bluuebunny/crossref_metadata_2025_split huggingface dataset:
The expression and significance of AKR1B10 in laryngeal squamous cell carcinoma
Authors: Liu Jixuan , Ban Hongyan , Liu Yafang , Ni Jinsong 
Published: April 2021

Abstract
Aldosterone reductase family 1 member B10 (AKR1B10) is a nicotinamide adenine dinucleotide phosphate (NADPH) (reduced coenzyme II)-dependent oxidoreductase, and its biological functions include carbonyl detoxification, hormone metabolism, osmotic adjustment, and lipid synthesis. Studies suggested that AKR1B10 is a new biomarker for cancer based on its overexpression in epithelial tumors, such as breast cancer, cervical cancer, and lung cancer. At present, studies on the expression of AKR1B10 in laryngeal cancer have not been reported. However, we found that AKR1B10 is upregulated in laryngeal carcinoma, and its expression was negatively correlated with the degree of differentiation. In addition, AKR1B10 expression was positively correlated with tumor size; lymph node metastasis; long-term drinking; and Ki-67, mutant p53, and matrix metalloproteinase 2 expression. AKR1B10 was overexpressed in Hep-2 laryngeal carcinoma cells. Oleanolic acid inhibited AKR1B10 activity and expression in Hep-2 cells and suppressed Hep-2 cell proliferation, migration, and invasion. Therefore, AKR1B10 may be related to the development of laryngeal carcinoma, suggesting its use as a prognostic indicator for laryngeal cancer.
Successful Treatment of Recurrent Hyperpyrexia, Stroke, Intracardiac Thrombosis and Inflammatory Pseudotumor Secondary to Behçet’s Syndrome With Drug Therapy Alone
Authors: Wang Shuolin , Zhang Lei , Li Tian-fang , Liang Xu , Gao Yajing , Liu Shengyun 
Published: April 2021

Abstract
BackgroundBehçet’s syndrome (BS) is an inflammatory vessel disease characterized by recurrent oral and genital ulcers. It is a rare disorder that affects blood vessels throughout the body. It can affect any bodily system, including the skin, joints and cardiovascular, respiratory, central nervous and degestive systems. But cerebral infarction related to cerebral artery, intracardiac thrombosis (ICT) and inflammatory pseudotumor (IPT) are complications hard to see. And there is no effective therapy in clinic.Case presentationWe report the case of a 17-year-old patient with a two-month history of recurrent hyperpyrexia without obvious infection symptoms. He had a medical history of cerebral infarction ten months ago. Antinuclear antibody (ANA), antiphospholipid antibodies, parasite antibodies and antineutrophil cytoplasmic antibodies (ANCA) were all negative, consequently. Echocardiography demonstrates heterogeneous echoes in the right ventricle and apex. He was suspected to have cardiac myxomas and infective endocarditis and underwent thoracotomy afterwards. Histological examinations showed the specimen is inflammatory mass of vascular origin and intracardiac thrombus (ICT). However, the hyperpyrexia and intracardiac masses relapsed in two months. The antibiotic treatment failed to control the temperature and he was diagnosed as BS and treated with prednisone, aspirin and oral cyclophosphamide. Since then, the body temperature turned to normal and the size of intracardiac mass maintained stable. Conclusion﻿BS should be considered as a causative factor in young man with stroke, intracardiac masses and hyperpyrexia. Glucocorticoid and immunosuppressive agents may be effective for IPT and ICT in patient with BS.
Variation of Femoral Component Size by Reference Points and Target Alignments in Total Knee Arthroplasty
Authors: Ishibashi Shojiro , Mizu-uchi Hideki , Kawahara Shinya , Tsushima Hidetoshi , Akasaki Yukio , Nakashima Yasuharu 
Published: April 2021

Abstract
Selecting appropriately sized components is important in total knee arthroplasty because they can affect postoperative knee function and pain. This study investigated size differences of 19 different femoral component placements from the standard position by three-dimensional virtual surgery using three-dimensional bone models of 101 varus osteoarthritic knees. Distal femoral bone was cut perpendicular to the femoral mechanical axis (MA) in the coronal plane. Twenty different component placements consisting of five cutting directions (perpendicular to MA, 3° and 5° extension/flexion relative to MA in the sagittal plane), two rotational alignments (clinical and surgical epicondylar axes), and two rotational types of anterior reference guide (central and medial) were simulated. The mean anteroposterior dimension of the standard position was 55.5 mm which means that the difference compared to 19 different methods ranged from -1.2 ± 0.2 mm to 7.1 ± 1.3 mm. Multiple regression analysis revealed that flexion cutting direction, surgical epicondylar axis, and central were associated with smaller component size. In conclusion, the femoral component size can be affected easily by not only cutting direction but also the reference guide type and the target alignment. Our findings could provide surgeons with clinically useful information to fine-tune for unintended loose or tight joint gaps by adjusting the component size.
A signiﬁcant effect of the HUWE1 copy number on autistic spectrum disorder and the development of zebraﬁsh
Authors: Wu Haojuan , Liang Yan , Li Juan , Zhang Xueguang , Xu Baoshan , Wang Xiang , Cheng Juan , Dinnyes Andras , Xie Jiang , Xu wenming 
Published: April 2021

