bluuebunny/crossref_metadata_2025_split huggingface dataset:
Self-testing for proteinuria in pregnancy: a systematic review and meta-analysis
Authors: Yeh Ping Teresa , Rhee Dong Keun , Kennedy Caitlin Elizabeth , Zera Chloe A. , Tunçalp Özge , Lucido Briana , Narasimhan Manjulaa 
Published: August 2022

ABSTRACTBackgroundSelf-testing for proteinuria may help identify preeclampsia risk during pregnancy, increase end-user empowerment, and reduce burden on health systems. We conducted this systematic review of the impact of proteinuria self-testing during pregnancy to expand the evidence base for the World Health Organization consolidated guideline on self-care interventions.MethodsWe comprehensively searched for articles comparing the effect of proteinuria self-testing with clinic-based testing among pregnant individuals receiving antenatal care on the following outcomes: maternal mortality or near-miss; adverse pregnancy outcomes; eclampsia or pre-eclampsia; long-term diseases; follow-up care and appropriate management; self-efficacy, self-determination, autonomy, and empowerment; mental health and well-being; adverse events and social harms; device-related issues; intra-uterine growth restriction; preterm birth; and stillbirth or perinatal death. After abstract screening and full-text review, we systematically extracted data using standardized forms and summarized the relative risks of outcomes between self-testing and clinic-based testing for proteinuria. We also assessed values and preferences and costs of self-testing.ResultsThree publications were identified for the effectiveness review; two for values/preferences, and none for the cost review, mostly from high-income countries. Overall, there was no statistically significant difference between self-testing and inpatient care for proteinuria among women with hypertension for any of the outcomes with data available. In general, both women and providers were supportive of proteinuria self-testing because it allows a greater role in self-care and fewer clinic visits, though some emphasized the need to train end-users for proper testing and appropriate follow-up actions.ConclusionsVery limited evidence suggests that self-testing for proteinuria results in comparable maternal and fetal outcomes as provider-testing for hypertensive pregnant individuals, and is generally acceptable to end-users and providers despite some concerns. No evidence of effectiveness was available for the general pregnant population. This evidence base supports its feasibility as an additional option for identifying individuals at risk of preeclampsia.Systematic review registration numberPROSPERO CRD42021233845
Methylation of the glucocorticoid receptor gene (NR3C1) in dyads mother-child exposed to intimate partner violence in Cameroon: Association with anxiety symptoms
Authors: Wadji Dany Laure , Morina Naser , Martin-Soelch Chantal , Wicky Chantal 
Published: August 2022

AbstractBackgroundThe glucocorticoid receptor (GR), which is encoded by theNR3C1(Nuclear Receptor Subfamily 3 Group C Member 1) gene plays an important role in the modulation of the hypothalamic-pituitary-adrenal (HPA) axis activity by providing feedback regulation which allows termination of the stress response. Little is known about epigenetic programming at the level of NGFI-A putative binding site (CpG) of theNR3C1exon 1F in dyads mother-child exposed to intimate partner violence (IPV) more specifically in an unstudied region such as the Sub-Saharan Africa where levels of violence are very high.ObjectiveExamineNR3C1exon 1F methylation in response to IPV and possible association with cortisol concentration and mental health.MethodWe recruited 20 mother–child dyads exposed to IPV and a control group of 20 mother–child dyads not exposed to IPV. We administered self-reported questionnaires to measure mother’s mental health and collected saliva samples for cortisol dosage and bisulfite sequencing of DNA methylation.ResultsRegarding the mothers, our results showed a significant difference in methylation level at CpG 16-21 sites of theNR3C1exon 1F promoter region between the groups. In the exposed group as compared to the control group, there was a significant positive association between the level of methylation at CpG 16-21 sites and mother’s mental health in particular anxiety symptoms. However, we did not find any significant correlation between methylation level and cortisol concentration. In children, we did not find any significant result.ConclusionThis study highlights a NGFI-A putative binding site (CpG 16-21) that is more methylated in mothers exposed to IPV and which may have the potential to confer vulnerability for psychopathologies.
Effect of Acute Cardiovascular Exercise on Cerebral Blood Flow: A Systematic Review
Authors: Mulser Lisa , Moreau David 
Published: August 2022

