bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phylogeny of Coreoidea based on mitochondrial genomes show the paraphyly of Coreidae and Alydidae
Authors: Dong Xue , Wang Kaibin , Tang Zechen , Zhang Yaoyao , Yi Wenbo , Xue Huaijun , Zheng Chenguang , Bu Wenjun 
Published: February 2022

AbstractCoreoidea (Insecta: Hemiptera: Heteroptera) is a widely distributed and agriculturally important bugs. However, the phylogeny of Coreoidea lacked consensus on higher‐level relationships and several studies by comparative morphological characters and molecular data suggested the non‐monophyly of two families: Coreidae and Alydidae. The mitochondrial genome (mitogenome) has long been thought to be a significant marker to understand phylogenetic relationships, but the mitogenome in Alydidae is scarce to date. In the present study, we gathered the mitogenomes of 28 species from four families of Coreoidea excluding Hyocephalidae (Alydidae, Coreidae, Rhopalidae, and Stenocephalidae), including four newly sequenced mitogenomes of Alydidae, and conducted mitogenomic organization and phylogenetic studies. We used maximum likelihood and Bayesian inference methods to infer the higher‐level phylogeny from the perspective of mitogenomes, primarily to investigate the phylogenetic relationship betweeen Coreidae and Alydidae. We add evidence that neither Alydidae nor Coreidae are monophyletic based on mitogenomes. Newly sequenced mitogenomes of Alydidae have traditional gene structure and gene rearrangement was not found. Alydinae was always recovered as closely related to Pseudophloeinae of the coreid subfamily with high support. The placement of the coreid subfamily Hydarinae and alydid subfamily Micrelytrinae are unstable depending on approach used. In terms of the length and nucleotide composition of the protein coding genes in mitogenomes, Pseudophloeinae and Hydarinae of coreid were more similar to Alydidae. The unsettled classification issues of Coreidae and Alydidae by mitogenomes were demonstrated in this work, indicating that further study is needed.
A cross‐sectional study of brownfields and birth defects
Authors: Slawsky Erik D. , Weaver Anne M. , Luben Thomas J. , Rappazzo Kristen M. 
Published: February 2022

AbstractBackgroundBrownfields are a multitude of abandoned and disused sites, spanning many former purposes. Brownfields represent a heterogenous yet ubiquitous exposure for many Americans, which may contain hazardous wastes and represent urban blight. Neonates and pregnant individuals are often sensitive to subtle environmental exposures. We evaluate whether residential brownfield exposure is associated with birth defects.MethodsUsing North Carolina birth records from 2003 to 2015, we sampled 753,195 births with 39,495 defects identified. We examined defect groups and 30 distinct phenotypes. Number of brownfields within 2,000 m of the residential address at birth was summed. We utilized mixed effects multivariable logistic regression models adjusted for demographic and environmental covariates available from birth records, 2010 Census, and EPA's Environmental Quality Index to estimate odds ratios (OR) and 95% confidence intervals (CI).ResultsWe observed positive associations between cardiovascular and external defect groups (OR [95% CI]: 1.07 [1.02–1.13] and 1.17 [1.01–1.35], respectively) and any brownfield exposure. We also observed positive associations with atrial septal and ventricular septal defects (1.08 [1.01–1.16] and 1.15 [1.03–1.28], respectively), congenital cataracts (1.38 [0.98–1.96]), and an inverse association with gastroschisis (0.74 [0.58–0.94]). Effect estimates for several additional defects were positive, though we observed null associations for most group and individual defects. Additional analyses indicated an exposure–response relationship for several defects across levels of brownfield exposure.ConclusionsOur results indicate that residential proximity to brownfields is associated with birth defects, especially cardiovascular and external defects. In‐depth analyses of individual defects and specific contaminants or brownfield sites may reveal additional novel associations.
Essential roles of exosome and circRNA_101093 on ferroptosis desensitization in lung adenocarcinoma
Authors: Zhang Xiao , Xu Yunhua , Ma Lifang , Yu Keke , Niu Yongjie , Xu Xin , Shi Yi , Guo Susu , Xue Xiangfei , Wang Yikun , Qiu Shiyu , Cui Jiangtao , Wang Hong , Tian Xiaoting , Miao Yayou , Meng Fanyu , Qiao Yongxia , Yu Yongchun , Wang Jiayi 
Published: February 2022

