bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of learning style and general self-efficacy on satisfaction of e-Learning in dental students
Authors: Baherimoghadam Tahereh , Hamedani Shahram , mehrabi Manoosh , Naseri Navid , Marzban Nooshin 
Published: August 2021

Abstract
Introduction
The COVID-19 pandemic has had a significant impact on education. e-Learning has been becoming most popular. Satisfaction of the student is one of important goal of e-Learning, therefore factors affecting this satisfaction should be considered extensively. This study aims to evaluate the effect of learning style and General Self-Efficacy (GSE) on satisfaction of e-Learning in dental student.

Method
Electronic questionnaires were sent to 85 fifth and sixth-year students who had passed the face-to-face orthodontics course in the previous semester and were studying online orthodontics at the time of this study. Three questionnaires were used including Soloman and Felder learning styles index, General self-efficacy questionnaire and Satisfaction questionnaire for online education.

Results
The results of the reliability test showed that Cronbach’s alpha index for the self-efficacy and satisfaction questionnaire was 0.836 and 0.96, respectively. The correlation between satisfaction and the dimensions of learning style showed that the active dimension of processing information had a significant relationship with the level of satisfaction. In the understanding dimension, a relatively strong correlation was observed in the Global dimension. Moderate significant relationship between the total score of self-efficacy and the level of satisfaction has been found.

Conclusion
The results of the present study highlight the necessity of more studies regarding defining effective on student satisfaction during e-Learning. GSES and active learning style in the processing dimension and global learning style in the understanding dimension affect students' satisfaction.
Exploring the experiences of nurses’ moral distress in long-term care of older adults: a phenomenological study
Authors: Nikbakht Nasrabadi Alireza , Wibisono Ahmad Hasyim , Allen Kelly-Ann , Yaghoobzadeh Ameneh , Bit-Lian Yee 
Published: August 2021

Abstract
Background
Moral distress is a poorly defined and frequently misunderstood phenomenon, and little is known about its triggering factors during ICU end-of-life decisions for nurses in Iran. This study aimed to explore the experiences of nurses’ moral distress in the long-term care of older adults via a phenomenological study.

Methods
A qualitative, phenomenological study was conducted with 9 participants using in-depth semi-structured interviews. The purpose was to gain insight into the lived experiences and perceptions of moral distress among ICU nurses in hospitals affiliated with Tehran University of Medical Sciences during their long-term care of older adults.

Results
Five major themes are identified from the interviews: advocating, defense mechanisms, burden of care, relationships, and organizational issues. In addition, several subthemes emerged including respectful end of life care, symptom management, coping, spirituality, futile care, emotional work, powerlessness, relationships between patients and families, relationships with healthcare teams, relationships with institutions, inadequate staffing, inadequate training, preparedness, education/mentoring, workload, and support.

Conclusions
This qualitative study contributes to the limited knowledge and understanding of the challenges nurses face in the ICU. It also offers possible implications for implementing supportive interventions.
Asymmetric expansions of FT and TFL1 lineages characterize differential evolution of the EuPEBP family in the major angiosperm lineages
Authors: Bennett Tom , Dixon Laura E. 
Published: August 2021

Abstract
Background
In flowering plants, precise timing of the floral transition is crucial to maximize chances of reproductive success, and as such, this process has been intensively studied. FLOWERING LOCUS T (FT) and TERMINAL FLOWER1 (TFL1) have been identified as closely related eukaryotic phosphatidylethanolamine-binding proteins (‘EuPEBPs’) that integrate multiple environmental stimuli, and act antagonistically to determine the optimal timing of the floral transition. Extensive research has demonstrated that FT acts similar to hormonal signals, being transported in the phloem from its primary site of expression in leaves to its primary site of action in the shoot meristem; TFL1 also appears to act as a mobile signal. Recent work implicates FT, TFL1, and the other members of the EuPEBP family, in the control of other important processes, suggesting that the EuPEBP family may be key general regulators of developmental transitions in flowering plants. In eudicots, there are a small number of EuPEBP proteins, but in monocots, and particularly grasses, there has been a large, but uncharacterized expansion of EuPEBP copy number, with unknown consequences for the EuPEBP function.

