bluuebunny/crossref_metadata_2025_split huggingface dataset:
A hydraulic conductivity model of frozen soils with the consideration of water films
Authors: Ming Feng , Pei Wansheng , Zhang Mingyi , Chen Lei 
Published: December 2021

AbstractAccurate evaluation of water migration in frozen soils requires the determination of hydraulic conductivity. Most classical predictive models of hydraulic conductivity rely on the pore bundle concept that only accounts for capillary flow and neglects the water film flow. This may underestimate the hydraulic conductivity of frozen soil. In this study, water in the capillary tube was divided into free water and water films with different dynamic viscosities. Then, a novel prediction model for hydraulic conductivity of frozen soil was proposed based on the capillary flow theory. The model parameters can be easily obtained from laboratory tests. The predicted results showed good agreement with tested hydraulic conductivity of 12 frozen soils. When the temperature decreases from 0 to −1°C, the contribution of water films to the hydraulic conductivity of frozen soil becomes large, up to 20%. To further develop the predictive power of the model, the hydraulic conductivity determined by relative change method was recommended. The use of relative hydraulic conductivity can provide a simple form to quantify the influence of unfrozen water content on the hydraulic conductivity of frozen soils.Highlights
Free water and water films have different dynamic viscosities in the model.
Soil freezing curve was used to predict the hydraulic conductivity of frozen soils.
Water film has about 20% contribution to hydraulic conductivity of frozen clay.
Changes in perspective needed to forge ‘no‐regret’ forest‐based climate change mitigation strategies
Authors: Erb Karl‐Heinz , Haberl Helmut , Le Noë Julia , Tappeiner Ulrike , Tasser Erich , Gingrich Simone 
Published: December 2021

AbstractForest‐based mitigation strategies will play a pivotal role in achieving the rapid and deep net‐emission reductions required to prevent catastrophic climate change. However, large disagreement prevails on how to forge forest‐based mitigation strategies, in particular in regions where forests are currently growing in area and carbon density. Two opposing viewpoints prevail in the current discourse: (1) A widespread viewpoint, specifically in countries in the Global North, favours enhanced wood use, including bioenergy, for substitution of emissions‐intensive products and processes. (2) Others instead focus on the biophysical, resource‐efficiency and time‐response advantages of forest conservation and restoration for carbon sequestration and biodiversity conservation, whilst often not explicitly specifying how much wood extraction can still safeguard these ecological benefits. We here argue for a new perspective in sustainable forest research that aims at forging “no‐regret” forest‐based climate change mitigation strategies. Based on the consideration of forest growth dynamics and the opportunity carbon cost associated with wood use, we suggest that, instead of taking (hypothetical) wood‐for‐fossil substitution as starting point in assessments of carbon implications of wood products and services, analyses should take the potential and desired carbon sequestration of forests as starting point and quantify sustainable yield potentials compatible with those carbon sequestration potentials. Such an approach explicitly addresses the possible benefits provided by forests as carbon sinks, brings research on the permanence and vulnerability of C‐stocks in forests, of substitution effects, as well as explorations of demand‐side strategies to the forefront of research and, in particular, aligns better with the urgency to find viable climate solutions.
Testing the effects on information use by older versus younger women of modality and narration style in a hospital report card
Authors: Yılmaz Nida Gizem , Timmermans Danielle R. M. , Portielje Johanneke , Van Weert Julia C. M. , Damman Olga C. 
Published: December 2021