AbstractBackgroundResistance to ferroptosis, a regulated cell death caused by iron‐dependent excessive accumulation of lipid peroxides, has recently been linked to lung adenocarcinoma (LUAD). Intracellular antioxidant systems are required for protection against ferroptosis. The purpose of the present study was to investigate whether and how extracellular system desensitizes LUAD cells to ferroptosis.MethodsEstablished human lung fibroblasts MRC‐5, WI38, and human LUAD H1650, PC9, H1975, H358, A549, and H1299 cell lines, tumor and matched normal adjacent tissues of LUAD, and plasma from healthy individuals and LUAD patients were used in this study. Immunohistochemistry and immunoblotting were used to analyze protein expression, and quantitative reverse transcription‐PCR was used to analyze mRNA expression. Cell viability, cell death, and the lipid reactive oxygen species generation were measured to evaluate the responses to ferroptosis. Exosomes were observed using transmission electron microscope. The localization of arachidonic acid (AA) was detected using click chemistry labeling followed by confocal microscopy. Interactions between RNAs and proteins were detected using RNA pull‐down, RNA immunoprecipitation and photoactivatable ribonucleoside‐enhanced crosslinking and immunoprecipitation methods. Proteomic analysis was used to investigate RNA‐regulated proteins, and metabolomic analysis was performed to analyze metabolites. Cell‐derived xenograft, patient‐derived xenograft, cell‐implanted intrapulmonary LUAD mouse models and plasma/tissue specimens from LUAD patients were used to validate the molecular mechanism.ResultsPlasma exosome from LUAD patients specifically reduced lipid peroxidation and desensitized LUAD cells to ferroptosis. A potential explanation is that exosomal circRNA_101093 (cir93) maintained an elevation in intracellular cir93 in LUAD to modulate AA, a poly‐unsaturated fatty acid critical for ferroptosis‐associated increased peroxidation in the plasma membrane. Mechanistically, cir93 interacted with and increased fatty acid‐binding protein 3 (FABP3), which transported AA and facilitated its reaction with taurine. Thus, global AA was reduced, whereas N‐arachidonoyl taurine (NAT, the product of AA and taurine) was induced. Notably, the role of NAT in suppressing AA incorporation into the plasma membrane was also revealed. In pre‐clinical in vivo models, reducing exosome improved ferroptosis‐based treatment.ConclusionExosome and cir93 are essential for desensitizing LUAD cells to ferroptosis, and blocking exosome may be helpful for future LUAD treatment.
The survival benefit of increasing the number of active drugs for metastatic colorectal cancer: A multicenter retrospective study
Authors: Kawakami Takeshi , Masuishi Toshiki , Kawamoto Yasuyuki , Go Hirofumi , Kato Kyoko , Kumanishi Ryosuke , Sawada Kentaro , Yuki Satoshi , Yamamoto Kouji , Komatsu Yoshito , Muro Kei , Fushiki Kunihiro , Shirasu Hiromichi , Yamazaki Kentaro 
Published: February 2022

AbstractBackgroundThe development of chemotherapy and treatment strategies for metastatic colorectal cancer (mCRC) have provided patients with significant survival benefits. Currently, molecular targeting agents and late‐line treatment with regorafenib and trifluridine/tipiracil (FTD/TPI) are available. However, the impact of this increase in drug availability on overall survival (OS) in mCRC remains a clinical question.MethodsWe retrospectively collected data on consecutive mCRC patients who were treated at three institutions in Japan. We divided the patients into three cohorts: patients who initiated first‐line treatment from Jan 2005 to Dec 2006 (cohort A: only cytotoxic drugs available), Jan 2007 to Dec 2011 (cohort B: molecular targeting drugs available), and Jan 2012 to Sep 2016 (cohort C: late‐line treatment available).ResultsA total of 1409 consecutive patients were analyzed. The median survival time (MST) in cohorts A, B, and C was 18.6, 25.4, and 26.4 months, respectively. The hazard ratio (HR) for cohort B versus A was 0.81 (95% CI 0.68–0.97), for cohort C versus A was 0.74 (95% CI 0.61–0.89), and for cohort C versus B was 0.92 (0.81–1.03). The median number of administered drugs (range) was 3 (1–5) in cohort A, 4 (1–7) in cohort B, and 4 (1–7) in cohort C. The increase in drug availability extended the MST from 15.5 months in patients treated with ≤3 drugs to 36.0–37.3 months in patients treated with six to seven drugs.ConclusionThe development of chemotherapy including late‐line treatments could improve the prognosis of mCRC patients.
Improved agronomic biofortification of sweetcorn achieved using foliar rather than soil Zn applications
Authors: Cheah Zhong Xiang , Harper Stephen M. , O'Hare Tim J. , Kopittke Peter M. , Bell Michael J. 
Published: February 2022