Results
To systematically characterize the evolution of EuPEBP proteins in flowering plants, and in land plants more generally, we performed a high-resolution phylogenetic analysis of 701 PEBP sequences from 208 species. We refine previous models of EuPEBP evolution in early land plants, demonstrating the algal origin of the family, and pin-pointing the origin of the FT/TFL1 clade at the base of monilophytes. We demonstrate how a core set of genes (MFT1, MFT2, FT, and TCB) at the base of flowering plants has undergone differential evolution in the major angiosperm lineages. This includes the radical expansion of the FT family in monocots into 5 core lineages, further re-duplicated in the grass family to 12 conserved clades.

Conclusions
We show that many grass FT proteins are strongly divergent from other FTs and are likely neo-functional regulators of development. Our analysis shows that monocots and eudicots have strongly divergent patterns of EuPEBP evolution.
Multiple malignant tumors in a patient with familial chordoma, a case report
Authors: Sumransub Nuttavut , Murugan Paari , Marette Shelly , Clohisy Denis R. , Skubitz Keith M. 
Published: August 2021

Abstract
Background
Chordoma is a rare bone tumor that is typically resistant to chemotherapy and is associated with genetic abnormalities of the T-box transcription factor T (TBXT) gene, which encodes the transcription factor brachyury. Brachyury is felt to be a major contributor to the development of chordomas.

Case presentation
We describe a 67-year-old woman who developed an undifferentiated pleomorphic sarcoma in her thigh. Despite treatment with standard chemotherapy regimens, she had a rapidly progressive course of disease with pulmonary metastases and passed away 8 months from diagnosis with pulmonary complications. Her medical history was remarkable in that she had a spheno-occipital chordoma at age 39 and later developed multiple other tumors throughout her life including Hodgkin lymphoma and squamous cell carcinoma and basal cell carcinoma of the skin. She had a family history of chordoma and her family underwent extensive genetic study in the past and were found to have a duplication of the TBXT gene.

Conclusions
Brachyury has been found to associate with tumor progression, treatment resistance, and metastasis in various epithelial cancers, and it might play roles in tumorigenesis and aggressiveness in this patient with multiple rare tumors and germ line duplication of the TBXT gene. Targeting this molecule may be useful for some malignancies.
The oncogenic role of HIF-1α/miR-182-5p/ZFP36L1 signaling pathway in nasopharyngeal carcinoma
Authors: Wang Gang , Zhou Fangzheng , Ou Tong , Sun Haiyan , Shan Zhirui , Lu Yingshen , Chen Gui , Yuan Simin , Zhang Xiaowen , Wu Song 
Published: August 2021

Abstract
Background
Accumulating evidence indicates that dysregulation of miR-182-5p can serve as diagnostic and prognostic biomarkers for some cancers, whereas the role of miR-182-5p has not been explored in nasopharyngeal carcinoma (NPC). Our study aims to elucidate the biological function of miR-182-5p in NPC and the potential molecular mechanism involved.

Methods
Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine miR-182-5p expression in NPC primary tissues and cell lines. Immunohistochemistry (IHC) for ZFP36L1 was conducted in NPC samples. Western blot was used to evaluate protein expression in cell lines. A series of functional assays were carried out to evaluate the roles of miR-182-5p and ZFP36L1 in tumor development and progression of NPC. Bioinformatics tools and luciferase reporter assays were utilized to identify the potential mechanisms of action. Moreover, rescue experiments were applied to explore whether ZFP36L1 mediated the effects of miR-182-5p in NPC.

Results
Up-regulation of miR-182-5p was significantly associated with tumor development and poor prognosis in patients with NPC. Functional study demonstrated that miR-182-5p overexpression enhanced, whereas suppression of miR-182-5p impeded NPC cell proliferation, migration, tumorigenesis and metastasis. Mechanistically, miR-182-5p interacted with ZFP36L1 at two sites in its 3′ un-translated region (UTR) and repressed ZFP36L1 expression in NPC. Consistently, an inverse correlation was observed between the expression levels of miR-182-5p and ZFP36L1 using clinical NPC tissues, and down-regulation of ZFP36L1 in NPC predicts poor survival. Furthermore, overexpression of miR-182-5p in NPC was partly attributable to the transcriptional activation effect induced by hypoxia-inducible factor 1α (HIF-1α).