AbstractBackgroundHospital report cards (HRCs) are usually presented in a textual and factual format, likely hampering information processing.ObjectiveThis study aimed to investigate the effects of audiovisual and narrative information in HRCs on user responses, and to test differences between older and younger women.DesignA 2 (modality [textual vs. audiovisual]) × 3 (narration style [factual vs. process narrative vs. experience narrative]) online experiment was conducted. Information about breast cancer care was used as a case example. Age (younger [<65] vs. older [≥65]) was included as a potential effect modifier.Setting and ParticipantsA total of 631 disease‐naïve women (Mage = 56.06) completed an online survey. The outcomes were perceived cognitive load, satisfaction, comprehension, information recall and decisional conflict. Data were analysed using AN(C)OVAs.ResultsAudiovisual (vs. textual) information resulted in higher information satisfaction across age groups, but was associated with lower comprehension in older women. An experience narrative (vs. factual information) increased satisfaction with attractiveness and emotional support of the information only in older women. A three‐way interaction effect was found, suggesting that older women were most satisfied with the comprehensibility of audiovisual factual or textual process narrative information. Younger women were most satisfied with the comprehensibility of audiovisual process narrative or textual factual information.Discussion and ConclusionAudiovisual and narrative information in an HRC showed beneficial effects on satisfaction measures. In particular, audiovisual information could be incorporated into HRCs to increase satisfaction with information.Public ContributionLay persons helped in optimizing the visuals used in the stimulus materials by checking for clarity.
Operationalizing a patient engagement plan for health research: Sharing a codesigned planning template from a national clinical trial
Authors: Etchegary Holly , Pike Andrea , Patey Andrea M. , Gionet Erin , Johnston Brian , Goold Susan , Francis Vanessa , Grimshaw Jeremy , Hall Amanda ,   De‐Implementing Wisely Research Group
Published: December 2021

AbstractIntroductionEngaging with patients about their lived experience of health and illness and their experience within the healthcare system can help inform the provision of care, health policies and health research. In the context of health research, however, operationalizing the levels of patient engagement is not straightforward. We suggest that a key challenge to the routine inclusion of patients as partners in health research is a lack of tangible guidance regarding how this can be accomplished.MethodsIn this article, we provide guidance on how to codesign and operationalize a concrete patient engagement plan for any health research project.ResultsWe illustrate a seven‐step approach using the example of a national clinical trial in Canada and provide a patient engagement planning template for use in any health research project.ConclusionSuch concrete guidance should improve the design and reporting of patient engagement in health research.Patient or Public ContributionThe De‐Implementing Wisely Research group is informed by a national 9‐member patient partner council (PPC). The research team includes three lead patient partners who are coinvestigators on the grant that funds the program of research. Members of the council advise on all aspects of the study design and implementation. The ideas presented in this paper were informed by regular communication and planning with the PPC; specific contributions of lead patient partner authors are outlined as follows: Brian Johnston, Susan Goold and Vanessa Francis are patient partners with a wide breadth of experience in the healthcare system and health research projects. The guidance in this article draws on their lived and professional expertise. All patient partner authors contributed to the planning of the manuscript, participated in meetings to develop content and provided critical manuscript edits and comments on drafts.
Longitudinal population‐based study of progression rates for borderline thyroid‐stimulating hormone abnormalities
Authors: Endall Ryan , Stokes Brian , Otahal Petr , Burgess John 
Published: December 2021

AbstractBackgroundCurrent guidelines recommend thyroid‐stimulating hormone (TSH) for initial biochemical evaluation of thyroid function, with borderline TSH abnormalities a common finding. The likelihood of a borderline TSH progressing to overt abnormality is not well characterised at the population level.AimsTo determine risk factors and likelihood for progression of borderline TSH to overt abnormality.MethodsPopulation‐based retrospective longitudinal data‐linkage study for TSH tests performed in Tasmania (1996–2013). Kaplan–Meier methodology was used to summarise conversion time for overt TSH elevation (≥10 mU/L) and overt suppression (≤0.1 mU/L) in patients whose initial TSH was borderline elevated (BeTSH; 4.0–9.99 mU/L) and borderline suppressed (BsTSH; 0.10–0.39 mU/L) respectively. Main outcome measures are the progression from borderline to overt TSH abnormality.ResultsA total of 1 296 060 TSH tests was performed on 367 917 patients. Of these, 14 507 (3.9%) patients had BeTSH on initial assessment; mean age 51.4 ± 21.8 years and median TSH of 5.0 mU/L (interquartile range (IQR) 4.4, 5.2). Patients aged ≥80 years were most likely to progress (hazard ratio (HR) = 2.09 compared with age <20 years reference group (95% confidence interval (CI): 1.64, 2.68)). Patients aged 20–39 years had the second‐highest rate of progression (HR = 1.49 (95% CI: 1.18, 1.88)). Seven thousand, eight hundred and eighty‐three (2.14%) patients had BsTSH; mean age 50.7 ± 22.1 years and median TSH 0.30 mU/L (IQR 0.22, 0.35). Patients aged 60–79 years had the highest rate of progression to overt TSH suppression (HR = 2.47 compared with age <20 years reference group (95% CI: 1.88, 3.22)).ConclusionsFollow‐up intervals for patients with borderline TSH abnormalities should take into account patient age as a progression risk factor.
Role of HrcA in stress management in Mycobacterium tuberculosis
Authors: Hakiem Owais R. , Batra Janendra K. 
Published: December 2021