AbstractBackground and ObjectivesThis field and glasshouse study evaluates the relative effectiveness of agronomic zinc biofortification strategies to increase the Zn concentration in sweetcorn (Zea mays) kernels for human health, using applications of Zn fertilizer to the root‐zone or to foliage.FindingsPlants accumulated additional Zn as the rate of Zn applied to the root‐zone increased, but most was retained in the stems and foliage and little was translocated into the kernels (≤7%). A large proportion of the additional Zn stored in the foliage was in the form of Zn‐phytate. In contrast, in field‐grown plants where soil Zn was adequate for maximizing commercial yields, Zn applications to foliage increased kernel Zn concentrations by up to 100%. ZnSO4·7H2O was more effective to use in foliar applications compared with Zn‐EDTA.ConclusionThe elevated kernel concentrations recorded for two varieties (59.1 and 71.1 mg Zn kg−1) were greater than all previously reported biofortification responses from maize. These concentrations also matched or exceeded the HarvestPlus target of 60 mg Zn kg−1 for maize.Significance and NoveltyWith a total kernel Zn content of 3.6 mg Zn per cob, approximately 25%–45% of the recommended dietary Zn intake could be met with one cob of Zn‐biofortified sweetcorn.
Cover Image
Authors: Cheng Kang‐jie , Liu Yun‐feng , Wang Russell , Yuan Zi‐xi , Jiang Xian‐feng , Dong Xing‐tao 
Published: February 2022

AbstractThe cover image is based on the Basic Research Biomechanical behavior of mandible with posterior marginal resection using finite element analysis by Kang‐jie Cheng et al., https://doi.org/10.1002/cnm.3549.

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Improving Thermal Stability of Enzymatic Micromotors by a Temperature‐Sensitive Smart Polymeric Shell
Authors: Wang Shengnan , Xu Dandan , Liu Xiaoxia , Wang Yong , Ye Heng , Ma Xing 
Published: February 2022

AbstractEnzyme‐powered micromotors using biocompatible substances as fuel are promising candidates in biomedical applications due to their potential autonomous movement in biological fluid and supreme biocompatibility. However, the inherent fragility of enzymes in complex environment hinders their application in practice. Herein, the smart temperature‐responsive poly(N‐isopropylacrylamide) (PNIPAM) is introduced to SiO2@urease micromotors to increase the stability of the enzyme engine by the confinement effect derived from shrinkage of PNIPAM at temperatures above its lower critical solution temperature (LCST). As a result, the structure transformation and subunit dissociation of the enzyme are suppressed, leading to improved thermal stability of the urease engine. A systematic comparison of PNIPAM protected and bare SiO2@urease micromotors after thermal treatments at identical temperatures for various time intervals has clearly revealed the enhancement of stability against thermal deformation by PNIPAM integration. This work, paving a way to the development of thermally stable enzyme‐powered micromotors, can greatly raise the prospect of the intelligent micromachines toward practical biomedical applications.
Multilocational screening identifies new drought‐tolerant, warm‐season turfgrasses
Authors: Katuwal Krishna B , Jespersen David , Bhattarai Uttam , Chandra Ambika , Kenworthy Kevin E , Milla‐Lewis Susana R , Schwartz Brian Matthew , Wu Yanqi , Raymer Paul 
Published: February 2022