Conclusions
Our data suggests that miR-182-5p facilitates cell proliferation and migration in NPC through its ability to down-regulate ZFP36L1 expression, and that the HIF-1α/miR-182-5p/ZFP36L1 axis may serve as a novel therapeutic target in the management of NPC.
Effect of a single dose of oral azithromycin on malaria parasitaemia in children: a randomized controlled trial
Authors: Coulibaly Boubacar , Sié Ali , Dah Clarisse , Bountogo Mamadou , Ouattara Mamadou , Compaoré Adama , Nikiema Moustapha , Tiansi Jérôme Nankoné , Sibiri Nestor Dembélé , Brogdon Jessica M. , Lebas Elodie , Doan Thuy , Porco Travis C. , Lietman Thomas M. , Oldenburg Catherine E. 
Published: August 2021

Abstract
Background
Azithromycin has recently been shown to reduce all-cause childhood mortality in sub-Saharan Africa. One potential mechanism of this effect is via the anti-malarial effect of azithromycin, which may help treat or prevent malaria infection. This study evaluated short- and longer-term effects of azithromycin on malaria outcomes in children.

Methods
Children aged 8 days to 59 months were randomized in a 1:1 fashion to a single oral dose of azithromycin (20 mg/kg) or matching placebo. Children were evaluated for malaria via thin and thick smear and rapid diagnostic test (for those with tympanic temperature ≥ 37.5 °C) at baseline and 14 days and 6 months after treatment. Malaria outcomes in children receiving azithromycin versus placebo were compared at each follow-up timepoint separately.

Results
Of 450 children enrolled, 230 were randomized to azithromycin and 220 to placebo. Children were a median of 26 months and 51% were female, and 17% were positive for malaria parasitaemia at baseline. There was no evidence of a difference in malaria parasitaemia at 14 days or 6 months after treatment. In the azithromycin arm, 20% of children were positive for parasitaemia at 14 days compared to 17% in the placebo arm (P = 0.43) and 7.6% vs. 5.6% in the azithromycin compared to placebo arms at 6 months (P = 0.47).

Conclusions
Azithromycin did not affect malaria outcomes in this study, possibly due to the individually randomized nature of the trial.
Trial registration This study is registered at clinicaltrials.gov (NCT03676751; registered 19 September 2018).
Hypoxia-inducible transcription factor-1α inhibition by topotecan protects against lipopolysaccharide-induced inflammation and apoptosis of cardiomyocytes
Authors: Zhang Ying , Xu Yi , Zhou Ke , Kao Guoying , Yan Meng , Xiao Jun 
Published: August 2021

Abstract
Background
Myocarditis, an inflammatory disease of the myocardium, is a serious hazard to human life due to the expansion of inflammatory lesions in the myocardium. The aim of this study was to investigate the role of hypoxia-inducible transcription factor (HIF)-1α and its inhibitor topotecan in the pathogenesis of myocarditis.

Methods
H9c2 cardiomyoblasts was stimulated with lipopolysaccharide (LPS) to simulate myocarditis model in vitro. The levels of myocardial damage markers were determined using commercially available kits. Western blotting was used to evaluate HIF-1α expression after LPS challenge. Then, after HIF-1α silencing, the contents of inflammatory factors were determined with enzyme-linked immunosorbent assay (ELISA). Cell viability was tested by means of a cell counting kit-8 (CCK-8) assay. Cell apoptosis was assessed by flow cytometry, and the expression of apoptotic proteins was examined using western blot analysis. Subsequently, HIF-1α was overexpressed and topotecan was employed to treat H9c2 cells under LPS exposure condition. The biological functions were detected again.

