bluuebunny/crossref_metadata_2025_split huggingface dataset:
Patient participation in dialysis care—A qualitative study of patients’ and health professionals’ perspectives
Authors: Årestedt Liselott , Martinsson Caroline , Hjelm Carina , Uhlin Fredrik , Eldh Ann Catrine 
Published: September 2019

AbstractBackground and objectiveEnd‐stage renal disease (ESRD) affects a multitude of aspects in the patient's daily life, often entailing their own involvement in various aspects of the treatment. Although patient participation is a core health‐care value, what the concept signifies is not yet fully known. The purpose of this paper is to conceptualize patient participation in dialysis care, depicting patients’ and health‐care professionals’ perspectives.DesignThis explorative study employed qualitative interviews and content analysis.Setting and participantsSeven focus group discussions engaging 42 key informants were performed, including patients, staff and managers with experience of dialysis care.ResultsIn dialysis care, patient participation connotes a sharing of information and knowledge, the learning of and planning of care, including partaking in shared decisions with regards to treatment and management, and being involved in the management of one's own health‐care treatment and/or self‐care activities. Although these attributes were illustrated by all stakeholders, their significance varied: patients suggested that their preferences regarding primary aspects of participation vary, while staff considered patients’ performance of dialysis to be the ultimate form of participation. Further, while patients considered multiple ways to execute participation, staff suggested that aspects such as sharing information were a route to, rather than actual, involvement.ConclusionsWithout a common understanding to denote the idea of patient participation, staff and patients are exposed to a potential deficit in terms of facilitating patient participation in everyday encounters of dialysis treatment. Further studies and means to serve a mutual understanding are needed.
Understanding the decision to screen for lung cancer or not: A qualitative analysis
Authors: Draucker Claire Burke , Rawl Susan M. , Vode Emilee , Carter‐Harris Lisa 
Published: September 2019

AbstractBackgroundAlthough new screening programmes with low‐dose computed tomography (LDCT) for lung cancer have been implemented throughout the United States, screening uptake remains low and screening‐eligible persons' decisions to screen or not remain poorly understood.ObjectiveTo describe how current and former long‐term smokers explain their decisions regarding participation in lung cancer screening.DesignPhone interviews using a semi‐structured interview guide were conducted to ask screening‐eligible persons to describe their decisions regarding screening with LDCT. The interviews were transcribed and analysed with conventional content analytic techniques.Setting and participantsA subsample of 40 participants (20 who had screened and 20 who had not) were drawn from the sample of a survey study whose participants were recruited by Facebook targeted advertisements.ResultsThe sample was divided into the following five groups based on their decisions regarding lung cancer screening participation: Group 1: no intention to be screened, Group 2: no deliberate consideration but somewhat open to being screened, Group 3: deliberate consideration but no definitive decision to be screened, Group 4: intention to be screened and Group 5: had been screened. Reasons for screening participation decisions are described for each group. Across groups, data revealed that screening‐eligible persons have a number of misconceptions regarding LDCT, including that a scan is needed only if one is symptomatic or has not had a chest x‐ray. A physician recommendation was a key influence on decisions to screen.Discussion and conclusionsEducation initiatives aimed at providers and long‐term smokers regarding LDCT is needed. Quality patient/provider communication is most likely to improve screening rates.
Functional properties and structural characteristics of phosphorylated pea protein isolate
Authors: Liu Yanhong , Wang Dezhen , Wang Jiahao , Yang Yang , Zhang Lingling , Li Jia , Wang Shuo 
Published: September 2019

SummaryIn order to expand the application of pea proteins in the food industry, pea protein isolate (PPI) was chemically phosphorylated to improve its functional properties. Based on the comprehensive membership value (CMV) degree, the optimal condition for PPI phosphorylation modification was as follows: pH 12, modification temperature at 70 °C and an addition of 7.0% (w/v) sodium tripolyphosphate (STP). Under this condition, the solubility, emulsifying property, emulsifying stability, foaming property and oil absorption capacity of the modified PPI were improved substantially. In addition, the structure of modified PPI was characterised by scanning electron microscope (SEM) and Fourier transform infrared (FTIR) spectroscopy. The results showed that the modified PPI had a smooth and uniform lamellar structure, where the content of α‐helix and β‐sheet structure increased, but the content of β‐corner and random coil structure decreased. The thermodynamic properties were analysed by differential scanning calorimetry (DSC) and the results showed that ∆H of the modified PPI increased significantly. Finally, the optimum phosphorylated PPI was mixed with 0.4% (w/v) xanthan gum to form PPI fat mimics (PPI‐FM). PPI‐FM was added into mango mousse cake to reduce the amount of light cream, and the result showed up to 20% of light cream could be substituted.
Thermochemistry of calcium rare‐earth silicate oxyapatites
Authors: Costa Gustavo , Harder Bryan J. , Bansal Narottam P. , Kowalski Benjamin A. , Stokes Jamesa L. 
Published: September 2019

