scholarly journals AB0386 CORONAVIRUS INFECTION AND VASCULITIS: IDENTIFYING ASSOCIATIONS MINING THE BIOMEDICAL LITERATURE

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1220.1-1221
Author(s):  
A. Rodriguez-Pla ◽  
R. Cartin-Ceba
Keyword(s):  
Hepatitis Virus ◽  
Dominant Role ◽  
Semantic Networks ◽  
Biomedical Literature ◽  
Cutaneous Lesions ◽  
Inflammatory Reactions ◽  
Search String ◽  
Pubmed Database ◽  
Increased Risk ◽  
Central Term

Background:Based on recent publications suggesting an association between COVID-19 and vascularInflammation.Objectives:Our aim was to explore new associations between coronavirus infections and vasculitis utilizing semantic mining of PubMed results.Methods:The following literature search string: “(vasculitis OR vascular inflammation OR vascular damage) AND (coronavirus OR SARS virus OR MERS-CoV OR Covid-19)” was used to retrieve abstracts from the whole PubMed database, using Semantic MEDLINE 2. on 6/7/2020. This application represents a network of semantic predications (triples of the form subject-predicate-object, e.g. COVID-19 causes Disease) on a knowledge graph. The system allows for choosing the maximum number of nodes represented, the central topic, and the length of the network. For our network we chose to display all relations, COVID-19 (31 edges) as the central term, 3 lengths, and selecting the most informative nodes. Automatic summarization eliminated the less informative predications.Results:The search string retrieved 152 citations from PubMed and identified 1,028 predications. Thenetwork (Figure 1), displayed using COVID-19 as the central term, consisted of 72 nodes and 140 edges. The 5 most connected nodes were ’Patients: 19 nodes’, COVID-19: 13’, ‘Inflammation: 13’, ’Lung: 11’, and ‘Disease: 11’. Multiple links have been found between coronavirus and vasculitis. Animal coronaviruses, including the one causing feline infectious peritonitis (FIP), the murine coronavirus mouse hepatitis virus (MHV), the SARS-CoV in transgenic mice and coronavirus in ferrets, are known to cause vasculitis in animals. It is known that coronaviruses that infect animals can evolve and become new human coronaviruses. SARS produces inflammation in blood vessels. In 2005, a link between the coronavirus HCoV-NL63 or New Haven Coronavirus (HCoV-NH) and KD was reported,although later studies concluded that HCoV-NH did not play a dominant role in the etiology orpathogenesis of KD. In 2014, serological testing suggested the possible involvement of CoV-229E in the development of KD. There has also been a report of KD patients being infected by coronavirus OC43/HKU1.COVID-19 may infect the vessels and trigger inflammatory reactions like those of vasculitis, including vasculitis-like cutaneous lesions. COVID-19 patients develop thrombosis, and increased risk of thrombosis is also present in primary vasculitic syndromes. Children, many of whom tested positive for COVID-19 antibodies, developed Multisystem Inflammatory Syndrome in Children (MIS-C), an inflammatory condition similar to Kawasaki Disease (KD).Conclusion:Knowledge integration and discovery methods are an efficient and powerful way of retrieving and analyzing relevan information from multiple papers. Their main advantages are finding relations among biomedical concepts, generating new hypotheses, and opening them to literature-based discovery.SARS-CoV-2 may cause vasculitis or vasculitis-like syndromes. The KD-like syndrome reported mainly in children with COVID-19 revives the previous suspicion of coronavirus as a possible triggering agent of KD and the decades-old hypothesis of infection involvement in the pathogenesis of vasculitis.References:[1]Rindflesch TC,et al. Semantic MEDLINE: An advanced information management application for biomedicine. Information Services & Use 2011;31:15-21.Figure 1.Semantic Networks Resulting from Pubmed. All relations COVID-19 (edges:140) 3 lengths Max nodes: F (all nodes considered relevant).Disclosure of Interests:None declared

scholarly journals AB0408 SYSTEMIC SCLERODERMA AND ENVIRONMENTAL RISK FACTORS: IDENTIFYING ASSOCIATIONS MINING THE BIOMEDICAL LITERATURE

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1232.2-1233
Author(s):  
A. Rodriguez-Pla
Keyword(s):  
Occupational Exposure ◽  
Environmental Factors ◽  
Autoimmune Diseases ◽  
Vinyl Chloride ◽  
Semantic Network ◽  
Biomedical Literature ◽  
Systemic Scleroderma ◽  
Search String ◽  
Hla Genes ◽  
Pubmed Database

