bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sports participation and alcohol use revisited: A longitudinal study of Norwegian postmillennial adolescents
Authors: Brunborg Geir Scott , Halkjelsvik Torleif Bjordal , Moan Inger Synnøve 
Published: April 2022

AbstractIntroductionRecent developments in health behavior among adolescents may have been accompanied by changes in risk factors for alcohol use. Focusing on postmillennial cohorts of adolescents, we revisit the question of whether sports participation is a risk factor for alcohol use.MethodThis study analyses data from four waves (2017−2020) of the MyLife longitudinal study. Participants were 3425 (45% boys) Norwegian adolescents attending middle school in 2017 (age range: 12−15 years). Annual questionnaire assessments included questions about frequency of sports practice, frequency of alcohol use/heavy episodic drinking, parental cohabitation, unstructured leisure time, sensation‐seeking, and behavioral problems. We employed growth curve models (N = 2682) and fixed effects models (N = 3131).ResultsOverall, we did not find systematic differences in initial alcohol use or development over time according to sports practice frequency at the first assessment. However, adolescents with the highest initial sports frequency had slightly lower initial alcohol use and a steeper increase (initial use: b = −0.06, p = .351; linear slope: b = −0.12, p = .218; quadratic curvature: b = 0.09, p = .004). There was no, or only a weak negative, association between change in sports practice and change in alcohol use after adjusting for potential time‐varying confounders, b = −0.03, p = .065.ConclusionContrary to most previous research, we found little evidence for an association between sports participation and alcohol use among Norwegian adolescents born after 2000. Sports activities might not require particular attention in the prevention of alcohol use.
Avoidance/emotion‐focused coping mediates the relationship between distress tolerance and problematic Internet use in a representative sample of adolescents in Taiwan: One‐year follow‐up
Authors: Lin Min‐Pei 
Published: April 2022

AbstractIntroductionBased on the theoretical frameworks of the Theory of Triadic Influence (TTI), this longitudinal study was designed to examine the mediating role of avoidance/emotion‐focused coping in the relationship between distress tolerance and problematic Internet use (PIU) in a large representative sample of senior high school students in Taiwan.MethodsThrough a 1‐year follow‐up design, 2170 participants were recruited from high schools throughout Taiwan using both stratified and cluster sampling in time 1 (T1), and 1832 students were followed‐up 1 year later (T2).ResultsStructure equation modeling and bootstrap analyses results showed that after controlling for PIU measured at T1, PIU (T2) was significantly predicted by distress tolerance (T1) and fully mediated through avoidance/emotion‐focused coping (T2).ConclusionsThe results not only support the TTI framework, but can also serve as a reference to help educational agencies and mental health organizations create policies and design programs that will help in the prevention of PIU among adolescents. The mediating role of avoidance/emotion‐focused coping in the relationship between distress tolerance and PIU was discussed.
The protective effect of resveratrol on diazinon‐induced oxidative stress and glucose hemostasis disorder in rats' liver
Authors: Mehri Fereshteh , Ranjbar Akram , Shirafkan Naghmeh , Asl Sara S. , Esfahani Maryam 
Published: April 2022

