bluuebunny/crossref_metadata_2025_split huggingface dataset:
Why Resilience in Health Care Systems is More than Coping with Disasters: Implications for Health Care Policy
Authors: Behrens Doris A. , Rauner Marion S. , Sommersguter-Reichmann Margit 
Published: April 2022

AbstractHealth care systems need to be resilient to deal with disasters like the global spread of the Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2) on top of serving the changing needs of a multi-morbid, ageing and often dispersed population. This paper identifies, discusses and augments critical dimensions of resilience retrieved from the academic literature. It pulls together an integrated concept of resilience characterised by organisational capabilities. Our concept does not focus on the micro-level like most resilience literature in health care but addresses the system level with many stakeholders involved. Distinguishing exogenous shocks to the health care system into adverse events and planned innovations provides the basis for our conclusions and insights. It becomes apparent only when dealing with planned interventions that transformative capabilities are indispensable to cope with sudden increases in health care pressures. Due to the current focus on absorptive and adaptive resilience, organisations over-rely on management capabilities that cannot generate a lasting increase in functionality. Therefore, reducing the resilience discussion to bouncing back from adverse events could deceive organisations into cultivating a suboptimal mix of organisational capabilities lacking transformative capabilities, which pave the way for a structural change that aims at a sustainably higher functionality.
Trends in antibiotic use before and during the coronavirus disease 2019 (COVID-19) pandemic across an integrated health system with different antimicrobial stewardship program models trends in antibiotic use by ASP model
Authors: Peterson Jennifer M. , White Kristina , Muehling Emily , Ebert Steven C. , Lambi Lisa , Thieman Corey , Peterson Nathan , Deuel Kia , Bushman Amanda M. , Kumar Sudhir , Best Leyla A. , Rosa Rossana 
Published: April 2022

Abstract
Changes in antimicrobial use during the pandemic in relation to long-term trends in utilization among different antimicrobial stewardship program models have not been fully characterized. We analyzed data from an integrated health system using joinpoint regression and found temporal fluctuations in prescribing as well as continuation of existing trends.
Time Savings vs. Access-Based Benefit Assessment of New York’s Second Avenue Subway
Authors: Wang Yadi , Levinson David 
Published: April 2022

AbstractUnder the current practice of benefit-cost analysis, the direct economic benefits produced by a newly built transit facility are assessed based on how it affects travel time and various costs that are associated with transport needs and travel behavior. However, the time-saving-based benefit calculation approach has been questioned and criticized. Given the strong correlation between accessibility and land value, we propose the access-based land value benefit assessment as an alternative, and apply this assessment method to analyzing the Second Avenue Subway project in Manhattan, New York. The primary principle of the access-based method is that the economic value of a transport project’s intangible gains is largely capitalized by nearby properties’ value appreciation, which is directly caused by improved transport accessibility. We find that: (i) the actual travel time saving is lower than originally forecast; (ii) a strong positive correlation between residential property value and job accessibility by transit is observed; (iii) the appreciation in sold property value and rented property value both far exceed total project cost; and (iv) such results support the decision to approve and construct the Second Avenue Subway.
Making Sense of Shame in Response to Racism
Authors: Webster Aness Kim 
Published: April 2022

AbstractSome people of colour feel shame in response to racist incidents. This phenomenon seems puzzling since, plausibly, they have nothing to feel shame about. This puzzle arises because we assume that targets of racism feel shame about their race. However, I propose that when an individual is racialised as non-White in a racist incident, shame is sometimes prompted, not by a negative self-assessment of her race, but by her inability to choose when her stigmatised race is made salient. I argue that this can make sense ofsomeshame responses to racism. My account also helps to highlight some of the emotional and cognitive costs of racism that have their root in shame as well as a new form of hermeneutical injustice and distinctive communicative harms, contributing to a fuller picture of what is objectionable about racism.
Structuring prosecutorial power
Authors: Sepulveda Carla , Wilenmann Javier 
Published: April 2022