AbstractThe calcium rare‐earth (RE) silicate oxyapatite, Ca2RE8(SiO4)6O2 (RE = Yb, Er, Y, Dy, Nd, Gd, and Sm), powders were synthesized by the solid‐state reaction method and characterized by X‐ray diffraction (XRD), Raman spectroscopy, and elemental composition analysis. The thermodynamic properties of the oxyapatites have been investigated using high‐temperature oxide melt calorimetry in molten 2PbO–B2O3 solvent at 805°C. The energetics of the oxyapatites related to ionic substitution on two crystallographic sites, M(1) and M(2), are discussed. The enthalpy of formation from the oxides becomes more exothermic as the ionic potential decreases or the ionic radius of the REs increases, which indicates increasing energetic stability in this order.
Is Managerial Myopia a Persistent Governance Problem?
Authors: Denis David J. 
Published: September 2019

Critics of U.S. corporations have long argued that companies are overly focused on short‐term results and, as a consequence, sacrifice their own long‐run value and competitiveness. These criticisms have expanded in recent years to include those from prominent politicians, investors, consultants, and academics. If such criticisms have merit, they would imply a massive governance failure in which there has been decades of underinvestment with little adjustment on the part of managers, boards, or the market for corporate control.This article evaluates the economic underpinnings of these criticisms and analyzes their implications in the context of empirical evidence produced by several decades of research on corporate investment policies, the outcomes of corporate control events, investor horizons, and the market pricing of companies with little if any earnings. In reviewing the findings of these studies, the author finds little evidence to support the view that U.S. companies sacrifice long‐run value and competitiveness by systematically underinvesting.First, although U.S. companies have indeed cut back on tangible investments such as property, plant, and equipment, these cutbacks have been more than offset by the dramatic growth in investment in intangibles, such as spending on developing knowledge capital, brand‐building, and IT infrastructure. Second, when subjected to events that have the effect of reducing managerial control over investment policies and transferring control to outside investors—such as leveraged buyouts and recapitalizations, forced CEO dismissals, and shareholder activist campaigns—companies tend to reduce, not increase, investment spending. In fact, it is difficult to find any corporate control threats that have had the goal or effect of increasing investment. Third, and at the same time, the rising concentration of large institutional investors, including indexers such as BlackRock and Vanguard, suggests that investors have become, if anything, more long‐term oriented over time. Fourth, there is no evidence that the market shuns companies that have yet to report large (or indeed any) earnings. These findings suggest that curbing overinvestment, and not discouraging myopia and underinvestment, may well still be the larger corporate governance challenge facing investors when monitoring and attempting to influence the performance of U.S. companies.
Are Performance Shares Shareholder Friendly?
Authors: Hodak Marc 
Published: September 2019

Performance shares, or PSUs, have become the largest element of pay for top executives in corporate America. Their spread was ignited by institutional investors looking for more “shareholder‐friendly” equity awards—as opposed to restricted stock and stock options, which have been characterized as “non‐performance” equity. Although that characterization has been challenged by many directors and compensation professionals, proxy advisers like Institutional Shareholder Services have continued to insist that the majority of stock be granted based on performance, compelling public companies to conform to that standard.With over a decade of experience with PSUs, the evidence is in regarding their net effect:
PSUs greatly complicate long‐term incentives. Pay disclosures are dominated by discussion of PSUs, including metrics, goals, performance and vesting, and any differences in one grant year versus the next over three overlapping periods.
PSUs may be contributing to the increase in pay. Companies issuing a significant portion of their long‐term incentives in the form of PSUs have been granting about 35% more in value than companies granting only restricted stock and stock options.
Shareholders don't appear to be getting anything for that added complexity and cost. S&P 500 companies using PSUs have underperformed their sector peers, and companies using solely “non‐performance” equity have significantly outperformed their sector peers, and in every single year over the last decade.
Given these findings on PSUs, it is time for institutional investors and their proxy advisors to reconsider their view of these vehicles as “shareholder‐friendly,” and rethink their unqualified promotion of their use by the companies they invest in.
Role of cardiac progenitor cell‐derived exosome‐mediated microRNA‐210 in cardiovascular disease
Authors: Wang Lirong , Jia Qiujin , Xinnong Chen , Xie Yingyu , Yang Yaqian , Zhang Ao , Liu Runteng , Zhuo Yuan , Zhang Junping 
Published: September 2019