Abstract
Autistic spectrum disorder (ASD) is a complex neurodevelopmental disorder. The copy number variation (CNV) of genes in the X-chromosome is speculated to play a critical role in ASD. The HECT, UBA and WWE domain containing the E3 ubiquitin protein ligase 1 (HUWE1) gene is located on the X-chromosome and is associated with neurodevelopment. However, the CNV of HUWE1 has not been linked to ASD. In this study, we identified increased copy numbers of HUWE1 in ASD patients compared to the controls. Moreover, an elevated severity of ASD phenotype was observed in patients with more HUWE1 copy numbers. In vitro, overexpression HUWE1 could decrease the proliferation of nervous system derived cells and promote their apoptosis, declining the G2/M phase transition. The functional assay showed that HUWE1, an E3 ubiquitin protein ligase, regulated the ubiquitination degradation of key mediators in the Wnt/β-catenin signaling pathway, which is involved in neurodevelopment. Consistent with the ASD patients, overexpression of huwe1 in zebrafish embryos caused defective brain development, small eyes, cardiac edema and a curly spinal cord, supporting the pivotal role of the HUWE1 CNV in neurodevelopmental disorders. In this study, we demonstrated the role of the HUWE1 CNV for complement pathway factors in the origin of ASD for the first time. Genetic analysis of the HUWE1 copy number could inform the clinical counseling of ASD patients.
Vitamin D levels are associated with low-density lipoprotein cholesterol in Chinese children with type 1 diabetes
Authors: Shu Jianbo , Wang Xinhui , Zhang Mingying , Zhi Xiufang , Guan Jun , Gu Chunyu , Pu Linjie , Gao Long , Cai Chunquan , Yang Wei , Lv Ling 
Published: April 2021

Abstract
Objective There is an increased level of low-density lipoprotein cholesterol (LDL-C)in children with type 1 diabetes mellitus(T1DM). In addition, the Vitamin D level in T1DM patients is usually below the normal reference range. The aim of this study was to explore the relationship between Vitamin D levels and LDL-C in Chinese children with T1DM. Methods A retrospective cross-sectional study was conducted in the Endocrine inpatient wards of Tianjin Children’s Hospital, 143 children with T1DM were included. The related clinical and laboratory examinations, including anthropometric parameters, lipid profiles, and Vitamin D levels, were collected in all subjects. Results The univariate analysis results did not show a significant correlation between Vitamin D levels and LDL-C (P=0.634). Furthermore, a nonlinear relationship was observed between Vitamin D levels and LDL-C by smooth curve fitting after adjusting for potential confounders. A multivariate piecewise linear regression model revealed a significant negative association between LDL-C and Vitamin D levels when LDL-C was greater than 3.1 mmol/L(β -2.9, 95% CI -5.4,-0.5; P=0.022). However, we did not observe a significant relationship between LDL-C and Vitamin D levels when LDL-C was lower than 3.1 mmol/L(β 2.4, 95% CI -0.2,5.1; P=0.076).Conclusions This study identified a nonlinear relationship between Vitamin D levels and LDL-C independent of other potential confounding factors, suggesting that the deficiency or insufficiency of Vitamin D in T1DM children with high LDL-C levels should be considered, especially LDL-C is higher than 3.1 mmol/L, which provides evidence of the timing about Vitamin D supplementation in T1DM children.
The Effects of a Mitochondrial Targeted Peptide (Elamipretide/SS31) on BAX Recruitment and Activation During Apoptosis
Authors: Grosser Joshua , Fehrman Rachel , Keefe Dennis , Redmon Martin , Nickells Robert 
Published: April 2021

