland area continuously expanding to the whole study area, and this growth trend persists until 2020; (4) the dataset of changes in the cropland of administrative districts in Northeast China, reconstructed based on multiple data sources and improved historical cropland reconstruction methods, significantly enhances time resolution and reliability. Additionally, the dataset shows relatively better credibility assessment results, which can provide a refined database for historical land use and land cover change (LUCC) dataset reconstruction, carbon emission estimation, climate data construction, etc. The dataset can be downloaded from https://doi.org/10.6084/m9.figshare.25450468.v2 (Jia et al., 2024).

Published
2024
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2. Shape-from-Shading Derived DEMs from ShadowCam Images in Permanently Shadowed Regions at the Lunar South Pole: A First Look

Author

R. Jia, B. Wu, and P. Mahanti

Subjects
Technology, Engineering (General). Civil engineering (General), TA1-2040, Applied optics. Photonics, TA1501-1820
Abstract

The lunar south pole, particularly its permanently shadowed regions (PSRs), has been the focus of future lunar exploration. The solar altitude angle at the lunar south pole is less than ∼ 2°, resulting in the PSRs not being directly illuminated and the possible existence of water ice in the PSRs due to the low temperatures. High-resolution digital elevation models (DEMs) in PSRs are crucial for future exploration missions and scientific research. However, existing image datasets (e.g., LROC NAC images) cannot penetrate the PSRs. Laser altimetry (e.g., LOLA) can measure the PSRs, but the DEMs derived from LOLA suffer from noises and interpolation defects. ShadowCam is a newly deployed camera onboard the Korea Pathfinder Lunar Orbiter, with a high imaging sensitivity. ShadowCam can capture the faint secondary illumination within PSRs, revealing previously indistinguishable topographic features in persistent darkness. Based on our existing Shape-from-Shading (SfS) pipeline for generating high-resolution DEMs from monocular images, we introduce a novel SfS approach that utilizes secondary illumination and reflectance to reconstruct pixel-wise high-resolution DEMs from ShadowCam images in PSRs. The approach consists of three steps: (1) modeling the secondary illumination on the target surfaces in PSRs based on the view factor; (2) optimizing a low-resolution LOLA DEM using the secondary illumination model; (3) refining the DEM to pixel-wise resolution based on SfS using the ShadowCam images. A test area (approximately 1 km × 1 km) within the PSR in the Shackleton crater near the lunar south pole is used for experimental evaluation. The results show that the DEM generated by the proposed approach is highly consistent with the direct LOLA measurements, particularly in small-scale topographic features such as crater floors and rims that are absent from the LOLA DEM. A first look at the results indicates that the proposed approach has great potential for generating high-resolution DEMs from ShadowCam images in PSRs, which can aid future exploration missions targeting the PSRs at the lunar south pole and support related scientific research on the water ice in the PSRs.

Published
2024
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3. The potential role of R2R3-MYB gene family in the phenylpropanoid pathway and regulatory mechanism in Fragaria × ananassa

Author

R. Jia, C.L. Ma, X.W. Jiang, and H.Q. Li

Subjects
fragaria × ananassa, gene expression pattern, mirna, phylogenetic relationship, protein-protein interaction, r2r3-myb gene family, Biology (General), QH301-705.5, Plant ecology, QK900-989
Abstract

It is common knowledge that R2R3-MYB transcription factors play significant roles in plant biological and physiological processes, especially in the phenylpropanoid metabolism pathway. The cultivated strawberry (Fragaria × ananassa Duch.) is an octoploid (2n = 8x = 56) species from the Rosaceae family and it is also an important fruit crop species. However, the function of R2R3-MYB genes in strawberry remains largely unknown. Here, based on the genome of the cultivated strawberry cv. Reikou, 66 FanMYB genes were found and systematically analyzed. RNA-seq analysis revealed that some FanMYBs exhibited tissue-specific expressions and were methyl jasmonate (MeJA)-responsive. Phylogenetic relationships and protein-protein interaction analysis suggested that 13 FanMYBs were likely associated with phenylpropanoid metabolism. Out of these genes, FanMYB22, FanMYB36, FanMYB47, FanMYB49, and FanMYB63 were post-transcriptionally regulated by miR858 according to the degradome data analysis, suggesting the conservation and complex regulation network in F. × ananassa. Current findings provide a useful resource for future research on the function of FanMYBs and the regulatory mechanism of the phenylpropanoid pathway in strawberry.

Published
2023
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4. Antagonistic effects of drought and sand burial enable the survival of the biocrust moss Bryum argenteum in an arid sandy desert

Author

R. Jia, Y. Zhao, Y. Gao, R. Hui, H. Yang, Z. Wang, and Y. Li

Subjects
Ecology, QH540-549.5, Life, QH501-531, Geology, QE1-996.5
Abstract

Biocrust moss is an essential soil surface bio-cover. It can represent the latest succession stage among the diverse range of surface-dwelling cryptogams (e.g., cyanobacteria, green algae, and lichen, which are also referred to as biocrusts), and it can make a major contribution to soil stability and fertility in many arid sandy desert ecosystems. The soil surface represents a very large ecological niche that is poikilohydric in nature. Biocrust moss is therefore highly susceptible to drought and sand burial, which are two ubiquitous stressors in arid sandy deserts. However, little information is available regarding the mechanism by which biocrust moss can survive and flourish in these habitats when stressed simultaneously by the two stressors. The combined effects of drought and sand burial were evaluated in a field experiment using the predominant biocrust moss, Bryum argenteum Hedw., in the Tengger Desert, China. Drought was simulated by applying distilled water in three artificial rainfall regimes at 8-day intervals in spring and autumn: 4 and 6 mm (average rainfall, control), 2 and 3 mm (double drought), and 1 and 1.5 mm (4-fold drought), respectively. The effect of sand burial was determined by applying six treatments, i.e., sand depths of 0 (control), 0.5, 1, 2, 4, and 10 mm. The four parameters of chlorophyll a content, PSII photochemical efficiency, regeneration potential, and shoot upgrowth were evaluated in the moss. It was found that the combined effects of drought and sand burial did not exacerbate the single negative effects of the four parameters tested. Drought significantly ameliorated the negative effects of deep-sand burial on the retention of chlorophyll a content, PSII photochemical efficiency, and the regeneration potential of B. argenteum. Sand burial diminished and even reversed the negative effects of drought on the maintenance of chlorophyll a content, PSII photochemical efficiency, and regeneration potential. Although drought and sand burial imposed an additive negative effect on shoot upgrowth, which suggested a trade-off between growth ability and stress tolerance, their mutually antagonistic effect on the physiological vigor of B. argenteum provided an opportunity for the biocrust moss to overcome the two co-occurring stressors. In addition to providing a strong stress tolerance, drought and sand burial may provide an important mechanism for the biodiversity maintenance of biocrust mosses in arid sandy ecosystems.

Published
2018
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5. Modeling study on the transport of summer dust and anthropogenic aerosols over the Tibetan Plateau

Author

Y. Liu, Y. Sato, R. Jia, Y. Xie, J. Huang, and T. Nakajima

Subjects
Physics, QC1-999, Chemistry, QD1-999
Abstract

The Tibetan Plateau (TP) is located at the juncture of several important natural and anthropogenic aerosol sources. Satellites have observed substantial dust and anthropogenic aerosols in the atmosphere during summer over the TP. These aerosols have distinct effects on the earth's energy balance, microphysical cloud properties, and precipitation rates. To investigate the transport of summer dust and anthropogenic aerosols over the TP, we combined the Spectral Radiation-Transport Model for Aerosol Species (SPRINTARS) with a non-hydrostatic regional model (NHM). The model simulation shows heavily loaded dust aerosols over the northern slope and anthropogenic aerosols over the southern slope and the east of the TP. The dust aerosols are primarily mobilized around the Taklimakan Desert, where a portion of the aerosols are transported eastward due to the northwesterly current; simultaneously, a portion of the particles are transported southward when a second northwesterly current becomes northeasterly because of the topographic blocking of the northern slope of the TP. Because of the strong upward current, dust plumes can extend upward to approximately 7–8 km a.s.l. over the northern slope of the TP. When a dust event occurs, anthropogenic aerosols that entrained into the southwesterly current via the Indian summer monsoon are transported from India to the southern slope of the TP. Simultaneously, a large amount of anthropogenic aerosol is also transported from eastern China to the east of the TP by easterly winds. An investigation on the transport of dust and anthropogenic aerosols over the plateau may provide the basis for determining aerosol impacts on summer monsoons and climate systems.

Published
2015
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6. Insecticidal activities and mechanism of extracts from neem leaves against Oxya chinensis

Author

L. Li, X. Song, Z. Yin, R. Jia, and Y. Zou

Subjects
folhas nem, Oxya chinesis, atividade inseticida, Animal culture, SF1-1100
Abstract

ABSTRACT In this study, neem leaves were successively extracted with petroleum ether, 95% ethanol and water and the insecticidal activities of these extracts against Oxya chinensis larvae were measured. The results showed that 95% ethanol extract gave the highest extraction yield and insecticidal activity, and it was further extracted with five different solvents. The petroleum ether extract from the 95% ethanol extract possessed the highest insecticidal activity with median lethal concentration values ranging from 14.93 to 55.66mg/mL. The gas chromatography-mass spectrometer analysis showed that the petroleum ether extract mainly composed of alkanes, olefin, esters and amide. The pathological examination revealed that the prominent lesions, including reduced regenerative cells in midgut and swelled and degenerated cylindrical cells, were observed in the 5th instar Oxya chinensis after treatment. The ultrastructural features showed that the cylindrical cells, microvilli and mitochondria were seriously damaged. These results suggested that the petroleum ether extract from neem leaves had potent insecticidal activity and could be a candidate insecticide.

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8. Novel <scp>MSH6</scp> mutation predicted metastasis in eyelid and periocular squamous cell carcinoma

Author

Y. Luo, Y. Rao, X. Gu, P. Chai, Y. Yang, J. Lin, X. Xu, R. Jia, and S. Xu

Subjects
DNA-Binding Proteins, Infectious Diseases, Mutation, Carcinoma, Squamous Cell, Humans, Eyelids, Dermatology
Abstract

Our previous research revealed the relative local aggressiveness of eyelid and periocular squamous cell carcinoma (EPSCC), but its distinct genetic characteristics involved remain unknown.We conducted this study based on next-generation sequencing to identify the genetic distinctiveness of EPSCC and damaging mutations for possible aetiology and poor prognosis.We performed sequencing using a 556-gene panel (SmartOnco) in 48 EPSCCs. Cox hazards model was applied to explore mutated genes that increase the risk of metastasis and death. Pathogenesis of the mutations was predicted by sequence alignment algorithms.The most commonly mutated genes were KMT2C (N = 17, 35%), LRP1B (N = 14, 29%), KMT2D (N = 12, 25%), PTCH1 (N = 10, 21%) and TP53 (N = 10, 21%). DNA mismatch repair (MMR) genes (42%) like MSH6 (19%) and MLH3 (12%) were among the most frequently mutated genes. Cell cycle regulators including TP53 (21%) and CDKN2A (10%) were less frequently mutated than in other squamous cell carcinomas (SCCs). Ultraviolet exposure, MMR deficiency and ageing were the main aetiology. Of note, KMT2C has a deleterious mutation hotspot. Patients burdened with MSH6 mutation has a higher risk of overall metastasis (P = 0.045, HR = 5.165) and nodal metastasis (P = 0.022, HR = 14.038). Moreover, a hotspot mutation MSH6EPSCCs displayed a unique mutation profile from cutaneous SCCs and mucosal SCCs. We have identified novel damaging mutations in epigenetic regulators like KMT2C boosted early onset of EPSCCs in addition to UVR, ageing or MMR deficiency. And malfunction of MMR genes worsened prognosis.