AbstractProsecutors play a decisive role in contemporary criminal justice. Their decisions greatly influence the output of the system, as well as the behaviour of other criminal justice institutions. By harnessing the power to filter, select and segment the work of criminal justice, prosecutors provide structure to an otherwise unbalanced field. They thus play a key structuring role. However, the prosecutors’ position and the problems that emanate from it have mostly been studied in terms of their power and discretion. We contend that this approach neglects the core problems and challenges connected to the prosecutorial function in contemporary criminal justice and offer a reconstruction of the formal and informal influences that shape the behaviour of prosecutors in providing for structure.
Change in the inflammatory potential of diet over 10 years and subsequent mortality: the Multiethnic Cohort Study
Authors: Park Song-Yi , Lozano Chloe P. , Shvetsov Yurii B. , Boushey Carol J. , Wirth Michael D. , Shivappa Nitin , Hébert James R. , Haiman Christopher A. , Wilkens Lynne R. , Le Marchand Loïc 
Published: April 2022

AbstractDietary inflammatory potential assessed by the Dietary Inflammatory Index (DII®) has been associated with health outcomes. However, longitudinal changes in the DII in relation to health outcomes rarely have been studied. This study aimed to examine change in the DII score over 10 years and its association with subsequent mortality in the Multiethnic Cohort. The analysis included 56 263 African American, Japanese American, Latino, Native Hawaiian and White participants who completed baseline (45–75 years) and 10-year follow-up surveys, including a FFQ. Mean energy-adjusted DII (E-DII) decreased over 10 years in men (from −0·85 to −1·61) and women (from −1·80 to −2·47), reflecting changes towards a more anti-inflammatory diet. During an average follow-up of 13·0 years, 16 363 deaths were identified. In multivariable Cox models, compared with anti-inflammatory stable individuals, risk of all-cause mortality was increased with pro-inflammatory change in men (hazard ratio (HR) = 1·13, 95 % CI 1·03, 1·23) and women (HR = 1·22, 95 % CI 1·13, 1·32). Per one-point increase in E-DII score over time, HR was 1·02 (95 % CI 1·00, 1·03) for men and 1·06 (95 % CI 1·04, 1·07) for women (Pfor heterogeneity < 0·001). While no heterogeneity by race and ethnicity was observed for men, the increased risk per one-point increase among women was stronger in non-Whites than in Whites (Pfor heterogeneity = 0·004). Our findings suggest that a change towards a more pro-inflammatory diet is associated with an increased risk of mortality both in men and women, and that the association is stronger in women, especially non-White women, than in men.
Dignity and time perspective: A pilot explorative study in cancer patients
Authors: Andreis Federica , Mirandola Mara , Wedenissow Anna Chiara , Runcan Mariana , Malighetti Clelia , Meriggi Fausto , Zaniboni Alberto 
Published: April 2022

AbstractObjectivesThis study investigated the possible correlation between emotional distress linked to dignity and dysfunctional temporal orientations in the oncological context.MethodsWe conducted an exploratory study between December 2020 and February 2021, referring to a sample of 107 patients in active treatment for solid tumors belonging to the Oncology Department of the Fondazione Poliambulanza (Brescia, Italy). We administered two self-report questionnaires: the Patient Dignity Inventory (PDI-IT) (Italian version, Grassi L, Costantini A, Caruso R, et al. (2017) Dignity and psychosocial-related variables in advanced and nonadvanced cancer patients by using the patient dignity inventory-Italian version. Journal of Pain and Symptom Management 53(2), 279–287), as a measure of perceived level of dignity, and the Italian version of the Zimbardo Time Perspective Inventory scale (ZTPI) (Zimbardo PG and Boyd JN (2009) Il paradosso del tempo. La nuova psicologia del tempo che cambierà la tua vita. Milano: Mondadori), as a measure of the experiential dimensions of time, such as past, present, and future.ResultsFrom the PDI-IT emerged that our sample reported high levels of physical and psychological distress. Furthermore, we founded higher distress in patients under 55 years (p = 0.04) and lower distress in retired patients (p = 0.01). The ZTPI showed in our patients prevailing orientations to the past-positive (39.3%) and the future (37.4%). We noticed a gender difference: men were mainly oriented to the future while women to the past-positive. Moreover, married subjects reported a prevalent orientation to past-positive and the future. Finally, data analysis found moderate positive correlation between the “Negative Past” dimension of ZTPI and high levels of physical (r = 0.203, p = 0.03) and psychological distress (r = 236, p = 0.01).Significance of resultsIn our experience in oncology, dignity and time perspective play a central role as indicators of the quality of care. Our study shows the importance of a treatment path that integrates the constructs of Dignity and Time Perspective to favor a better psychological adaptation.
A Coupled Geochemical‐Geodynamic Approach for Predicting Mantle Melting in Space and Time
Authors: Ball P. W. , Duvernay T. , Davies D. R. 
Published: April 2022