AbstractCardiac progenitor cells are considered to be one of the most promising stem cells for heart regeneration and repair. The cardiac protective effect of CPCs is mainly achieved by reducing tissue damage and/or promoting tissue repair through a paracrine mechanism. Exosome is a factor that plays a major role in the paracrine effect of CPCs. By delivering microRNAs to target cells and regulating their functions, exosomes have shown significant beneficial effects in slowing down cardiac injury and promoting cardiac repair. Among them, miRNA‐210 is an important anoxic‐related miRNA derived from CPCs exosomes, which has great cardiac protective effect of inhibiting myocardial cell apoptosis, promoting angiogenesis and improving cardiac function. In addition, circulating miR‐210 may be a useful biomarker for the prediction or diagnosis of related cardiovascular diseases. In this review, we briefly reviewed the mechanism of miR‐210 derived from CPCs exosomes in cardiac protection in recent years.
PCSK9 inhibitor improves cardiac function and reduces infarct size in rats with ischaemia/reperfusion injury: Benefits beyond lipid‐lowering effects
Authors: Palee Siripong , McSweeney Christian M. , Maneechote Chayodom , Moisescu Dalila M. , Jaiwongkam Thidarat , Kerdphoo Sasiwan , Chattipakorn Siriporn C. , Chattipakorn Nipon 
Published: September 2019

AbstractDuring acute cardiac ischaemia/reperfusion (I/R), an increased plasma proprotein convertase subtilisin/kexin 9 (PCSK9) level instigates inflammatory and oxidative processes within ventricular myocytes, resulting in cardiac dysfunction. Therefore, PCSK9 inhibitor (PCSK9i) might exert cardioprotection against I/R injury. However, the effects of PCSK9i on the heart during I/R injury have not been investigated. The effects of PCSK9i given at different time‐points during I/R injury on left ventricular (LV) function were investigated. Male Wistar rats were subjected to cardiac I/R injury and divided into 3 treatment groups (n = 10/group): pre‐ischaemia, during ischaemia and upon onset of reperfusion. The treatment groups received PCSK9i (Pep2‐8, 10 μg/kg) intravenously. A control group (n = 10) received saline solution. During the I/R protocol, arrhythmia scores and LV function were determined. Then, the infarct size, mitochondrial function, mitochondrial dynamics and level of apoptosis were determined. PCSK9i given prior to ischaemia exerted cardioprotection through protection of cardiac mitochondrial function, decreased infarct size and improved LV function, compared with control. PCSK9i administered during ischaemia and upon the onset of reperfusion did not provide any of those benefits. PCSK9i administered before ischaemia exerts cardioprotection, as demonstrated by the attenuation of infarct size and cardiac arrhythmia during cardiac I/R injury. The attenuation is associated with improved mitochondrial function and connexin43 phosphorylation, leading to improved LV function.
Preclinical evaluation of exemestane as a novel chemotherapy for gastric cancer
Authors: Yang Juan‐Cheng , Chang Ning , Wu Deng‐Chyang , Cheng Wei‐Chung , Chung Wei‐Min , Chang Wei‐Chun , Lei Fu‐Ju , Liu Chung‐Jung , Wu I‐Chen , Lai Hsueh‐Chou , Ma Wen‐Lung 
Published: September 2019