AbstractDuring periods of drought, the irrigation needs of current warm‐season turfgrass cultivars and frequent municipal water use restrictions present a major challenge to the turfgrass industry. Turfgrass breeding programs have responded by placing more emphasis on improved drought response. During 2012–2013, 560 genotypes of four warm‐season turfgrass species developed by five southern breeding programs were evaluated for drought response in replicated field trials at seven locations. Breeders selected 35 genotypes as drought‐tolerant selections (DTS) for further evaluation. The objectives of this study were to verify superior drought response among DTS under short‐term drought conditions and to assess the effectiveness of this approach as a viable breeding strategy to improve drought response in warm‐season turfgrasses. Forty‐seven genotypes including standard commercial cultivars of zoysiagrass (Zoysia spp. Willd.), bermudagrass [Cynodon spp. (L.) Pers.], St. Augustinegrass [Stenotaphrum secundatum (Walt.) Kuntze], and seashore paspalum (Paspalum vaginatum Swartz) were exposed to dry‐downs in three consecutive years by withholding irrigation and excluding rainfall. Significant differences in drought performance were seen across genotypes over the multiyear study. Statistical contrasts found that DTS of zoysiagrass, St. Augustinegrass, and seashore paspalum generally performed better than the standard cultivars. Top‐performing DTS zoysiagrass and St. Augustinegrass genotypes maintained >50% green cover longer than the average of the standard cultivars. Based on this research, multilocational screening for drought tolerance was effective in selection of new genotypes with superior performance to standard cultivars and continued screening of turfgrass germplasm to identify new drought‐tolerant genotypes is warranted.
Enhanced Phase‐Change Heat Transfer by Surface Wettability Control
Authors: Zhou Lei , He Wen , Wang Miao , Hou Xu 
Published: February 2022

AbstractThe phase‐change heat‐transfer coefficient can be improved by several orders of magnitude through the design of micro‐nanostructures on typical surfaces. However, with the rapid development of intelligent and integrated devices, there is an increasing desire to regulate the heat exchange form of the surface to adapt to various environmental requirements. This study concerns the design of a carbon nanotube array‐based phase‐change heat‐transfer surface, which can switch its wettability between superhydrophobicity and superhydrophilicity. By installing this surface on a device that integrates boiling heat transfer and condensation heat transfer, the device can independently adjust the surface wettability for different heat‐transfer requirements. As a result, this surface can enhance condensation heat‐transfer coefficient over 90 % in the superhydrophobic state and enhance the boiling heat‐transfer coefficient over 41 % in the superhydrophilic state. Surfaces with controllable wettability can aid development of a new generation of smart control technologies to actively regulate system and device temperatures.
Os1B11N12/C2N as an Efficient Electrocatalyst for Nitrogen Reduction Reaction
Authors: Yang Xue J. , Wen Zi , Wang Zhi L. , Jiang Qing 
Published: February 2022

AbstractAmmonia is one of the most important fertilizer feedstocks and chemical precursor besides a promising hydrogen carrier. However, the electrochemical reduction of nitrogen to ammonia is impeded by the low selectivity and high limiting potential of reported catalysts. Herein, the nitrogen reduction reaction (NRR) on Os‐doped BN cluster supported on C2N (Os1B11N12/C2N) was investigated systematically based on density functional theory calculations. It was found that the adjustment of BN cluster on the upper d‐band edge of Os atom enabled the optimal adsorption strength for NRR intermediates. Consequently, Os1B11N12/C2N exhibited high catalytic activity for NRR with the limiting potential of −0.34 V and a remarkable suppressive effect on the hydrogen evolution reaction. This work is not only beneficial for understanding the mechanism of NRR but also provides a fundamental guidance for rational design of catalysts for NRR.
Src kinase as a potential therapeutic target in non‐alcoholic and alcoholic steatohepatitis
Authors: Kurniawan Dhadhang Wahyu , Booijink Richell , Jajoriya Arun Kumar , Dhawan Garima , Mishra Divya , Oosterhuis Dorenda , Argemi Josepmaria , Storm Gert , Olinga Peter , Bataller Ramon , Mohanty Sujit Kumar , Mishra Durga Prasad , Prakash Jai , Bansal Ruchi 
Published: February 2022

