bluuebunny/crossref_metadata_2025_split huggingface dataset:
Employment of U‐Shape Technique at Reentry Surgery for Papillae Coronal Migration on the Rehabilitation of Anterior Single Implant: 3‐Year Follow‐Up Case Report
Authors: S. Brum Renata , Galarraga Maria Elisa , Magrin Gabriel , Ruales‐Carrera Edwin , Escobar‐Ramos Mario , Rodriguez‐Ivich Jair , Cardoso Antônio Carlos , Volpato Claudia 
Published: May 2020

IntroductionThe rehabilitation of a maxillary single dental implant represents a great challenge at clinical practice. Harmony among the implant‐supported crown and adjacent teeth is required in which concerns pink and white esthetics. The aim of the present case report is to depict a multidisciplinary treatment in which the U‐shape flap technique for papillae preservation at second stage surgery was used.Case PresentationOne female patient presenting an un‐rehabilitated dental implant at the left central incisor position sought treatment at the Centre of Education and Research on Dental Implants (CEPID). Alterations of color, shape, and position were observed on the anterior maxillary teeth. For proper treatment planning, radiograph, wax‐up, and mock‐up were performed. Second stage surgery was performed by the U‐shape flap technique. A trunnion abutment was installed at the implant and a provisional subcontoured cemented crown was manufactured. Dental bleaching, feldspathic veneers, and a ceramic crown were performed. Oral hygiene instructions were recommended. Follow‐up appointments were set at 1.5 and 3 years after restoration placement. After 3‐year follow‐up, soft tissue stability and health were preserved and papillae coronal migration around the single dental implant was observed. A complication‐free treatment was reached, and patient demonstrated satisfaction towards esthetic and function.ConclusionsThe use of U‐shape technique at second stage surgery associated to adequate prosthetic contour improved soft tissue esthetic outcomes, while the multidisciplinary treatment planning provided adequate solutions, refining harmony between dental and implant‐supported components.
STAT1 determines aggressiveness of glioblastoma both in vivo and in vitro through wnt/β‐catenin signalling pathway
Authors: Zhao Li , Li Xiangquan , Su Jing , Wang Gong Fenfei , Lu Junjie , Wei Yuzhen 
Published: May 2020

Glioblastoma is one of the most malignant tumors and causes the high mortality in cancer patients. Currently, there is no highly efficient therapy against glioblastoma. Therefore, searching for a new molecular target to anti‐glioblastoma therapy is urgent and necessary. In this study, we elucidated the role of Signal transducer and activator of transcription 1 (STAT1) in proliferation, migration and apoptosis of glioblastoma cells. We found that STAT1 downregulation could weaken the aggressiveness of glioblastoma cells. Besides, the glioblastoma growth in vivo was also inhibited with the STAT1 downregulation by shRNA as well as by pharmacological stimulation withSTAT1inhibitors. This negative regulation of tumor growth was accompanied by the inhibition in epithelial‐mesenchymal transition (EMT), whereas the STAT1 overexpression promoted EMT. Furthermore, the involvement of wnt/β‐catenin was observed in STAT1 downregulation mediated weakness in glioblastoma aggressiveness since application of activator wnt agonist 1 could counteract the inhibitory effect induced by STAT1 downregulation. Collectively, this work provided the evidence to support the conclusion that STAT1 can regulate the glioblastoma growth and migration, potentially serving as a therapeutic target against glioblastoma.Significance of the studyGlioblastoma is one of the most malignant tumors with very high mortality. Until now, there is no efficient therapy against glioblastoma. In this study, we found downregulation of Signal transducer and activator of transcription 1 (STAT1) could weaken the aggressiveness of glioblastoma cells through inhibition in epithelial‐mesenchymal transition, mediated through wnt/β‐catenin signalling pathway. Thus, this work supported the regulatory role of STAT1 in glioblastoma growth and migration. This potentially serves as a new therapeutic target against glioblastoma.
Study of the effect of operative conditions on the decolourization of azo dye solutions by using hydrodynamic cavitation at the lab scale
Authors: Innocenzi Valentina , Prisciandaro Marina , Vegliò Francesco 
Published: May 2020

