bluuebunny/crossref_metadata_2025_split huggingface dataset:
Working without Wages: Network Structure and Migrant Construction Workers’ Protests in China
Authors: Wei Haitao , Chan Cheris Shun-ching 
Published: July 2022

AbstractMigrant construction workers are among the most vulnerable working populations in China as they are prone to facing the problem of wage arrears under the multi-tier subcontracting system. Based on ethnographic research of migrant construction workers in Tianjin, Shenzhen, Nanchang and Shaoguan, we examine workers’ divergent responses to wage arrears. While extant literature focuses on the positive role of informal networks in facilitating collective action, our findings indicate that the network structure between labour subcontractors and migrant workers plays a key role in enabling or constraining labour protests. We identify two network structures: the satellite network – characterized by arm's-length relationships between subcontractors and clusters of workers; and the spider-web network – characterized by strong relationships between subcontractors and their workers. We found that workers in satellite networks were prone to stage protests over wage arrears, but those in spider-web networks never held collective actions when facing the same problem. We argue that strongguanxiis a double-edged sword for the mobilization of labour protests and that workers’ responses to wage arrears are mediated through the network structure. Future studies may further scrutinize the role of a social network and its operating mechanisms in shaping workers’ working conditions and labour politics.
Persisting gastrointestinal symptoms and post-infectious irritable bowel syndrome following SARS-CoV-2 infection: results from the Arizona CoVHORT
Authors: Austhof Erika , Bell Melanie L. , Riddle Mark S. , Catalfamo Collin , McFadden Caitlyn , Cooper Kerry , Scallan Walter Elaine , Jacobs Elizabeth , Pogreba-Brown Kristen 
Published: July 2022

AbstractIn this study, we aimed to examine the association between gastrointestinal (GI) symptom presence during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the prevalence of GI symptoms and the development of post-infectious irritable bowel syndrome (PI-IBS). We used data from a prospective cohort and logistic regression to examine the association between GI symptom status during confirmed SARS-CoV-2 infection and prevalence of persistent GI symptoms at ≥45 days. We also report the incidence of PI-IBS following SARS-CoV-2 infection. Of the 1475 participants in this study, 33.8% (n= 499) had GI symptoms during acute infection. Cases with acute GI symptoms had an odds of persisting GI symptoms 4 times higher than cases without acute GI symptoms (odds ratio (OR) 4.29, 95% confidence interval (CI) 2.45–7.53); symptoms lasted on average 8 months following infection. Of those with persisting GI symptoms, 67% sought care for their symptoms and incident PI-IBS occurred in 3.0% (n= 15) of participants. Those with acute GI symptoms after SARS-CoV-2 infection are likely to have similar persistent symptoms 45 days and greater. These data indicate that attention to a potential increase in related healthcare needs is warranted.
Critical CHD screening programme: a 3-year multicentre experience in Mexico
Authors: Gómez-Gutiérrez René , Galindo-Hayashi José M. , Cantú-Reyna Consuelo , Vazquez-Cantu Diana L. , Britton-Robles Cecilia , Cruz-Camino Héctor 
Published: July 2022

AbstractIntroduction:CHDs are the most common type of birth defect. One in four newborns with a heart defect has a critical CHD. In Mexico, there is a lack of data available to determine its prevalence. Pulse oximetry screening programmes have been implemented worldwide, reporting opportunity areas in algorithm interpretation and data management. Our study aims to share preliminary results of a 3-year experience of a multicentre pulse oximetry screening programme that addresses critical challenges.Materials and methods:This retrospective study examined the reports of newborns screened from February 2016 to July 2019 from five hospitals. Two algorithms –the New Jersey and the American Academy of Pediatrics– were implemented over consecutive periods. The algorithms’ impact was assessed through the calculation of the false-positive rate in an eligible population.Results:A total of 8960 newborns were eligible for the study; from it, 32.27% were screened under the New Jersey and 67.72% under the American Academy of Pediatrics algorithm – false-positive rate: 1% (CI 95: ± 0.36%) and 0.71% (CI 95: ± 0.21%), respectively. Seventy-nine newborns were referred, six were diagnosed with critical CHD, and six with CHD. The critical CHD estimated prevalence was 6.69:10,000 newborns (CI 95: ± 5.36). Our results showed that the algorithm was not related to the observable false-positive rate reduction.Discussion:Other factors may play a role in decreasing the false-positive rate. Our experience implementing this programme was that a systematic screening process led to more confident results, newborn’s report interpretation, and follow-up.
Neighborhood inequalities and the decline of infant mortality in São Paulo
Authors: Gusmano Michael K. , Grafova Irina , Ayoub Rafael , Weisz Daniel , Rodwin Victor G. 
Published: July 2022