AbstractA single bout of cardiovascular exercise can have a cascade of physiological effects, including increased blood flow to the brain. This effect has been documented across multiple modalities, yet studies have reported mixed findings. Here, we systematically review evidence for the acute effect of cardiovascular exercise on cerebral blood flow across a range of neuroimaging techniques and exercise characteristics. Based on 52 studies and a combined sample size of 1,174 individuals, our results indicate that the acute effect of cardiovascular exercise on cerebral blood flow generally follows an inverted U-shaped relationship, whereby blood flow increases early on but eventually decreases as exercise continues. However, we also find that this effect is not uniform across studies, instead varying across a number of key variables including exercise characteristics, brain regions, and neuroimaging modalities. As the most comprehensive synthesis on the topic to date, this systematic review sheds light on the determinants of exercise-induced change in cerebral blood flow, a necessary step toward personalized interventions targeting brain health across a range of populations.
A pan-cancer analysis of the oncogenic role of COVID-19 risk gene Leucine Zipper Transcription Factor-Like Protein 1 (LZTFL1) in human tumors
Authors: Mo Jihao , Zhang Zhenzhen , Wang Daping , Su Mingqin , Hu Jian , Liu Yakun , Wang Lei , Wang Meimei 
Published: August 2022

AbstractPopulation-based studies showed that COVID-19 infection causes higher death rate in cancer patients. However, the molecular mechanism of COVID-19 with cancer is still largely unknown. Here we analyzed the Leucine Zipper Transcription Factor-Like Protein 1 (LZTFL1) which is the most significant gene associated with COVID-19. First, we explored the potential oncogenic roles of LZTFL1 through transcriptome data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. LZTFL1 is significantly low expressed in 11 of 34 kinds of cancers we analyzed. Consistent with the mRNA expression data, the protein expression of LZTFL1 in lung adenocarcinoma (LUAD), clear cell renal cell carcinoma (ccRCC), Uterine corpus endometrial carcinoma (UCEC), and ovarian cancer (OV) patients are significantly decreased compared to healthy tissues. The survival analysis from the Kidney renal clear cell carcinoma (KIRC), Rectum adenocarcinoma (READ), and Uveal Melanoma (UVM), the LZTFL1 high expression group have a significantly higher survival rate compared to the low expression group. Taken together, LZTFL1 acts as a cancer suppressor gene for several cancers. Moreover, LZTFL1 expression was associated with the cancer-associated fibroblast infiltration in several tumors including Bladder Urothelial Carcinoma (BLCA), Breast invasive carcinoma (BRCA), Esophageal carcinoma (ESCA), Head and Neck squamous cell carcinoma (HNSC), Lung squamous cell carcinoma (LUSC), and Pancreatic adenocarcinoma (PAAD). Gene ontology analysis showed that cilium organization, positive regulation of establishment of protein localization to telomere and SRP-dependent cotranslational protein targeting to the membrane were involved in the function mechanisms related to LZTFL1. Our studies offer a relatively comprehensive understanding of the oncogenic roles of LZTFL1 across different kinds of tumors.
Syncope and subsequent traffic crash: A responsibility analysis
Authors: Staples John A , Erdelyi Shannon , Merchant Ketki , Yip Candace , Khan Mayesha , Redelmeier Donald A , Chan Herbert , Brubacher Jeffrey R 
Published: August 2022