Background:A debate still exists concerning the role of occupational and environmental factors in the pathogenesis of systemic scleroderma (SSc).Objectives:Our aim was to explore associations between SSc and environmental factors utilizing an automatic semantic interpretation of PubMed results.Methods:The literature search string: (“systemic sclerosis” OR “scleroderma”) AND (“occupational exposure” OR “environmental” OR “risk factor”) was used to retrieve abstracts from the entire PubMed database, using Semantic MEDLINE 2, on 6/14/2020. This application represents a network of semantic predications (triples of the form subject-predicate (or relation) -object, e.g. Occupational Exposure causes Systemic Scleroderma) on a knowledge graph. Subject and object arguments of each predication are concepts from the Unified Medical Language System (UMLS) Metathesaurus and the relation is taken from the UMLS Semantic Network. The system allows for choosing the central topic (“Systemic Scleroderma”), the length of the network (3 nodes), and automatic summarization, eliminating the less informative predications.Results:The search string retrieved 864 citations and identified 6,397 predications by using 34 types of relations. Initially, we focused our attention on the ‘CAUSES’ type of relation (Figure 1), displaying a network with 59 nodes and 57 edges.The central concepts of this network, identified as having causal relationship with SSc are autoimmune diseases/autoimmunity, chemicals such as bleomycin, occupational and environmental exposure, especially silica, vinyl chloride and trichloroethylene, genes, including HLA and non-HLA genes, genetic polymorphisms, transcription factors (TFs) such as Fli1 and KLF5, and fibrosis. Eosinophilia-myalgia syndrome, toxic oil syndrome and infection were all causally linked to autoimmune diseases. Minerals were associated with occupational exposure and with autoimmune diseases. Concepts causally linked to fibrosis were rare diseases, HLA genes, other non-HLA genes, such as STAT4, IR4, IR5, TLR4, TLR7 and Rho-associated Kinase, and vinyl chloride monomer. Pathogenic factors associated with SSc were endothelial dysfunction and extracellular matrix proteins. Many of the papers in the network also suggested that hormonal factors are involved.Conclusion:Inspection on the knowledge graphs reveals concepts central to research on the etiopathogenesis of SSc. The relations in which these concepts participate, provide more specific information. The Semantic MEDLINE graph supports the kind of patterns that underpin literature-based discovery.Although the pathogenesis of SSc remains elusive, it is accepted that initial vascular damage driven by autoimmunity and environmental factors causes abnormalities in the vasculature resulting in the activation of fibroblasts in various organs. Silica and solvents such as trichloroethylene seem to be the most consistently suspected environmental agents in SSc.References:[1]Rindflesch TC,et al. Semantic MEDLINE: An advanced information management application for biomedicine. Information Services & Use 2011;31:15-21.Figure 1.Semantic Network of Casual Relationships of Systemic Scleroderma.Disclosure of Interests:None declared

scholarly journals Exploring the Relationship between Biologics and Postoperative Surgical Morbidity in Ulcerative Colitis: A Review

2021 ◽  
Vol 10 (4) ◽  
pp. 710
Author(s):  
Abel Botelho Quaresma ◽  
Fernanda da Silva Barbosa Baraúna ◽  
Fábio Vieira Teixeira ◽  
Rogério Saad-Hossne ◽  
Paulo Gustavo Kotze
Keyword(s):  
Ulcerative Colitis ◽  
Postoperative Complications ◽  
Meta Analysis ◽  
Qualitative Evaluation ◽  
Complication Rates ◽  
Surgical Morbidity ◽  
Randomized Studies ◽  
Pubmed Database ◽  
Increased Risk ◽  
The Impact

Background: With the paradigm shift related to the overspread use of biological agents in the treatment of inflammatory bowel diseases (IBD), several questions emerged from the surgical perspective. Whether the use of biologicals would be associated with higher rates of postoperative complications in ulcerative colitis (UC) patients still remains controversial. Aims: We aimed to analyze the literature, searching for studies that correlated postoperative complications and preoperative exposure to biologics in UC patients, and synthesize these data qualitatively in order to check the possible impact of biologics on postoperative surgical morbidity in this population. Methods: Included studies were identified by electronic search in the PUBMED database according to the PRISMA (Preferred Items of Reports for Systematic Reviews and Meta-Analysis) guidelines. The quality and bias assessments were performed by MINORS (methodological index for non-randomized studies) criteria for non-randomized studies. Results: 608 studies were initially identified, 22 of which were selected for qualitative evaluation. From those, 19 studies (17 retrospective and two prospective) included preoperative anti-TNF. Seven described an increased risk of postoperative complications, and 12 showed no significant increase postoperative morbidity. Only three studies included surgical UC patients with previous use of vedolizumab, two retrospective and one prospective, all with no significant correlation between the drug and an increase in postoperative complication rates. Conclusions: Despite conflicting results, most studies have not shown increased complication rates after abdominal surgical procedures in patients with UC with preoperative exposure to biologics. Further prospective studies are needed to better establish the impact of preoperative biologics and surgical complications in UC.