AbstractThis paper documents changes in infant mortality (IM) rates in São Paulo, Brazil, between 2003 and 2013 and examines the association among neighborhood characteristics and IM. We investigate the extent to which increased use of health care services and improvements in economic and social conditions are associated with reductions in IM. Using data from the Brazilian Census and the São Paulo Secretaria Municipal da Saúde/SMS, we conducted a longitudinal analysis of panel data in all 96 districts of São Paulo for every year between 2003 and 2013. Our regression model includes district level measures that reflect economic, health care and social determinants of IM. We find that investments in health care have contributed to lower IM rates in the city, but the direct effect of increased spending is most evident for people living in São Paulo's middle- and high-income neighborhoods. Improvements in social conditions were more strongly associated with IM declines than increases in the use of health care among São Paulo's low-income neighborhoods. To reduce health inequalities, policies should target benefits to lower-income neighborhoods. Subsequent research should document the consequences of recent changes in Brazil's economic capacity and commitment to public health spending for population health.
Association between maternal prenatal psychological distress and autism spectrum disorder among 3-year-old children: The Japan Environment and Children’s Study
Authors: Nishigori Toshie , Hashimoto Koichi , Mori Miyuki , Suzuki Taeko , Watanabe Madoka , Imaizumi Karin , Murata Tsuyoshi , Kyozuka Hyo , Ogata Yuka , Sato Akiko , Shinoki Kosei , Yasumura Seiji , Fujimori Keiya , Nishigori Hidekazu , Hosoya Mitsuaki ,   The Japan Environment and Children’s Study Group
Published: July 2022

AbstractMaternal prenatal psychological distress, which includes depression and anxiety, affects the onset of autism spectrum disorder (ASD). However, there is no consistent knowledge regarding at which term during pregnancy psychological distress affects the risk of ASD among children. We used a dataset obtained from the Japan Environment and Children’s Study, which is a nationwide prospective birth cohort study, to evaluate the association between the six-item Kessler Psychological Distress Scale (K6) and ASD among 3-year-old children. A total of 78,745 children were analyzed, and 355 of them were diagnosed with ASD (0.45%). The maternal K6 was administered twice during pregnancy: at a median of 15.1 weeks (M-T1) and at that of 27.4 weeks (M-T2) of gestation. Multivariate logistic regression analyses demonstrated that the group with a maternal K6 score of ≥5 at both M-T1 and M-T2 was significantly associated with ASD among the children (adjusted odds ratio, 1.440; 95% confidence interval, 1.104–1.877) compared to the group with a score of ≤4 at both M-T1 and M-T2. There was no significant difference between the group with a score of ≥5 only at M-T1 or M-T2 and that with a score of ≤4 at both M-T1 and M-T2. In conclusion, from the first to the second half of pregnancy, continuous maternal psychological distress was associated with ASD among 3-year-old children. Contrarily, in the group without persistent maternal psychological distress during pregnancy, there was no significant association.
Explaining Solar Flare‐Induced Ionospheric Ion Upflow at Millstone Hill (42.6°N)
Authors: Liu Xuanqing , Liu Jing , Wang Wenbin , Zhang Shun‐Rong , Zhang Kedeng , Lei Jiuhou , Liu Libo , Chen Xuetao , Li Shuhan , Zhang Qing‐He , Xing Zan‐Yang 
Published: July 2022