AbstractThis study was intended to assess the possible protective effect of resveratrol (Res) against oxidative stress and glucose hemostasis disorder in rats exposed to diazinon (DZN) for 4 weeks. Totally 25 Sprague‐Dawley rats were divided randomly into five groups: Control (orally received corn oil), DZN group (orally received 70 mg/kg/day), and Res groups (received DZN 70 mg/kg/day plus Res doses of 5, 10, and 20 mg/kg bodyweight/‐day), respectively. DZN significantly inhibited serum acetylcholinesterase enzyme (Ach E), serum and liver catalase, glutathione peroxidase activities, also total antioxidant capacities. On the other hand, DZN increased serum and liver malondialdehyde. DZN significantly increased Forkhead box protein O1 (Foxo1) expression and decreased phosphatase and tensin homolog (PTEN) and sirtuin 1 (Sirt‐1) expression. DZN impaired glucose hemostasis. Instead, Res treatment significantly reversed status of oxidative stress and antioxidant enzymes activities induced by DZN. Also, Res improved glucose hemostasis. Res increased PTEN and Sirt‐1 expression and reduced Foxo1 expression. Res administration ameliorated liver histopathological changes induced by DZN. These data confirmed that DZN significantly enhances oxidative stress and impairs glucose hemostasis. While Res showed a protective effect against the toxicity induced by DZN in rats.
Silencing ATF4 inhibits JMJD3‐dependent JUNB/ETS1 axis and mitigates cerebral ischemic injury
Authors: Wu Gang , Zhang Xi'an , Li Shijun , Wang Lina , Bai Jie , Wang Hanxiang , Shu Qing 
Published: April 2022

AbstractActivating transcription factor 4 (ATF4) is known to play an important role in cerebral ischemia through apoptosis and neuron regulation. Histone demethylase JMJD3, specifically removing the methylation of H3K27me3, is highlighted to attenuate cerebral ischemic injury. However, few studies have explored the interaction between ATF4 and JMJD3 in this disease. Thus, we intended to explore the effect of ATF4 on cerebral ischemia. We first constructed a mouse model of middle cerebral artery occlusion (MCAO) and cultured PC12 cells. Specifically, the regulatory function of ATF4 and demethylase JMJD3 on the ischemic injury was explored via using ectopic expression and depletion by determination of modified neurologic severity score, blood–brain barrier, brain water content, apoptosis, infarct size, oxidative stress, and inflammation. Moreover, the interaction among ATF4, JUNB, JMJD3, and ETS1 was assessed by western blot analysis, immunofluorescence, immunoprecipitation, and dual‐luciferase reporter gene assay. These data showed that ATF4 and JMJD3 were upregulated in the MCAO model and PC12 cells. In addition, ectopic expression of ATF4 aggravated the ischemic injury through demethylation of JMJD3. Meanwhile, JMJD3 upregulated JUNB expression by inhibiting H3K21me2/3 enrichment and promoted ETS1 expression as well. Altogether, ATF4 could exacerbate cerebral ischemic injury through JMJD3‐dependent upregulation of JUNB/ETS1 expression, suggesting a potential theoretical basis of treatment for cerebral ischemic injury.
Overreact, an in silico lab: Automative quantum chemical microkinetic simulations for complex chemical reactions
Authors: Schneider Felipe S. S. , Caramori Giovanni F. 
Published: April 2022

AbstractToday's demand for precisely predicting chemical reactions from first principles requires research to go beyond Gibbs' free energy diagrams and consider other effects such as concentrations and quantum tunneling. The present work introduces overreact, a novel Python package for propagating chemical reactions over time using data from computational chemistry only. The overreact code infers all differential equations and parameters from a simple input that consists of a set of chemical equations and quantum chemistry package outputs for each chemical species. We evaluate some applications from the literature: gas‐phase eclipsed‐staggered isomerization of ethane, gas‐phase umbrella inversion of ammonia, gas‐phase degradation of methane by chlorine radical, and three solvation‐phase reactions. Furthermore, we comment on a simple solvation‐phase acid–base equilibrium. We show how it is possible to achieve reaction profiles and information matching experiments.
Subversion of the immune response of human pathogenic spirochetes
Authors: Huang Jielite , Chen Jinlin , Xie Yafeng , Liu Zhuoran 
Published: April 2022

