bluuebunny/crossref_metadata_2025_split huggingface dataset:
Overexpressed VDAC1 in breast cancer as a novel prognostic biomarker and correlates with immune infiltrates
Authors: Fang Yutong , Liu Junpeng , Zhang Qunchen , She Chuanghong , Zheng Rongji , Zhang Rendong , Chen Zexiao , Chen Chunfa , Wu Jundong 
Published: June 2022

Abstract
Background
More and more evidence suggests that cancer is a mitochondrial metabolic disease recently and mitochondria dysfunction is critical to tumorigenesis. As a gatekeeper of mitochondria, the voltage-dependent anion channel 1 (VDAC1) is associated with the development of breast cancer (BC). However, its potential mechanism and clinical significance remain unclear; thus, in this research, we aimed to explore it.

Methods
VDAC1 expression in BC tissues and normal tissues was obtained from The Cancer Genome Atlas (TCGA) and validated by datasets from the gene expression omnibus (GEO) database. Then, the relationships between VDAC1 expression and clinicopathological features were analyzed. Receiver operating characteristics (ROC) curves were used to identify the diagnostic value of VDAC1. The prognostic value was evaluated by Kaplan-Meier survival curves and Cox regression analysis. VDAC1 with its co-expression genes were subjected to enrichment analysis to explore potential mechanisms in BC and the protein-protein interaction (PPI) network was constructed. At last, the association between VDAC1 expression and infiltration levels of immune cell infiltration by various methods, as well as their corresponding markers, was analyzed. We also analyzed the correction between VDAC1 expression and eight immune checkpoint genes and the tumor immune dysfunction and exclusion (TIDE) scores of each BC sample in TCGA were calculated and the differences between high and low VDAC1 expression groups were analyzed.

Results
VDAC1 expression was remarkably elevated in BC (p < 0.001), and high expression of VDAC1 was associated with the positive expression of ER (p = 0.004), PR (p = 0.033), and HER2 (p = 0.001). ROC analysis suggested that VDAC1 had diagnosed value in BC. The Kaplan-Meier analysis suggested that higher expression of VDAC1 was associated with shorter overall survival (OS), and further Cox regression analysis revealed that VDAC1 was an independent factor of unfavorable prognosis in BC patients. Enrichment analysis of VDAC1 and its co-expression suggested that VDAC1 was related to the regulation of mitochondrial energy metabolism and protein modification, and the HIF-1 singing pathway might be the potential mechanism in BC. Notably, we found that VDAC1 expression was infiltration levels of most types of immune cells, as well as the expression of marker genes of immune cells. The ICGs PDCD1, CTLA4, LAG3, SIGLEC15, and TIGIT were negatively corrected with VDAC1 expression in BC. TIDE scores between the low and high expression groups showed no difference.

Conclusion
Overexpressed VDAC1 in BC could be severed as a novel biomarker for diagnosis and VDAC1 was an independent factor for adverse prognosis prediction. Our study revealed that VDAC1 might inhibit tumor immunity and might be a novel therapeutic target in BC.
Cellular inhibitor of apoptosis 2 (cIAP2) restricts neuroinflammation during experimental autoimmune encephalomyelitis
Authors: Biswas Debolina D. , Martin Rebecca K. , Brown LaShardai N. , Mockenhaupt Karli , Gupta Angela S. , Surace Michael J. , Tharakan Anuj , Yester Jessie W. , Bhardwaj Reetika , Conrad Daniel H. , Kordula Tomasz 
Published: June 2022