AbstractCYP19A1/aromatase (Ar) is a prognostic biomarker of gastric cancer (GCa). Ar is a critical enzyme for converting androstenedione to oestradiol in the steroidogenesis cascade. For decades, Ar has been targeted with Ar inhibitors (ARIs) in gynaecologic malignancies; however, it is unexplored in GCa. A single‐cohort tissue microarray examination was conducted to study the association between Ar expression and disease outcome in Asian patients with GCa. The results revealed that Ar was a prognostic promoter. Bioinformatics analyses conducted on a Caucasian‐based cDNA microarray databank showed Ar to be positively associated with GCa prognosis for multiple clinical modalities, including surgery, 5‐Fluorouracil (5‐FU) for adjuvant chemotherapy, or HER2 positivity. These findings imply that targeting Ar expression exhibits a potential for fulfilling unmet medical needs. Hence, Ar‐targeting compounds were tested, and the results showed that exemestane exhibited superior cancer‐suppressing efficacy to other ARIs. In addition, exemestane down‐regulated Ar expression. Ablating Ar abundance with short hairpin (sh)Ar could also suppress GCa cell growth, and adding 5‐FU could facilitate this effect. Notably, adding oestradiol could not prevent exemestane or shAr effects, implicating a nonenzymatic mechanism of Ar in cancer growth. Regarding translational research, treatment with exemestane alone exhibited tumour suppression efficacy in a dose‐dependent manner. Combining subminimal doses of 5‐FU and exemestane exerted an excellent tumour suppression effect without influencing bodyweight. This study validated the therapeutic potentials of exemestane in GCa. Combination of metronomic 5‐FU and exemestane for GCa therapy is recommended.
LINC01133 inhibits breast cancer invasion and metastasis by negatively regulating SOX4 expression through EZH2
Authors: Song Zhiwang , Zhang Xia , Lin Yun , Wei Youzhen , Liang Shujing , Dong Chunyan 
Published: September 2019

AbstractMounting evidence highlights long non‐coding RNAs (lncRNAs) as crucial regulators in multiple types of biological processes and contributing to tumourigenesis. LINC01133, located in chromosome 1q23.2, was a recently identified novel lncRNA with a length of 1154nt. It was involved in the development of colorectal cancer and non‐small cell lung cancer. However, its clinical relevance, biological functions and potential molecular mechanism in breast cancer are still unclear. In this study, we found that the LINC01133 expression was significantly down‐regulated in breast cancer samples and was associated with progression and poor prognosis of breast cancer. Further experiments demonstrated that overexpression of LINC01133 inhibited invasion and metastasis in breast cancer both in vitro and in vivo. Mechanistic investigations revealed that LINC01133 repressed SOX4 expression by recruiting EZH2 to SOX4 promoter. Moreover, rescue experiments further confirmed that LINC01133 functional acted as an anti‐oncogene, at least partly, via repressing SOX4 in breast cancer. Taken together, these findings imply that LINC01133 could serve as a novel prognostic biomarker and potential therapeutic target for breast cancer.
ALPK1 regulates streptozotocin‐induced nephropathy through CCL2 and CCL5 expressions
Authors: Lee Chi‐Pin , Nithiyanantham Srinivasan , Hsu Hui‐Ting , Yeh Kun‐Tu , Kuo Tzer‐Min , Ko Ying‐Chin 
Published: September 2019

AbstractALPK1 is associated with chronic kidney disease, gout and type 2 diabetes mellitus. Raised renal ALPK1 level in patients with diabetes was reported. Accelerated fibrotic nephropathies were observed in hyperglycaemic mice with up‐regulated ALPK1. The aim of this study was to identify the mediators contributing to ALPK1 effect involving in nephropathies induction. The haematoxylin and eosin staining, Masson's trichrome and immunohistochemical analysis of ALPK1, NFkB, CCL2 and CCL5 were performed in the mice kidney. Cytokine antibody array analysis was performed in streptozotocin‐treated wild‐type mice (WT‐STZ) and streptozotocin‐treated ALPK1 transgenic mice (TG‐STZ). The ALPK1 levels were measured in mice kidney and in cultured cells. We found that the higher levels of renal CCL2/MCP‐1, CCL5/Rantes and G‐CSF expression in TG‐STZ compared with the WT‐STZ. Glucose increased ALPK1 expressions in monocytic THP1 and human kidney‐2 cells. The protein expression of ALPK1, NFkB and lectin was up‐regulated in glucose‐treated HK‐2 cells. Knockdown of ALPK1 reduced CCL2 and CCL5 mRNA levels, whereas overexpressed ALPK1 increased CCL2 and CCL5 in cultured kidney cells. Taken together, these results show that high glucose increases ALPK1 and chemokine levels in the kidney. Elevated ALPK1 expression enhances renal CCL2 and CCL5 expressions in vivo and in vitro. ALPK1 is a mediator for CCL2 and CCL5 chemokine up‐regulation involving in diabetic nephropathies induction.
Mitofusin2, a rising star in acute‐on‐chronic liver failure, triggers macroautophagy via the mTOR signalling pathway
Authors: Xue Ran , Zhu Xuemin , Jia Lin , Wu Jing , Yang Jing , Zhu Yueke , Meng Qinghua 
Published: September 2019