AbstractSpirochetes are a large group of prokaryotes that originated from Gram‐negative bacteria and are capable of causing a variety of human and animal infections. However, the pathogenesis of spirochetes remains unclear, as different types of spirochetes play pathogenic roles through different pathogenic substances and mechanisms. To survive and spread in the host, spirochetes have evolved complicated strategies to evade host immune responses. In this review, we aimed to provide a comprehensive overview of immune evasion strategies in spirochetes infection. These strategies can be explained from the following points: (i) Antigenic variation: random, unidirectional, and segmental conversion of the gene to evade immune surveillance; (ii) Overcoming the attack of the complement system: recruitment of host complement regulators, cleavage of complement components and inhibition of complement activation to evade immune defenses; (iii) Interfering with immune cells to regulating the immune system; (iv) Persistent infection: invading and colonizing the host cell to escape immune damage.
Inosine monophosphate dehydrogenase type1 sustains tumor growth in hepatocellular carcinoma
Authors: Jia Xiaoyuan , Liu Yao , Cheng Yan , Wang Yin , Kang Hui , Ma Zhongren , Chen Kan 
Published: April 2022

AbstractBackgroundInosine monophosphate dehydrogenase (IMPDH) is the key enzyme in the biosynthesis of purine nucleotides. IMPDH1 and IMPDH2 are the two isoforms of IMPDH and they share 84% amino acid similarity and virtually indistinguishable catalytic activity. Although high expression of IMPDH2 has been reported in various cancers, the roles of IMPDH1 in hepatocellular carcinoma (HCC) are largely unknown.MethodsThe expression and the clinical relevance of IMPDH1 in 154 HCC patients were detected by immunohistochemistry analysis. The stable IMPDH1 knockdown HuH7 cells were established by lentiviral RNAi approach. The single cell proliferation was detected by colony‐forming unit assay. The tumor initiation and growth ability were measured by using xenograft tumor model in immunodeficient mice. The effect of IMPDH1 on cellular signaling pathways was analyzed by genome‐wide transcriptomic profiling.ResultsThe expression of IMPDH1 is upregulated in tumor tissue compared with adjacent liver tissue, and higher expression of IMPDH1 is associated with better patient cumulative survival. In experimental models, loss of IMPDH1 in HCC cells inhibits the ability of single cell colony formation in vitro, and reduces the efficiency of tumor initiation and growth in immunodeficient mice. Consistently, loss of IMPDH1 results in distinct alterations of signaling pathways revealed by genome‐wide transcriptomic profiling.ConclusionIMPDH1 sustains HCC growth and progression.
The investigation of in vitro effects of farnesol at different cancer cell lines
Authors: Yilmaz Öztürk Betül , Feyzullazade Narmın , Dağ İlknur , Şengel Tayfun 
Published: April 2022

AbstractFarnesol (trans, trans‐3,7,11‐trimethyl‐2,6,10‐dodecatriene‐1‐ol) is an essential oil component that can be found in a variety of plants. In this study, in vitro effects of farnesol on human lung cancer A549 cell line, colon adenocarcinoma (Caco‐2) cell line and healthy human lung epithelial BEAS‐2B cell lines, WST‐1 cytotoxicity test, dual staining of cell survival (DAPI‐PI) analysis, micronucleus test, and transmission electron microscopy (TEM). Farnesol acted in a concentration‐dependent manner at the dose ranges studied for cancer cell lines, and while at certain doses it reduced proliferation, interestingly at higher concentrations it induced growth more than the control. In the healthy BEAS‐2B cell line, it was tested over a wide range of doses and at all studied concentrations, it did not suppress cellular growth, but rather increased. This seems promising in that farnesol harms cancer cell lines but does not cause significant damage to healthy cells. Obtained TEM data after treatment with farnesol at IC50 dose showed both autophagic and apoptotic findings in cancer cell lines compared to control, and normal findings exhibited in BEAS‐2B cell line, cell survival, and micronucleus analyzes showed the presence of apoptotic findings and chromosomal damage as a result of farnesol application in cancer cell lines.Research Highlights
Farnesol has dose‐dependent effects on human lung cancer and colon adenocarcinoma cell lines, with no significant damaging effects on healthy human lung epithelial cell lines.
TEM, cell survival, and micronucleus findings support the findings of autophagic, apoptotic, and chromosomal damage on cancer cell lines.
Use of SMOF lipid emulsion in very preterm infants does not affect the incidence of bronchopulmonary dysplasia–free survival
Authors: Ndiaye Aissatou B.K.T. , Mohamed Ibrahim , Pronovost Etienne , Angoa Georgina , Piedboeuf Bruno , Lemyre Brigitte , Afifi Jehier , Qureshi Mosarrat , Sériès Thibaut , Guillot Mireille , Simonyan David , Yusuf Kamran , Lavoie Pascal M. , Fraser William D. , Mâsse Benoît , Nuyt Anne Monique , Lacaze‐Masmonteil Thierry , Marc Isabelle 
Published: April 2022