Published
2022
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11. [Risk factors of postoperative voiding dysfunction in children with congenital anorectal malformation]

Author

R, Jia, C P, Song, Q F, Dou, H Q, Zhang, and J G, Wen

Subjects
Male, Urodynamics, Risk Factors, Humans, Urination, Female, Postoperative Period, Child, Anorectal Malformations
Abstract

This study analyzed the clinical data of children with anorectal malformation (ARM)who underwent surgery from 2006 to 2021, and explored the related factors of postoperative voiding dysfunction (VD).A total of 60 children including 51 males and 9 females, aged 4-15 years, were enrolled. During follow up, normal voiding function were found in 43 cases, VD in 17 cases. It was found that middle to high clinical classification (本研究分析2006年至2021年手术治疗的先天性肛门直肠畸形（ARM）患儿的临床资料，探讨ARM患儿术后排尿异常的相关因素。共纳入患儿60例，其中男51例、女9例，年龄4~15岁。其中，43例排尿正常，17例排尿异常。通过尿动力学检查随访发现中-高位临床分型（

Published
2022

13. Utility of Fine-Needle Aspirations to Diagnose Pediatric Thyroid Nodules

Author

Jalal B. Jalaly, N. Scott Adzick, Tricia R. Bhatti, Ken Kazahaya, Aime T. Franco, Zubair W. Baloch, Julia A Baran, Cindy McGrath, Lindsay Sisko, Ganesh Krishnamurthy, Lea F. Surrey, Amber Isaza, Margaret R Jia, Fernando Escobar, Sogol Mostoufi-Moab, Andrew J. Bauer, and Tasleema Patel

Subjects
Thyroid nodules, medicine.medical_specialty, business.industry, Endocrinology, Diabetes and Metabolism, Biopsy, Fine-Needle, Thyroid Gland, MEDLINE, medicine.disease, Endocrinology, Pediatrics, Perinatology and Child Health, medicine, Humans, Thyroid Nodule, Radiology, Child, business, Retrospective Studies
Abstract

Introduction: Risk of malignancy for pediatric thyroid nodules classified according to The Bethesda System for Reporting Thyroid Cytopathology (TBSRTC) is not well defined. Correlations between risk of malignancy and ancillary clinical data remain inconclusive. We report a single institutional experience of fine-needle aspiration (FNA) to improve upon current management paradigm of thyroid nodules. Methods: A retrospective chart review of 575 thyroid nodules was performed of 324 patients who underwent 340 FNAs between 2008 and 2018 at the Children’s Hospital of Philadelphia. Demographics, ultrasound (US) characteristics, FNA cytology, surgical pathology, and ancillary data were reviewed. Results: The rate of malignancy according to TBSRTC was 0.0% for category I, 0.8% for category II, 15.6% for category III, 54.5% for category IV, 100.0% for category V, and 100.0% for category VI. The cumulative Thyroid Imaging Reporting and Data System (TI-RADS) score was significantly correlated with benign and malignant nodules on pathology (p < 2.2e−16). Distribution of TI-RADS for cytologically indeterminate nodules with benign or malignant pathology revealed significant differences for composition (p = 3.20e−8) and echogenic foci (p = 0.005) but not for echogenicity (p = 0.445), shape (p = 0.160), margins (p = 0.220), and size (p = 0.105). Distributions of thyroid-stimulating hormone levels between benign and malignant patients was significant (p = 1.58e−3). Conclusions: Nodules with TI-RADS scores >3 should undergo FNA, irrespective of size; surgical resection is recommended for nodules classified as TBSRTC category IV and V due to high risk of malignancy. US surveillance instead of FNA can be performed for nodules with TI-RADS scores ≤3.

Published
2021
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21. Solving crustal heat transfer for thermochronology using physics-informed neural networks

Author

R. Jiao, S. Cai, and J. Braun

Subjects
Geology, QE1-996.5, Stratigraphy, QE640-699
Abstract

We present a deep-learning approach based on the physics-informed neural networks (PINNs) for estimating thermal evolution of the crust during tectonic uplift with a changing landscape. The approach approximates the temperature field of the crust with a deep neural network, which is trained by optimizing the heat advection–diffusion equation, assuming initial and boundary temperature conditions that follow a prescribed topographic history. From the trained neural network of temperature field and the prescribed velocity field, one can predict the temperature history of a given rock particle that can be used to compute the cooling ages of thermochronology. For the inverse problem, the forward model can be combined with a global optimization algorithm that minimizes the misfit between predicted and observed thermochronological data, in order to constrain unknown parameters in the rock uplift history or boundary conditions. We demonstrate the approach with solutions of one- and three-dimensional forward and inverse models of the crustal thermal evolution, which are consistent with results of the finite-element method. As an example, the three-dimensional model simulates the exhumation and post-orogenic topographic decay of the Dabie Shan, eastern China, whose post-orogenic evolution has been constrained by previous thermochronological data and models. This approach takes advantage of the computational power of machine learning algorithms, offering a valuable alternative to existing analytical and numerical methods, with great adaptability to diverse boundary conditions and easy integration with various optimization schemes.

Published
2024
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22. Simulation of edge cracking using shear GTN damage model during hot plate rolling of magnesium alloys

Author

C C Zhao, J L Liu, Z X Li, R Jia, Z Q Huang, and T Wang

Subjects
General Medicine
Abstract

Edge cracks are a more prominent problem during the rolling process of magnesium alloy sheets. The hexagonal structure of magnesium alloys and the product defects caused by the second phase impurities mixed in the sheets are the main causes of edge cracking. Conventional hot-rolled edge cracking simulations can only characterize the edge damage of the sheets numerically, however, the actual crack morphology is ignored. In this paper, the Gurson-Tvergaard-Needleman (GTN) damage model coupled with a continuous medium shear damage model was developed for improving the applicability of the model at low-stress triaxiality. Powell’s “Dogleg” method was used in the numerical solution of the damage model instead of the traditional Newton-Raphson method and the Vumat subroutine was written for the finite element simulation by the stress return algorithm. The damage model parameters were calibrated by a shear specimen. The results showed a good agreement between the simulated crack morphology and the experiment.

Published
2022
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25. The Relationships among Topographically-driven Habitats, Dominant Species and Vertical Layers in Temperate Forest in China

Author

Xueying Wang, Zhiliang Yuan, Peikun Li, H. R. Jia, Yanhui Chen, and Yongzhong Ye

Subjects
Canopy, 0303 health sciences, Forest dynamics, Ecology, 030302 biochemistry & molecular biology, Temperate forest, 04 agricultural and veterinary sciences, Interspecific competition, 03 medical and health sciences, Geography, Habitat, Forest ecology, 040103 agronomy & agriculture, 0401 agriculture, forestry, and fisheries, China, Ecology, Evolution, Behavior and Systematics
Abstract

The relationships among topography, topographically-driven habitats, dominant species and vertical layers in forest ecosystem are often complicate. In this study, based on the five 1 ha forest dynamics plots in China, we examined these relationships in different communities of temperate forest in China through structural equation model and torus-translation test. Our results showed that (1) the dominant species is an important factor that affects the forest vertical layers; (2) interspecific competition is prevalent between dominant species and canopy layer; (3) the species in each vertical layer have varying topographical habitat preferences. These findings shed new light to the species coexistence among forest vertical layers in temperate forest.

Published
2019
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26. Phageome-based vaccination and human innate immune modulation could be a useful strategy to control human Coronavirus infections

Author

M, Abaidullah, S, Peng, M, Kamran, X, Song, A, Ali Sher, Y, Chen, A, Rehman, L, Lin, R, Jia, and Z, Yin

Subjects
SARS-CoV-2, Virome, Vaccination, COVID-19, Humans, Immunity, Innate
Abstract

Human Coronavirus (CoV) infections, including SARS-COV, MERS-COV, and SARS-CoV-2, usually cause fatal lower and upper respiratory tract infections due to exacerbated expression of pro-inflammatory cytokines and chemokines. We aim to summarize different aspects, such as CoV immune evasion mechanisms and host innate immune response to these infections, and their role in pathogenesis. We have also elaborated the up-to-date findings on different vaccine development strategies and progress against CoVs in both humans and non-human models. Most importantly, we have described the Phageome-human immune interaction, its therapeutic usage as anti-viral, anti-inflammatory agent, and implications for multiple vaccine development systems. The data suggest that endogenous phages might play a vital role in eliminating the infection and regulating the body's immune system. Considering the innate-immune-induced pathogenesis against CoVs and the therapeutic aptitude of phageome, we propose that the prophylactic administration of phages and phage-based vaccines could be a useful strategy to control the emerging CoV infections.