AbstractPrevious studies have shown that solar flares can significantly affect Earth's ionosphere and induce ion upflow with a magnitude of ∼110 m/s in the topside ionosphere (∼570 km) at Millstone Hill (42.61°N, 71.48°W). We use simulations from the Thermosphere‐Ionosphere‐Electrodynamics General Circulation Model (TIEGCM) and observations from Incoherent Scatter Radar (ISR) at Millstone Hill to reveal the mechanism of ionospheric ion upflow near the X9.3 flare peak (07:16 LT) on 6 September 2017. The ISR observed ionospheric upflow was captured by the TIEGCM in both magnitude and morphology. The term analysis of the F‐region ion continuity equation during the solar flare shows that the ambipolar diffusion enhancement is the main driver for the upflow in the topside ionosphere, while ion drifts caused by electric fields and neutral winds play a secondary role. Further decomposition of the ambipolar diffusive velocity illustrates that flare‐induced changes in the vertical plasma density gradient is responsible for ion upflow. The changes in the vertical plasma density gradient are mainly due to solar extreme ultraviolet (EUV, 15.5–79.8 nm) induced electron density and temperature enhancements at the F2‐region ionosphere with a minor and indirectly contribution from X‐ray (0–15.5 nm) and ultraviolet (UV, 79.8–102.7 nm).
GFI1B acts as a metabolic regulator in hematopoiesis and acute myeloid leukemia
Authors: Liu Longlong , Patnana Pradeep Kumar , Xie Xiaoqing , Frank Daria , Nimmagadda Subbaiah Chary , Su Minhua , Zhang Donghua , Koenig Thorsten , Rosenbauer Frank , Liebmann Marie , Klotz Luisa , Xu Wendan , Vorwerk Jan , Neumann Felix , Hüve Jana , Unger Andreas , Okun Jürgen Günther , Opalka Bertram , Khandanpour Cyrus 
Published: July 2022

AbstractRecent studies highlighted the role of transcription factors in metabolic regulation during hematopoiesis and leukemia development. GFI1B is a transcriptional repressor that plays a critical role in hematopoiesis, and its expression is negatively related to the prognosis of acute myeloid leukemia (AML) patients. We earlier reported a change in the metabolic state of hematopoietic stem cells upon Gfi1b deletion. Here we explored the role of Gfi1b in metabolism reprogramming during hematopoiesis and leukemogenesis. We demonstrated that Gfi1b deletion remarkably activated mitochondrial respiration and altered energy metabolism dependence toward oxidative phosphorylation (OXPHOS). Mitochondrial substrate dependency was shifted from glucose to fatty acids upon Gfi1b deletion via upregulating fatty acid oxidation (FAO). On a molecular level, Gfi1b epigenetically regulated multiple FAO-related genes. Moreover, we observed that metabolic phenotypes evolved as cells progressed from preleukemia to leukemia, and the correlation between Gfi1b expression level and metabolic phenotype was affected by genetic variations in AML cells. FAO or OXPHOS inhibition significantly impeded leukemia progression of Gfi1b-KO MLL/AF9 cells. Finally, we showed that Gfi1b-deficient AML cells were more sensitive to metformin as well as drugs implicated in OXPHOS and FAO inhibition, opening new potential therapeutic strategies.
Donor genetic determinant of thymopoiesis rs2204985 impacts clinical outcome after single HLA mismatched hematopoietic stem cell transplantation
Authors: Tsamadou Chrysanthi , Gowdavally Sowmya , Platzbecker Uwe , Sala Elisa , Valerius Thomas , Wagner-Drouet Eva , Wulf Gerald , Kröger Nicolaus , Murawski Niels , Einsele Hermann , Schaefer-Eckart Kerstin , Freitag Sebastian , Casper Jochen , Kaufmann Martin , Dürholt Mareike , Hertenstein Bernd , Klein Stefan , Ringhoffer Mark , Frank Sandra , Neuchel Christine , Rode Immanuel , Schrezenmeier Hubert , Mytilineos Joannis , Fuerst Daniel 
Published: July 2022

AbstractA common genetic variant within the T cell receptor alpha (TCRA)-T cell receptor delta (TCRD) locus (rs2204985) has been recently found to associate with thymic function. Aim of this study was to investigate the potential impact of donor rs2204985 genotype on patient’s outcome after unrelated hematopoietic stem cell transplantation (uHSCT). 2016 adult patients were retrospectively analyzed. rs2204985 genotyping was performed by next generation sequencing, p < 0.05 was considered significant and donor rs2204985 GG/AG genotypes were set as reference vs. the AA genotype. Multivariate analysis of the combined cohort regarding the impact of donor’s rs2204985 genotype indicated different risk estimates in 10/10 and 9/10 HLA matched transplantations. A subanalysis on account of HLA incompatibility revealed that donor AA genotype in single HLA mismatched cases (n = 624) associated with significantly inferior overall- (HR: 1.48, p = 0.003) and disease-free survival (HR: 1.50, p = 0.001). This effect was driven by a combined higher risk of relapse incidence (HR: 1.40, p = 0.026) and non-relapse mortality (HR: 1.38, p = 0.042). This is the first study to explore the role of rs2204985 in a clinical uHSCT setting. Our data suggest that donor rs2204985 AA genotype in combination with single HLA mismatches may adversely impact post-HSCT outcome and should thus be avoided.
FAK mediates LPS-induced inflammatory lung injury through interacting TAK1 and activating TAK1-NFκB pathway
Authors: Chen Xi , Zhao Ying , Wang Xu , Lin Yimin , Zhao Weixin , Wu Di , Pan Jingye , Luo Wu , Wang Yi , Liang Guang 
Published: July 2022

