bluuebunny/crossref_metadata_2025_split huggingface dataset:
DeepToA: an ensemble deep-learning approach to predicting the theater of activity of a microbiome
Authors: Zeng Wenhuan , Gautam Anupam , Huson Daniel H 
Published: August 2022

Abstract

Motivation
Metagenomics is the study of microbiomes using DNA sequencing. A microbiome consists of an assemblage of microbes that is associated with a ‘theater of activity’ (ToA). An important question is, to what degree does the taxonomic and functional content of the former depend on the (details of the) latter? Here, we investigate a related technical question: Given a taxonomic and/or functional profile estimated from metagenomic sequencing data, how to predict the associated ToA? We present a deep-learning approach to this question. We use both taxonomic and functional profiles as input. We apply node2vec to embed hierarchical taxonomic profiles into numerical vectors. We then perform dimension reduction using clustering, to address the sparseness of the taxonomic data and thus make the problem more amenable to deep-learning algorithms. Functional features are combined with textual descriptions of protein families or domains. We present an ensemble deep-learning framework DeepToA for predicting the ToA of amicrobial community, based on taxonomic and functional profiles. We use SHAP (SHapley Additive exPlanations) values to determine which taxonomic and functional features are important for the prediction.

Results
Based on 7560 metagenomic profiles downloaded from MGnify, classified into 10 different theaters of activity, we demonstrate that DeepToA has an accuracy of 98.30%. We show that adding textual information to functional features increases the accuracy.

Availability and implementation
Our approach is available at http://ab.inf.uni-tuebingen.de/software/deeptoa.

Supplementary information
Supplementary data are available at Bioinformatics online.
scFeatures: multi-view representations of single-cell and spatial data for disease outcome prediction
Authors: Cao Yue , Lin Yingxin , Patrick Ellis , Yang Pengyi , Yang Jean Yee Hwa 
Published: August 2022

Abstract

Motivation
With the recent surge of large-cohort scale single cell research, it is of critical importance that analytical methods can fully utilize the comprehensive characterization of cellular systems that single cell technologies produce to provide insights into samples from individuals. Currently, there is little consensus on the best ways to compress information from the complex data structures of these technologies to summary statistics that represent each sample (e.g. individuals).

Results
Here, we present scFeatures, an approach that creates interpretable cellular and molecular representations of single-cell and spatial data at the sample level. We demonstrate that summarizing a broad collection of features at the sample level is both important for understanding underlying disease mechanisms in different experimental studies and for accurately classifying disease status of individuals.

Availability and implementation
scFeatures is publicly available as an R package at https://github.com/SydneyBioX/scFeatures. All data used in this study are publicly available with accession ID reported in the Section 2.

Supplementary information
Supplementary data are available at Bioinformatics online.
Demographic trends in the incidence of malignant appendiceal tumours in England between 1995 and 2016: Population-based analysis
Authors: Orchard Philippa , Preece Ryan , Thomas Michael G , Dixon Steven W , Wong Newton A C S , Chambers Adam C , Messenger David E 
Published: August 2022

Abstract

Aims
Recent data suggest that the incidence of malignant appendiceal tumours is increasing. This study aimed to determine temporal trends in the incidence of malignant appendiceal tumours within England and a possible influence by demographic factors.

Methods
All incident cases of appendiceal tumours in patients aged 20 years and above were identified from the National Cancer Registration and Analysis Service database between 1995 and 2016 using ICD-9/10 codes. Cancers were categorized according to histology. Joinpoint regression analysis was used to investigate changes in age-standardized incidence rates by age, sex, histological subtype and index of multiple deprivation quintiles, based on socioeconomic domains (income, employment, education, health, crime, barriers to housing and services and living environment). Average annual per cent changes (AAPCs) were estimated by performing Monte-Carlo permutation analysis.

Results
A total of 7333 tumours were diagnosed and 7056 patients were analysed, comprising 3850 (54.6 per cent) neuroendocrine tumours (NETs), 1892 (26.8 per cent) mucinous adenocarcinomas and 1314 (18.6 per cent) adenocarcinoma (not otherwise specified). The overall incidence of appendiceal tumours increased from 0.3 per 100 000 to 1.6 per 100 000 over the study interval. Incidence rate increases of comparable magnitude were observed across all age groups, but the AAPC was highest among patients aged 20–29 years (15.6 per cent, 95 per cent c.i 12.7–18.6 per cent) and 30–39 years (14.2 per cent, 12.2–16.2 per cent) and lowest among those aged 70–79 years (6.8 per cent, 5.7–8.0 per cent). Similar incidence rate increases were reported across all socioeconomic deprivation quintiles and in both sexes. Analysis by grade of NET showed that grade 1 tumours accounted for 63 per cent between 2010 and 2013, compared with 2 per cent between 2000 and 2003.