AbstractIn the present study, the potentiality of hydrodynamic cavitation (HC) for the degradation of methyl orange from synthetic aqueous solutions is presented. Hydrodynamic cavitation was set up at laboratory scale using a Venturi tube. Solutions of methyl orange (MO) were subjected to cavitation in order to investigate the efficiency and the potential of this technique for azo dye degradation. Moreover, a HC/H2O2/TiO2 hybrid system was tested with the aim to verify its potential positive impact on the decolourization process and define the best conditions, among those investigated, to remove azo dye from synthetic solutions. The results obtained in this study showed that the maximum efficiency was close to 30% using a Venturi tube at an operating pressure of 400 kPa. The presence of additives, such as titanium dioxide and hydrogen peroxide, increased the performance of the degradation process to slightly above 70%.
Pax9's dual roles in modulating Wnt signaling during murine palatogenesis
Authors: Jia Shihai , Zhou Jing , D'Souza Rena N. 
Published: May 2020

AbstractBackgroundDespite the strides made in understanding the complex network of key regulatory genes and cellular processes that drive palate morphogenesis, patients suffering from these conditions face treatment options that are limited to complex surgeries and multidisciplinary care throughout life. Hence, a better understanding of how molecular interactions drive palatal growth and fusion is critical for the development of treatment and preventive strategies for cleft palates in humans. Our previous work demonstrated that Pax9‐dependent Wnt signaling is critical for the growth and fusion of palatal shelves. We showed that controlled intravenous delivery of small molecule Wnt agonists specifically blocks the action of Dkks (inhibitors of Wnt signaling) and corrects secondary palatal clefts in Pax9−/− mice. While these data underscore the importance of the functional upstream relationship of Pax9 to the Wnt pathway, not much is known about how the genetic nature of Pax9's interactions in vivo and how it modulates the actions of these downstream effectors during palate formation.ResultsHere, we show that the genetic reduction of Dkk1 during palatogenesis corrected secondary palatal clefts in Pax9−/− mice with restoration of Wnt signaling activities. In contrast, genetically induced overexpression of Dkk1 mice phenocopied the defects in tooth and palate development visible in Pax9−/− strains. Results of ChIP‐qPCR assays showed that Pax9 can bind to regions near the transcription start sites of Dkk1 and Dkk2 as well as the intergenic region of Wnt9b and Wnt3 ligands that are downregulated in Pax9−/− palates.ConclusionsTaken together, these data suggest that the molecular mechanisms underlying Pax9's role in modulating Wnt signaling activity likely involve the inhibition of Dkk expression and the control of Wnt ligands during palatogenesis.
FGF signaling is required for chemokinesis and ventral migration of trunk neural crest cells
Authors: Dunkel Haley , Chaverra Martha , Bradley Roger , Lefcort Frances 
Published: May 2020

AbstractBackgroundNeural crest cells (NCCs) delaminate from the neural tube (NT) and migrate ventrally to generate the trunk peripheral nervous system (PNS). Although several signaling pathways have been identified that steer NCCs once they are on their ventral trajectory, no molecules have been identified that are required for the initial migration between the NT and the dorsal root ganglion. Given the critical role of fibroblast growth factor (FGF) signaling in embryogenesis, we investigated its function in this initial migration.ResultsFGFR1 signaling is required for the migration of newly delaminated NCCs onto the ventral pathway. Live imaging of migrating NCCs revealed that inhibition of FGFR1 signaling caused the dorsally stalled NCCs to lose their dorsal/ventral oriented polarity and instead adopt a rounded morphology while dynamically extending filopodia. FGF8, an FGFR1 ligand, increased motility of NCCs away from the NT by acting chemokinetically. Finally, we provide evidence that inhibition of FGFR1‐mediated chemokinesis is partially rescued by increasing Akt signaling, inhibiting RhoA, and activation of N‐cadherin signaling.ConclusionThese data support a model in which NCCs are stimulated chemokinetically by FGF:FGFR1 signaling, and that this activation positions and orients NCCs on their ventral migratory route—a process that is essential for patterning the trunk PNS.
A High Capacity and Working Voltage Potassium‐Based Dual Ion Batteries
Authors: Zhang Meng , Zhong Jiang , Kong Weiqing , Wang Lei , Wang Tao , Fei Huilong , Luo Haiyan , Zhu Jian , Hu Jiawen , Lu Bingan 
Published: May 2020