Abstract

Aim
The current study aims to understand the role of HrcA in stress response of M. tuberculosis.

Methods and Results
In this study, using an hrcA knock out mutant of M. tuberculosis it is demonstrated that the heat shock repressor, HrcA is important for countering environmental stresses pathogen faces within the host during the infection process. Also, with scanning electron microscopy, it has been shown that HrcA plays a role in maintaining the morphology and cell size of the pathogen as disruption of the hrcA gene resulted in significantly elongated bacilli. Furthermore, heat shock proteins like ClpC1, ClpB, DnaK, GroEL2, GroEL1, DnaJ2 and GroES were detected in the secretome of M. tuberculosis by mass spectrometric analysis. The study also demonstrates a strong humoral response against M. tuberculosis heat shock proteins in H37Rv-infected mice sera.

Conclusion
The study establishes that though hrcA is not an essential gene for M. tuberculosis, it regulates the expression of heat shock proteins during infection and disruption of hrcA gives a survival advantage to the pathogen during stress conditions.

Significance and Impact of the Study
HrcA plays an important role in maintaining a fine balance of heat shock proteins during infection to give adequate survival advantage and also evade immune detection.
Economics and outcomes of sotalol in‐patient dosing approaches in patients with atrial fibrillation
Authors: Varela Daniel L. , Burnham Tyson S. , T. May Heidi , L. Bair Tami , Steinberg Benjamin A. , B. Muhlestein Joseph , L. Anderson Jeffrey , U. Knowlton Kirk , Jared Bunch Thomas 
Published: December 2021

AbstractIntroductionThere exists variability in the administration of in‐patient sotalol therapy for symptomatic atrial fibrillation (AF). The impact of this variability on patient in‐hospital and 30‐day posthospitalization costs and outcomes is not known. Also, the cost impact of intravenous sotalol, which can accelerate drug loading to therapeutic levels, is unknown.MethodsOne hundred and thirty‐three AF patients admitted for oral sotalol initiation at an Intermountain Healthcare Hospital from January 2017 to December 2018 were included. Patient and dosing characteristics were described descriptively and the impact of dosing schedule was correlated with daily hospital costs/clinical outcomes during the index hospitalization and for 30 days. The Centers for Medicare and Medicaid Services reimbursement for 3‐day sotalol initiation is $9263.51. Projections of cost savings were made considering a 1‐day load using intravenous sotalol that costs $2500.00 to administer.ResultsThe average age was 70.3 ± 12.3 years and 60.2% were male with comorbidities of hypertension (83%), diabetes (36%), and coronary artery disease (53%). The mean ejection fraction was 59.9 ± 7.8% and the median corrected QT interval was 453.7 ± 37.6 ms before sotalol dosing. No ventricular arrhythmias developed, but bradycardia (<60 bpm) was observed in 37.6% of patients. The average length of stay was 3.9 ± 4.6 (median: 2.2) days. Postdischarge outcomes and rehospitalization rates stratified by length of stay were similar. The cost per day was estimated at $2931.55 (1. $2931.55, 2. $5863.10, 3. $8794.65, 4. $11 726.20).ConclusionsIn‐patient oral sotalol dosing is markedly variable and results in the potential of both cost gain and loss to a hospital. In consideration of estimated costs, there is the potential for $871.55 cost savings compared to a 2‐day oral load and $3803.10 compared to a 3‐day oral load.
Leadless pacemaker perforations: Clinical consequences and related device and user problems
Authors: Hauser Robert G. , Gornick Charles C. , Abdelhadi Raed H. , Tang Chuen Y. , Kapphahn‐Bergs Melanie , Casey Susan A. , Okeson Brynn K. , Steele Elizabeth A. , Sengupta Jay D. 
Published: December 2021