AbstractBackgroundImmune activation, neuroinflammation, and cell death are the hallmarks of multiple sclerosis (MS), which is an autoimmune demyelinating disease of the central nervous system (CNS). It is well-documented that the cellular inhibitor of apoptosis 2 (cIAP2) is induced by inflammatory stimuli and regulates adaptive and innate immune responses, cell death, and the production of inflammatory mediators. However, the impact of cIAP2 on neuroinflammation associated with MS and disease severity remains unknown.MethodsWe used experimental autoimmune encephalomyelitis (EAE), a widely used mouse model of MS, to assess the effect of cIAP2 deletion on disease outcomes. We performed a detailed analysis on the histological, cellular, and molecular levels. We generated and examined bone-marrow chimeras to identify the cIAP2-deficient cells that are critical to the disease outcomes.ResultscIAP2−/−mice exhibited increased EAE severity, increased CD4+T cell infiltration, enhanced proinflammatory cytokine/chemokine expression, and augmented demyelination. This phenotype was driven by cIAP2-deficient non-hematopoietic cells. cIAP2 protected oligodendrocytes from cell death during EAE by limiting proliferation and activation of brain microglia. This protective role was likely exerted by cIAP2-mediated inhibition of the non-canonical NLRP3/caspase-8-dependent myeloid cell activation during EAE.ConclusionsOur findings suggest that cIAP2 is needed to modulate neuroinflammation, cell death, and survival during EAE. Significantly, our data demonstrate the critical role of cIAP2 in limiting the activation of microglia during EAE, which could be explored for developing MS therapeutics in the future.
ALK rearrangement-associated renal cell carcinoma morphologically mimicking mucinous tubular and spindle cell carcinoma: a case report
Authors: Kai Keita , Tobu Shohei , Kido Shinichi , Mikami Shuji , Takeuchi Kengo , Dobashi Akito , Togashi Yuki , Noguchi Mitsuru , Aishima Shinichi 
Published: June 2022

Abstract
Background
Anaplastic lymphoma kinase rearrangement-associated renal cell carcinoma (ALK-RCC) is an extremely rare tumor and ALK-RCC that mimics mucinous tubular and spindle cell carcinoma (MTSCC) has been very reported only in one instance.

Case presentation
A 42-year-old Japanese woman was admitted to our hospital for the treatment of a left renal tumor measuring 5 cm in maximum dimension. She underwent a laparoscopic left nephrectomy. Histologically, the tumor formed tubular or focally papillary structures with a small amount of spindle-shaped tumor cells against the background of prominent extracellular mucin. Although the tumor cells were negative for immunohistochemistry (IHC) of alpha-methylacyl-CoA racemase (AMACR) and lymph node metastasis was presented (these are atypical findings for MTSCC), we initially diagnosed the tumor as MTSCC based on its morphological characteristics with mucin deposition. However, an additional IHC analysis revealed that the tumor cells were diffusely positive for ALK-IHC. In addition, TPM3 exon 8 – ALK exon 20 fusion gene was detected by RNA sequencing. The tumor was thus correctly diagnosed as ALK rearrangement-associated renal cell carcinoma (ALK-RCC).

Conclusions
Since the use of molecular targeted therapy with an ALK inhibitor for ALK-RCC is promising, the correct pathological diagnosis of ALK-RCC is quite important. We strongly recommend that ALK-IHC be routinely performed for renal tumors with negative AMACR staining that mimic MTSCC.
Initiation and elongation factor co-expression correlates with recurrence and survival in epithelial ovarian cancer
Authors: Sobočan Monika , Brunialti Daniela , Sprung Sussanne , Schatz Christoph , Knez Jure , Kavalar Rajko , Takač Iztok , Haybaeck Johannes 
Published: June 2022

AbstractHigh grade epithelial ovarian cancer (EOC) represents a diagnostic and therapeutic challenge due to its aggressive features and short recurrence free survival (RFS) after primary treatment. Novel targets to inform our understanding of the EOC carcinogenesis in the translational machinery can provide us with independent prognostic markers and provide drugable targets. We have identified candidate eukaryotic initiation factors (eIF) and eukaryotic elongation factors (eEF) in the translational machinery for differential expression in EOC through in-silico analysis. We present the analysis of 150 ovarian tissue microarray (TMA) samples on the expression of the translational markers eIF2α, eIF2G, eIF5 (eIF5A and eIF5B), eIF6 and eEF1A1. All translational markers were differentially expressed among non-neoplastic ovarian samples and tumour samples (borderline tumours and EOC). In EOC, expression of eIF5A was found to be significantly correlated with recurrence free survival (RFS) and expression of eIF2G and eEF1A1 with overall survival (OS). Expression correlation among factor subunits showed that the correlation of eEF1A1, eIF2G, EIF2α and eIF5A were significantly interconnected. eIF5A was also correlated with eIF5B and eIF6. Our study demonstrates that EOCs have different translational profile compared to benign ovarian tissue and that eIF5A is a central dysregulated factor of the translation machinery.
Effect of plant waste addition as exogenous nutrients on microbial remediation of petroleum-contaminated soil
Authors: Shi Lei , Liu Zhongzheng , Yang Liangyan , Fan Wangtao 
Published: June 2022