Potassium‐based dual ion batteries (KDIBs) have attracted significant attention owing to high working voltage, high safety, low processing cost, and environmental friendliness. Nevertheless, one great challenge for practical KDIBs is to develop suitable anode materials with high specific capacity. Herein, we report an architecture of hierarchically porous antimony nanoparticles/carbon nanofibers (HPSbCNFs) as flexible, free‐standing anode for high‐performance KDIBs. The HPSbCNFs with hierarchically porous structure, and high‐content nitrogen doping, not only offer sufficient free space to tolerate the repetitive volume expansion of Sb nanoparticles during long‐term cycling, but also greatly facilitate the transport of electrons and ions within electrode, ensuring high material utilization ratio. Thus, the KDIBs, constituted by HPSbCNFs‐700 (calcined at 700 °C) anode and graphite cathode, exhibited a high reversible capacity of 440 mAh g−1with high discharge medium voltage of 4.5 V at a specific current of 200 mA g−1(the highest capacity for all KDIBs normalized by the mass of the anode), and excellent cyclic life. Outstanding electrochemical reversibility of the KDIBs was further demonstrated byex situXRD,ex situRaman spectrum, and HRTEM. These results suggest the as‐designed HPSbCNFs‐700 with high‐capacity and long‐term cycling stability is a promising anode material for high‐performance KDIBs.
Improving exercise capacity and quality of life using non‐invasive heart failure treatments: evidence from clinical trials
Authors: von Haehling Stephan , Arzt Michael , Doehner Wolfram , Edelmann Frank , Evertz Ruben , Ebner Nicole , Herrmann‐Lingen Christoph , Garfias Macedo Tania , Koziolek Michael , Noutsias Michel , Schulze P. Christian , Wachter Rolf , Hasenfuß Gerd , Laufs Ulrich 
Published: May 2020

AbstractEndpoints of large‐scale trials in chronic heart failure have mostly been defined to evaluate treatments with regard to hospitalizations and mortality. However, patients with heart failure are also affected by very severe reductions in exercise capacity and quality of life. We aimed to evaluate the effects of heart failure treatments on these endpoints using available evidence from randomized trials. Interventions with evidence for improvements in exercise capacity include physical exercise, intravenous iron supplementation in patients with iron deficiency, and – with less certainty – testosterone in highly selected patients. Erythropoiesis‐stimulating agents have been reported to improve exercise capacity in anaemic patients with heart failure. Sinus rhythm may have some advantage when compared with atrial fibrillation, particularly in patients undergoing pulmonary vein isolation. Studies assessing treatments for heart failure co‐morbidities such as sleep‐disordered breathing, diabetes mellitus, chronic kidney disease and depression have reported improvements of exercise capacity and quality of life; however, the available data are limited and not always consistent. The available evidence for positive effects of pharmacologic interventions using angiotensin‐converting enzyme inhibitors, angiotensin receptor blockers, beta‐blockers, and mineralocorticoid receptor antagonists on exercise capacity and quality of life is limited. Studies with ivabradine and with sacubitril/valsartan suggest beneficial effects at improving quality of life; however, the evidence base is limited in particular for exercise capacity. The data for heart failure with preserved ejection fraction are even less positive, only sacubitril/valsartan and spironolactone have shown some effectiveness at improving quality of life. In conclusion, the evidence for state‐of‐the‐art heart failure treatments with regard to exercise capacity and quality of life is limited and appears not robust enough to permit recommendations for heart failure. The treatment of co‐morbidities may be important for these patient‐related outcomes. Additional studies on functional capacity and quality of life in heart failure are required.
Murine iNKT cells are depleted by liver damage via activation of P2RX7
Authors: Bovens Astrid A. , Wesselink Thomas H. , Behr Felix M. , Kragten Natasja A. M. , van Lier René A. W. , van Gisbergen Klaas P. J. M. , Stark Regina 
Published: May 2020

AbstractInvariant natural killer T cells (iNKT) constitute up to 50% of liver lymphocytes and contribute to immunosurveillance as well as pathogenesis of the liver. Systemic activation of iNKT cells induces acute immune‐mediated liver injury. However, how tissue damage events regulate iNKT cell function and homeostasis remains unclear. We found that specifically tissue‐resident iNKT cells in liver and spleen express the tissue‐damage receptor P2RX7 and the P2RX7‐activating ectoenzyme ARTC2. P2RX7 expression restricted formation of iNKT cells in the liver suggesting that liver iNKT cells are actively restrained under homeostatic conditions. Deliberate activation of P2RX7 in vivo by exogenous NAD resulted in a nearly complete iNKT cell ablation in liver and spleen in a P2RX7‐dependent manner. Tissue damage generated by acetaminophen‐induced liver injury reduced the number of iNKT cells in the liver. The tissue‐damage‐induced iNKT cell depletion was driven by P2RX7 and localized to the site of injury, as iNKT cells in the spleen remained intact. The depleted liver iNKT cells reconstituted only slowly compared to other lymphocytes such as regulatory T cells. These findings suggest that tissue‐damage‐mediated depletion of iNKT cells acts as a feedback mechanism to limit iNKT cell‐induced pathology resulting in the establishment of a tolerogenic environment.
What can we learn from the return predictability over the business cycle?
Authors: Liu Li , Pan Zhiyuan , Wang Yudong 
Published: May 2020