scholarly journals In Silico Exploration of the Potential Role of Acetaminophen and Pesticides in the Etiology of Autism Spectrum Disorder

Toxics ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 97
Author(s):  
Tristan Furnary ◽  
Rolando Garcia-Milian ◽  
Zeyan Liew ◽  
Shannon Whirledge ◽  
Vasilis Vasiliou
Keyword(s):  
Autism Spectrum Disorder ◽  
Prenatal Exposure ◽  
Pesticide Exposure ◽  
Neurodevelopmental Disorder ◽  
Autism Spectrum ◽  
Biomedical Literature ◽  
Spectrum Disorder ◽  
Biological Processes ◽  
Genetic Associations ◽  
Increased Risk

Recent epidemiological studies suggest that prenatal exposure to acetaminophen (APAP) is associated with increased risk of Autism Spectrum Disorder (ASD), a neurodevelopmental disorder affecting 1 in 59 children in the US. Maternal and prenatal exposure to pesticides from food and environmental sources have also been implicated to affect fetal neurodevelopment. However, the underlying mechanisms for ASD are so far unknown, likely with complex and multifactorial etiology. The aim of this study was to explore the potential effects of APAP and pesticide exposure on development with regards to the etiology of ASD by highlighting common genes and biological pathways. Genes associated with APAP, pesticides, and ASD through human research were retrieved from molecular and biomedical literature databases. The interaction network of overlapping genetic associations was subjected to network topology analysis and functional annotation of the resulting clusters. These genes were over-represented in pathways and biological processes (FDR p < 0.05) related to apoptosis, metabolism of reactive oxygen species (ROS), and carbohydrate metabolism. Since these three biological processes are frequently implicated in ASD, our findings support the hypothesis that cell death processes and specific metabolic pathways, both of which appear to be targeted by APAP and pesticide exposure, may be involved in the etiology of ASD. This novel exposures-gene-disease database mining might inspire future work on understanding the biological underpinnings of various ASD risk factors.

scholarly journals Relevance of hMLH1 -93G>A, 655A>G and 1151T>A polymorphisms with colorectal cancer susceptibility: a meta-analysis based on 38 case-control studies

2018 ◽  
Vol 64 (10) ◽  
pp. 942-951 ◽  
Author(s):  
Mohammad Zare ◽  
Jamal Jafari-Nedooshan ◽  
Mohammadali Jafari ◽  
Hossein Neamatzadeh ◽  
Seyed Mojtaba Abolbaghaei ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Asian Population ◽  
Case Control ◽  
Biomedical Literature ◽  
Case Control Studies ◽  
Increased Risk ◽  
Comprehensive Search ◽  
Meta Analyses

SUMMARY OBJECTIVE: There has been increasing interest in the study of the association between human mutL homolog 1 (hMLH1) gene polymorphisms and risk of colorectal cancer (CRC). However, results from previous studies are inconclusive. Thus, a meta-analysis was conducted to derive a more precise estimation of the effects of this gene. METHODS: A comprehensive search was conducted in the PubMed, EMBASE, Chinese Biomedical Literature databases until January 1, 2018. Odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of the association. RESULTS: Finally, 38 case-control studies in 32 publications were identified met our inclusion criteria. There were 14 studies with 20668 cases and 19533 controls on hMLH1 −93G>A, 11 studies with 5,786 cases and 8,867 controls on 655A>G and 5 studies with 1409 cases and 1637 controls on 1151T>A polymorphism. The combined results showed that 655A>G and 1151T>A polymorphisms were significantly associated with CRC risk, whereas −93G>A polymorphism was not significantly associated with CRC risk. As for ethnicity, −93G>A and 655A>G polymorphisms were associated with increased risk of CRC among Asians, but not among Caucasians. More interestingly, subgroup analysis indicated that 655A>G might raise CRC risk in PCR-RFLP and HB subgroups. CONCLUSION: Inconsistent with previous meta-analyses, this meta-analysis shows that the hMLH1 655A>G and 1151T>A polymorphisms might be risk factors for CRC. Moreover, the −93G>A polymorphism is associated with the susceptibility of CRC in Asian population.