Abstract
Purpose
This study investigates the feasibility of bio-enhanced microbial remediation of petroleum-contaminated soil, and analyzes the effect of different plant wastes as exogenous stimulants on microbial remediation of petroleum-contaminated soil and the effect on soil microbial community structure, in order to guide the remediation of soil in long-term petroleum-contaminated areas with nutrient-poor soils.

Methods
The study was conducted in a representative oil extraction area in the Loess Hills, a typical ecologically fragile area in China. Through indoor simulated addition tests, combined with the determination of soil chemical and microbiological properties, the degradation efficiency of petroleum pollutants and the response characteristics of soil microbial community structure to the addition of different plant wastes in the area were comprehensively analyzed to obtain the optimal exogenous additive and explore the strengthening mechanism of plant wastes on microbial remediation of petroleum-contaminated soil.

Results
Compared with the naturally decaying petroleum-contaminated soil, the addition of plant waste increased the degradation rate of petroleum pollutants, that is, it strengthened the degradation power of indigenous degrading bacteria on petroleum pollutants, among which the highest degradation rate of petroleum pollutants was achieved when the exogenous additive was soybean straw; compared with the naturally decaying petroleum-contaminated soil, the addition of soybean straw and dead and fallen leaves of lemon mallow made the microbial species in the contaminated soil significantly reduced and the main dominant flora changed, but the flora capable of degrading petroleum pollutants increased significantly; the addition of exogenous nutrients had significant effects on soil microbial diversity and community structure.

Conclusions
Soybean straw can be added to the contaminated soil as the optimal exogenous organic nutrient system, which improves the physicochemical properties of the soil and gives a good living environment for indigenous microorganisms with the function of degrading petroleum pollutants, thus activating the indigenous degrading bacteria in the petroleum-contaminated soil and accelerating their growth and proliferation and new city metabolic activities, laying a foundation for further obtaining efficient, environmentally friendly and low-cost microbial enhanced remediation technology solutions. The foundation for further acquisition of efficient, environmentally friendly, and low-cost microbial-enhanced remediation technology solutions. It is important for improving soil remediation in areas with long-term oil contamination and nutrient-poor soils.
KIF2A decreases IL-33 production and attenuates allergic asthmatic inflammation
Authors: Wang Zhengxia , Wu Jingjing , Jiang Jingxian , Ma Qiyun , Song Meijuan , Xu Tingting , Liu Yanan , Chen Zhongqi , Bao Yanmin , Huang Mao , Zhang Mingshun , Ji Ningfei 
Published: June 2022

Abstract
Background
The microtubule-dependent molecular motor protein Kinesin Family Member 2A (KIF2A) is down-regulated in asthmatic human airway epithelium. However, little is known about the roles of KIF2A as well as the possible underlying mechanisms in asthma.

Methods
House dust mite (HDM) extract was administered to establish a murine model of asthma. The expression of KIF2A, IL-33 and the autophagy pathways were detected. The plasmid pCMV-KIF2A was used to overexpress KIF2A in the airway epithelial cells in vitro and in vivo. IL-4, IL-5, IL-33 and other cytokines in bronchoalveolar lavage fluid (BALF) and lung tissues homogenates were measured.

Results
In response to the challenge of house dust mite (HDM) in vitro and in vivo, airway epithelial cells displayed decreased production of KIF2A. Meanwhile, autophagy and IL-33 were increased in HMD-treated epithelial cells. Mechanistically, KIF2A decreased autophagy via suppressing mTORC1 pathway in HDM-treated epithelial cells, which contributed to the reduced production of IL-33. Moreover, in vivo KIF2A transfection reduced IL-33 and autophagy in the lung, leading to the attenuation of allergic asthma.