Conclusions
The incidence rate of malignant appendiceal tumours has increased significantly since 1995 and is mainly attributed to an increase in NETs. The increased diagnosis of low-grade NETs may in part be due to changes in pathological classification systems.
Rescue of lysosomal function as therapeutic strategy for SPG15 hereditary spastic paraplegia
Authors: Vantaggiato Chiara , Orso Genny , Guarato Giulia , Brivio Francesca , Napoli Barbara , Panzeri Elena , Masotti Simona , Santorelli Filippo Maria , Lamprou Maria , Gumeni Sentiljana , Clementi Emilio , Bassi Maria Teresa 
Published: August 2022

AbstractSPG15 is a hereditary spastic paraplegia subtype caused by mutations in Spastizin, a protein encoded by the ZFYVE26 gene. Spastizin is involved in autophagosome maturation and autophagic lysosome reformation and SPG15-related mutations lead to autophagic lysosome reformation defects with lysosome enlargement, free lysosome depletion and autophagosome accumulation. Symptomatic and rehabilitative treatments are the only therapy currently available for patients. Here, we targeted autophagy and lysosomes in SPG15 patient-derived cells by using a library of autophagy-modulating compounds. We identified a rose of compounds affecting intracellular calcium levels, the calcium-calpain pathway or lysosomal functions, which reduced autophagosome accumulation. The six most effective compounds were tested in vivo in a new SPG15 loss of function Drosophila model that mimicked the reported SPG15 phenotype, with autophagosome accumulation, enlarged lysosomes, reduced free lysosomes, autophagic lysosome reformation defects and locomotor deficit. These compounds, namely verapamil, Bay K8644, 2′,5′-dideoxyadenosine, trehalose, Small-Molecule Enhancer of Rapamycin 28 and trifluoperazine, improved lysosome biogenesis and function in vivo, demonstrating that lysosomes are a key pharmacological target to rescue SPG15 phenotype. Among the others, the Small-Molecule Enhancer of Rapamycin 28 was the most effective, rescuing both autophagic lysosome reformation defects and locomotor deficit, and could be considered as a potential therapeutic compound for this hereditary spastic paraplegia subtype.
DJ-1 is an essential downstream mediator in PINK1/parkin-dependent mitophagy
Authors: Imberechts Dorien , Kinnart Inge , Wauters Fieke , Terbeek Joanne , Manders Liselot , Wierda Keimpe , Eggermont Kristel , Madeiro Rodrigo Furtado , Sue Carolyn , Verfaillie Catherine , Vandenberghe Wim 
Published: August 2022

Abstract
Loss-of-function mutations in the PRKN, PINK1 and PARK7 genes (encoding parkin, PINK1 and DJ-1, respectively) cause autosomal recessive forms of Parkinson’s disease. PINK1 and parkin jointly mediate selective autophagy of damaged mitochondria (mitophagy), but the mechanisms by which loss of DJ-1 induces Parkinson’s disease are not well understood. Here, we investigated PINK1/parkin-mediated mitophagy in cultured human fibroblasts and induced pluripotent stem cell-derived neurons with homozygous PARK7 mutations. We found that DJ-1 is essential for PINK1/parkin-mediated mitophagy. Loss of DJ-1 did not interfere with PINK1 or parkin activation after mitochondrial depolarization but blocked mitophagy further downstream by inhibiting recruitment of the selective autophagy receptor optineurin to depolarized mitochondria. By contrast, starvation-induced, non-selective autophagy was not affected by loss of DJ-1. In wild-type fibroblasts and induced pluripotent stem cell-derived dopaminergic neurons, endogenous DJ-1 translocated to depolarized mitochondria in close proximity to optineurin. DJ-1 translocation to depolarized mitochondria was dependent on PINK1 and parkin and did not require oxidation of cysteine residue 106 of DJ-1. Overexpression of DJ-1 did not rescue the mitophagy defect of PINK1- or parkin-deficient cells. These findings position DJ-1 downstream of PINK1 and parkin in the same pathway and suggest that disruption of PINK1/parkin/DJ-1-mediated mitophagy is a common pathogenic mechanism in autosomal recessive Parkinson’s disease.
GFPT1 promotes the proliferation of cervical cancer via regulating the ubiquitination and degradation of PTEN
Authors: Li Dailing , Guan Mingmei , Cao Xiaofei , Zha Zhi Qiang , Zhang Peiling , Xiang Hong , Zhou Yun , Peng Qian , Xu Zhixiang , Lu Lin , Liu Guolong 
Published: August 2022