AbstractGeodynamic simulations underpin our understanding of upper‐mantle processes, but their predictions require validation against observational data. Widely used geophysical datasets provide limited constraints on dynamic processes into the geological past, whereas under‐exploited geochemical observations from volcanic lavas at Earth's surface constitute a valuable record of mantle processes back in time. Here, we describe a new peridotite‐melting parameterization, BDD21, that can predict the incompatible‐element concentrations of melts within geodynamic simulations, thereby providing a means to validate these simulations against geochemical datasets. Here, BDD21's functionality is illustrated using the Fluidity computational modeling framework, although it is designed so that it can be integrated with other geodynamic software. To validate our melting parameterization and coupled geochemical‐geodynamic approach, we develop 2‐D single‐phase flow simulations of melting associated with passive upwelling beneath mid‐oceanic ridges and edge‐driven convection adjacent to lithospheric steps. We find that melt volumes and compositions calculated for mid‐oceanic ridges at a range of mantle temperatures and plate spreading rates closely match those observed at present‐day ridges with the same conditions. Our lithospheric step simulations predict spatial and temporal melting trends that are consistent with those recorded at intraplate volcanic provinces in similar geologic settings. Taken together, these results suggest that our coupled geochemical‐geodynamic approach can accurately predict a suite of present‐day geochemical observations. Since our results are sensitive to small changes in upper‐mantle thermal and compositional structure, this novel approach provides a means to improve our understanding of the mantle's thermo‐chemical structure and flow regime into the geological past.
Progression in translational research on spinal cord injury based on microenvironment imbalance
Authors: Fan Baoyou , Wei Zhijian , Feng Shiqing 
Published: April 2022

AbstractSpinal cord injury (SCI) leads to loss of motor and sensory function below the injury level and imposes a considerable burden on patients, families, and society. Repair of the injured spinal cord has been recognized as a global medical challenge for many years. Significant progress has been made in research on the pathological mechanism of spinal cord injury. In particular, with the development of gene regulation, cell sequencing, and cell tracing technologies, in-depth explorations of the SCI microenvironment have become more feasible. However, translational studies related to repair of the injured spinal cord have not yielded significant results. This review summarizes the latest research progress on two aspects of SCI pathology: intraneuronal microenvironment imbalance and regenerative microenvironment imbalance. We also review repair strategies for the injured spinal cord based on microenvironment imbalance, including medications, cell transplantation, exosomes, tissue engineering, cell reprogramming, and rehabilitation. The current state of translational research on SCI and future directions are also discussed. The development of a combined, precise, and multitemporal strategy for repairing the injured spinal cord is a potential future direction.
Hsa_circRNA_0088036 acts as a ceRNA to promote bladder cancer progression by sponging miR-140-3p
Authors: Yang Jun , Qi Manlong , Fei Xiang , Wang Xia , Wang Kefeng 
Published: April 2022

AbstractCircular RNAs (circRNAs) are a class of non-coding RNAs that play vital roles in cancer biology. However, the potential role of hsa_circRNA_0088036 in bladder cancer (BCa) remains unknown. Hsa_circRNA_0088036 was identified by microarray analysis and validated by quantitative real-time polymerase chain reaction. Functional assays were conducted to confirm the effects of hsa_circRNA_0088036 on the growth, migration, invasion, tumorigenesis, and metastasis of BCa cells. The luciferase reporter assay and RNA pull down assay were performed to investigate the interactions between hsa_circRNA_0088036, miR-140-3p, and forkhead box protein Q1 (FOXQ1). Upregulated expression of hsa_circRNA_0088036 in BCa tissues and cell lines was positively correlated with overall survival and clinicopathologic characteristics. Knockdown of hsa_circRNA_0088036 inhibited the growth, migration, and invasion of BCa cells both in vivo and in vitro. Mechanistically, hsa_circRNA_0088036 could directly interact with miR-140-3p and act as a miRNA sponge to modulate FOXQ1 expression. Knockdown of hsa_circRNA_0088036 inhibited the proliferation, migration, and metastasis of BCa cells via miR-140-3p/FOXQ1 signaling, suggesting that hsa_circRNA_0088036 is a potential biomarker and therapeutic target for BCa.
Ischemia-induced cleavage of OPA1 at S1 site aggravates mitochondrial fragmentation and reperfusion injury in neurons
Authors: Li Xiang , Li Haiying , Xu Zhongmou , Ma Cheng , Wang Tianyi , You Wanchun , Yu Zhengquan , Shen Haitao , Chen Gang 
Published: April 2022