Conclusion
KIF2A suppressed mTORC1-mediated autophagy and decreased the production of epithelial-derived cytokine IL-33 in allergic airway inflammation. These data indicate that KIF2A may be a novel target in allergic asthma.
WDFY3 mutation alters laminar position and morphology of cortical neurons
Authors: Schaaf Zachary A. , Tat Lyvin , Cannizzaro Noemi , Panoutsopoulos Alexios A. , Green Ralph , Rülicke Thomas , Hippenmeyer Simon , Zarbalis Konstantinos S. 
Published: June 2022

Abstract
Background
Proper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology.

Methods
Here, in an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild-type cells concomitantly in vivo using immunofluorescent techniques.

Results
We revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages.

Limitations
While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients or some of the other neurodevelopmental conditions associated with WDFY3 mutation.

Conclusions
Our genetic approach revealed several cell autonomous requirements of WDFY3 in neuronal development that could underlie the pathogenic mechanisms of WDFY3-related neurodevelopmental conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for WDFY3 in regulating neuronal function and interconnectivity in postnatal life.
Post-synaptic specialization of the neuromuscular junction: junctional folds formation, function, and disorders
Authors: Zou Suqi , Pan Bing-Xing 
Published: June 2022

AbstractPost-synaptic specialization is critical to the neurotransmitter release and action potential conduction. The neuromuscular junctions (NMJs) are the synapses between the motor neurons and muscle cells and have a more specialized post-synaptic membrane than synapses in the central nervous system (CNS). The sarcolemma within NMJ folded to form some invagination portions called junctional folds (JFs), and they have important roles in maintaining the post-synaptic membrane structure. The NMJ formation and the acetylcholine receptor (AChR) clustering signal pathway have been extensively studied and reviewed. Although it has been suggested that JFs are related to maintaining the safety factor of neurotransmitter release, the formation mechanism and function of JFs are still unclear. This review will focus on the JFs about evolution, formation, function, and disorders. Anticipate understanding of where they are coming from and where we will study in the future.
The Alberta Wildland Fuels Inventory Program (AWFIP): data description and reference tables
Authors: Phelps Nathan , Cameron Hilary , Forbes Air M. , Schiks Tom , Schroeder Dave , Beverly Jennifer L. 
Published: June 2022

Key message
This document describes a dataset obtained from a field sampling program conducted in Alberta, Canada. Field data were used to describe the structure and composition of forest stands, including several fuel loads (e.g., surface, understory, canopy fuels). The dataset can be downloaded from https://doi.org/10.17605/OSF.IO/FZ8E4 and metadata is available at https://metadata-afs.nancy.inra.fr/geonetwork/srv/fre/catalog.search#/metadata/527efb49-43b4-43eb-88b2-70535ff99fc5

Abstract
We present a quality-checked and curated dataset obtained from a field sampling program conducted in the province of Alberta, Canada. Field data were used to describe the structure and composition of forest stands documented in 476 sampling events. Each sampling event record consists of 42 different variables, including several fuel loads (e.g., surface, understory, canopy fuels). The dataset has been created for operational and research applications including but not limited to fuel classification, estimation of fuel attributes from remote sensing technologies, fuel treatment planning, fire behavior prediction, and use in high resolution fire growth models.
Comparison of clinical characteristics and hospital mortality in critically ill patients without COVID-19 before and during the COVID-19 pandemic: a multicenter, retrospective, propensity score-matched study
Authors: Kim Sua , Choi Hangseok , Sim Jae Kyeom , Jung Won Jai , Lee Young Seok , Kim Je Hyeong 
Published: June 2022

Abstract
Background
The high transmission and fatality rates of coronavirus disease 2019 (COVID-19) strain intensive care resources and affect the treatment and prognosis of critically ill patients without COVID-19. Therefore, this study evaluated the differences in characteristics, clinical course, and prognosis of critically ill medical patients without COVID-19 before and during the COVID-19 pandemic.