AbstractIn this paper, we forecast stock returns using time‐varying parameter (TVP) models with parameters driven by economic conditions. An in‐sample specification test shows significant variation in the parameters. Out‐of‐sample results suggest that the TVP models outperform their constant coefficient counterparts. We also find significant return predictability from both statistical and economic perspectives with the application of TVP models. The out‐of‐sampleR2of an equal‐weighted combination of TVP models is as high as 2.672%, and the gains in the certainty equivalent return are 214.7 basis points. Further analysis indicates that the improvement in predictability comes from the use of information on economic conditions rather than simply from allowing the coefficients to vary with time.
Variability in retinoblastoma genome stability is driven by age and not heritability
Authors: Polski Ashley , Xu Liya , Prabakar Rishvanth K. , Gai Xiaowu , Kim Jonathan W. , Shah Rachana , Jubran Rima , Kuhn Peter , Cobrinik David , Hicks James , Berry Jesse L. 
Published: May 2020

AbstractRetinoblastoma (RB) is a childhood intraocular cancer initiated by biallelic inactivation of the RB tumor suppressor gene (RB1−/−). RB can be hereditary (germline RB1 pathogenic allele is present) or non‐hereditary. Somatic copy number alterations (SCNAs) contribute to subsequent tumorigenesis. Previous studies of only enucleated RB eyes have reported associations between heritability status and the prevalence of SCNAs. Herein, we use an aqueous humor (AH) liquid biopsy to investigate RB genomic profiles in the context of germline RB1 status, age, and International Intraocular Retinoblastoma Classification (IIRC) clinical grouping for both enucleated and salvaged eyes. Between 2014 and 2019, AH was sampled from a total of 54 eyes of 50 patients. Germline RB1 status was determined from clinical blood testing, and cell‐free DNA from AH was analyzed for SCNAs. Of the 50 patients, 23 (46.0%; 27 eyes) had hereditary RB, and 27 (54.0%, 27 eyes) had non‐hereditary RB. Median age at diagnosis was comparable between hereditary (13 ± 10 months) and non‐hereditary (13 ± 8 months) eyes (P = 0.818). There was no significant difference in the prevalence or number of SCNAs based on (1) hereditary status (P > 0.56) or (2) IIRC grouping (P > 0.47). There was, however, a significant correlation between patient age at diagnosis, and (1) number of total SCNAs (r[52] = 0.672, P < 0.00001) and (2) number of highly‐recurrent RB SCNAs (r[52] = 0.616, P < 0.00001). This evidence does not support the theory that specific molecular or genomic subtypes exist between hereditary and non‐hereditary RB; rather, the prevalence of genomic alterations in RB eyes is strongly related to patient age at diagnosis.
Gamma‐glutamyl transferase variability and risk of dementia: A nationwide study
Authors: Lee You‐Bin , Han Kyungdo , Park Sanghyun , Kim Seon Mee , Kim Nan Hee , Choi Kyung Mook , Baik Sei Hyun , Park Yong Gyu , Yoo Hye Jin 
Published: May 2020

ObjectivesVariability in various biomarkers has emerged as a new clinical indicator for diseases including neurodegenerative disorders. Gamma‐glutamyl transferase (GGT) has a potential to be involved in the pathogenesis of dementia due to its function as a marker of oxidative stress and atherosclerosis. We investigated the association between baseline GGT, GGT variability, and dementia risk for the first time in a large population.MethodsThe Korean National Health Insurance Service datasets of claims and preventive health check‐ups from 2004 to 2016 were used for this retrospective longitudinal study. The risk of incident dementia (all‐cause dementia, Alzheimer's disease, and vascular dementia) was analyzed according to sex‐specific quartiles of baseline GGT and GGT variability, and groups categorized by baseline GGT and GGT variability in ≥40‐year‐old individuals without baseline dementia (N = 6 046 442; mean follow‐up 6.32 years).ResultsDuring follow‐up, 166 851 cases of new dementia developed. The fully adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for incident dementia increased in the higher quartiles of baseline GGT and GGT variability (HR [95% CI]: Q2, 1.034 [1.019‐1.049]; Q3, 1.090 [1.075‐1.105]; Q4, 1.212 [1.196‐1.229]). The association between GGT variability quartiles and dementia risk remained significant even after adjusting for log‐transformed baseline GGT level. The fully adjusted HRs for dementia was highest in the group with high baseline GGT concentration and the highest GGT variability quartile [HR (95% CI): 1.273 (1.250‐1.296)].ConclusionsNot only baseline GGT level, but also GGT variability may be an independent predictor of dementia, and might be used for risk stratification for future dementia.
Association of prediagnostic vitamin D status with mortality among colorectal cancer patients differs by common, inherited vitamin D‐binding protein isoforms
Authors: Gibbs David Corley , Bostick Roberd M. , McCullough Marjorie L. , Um Caroline Y. , Flanders W. Dana , Jenab Mazda , Weiderpass Elisabete , Gylling Björn , Gram Inger T. , Heath Alicia K. , Colorado‐Yohar Sandra , Dahm Christina C. , Bueno‐de‐Mesquita Bas , Perez‐Cornago Aurora , Trichopoulou Antonia , Tumino Rosario , Kühn Tilman , Fedirko Veronika 
Published: May 2020