AbstractBackgroundPhysicians are often asked to counsel patients about driving safety after syncope, yet little empirical data guides such advice.MethodsWe identified a population-based retrospective cohort of 9,507 individuals with a driver license who were discharged from any of six urban emergency departments (EDs) with a diagnosis of ‘syncope and collapse’. We examined all police-reported crashes that involved a cohort member as a driver and occurred between 1 January 2010 and 31 December 2016. We categorized crash-involved drivers as ‘responsible’ or ‘non-responsible’ for their crash using detailed police-reported crash data and a validated responsibility scoring tool. We then used logistic regression to test the hypothesis that recent syncope was associated with driver responsibility for crash.ResultsOver the 7-year study interval, cohort members were involved in 475 police-reported crashes: 210 drivers were deemed responsible and 133 drivers were deemed non-responsible for their crash; the 132 drivers deemed to have indeterminate responsibility were excluded from further analysis. An ED visit for syncope occurred in the three months leading up to crash in 11 crash-responsible drivers and in 5 crash-non-responsible drivers, suggesting that recent syncope was not associated with driver responsibility for crash (adjusted odds ratio, 1.31; 95%CI, 0.40-4.74; p=0.67). However, all drivers with cardiac syncope were deemed responsible, precluding calculation of an odds ratio for this important subgroup.ConclusionsRecent syncope was not significantly associated with driver responsibility for traffic crash. Clinicians and policymakers should consider these results when making fitness-to-drive recommendations after syncope.Key MessagesWhat is already known on this topic: Clinicians are often asked to counsel patients about driving safety after syncope, yet little empirical data guides such advice.What this study adds: In contrast to prior studies, we found no significant association between an emergency department visit for syncope and driver responsibility for a subsequent motor vehicle crash.How this study might affect research, practice or policy: These findings might reassure clinicians, patients and policymakers that current driving restrictions after first-episode syncope adequately mitigate the risk of subsequent crash.
A cell-autonomous role for primary cilia in long-range commissural axon guidance
Authors: Dumoulin Alexandre , Wilson Nicole H. , Tucker Kerry L. , Stoeckli Esther T. 
Published: August 2022

SummaryCiliopathies are characterized by the absence or dysfunction of primary cilia. Despite the fact that cognitive impairments are a common feature of ciliopathies, how cilia dysfunction affects neuronal development has not been characterized in detail. Here, we show that the primary cilium is required cell-autonomously by neurons during neural circuit formation. In particular, the primary cilium is crucial during axonal pathfinding for the switch in responsiveness of axons at a choice point, or intermediate target. Utilizing animal models and in vivo, ex vivo, as well as in vitro experiments, we provide evidence for a critical role of the primary cilium in long-range axon guidance. The primary cilium on the cell body of commissural neurons transduces long-range guidance signals sensed by growth cones navigating an intermediate target. In extension of our finding that Shh is required for the rostral turn of post-crossing commissural axons, we show here that the cilium is required for a transcriptional change of axon guidance receptors, which in turn mediate the repulsive response to floorplate-derived Shh shown by post-crossing commissural axons.
Bioinformatics analysis in identifying significantly expressed immune related genes in influenza A virus infection
Authors: Olaniyi Ayinde , Oluwabunmi Alabi , Oluwatobi Oguntoye 
Published: August 2022

AbstractThis study is done to identify significantly expressed genes of influenza A virus infection in human, facilitated by the idea of checking for the presence of immune related genes in these significantly expressed genes, followed by the analysis of their potential mechanism and pathway. Considering the usage of microarray dataset, the gene expression profile GSE66597 was downloaded from the gene expression omnibus(GEO) database, and then a subsequent generation of differentially expressed genes(DEGs) using the GEO2R tool. A total of 1107 genes was generated with 703 upregulated and 404 downregulated genes. The protein-protein interaction (PPI) network was constructed using string and Cytoscape software which resulted in generating the core genes, hub genes, and bottleneck genes. Subsequent Venn diagram analysis finally gave the six candidate genes CRP, CCL5, IL17A, STAT1, CD34, SPI1, subjected to gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) for enrichment and pathway analysis respectively. Out of the initial six candidate genes, four of these genes CRP, CCL5, IL17A, are immune related, and initiated particularly by the presence of influenza A virus.
Hepatic MCPIP1 protein levels are reduced in NAFLD patients and are predominantly expressed in cholangiocytes and liver endothelium
Authors: Pydyn Natalia , Kadluczka Justyna , Major Piotr , Hutsch Tomasz , Wołoszyn Kinga , Malczak Piotr , Radkowiak Dorota , Budzynski Andrzej , Miekus Katarzyna , Jura Jolanta , Kotlinowski Jerzy 
Published: August 2022