Abstract
Cervical cancer demonstrates the fourth incidence and death rate in females worldwide. Glutamine--fructose-6-phosphate transaminase 1 (GFPT1), the first rate-limited enzyme of the hexosamine biosynthesis pathway, has been reported to promote the progression of cancers. However, the prognostic value and roles of GFPT1 in cervical cancer are largely unknown. Transcription expression data for cervical cancer were downloaded from public databases. GFPT1 overexpressed and knockdown cell lines were constructed. Colony formation assays, Edu assays and 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays were used to measure the proliferation capabilities of cervical cancer cells. Western blot, Immunofluorescence and co-immunoprecipitation assays were performed to verify the interaction between GFPT1and Phosphatase and tensin homolog (PTEN). Animal assays were applied to verify the results in vivo. GFPT1 expression was higher in cervical cancer cell lines. The proliferation capabilities of cervical cancer cells were suppressed in GFPT1 knockdown cells and GFPT1 inhibitor L-DON treated cells. And overexpression of GFPT1 promoted cell proliferation. PTEN was up-regulated in GFPT1 knockdown cells and downregulated in GFPT1 overexpression cells. Immunofluorescence and co-immunoprecipitation results showed that GFPT1 was co-localized and interacted with PTEN. GFPT1 promoted the ubiquitination and degradation of PTEN. Silence of PTEN offsets the growth inhibition of cervical cancer caused by GFPT1 knockdown. Animal assays showed that GFPT1 promoted the proliferation of cervical cancer in vivo. Our study revealed that GFPT1 could promote the progression of cervical cancer by regulating PTEN expression. Our study highlights the GFPT1-PTEN regulation as a potential therapy target for cervical cancer. .
Persistence of Severe Acute Respiratory Syndrome Coronavirus 2 Omicron Variant in Children and Utility of Rapid Antigen Testing as an Indicator of Culturable Virus
Authors: Lohse Zoe M , Shapiro Jerne J , Lednicky John A , Cash Melanie N , Jun Inyoung , Mavian Carla N , Tagliamonte Massimiliano S , Saleem Cyrus , Yang Yang , Nelson Eric J , Salemi Marco , Ryan Kathleen A , Morris J Glenn 
Published: August 2022

Abstract
We screened 65 longitudinally collected nasal swab samples from 31 children aged 0–16 years who were positive for severe acute respiratory syndrome coronavirus 2 Omicron BA.1. By day 7 after onset of symptoms, 48% of children remained positive by rapid antigen test. In a sample subset, we found 100% correlation between antigen test results and virus culture.
Physiological Differences Between Seasonal Dimorphs of Agonoscena pistaciae (Hemiptera: Aphalaridae) Elicit Distinct Host Plant Responses, Informing Novel Pest Management Insights
Authors: Homayoonzadeh Mohammad , Michaud J P , Esmaeily Mojtaba , Talebi Khalil , Allahyari Hossein , Wright Denis J 
Published: August 2022