AbstractBackgroundCardiac perforation during leadless pacemaker implantation is more likely to require intervention than perforation by a transvenous lead. This study reports the consequences of Micra pacemaker perforations and related device and operator use problems based on information the manufacturer has submitted to the Food and Drug Administration (FDA).MethodsFDA's Manufacturer and User Facility Device Experience (MAUDE) database was searched for Micra perforations. Data extracted included deaths, major adverse clinical events (MACEs), and device and/or operator use problems.ResultsBetween 2016 and July 2021, 563 perforations were reported within 30 days of implant and resulted in 150 deaths (27%), 499 cardiac tamponades (89%), 64 pericardial effusions (11%), and 146 patients (26%) required emergency surgery. Half of perforations were associated with 139 (25%) device problems, 78 (14%) operator use problems, and 62 (11%) combined device and operator use problems. Inadequate electrical measurements or difficult positioning were the most frequent device problems (n = 129); non‐septal implants and perforation of other structures were the most frequent operator use problems (n = 69); a combined operator use and device problem resulted in 62 delivery system perforations. No device or operator use problem was identified for 282 perforations (50%), but they were associated with 78 deaths, 245 tamponades, and 57 emergency surgeries.ConclusionThe Micra perforations reported in MAUDE are often associated with death and major complications requiring emergency intervention. Device and use problems account for at least half of perforations. Studies are needed to identify who is at risk for a perforation and how MACE can be avoided or mitigated.
The G to A transformation of rs4702 polymorphism in 3’UTR of FURIN reduced the risk of radiotherapy‐induced cognitive impairment in glioma patients
Authors: Yang Sen , Fu Zhan‐Zhao , Zhang Yan‐qiu , Fu Bao‐hong , Dong Lixin 
Published: December 2021

AbstractThe G allele of rs4702 polymorphism has been reported to reduce the production of mature BDNF and FURIN, both of which were closely associated with cognitive functions. Real‐time PCR, ELISA and luciferase assay were performed to explore the interactions between miR‐338‐3p, FURIN and BDNF. T‐RFLP was used to assess the intestinal flora in the stool samples of glioma patients after radiotherapy. We grouped the 106 glioma patients recruited according to the rs4702 polymorphism. The results showed no obvious correlation between rs4702 polymorphism and the expression of miR‐338‐3p. However, rs4702‐A was associated with increased expression of FURIN and BDNF in the serum and PBMC of glioma patients after radiotherapy. Besides, the study found that rs4702‐A was remarkably associated with increased enterotype I and decreased enterotype III in the stool of glioma patients after radiotherapy. Rs4702‐A was also proved to be closely associated with increased MMSE, role functioning and social functioning at three months after radiotherapy. Furthermore, miR‐338‐3p repressed the expression of FURIN‐G. Compared with G allele, the presence of A allele of rs4702 polymorphism in FURIN could obstruct the suppressive effect of miR‐338‐3p upon the expression of FURIN and BDNF in intestinal flora. Therefore, the carriers of A allele will be challenged with less risk of radiotherapy‐induced cognitive impairment.
Studying the mechanism of sperm DNA damage caused by folate deficiency
Authors: Wang Wei , Peng Meilin , Yuan Hongfang , Liu Chunyan , Zhang Yuan , Fang Yiwei , Su Yufang , Zhang Xinzong , Zhang Huiping , Tang Yunge , Zhao Kai 
Published: December 2021