AbstractAcute‐on‐chronic liver failure (ACLF) is a life‐threatening syndrome with poor prognosis. Several studies have begun to prove that mitochondria play a crucial role in liver failure. Mitofusin2 (Mfn2) plays a key role in maintaining the integrity of mitochondrial morphology and function. However, the role and underlying mechanisms of Mfn2 on cell autophagy of ACLF remain unclear. Our aim was to explore the effect of Mfn2 on several biological functions involving cell autophagy in ACLF. In this study, we constructed an ACLF animal model and a hepatocyte autophagy model, using adenovirus and lentivirus to deliver Mfn2 to liver cells, in order to assess the effect of Mfn2 on autophagy and apoptosis in ACLF. Furthermore, we explored the biological mechanism of Mfn2‐induced autophagy of ACLF using Western blotting, RT‐PCR and electron microscopy. We found that Mfn2 significantly attenuated ACLF, characterized by ameliorated gross appearance and microscopic histopathology of liver, and reduced serum AST, ALT, and TBIL levels. Mfn2 improved the expressions of LC3‐II, Atg5 and Bcl‐2 and down‐regulated the expression of P62 and Bax in ACLF. Like rapamycin, Mfn2 also significantly inhibited the expressions of p‐PI3K, p‐Akt and p‐mTOR in ACLF. In conclusion, our findings suggest that Mfn2 influences multiple biological functions of ACLF via the PI3K/Akt/mTOR signalling pathway. This study will provide a reliable theoretical basis for the application of Mfn2 as an effective target for ACLF treatment, reversing or delaying the process of ACLF.
Down‐regulation of interferon regulatory factor 2 binding protein 2 suppresses gastric cancer progression by negatively regulating connective tissue growth factor
Authors: Yao Yangyang , Wang Yi , Li Li , Xiang Xiaojun , Li Junhe , Chen Jun , Liu Zhen , Huang Shanshan , Xiong Jianping , Deng Jun 
Published: September 2019

AbstractInterferon regulatory factor 2 binding protein 2 (IRF2BP2) is a transcriptional repressor involved in regulating gene expression and other biological processes, including tumorigenesis. However, the clinical significance and roles of IRF2BP2 in human gastric cancer (GC) remain uncertain. Clinical GC tissues were obtained from GC patients at the First Affiliated Hospital of Nanchang University. Immunohistochemistry (IHC) was conducted to detect the IRF2BP2 protein in clinical paraffin specimens. Cell proliferation, migration and invasion were evaluated by MTT, colony formation assays and transwell assays. Co‐immunoprecipitation was conducted to detect the interaction between TEA domain family members 4 (TEAD4) and vestigial‐like family member 4 (VGLL4) or Yes‐associated protein 1 (YAP1). Dual‐luciferase reporter assay was used to confirm the binding of miR‐101‐3p to the 3′‐UTR. The expression of IRF2BP2 was significantly higher in GC tissues than in normal tissues. Patients with higher IRF2BP2 protein expression had lower survival. IRF2BP2 knockdown inhibited proliferation, migration, invasion and epithelial‐mesenchymal transition in GC cells. IRF2BP2 knockdown decreased the mRNA and protein levels of connective tissue growth factor (CTGF). The interaction between IRF2BP2 and VGLL4 increased the binding of TEAD4 to YAP1, resulting in the transcriptional coactivation of CTGF. In addition, miR‐101‐3p suppressed the expression of CTGF by directly targeting the 3′‐UTR of IRF2BP2. Taken together, these findings provide a model for the role of miR‐101‐3p‐IRF2BP2‐CTGF signalling axis in GC and a novel insight into the mechanism of GC progression and metastasis.