AbstractNon‐alcoholic steatohepatitis (NASH) and alcohol‐associated steatohepatitis (ASH) are the major cause of liver‐related mortality with limited therapeutic options available. In this study, we investigated the role of Src tyrosine kinase in the pathogenesis of (N)ASH. We examined Src kinase expression in livers from patients with NASH, ASH, cirrhosis and biliary atresia, and from preclinical mouse models: methionine choline deficient (MCD)‐diet‐induced NASH, Lieber–DeCarli ethanol (EtOH)‐diet‐induced ASH, carbon tetrachloride (CCl4)‐ and bile duct ligation (BDL)‐induced liver fibrosis. Functional studies, using Src kinase inhibitor KX2‐391, were performed in NASH and ASH mouse models, and in relevant in vitro models. Transcriptomic analysis revealed increased Src kinase expression in human and mouse diseased livers that positively correlated with disease progression. Src kinase inhibition ameliorated lipid biosynthesis (steatosis); monocytes/macrophages infiltration and inflammatory cytokines expression (inflammation) and hepatic stellate cells (HSCs) activation and collagen expression (fibrosis) in MCD‐diet and EtOH‐diet induced liver disease mouse models. In vitro Src inhibition attenuated FFA‐induced hepatocytic lipid accumulation, LPS/IFNγ‐induced nitric oxide release and expression of several inflammatory signatures in macrophages and TGFβ‐induced HSCs activation, contractility and collagen expression. Moreover, Src inhibition diminished gene expression of inflammatory markers in LPS/IFNγ‐stimulated BMDMs and LPS‐stimulated PCLS, and reduced FA accumulation, macrophage activation and collagen deposition in 3D human liver spheroids. Mechanistic studies further revealed that Src kinase mediated the effects through FAK/PI3K/AKT pathway. Our results demonstrate a multicellular and functional role of Src kinase highlighting Src kinase as a promising therapeutic target in (non)alcoholic steatohepatitis.
Osteomodulin attenuates smooth muscle cell osteogenic transition in vascular calcification
Authors: Skenteris Nikolaos T. , Seime Till , Witasp Anna , Karlöf Eva , Wasilewski Grzegorz B. , Heuschkel Marina A. , Jaminon Armand M.G. , Oduor Loureen , Dzhanaev Robert , Kronqvist Malin , Lengquist Mariette , Peeters Frederique E.C.M. , Söderberg Magnus , Hultgren Rebecka , Roy Joy , Maegdefessel Lars , Arnardottir Hildur , Bengtsson Eva , Goncalves Isabel , Quertermous Thomas , Goettsch Claudia , Stenvinkel Peter , Schurgers Leon J. , Matic Ljubica 
Published: February 2022

AbstractRationaleVascular calcification is a prominent feature of late‐stage diabetes, renal and cardiovascular disease (CVD), and has been linked to adverse events. Recent studies in patients reported that plasma levels of osteomodulin (OMD), a proteoglycan involved in bone mineralisation, associate with diabetes and CVD. We hypothesised that OMD could be implicated in these diseases via vascular calcification as a common underlying factor and aimed to investigate its role in this context.Methods and resultsIn patients with chronic kidney disease, plasma OMD levels correlated with markers of inflammation and bone turnover, with the protein present in calcified arterial media. Plasma OMD also associated with cardiac calcification and the protein was detected in calcified valve leaflets by immunohistochemistry. In patients with carotid atherosclerosis, circulating OMD was increased in association with plaque calcification as assessed by computed tomography. Transcriptomic and proteomic data showed that OMD was upregulated in atherosclerotic compared to control arteries, particularly in calcified plaques, where OMD expression correlated positively with markers of smooth muscle cells (SMCs), osteoblasts and glycoproteins. Immunostaining confirmed that OMD was abundantly present in calcified plaques, localised to extracellular matrix and regions rich in α‐SMA+ cells. In vivo, OMD was enriched in SMCs around calcified nodules in aortic media of nephrectomised rats and in plaques from ApoE−/− mice on warfarin. In vitro experiments revealed that OMD mRNA was upregulated in SMCs stimulated with IFNγ, BMP2, TGFβ1, phosphate and β‐glycerophosphate, and by administration of recombinant human OMD protein (rhOMD). Mechanistically, addition of rhOMD repressed the calcification process of SMCs treated with phosphate by maintaining their contractile phenotype along with enriched matrix organisation, thereby attenuating SMC osteoblastic transformation. Mechanistically, the role of OMD is exerted likely through its link with SMAD3 and TGFB1 signalling, and interplay with BMP2 in vascular tissues.ConclusionWe report a consistent association of both circulating and tissue OMD levels with cardiovascular calcification, highlighting the potential of OMD as a clinical biomarker. OMD was localised in medial and intimal α‐SMA+ regions of calcified cardiovascular tissues, induced by pro‐inflammatory and pro‐osteogenic stimuli, while the presence of OMD in extracellular environment attenuated SMC calcification.