AbstractAcute lung injury (ALI), characterized by inflammatory damage, is a major clinical challenge. Developing specific treatment options for ALI requires the identification of novel targetable signaling pathways. Recent studies reported that endotoxin lipopolysaccharide (LPS) induced a TLR4-dependent activation of focal adhesion kinase (FAK) in colorectal adenocarcinoma cells, suggesting that FAK may be involved in LPS-induced inflammatory responses. Here, we investigated the involvement and mechanism of FAK in mediating LPS-induced inflammation and ALI. We show that LPS phosphorylates FAK in macrophages. Either FAK inhibitor, site-directly mutation, or siRNA knockdown of FAK significantly suppresses LPS-induced inflammatory cytokine production in macrophages. FAK inhibition also blocked LPS-induced activation of MAPKs and NFκB. Mechanistically, we demonstrate that activated FAK directly interacts with transforming growth factor-β-activated kinase-1 (TAK1), an upstream kinase of MAPKs and NFκB, and then phosphorylates TAK1 at Ser412. In a mouse model of LPS-induced ALI, pharmacological inhibition of FAK suppressed FAK/TAK activation and inflammatory response in lung tissues. These activities resulted in the preservation of lung tissues in LPS-challenged mice and increased survival during LPS-induced septic shock. Collectively, our results illustrate a novel FAK-TAK1-NFκB signaling axis in LPS-induced inflammation and ALI, and support FAK as a potential target for the treatment of ALI.
The contribution of common regulatory and protein-coding TYR variants to the genetic architecture of albinism
Authors: Michaud Vincent , Lasseaux Eulalie , Green David J. , Gerrard Dave T. , Plaisant Claudio ,   UK Biobank Eye and Vision Consortium, Fitzgerald Tomas , Birney Ewan , Arveiler Benoît , Black Graeme C. , Sergouniotis Panagiotis I. 
Published: July 2022

AbstractGenetic diseases have been historically segregated into rare Mendelian disorders and common complex conditions. Large-scale studies using genome sequencing are eroding this distinction and are gradually unmasking the underlying complexity of human traits. Here, we analysed data from the Genomics England 100,000 Genomes Project and from a cohort of 1313 individuals with albinism aiming to gain insights into the genetic architecture of this archetypal rare disorder. We investigated the contribution of protein-coding and regulatory variants both rare and common. We focused on TYR, the gene encoding tyrosinase, and found that a high-frequency promoter variant, TYR c.−301C>T [rs4547091], modulates the penetrance of a prevalent, albinism-associated missense change, TYR c.1205G>A (p.Arg402Gln) [rs1126809]. We also found that homozygosity for a haplotype formed by three common, functionally-relevant variants, TYR c.[−301C;575C>A;1205G>A], is associated with a high probability of receiving an albinism diagnosis (OR>82). This genotype is also associated with reduced visual acuity and with increased central retinal thickness in UK Biobank participants. Finally, we report how the combined analysis of rare and common variants can increase diagnostic yield and can help inform genetic counselling in families with albinism.
Late quaternary biotic homogenization of North American mammalian faunas
Authors: Fraser Danielle , Villaseñor Amelia , Tóth Anikó B. , Balk Meghan A. , Eronen Jussi T. , Andrew Barr W. , Behrensmeyer A. K. , Davis Matt , Du Andrew , Tyler Faith J. , Graves Gary R. , Gotelli Nicholas J. , Jukar Advait M. , Looy Cindy V. , McGill Brian J. , Miller Joshua H. , Pineda-Munoz Silvia , Potts Richard , Shupinski Alex B. , Soul Laura C. , Kathleen Lyons S. 
Published: July 2022