Abstract
We examined differences in the physiology and life history between dimorphs of the common pistachio psyllid, Agonoscena pistaciae (Burckhardt and Lauterer) (Hemiptera: Aphalaridae), and how they differ in elicitating host plant production of key metabolites and volatile compounds involved in the recruitment of herbivores and natural enemies. Summer morphs had higher activities of glutathione S-transferase, carboxylesterase, acetylcholinesterase, and cytochrome P450 monooxygenase, superoxide dismutase, catalase, peroxidase, phenoloxidase, and a higher total protein content compared to winter morphs, whereas the latter had higher amounts of lipid, carbohydrate, and glycogen. Winter morphs were heavier, with a higher chitin content and longer preoviposition period, but greater fecundity and longevity than summer morphs. A lower LC50 to thiamethoxam for winter morphs resulted in higher mortality following exposure to the recommended rate of this insecticide in a greenhouse trial. Feeding by winter morphs elicited more strongly the release of volatile compounds known to be attractive to other herbivores, whereas feeding by summer morphs elicited more strongly the release of volatiles implicated in the attraction of natural enemies. Feeding by psyllids increased the concentrations of nitrogenous compounds, carbohydrates, vitamins, and amino acids in plants, the winter morph eliciting larger changes and more improved host plant quality. We conclude that winter morphs are more vulnerable targets for chemical control in early spring, whereas management of summer morphs could rely more on conservation biological control.
Critical Care Cardiology Trials Network (CCCTN): a cohort profile
Authors: Metkus Thomas S , Baird-Zars Vivian M , Alfonso Carlos E , Alviar Carlos L , Barnett Christopher F , Barsness Gregory W , Berg David D , Bertic Mia , Bohula Erin A , Burke James , Burstein Barry , Chaudhry Sunit-Preet , Cooper Howard A , Daniels Lori B , Fordyce Christopher B , Ghafghazi Shahab , Goldfarb Michael , Katz Jason N , Keeley Ellen C , Keller Norma M , Kenigsberg Benjamin , Kontos Michael C , Kwon Younghoon , Lawler Patrick R , Leibner Evan , Liu Shuangbo , Menon Venu , Miller P Elliott , Newby L Kristin , O'Brien Connor G , Papolos Alexander I , Pierce Matthew J , Prasad Rajnish , Pisani Barbara , Potter Brian J , Roswell Robert O , Sinha Shashank S , Shah Kevin S , Smith Timothy D , Snell R Jeffrey , So Derek , Solomon Michael A , Ternus Bradley W , Teuteberg Jeffrey J , van Diepen Sean , Zakaria Sammy , Morrow David A 
Published: August 2022

AbstractAimsThe aims of the Critical Care Cardiology Trials Network (CCCTN) are to develop a registry to investigate the epidemiology of cardiac critical illness and to establish a multicentre research network to conduct randomised clinical trials (RCTs) in patients with cardiac critical illness.Methods and resultsThe CCCTN was founded in 2017 with 16 centres and has grown to a research network of over 40 academic and clinical centres in the United States and Canada. Each centre enters data for consecutive cardiac intensive care unit (CICU) admissions for at least 2 months of each calendar year. More than 20 000 unique CICU admissions are now included in the CCCTN Registry. To date, scientific observations from the CCCTN Registry include description of variations in care, the epidemiology and outcomes of all CICU patients, as well as subsets of patients with specific disease states, such as shock, heart failure, renal dysfunction, and respiratory failure. The CCCTN has also characterised utilization patterns, including use of mechanical circulatory support in response to changes in the heart transplantation allocation system, and the use and impact of multidisciplinary shock teams. Over years of multicentre collaboration, the CCCTN has established a robust research network to facilitate multicentre registry-based randomised trials in patients with cardiac critical illness.ConclusionThe CCCTN is a large, prospective registry dedicated to describing processes-of-care and expanding clinical knowledge in cardiac critical illness. The CCCTN will serve as an investigational platform from which to conduct randomised controlled trials in this important patient population.
Pulmonary artery banding as adjunct therapy for ventricular recovery after anomalous left coronary artery from the pulmonary artery repair: a case report
Authors: Mets Gilles , Bové Thierry , François Katrien , Panzer Joseph 
Published: August 2022

Abstract
Anomalous left coronary artery from the pulmonary artery is a rare congenital coronary anomaly commonly associated with severe but reversible left ventricular dysfunction. We present an anomalous left coronary artery from the pulmonary artery case of persisting left ventricular failure with inability to wean off the ventilator and inotropes after successful coronary reimplantation, in whom pulmonary artery banding enhanced myocardial recovery.
Reoperative aortic valve replacement after bio-Bentall using a double sewing ring technique
Authors: Ikeno Yuki , Motoki Tatsuo , Kurushima Atsushi , Fukumura Yoshiaki 
Published: August 2022

Abstract
We report an 89-year-old haemodialysis patient with a structural valve deterioration following a Bentall–de Bono operation with a tissue valve using the double sewing ring technique. The bioprosthesis was extracted easily, and the aortic valve replacement was performed without any complications in a high-risk patient. This procedure may be feasible given the prospects of reoperation.
Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement
Authors: Kronenberg Florian , Mora Samia , Stroes Erik S G , Ference Brian A , Arsenault Benoit J , Berglund Lars , Dweck Marc R , Koschinsky Marlys , Lambert Gilles , Mach François , McNeal Catherine J , Moriarty Patrick M , Natarajan Pradeep , Nordestgaard Børge G , Parhofer Klaus G , Virani Salim S , von Eckardstein Arnold , Watts Gerald F , Stock Jane K , Ray Kausik K , Tokgözoğlu Lale S , Catapano Alberico L 
Published: August 2022