AbstractBackgroundWe aim to assess whether the docosahexaenoic acid (DHA)–containing lipid emulsion (LE) SMOFlipid 20% (Fresenius Kabi Canada Ltd) is associated with bronchopulmonary dysplasia (BPD)–free survival at 36 weeks' postmenstrual age in very preterm infants.MethodsThis cohort study is nested in the MOBYDIck randomized clinical trial (NCT02371460), which investigated the effect of maternal DHA supplementation on BPD‐free survival in breastfed very preterm infants born between 23 0/7 and 28 6/7 weeks' gestation in 16 Canadian neonatal intensive care units (2015–2018). Parenteral SMOF‐LE was given to the infants according to the sites' routine care protocols. Relative risks (RRs) were estimated using a modified Poisson regression model with generalized estimating equations taking into account recruitment site, multiple birth, DHA supplementation, birth weight, sex, and gestational age.ResultsAmong 528 infants (mean gestational age, 26.5 weeks [SD, 1.6]), 272 received SMOF‐LE. Overall, 56.7% of the infants in the SMOF‐LE group and 59.7% infants in the non–SMOF‐LE group survived without BPD (adjusted RR, 0.94 [95% CI, 0.77–1.14]; P = 0.51). BPD rates were 39.3% in the SMOF‐LE group vs 34.1% in the non–SMOF‐LE group (adjusted RR, 1.10 [95% CI, 0.82–1.47]; P = 0.53). Severe BPD rates were 31.8% in the SMOF‐LE group vs 28.8% in the non–SMOF‐LE group (adjusted P = 0.59). Mortality was not significantly different between the SMOF‐LE (6.7%) and non–SMOF‐LE groups (9.5%; adjusted P = 0.40).ConclusionIn very preterm infants, intravenous DHA‐containing SMOF‐LE during the neonatal period was not associated with BPD‐free survival.
Interferon activated gene 204 protects against bone loss in experimental periodontitis
Authors: Swanson Karen V. , Girnary Mustafa , Alves Tomaz , Ting Jenny PY , Divaris Kimon , Beck Jim , Pucinelli Carolina Maschietto , da Silva Raquel Assed Bezerra , Uyan Dilek , Wilson Justin E. , Seaman William T. , Webster‐Cyriaque Jennifer , Vias Nishma , Jiao Yizu , Cantley Lloyd , Marlier Arnaud , Arnold Roland R. , Marchesan Julie T. 
Published: April 2022