AbstractNonalcoholic fatty liver disease (NAFLD) is characterized by the excessive accumulation of fat in hepatocytes. NAFLD can range from simple steatosis to the aggressive form called nonalcoholic steatohepatitis (NASH), which is characterized by both fatty liver and liver inflammation. Without proper treatment, NAFLD may further progress to lifethreatening complications, such as fibrosis, cirrhosis or liver failure. Monocyte chemoattractant protein-induced protein 1 (MCPIP1, alias Regnase 1) is a negative regulator of inflammation, acting through the cleavage of transcripts coding for proinflammatory cytokines and the inhibition of NFκB activity.In this study, we investigated MCPIP1 expression in the liver and peripheral blood mononuclear cells (PBMCs) collected from a cohort of 36 control and NAFLD patients hospitalized due to bariatric surgery or primary inguinal hernia laparoscopic repair. Based on liver histology data (H&E and Oil Red O staining), 12 patients were classified into the nonalcoholic fatty liver (NAFL) group, 19 into the NASH group and 5 into the control (non-NAFLD) group. Biochemical characterization of patient plasma was followed by expression analysis of genes regulating inflammation and lipid metabolism. The MCPIP1 protein level was reduced in the livers of NAFL and NASH patients in comparison to non-NAFLD control individuals. Additionally, in all groups of patients, immunohistochemical staining showed that the expression of MCPIP1 was higher in the portal fields and bile ducts in comparison to the liver parenchyma and central vein. The liver MCPIP1 protein level negatively correlated with hepatic steatosis but not with patient BMI or any other analyte. The MCPIP1 level in PBMCs did not differ between NAFLD patients and control patients. Similarly, in patients’ PBMCs there were no differences in the expression of genes regulating β-oxidation (ACOX1, CPT1A, and ACC1) and inflammation (TNF, IL1B, IL6, IL8, IL10, and CCL2), or transcription factors controlling metabolism (FAS, LCN2, CEBPB, SREBP1, PPARA, and PPARG).We have demonstrated that MCPIP1 protein levels are reduced in NAFLD patients, but further research is needed to investigate the specific role of MCPIP1 in NAFL initiation and the transition to NASH.
DeepGAMI: Deep biologically guided auxiliary learning for multimodal integration and imputation to improve phenotype prediction
Authors: Chandrashekar Pramod Bharadwaj , Wang Jiebiao , Hoffman Gabriel E. , He Chenfeng , Jin Ting , Alatkar Sayali , Khullar Saniya , Bendl Jaroslav , Fullard John F. , Roussos Panagiotis , Wang Daifeng 
Published: August 2022

AbstractGenotype-phenotype association is found in many biological systems, such as brain-related diseases and behavioral traits. Despite the recent improvement in the prediction of phenotypes from genotypes, they can be further improved and explainability of these predictions remains challenging, primarily due to complex underlying molecular and cellular mechanisms. Emerging multimodal data enables studying such mechanisms at different scales from genotype to phenotypes involving intermediate phenotypes like gene expression. However, due to the black-box nature of many machine learning techniques, it is challenging to integrate these multi-modalities and interpret the biological insights in prediction, especially when some modality is missing. Biological knowledge has recently been incorporated into machine learning modeling to help understand the reasoning behind the choices made by these models.To this end, we developed DeepGAMI, an interpretable deep learning model to improve genotype-phenotype prediction from multimodal data. DeepGAMI uses prior biological knowledge to define the neural network architecture. Notably, it embeds an auxiliary-learning layer for cross-modal imputation while training the model from multimodal data. Using this pre-trained layer, we can impute latent features of additional modalities and thus enable predicting phenotypes from a single modality only. Finally, the model uses integrated gradient to prioritize multimodal features and links for phenotypes. We applied DeepGAMI to multiple emerging multimodal datasets: (1) population-level genotype and bulk-tissue gene expression data for predicting schizophrenia, (2) population-level genotype and gene expression data for predicting clinical phenotypes in Alzheimer’s Disease, (3) gene expression and electrophysiological data of single neuronal cells in the mouse visual cortex, and (4) cell-type gene expression and genotype data for predicting schizophrenia. We found that DeepGAMI outperforms existing state-of-the-art methods and provides a profound understanding of gene regulatory mechanisms from genotype to phenotype, especially at cellular resolution. DeepGAMI is an open-source tool and is available at https://github.com/daifengwanglab/DeepGAMI.
In-vivo Measurement of Radio Frequency Electric Fields in Mice Brain
Authors: Yaghmazadeh Omid , Schoenhardt Seth , Sarabandi Arya , Sabet Ali , Sabet Kazem , Safari Fatemeh , Alon Leeor , Buzsáki György 
Published: August 2022