Results
LPS significantly elevated the levels of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB) and cardiac troponin-I (cTn-I) in supernatant of H9c2 cell lysates. Additionally, LPS led to the notably upregulated expression of HIF-1α. HIF-1α-knockdown markedly decreased the concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 compared with the LPS-induced group. Moreover, the cell viability was conspicuously enhanced and cell apoptotic ratio was remarkably reduced, accompanied by downregulated expression of Bax, Bim, caspase 3 and caspase 9 after HIF-1α silencing. Consistently, HIF-1α gain-of-function significantly promoted the production of inflammatory cytokines and cell apoptosis, which was partially counteracted by topotecan administration.

Conclusion
To conclude, these findings demonstrated that HIF-1α inhibition by topotecan ameliorates LPS-induced myocarditis in vitro, providing a new approach in the treatment of myocarditis.
Blau syndrome: a case report from Palestine
Authors: Iriqat Salam , Safieh Mohammed Abu , Fatouleh Manuel , Alkaiyat Abdulsalam 
Published: August 2021

Abstract
Background
This case study documents the first familial case of Blau syndrome (BS) in Palestine characterized with mutation in CARD15/NOD2.

Case presentation
Eighteen years old female was initially misdiagnosed with Juvenile idiopathic arthritis (JIA). The patient had been on steroids and methotrexate treatment for the last 16 years, but did not respond well to treatment. Initial examination at Saint John of Jerusalem Eye Hospital Group clinic showed bilateral intermediate uveitis with camptodactyly. The patient’s sister (aged 19 years) had bilateral intermediate uveitis and camptodactyly. Both eyes of their father had signs of old posterior uveitis. Father’s left eye showed 360 degrees posterior synechia, mature cataract with old Keratic precipitates (KPs). He also had camptodactyly. The patient was referred to pediatric rheumatologist to rule out sarcoidosis.
Lung CT scan showed bronchiectasis, genetic consultation followed. Complete eye examination, full history, refraction, and Optical coherence tomography (oct) were done. Systemic and topical steroid therapy could not control the ocular inflammation. The family then was referred to a geneticist. Genetic analyses showed that the proband and all three family members had an R334q mutation in the CARD15/Nod2 gene.

Conclusions
BS should be considered in the differential diagnosis of childhood uveitis, especially in low and middle income countries where it is misdiagnosed in many cases, which delay appropriate diagnosis and thus control. Genetic analysis of the CARD15/Nod2 gene is helpful in the diagnosis. Steroids alone are not enough to control the disease, other immunosuppressants and biologics are needed.
Hippocampal glucose uptake as a surrogate of metabolic change of microglia in Alzheimer’s disease
Authors: Choi Hongyoon , Choi Yoori , Lee Eun Ji , Kim Hyun , Lee Youngsun , Kwon Seokjun , Hwang Do Won , Lee Dong Soo ,   for the Alzheimer’s Disease Neuroimaging Initiative
Published: August 2021

Abstract

Background
Dynamically altered microglia play an important role in the progression of Alzheimer’s disease (AD). Here, we found a close association of the metabolic reconfiguration of microglia with increased hippocampal glucose uptake on [18F]fluorodeoxyglucose (FDG) PET.

Methods
We used an AD animal model, 5xFAD, to analyze hippocampal glucose metabolism using both animal FDG PET and ex vivo FDG uptake test. Cells of the hippocampus were isolated to perform single-cell RNA-sequencing (scRNA-seq). The molecular features of cells associated with glucose metabolism were analyzed at a single-cell level. In order to apply our findings to human brain imaging study, brain FDG PET data obtained from the Alzheimer’s Disease Neuroimaging Initiative were analyzed. FDG uptake in the hippocampus was compared according to the diagnosis, AD, mild cognitive impairment, and controls. The correlation analysis between hippocampal FDG uptake and soluble TREM2 in cerebrospinal fluid was performed.