AbstractBackgroundPeriodontal destruction can be the result of different known and yet‐to‐be‐discovered biological pathways. Recent human genetic association studies have implicated interferon‐gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) with high periodontal interleukin (IL)‐1β levels and more destructive disease, but mechanistic evidence is lacking. Here, we sought to experimentally validate these observational associations and better understand IFI16 and AIM2's roles in periodontitis.MethodsPeriodontitis was induced in Ifi204–/– (IFI16 murine homolog) and Aim2–/– mice using the ligature model. Chimeric mice were created to identify the main source cells of Ifi204 in the periodontium. IFI16‐silenced human endothelial cells were treated with periodontal pathogens in vitro. Periodontal tissues from Ifi204–/– mice were evaluated for alveolar bone (micro‐CT), cell inflammatory infiltration (MPO+ staining), Il1b (qRT‐PCR), and osteoclast numbers (cathepsin K+ staining).ResultsIfi204‐deficient mice> exhibited >20% higher alveolar bone loss than wild‐type (WT) (P < 0.05), while no significant difference was found in Aim2–/– mice. Ifi204's effect on bone loss was primarily mediated by a nonbone marrow source and was independent of Aim2. Ifi204‐deficient mice had greater neutrophil/macrophage trafficking into gingival tissues regardless of periodontitis development compared to WT. In human endothelial cells, IFI16 decreased the chemokine response to periodontal pathogens. In murine periodontitis, Ifi204 depletion elevated gingival Il1b and increased osteoclast numbers at diseased sites (P < 0.05).ConclusionsThese findings support IFI16's role as a novel regulator of inflammatory cell trafficking to the periodontium that protects against bone loss and offers potential targets for the development of new periodontal disease biomarkers and therapeutics.
Development and Validation of Automated Magnetic Resonance Parkinsonism Index 2.0 to Distinguish Progressive Supranuclear Palsy‐Parkinsonism From Parkinson's Disease
Authors: Quattrone Andrea , Bianco Maria G. , Antonini Angelo , Vaillancourt David E. , Seppi Klaus , Ceravolo Roberto , Strafella Antonio P. , Tedeschi Gioacchino , Tessitore Alessandro , Cilia Roberto , Morelli Maurizio , Nigro Salvatore , Vescio Basilio , Arcuri Pier Paolo , De Micco Rosa , Cirillo Mario , Weis Luca , Fiorenzato Eleonora , Biundo Roberta , Burciu Roxana G. , Krismer Florian , McFarland Nikolaus R. , Mueller Christoph , Gizewski Elke R. , Cosottini Mirco , Del Prete Eleonora , Mazzucchi Sonia , Quattrone Aldo 
Published: April 2022

AbstractBackgroundDifferentiating progressive supranuclear palsy‐parkinsonism (PSP‐P) from Parkinson's disease (PD) is clinically challenging.ObjectiveThis study aimed to develop an automated Magnetic Resonance Parkinsonism Index 2.0 (MRPI 2.0) algorithm to distinguish PSP‐P from PD and to validate its diagnostic performance in two large independent cohorts.MethodsWe enrolled 676 participants: a training cohort (n = 346; 43 PSP‐P, 194 PD, and 109 control subjects) from our center and an independent testing cohort (n = 330; 62 PSP‐P, 171 PD, and 97 control subjects) from an international research group. We developed a new in‐house algorithm for MRPI 2.0 calculation and assessed its performance in distinguishing PSP‐P from PD and control subjects in both cohorts using receiver operating characteristic curves.ResultsThe automated MRPI 2.0 showed excellent performance in differentiating patients with PSP‐P from patients with PD and control subjects both in the training cohort (area under the receiver operating characteristic curve [AUC] = 0.93 [95% confidence interval, 0.89–0.98] and AUC = 0.97 [0.93–1.00], respectively) and in the international testing cohort (PSP‐P versus PD, AUC = 0.92 [0.87–0.97]; PSP‐P versus controls, AUC = 0.94 [0.90–0.98]), suggesting the generalizability of the results. The automated MRPI 2.0 also accurately distinguished between PSP‐P and PD in the early stage of the diseases (AUC = 0.91 [0.84–0.97]). A strong correlation (r = 0.91, P < 0.001) was found between automated and manual MRPI 2.0 values.ConclusionsOur study provides an automated, validated, and generalizable magnetic resonance biomarker to distinguish PSP‐P from PD. The use of the automated MRPI 2.0 algorithm rather than manual measurements could be important to standardize measures in patients with PSP‐P across centers, with a positive impact on multicenter studies and clinical trials involving patients from different geographic regions. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society
The design of a novel direction modulated brachytherapy vaginal cylinder applicator for optimizing coverage of the apex
Authors: Meftahi Moeen , Fields Emma , Guy Christopher , Song William Y. 
Published: April 2022