Published
2021

29. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Author

D. KLIONSKY, A. ABDEL-AZIZ, S. ABDELFATAH, M. ABDELLATIF, A. ABDOLI, S. ABEL, H. ABELIOVICH, M. ABILDGAARD, Y. ABUDU, A. ACEVEDO-AROZENA, I. ADAMOPOULOS, K. ADELI, T. ADOLPH, A. ADORNETTO, E. AFLAKI, G. AGAM, A. AGARWAL, B. AGGARWAL, M. AGNELLO, P. AGOSTINIS, J. AGREWALA, A. AGROTIS, P. AGUILAR, S. AHMAD, Z. AHMED, U. AHUMADA-CASTRO, S. AITS, S. AIZAWA, Y. AKKOC, T. AKOUMIANAKI, H. AKPINAR, A. AL-ABD, L. AL-AKRA, A. AL-GHARAIBEH, M. ALAOUI-JAMALI, S. ALBERTI, E. ALCOCER-GOMEZ, C. ALESSANDRI, M. ALI, M. AL-BARI, S. ALIWAINI, J. ALIZADEH, E. ALMACELLAS, A. ALMASAN, A. ALONSO, G. ALONSO, N. ALTAN-BONNET, D. ALTIERI, S. ALVES, C. DA COSTA, M. ALZAHARNA, M. AMADIO, C. AMANTINI, C. AMARAL, S. AMBROSIO, A. AMER, V. AMMANATHAN, Z. AN, S. ANDERSEN, S. ANDRABI, M. ANDRADE-SILVA, A. ANDRES, S. ANGELINI, D. ANN, U. ANOZIE, M. ANSARI, P. ANTAS, A. ANTEBI, Z. ANTON, T. ANWAR, L. APETOH, N. APOSTOLOVA, T. ARAKI, Y. ARAKI, K. ARASAKI, W. ARAUJO, J. ARAYA, C. ARDEN, M. AREVALO, S. ARGUELLES, E. ARIAS, J. ARIKKATH, H. ARIMOTO, A. ARIOSA, D. ARMSTRONG-JAMES, L. ARNAUNE-PELLOQUIN, A. AROCA, D. ARROYO, I. ARSOV, R. ARTERO, D. ASARO, M. ASCHNER, M. ASHRAFIZADEH, O. ASHUR-FABIAN, A. ATANASOV, A. AU, P. AUBERGER, H. AUNER, L. AURELIAN, R. AUTELLI, L. AVAGLIANO, Y. AVALOS, S. AVEIC, C. AVELEIRA, T. AVINWITTENBERG, Y. AYDIN, S. AYTON, S. AYYADEVARA, M. AZZOPARDI, M. BABA, J. BACKER, S. BACKUES, D. BAE, O. BAE, S. BAE, E. BAEHRECKE, A. BAEK, S. BAEK, G. BAGETTA, A. BAGNIEWSKA-ZADWORNA, H. BAI, J. BAI, X. BAI, Y. BAI, N. BAIRAGI, S. BAKSI, T. BALBI, C. BALDARI, W. BALDUINI, A. BALLABIO, M. BALLESTER, S. BALAZADEH, R. BALZAN, R. BANDOPADHYAY, S. BANERJEE, Y. BAO, M. BAPTISTA, A. BARACCA, C. BARBATI, A. BARGIELA, D. BARILA, P. BARLOW, S. BARMADA, E. BARREIRO, G. BARRETO, J. BARTEK, B. BARTEL, A. BARTOLOME, G. BARVE, S. BASAGOUDANAVAR, D. BASSHAM, R. JR, A. BASU, H. BATOKO, I. BATTEN, E. BAULIEU, B. BAUMGARNER, J. BAYRY, R. BEALE, I. BEAU, F. BEAUMATIN, L. BECHARA, G. BECK, M. BEERS, J. BEGUN, C. BEHRENDS, G. BEHRENS, R. BEI, E. BEJARANO, S. BEL, C. BEHL, A. BELAID, N. BELGAREH-TOUZE, C. BELLAROSA, F. BELLEUDI, M. PEREZ, R. BELLO-MORALES, J. BELTRAN, S. BELTRAN, D. BENBROOK, M. BENDORIUS, B. BENITEZ, I. BENITO-CUESTA, J. BENSALEM, M. BERCHTOLD, S. BEREZOWSKA, D. BERGAMASCHI, M. BERGAMI, A. BERGMANN, L. BERLIOCCHI, C. BERLIOZ-TORRENT, A. BERNARD, L. BERTHOUX, C. BESIRLI, S. BESTEIRO, V. BETIN, R. BEYAERT, J. BEZBRADICA, K. BHASKAR, I. BHATIA-KISSOVA, R. BHATTACHARYA, S. BHATTACHARYA, S. BHATTACHARYYA, M. BHUIYAN, S. BHUTIA, L. BI, X. BI, T. BIDEN, K. BIJIAN, V. BILLES, N. BINART, C. BINCOLETTO, A. BIRGISDOTTIR, G. BJORKOY, G. BLANCO, A. BLAS-GARCIA, J. BLASIAK, R. BLOMGRAN, K. BLOMGREN, J. BLUM, E. BOADA-ROMERO, M. BOBAN, K. BOESZEBATTAGLIA, P. BOEUF, B. BOLAND, P. BOMONT, P. BONALDO, S. BONAM, L. BONFILI, J. BONIFACINO, B. BOONE, M. BOOTMAN, M. BORDI, C. BORNER, B. BORNHAUSER, G. BORTHAKUR, J. BOSCH, S. BOSE, L. BOTANA, J. BOTAS, C. BOULANGER, M. BOULTON, M. BOURDENX, B. BOURGEOIS, N. BOURKE, G. BOUSQUET, P. BOYA, P. BOZHKOV, L. BOZI, T. BOZKURT, D. BRACKNEY, C. BRANDTS, R. BRAUN, G. BRAUS, R. BRAVO-SAGUA, J. BRAVO-SAN PEDRO, P. BREST, M. BRINGER, A. BRIONES-HERRERA, V. BROADDUS, P. BRODERSEN, E. ALVAREZ, J. BRODSKY, S. BRODY, P. BRONSON, J. BRONSTEIN, C. BROWN, R. BROWN, P. BRUM, J. BRUMELL, N. BRUNETTI-PIERRI, D. BRUNO, R. BRYSON-RICHARDSON, C. BUCCI, C. BUCHRIESER, M. BUENO, L. BUITRAGO-MOLINA, S. BURASCHI, S. BUCH, J. BUCHAN, E. BUCKINGHAM, H. BUDAK, M. BUDINI, G. BULTYNCK, F. BURADA, J. BURGOYNE, M. BURON, V. BUSTOS, S. BUTTNER, E. BUTTURINI, A. BYRD, I. CABAS, S. CABRERA-BENITEZ, K. CADWELL, J. CAI, L. CAI, Q. CAI, M. CAIRO, J. CALBET, G. CALDWELL, K. CALDWELL, J. CALL, R. CALVANI, A. CALVO, M. BARRERA, N. CAMARA, J. CAMONIS, N. CAMOUGRAND, M. CAMPANELLA, E. CAMPBELL, F. CAMPBELL-VALOIS, S. CAMPELLO, I. CAMPESI, J. CAMPOS, O. CAMUZARD, J. CANCINO, D. DE ALMEIDA, L. CANESI, I. CANIGGIA, B. CANONICO, C. CANTI, B. CAO, M. CARAGLIA, B. CARAMES, E. CARCHMAN, E. CARDENAL-MUNOZ, C. CARDENAS, L. CARDENAS, S. CARDOSO, J. CAREW, G. CARLE, G. CARLETON, S. CARLONI, D. CARMONA-GUTIERREZ, L. CARNEIRO, O. CARNEVALI, J. CAROSI, S. CARRA, A. CARRIER, L. CARRIER, B. CARROLL, A. CARTER, A. CARVALHO, M. CASANOVA, C. CASAS, J. CASAS, C. CASSIOLI, E. CASTILLO, K. CASTILLO, S. CASTILLO-LLUVA, F. CASTOLDI, M. CASTORI, A. CASTRO, M. CASTRO-CALDAS, J. CASTRO-HERNANDEZ, S. CASTRO-OBREGON, S. CATZ, C. CAVADAS, F. CAVALIERE, G. CAVALLINI, M. CAVINATO, M. CAYUELA, P. RICA, V. CECARINI, F. CECCONI, M. CECHOWSKA-PASKO, S. CENCI, V. CEPERUELO-MALLAFRE, J. CERQUEIRA, J. CERUTTI, D. CERVIA, V. CETINTAS, S. CETRULLO, H. CHAE, A. CHAGIN, C. CHAI, G. CHAKRABARTI, O. CHAKRABARTI, T. CHAKRABORTY, M. CHAMI, G. CHAMILOS, D. CHAN, E. CHAN, H. CHAN, M. CHAN, Y. CHAN, P. CHANDRA, C. CHANG, H. CHANG, K. CHANG, J. CHAO, T. CHAPMAN, N. CHARLET-BERGUERAND, S. CHATTERJEE, S. CHAUBE, A. CHAUDHARY, S. CHAUHAN, E. CHAUM, F. CHECLER, M. CHEETHAM, C. CHEN, G. CHEN, J. CHEN, L. CHEN, M. CHEN, N. CHEN, Q. CHEN, R. CHEN, S. CHEN, W. CHEN, X. CHEN, Y. CHEN, Z. CHEN, H. CHENG, J. CHENG, S. CHENG, W. CHENG, X. CHENG, Y. CHENG, Z. CHENG, H. CHEONG, J. CHEONG, B. CHERNYAK, S. CHERRY, C. CHEUNG, K. CHEUNG, E. CHEVET, R. CHI, A. CHIANG, F. CHIARADONNA, R. CHIARELLI, M. CHIARIELLO, N. CHICA, S. CHIOCCA, M. CHIONG, S. CHIOU, A. CHIRAMEL, V. CHIURCHIU, D. CHO, S. CHOE, A. CHOI, M. CHOI, K. CHOUDHURY, N. CHOW, C. CHU, J. CHUA, H. CHUNG, K. CHUNG, S. CHUNG, Y. CHUNG, V. CIANFANELLI, I. CIECHOMSKA, M. CIFUENTES, L. CINQUE, S. CIRAK, M. CIRONE, M. CLAGUE, R. CLARKE, E. CLEMENTI, E. COCCIA, P. CODOGNO, E. COHEN, M. COHEN, T. COLASANTI, F. COLASUONNO, R. COLBERT, A. COLELL, N. COLL, M. COLLINS, M. COLOMBO, D. COLON-RAMOS, L. COMBARET, S. COMINCINI, M. COMINETTI, A. CONSIGLIO, A. CONTE, F. CONTI, V. CONTU, M. COOKSON, K. COOMBS, I. COPPENS, M. CORASANITI, D. CORKERY, N. CORDES, K. CORTESE, M. COSTA, S. COSTANTINO, P. COSTELLI, A. COTO-MONTES, P. CRACK, J. CRESPO, A. CRIOLLO, V. CRIPPA, R. CRISTOFANI, T. CSIZMADIA, A. CUADRADO, B. CUI, J. CUI, Y. CUI, E. CULETTO, A. CUMINO, A. CYBULSKY, M. CZAJA, S. CZUCZWAR, S. D'ADAMO, M. D'AMELIO, D. D'ARCANGELO, A. D'LUGOS, G. D'ORAZI, J. DA SILVA, H. DAFSARI, R. DAGDA, Y. DAGDAS, M. DAGLIA, X. DAI, Y. DAI, J. DAL COL, P. DALHAIMER, L. DALLA VALLE, T. DALLENGA, G. DALMASSO, M. DAMME, I. DANDO, N. DANTUMA, A. DARLING, H. DAS, S. DASARATHY, S. DASARI, S. DASH, O. DAUMKE, A. DAUPHINEE, J. DAVIES, V. DAVILA, R. DAVIS, T. DAVIS, S. NAIDU, F. DE AMICIS, K. DE BOSSCHER, F. DE FELICE, L. DE FRANCESCHI, C. DE LEONIBUS, M. BARBOSA, G. DE MEYER, A. DE MILITO, C. DE NUNZIO, C. DE PALMA, M. DE SANTI, C. DE VIRGILIO, D. DE ZIO, J. DEBNATH, B. DEBOSCH, J. DECUYPERE, M. DEEHAN, G. DEFLORIAN, J. DEGREGORI, B. DEHAY, G. DEL RIO, J. DELANEY, L. DELBRIDGE, E. DELORME-AXFORD, M. DELPINO, F. DEMARCHI, V. DEMBITZ, N. DEMERS, H. DENG, Z. DENG, J. DENGJEL, P. DENT, D. DENTON, M. DEPAMPHILIS, C. DER, V. DERETIC, A. DESCOTEAUX, L. DEVIS, S. DEVKOTA, O. DEVUYST, G. DEWSON, M. DHARMASIVAM, R. DHIMAN, D. DI BERNARDO, M. DI CRISTINA, F. DI DOMENICO, P. DI FAZIO, A. DI FONZO, G. DI GUARDO, G. DI GUGLIELMO, L. DI LEO, C. DI MALTA, A. DI NARDO, M. DI RIENZO, F. DI SANO, G. DIALLINAS, J. DIAO, G. DIAZ-ARAYA, I. DIAZ-LAVIADA, J. DICKINSON, M. DIEDERICH, M. DIEUDE, I. DIKIC, S. DING, W. DING, L. DINI, M. DINIC, A. DINKOVA-KOSTOVA, M. DIONNE, J. DISTLER, A. DIWAN, I. DIXON, M. DJAVAHERI-MERGNY, I. DOBRINSKI, O. DOBROVINSKAYA, R. DOBROWOLSKI, R. DOBSON, S. EMRE, M. DONADELLI, B. DONG, X. DONG, Z. DONG, G. II, V. DOTSCH, H. DOU, J. DOU, M. DOWAIDAR, S. DRIDI, L. DRUCKER, A. DU, C. DU, G. DU, H. DU, L. DU, A. DU TOIT, S. DUAN, X. DUAN, S. DUARTE, A. DUBROVSKA, E. DUNLOP, N. DUPONT, R. DURAN, B. DWARAKANATH, S. DYSHLOVOY, D. EBRAHIMI-FAKHARI, L. ECKHART, C. EDELSTEIN, T. EFFERTH, E. EFTEKHARPOUR, L. EICHINGER, N. EID, T. EISENBERG, N. EISSA, S. EISSA, M. EJARQUE, A. EL