Results
In the animal study, 8- and 12-month-old 5xFAD mice showed higher FDG uptake in the hippocampus than wild-type mice. Cellular FDG uptake tests showed that FDG activity in hippocampal microglia was increased in the AD model, while FDG activity in non-microglial cells of the hippocampus was not different between the AD model and wild-type. scRNA-seq data showed that changes in glucose metabolism signatures including glucose transporters, glycolysis and oxidative phosphorylation, mainly occurred in microglia. A subset of microglia with higher glucose transporters with defective glycolysis and oxidative phosphorylation was increased according to disease progression. In the human imaging study, we found a positive association between soluble TREM2 and hippocampal FDG uptake. FDG uptake in the hippocampus at the baseline scan predicted mild cognitive impairment conversion to AD.

Conclusions
We identified the reconfiguration of microglial glucose metabolism in the hippocampus of AD, which could be evaluated by FDG PET as a feasible surrogate imaging biomarker for microglia-mediated inflammation.
Electrocardiographic abnormalities in medically screened German military aircrew
Authors: Guettler Norbert , Sammito Stefan 
Published: August 2021

Abstract
Background
A resting electrocardiogram (ECG) is a well-tolerated, non-invasive, and inexpensive test for overt electrical signs of cardiac pathology and is widely used in the screening of aircrew and other high-hazard occupations. Given the low number of pathological results leading to disqualification or restriction however, there is an ongoing debate as to how often screening ECGs should be performed in different age groups.

Methods
We restrospectively analyzed 8275 resting 12-lead ECGs registered between 2007 and 2020 in the German Air Force Centre of Aerospace Medicine. Findings were categorized according to consensus recommendations published by the NATO Working Group on Occupational Cardiology in Military Aircrew, based on ECG screening criteria published for athletes which were used at the time of registration. Age, sex, height, weight, and body mass index of the probands were also captured. Additionally, 4839 pilot and non-pilot aircrew members were analyzed longitudinally over a maximum period of 13.4 years.

Results
Out of all the ECGs only 18 revealed findings requiring further investigation, and only one individual was temporarily disqualified because of a ventricular pre-excitation (delta wave) as a sign of an antegrade conducting accessory pathway. The longitudinal analysis of 25,829 ECGs revealed 28 abnormalities requiring further investigation, and only two ECG findings (in probands aged 48.8 and 59.1 years) led to temporary, or permanent disqualification. In a third case, the ECG showed signs of a myocardial infarction, which was already known from the proband’s history.

Conclusions
Initial ECG screening for asymptomatic aircrew revealed extremely low numbers of individuals requiring further investigation in our cohort. This would appear to justify an initial screening ECG and follow-up ECGs at certain intervals starting at a certain age, but routine ECG screening of applicants in professions with a higher risk tolerance or frequent, e.g. annual, follow-up ECGs in younger aircrew is not supported by our data because of the minimal yield of ECG findings requiring further investigation.
Case report: Rare myeloid sarcoma development following renal transplantation with KRAS and DNMT3A gene mutations
Authors: Wu Danyang , Lu Xiaoxuan , Yan Xiaojing , Gao Ran 
Published: August 2021

Abstract
Background
A high incidence of malignant tumors, such as post-transplant lymphoproliferative disorders (PTLD), Kaposi sarcoma, and renal cancer is common in solid organ and bone marrow transplant recipients. However, myeloid sarcoma (MS) after renal transplantation has rarely been reported and the diagnosis is challenging due to its low incidence.

Case presentation
Here, we report a rare case of a 49-year-old man who developed myeloid sarcoma (MS) in the transplanted kidney two years after renal transplantation. Next-generation sequencing (NGS) showed mutations of KRAS and DNMT3A genes in the MS, and no gene mutations in the bone marrow. He presented a normal karyotype of 46, XY. Following treatment with 6 cycles of systemic chemotherapy, the patient was in satisfactory condition with stable serum creatinine (sCr) levels at the 1-year follow-up. In addition, we performed a detailed review with emphasis on the clinical manifestations, and the diagnostic and therapeutic processes of another 7 patients who developed MS following renal transplantation.

Conclusions
Our report illustrates the clinical utility of comprehensive genomic profiling in benefiting the diagnosis of MS, the selection of therapeutic strategy and the determination of whether MS is donor-derived.