Abstract
Objective: Elamipretide (SS31) is a mitochondria-targeted peptide that has reported functions of stabilizing mitochondrial cristae structure and improving mitochondrial bioenergetics. Several studies have documented cell protective features of this peptide, including impairment of intrinsic apoptosis by inhibiting the recruitment and activation of the pro-apoptotic BAX protein. We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively. Result: In nucleofected and plated ARPE-19 cells, elamipretide accelerated the formation of larger mitochondria. In the presence of the apoptotic stimulator, staurosporine, cells treated with elamipretide exhibited moderately slower rates of BAX recruitment. Peptide treatment, however, did not significantly delay the onset of BAX recruitment or the final total amount of BAX that was recruited. Additionally, elamipretide showed no impairment or delay of cytochrome c release or mitochondrial fragmentation, two events associated with normal BAX activation during cell death. These results indicate that the protective effect of elamipretide is not at the level of BAX activity to induce pro-apoptotic mitochondrial dysfunction after the initiation of staurosporine-induced apoptosis.
Quantitative analysis of membrane-mediated interactions and aggregation of flexible peripheral proteins orchestrating large-scale membrane remodeling
Authors: Sadeghi Mohsen , Noé Frank 
Published: April 2021

Abstract
Shaping and remodeling of biomembranes is essential for cellular trafficking, with membrane-binding peripheral proteins playing the key role in it. Significant membrane remodeling as in endo- and exocytosis is often due to clusters or aggregates of many proteins whose interactions may be direct or mediated via the membrane. While computer simulation could be an important tool to disentangle these interactions and understand what drives cooperative protein interactions in membrane remodeling, this has so far been extremely challenging: protein-membrane systems involve time- and lengthscales that make detailed atomistic simulations impractical, while most coarse-grained models lack the degree of detail needed to resolve the dynamics and physical effect of protein and membrane flexibility. Here, we develop a coarse-grained model of the bilayer membrane bestrewed with rotationally-symmetric flexible membrane-bound proteins. We show how this model can be parameterized based on local curvatures, protein flexibility, and the in-plane dynamics of proteins. We measure the effective interaction potential for the membrane-mediated interactions between peripheral proteins. Furthermore, we investigate the kinetics, equilibrium distributions, and the free energy landscape governing the formation and break-up of protein clusters on the surface of the membrane. We demonstrate how the flexibility of the protein plays a deciding role in highly selective macroscopic aggregation behavior. Finally, we present large-scale simulations of membrane tubulation, and discuss the sequence of events and the stability of intermediates.
Chronic Cadmium Exposure Impairs Macrophage Mitochondrial Homeostasis and Promotes Macrophage Polarization Contributing to Atherosclerosis via Regulating RIPK3&nbsp;Signaling
Authors: Zhang Jiexin , Feng Weijing , Chen Peier , Ning Xiaodong , Ou Caiwen , Chen Minsheng 
Published: April 2021

Abstract
Background: Chronic cadmium (Cd) exposure can contribute to the progression of cardiovascular disease (CVD), especially atherosclerosis (AS), but the underlying mechanism is unclear. Since mitochondrial homeostasis is emerging as a core player in the development of CVD, it might serve as a potential mechanism linking Cd exposure and AS. Here, we aimed to investigate the Cd-induced AS through macrophage polarization and tried to find out the mechanism of mitochondrial dysfunction caused by Cd exposure. Methods and results: In vitro, flow cytometry showed that Cd exposure markedly promoted M1-type polarization of macrophages, manifesting as the increasing expression of NF-kB, NLRP3 and their downstream inflammatory factors, IL-1β and IL-6. Mitochondrial function test revealed that the decreasing mitochondrial membrane potential and increasing superoxide (mROS) and mitochondrial fission were involved in Cd-induced macrophage polarization. Transmission electron microscope observation and immunofluorescence both identified the decrease of mitophage after Cd exposure. And improving mitochondrial function above significantly restored the balance of macrophage polarization. In vivo, Cd exposure was positively correlated with blood Cd concentration, and oil red O staining showed higher blood Cd significantly increased the area of AS plaques. Besides, M1-type polarization of macrophages and mitochondrial dysfunction were observed in mouse aortic roots through immunofluorescence and western blot as the dosage of Cd increasing. And the administered NAC or Mdivi-1, which decreased mROS or mitochondrial fission, markedly attenuated AS plaques and macrophage M1-type polarization in Cd-treated group. Finally, the up-regulated expressions of RIPK3 and p-MLKL were observed both in vitro and in vivo. And knocking out RIPK3 with decreasing expression of p-MLKL followed did improve mitochondrial dysfunction caused by Cd which effectively reversed macrophage polarization. Conclusion: Cd exposure activated RIPK3 pathway and impaired mitochondrial homeostasis, resulting in macrophage polarization to a pro-inflammatory phenotype and subsequent AS. These findings suggest that improving mitochondrial homeostasis may provide a potential therapeutic target for AS induced by chronic Cd exposure.
Biofilm Growth By Listeria Monocytogenes On Stainless Steel and Expression of Biofilm-Related Genes Under Stressing Conditions
Authors: Silva Danilo Augusto Lopes da , Tavares Rafaela de Melo , Camargo Anderson Carlos , Yamatogi Ricardo Seiti , Martinis Elaine Cristina Pereira De , Nero Luis Augusto 
Published: April 2021