AbstractPurposeHigh‐dose‐rate (HDR) vaginal cuff brachytherapy is an effective adjuvant therapy for women with stage I endometrial cancer. Although infrequent, failures do occur, most frequently at the vaginal vault. A potential cause of failure is insufficient dosimetric coverage at the vaginal apex due to cold spots from the anisotropic dose distribution of the source. Here, we propose a novel direction modulated brachytherapy (DMBT)‐concept vaginal cylinder (VC) applicator that resolves this dosimetric issue.Methods and materialsThe novel DMBT‐VC applicator was designed and simulated with the GEANT4 Monte Carlo code. The outer cylinder material chosen was polyphenylsulfone (PPSU) plastic, and the central part was a detachable rod, housing a single lumen made of either polyether ether ketone (PEEK) plastic or an MR‐compatible tungsten alloy. The PPSU‐based outer cylinder, together with the inner PEEK rod provides the dose distribution of a conventional VC applicator. The PEEK rod is then replaced with an MR‐compatible tungsten alloy rod of the same dimensions to generate directional “pencil‐like” beams to compensate for the anisotropic cold spots. Two widely used192Ir HDR sources, VS2000 and GammaMedPlus, were also simulated.ResultsThe novel DMBT‐VC applicator was able to remove the underdosage at the apex due to the anisotropy effect regardless of the HDR sources without unnecessarily increasing the dose to the periphery of the applicator. Also, further directional modulation to reach deeper in the apex by up to 14 mm beyond the VC surface was achievable, again without increasing the peripheral doses. Total treatment dwell times increased only by 7–13%.ConclusionsThe novel DMBT‐VC applicator provides improved dose coverage at the vaginal apex by overcoming the classical anisotropy issue ubiquitous to all HDR brachytherapy sources. The next step in development of the device is manufacturing a prototype for clinical testing.
Neurocognitive outcomes in survivors of childhood acute lymphoblastic leukemia: Experience from a tertiary care center in India
Authors: CR Vishwa , Das Gargi , Seth Rachna , Sapra Savita , Sri Prasanth , Meena Jagdish Prasad , Gupta Aditya Kumar , Sreenivas Vishnu 
Published: April 2022

AbstractBackgroundData of neurocognitive deficits in survivors of acute lymphoblastic leukemia (ALL) is scarce from low middle‐income countries (LMICs), and is influenced by biological and cultural variations. The objective of this study was to assess the prevalence and spectrum of neurocognitive deficits in a cohort of survivors from India.ProcedureSeventy survivors of childhood ALL were evaluated for neurocognitive deficits by the Indian adaptation of Wechsler Intelligence Scale for Children ‐ Fourth Edition (WISC‐IVINDIA). The prevalence of neurocognitive deficits was calculated based on the full‐scale intelligence quotient (FSIQ), and scores in discrete domains like verbal comprehension, perceptual reasoning, working memory, and processing speed were calculated and compared to demographics, treatment, and sociocultural factors.ResultsThe mean (SD) current age and time since diagnosis was 10.5 (±3.2) years and 5 (±2.8) years, respectively. The mean FSIQ was 86.1 ± 20.5, with significant neurocognitive deficit (FSIQ <90) being prevalent in 50% (95% CI: 38%–62%) of the cohort. The proportion of survivors with deficits in individual domains of verbal comprehension, perceptual reasoning, working memory, and processing speed were 49%, 50%, 47%, and 44%, respectively. The odds of having neurocognitive deficits were higher when a child belonged to lower socioeconomic strata (OR 5.7, p = .004), parents with lower education attainment (OR 4.3, p = .041), and whose birth order was higher (OR 20.1, p = .005). Age at diagnosis/assessment, chemotherapy received, or dose of radiotherapy did not have a direct impact on neurocognition.Conclusions and relevanceRates of neurocognitive deficits are higher in survivors in LMICs, with socioeconomic variables contributing more than the direct neurotoxic effects of treatment.