AbstractNeuronal mitochondrial dynamics are disturbed after ischemic stroke. Optic atrophy 1 (OPA1) and its GTPase activity are involved in maintaining mitochondrial cristae and inner membrane fusion. This study aimed to explore the role of OMA1-mediated OPA1 cleavage (S1-OPA1) in neurons exposed to cerebral ischemia and reperfusion. After oxygen-glucose deprivation (OGD) for 60 min, we found that mitochondrial fragmentation occurred successively in the axon and soma of neurons, accompanied by an increase in S1-OPA1. In addition, S1-OPA1 overexpression significantly aggravated mitochondrial damage in neurons exposed to OGD for 60 min and 24 h after OGD/R, characterized by mitochondrial fragmentation, decreased mitochondrial membrane potential, mitochondrial cristae ultrastructural damage, increased superoxide production, decreased ATP production and increased mitochondrial apoptosis, which was inhibited by the lysine 301 to alanine mutation (K301A). Furthermore, we performed neuron-specific overexpression of S1-OPA1 in the cerebral cortex around ischemia of middle cerebral artery occlusion/reperfusion (MCAO/R) mice. The results further demonstrated in vivo that S1-OPA1 exacerbated neuronal mitochondrial ultrastructural destruction and injury induced by cerebral ischemia-reperfusion, while S1-OPA1-K301 overexpression had no effect. In conclusion, ischemia induced neuronal OMA1-mediated cleavage of OPA1 at the S1 site. S1-OPA1 aggravated neuronal mitochondrial fragmentation and damage in a GTPase-dependent manner, and participated in neuronal ischemia-reperfusion injury.
HIF-1α-regulated lncRNA-TUG1 promotes mitochondrial dysfunction and pyroptosis by directly binding to FUS in myocardial infarction
Authors: Wang Yong-Wang , Dong Hong-Zhi , Tan Yong-Xing , Bao Xu , Su Ying-Man , Li Xin , Jiang Fang , Liang Jing , Huang Zhen-Cai , Ren Yan-Ling , Xu Yu-Li , Su Qiang 
Published: April 2022

AbstractMyocardial infarction (MI) is a fatal heart disease that affects millions of lives worldwide each year. This study investigated the roles of HIF-1α/lncRNA-TUG1 in mitochondrial dysfunction and pyroptosis in MI. CCK-8, DHE, lactate dehydrogenase (LDH) assays, and JC-1 staining were performed to measure proliferation, reactive oxygen species (ROS), LDH leakage, and mitochondrial damage in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Enzyme-linked immunoassay (ELISA) and flow cytometry were used to detect LDH, creatine kinase (CK), and its isoenzyme (CK-MB) levels and caspase-1 activity. Chromatin immunoprecipitation (ChIP), luciferase assay, and RNA-immunoprecipitation (RIP) were used to assess the interaction between HIF-1α, TUG1, and FUS. Quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, and immunohistochemistry were used to measure HIF-1α, TUG1 and pyroptosis-related molecules. Hematoxylin and eosin (HE), 2,3,5-triphenyltetrazolium chloride (TTC), and terminal deoxynucleotidyl transferase dUTP risk end labelling (TUNEL) staining were employed to examine the morphology, infarction area, and myocardial injury in the MI mouse model. Mitochondrial dysfunction and pyroptosis were induced in H/R-treated cardiomyocytes, accompanied by an increase in the expression of HIF-α and TUG1. HIF-1α promoted TUG1 expression by directly binding to the TUG1 promoter. TUG1 silencing inhibited H/R-induced ROS production, mitochondrial injury and the expression of the pyroptosis-related proteins NLRP3, caspase-1 and GSDMD. Additionally, H/R elevated FUS levels in cardiomyocytes, which were directly inhibited by TUG1 silencing. Fused in sarcoma (FUS) overexpression reversed the effect of TUG1 silencing on mitochondrial damage and caspase-1 activation. However, the ROS inhibitor N-acetylcysteine (NAC) promoted the protective effect of TUG1 knockdown on H/R-induced cardiomyocyte damage. The in vivo MI model showed increased infarction, myocardial injury, ROS levels and pyroptosis, which were inhibited by TUG1 silencing. HIF-1α targeting upregulated TUG1 promotes mitochondrial damage and cardiomyocyte pyroptosis by combining with FUS, thereby promoting the occurrence of MI. HIF-1α/TUG1/FUS may serve as a potential treatment target for MI.
MAT2A facilitates PDCD6 methylation and promotes cell growth under glucose deprivation in cervical cancer
Authors: Luo Hui , Song Yizuo , Zhang Jian-an , Liu Yi , Chen Fengyun , Wang Zhiwei , Zhu Xueqiong 
Published: April 2022