AbstractSperm DNA injury is one of the common causes of male infertility. Folic acid deficiency would increase the methylation level of the important genes, including those involved in DNA double‐strand break (DSB) repair pathway. In the early stages, we analysed the correlation between seminal plasma folic acid concentration and semen parameters in 157 infertility patients and 91 sperm donor volunteers, and found that there was a significant negative correlation between seminal folic acid concentration and sperm DNA Fragmentation Index (DFI; r = −0.495, p < 0.01). Then through reduced representation bisulphite sequencing, global DNA methylation of sperm of patients in the low folic acid group and the high folic acid group was analysed, it was found that the methylation level in Rad54 promoter region increased in the folic acid deficiency group compared with the normal folic acid group. Meanwhile, the results of animal model and spermatocyte line (GC‐2) also found that folic acid deficiency can increase the methylation level in Rad54 promoter region, increased sperm DFI in mice, increased the expression of γ‐H2AX, that is, DNA injury marker protein, and increased sensitivity of GC‐2 to external damage and stimulation. The study indicates that the expression of Rad54 is downregulated by folic acid deficiency via DNA methylation. This may be one of the mechanisms of sperm DNA damage caused by folate deficiency.
Expression and significance of SOX B1 genes in glioblastoma multiforme patients
Authors: Pan Cunyao , Liang Lanlan , Wang Zirou , Zhang Baoyi , Li Qionglin , Tian Yingrui , Yu Yijing , Chen Zhaoli , Wang Xinxing , Liu Hui 
Published: December 2021

AbstractThe overall survival of glioblastoma multiforme (GBM) patients remains poor. To improve patient outcomes, effective diagnostic and prognostic biomarkers for GBM are needed. In this study, we first applied bioinformatic analyses to identify biomarkers for GBM, focusing on SOX (sex‐determining region on the Y chromosome (SRY)‐related high mobility group (HMG) box) B1 family members. The ONCOMINE, GEPIA, LinkedOmics and CCLE databases were used to assess mRNA expression levels of the SOX B1 family members in different cancers and normal tissue. Further bioinformatic analysis was performed using the ONCOMINE database in combination with the LinkedOmics data set to identify the prognostic value of SOX B1 family members for GBM. We found mRNA expression levels of all tested SOX B1 genes were significantly increased in GBM. In the LinkedOmics database, increased expression of SOX3 indicated a better overall survival. In GEPIA databases, increased expression of all SOX B1 family members suggested an improved overall survival, but none of them were statistically different. Then, Transwell assays and wound healing were employed to evaluate the motility and invasive captivity of U251 cells when silencing SOX2 and SOX3. We found exogenous inhibition of SOX2 appeared to reduce the migration and invasion of U251 cells in vitro. Collectively, our research suggested that SOX2 might serve as a cancer‐promoting gene to identify high‐risk GBM patients, and SOX3 had the potential to be a prognostic biomarker for GBM patients.
AR imposes different effects on ZFHX3 transcription depending on androgen status in prostate cancer cells
Authors: Fu Xing , Zhang Zhiqian , Liu Mingcheng , Li Juan , A Jun , Fu Liya , Huang Chenyang , Dong Jin‐Tang 
Published: December 2021

AbstractBoth androgen receptor (AR) and the ZFHX3 transcription factor modulate prostate development. While AR drives prostatic carcinogenesis, ZFHX3 is a tumour suppressor whose loss activates the PI3K/AKT signalling in advanced prostate cancer (PCa). However, it is unknown whether ZFHX3 and AR are functionally related in PCa cells and, if so, how. Here, we report that in AR‐positive LNCaP and C4‐2B PCa cells, androgen upregulates ZFHX3 transcription via androgen‐induced AR binding to the androgen‐responsive elements (AREs) of the ZFHX3 promoter. Androgen also upregulated ZFHX3 transcription in vivo, as castration dramatically reduced Zfhx3 mRNA and protein levels in mouse prostates, and ZFHX3 mRNA levels correlated with AR activities in human PCa. Interestingly, the binding of AR to one ARE occurred in the absence of androgen, and the binding repressed ZFHX3 transcription as this repressive binding was interrupted by androgen treatment. The enzalutamide antiandrogen prevented androgen from inducing ZFHX3 transcription and caused excess ZFHX3 protein degradation. In human PCa, ZFHX3 was downregulated and the downregulation correlated with worse patient survival. These findings establish a regulatory relationship between AR and ZFHX3, suggest a role of ZFHX3 in AR function and implicate ZFHX3 loss in the antiandrogen therapies of PCa.