AbstractLower prediagnostic circulating 25‐hydroxyvitamin D (25[OH]D)—considered the best marker of total vitamin D exposure—is associated with higher mortality risk among colorectal cancer (CRC) patients. However, it is unknown whether this association differs by the vitamin D‐binding protein (GC) isoform Gc2 (encoded by GC rs4588*C>A, Thr436Lys), which may substantially affect vitamin D metabolism and modify associations of 25(OH)D with colorectal neoplasm risk. Prediagnostic 25(OH)D‐mortality associations according to Gc2 isoform were estimated using multivariable Cox proportional hazards regression among 1281 CRC cases (635 deaths, 483 from CRC) from two large prospective cohorts conducted in the United States (Cancer Prevention Study‐II) and Europe (European Prospective Investigation into Cancer and Nutrition). 25(OH)D measurements were calibrated to a single assay, season standardized, and categorized using Institute of Medicine recommendations (deficient [<30], insufficient [30 ‐ <50], sufficient [≥50 nmol/L]). In the pooled analysis, multivariable‐adjusted hazard ratios (HRs) for CRC‐specific mortality associated with deficient relative to sufficient 25(OH)D concentrations were 2.24 (95% CI 1.44‐3.49) among cases with the Gc2 isoform, and 0.94 (95% CI 0.68‐1.22) among cases without Gc2 (Pinteraction = .0002). The corresponding HRs for all‐cause mortality were 1.80 (95% CI 1.24‐2.60) among those with Gc2, and 1.12 (95% CI 0.84‐1.51) among those without Gc2 (Pinteraction = .004). Our findings suggest that the association of prediagnostic vitamin D status with mortality among CRC patients may differ by functional GC isoforms, and patients who inherit the Gc2 isoform (GC rs4588*A) may particularly benefit from higher circulating 25(OH)D for improved CRC prognosis.
Imperatorin and β-sitosterol have synergistic activities in alleviating collagen-induced arthritis
Authors: Guo Qingqing , Li Li , Zheng Kang , Zheng Guang , Shu Haiyang , Shi Yingjie , Lu Cheng , Shu Jun , Guan Daogang , Lu Aiping , He Xiaojuan 
Published: May 2020

Abstract
Rheumatoid arthritis (RA) is a chronic disease with complex molecular network of pathophysiology, single drug is usually not full satisfactory because it is almost impossible to target the whole molecular network of the disease. Drug combinations that act synergistically with each another is an effective strategy in RA therapy. In this study, we aimed to establish a new strategy to search effective synergized compounds from Chinese herbal medicine (CHM) used in RA. Based on multi-information integrative approaches, imperatorin (IMP) and β-sitosterol (STO) were predicted as the most effective pair for RA therapy. Further animal experiments demonstrated that IMP+STO treatment ameliorated arthritis severity of collagen-induced arthritis (CIA) rats in a synergistic manner, whereas IMP or STO administration separately had no such effect. RNA sequencing and IPA analysis revealed that the synergistic mechanism of IMP+STO treatment was related to its regulatory effect on 5 canonical signaling pathways, which were not found when IMP or STO used alone. Moreover, LTA, CD83, and SREBF1 were 3 important targets for synergistic mechanism of IMP+STO treatment. The levels of these 3 genes were significantly up-regulated in IMP+STO group compared to model group, whereas IMP or STO administration separately had no effect on them. In conclusion, this study found that IMP and STO were 2 synergistic compounds from the CHM in RA therapy, whose synergistic mechanism was closely related to regulate the levels of LTA, CD83, and SREBF1.