ANDALOUSSI, N. EL-HAGE, S. EL-NAGGAR, A. ELEUTERI, E. EL-SHAFEY, M. ELGENDY, A. ELIOPOULOS, M. ELIZALDE, P. ELKS, H. ELSASSER, E. ELSHERBINY, B. EMERLING, N. EMRE, C. ENG, N. ENGEDAL, A. ENGELBRECHT, A. ENGELSEN, J. ENSERINK, R. ESCALANTE, A. ESCLATINE, M. ESCOBAR-HENRIQUES, E. ESKELINEN, L. ESPERT, M. EUSEBIO, G. FABRIAS, C. FABRIZI, A. FACCHIANO, F. FACCHIANO, B. FADEEL, C. FADER, A. FAESEN, W. FAIRLIE, A. FALCO, B. FALKENBURGER, D. FAN, J. FAN, Y. FAN, E. FANG, Y. FANG, M. FANTO, T. FARFEL-BECKER, M. FAURE, G. FAZELI, A. FEDELE, A. FELDMAN, D. FENG, J. FENG, L. FENG, Y. FENG, W. FENG, T. ARAUJO, T. FERGUSON, J. FERNANDEZ-CHECA, S. FERNANDEZVELEDO, A. FERNIE, A. FERRANTE, A. FERRARESI, M. FERRARI, J. FERREIRA, S. FERRO-NOVICK, A. FIGUERAS, R. FILADI, N. FILIGHEDDU, E. FILIPPICHIELA, G. FILOMENI, G. FIMIA, V. FINESCHI, F. FINETTI, S. FINKBEINER, E. FISHER, P. FISHER, F. FLAMIGNI, S. FLIESLER, T. FLO, I. FLORANCE, O. FLOREY, T. FLORIO, E. FODOR, C. FOLLO, E. FON, A. FORLINO, F. FORNAI, P. FORTINI, A. FRACASSI, A. FRALDI, B. FRANCO, R. FRANCO, F. FRANCONI, L. FRANKEL, S. FRIEDMAN, L. FROHLICH, G. FRUHBECK, J. FUENTES, Y. FUJIKI, N. FUJITA, Y. FUJIWARA, M. FUKUDA, S. FULDA, L. FURIC, N. FURUYA, C. FUSCO, M. GACK, L. GAFFKE, S. GALADARI, A. GALASSO, M. GALINDO, S. KANKANAMALAGE, L. GALLUZZI, V. GALY, N. GAMMOH, B. GAN, I. GANLEY, F. GAO, H. GAO, M. GAO, P. GAO, S. GAO, W. GAO, X. GAO, A. GARCERA, M. GARCIA, V. GARCIA, F. GARCIA-DEL PORTILLO, V. GARCIA-ESCUDERO, A. GARCIAGARCIA, M. GARCIA-MACIA, D. GARCIA-MORENO, C. GARCIA-RUIZ, P. GARCIA-SANZ, A. GARG, R. GARGINI, T. GAROFALO, R. GARRY, N. GASSEN, D. GATICA, L. GE, W. GE, R. GEISS-FRIEDLANDER, C. GELFI, P. GENSCHIK, I. GENTLE, V. GERBINO, C. GERHARDT, K. GERMAIN, M. GERMAIN, D. GEWIRTZ, E. AFSHAR, S. GHAVAMI, A. GHIGO, M. GHOSH, G. GIAMAS, C. GIAMPIETRI, A. GIATROMANOLAKI, G. GIBSON, S. GIBSON, V. GINET, E. GINIGER, C. GIORGI, H. GIRAO, S. GIRARDIN, M. GIRIDHARAN, S. GIULIANO, C. GIULIVI, S. GIURIATO, J. GIUSTINIANI, A. GLUSCHKO, V. GODER, A. GOGINASHVILI, J. GOLAB, D. GOLDSTONE, A. GOLEBIEWSKA, L. GOMES, R. GOMEZ, R. GOMEZ-SANCHEZ, M. GOMEZ-PUERTO, R. GOMEZ-SINTES, Q. GONG, F. GONI, J. GONZALEZ-GALLEGO, T. GONZALEZ-HERNANDEZ, R. GONZALEZ-POLO, J. GONZALEZ-REYES, P. GONZALEZ-RODRIGUEZ, I. GOPING, M. GORBATYUK, N. GORBUNOV, R. GOROJOD, S. GORSKI, S. GORUPPI, C. GOTOR, R. GOTTLIEB, I. GOZES, D. GOZUACIK, M. GRAEF, M. GRALER, V. GRANATIERO, D. GRASSO, J. GRAY, D. GREEN, A. GREENHOUGH, S. GREGORY, E. GRIFFIN, M. GRINSTAFF, F. GROS, C. GROSE, A. GROSS, F. GRUBER, P. GRUMATI, T. GRUNE, X. GU, J. GUAN, C. GUARDIA, K. GUDA, F. GUERRA, C. GUERRI, P. GUHA, C. GUILLEN, S. GUJAR, A. GUKOVSKAYA, I. GUKOVSKY, J. GUNST, A. GUNTHER, A. GUNTUR, C. GUO, H. GUO, L. GUO, M. GUO, P. GUPTA, A. FERNANDEZ, S. GUPTA, V. GUPTA, A. GUSTAFSSON, D. GUTTERMAN, H. RANJITHA, A. HAAPASALO, J. HABER, S. HADANO, A. HAFREN, M. HAIDAR, B. HALL, G. HALLDEN, A. HAMACHER-BRADY, A. HAMANN, M. HAMASAKI, W. HAN, M. HANSEN, P. HANSON, Z. HAO, M. HARADA, L. HARHAJI-TRAJKOVIC, N. HARIHARAN, N. HAROON, J. HARRIS, T. HASEGAWA, N. NAGOOR, J. HASPEL, V. HAUCKE, W. HAWKINS, B. HAY, C. HAYNES, S. HAYRABEDYAN, T. HAYS, C. HE, Q. HE, R. HE, Y. HE, Y. HEAKAL, A. HEBERLE, J. HEJTMANCIK, G. HELGASON, V. HENKEL, M. HERB, A. HERGOVICH, A. HERMAN-ANTOSIEWICZ, A. HERNANDEZ, C. HERNANDEZ, S. HERNANDEZ-DIAZ, V. HERNANDEZ-GEA, A. HERPIN, J. HERREROS, J. HERVAS, D. HESSELSON, C. HETZ, V. HEUSSLER, Y. HIGUCHI, S. HILFIKER, J. HILL, W. HLAVACEK, E. HO, I. HO, P. HO, S. HO, W. HO, G. HOBBS, M. HOCHSTRASSER, P. HOET, D. HOFIUS, P. HOFMAN, A. HOHN, C. HOLMBERG, J. HOMBREBUENO, C. HONG, Y. HONG, L. HOOPER, T. HOPPE, R. HOROS, Y. HOSHIDA, I. HSIN, H. HSU, B. HU, D. HU, L. HU, M. HU, R. HU, W. HU, Y. HU, Z. HU, F. HUA, J. HUA, Y. HUA, C. HUAN, C. HUANG, H. HUANG, K. HUANG, M. HUANG, R. HUANG, S. HUANG, T. HUANG, X. HUANG, Y. HUANG, T. HUBER, V. HUBERT, C. HUBNER, S. HUGHES, W. HUGHES, M. HUMBERT, G. HUMMER, J. HURLEY, S. HUSSAIN, P. HUSSEY, M. HUTABARAT, H. HWANG, S. HWANG, A. IENI, F. IKEDA, Y. IMAGAWA, Y. IMAI, C. IMBRIANO, M. IMOTO, D. INMAN, K. INOKI, J. IOVANNA, R. IOZZO, G. IPPOLITO, J. IRAZOQUI, P. IRIBARREN, M. ISHAQ, M. ISHIKAWA, N. ISHIMWE, C. ISIDORO, N. ISMAIL, S. ISSAZADEH-NAVIKAS, E. ITAKURA, D. ITO, D. IVANKOVIC, S. IVANOVA, A. IYER, J. IZQUIERDO, M. IZUMI, M. JAATTELA, M. JABIR, W. JACKSON, N. JACOBO-HERRERA, A. JACOMIN, E. JACQUIN, P. JADIYA, H. JAESCHKE, C. JAGANNATH, A. JAKOBI, J. JAKOBSSON, B. JANJI, P. JANSENDURR, P. JANSSON, J. JANTSCH, A. JASSEY, S. JEAN, H. JELTSCHDAVID, P. JENDELOVA, A. JENNY, T. JENSEN, N. JESSEN, J. JEWELL, J. JI, L. JIA, R. JIA, L. JIANG, Q. JIANG, R. JIANG, T. JIANG, X. JIANG, Y. JIANG, M. JIMENEZ-SANCHEZ, E. JIN, F. JIN, H. JIN, L. JIN, M. JIN, S. JIN, E. JO, C. JOFFRE, T. JOHANSEN, G. JOHNSON, S. JOHNSTON, E. JOKITALO, M. JOLLY, L. JOOSTEN, J. JORDAN, B. JOSEPH, D. JU, J. JU, E. JUAREZ, D. JUDITH, G. JUHASZ, Y. JUN, C. JUNG, S. JUNG, Y. JUNG, H. JUNGBLUTH, J. JUNGVERDORBEN, S. JUST, K. KAARNIRANTA, A. KAASIK, T. KABUTA, D. KAGANOVICH, A. KAHANA, R. KAIN, S. KAJIMURA, M. KALAMVOKI, M. KALIA, D. KALINOWSKI, N. KALUDERCIC, I. KALVARI, J. KAMINSKA, V. KAMINSKYY, H. KANAMORI, K. KANASAKI, C. KANG, R. KANG, S. KANG, S. KANIYAPPAN, T. KANKI, T. KANNEGANTI, A. KANTHASAMY, M. KANTOROW, O. KAPUY, M. KARAMOUZIS, M. KARIM, P. KARMAKAR, R. KATARE, M. KATO, S. KAUFMANN, A. KAUPPINEN, G. KAUSHAL, S. KAUSHIK, K. KAWASAKI, K. KAZAN, P. KE, D. KEATING, U. KEBER, J. KEHRL, K. KELLER, C. KELLER, J. KEMPER, C. KENIFIC, O. KEPP, S. KERMORGANT, A. KERN, R. KETTELER, T. KEULERS, B. KHALFIN, H. KHALIL, B. KHAMBU, S. KHAN, V. KHANDELWAL, R. KHANDIA, W. KHO, N. KHOBREKAR, S. KHUANSUWAN, M. KHUNDADZE, S. KILLACKEY, D. KIM, E. KIM, H. KIM, J. KIM, K. KIM, P. KIM, S. KIM, S. KIMBALL, A. KIMCHI, A. KIMMELMAN, T. KIMURA, M. KING, K. KINGHORN, C. KINSEY, V. KIRKIN, L. KIRSHENBAUM, S. KISELEV, S. KISHI, K. KITAMOTO, Y. KITAOKA, K. KITAZATO, R. KITSIS, J. KITTLER, O. KJAERULFF, P. KLEIN, T. KLOPSTOCK, J. KLUCKEN, H. KNOVELSRUD, R. KNORR, B. KO, F. KO, J. KO, H. KOBAYASHI, S. KOBAYASHI, I. KOCH, J. KOCH, U. KOENIG, D. KOGEL, Y. KOH, M. KOIKE, S. KOHLWEIN, N. KOCATURK, M. KOMATSU, J. KONIG, T. KONO, B. KOPP, T. KORCSMAROS, G. KORKMAZ, V. KOROLCHUK, M. KORSNES, A. KOSKELA, J. KOTA, Y. KOTAKE, M. KOTLER, Y. KOU, M. KOUKOURAKIS, E. KOUSTAS, A. KOVACS, T. KOVACS, D. KOYA, T. KOZAKO, C. KRAFT, D. KRAINC, H. KRAMER, A. KRASNODEMBSKAYA, C. KRETZ-REMY, G. KROEMER, N. KTISTAKIS, K. KUCHITSU, S. KUENEN, L. KUERSCHNER, T. KUKAR, A. KUMAR, D. KUMAR, S. KUMAR, S. KUME, C. KUMSTA, C. KUNDU, M. KUNDU, A. KUNNUMAKKARA, L. KURGAN, T. KUTATELADZE, O. KUTLU, S. KWAK, H. KWON, T. KWON, Y. KWON, I. KYRMIZI, A. LA SPADA, P. LABONTE, S. LADOIRE, I. LAFACE, F. LAFONT, D. LAGACE, V. LAHIRI, Z. LAI, A. LAIRD, A. LAKKARAJU, T. LAMARK, S. LAN, A. LANDAJUELA, D. LANE, J. LANE, C. LANG, C. LANGE, R. LANGER, P. LAPAQUETTE, J. LAPORTE, N. LARUSSO, I. LASTRES-BECKER, W. LAU, G. LAURIE, S. LAVANDERO, B. LAW, H. LAW, R. LAYFIELD, W. LE, H. LE