Methods
This retrospective cohort study included patients from three university-affiliated tertiary hospitals. Demographic data and data on the severity, clinical course, and prognosis of medical patients without COVID-19 admitted to the intensive care unit (ICU) via the emergency room (ER) before (from January 1 to May 31, 2019) and during (from January 1 to May 31, 2021) the COVID-19 pandemic were obtained from electronic medical records. Propensity score matching was performed to compare hospital mortality between patients before and during the pandemic.

Results
This study enrolled 1161 patients (619 before and 542 during the pandemic). During the COVID-19 pandemic, the Simplified Acute Physiology Score (SAPS) 3 and Sequential Organ Failure Assessment (SOFA) scores, assessed upon ER and ICU admission, were significantly higher than those before the pandemic (p < 0.05). The lengths of stay in the ER, ICU, and hospital were also longer (p < 0.05). Finally, the hospital mortality rates were higher during the pandemic than before (215 [39.7%] vs. 176 [28.4%], p < 0.001). However, in the propensity score-matched patients, hospital mortality did not differ between the groups (p = 0.138). The COVID-19 pandemic did not increase the risk of hospital mortality (odds ratio [OR] 1.405, 95% confidence interval [CI], 0.937–2.107, p = 0.100). SAPS 3, SOFA score, and do-not-resuscitate orders increased the risk of in-hospital mortality in the multivariate logistic regression model.

Conclusions
In propensity score-matched patients with similarly severe conditions, hospital mortality before and during the COVID-19 pandemic did not differ significantly. However, hospital mortality was higher during the COVID-19 pandemic in unmatched patients in more severe conditions. These findings imply collateral damage to non-COVID-19 patients due to shortages in medical resources during the COVID-19 pandemic. Thus, strategic management of medical resources is required to avoid these consequences.
Global evidence on the rapid adoption of telemedicine in primary care during the first 2 years of the COVID-19 pandemic: a scoping review protocol
Authors: Valdes Daniela , Alqazlan Lama , Procter Rob , Dale Jeremy 
Published: June 2022

Abstract
Background
Before the declaration of the COVID-19 pandemic in March 2020, primary care in most countries relied on face-to-face consultations, with relatively limited use of telemedicine. Lockdowns and social distancing measures during the early stages of the pandemic led to rapid, widely spread telemedicine adoption in healthcare settings. The rapid uptake that occurred following the onset of these pandemic-induced measures in countries such as the UK, Canada and New Zealand prompts questions around the drivers, extent and sustainability of this transformation in clinical practice at the global level, as the research in this area is still emerging. The purpose of this scoping review is to explore the global evidence surrounding the rapid adoption of telemedicine in primary care settings during the first 2 years of the COVID-19 pandemic through three lenses: patient experience, health inequalities and patient-clinician trust, with the purpose of identifying elements contributing to the sustainability of this innovation.

Methods
A draft protocol was tested through an initial search on Ovid Medline, Web of Science and Google Scholar with additional searches on the Cochrane Database. This informed the final selection of terms which will be used to search Ovid, Web of Science, Google Scholar, PROSPERO, Cochrane Library and others, filtering for studies from the pandemic declaration onwards. Additional grey literature reports will be sourced through simplified searches on Google in widely spoken languages. Duplicates will be removed by screening titles. Abstracts and grey literature text extracts will be screened based on pre-set eligibility criteria by two researchers. Abstracts (and extracts in the case of grey literature) will be mapped against the domains of the Non-adoption, Abandonment, and challenges to Scale-up, Spread and Sustainability (NASSS) framework by two researchers. Data will be presented in table format.

Discussion
This review will map the current literature to identify current gaps in evidence related to the adoption of telemedicine after the declaration of the pandemic in March 2020. The use of simplified searches in the several spoken languages in the world is aimed at capturing more immediate non-academic reflections and experiences on this major service change at a global level.

Systematic review registration
The study has been registered on Open Science Framework and can be accessed through the following URL: https://osf.io/4z5ut/