Cannabis consumption and psychosis or schizophrenia development

2018 ◽  
Vol 64 (7) ◽  
pp. 690-704 ◽  
Author(s):  
María Bettina Ortiz-Medina ◽  
Marta Perea ◽  
Julio Torales ◽  
Antonio Ventriglio ◽  
Giovanna Vitrani ◽  
...  
Keyword(s):  
Cannabis Use ◽  
Psychotic Symptoms ◽  
Current State ◽  
Gene Environment ◽  
Pubmed Database ◽  
Increased Risk ◽  
Vulnerable People ◽  
Cannabis Consumption ◽  
The Relationship

Objective: Cannabis consumption produces psychopathology, in some cases psychotic episodes, which are of our interest in this work. However, the relationship between cannabis use and psychosis has not been fully elucidated. The objectives of this work are to (1) review the current state of knowledge on the association of cannabis use with the risk of the development of psychosis or psychotic symptoms in people without schizophrenia and (2) assess the consistency of the hypothesis that cannabis use is associated with increased risk of psychosis in people without schizophrenia. Method: This work included research done in humans until May 2018 with the keywords ‘cannabis’ and ‘psychosis’, published in English and Spanish, in the PubMed database. Results: In all, 66 papers were analyzed, of which 23 were cohort trials and 43 were reviews. Conclusion: Cannabis use doubles the risk of developing psychosis in vulnerable people. There even exists a relationship regarding the dose used and the age of first use. Gene–environment interactions that modulate the association between cannabis use and the presence of psychosis have also been described.

scholarly journals The effect of off-hours hospital admission on mortality and clinical outcomes for patients with upper gastrointestinal hemorrhage: A systematic review and meta-analysis of 20 cohorts

2017 ◽  
Vol 6 (3) ◽  
pp. 367-381 ◽  
Author(s):  
Xian Feng Xia ◽  
Philip Wai Yan Chiu ◽  
Kelvin Kam Fai Tsoi ◽  
Francis Ka Leung Chan ◽  
Joseph Jao Yiu Sung ◽  
...  
Keyword(s):  
Hospital Admission ◽  
Gastrointestinal Hemorrhage ◽  
Meta Analysis ◽  
Biomedical Literature ◽  
Upper Gastrointestinal Hemorrhage ◽  
Risk Of Mortality ◽  
Increased Risk ◽  
Public Holidays ◽  
To Receive ◽  
Upper Gastrointestinal

Objective The objective of this article is to evaluate the relationship between off-hours hospital admission (weekends, public holidays or nighttime) and mortality for upper gastrointestinal hemorrhage (UGIH). Methods Medline, Embase, Scopus, and the Chinese Biomedical Literature were searched through December 2016 to identify eligible records for inclusion in this meta-analysis. A random-effects model was applied. Results Twenty cohort studies were included for analysis. Patients with UGIH who were admitted during off-hours had a significantly higher mortality and were less likely to receive endoscopy within 24 hours of admission. In comparison to variceal cases, patients with nonvariceal bleeding showed a higher mortality when admitted during off-hours. However, for studies conducted in hospitals that provided endoscopy outside normal hours, off-hours admission was not associated with an increased risk of mortality. Conclusion Our study showed a higher mortality for patients with nonvariceal UGIH who were admitted during off-hours, while this effect might be offset in hospitals with a formal out-of-hours endoscopy on-call rotation.

scholarly journals Association between interleukin-17F rs763780 polymorphism and psoriasis risk: A meta-analysis

2021 ◽  
Vol 0 ◽  
pp. 1-6
Author(s):  
Zhi Xiang ◽  
Zhimin Hao ◽  
Pangen Cui ◽  
Lin Lin ◽  
Min Chen ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Genetic Mutation ◽  
Case Control ◽  
Biomedical Literature ◽  
Cochrane Central Register ◽  
Odds Ratios ◽  
Case Control Studies ◽  
Functional Sites ◽  
Increased Risk ◽  
Interleukin 17F