STUNFF, A. LEARY, J. LEBRUN, L. LECK, J. LEDUC-GAUDET, C. LEE, D. LEE, E. LEE, G. LEE, H. LEE, J. LEE, M. LEE, S. LEE, W. LEE, Y. LEE, C. LEFEBVRE, R. LEGOUIS, Y. LEI, S. LEIKIN, G. LEITINGER, L. LEMUS, S. LENG, O. LENOIR, G. LENZ, H. LENZ, P. LENZI, Y. LEON, A. LEOPOLDINO, C. LESCHCZYK, S. LESKELA, E. LETELLIER, C. LEUNG, P. LEUNG, J. LEVENTHAL, B. LEVINE, P. LEWIS, K. LEY, B. LI, D. LI, J. LI, K. LI, L. LI, M. LI, P. LI, Q. LI, S. LI, T. LI, W. LI, X. LI, Y. LI, Z. LI, J. LIAN, C. LIANG, Q. LIANG, W. LIANG, Y. LIANG, G. LIAO, L. LIAO, M. LIAO, Y. LIAO, M. LIBRIZZI, P. LIE, M. LILLY, H. LIM, T. LIMA, F. LIMANA, C. LIN, D. LIN, F. LIN, J. LIN, K. LIN, L. LIN, P. LIN, Q. LIN, S. LIN, W. LIN, X. LIN, Y. LIN, R. LINDEN, P. LINDNER, S. LING, P. LINGOR, A. LINNEMANN, Y. LIOU, M. LIPINSKI, S. LIPOVSEK, V. LIRA, N. LISIAK, P. LITON, C. LIU, F. LIU, H. LIU, J. LIU, L. LIU, M. LIU, Q. LIU, W. LIU, X. LIU, Y. LIU, J. LIVINGSTON, G. LIZARD, J. LIZCANO, S. LJUBOJEVIC-HOLZER, M. LLEONART, D. LLOBET-NAVAS, A. LLORENTE, C. LO, D. LOBATO-MARQUEZ, Q. LONG, Y. LONG, B. LOOS, J. LOOS, M. LOPEZ, G. LOPEZ-DOMENECH, J. LOPEZ-GUERRERO, A. LOPEZ-JIMENEZ, I. LOPEZ-VALERO, M. LORENOWICZ, M. LORENTE, P. LORINCZ, L. LOSSI, S. LOTERSZTAJN, P. LOVAT, J. LOVELL, A. LOVY, G. LU, H. LU, J. LU, M. LU, S. LU, A. LUCIANI, J. LUCOCQ, P. LUDOVICO, M. LUFTIG, M. LUHR, D. LUIS-RAVELO, J. LUM, L. LUNA-DULCEY, A. LUND, V. LUND, J. LUNEMANN, P. LUNINGSCHROR, H. LUO, R. LUO, S. LUO, Z. LUO, C. LUPARELLO, B. LUSCHER, L. LUU, A. LYAKHOVICH, K. LYAMZAEV, A. LYSTAD, L. LYTVYNCHUK, A. MA, C. MA, M. MA, N. MA, Q. MA, X. MA, Y. MA, Z. MA, O. MACDOUGALD, F. MACIAN, G. MACINTOSH, J. MACKEIGAN, K. MACLEOD, S. MADAY, F. MADEO, M. MADESH, T. MADL, J. MADRIGAL-MATUTE, A. MAEDA, Y. MAEJIMA, M. MAGARINOS, P. MAHAVADI, E. MAIANI, K. MAIESE, P. MAITI, M. MAIURI, B. MAJELLO, M. MAJOR, E. MAKAREEVA, F. MALIK, K. MALLILANKARAMAN, W. MALORNI, A. MALOYAN, N. MAMMADOVA, G. MAN, F. MANAI, J. MANCIAS, E. MANDELKOW, M. MANDELL, A. MANFREDI, M. MANJILI, R. MANJITHAYA, P. MANQUE, B. MANSHIAN, R. MANZANO, C. MANZONI, K. MAO, C. MARCHESE, S. MARCHETTI, A. MARCONI, F. MARCUCCI, S. MARDENTE, O. MARENINOVA, M. MARGETA, M. MARI, S. MARINELLI, O. MARINELLI, G. MARINO, S. MARIOTTO, R. MARSHALL, M. MARTEN, S. MARTENS, A. MARTIN, K. MARTIN, S. MARTIN, A. MARTIN-SEGURA, M. MARTIN-ACEBES, I. MARTIN-BURRIEL, M. MARTIN-RINCON, P. MARTIN-SANZ, J. MARTINA, W. MARTINET, A. MARTINEZ, J. MARTINEZ, M. VELAZQUEZ, N. MARTINEZ-LOPEZ, M. MARTINEZ-VICENTE, D. MARTINS, U. LANGE, O. LOPEZ-PEREZ, J. MARTINS, W. MARTINS, T. MARTINS-MARQUES, E. MARZETTI, S. MASALDAN, C. MASCLAUX-DAUBRESSE, D. MASHEK, V. MASSA, L. MASSIEU, G. MASSON, L. MASUELLI, A. MASYUK, T. MASYUK, P. MATARRESE, A. MATHEU, S. MATOBA, S. MATSUZAKI, P. MATTAR, A. MATTE, D. MATTOSCIO, J. MAURIZ, M. MAUTHE, C. MAUVEZIN, E. MAVERAKIS, P. MAYCOTTE, J. MAYER, G. MAZZOCCOLI, C. MAZZONI, J. MAZZULLI, N. MCCARTY, C. MCDONALD, M. MCGILL, S. MCKENNA, B. MCLAUGHLIN, F. MCLOUGHLIN, M. MCNIVEN, T. MCWILLIAMS, F. MECHTA-GRIGORIOU, T. MEDEIROS, D. MEDINA, L. MEGENEY, K. MEGYERI, M. MEHRPOUR, J. MEHTA, A. MEIJER, J. MEJLVANG, A. MELENDEZ, A. MELK, G. MEMISOGLU, A. MENDES, D. MENG, F. MENG, T. MENG, R. MENNA-BARRETO, M. MENON, C. MERCER, A. MERCIER, J. MERGNY, A. MERIGHI, S. MERKLEY, G. MERLA, V. MESKE, A. MESTRE, S. METUR, C. MEYER, H. MEYER, W. MI, J. MIALET-PEREZ, J. MIAO, L. MICALE, Y. MIKI, E. MILAN, D. MILLER, S. MILLER, S. MILLWARD, I. MILOSEVIC, E. MININA, H. MIRZAEI, M. MIRZAEI, A. MISHRA, N. MISHRA, P. MISHRA, M. MARJANOVIC, R. MISASI, A. MISRA, G. MISSO, C. MITCHELL, G. MITOU, T. MIURA, S. MIYAMOTO, M. MIYAZAKI, T. MIYAZAKI, K. MIYAZAWA, N. MIZUSHIMA, T. MOGENSEN, B. MOGRABI, R. MOHAMMADINEJAD, Y. MOHAMUD, A. MOHANTY, S. MOHAPATRA, T. MOHLMANN, A. MOHMMED, A. MOLES, K. MOLEY, M. MOLINARI, V. MOLLACE, A. MULLER, B. MOLLEREAU, F. MOLLINEDO, C. MONTAGNA, M. MONTEIRO, A. MONTELLA, L. MONTES, B. MONTICO, V. MONY, G. COMPAGNONI, M. MOORE, M. MOOSAVI, A. MORA, M. MORA, D. MORALES-ALAMO, R. MORATALLA, P. MOREIRA, E. MORELLI, S. MORENO, D. MORENO-BLAS, V. MORESI, B. MORGA, A. MORGAN, F. MORIN, H. MORISHITA, O. MORITZ, M. MORIYAMA, Y. MORIYASU, M. MORLEO, E. MORSELLI, J. MORUNO-MANCHON, J. MOSCAT, S. MOSTOWY, E. MOTORI, A. MOURA, N. MOUSTAID-MOUSSA, M. MRAKOVCIC, G. MUCINOHERNANDEZ, A. MUKHERJEE, S. MUKHOPADHYAY, J. LEVY, V. MULERO, S. MULLER, C. MUNCH, A. MUNJAL, P. MUNOZ-CANOVES, T. MUNOZ-GALDEANO, C. MUNZ, T. MURAKAWA, C. MURATORI, B. MURPHY, J. MURPHY, A. MURTHY, T. MYOHANEN, I. MYSOREKAR, J. MYTYCH, S. NABAVI, M. NABISSI, P. NAGY, J. NAH, A. NAHIMANA, I. NAKAGAWA, K. NAKAMURA, H. NAKATOGAWA, S. NANDI, M. NANJUNDAN, M. NANNI, G. NAPOLITANO, R. NARDACCI, M. NARITA, M. NASSIF, I. NATHAN, M. NATSUMEDA, R. NAUDE, C. NAUMANN, O. NAVEIRAS, F. NAVID, S. NAWROCKI, T. NAZARKO, F. NAZIO, F. NEGOITA, T. NEILL, A. NEISCH, L. NERI, M. NETEA, P. NEUBERT, T. NEUFELD, D. NEUMANN, A. NEUTZNER, P. NEWTON, P. NEY, I. NEZIS, C. NG, T. NG, H. NGUYEN, L. NGUYEN, H. NI, C. CHEALLAIGH, Z. NI, M. NICOLAO, F. NICOLI, M. NIETO-DIAZ, P. NILSSON, S. NING, R. NIRANJAN, H. NISHIMUNE, M. NISO-SANTANO, R. NIXON, A. NOBILI, C. NOBREGA, T. NODA, U. NOGUEIRA-RECALDE, T. NOLAN, I. NOMBELA, I. NOVAK, B. NOVOA, T. NOZAWA, N. NUKINA, C. NUSSBAUM-KRAMMER, J. NYLANDSTED, T. O'DONOVAN, S. O'LEARY, E. O'ROURKE, M. O'SULLIVAN, T. O'SULLIVAN, S. ODDO, I. OEHME, M. OGAWA, E. OGIER-DENIS, M. OGMUNDSDOTTIR, B. OGRETMEN, G. OH, S. OH, Y. OH, T. OHAMA, Y. OHASHI, M. OHMURAYA, V. OIKONOMOU, R. OJHA, K. OKAMOTO, H. OKAZAWA, M. OKU, S. OLIVAN, J. OLIVEIRA, M. OLLMANN, J. OLZMANN, S. OMARI, M. OMARY, G. ONAL, M. ONDREJ, S. ONG, A. ONNIS, J. ORELLANA, S. ORELLANA-MUNOZ, M. ORTEGA-VILLAIZAN, X. ORTIZ-GONZALEZ, E. ORTONA, H. OSIEWACZ, A. OSMAN, R. OSTA, M. OTEGUI, K. OTSU, C. OTT, L. OTTOBRINI, J. OU, T. OUTEIRO, I. OYNEBRATEN, M. OZTURK, G. PAGES, S. PAHARI, M. PAJARES, U. PAJVANI, R. PAL, S. PALADINO, N. PALLET, M. PALMIERI, G. PALMISANO, C. PALUMBO, F. PAMPALONI, L. PAN, Q. PAN, W. PAN, X. PAN, G. PANASYUK, R. PANDEY, U. PANDEY, V. PANDYA, F. PANENI, S. PANG, E. PANZARINI, D. PAPADEMETRIO, E. PAPALEO, D. PAPINSKI, D. PAPP, E. PARK, H. PARK, J. PARK, S. PARK, A. PAROLA, J. PARYS, A. PASQUIER, B. PASQUIER, J. PASSOS, N. PASTORE, H. PATEL, D. PATSCHAN, S. PATTINGRE, G. PEDRAZA-ALVA, J. PEDRAZA-CHAVERRI, Z. PEDROZO, G. PEI, J. PEI, H. PELED-ZEHAVI, J. PELLEGRINI, J. PELLETIER, M. PENALVA, D. PENG, Y. PENG, F. PENNA, M. PENNUTO, F. PENTIMALLI, C. PEREIRA, G. PEREIRA, L. PEREIRA, L. DE ALMEIDA, N. PERERA, A. PEREZOLIVA, M. PEREZ-PEREZ, P. PERIYASAMY, A. PERL, C. PERROTTA, I. PERROTTA, R. PESTELL, M. PETERSEN, I. PETRACHE, G. PETROVSKI, T. PFIRRMANN, A. PFISTER, J. PHILIPS, H. PI, A. PICCA, A. PICKRELL, S. PICOT, G. PIERANTONI, M. PIERDOMINICI, P. PIERRE, V. PIERREFITE-CARLE, K. PIERZYNOWSKA, F. PIETROCOLA, M. PIETRUCZUK, C. PIGNATA, F. PIMENTELMUINOS, M. PINAR, R. PINHEIRO, R. PINKAS-KRAMARSKI, P. PINTON, K. PIRCS, S. PIYA, P. PIZZO, T. PLANTINGA, H. PLATTA, A. PLAZA-ZABALA, M. PLOMANN, E. PLOTNIKOV, H. PLUN-FAVREAU, R. PLUTA, R. POCOCK, S. POGGELER, C. POHL, M. POIROT, A. POLETTI, M. PONPUAK, H. POPELKA, B. POPOVA, H. PORTA, S. ALCON, E. PORTILLA-FERNANDEZ, M. POST, M. POTTS, J. POULTON, T. POWERS, V. PRAHLAD, T. PRAJSNAR, D. PRATICO, R. PRENCIPE, M. PRIAULT, T. PROIKASCEZANNE, V. PROMPONAS, C. PROUD, R. PUERTOLLANO, L. PUGLIELLI, T. PULINILKUNNIL, D. PURI, R. PURI, J. PUYAL, X. QI, Y. QI, W. QIAN, L. QIANG, Y. QIU, J. QUADRILATERO, J. QUARLERI, N. RABEN, H. RABINOWICH, D. RAGONA, M. RAGUSA, N. RAHIMI, M. RAHMATI, V. RAIA, N. RAIMUNDO, N. RAJASEKARAN, S. RAO, A. RAMI, I. RAMIREZ-PARDO, D. RAMSDEN, F. RANDOW, P. RANGARAJAN, D. RANIERI, H. RAO, L. RAO, R. RAO, S. RATHORE, J. RATNAYAKA, E. RATOVITSKI, P. RAVANAN, G. RAVEGNINI, S. RAY, B. RAZANI, V. REBECCA, F. REGGIORI, A. REGNIER-VIGOUROUX, A. REICHERT, D. REIGADA, J. REILING, T. REIN, S. REIPERT, R. REKHA, H. REN, J. REN, W. REN, T. RENAULT, G. RENGA, K. REUE, K. REWITZ, B. RAMOS, S. RIAZUDDIN, T. RIBEIRO-RODRIGUES, J. RICCI, R. RICCI, V. RICCIO, D. RICHARDSON, Y. RIKIHISA, M. RISBUD, R. RISUENO, K. RITIS, S. RIZZA, R. RIZZUTO, H. ROBERTS, L. ROBERTS, K. ROBINSON, M. ROCCHERI, S. ROCCHI, G. RODNEY, T. RODRIGUES, V. SILVA, A. RODRIGUEZ, R. RODRIGUEZ-BARRUECO, N. RODRIGUEZ-HENCHE, H. RODRIGUEZ-ROCHA, J. ROELOFS, R. ROGERS, V. ROGOV, A. ROJO, K. ROLKA, V. ROMANELLO, L. ROMANI, A. ROMANO, P. ROMANO, D. ROMEO-GUITART, L. ROMERO, M. ROMERO, J. RONEY, C. RONGO, S. ROPERTO, M. ROSENFELDT, P. ROSENSTIEL, A. ROSENWALD, K. ROTH, L. ROTH, S. ROTH, K. ROUSCHOP, B. ROUSSEL, S. ROUX, P. ROVERE-QUERINI, A. ROY, A. ROZIERES, D. RUANO, D. RUBINSZTEIN, M. RUBTSOVA, K. RUCKDESCHEL, C. RUCKENSTUHL, E. RUDOLF, R. RUDOLF, A. RUGGIERI, A. RUPARELIA, P. RUSMINI, R. RUSSELL, G. RUSSO, M. RUSSO, R. RUSSO, O. RYABAYA, K. RYAN, K. RYU, M. SABATER-ARCIS, U. SACHDEV, M. SACHER, C. SACHSE, A. SADHU, J. SADOSHIMA, N. SAFREN, P. SAFTIG, A. SAGONA, G. SAHAY, A. SAHEBKAR, M. SAHIN, O. SAHIN, S. SAHNI, N. SAITO, S. SAITO, T. SAITO, R. SAKAI, Y. SAKAI, J. SAKAMAKI, K. SAKSELA, G. SALAZAR, A. SALAZAR-DEGRACIA, G. SALEKDEH, A. SALUJA, B. SAMPAIO-MARQUES, M. SANCHEZ, J. SANCHEZ-ALCAZAR, V. SANCHEZ-VERA, V. SANCHO-SHIMIZU, J. SANDERSON, M. SANDRI, S. SANTAGUIDA, L. SANTAMBROGIO, M. SANTANA, G. SANTONI, A. SANZ, P. SANZ, S. SARAN, M. SARDIELLO, T. SARGEANT, A. SARIN, C. SARKAR, S. SARKAR, M. SARRIAS, D. SARMAH, J. SARPARANTA, A. SATHYANARAYAN, R. SATHYANARAYANAN, K. SCAGLIONE, F. SCATOZZA, L. SCHAEFER, Z. SCHAFER, U. SCHAIBLE, A. SCHAPIRA, M. SCHARL, H. SCHATZL, C. SCHEIN, W. SCHEPER, D. SCHEURING, M. SCHIAFFINO, M. SCHIAPPACASSI, R. SCHINDL, U. SCHLATTNER, O. SCHMIDT, R. SCHMITT, S. SCHMIDT, I. SCHMITZ, E. SCHMUKLER, A. SCHNEIDER, B. SCHNEIDER, R. SCHOBER, A. SCHOIJET, M. SCHOTT, M. SCHRAMM, B. SCHRODER, K. SCHUH, C. SCHULLER, R. SCHULZE, L. SCHURMANNS, J. SCHWAMBORN, M. SCHWARTEN, F. SCIALO, S. SCIARRETTA, M. SCOTT, K. SCOTTO, A. SCOVASSI, A. SCRIMA, A. SCRIVO, D. SEBASTIAN, S. SEBTI, S. SEDEJ, L. SEGATORI, N. SEGEV, P. SEGLEN, I. SEILIEZ, E. SEKI, S. SELLECK, F. SELLKE, A. PEREZ-LARA, J. SELSBY, M. SENDTNER, S. SENTURK, E. SERANOVA, C. SERGI, R. SERRA-MORENO, H. SESAKI, C. SETTEMBRE, S. SETTY, G. SGARBI, O. SHA, J. SHACKA, J. SHAH, D. SHANG, C. SHAO, F. SHAO, S. SHARBATI, L. SHARKEY, D. SHARMA, G. SHARMA, K. SHARMA, P. SHARMA, S. SHARMA, H. SHEN, J. SHEN, M. SHEN, W. SHEN, Z. SHEN, R. SHENG, Z. SHENG, J. SHI, X. SHI, Y. SHI, K. SHIBA-FUKUSHIMA, J. SHIEH, Y. SHIMADA, S. SHIMIZU, M. SHIMOZAWA, T. SHINTANI, C. SHOEMAKER, S. SHOJAEI, I. SHOJI, B. SHRAVAGE, V. SHRIDHAR, C. SHU, H. SHU, K. SHUI, A. SHUKLA, T. SHUTT, V. SICA, A. SIDDIQUI, A. SIERRA, V. SIERRA-TORRE, S. SIGNORELLI, P. SIL, B. SILVA, J. SILVA, E. SILVA-PAVEZ, S. SILVENTE-POIROT, R. SIMMONDS, A. SIMON, H. SIMON, M. SIMONS, A. SINGH, L. SINGH, R. SINGH, S. SINGH, D. SINHA, R. SINHA, S. SINHA, A. SIRKO, K. SIROHI, E. SIVRIDIS, P. SKENDROS, A. SKIRYCZ, I. SLANINOVA, S. SMAILI, A. SMERTENKO, M. SMITH, S. SOENEN, E. SOHN, S. SOK, G. SOLAINI, T. SOLDATI, S. SOLEIMANPOUR, R. SOLER, A. SOLOVCHENKO, J. SOMARELLI, A. SONAWANE, F. SONG, H. SONG, J. SONG, K. SONG, Z. SONG, L. SORIA, M. SORICE, A. SOUKAS, S. SOUKUP, D. SOUSA, N. SOUSA, P. SPAGNUOLO, S. SPECTOR, M. BHARATH, D. ST CLAIR, V. STAGNI, L. STAIANO, C. STALNECKER, M. STANKOV, P. STATHOPULOS, K. STEFAN, S. STEFAN, L. STEFANIS, J. STEFFAN, A. STEINKASSERER, H. STENMARK, J. STERNECKERT, C. STEVENS, V. STOKA, S. STORCH, B. STORK, F. STRAPPAZZON, A. STROHECKER, D. STUPACK, H. SU, L. SU, A. SUAREZFONTES, C. SUBAUSTE, S. SUBBIAN, P. SUBIRADA, G. SUDHANDIRAN, C. SUE, X. SUI, C. SUMMERS, G. SUN, J. SUN, K. SUN, M. SUN, Q. SUN, Y. SUN, Z. SUN, K. SUNAHARA, E. SUNDBERG, K. SUSZTAK, P. SUTOVSKY, H. SUZUKI, G. SWEENEY, J. SYMONS, S. SZE, N. SZEWCZYK, C. TABOLACCI, F. TACKE, H. TAEGTMEYER, M. TAFANI, M. TAGAYA, H. TAI, S. TAIT, Y. TAKAHASHI, S. TAKATS, P. TALWAR, C. TAM, S. TAM, D. TAMPELLINI, A. TAMURA, C. TAN, E. TAN, Y. TAN, M. TANAKA, D. TANG, J. TANG, T. TANG, I. TANIDA, Z. TAO, M. TAOUIS, L. TATENHORST, N. TAVERNARAKIS, A. TAYLOR, G. TAYLOR, J. TAYLOR, E. TCHETINA, A. TEE, I. TEGEDER, D. TEIS, N. TEIXEIRA, F. TEIXEIRA-CLERC, K. TEKIRDAG, T. TENCOMNAO, S. TENREIRO, A. TEPIKIN, P. TESTILLANO, G. TETTAMANTI, P. THARAUX, K. THEDIECK, A. THEKKINGHAT, S. THELLUNG, J. THINWA, V. THIRUMALAIKUMAR, S. THOMAS, P. THOMES, A. THORBURN, L. THUKRAL, T. THUM, M. THUMM, L. TIAN, A. TICHY, A. TILL, V. TIMMERMAN, V. TITORENKO, S. TODI, K. TODOROVA, J. TOIVONEN, L. TOMAIPITINCA, D. TOMAR, C. TOMAS-ZAPICO, B. TONG, C. TONG, X. TONG, S. TOOZE, M. TORGERSEN, S. TORII, L. TORRES-LOPEZ, A. TORRIGLIA, C. TOWERS, R. TOWNS, S. TOYOKUNI, V. TRAJKOVIC, D. TRAMONTANO, Q. TRAN, L. TRAVASSOS, C. TRELFORD, S. TREMEL, I. TROUGAKOS, B. TSAO, M. TSCHAN, H. TSE, T. TSE, H. TSUGAWA, A. TSVETKOV, D. TUMBARELLO, Y. TUMTAS, M. TUNON, S. TURCOTTE, B. TURK, V. TURK, B. TURNER, R. TUXWORTH, J. TYLER, E. TYUTEREVA, Y. UCHIYAMA, A. UGUNKLUSEK, H. UHLIG, I. ULASOV, M. UMEKAWA, C. UNGERMANN, R. UNNO, S. URBE, E. URIBE-CARRETERO, S. USTUN, V. UVERSKY, T. VACCARI, M. VACCARO, B. VAHSEN, H. VAKIFAHMETOGLU-NORBERG, R. VALDOR, M. VALENTE, A. VALKO, R. VALLEE, A. VALVERDE, G. VAN DEN BERGHE, S. VAN DER VEEN, L. VAN KAER, J. VAN LOOSDREGT, S. VAN WIJK, W. VANDENBERGHE, I. VANHOREBEEK, M. VANNIER-SANTOS, N. VANNINI, M. VANRELL, C. VANTAGGIATO, G. VARANO, I. VARELA-NIETO, M. VARGA, M. VASCONCELOS, S. VATS, D. VAVVAS, I. VEGANAREDO, S. VEGA-RUBIN-DE-CELIS, G. VELASCO, A. VELAZQUEZ, T. VELLAI, E. VELLENGA, F. VELOTTI, M. VERDIER, P. VERGINIS, I. VERGNE, P. VERKADE, M. VERMA, P. VERSTREKEN, T. VERVLIET, J. VERVOORTS, A. VESSONI, V. VICTOR, M. VIDAL, C. VIDONI, O. VIEIRA, R. VIERSTRA, S. VIGANO, H. VIHINEN, V. VIJAYAN, M. VILA, M. VILAR, J. VILLALBA, A. VILLALOBO, B. VILLAREJO-ZORI, F. VILLARROYA, J. VILLARROYA, O. VINCENT, C. VINDIS, C. VIRET, M. VISCOMI, D. VISNJIC, I. VITALE, D. VOCADLO, O. VOITSEKHOVSKAJA, C. VOLONTE, M. VOLTA, M. VOMERO, C. VON HAEFEN, M. VOOIJS, W. VOOS, L. VUCICEVIC, R. WADE-MARTINS, S. WAGURI, K. WAITE, S. WAKATSUKI, D. WALKER, M. WALKER, S. WALKER, J. WALTER, F. WANDOSELL, B. WANG, C. WANG, D. WANG, F. WANG, G. WANG, H. WANG, J. WANG, K. WANG, L. WANG, M. WANG, N. WANG, P. WANG, Q. WANG, W. WANG, X. WANG, Y. WANG, Z. WANG, G. WARNES, V. WARNSMANN, H. WATADA, E. WATANABE, M. WATCHON, T. WEAVER, G. WEGRZYN, A. WEHMAN, H. WEI, L. WEI, T. WEI, Y. WEI, O. WEIERGRABER, C. WEIHL, G. WEINDL, R. WEISKIRCHEN, A. WELLS, R. WEN, X. WEN, A. WERNER, B. WEYKOPF, S. WHEATLEY, J. WHITTON, A. WHITWORTH, K. WIKTORSKA, M. WILDENBERG, T. WILEMAN, S. WILKINSON, D. WILLBOLD, B. WILLIAMS, R. WILLIAMS, P. WILLIAMSON, R. WILSON, B. WINNER, N. WINSOR, S. WITKIN, H. WODRICH, U. WOEHLBIER, T. WOLLERT, E. WONG, J. WONG, R. WONG, V. WONG, W. WONG, A. WU, C. WU, J. WU, K. WU, M. WU, S. WU, W. WU, X. WU, Y. WU, R. XAVIER, H. XIA, L. XIA, Z. XIA, G. XIANG, J. XIANG, M. XIANG, W. XIANG, B. XIAO, G. XIAO, H. XIAO, J. XIAO, L. XIAO, S. XIAO, Y. XIAO, B. XIE, C. XIE, M. XIE, Y. XIE, Z. XIE, M. XILOURI, C. XU, E. XU, H. XU, J. XU, L. XU, W. XU, X. XU, Y. XUE, S. YAKHINE-DIOP, M. YAMAGUCHI, O. YAMAGUCHI, A. YAMAMOTO, S. YAMASHINA, S. YAN, Z. YAN, Y. YANAGI, C. YANG, D. YANG, H. YANG, J. YANG, L. YANG, M. YANG, P. YANG, Q. YANG, S. YANG, W. YANG, X. YANG, Y. YANG, H. YAO, S. YAO, X. YAO, Y. YAO, T. YASUI, M. YAZDANKHAH, P. YEN, C. YI, X. YIN, Y. YIN, Z. YIN, M. YING, Z. YING, C. YIP, S. YIU, Y. YOO, K. YOSHIDA, S. YOSHII, T. YOSHIMORI, B. YOUSEFI, B. YU, H. YU, J. YU, L. YU, M. YU, S. YU, V. YU, W. YU, Z. YU, J. YUAN, L. YUAN, S. YUAN, Y. YUAN, Z. YUAN, J. YUE, Z. YUE, J. YUN, R. YUNG, D. ZACKS, G. ZAFFAGNINI, V. ZAMBELLI, I. ZANELLA, Q. ZANG, S. ZANIVAN, S. ZAPPAVIGNA, P. ZARAGOZA, K. ZARBALIS, A. ZAREBKOHAN, A. ZARROUK, S. ZEITLIN, J. ZENG, E. ZEROVNIK, L. ZHAN, B. ZHANG, D. ZHANG, H. ZHANG, J. ZHANG, K. ZHANG, L. ZHANG, M. ZHANG, P. ZHANG, S. ZHANG, W. ZHANG, X. ZHANG, Y. ZHANG, Z. ZHANG, H. ZHAO, L. ZHAO, S. ZHAO, T. ZHAO, X. ZHAO, Y. ZHAO, G. ZHENG, K. ZHENG, L. ZHENG, S. ZHENG, X. ZHENG, Y. ZHENG, Z. ZHENG, B. ZHIVOTOVSKY, Q. ZHONG, A. ZHOU, B. ZHOU, C. ZHOU, G. ZHOU, H. ZHOU, J. ZHOU, K. ZHOU, R. ZHOU, X. ZHOU, Y. ZHOU, Z. ZHOU, B. ZHU, C. ZHU, G. ZHU, H. ZHU, W. ZHU, Y. ZHU, H. ZHUANG, X. ZHUANG, K. ZIENTARA-RYTTER, C. ZIMMERMANN, E. ZIVIANI, T. ZOLADEK, W. ZONG, D. ZOROV, A. ZORZANO, W. ZOU, Z. ZOU, S. ZURYN, W. ZWERSCHKE, B. BRAND-SABERI, C. KENCHAPPA, S. OSHIMA, Y. RONG, J. SLUIMER, and C. STALLINGS