Abstract
This research was carried out to assess the ability of L. monocytogenes for adhesion and growth in biofilm on stainless steel coupons under different stressing conditions (NaCl, curing salts and quaternary ammonium compounds - QAC), besides determining the expression of different genes involved in biofilm formation and stress response. Results from crystal violet assay revealed that one isolate carrying a premature stop codon (PMSC) in agrC gene formed high-density biofilms in the presence of QAC or cure salts (7.5% and 10%). Reverse Transcriptase-qPCR results revealed that isolates of L. monocytogenes lineages I and II presented differences in transcriptional profile of genes related to biofilm formation and adaptation to environmental conditions. In conclusion, our results demonstrated how L. monocytogenes can survive, multiply and form biofilm under adverse conditions related to food processing environments. Differences in transcriptional expression were observed, highlighting the role of regulatory gene networks for particular serotypes under different stress responses.
Transcriptomic Assessment of Dietary Fish Meal Partial Replacement By Soybean Meal and Prebiotic Inclusion In The Liver of Juvenile Pacific Yellowtail (Seriola Lalandi)
Authors: Juárez Oscar E. , Delgado-Vega Rigoberto , Cruz Fabiola Lafarga De La , Lazo Juan Pablo , López-Landavery Edgar , Tovar Dariel , Galindo-Sánchez Clara E. 
Published: April 2021

Abstract
Seriola lalandi is an important species for aquaculture, due to its rapid growth, adaptation to captivity and formulated diets, and high commercial value. Due to the rise in fish meal (FM) price, efforts are made to replace it partially or entirely with vegetable meals in diets for carnivorous fish. The use of prebiotics when feeding vegetable meals has improved fish health. In this study, four experimental diets were assessed in juveniles, the control diet consisted of FM as the main protein source, the second diet included 2% GroBiotic®-A (FM-P), the third included FM with 25% replacement by soybean meal (SM25), and the fourth consisted in SM25 with 2% of GroBiotic®-A (SM25-P). RNA-seq of the liver tissue was performed, followed by differential expression analysis and functional annotation to identify genes affected by the diets. Growth was not affected by this level of FM replacement, but it was improved by the prebiotic. Annotation was achieved for 78,826 transcripts, of which 135 were up-regulated and 78 down-regulated among all treatments compared to the control. Transcriptomic profiles of control samples were clustered with those from fishes fed SM25 and SM25-P diets, and the most differentiated group was that one fed the FM-P diet. SM25-P showed the least amount of differentially expressed genes, maintaining general transcriptomic profiles of control diet in the liver, therefore this diet is a potential economic alternative to the FM diet, for S. lalandi juveniles. Assessment of the effects of this diet along the digestive tract is recommended.
Intermediate Field Directions Recorded in Pliocene Basalts in Styria (Austria): Evidence for Cryptochron C2r.2r-1
Authors: Schnepp Elisabeth , Arneitz Patrick , Ganerød Morgan , Scholger Robert , Fritz Ingomar , Egli Ramon , Leonhardt Roman 
Published: April 2021