AbstractThe underlying mechanisms of methionine adenosyltransferase 2 A (MAT2A)-mediated cervical cancer progression under nutrient stress are largely elusive. Therefore, our study aims to investigate molecular mechanism by which MAT2A-indcued cervical oncogenesis. The interaction between MAT2A and programmed cell death protein 6 (PDCD6) in cervical cancer cell lines was detected by immunoprecipitation, immunoblotting and mass spectrometric analysis. A panel of inhibitors that are linked to stress responsive kinases were utilized to detect related pathways by immunoblotting. Cell proliferation and apoptosis were investigated by CCK-8 and flow cytometry. Apoptosis related protein level of Bcl-2, Bax and Caspase-3 was also analyzed in cells with PDCD6 K90 methylation mutation. The association between MAT2A and PDCD6 was detected by immunohistochemistry and clinicopathological characteristics were further analyzed. We found that the interaction between MAT2A and PDCD6 is mediated by AMPK activation and facilitates PDCD6 K90 methylation and further promotes protein stability of PDCD6. Physiologically, expression of PDCD6 K90R leads to increased apoptosis and thus suppresses growth of cervical cancer cells under glucose deprivation. Furthermore, the clinical analysis indicates that the MAT2A protein level is positively associated with the PDCD6 level, and the high level of PDCD6 significantly correlates with poor prognosis and advanced stages of cervical cancer patients. We conclude that MAT2A facilitates PDCD6 methylation to promote cervical cancer growth under glucose deprivation, suggesting the regulatory role of MAT2A in cellular response to nutrient stress and cervical cancer progression.
Targeting matrix metallopeptidase 2 by hydroxyurea selectively kills acute myeloid mixed-lineage leukemia
Authors: Wang Ruiheng , Xie Shufeng , Zhu Shouhai , Sun Yong , Shi Bowen , Li Dan , Kang Ting , Wang Yuanli , Xu Zhenshu , Liu Han 
Published: April 2022

AbstractOncogene-induced tumorigenesis results in the variation of epigenetic modifications, and in addition to promoting cell immortalization, cancer cells undergo more intense cellular stress than normal cells and depend on other support genes for survival. Chromosomal translocations of mixed-lineage leukemia (MLL) induce aggressive leukemias with an inferior prognosis. Unfortunately, most MLL-rearranged (MLL-r) leukemias are resistant to conventional chemotherapies. Here, we showed that hydroxyurea (HU) could kill MLL-r acute myeloid leukemia (AML) cells through the necroptosis process. HU target these cells by matrix metallopeptidase 2 (MMP2) deficiency rather than subordinate ribonucleotide reductase regulatory subunit M2 (RRM2) inhibition, where MLL directly regulates MMP2 expression and is decreased in most MLL-r AMLs. Moreover, iron chelation of HU is also indispensable for inducing cell stress, and MMP2 is the support factor to protect cells from death. Our preliminary study indicates that MMP2 might play a role in the nonsense-mediated mRNA decay pathway that prevents activation of unfolding protein response under innocuous endoplasmic reticulum stress. Hence, these results reveal a possible strategy of HU application in MLL-r AML treatment and shed new light upon HU repurposing.