Subjects
flux, macroautophagy, phagophore, stress, vacuole, Autophagosome, LC3, lysosome, neurodegeneration, cancer
Abstract

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.

Published
2021

32. The changing vaccine landscape: rates of COVID-19 vaccine acceptance and hesitancy in young adults during vaccine rollout

Author

H Knight, R Jia, K Ayling, H Blake, JR Morling, AM Villalon, J Corner, C Denning, J Ball, K Bolton, G Figueredo, D Morris, P Tighe, and K Vedhara

Subjects
Public Health, Environmental and Occupational Health
Abstract

Aims: Development and rollout of vaccines offers the best opportunity for population protection against the SARS-CoV-2 (COVID-19) virus. However, hesitancy towards the vaccines might impede successful uptake in the United Kingdom, particularly in young adults who demonstrate the highest rates of hesitancy. This prospective study explored COVID-19 vaccine hesitancy in young adults and whether the reasons behind these attitudes changed during the initial stages of the United Kingdom’s vaccine rollout. Method: Data on vaccination intention were collected from a British university student cohort at three time points: October 2020, February 2021, and March 2021. This online survey included items on intention to receive a vaccine and a free-text response for the reasons behind this intention. Cochran’s Q tests examined changes in rates of hesitancy and acceptance over time and free-text responses were analysed thematically. Results: At baseline, 893 students provided data, with 476 participants completing all three time points. Hesitancy declined over time, with 29.4% of participants expressing hesitancy at baseline, reducing to 9.1% at wave 2 and 5.9% at wave 3. The most commonly endorsed themes for those willing to accept a vaccine were self-protection against COVID-19 and pro-social reasons, including protecting the population or unspecific others, and ending the pandemic/returning to normal life. The most commonly endorsed hesitancy themes related to ‘confidence’ in the vaccines and potential personal risk, including insufficient testing/scientific evidence, concern about side effects, and long-term effects. These reasons remained the most commonly endorsed at both waves 2 and 3. Conclusions: While a decline in hesitancy was observed over time, the key reasons behind both vaccine acceptance and hesitancy remained consistent. Reasons behind hesitancy aligned with those of the general public, providing support for the use of generalist interventions. Pro-social reasons frequently underpinned vaccine acceptance, so cohort-specific interventions targeting those factors may be of benefit.

Published
2022
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33. Relationship between onset of eclampsia and AGTR1 gene polymorphisms

Author

H-L, Xu, J, Cui, R, Jia, X, Liu, and Y-J, Wang

Subjects
Adult, Young Adult, Polymorphism, Genetic, Pregnancy, Humans, Eclampsia, Female, Receptor, Angiotensin, Type 1
Abstract

We aimed to study the correlations of angiotensin II receptor type 1 (AGTR1) gene polymorphisms with the occurrence and development of eclampsia.A total of 200 pregnant women with eclampsia admitted to our hospital from January 1, 2017 to September 30, 2019 were collected as observation group and 200 normal pregnant women during the same period were recruited in the control group. Genome sequencing was performed to detect the AGTR1 gene polymorphisms in the two groups. Expression level of AGTR1 in both groups was detected. The influences of AGTR1 on clinical data of pregnant women with eclampsia were analyzed.There were no significant differences in age (p=0.545), height (p=0.738), weight (p=0.695) and hypertension (p=0.372) between observation group and control group. However, significant differences were found in the distributions of alleles at AGTR1 rs1799870 (p=0.002) and AGTR1 rs52936049 (p=0.047) between groups. The frequencies of T allele at rs1799870 and rs52936044 in observation group were higher than those in the control group. In addition, the distributions of AGTR1 gene genotypes at rs1799870 (p=0.012), rs144520513 (p=0.008) and rs529360494 (p p =0.036) in observation group differed from those in control group. Observation group had higher frequencies of TT genotype at rs1799870, GG genotype at rs144520513 and TG genotype at rs529360494 than those in control group. Besides, the frequency of CGG haplotype (p=0.008) of AGTR1 gene in observation group was notably lower than that in the control group, while the frequency of TGT haplotype (p=0.012) of AGTR1 gene in the former was remarkably higher than that in the latter. Moreover, the linkage disequilibrium between rs529360494 and rs144520513 of AGTR1 gene was relatively high (D'=0.623). AGTR1 gene polymorphism rs529360494 showed an evident relationship with the expression of AGTR1 gene, and the expression of AGTR1 in pregnant women with eclampsia who carried TG genotype was markedly reduced (p0.05). Furthermore, AGTR1 gene polymorphism rs1799870 was associated with prothrombin time (PT) in pregnant women with eclampsia (p=0.046), and PT in those carrying genotype TC was shorter. Rs144520513 was related to the levels of triglyceride (TG) (p0.001) and low-density lipoprotein (LDL) (p0.001) in pregnant women with eclampsia, and TG and LDL levels were significantly lower.AGTR1 gene polymorphisms are closely associated with the onset and progression of eclampsia.

Published
2020

34. Low-dose IL-2 therapy limits the reduction in absolute numbers of circulating regulatory T cells in rheumatoid arthritis

Author

Sheng-Xiao Zhang, Jing Luo, Xue-Yu Liu, Xiaofeng Li, Ming Yan, Caihong Wang, Fang-Yuan Hu, G. Y. Liu, Jia Wang, R Jia, and Chong Gao

Subjects
030203 arthritis & rheumatology, 0301 basic medicine, Il-2 therapy, business.industry, Low dose, Diseases of the musculoskeletal system, medicine.disease, Immune tolerance, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, RC925-935, Rheumatology, Rheumatoid arthritis, Immunology, Medicine, Orthopedics and Sports Medicine, business, Homeostasis
Abstract

Background: Circulating regulatory T cells (Tregs) are responsible for mediating immune tolerance and maintaining immunological homeostasis. Decreases in Tregs may be involved in the onset of rheumatoid arthritis (RA). Low-dose interleukin-2 (IL-2) has been considered for the treatment of inflammatory diseases mediated by T cells. This study focused on the status of circulating CD4+T subsets and the clinical feasibility of IL-2 therapies in patients with RA. Methods: The subjects included 888 patients with RA and 100 healthy controls (HCs); 233 RA patients received IL-2 treatment with 0.5 million international units (MIU)/day from days 1 through 5. The demographic features, disease activity, and levels of CD4+T cells measured by modified flow cytometry were collected in all RA patients before and after treatment. Results: RA patients had lower absolute Treg counts (but not Th17) compared with HCs, which was associated with disease activity; previously treated RA patients had the fewest circulating Tregs ( p +T subsets. Moreover, post-treatment levels of markers of disease activity in RA patients treated with IL-2 were significantly lower than the baseline values ( p Conclusion: Decreased absolute counts of circulating CD4+T lymphocyte subsets were observed in patients with RA. Circulating Tregs, which mediate immune tolerance, may be involved in the pathogenesis and progression of RA; however, this was ameliorated by low-dose IL-2, without obvious side effects. Plain language summary Low-dose IL-2 treatment for rheumatoid arthritis • Circulating Tregs may be involved in the pathogenesis and progression of RA. • The absolute count of Tregs was significantly correlated with disease activity measures. • Low-dose IL-2 was able to effectively expade Tregs and help for RA patients’ symptoms remission without evaluated side effects.

Published
2020

35. The prokaryotic expression, polyclonal antibody preparation, and subcellular localization of the transmembrane protein NS2A of the duck Tembusu virus

Author

R Jia, D Zhu, Y. Wu, M Wang, B Jiang, Ch Yang, Q Yang, Mengmeng Liu, Sheng Po Chen, P Liu, X Zhao, W Zhang, and A Cheng

Subjects
lac operon, Viral Nonstructural Proteins, Antibodies, Viral, law.invention, Mice, Western blot, law, Antibody Specificity, Virology, medicine, Escherichia coli, Animals, Mice, Inbred BALB C, biology, medicine.diagnostic_test, Chemistry, Flavivirus, General Medicine, Subcellular localization, Molecular biology, Transmembrane protein, Infectious Diseases, Polyclonal antibodies, Virion assembly, biology.protein, Recombinant DNA, Antibody
Abstract

Duck Tembusu virus (DTMUV) is a single-stranded, positive-sense RNA arbovirus, belonging to the genus Flavivirus, the family Flaviviridae. As a transmembrane protein, non-structural protein 2A (NS2A) plays an important role in virion assembly, replication complex and antagonizing host immune response. Since NS2A protein contains many hydrophobic amino acids, it is hard to gain the full-length protein of NS2A for prokaryotic expression. Therefore, to make a deep study, prokaryotic expression and polyclonal antibody preparation of truncated DTMUV NS2A was performed. The truncated NS2A gene (178-450 bp) was obtained, and sub-cloned into the prokaryotic vector pGEX-4T-1 (pGEX-4T-1-NS2A178-450bp). Subsequently, the recombinant GST-NS2A60-150aa protein was successfully expressed in E. coli BL21 (DE3) with the induction by 0.3 mmol/l isopropyl β-D-thiogalactoside (IPTG) for 6 h at 37°C. The GST-NS2A60-150aa protein was extracted from the gel. The BALB/c mice were immunized with the purified recombinant NS2A protein to prepare polyclonal antibodies against the truncated NS2A protein. The titer of the polyclonal antibodies, determined by ELISA analysis, was 1:128,000. The specificity of the polyclonal antibodies (mPAb-DTMUV-NS2A60-150aa) were verified by Western blot analysis. Furthermore, the indirect immunofluorescence (IFA) was performed to explore the subcellular localization of NS2A. NS2A protein was, in the transfected cells, located mainly around nucleus in the endoplasmatic reticulum. Taken together, our study provided a useful tool for the further exploration of the biological functions and molecular mechanism of DTMUV NS2A. Keywords: duck Tembusu virus; non-structural protein 2A; prokaryotic expression; polyclonal antibodies; subcellular location.

Published
2020

36. Fluctuations of topological charge and chiral density in the early stage of high energy nuclear collisions

Author

Marco Ruggieri, Hong-Fei Zhang, M. R. Jia, and J. H. Liu

Subjects
Physics, Chiral anomaly, Quantum chromodynamics, High Energy Physics - Theory, Nuclear Theory, 010308 nuclear & particles physics, High Energy Physics::Lattice, Order (ring theory), Inverse, FOS: Physical sciences, 01 natural sciences, Nuclear Theory (nucl-th), High Energy Physics - Phenomenology, High Energy Physics - Phenomenology (hep-ph), High Energy Physics - Theory (hep-th), 0103 physical sciences, Saturation (graph theory), Production (computer science), 010306 general physics, Energy (signal processing), Topological quantum number, Mathematical physics
Abstract

We study systematically the topological charge density and the chiral density correlations in the early stage of high energy nuclear collisions: the intial condition is given by the McLerran-Venugopalan model and the evolution of the gluon fields is studied via the Classical Yang-Mills equations up to proper time $\tau\approx 1$ fm/c for an $SU(2)$ evolving Glasma. Topological charge is related to the gauge invariant $\bm E \cdot \bm B$ where $\bm E$ and $\bm B$ denote the color-electric and color-magnetic fields, while the chiral density is produced via the chiral anomaly of Quantum Chromodynamics. We study how the correlation lengths are related to the collision energy, and how the correlated domains grow up with proper time in the transverse plane for a boost invariant longitudinal expansion. We estimate the correlation lengths of both quantities, that after a short transient results of the order of the typical energy scale of the model, namely the inverse of the saturation scale. We estimate the proper time for the formation of a steady state in which the production of the chiral density in the transverse plane per unit rapidity slows down, as well as the amount of chiral density that would be present at the switch time between the Classical Yang-Mills evolution and the relativistic transport or hydro for the quark-gluon plasma phase., Comment: Statistics has been improved. A few comments on the Gauss Law and the gauge invariance of the results have been added. This version corresponds to the one accepted for publication on Phys. Rev. D

Published
2020
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38. Derivatives from Two Algae: Moisture Absorption-Retention Ability, Antioxidative and Uvioresistant Activity

Author

R. D. Cao, R. Jia, Y. Y. Yang, Peimin He, and C. E. Cai

Subjects
Moisture absorption, biology, Renewable Energy, Sustainability and the Environment, Chemistry, 020209 energy, Bioengineering, 02 engineering and technology, 010501 environmental sciences, biology.organism_classification, 01 natural sciences, Biomaterials, Algae, Environmental chemistry, 0202 electrical engineering, electronic engineering, information engineering, 0105 earth and related environmental sciences
Published
2018
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39. Construction of expression vectors of capsid proteins from goose parvovirus and investigation of the immunogenicity

Author

R Jia, P Liu, M Liu, S Chen, Anchun Cheng, D Zhu, X Chen, K Sun, M. S. Wang, Y Wu, M Tu, Q Yang, and F Liu

Subjects
viruses, Immunogenicity, virus diseases, Viral Vaccines, General Medicine, biochemical phenomena, metabolism, and nutrition, Biology, Virology, DNA vaccination, Parvoviridae Infections, Infectious Diseases, Goose, Immune system, Plasmid, Capsid, Parvovirinae, biology.animal, Humoral immunity, Leukocytes, Mononuclear, biology.protein, Animals, Capsid Proteins, Antibody
Abstract

Goose parvovirus (GPV) is a highly contagious and lethal disease in goslings and Muscovy ducklings, and is of concern to the waterfowl industry. With the aim of comparing the cellular immunogenicity of three capsid proteins of GPV, plasmids of pcDNA3.1(+)-VP1, pcDNA3.1(+)-VP2, and pcDNA3.1(+)-VP3 were constructed, and the recombinant protein VPs were expressed using an eukaryotic expression system. We detected the levels of immune-related genes (CD4, CD8α, IL-1β, IL-6, IFNα, IFNγ, and IFNλ) in both goose embryo fibroblasts (GEF) and goose peripheral blood mononuclear cells (PBMCs) cellular models. The immune response conferred by a VP2 DNA vaccine in vivo was observed in a time course. Our data suggested that the cellular immune response to VP2 and VP3 was stronger than that to VP1, while VP2 and VP3 shared similar cellular immune reactivity. In addition, vaccination with VP2 plasmid can induce high level of IgY antibody that continued to increase through 28 days post vaccination. Therefore, our findings shed light on the host cellular immune response against GPV capsid proteins. Keywords: GPV; capsid proteins; cellular immune response; humoral immunity.