AbstractThis 2022 European Atherosclerosis Society lipoprotein(a) [Lp(a)] consensus statement updates evidence for the role of Lp(a) in atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis, provides clinical guidance for testing and treating elevated Lp(a) levels, and considers its inclusion in global risk estimation. Epidemiologic and genetic studies involving hundreds of thousands of individuals strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes in different ethnicities; elevated Lp(a) is a risk factor even at very low levels of low-density lipoprotein cholesterol. High Lp(a) is associated with both microcalcification and macrocalcification of the aortic valve. Current findings do not support Lp(a) as a risk factor for venous thrombotic events and impaired fibrinolysis. Very low Lp(a) levels may associate with increased risk of diabetes mellitus meriting further study. Lp(a) has pro-inflammatory and pro-atherosclerotic properties, which may partly relate to the oxidized phospholipids carried by Lp(a). This panel recommends testing Lp(a) concentration at least once in adults; cascade testing has potential value in familial hypercholesterolaemia, or with family or personal history of (very) high Lp(a) or premature ASCVD. Without specific Lp(a)-lowering therapies, early intensive risk factor management is recommended, targeted according to global cardiovascular risk and Lp(a) level. Lipoprotein apheresis is an option for very high Lp(a) with progressive cardiovascular disease despite optimal management of risk factors. In conclusion, this statement reinforces evidence for Lp(a) as a causal risk factor for cardiovascular outcomes. Trials of specific Lp(a)-lowering treatments are critical to confirm clinical benefit for cardiovascular disease and aortic valve stenosis.
Dapagliflozin for heart failure according to body mass index: the DELIVER trial
Authors: Adamson Carly , Kondo Toru , Jhund Pardeep S , de Boer Rudolf A , Cabrera Honorio Jose Walter , Claggett Brian , Desai Akshay S , Alcocer Gamba Marco Antonio , Al Habeeb Waleed , Hernandez Adrian F , Inzucchi Silvio E , Kosiborod Mikhail N , Lam Carolyn S P , Langkilde Anna Maria , Lindholm Daniel , Bachus Erasmus , Litwin Sheldon E , Martinez Felipe , Petersson Magnus , Shah Sanjiv J , Vaduganathan Muthiah , Nguyen Vinh Pham , Wilderäng Ulrica , Solomon Scott D , McMurray John J V 
Published: August 2022

Abstract

Aims
Obesity is common and associated with unique phenotypic features in heart failure with preserved ejection fraction (HFpEF). Therefore, understanding the efficacy and safety of new therapies in HFpEF patients with obesity is important. The effects of dapagliflozin were examined according to body mass index (BMI) among patients in the Dapagliflozin Evaluation to Improve the LIVEs of Patients With PReserved Ejection Fraction Heart Failure trial.

Methods and results
Body mass index was analysed by World Health Organization (WHO) categories and as a continuous variable using restricted cubic splines. Body mass index ranged from 15.2 to 50 kg/m2 with a mean value of 29.8 (standard deviation ± 6.1) kg/m2. The proportions, by WHO category, were: normal weight 1343 (21.5%); overweight 2073 (33.1%); Class I obesity 1574 (25.2%); Class II obesity 798 (12.8%); and Class III obesity 415 (6.6%). Compared with placebo, dapagliflozin reduced the risk of the primary outcome to a similar extent across these categories: hazard ratio (95% confidence interval): 0.89 (0.69–1.15), 0.87 (0.70–1.08), 0.74 (0.58–0.93), 0.78 (0.57–1.08), and 0.72 (0.47–1.08), respectively (P-interaction = 0.82). The placebo-corrected change in Kansas City Cardiomyopathy Questionnaire total symptom score with dapagliflozin at 8 months was: 0.9 (−1.1, 2.8), 2.5 (0.8, 4.1), 1.9 (−0.1, 3.8), 2.7 (−0.5, 5.8), and 8.6 (4.0, 13.2) points, respectively (P-interaction = 0.03). The placebo-corrected change in weight at 12 months was: –0.88 (−1.28, –0.47), –0.65 (−1.04, –0.26), –1.42 (−1.89, –0.94), –1.17 (−1.94, –0.40), and –2.50 (−4.4, –0.64) kg (P-interaction = 0.002).

Conclusions
Obesity is common in patients with HFpEF and is associated with higher rates of heart failure hospitalization and worse health status. Treatment with dapagliflozin improves cardiovascular outcomes across the spectrum of BMI, leads to greater symptom improvement in patients with obesity, compared with those without, and has the additional benefit of causing modest weight loss.