Background: The polymorphism of interleukin-17F rs763780 has been found to have a probable association with increased risk of developing psoriasis. Aims: This study aims to get a more convincing estimation of the association between the interleukin-17F rs763780 T /C polymorphism and psoriasis risk. Methods: Two authors independently searched the databases including PubMed, EMBASE, Cochrane Central Register of Controlled Trials, Chinese National Knowledge Infrastructure, Wanfang and Chinese Biomedical Literature Databases for case–control studies which reported the odds ratios with 95% confidence intervals comparing genotype and allele frequencies of the interleukin-17F rs763780 polymorphism in patients with psoriasis versus participants without psoriasis. Results: A total of seven case–control studies incorporating 1824 cases and 1585 controls were identified. The pooled odds ratios indicated that interleukin-17F rs763780 C allele was a risk factor for psoriasis in allele frequency, recessive model and homozygote model (P < 0.05). Subgroup analysis by ethnicity further indicated that the C allele was closely related to increased risk of psoriasis in Asian populations (P < 0.05), but not in Caucasians. Limitations: Only a few studies on the interleukin-17F rs763780 polymorphism in psoriasis have been reported till date, thus the data is insufficient. Only one gene polymorphic site was selected for this study, and it is not clear whether other genetic mutation functional sites affect the gene. Further studies on confounding effects of other genetic polymorphisms are needed. Conclusion: The present meta-analysis results suggested that the interleukin-17F rs763780 T /C is significantly associated with psoriasis risk in Asians.

scholarly journals Cannabis Use and Risk of Schizophrenia: A Literature Review

2021 ◽  
Vol 6 (2) ◽  
Keyword(s):  
Positive Association ◽  
Epidemiological Studies ◽  
The Body ◽  
Cannabis Use ◽  
Normal Brain ◽  
Brain Functioning ◽  
Pubmed Database ◽  
Increased Risk ◽  
Meta Analyses ◽  
Study Designs

Background and Objective: Cannabis remains the most widely used illicit drug worldwide. The similarity in the chemical structure of tetrahydrocannabinol to the brain chemical anandamide allows the body to recognize it and alter normal brain functioning. The objective of this review article is to summarize the evidence for the association between cannabis and schizophrenia. Methods: A literature search was conducted using the PubMed database and other sources. The keywords used were “cannabis” and “psychosis” and “schizophrenia.” Fifty-two articles relevant to our topic have been selected for this review. Results: Evidence from observational epidemiological studies has shown a positive association between regular cannabis use and schizophrenia risk. Meta-analyses and Mendelian randomization studies support the evidence from observational study designs. Discussion and Conclusions: The association between cannabis and schizophrenia is biologically plausible. Moreover, there has been emerging evidence of genes interacting with cannabis use to confer a higher risk for schizophrenia. There are enough reason and sufficient epidemiological evidence to warn people about the risk of developing schizophrenia with cannabis use. Scientific Significance: The increasing legalization of cannabis for recreational use is of significant concern. Long-term cannabis use might predispose people to increased risk of developing schizophrenia. Health professionals have a major role to play by taking maximum advantage of social and psychological interventions to educate people about the potential danger associated with cannabis and avoid its use.

scholarly journals Nutrition as a modifiable factor in the onset and progression of pulmonary function impairment in COPD: a systematic review

2021 ◽  
Author(s):  
Lieke E J van Iersel ◽  
Rosanne J H C G Beijers ◽  
Harry R Gosker ◽  
Annemie M W J Schols
Keyword(s):  
Systematic Review ◽  
Pulmonary Function ◽  
Lung Disease ◽  
Nutrient Status ◽  
Dietary Quality ◽  
Airflow Limitation ◽  
Processed Meat ◽  
Pubmed Database ◽  
Increased Risk ◽  
Modifiable Factor

Abstract Context Chronic obstructive lung disease (COPD) is a progressive lung disease characterized by persistent airflow limitation. An increasing amount of evidence suggests an effect of dietary quality on the risk of COPD in the general population and pulmonary function decline in patients with COPD. Objective The association of dietary intake and nutrient status with COPD risk and onset, as well as pulmonary function decline (change in forced expiratory volume in 1 second, forced vital capacity, or the ratio of the former to the latter) in patients with COPD was investigated in this systematic review. Data Sources The PubMed database was searched by combining terms of pulmonary function or COPD with diet, nutrient status, or nutritional supplementation. Data Extraction Original studies and systematic reviews and meta-analyses were included. Articles obtained were independently screened for relevance on the bases of title and abstract by 2 researchers. Eventually, 89 articles were included in the analysis. Results The unhealthy Western-style diet is associated with an increased risk of COPD and an accelerated decline of pulmonary function. Intake of fruit, vegetables, dietary fibers, vitamins C and E, polyphenols, and β-carotene were individually associated with lower COPD risk, whereas consumption of processed meat was associated with higher COPD risk. Data on the effect of dietary quality on pulmonary function decline in patients with COPD are limited and inconsistent. Strong evidence for beneficial effects on pulmonary function decline was found only for vitamin D supplementation. Conclusion Considering the increasing burden of COPD, more attention should be given to dietary quality as a modifiable factor in disease development and progression in patients with COPD. Systematic Review Registration PROSPERO registration no. CRD42021240183.

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