AbstractBiotic homogenization—increasing similarity of species composition among ecological communities—has been linked to anthropogenic processes operating over the last century. Fossil evidence, however, suggests that humans have had impacts on ecosystems for millennia. We quantify biotic homogenization of North American mammalian assemblages during the late Pleistocene through Holocene (~30,000 ybp to recent), a timespan encompassing increased evidence of humans on the landscape (~20,000–14,000 ybp). From ~10,000 ybp to recent, assemblages became significantly more homogenous (>100% increase in Jaccard similarity), a pattern that cannot be explained by changes in fossil record sampling. Homogenization was most pronounced among mammals larger than 1 kg and occurred in two phases. The first followed the megafaunal extinction at ~10,000 ybp. The second, more rapid phase began during human population growth and early agricultural intensification (~2,000–1,000 ybp). We show that North American ecosystems were homogenizing for millennia, extending human impacts back ~10,000 years.
Halide perovskites as disposable epitaxial templates for the phase-selective synthesis of lead sulfochloride nanocrystals
Authors: Toso Stefano , Imran Muhammad , Mugnaioli Enrico , Moliterni Anna , Caliandro Rocco , Schrenker Nadine J. , Pianetti Andrea , Zito Juliette , Zaccaria Francesco , Wu Ye , Gemmi Mauro , Giannini Cinzia , Brovelli Sergio , Infante Ivan , Bals Sara , Manna Liberato 
Published: July 2022

AbstractColloidal chemistry grants access to a wealth of materials through simple and mild reactions. However, even few elements can combine in a variety of stoichiometries and structures, potentially resulting in impurities or even wrong products. Similar issues have been long addressed in organic chemistry by using reaction-directing groups, that are added to a substrate to promote a specific product and are later removed. Inspired by such approach, we demonstrate the use of CsPbCl3 perovskite nanocrystals to drive the phase-selective synthesis of two yet unexplored lead sulfochlorides: Pb3S2Cl2 and Pb4S3Cl2. When homogeneously nucleated in solution, lead sulfochlorides form Pb3S2Cl2 nanocrystals. Conversely, the presence of CsPbCl3 triggers the formation of Pb4S3Cl2/CsPbCl3 epitaxial heterostructures. The phase selectivity is guaranteed by the continuity of the cationic subnetwork across the interface, a condition not met in a hypothetical Pb3S2Cl2/CsPbCl3 heterostructure. The perovskite domain is then etched, delivering phase-pure Pb4S3Cl2 nanocrystals that could not be synthesized directly.
Waist circumference and risk of Parkinson’s disease
Authors: Park Kye-Yeung , Nam Ga Eun , Han Kyungdo , Park Hoon-Ki , Hwang Hwan-Sik 
Published: July 2022

AbstractAlthough many studies support the association of obesity with neurodegenerative diseases, such as Parkinson’s disease (PD), there are limited data regarding the association between abdominal obesity and PD, with mixed findings. The aim of this study was to examine the association of waist circumference (WC) with the risk of PD incidence. We retrospectively analyzed a large-scale nationwide cohort of 6,925,646 individuals aged ≥40 years who underwent the Korean National Health Screening during 2009. We performed multivariable Cox proportional hazards regression to evaluate the association of WC and abdominal obesity with PD risk and calculated hazard ratios (HRs) with 95% confidence intervals (CIs) of PD incidence. During a median follow-up period of 8.35 years, 33,300 cases of PD developed. PD incidence was positively associated with increases in WC (P for trend < 0.001). The risk of PD incidence tended to elevate as WC increased (P for trend < 0.001), indicating that the adjusted HRs of PD incidence in the highest WC group versus the reference group was 1.16 (95% CI, 1.10–1.23), whereas it was 0.91 (95% CI 0.84–0.98) in the lowest WC group. Individuals with abdominal obesity were significantly associated with an increased PD risk (HR 1.10, 95% CI: 1.07–1.13). These associations persisted even after adjustment for body mass index and stratification by sex. Even among non-obese individuals, abdominal obesity was associated with a higher PD risk (adjusted HR 1.13, 95% CI: 1.09–1.18). Taken together, higher WC and abdominal obesity were associated with increased PD risk. Even in non-obese individuals, abdominal obesity was associated with an increased PD risk.