Abstract
Pliocene volcanic rocks from South-East-Austria were paleomagnetically investigated. Samples were taken from 28 sites located on eight different volcanoes. Rock magnetic investigations revealed that magnetic carriers are Ti-rich or Ti-poor titanomagnetites with mainly pseudo-single-domain grain size. Characteristic remanent magnetization directions were obtained from alternating field as well as from thermal demagnetization. Four localities give reversed directions agreeing with the expected direction from secular variation. Another four localities of the Klöch-Königsberg volcanic complex (3) and the Neuhaus volcano (1) have reversed directions with shallow inclinations and declinations of about 240° while the locality Steinberg yields a positive inclination of about 30° and 200° declination. These aberrant directions cannot be explained by local or regional tectonic movements. All virtual geomagnetic pole positions are located on the southern hemisphere. Four virtual geomagnetic poles lie close to the geographic pole, while all others are concentrated in a narrow longitude sector offshore South America (310° to 355°) with low virtual geomagnetic pole latitudes ranging from − 15° to -70°. The hypothesis that a transitional geomagnetic field configuration was recorded during the short volcanic activity of these five localities is supported by 9 paleointensity results and 39Ar/40Ar dating. Virtual geomagnetic dipole moments range from 1.1 to 2.9·1022 Am2 for sites with low VGP latitudes about 60° and from 3.0 to 9.3·1022 Am2 for sites with higher virtual geomagnetic pole latitudes. The new 39Ar/40Ar ages of 2.51 ± 0.27 Ma for Klöch and 2.39 ± 0.03 Ma for Steinberg allow for the correlation of the Styrian transitional directions with cryptochron C2r.2r-1 of the geomagnetic polarity time scale.
Silencing of UBE2D1 Inhibited Cell Migration in Gastric Cancer, Decreasing Ubiquitination of SMAD4
Authors: Xie Honghu , He Yu , Wu Yugang , Lu Qicheng 
Published: April 2021

Abstract
Background: Gastric cancer (GC) is the second leading cause of cancer-related deaths. Because it is hard to diagnose at early stage, the overall 5 years survival rate is lower than 25%. High migration is the main hallmark of malignant cells at advanced stage of GC. Thus, it is urgent to find biomarkers for early diagnosis and more effective therapy of GC.Methods: In this study, silencing and overexpression lentiviruses targeting the ubiquitin-conjugating enzyme E2 D1 (UBE2D1), transwell, wound healing, and pulmonary metastasis mouse model were applied to analyze the function of UBE2D1 in vitro and in vivo. Real-time PCR and immunohistochemistry were used to elucidate the level of UBE2D1 in GC samples.Results: Silencing of UBE2D1 inhibited cell migration and the levels of Epithelial-mesenchymal transition (EMT) makers (MMP2 and MMP9) in AGS and MKN45 cells. Silencing of UBE2D1 inhibited cell metastasis in mouse model. On the contrary, UBE2D1 overexpression increased cell migration and the levels of MMP2 and MMP9 in MGC-803 cells. Further, silencing of UBE2D1 decreased the ubiquitination level of mothers against decapentaplegic homolog 4 (SMAD4), and the increase of cell migration induced by UBE2D1 overexpression could be reversed by SMAD4.Conclusion: Silencing of UBE2D1 inhibited cell migration through transforming growth factor β (TGF-β)/SMAD4 signaling pathway in GC.
Tracheal Intubation in Out-Of-Hospital Setting is Associated With A High Failure Rate of The First Attempt: A Multicenter Prospective Study
Authors: Galinski Michel , Wrobel Marion , Boyer Romain , Reuter Paul Georges , Ruscev Mirko , Debaty Guillaume , Gilles Bagou , Dehours Emilie , Bosc Juliane , Lorendeau Jean-Paul , Goddet Sybille , Marouf Kamelia , Catoire Pierre , Gil-Jardiné Cédric , Simonnet Bruno 
Published: April 2021

Abstract
BackgroundTracheal intubation in an out-of-hospital setting is a frequent and potentially difficult procedure. The risk of adverse events increases dramatically with the number of attempts. The failure rate of the first intubation attempt ranges from 5 to 32% and the risk factors are unclear. We evaluated the failure rate of the first intubation attempt in an out-of-hospital setting and identified variables potentially associated with such failure.MethodsThis was an observational prospective multicenter study performed over 17 months and involving 10 prehospital emergency medical units. Airway management for patients who needed tracheal intubation followed the national guidelines. Rapid sequence intubation with a sedative and myorelaxant drugs was systematically performed for spontaneously breathing patients. After each tracheal intubation, the operator was required to provide, by completing a data-collection form, information on operator and patient characteristics and the environmental conditions during the intubation. The primary endpoint was failure of the first intubation attempt.ResultsDuring the study period, 1546 patients were analyzed, of whom 59% had cardiac arrest, and 486 intubations failed on the first attempt (31.4% [95% confidence interval = 30.2–32.6]). A multivariate analysis revealed that the following 7 of 28 factors were associated with an increased risk of a failed first intubation attempt: operator with fewer than 50 prior intubations, small inter-incisor space, limited extension of the head, macroglossia, ear/nose/throat tumor, cardiac arrest, and vomiting. The frequency of adverse events was 13.4% and increased with each additional attempt.ConclusionsThe failure rate of the first attempt was high. Most risk factors could be identified only at the moment of occurrence and were not easily anticipated. Finally, the risk of complications increased with the number of attempts.