ABSTRACTWith development of novel technologies, radio frequency (RF) energy exposure is expanding at various wavelengths and power levels. These developments necessitate updated approaches of RF measurements in complex environments, particularly in live biological tissue. In this study, we introduce a technique for direct in-vivo measurement of electric fields in living tissue. Proof of principle in-vivo electric field measurements were conducted in rodent brains using Bismuth Silicon Oxide (BSO) crystals exposed to varying levels of RF energy. Electric field measurements were calibrated and verified using in-vivo temperature measurements using optical temperature fibers alongside electromagnetic field simulations of a transverse electromagnetic (TEM) cell.SIGNIFICANCEAccurate dosimetry of the absorbed radio frequency (RF) electric fields (E-Fields) by the live tissue is the keystone of environmental health considerations for this type of ever-growing non-ionizing radiation energy. The complexity of biological tissue and technical difficulties have made direct measurement of E-fields in live tissue challenging leading to application of ex-vivo and in-silico approaches. Here, we present a novel method for in-vivo direct measurement of RF E-fields in anesthetized mice brain using electro-optic sensors.
Changes in active-site geometry on X-ray photoreduction of a lytic polysaccharide monooxygenase active-site copper and saccharide binding
Authors: Tandrup Tobias , Muderspach Sebastian J. , Banerjee Sanchari , Santoni Gianluca , Ipsen Johan Ø. , Hernández-Rollán Cristina , Nørholm Morten H. H. , Johansen Katja S. , Meilleur Flora , Lo Leggio Leila 
Published: August 2022

The recently discovered lytic polysaccharide monooxygenases (LPMOs) are Cu-containing enzymes capable of degrading polysaccharide substrates oxidatively. The generally accepted first step in the LPMO reaction is the reduction of the active-site metal ion from Cu2+ to Cu+. Here we have used a systematic diffraction data collection method to monitor structural changes in two AA9 LPMOs, one from Lentinus similis (LsAA9_A) and one from Thermoascus aurantiacus (TaAA9_A), as the active-site Cu is photoreduced in the X-ray beam. For LsAA9_A, the protein produced in two different recombinant systems was crystallized to probe the effect of post-translational modifications and different crystallization conditions on the active site and metal photoreduction. We can recommend that crystallographic studies of AA9 LPMOs wishing to address the Cu2+ form use a total X-ray dose below 3 × 104 Gy, while the Cu+ form can be attained using 1 × 106 Gy. In all cases, we observe the transition from a hexacoordinated Cu site with two solvent-facing ligands to a T-shaped geometry with no exogenous ligands, and a clear increase of the θ2 parameter and a decrease of the θ3 parameter by averages of 9.2° and 8.4°, respectively, but also a slight increase in θT. Thus, the θ2 and θ3 parameters are helpful diagnostics for the oxidation state of the metal in a His-brace protein. On binding of cello-oligosaccharides to LsAA9_A, regardless of the production source, the θT parameter increases, making the Cu site less planar, while the active-site Tyr—Cu distance decreases reproducibly for the Cu2+ form. Thus, the θT increase found on copper reduction may bring LsAA9_A closer to an oligosaccharide-bound state and contribute to the observed higher affinity of reduced LsAA9_A for cellulosic substrates.