Published
2018
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40. Effects of Topographical Heterogeneity and Dispersal Limitation on Species Turnover in a Temperate Mountane Ecosystem: a Case Study in the Henan Province, China

Author

Shuai Niu, H. L. Wang, X. Zhang, H. R. Jia, Quan Chen, Zhiliang Yuan, Yun Chen, and Yongzhong Ye

Subjects
0106 biological sciences, Ecology, 010604 marine biology & hydrobiology, Ecology (disciplines), Elevation, food and beverages, Biology, 010603 evolutionary biology, 01 natural sciences, Temperate climate, Biological dispersal, Ecosystem, China, Ecology, Evolution, Behavior and Systematics, National nature reserve
Abstract

Species turnover patterns can be inconsistent due to differences in the dispersal ability of different growth forms. Here, species of trees, shrubs, herbs, and bryophytes in the Xiaoqinling National Nature Reserve in China were analyzed to determine patterns of species turnover along an elevation and spatial gradient. Variance partitioning was used to assess the relative contribution of topographic heterogeneity and dispersal limitation to species turnover. Our results suggest that the effect of dispersal limitation is more important than topographic heterogeneity on species turnover in temperate mountane ecosystems in the study area. Dispersal limitation has a greater effect on trees species turnover than on shrubs, herbs or bryophytes species turnover.

Published
2018
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41. Characteristics of cloud-to-ground lightning (CG) and differences between +CG and −CG strokes in China regarding the China National Lightning Detection Network

Author

R. Jiang, G. Zhang, S. Wang, B. Xue, Z. Xie, T. Yu, K. Wang, J. Ding, and X. Zhu

Subjects
Environmental technology. Sanitary engineering, TD1-1066, Geography. Anthropology. Recreation, Environmental sciences, GE1-350, Geology, QE1-996.5
Abstract

A lightning location system consisting of multiple ground-based stations is an effective means of lightning observation. The dataset from CNLDN (China National Lightning Detection Network) in 2016–2022 is employed to analyze the temporal and spatial lightning distributions and the differences between +CG (positive cloud-to-ground lightning) and −CG (negative cloud-to-ground lightning) strokes in China. On the annual scale, lightning activity is most prevalent during the summer months (June, July, and August), accounting for 72.6 % of the year. Spring sees more lightning than autumn, and winter has only a small amount in southeastern coastal areas. During the day, the frequency of lightning peaks at 15:00–17:00 CST (China standard time) and is lowest at 8:00–10:00 CST. For the period with high CG stroke frequency (summer of a year or afternoon of a day), the proportion of +CG strokes and the discharge peak current are relatively small. Winter in a year and morning or midnight in a day correspond to a greater +CG stroke proportion and discharge current. Spatially, low latitudes, undulating terrain, the seaside, and humid surfaces are favorable factors for lightning occurrence. Thus, the southeast coastland has the largest lightning stroke density, while the northwest deserts and basins and the western and northern Tibetan Plateau, with altitudes over 6000 m, have almost no lightning. The proportion of +CG strokes and the peak current are low in the southern region with high density but diverse in other regions. The Tibetan Plateau causes the diversity of lightning activity in China and lays the foundation for studying the impact of surface elevation on lightning. Results indicate that the +CG stroke proportion on the eastern and southern Tibetan Plateau is up to 15 %, larger than the plain regions. The peak current of −CG strokes is positively correlated with altitude, but +CG strokes show a negative correlation, resulting in a large difference in peak current between +CG and −CG on the plain and a small difference on the plateau.

Published
2023
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44. Fabrication of three-component hydrogen-bonded covalent-organic polymers for ciprofloxacin decontamination from water: adsorption mechanism and modeling

Author

F. Zhang, X. Lin, R. Jia, Z. Liu, M. Hong, A. Jia, Y. Li, and H. Zhang

Subjects
Materials science, Polymers and Plastics, 02 engineering and technology, 010402 general chemistry, 01 natural sciences, Catalysis, Biomaterials, symbols.namesake, Colloid and Surface Chemistry, Adsorption, Materials Chemistry, HOMO/LUMO, chemistry.chemical_classification, Hydrogen bond, Langmuir adsorption model, Polymer, 021001 nanoscience & nanotechnology, 0104 chemical sciences, Electronic, Optical and Magnetic Materials, Chemical engineering, chemistry, Ionic strength, Covalent bond, symbols, Density functional theory, 0210 nano-technology
Abstract

A three-component hydrogen-bonded covalent organic polymer, namely JLUE-HCOP-66, was fabricated via a facile multiple-linking-site solvothermal approach to overcome the weakness of poor function complexity and limited structure diversity of the pure covalent skeletons. The as-prepared JLUE-HCOP-66 polymers were employed to decontaminate ciprofloxacin (CIP), a popular F-quinolones (FQNs) antibiotic, from water and exhibited satisfactory adsorption performance. Specifically, JLUE-HCOP-66 polymers have high adsorption capacity with the maximum contribution of 111.1 mg/g according to the Langmuir model, good antiinterference to NaCl salts, and excellent regeneration property. The pH-dependent experiment results signified the probably dominated mechanism of electrostatic interaction. In addition, adsorption studies and structural characterization in combination illustrated that the pore-filling effect, hydrogen bonding formation might also govern the whole process, accompanied by electrostatic interaction, dipole-dipole complexation, π-π EDA interaction, and hydrophobic-hydrophobic interaction besides. Moreover, electrostatic potentials, as well as the frontier molecular orbital distributions (HOMO and LUMO) of CIP and JLUE-HCOP-66 fragment, were calculated using density functional theory to theoretically support the research. Furthermore, the response surface methodology (RSM) according to the CCD matrix was used to not only study the interactive and cooperative effects of initial CIP concentration, initial pH, ionic strength along with JLUE-HCOP-66 dosage on CIP removal using JLUE-HCOP-66 but also optimize the operation conditions. Given the peculiar structure and functional feature, this work could hopefully bring HCOPs into the practical applications of such challenging and persistent ciprofloxacin potent removal with further large-scale efficiency.

Published
2021
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47. 1165P Subgroup analysis by Ki-67 and primary tumour origins of the randomized, placebo-controlled phase III study of surufatinib in advanced well-differentiated extrapancreatic neuroendocrine tumours (SANET-ep)

Author

Z. Zhou, J. Xu, L. Shen, J. Li, C. Bai, Y. Chi, Z. Li, N. Xu, R. Jia, E. Li, T. Liu, Y. Bai, Y. Yuan, X. Li, X. Wang, J. Chen, W. Wang, J. He, and W. Su

Subjects
Oncology, medicine.medical_specialty, biology, business.industry, Subgroup analysis, Hematology, Placebo, Well differentiated, Internal medicine, Ki-67, medicine, biology.protein, business
Published
2020
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48. Ultrastructure of duck Tembusu virus observed by electron microscopy with negative staining

Author

X Luo, D Zhu, X Wang, S Chen, R Jia, Q Yang, Anchun Cheng, Y Liu, Xin Zhao, M Liu, Z Yin, H Shen, Y Wu, and M. S. Wang

Subjects
0301 basic medicine, 040301 veterinary sciences, viruses, Negative Staining, law.invention, Flavivirus Infections, 0403 veterinary science, 03 medical and health sciences, law, Virology, Animals, Lipid bilayer, Poultry Diseases, biology, Chemistry, Flavivirus, RNA, 04 agricultural and veterinary sciences, General Medicine, biology.organism_classification, Negative stain, Microscopy, Electron, 030104 developmental biology, Infectious Diseases, Ducks, Ectodomain, Capsid, Ultrastructure, Biophysics, Capsid Proteins, Electron microscope
Abstract

Duck Tembusu virus (DTMUV) is a newly emerging enveloped flavivirus. This study shows the ultrastructure of DTMUV using viral purification, negative staining and electron microscopy. Electron microscopic examinations revealed mature DTMUV particles with 50 to 75 nm in diameter and typical enveloped flavivirus structure that consists of the internal nucleocapsid, an inner layer of lipid bilayer and an external layer of E glycoprotein ectodomain. Particles appear to be mostly spherical. In particular, RNA core is deep colored and dense, both capsid and lipid bilayer are clearly visible, the capsid forms regular hexagon, and E glycoprotein ectodomain forms a fringe instead of visible spikes. Thus, this report about the clear ultrastructure of the DTMUV particles will be the major driving forces behind structural biology of DTMUV.

Published
2018

49. Multiple Virus Infections and the Characteristics of Chronic Bee Paralysis Virus in Diseased Honey Bees (Apis Mellifera L.) in China

Author

Qiang Wang, Ting Zhou, Xing Wang, Yan Y. Wu, Shu F. Xu, Ping L. Dai, Qing Y. Diao, and Hui R. Jia

Subjects
fungi, food and beverages, Plant Science, Chronic bee paralysis virus, Biology, chronic bee paralysis virus (cbpv), phylogeny, Virology, Virus, Honey Bees, diseased honey bees, QL1-991, law, Insect Science, law.legal_case, behavior and behavior mechanisms, apis mellifera l, multiple viruses, china, Zoology
Abstract

China has the largest number of managed honey bee colonies globally, but there is currently no data on viral infection in diseased A. mellifera L. colonies in China. In particular, there is a lack of data on chronic bee paralysis virus (CBPV) in Chinese honey bee colonies. Consequently, the present study investigated the occurrence and frequency of several widespread honey bee viruses in diseased Chinese apiaries, and we used the reverse transcription-polymerase chain reaction (RT-PCR) assay. Described was the relationship between the presence of CBPV and diseased colonies (with at least one of the following symptoms: depopulation, paralysis, dark body colorings and hairless, or a mass of dead bees on the ground surrounding the beehives). Phylogenetic analyses of CBPV were employed. The prevalence of multiple infections of honey bee viruses in diseased Chinese apiaries was 100%, and the prevalence of infections with even five and six viruses were higher than expected. The incidence of CBPV in diseased colonies was significantly higher than that in apparently healthy colonies in Chinese A. mellifera aparies, and CBPV isolates from China can be separated into Chinese-Japanese clade 1 and 2. The results indicate that beekeeping in China may be threatened by colony decline due to the high prevalence of multiple viruses with CBPV.

Published
2015

50. Ruscogenin suppresses mouse neutrophil activation: Involvement of protein kinase A pathway

Author

Boyang Yu, Junping Kou, Ying-sheng Gao, L.L. Wang, Yining Lin, Y.H. Liu, and R. Jia

Subjects
Male, Endocrinology, Diabetes and Metabolism, p38 mitogen-activated protein kinases, Clinical Biochemistry, Phospholipases A2, Cytosolic, Pharmacology, Biochemistry, Neutrophil Activation, Mice, chemistry.chemical_compound, Endocrinology, Superoxides, Spirostans, Animals, Protein kinase A, Molecular Biology, Protein kinase B, Mice, Inbred ICR, NADPH oxidase, biology, Kinase, Superoxide, Cell Biology, Cyclic AMP-Dependent Protein Kinases, Molecular biology, Enzyme Activation, p21-Activated Kinases, chemistry, biology.protein, Molecular Medicine, Phosphorylation, Signal transduction
Abstract

Ruscogenin, a natural steroidal sapogenin, presents in both food and medicinal plants. It has been found to exert significant anti-inflammatory activities. Considering that activation of neutrophil is a key feature of inflammatory diseases, this study was performed to investigate the inhibitory effect of ruscogenin and its underlying mechanisms responsible for neutrophil activation. Ruscogenin displayed potent antioxidative effects against Formyl-Met-Leu-Phe (FMLP)-induced extra- and intracellular superoxide generation in mouse bone marrow neutrophils, with IC50 values of 1.07±0.32 μM and 1.77±0.46 μM, respectively. Phorbol myristate acetate (PMA)-elicited extra- and intracellular superoxide generation were also suppressed by ruscogenin, with IC50 values of 1.56±0.46 μM and 1.29±0.49 μM, respectively. However, ruscogenin showed weak inhibition in NaF-induced response. Inhibition of superoxide generation was mediated neither by a superoxide-scavenging ability nor by a cytotoxic effect. Furthermore, ruscogenin inhibited the membrane translocation of p47phox and p67phox. It reduced FMLP-induced phosphorylation of cytosolic phospholipase A2 (cPLA2) and p21-activated kinase (PAK). The cellular cyclic adenosine monophosphate (cAMP) levels and protein kinase A (PKA) expression were increased by ruscogenin. Moreover, ruscogenin inhibited phosphorylation of protein kinase B (Akt), p38 mitogen-activated protein kinase (p38MAPK), extracellular signal-regulated kinase 1 and 2 (ERK1/2), and c-Jun N-terminal kinase (JNK). In addition, the inhibitory effects of ruscogenin on superoxide production and the phosphorylation of Akt, p38MAPK, and ERK1/2 were reversed by PKA inhibitor (H89), suggesting a PKA-dependent mechanism. In summary, our data suggest that ruscogenin inhibits activation of neutrophil through cPLA2, PAK, Akt, MAPKs, cAMP, and PKA signaling pathways. Increased PKA activity is associated with suppression of the phosphorylation of Akt, p38MAPK, and ERK1/2 pathways.

Published
2015
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