rm(list = ls())
######################################
library(easyPubMed)
library(XML)
library(RISmed)
######################################
i <- "TCDD"
my_query <- paste("nerve[TIAB] OR neuro[TIAB] OR nervous[TIAB] AND ",i,"[TIAB]", sep = "")
print(my_query)
## [1] "nerve[TIAB] OR neuro[TIAB] OR nervous[TIAB] AND TCDD[TIAB]"
#Possible E-utilities to supply to type are einfo, esearch, epost, esummary, elink, egquery, espell.
#The database name supplied to db can be any valid Entrez database, such as pubmed, protein, nlm, etc.
res1 <- tryCatch(EUtilsSummary(my_query,
type = "esearch",
db = "pubmed",
datetype = "pdat",
retmax = 12000,
mindate = 2010,
maxdate = 2020), error=function(err) NA)
print(res1)
## [1] "nerve[TIAB] OR neuro[TIAB] OR nervous[TIAB] AND TCDD[TIAB] AND 2010[PDAT] : 2020[PDAT]"
class(res1)
## [1] "EUtilsSummary"
## attr(,"package")
## [1] "RISmed"
#if (is.na(res1)) {
# abstracts <- NA
# }else{
QueryCount(res1) #[1] 21
## [1] 39
fetch <- EUtilsGet(res1, type = "efetch", db = "pubmed")
fetch
## PubMed query: nerve[TIAB] OR neuro[TIAB] OR nervous[TIAB] AND TCDD[TIAB] AND 2010[PDAT] : 2020[PDAT]
##
## Records: 39
#2.3
abstracts <- data.frame(Query = fetch@Query,
PMID = fetch@PMID,
YearReceived = fetch@YearReceived,
#MonthReceived = fetch@MonthReceived,
#DayReceived = fetch@DayReceived,
#HourReceived = fetch@HourReceived,
#MinuteReceived = fetch@MinuteReceived,
#YearPpublish = fetch@YearPpublish,
Author = as.character(fetch@Author),
ISSN = fetch@ISSN,
#Title = fetch@Title,
ArticleTitle = fetch@ArticleTitle,
ELocationID = fetch@ELocationID,
AbstractText = fetch@AbstractText,
#Language = fetch@Language,
#MedlineTA = fetch@MedlineTA,
#NlmUniqueID = fetch@NlmUniqueID,
#ISSNLinking = fetch@ISSNLinking,
#PublicationStatus = fetch@PublicationStatus,
#ArticleId = fetch@ArticleId,
Volume = fetch@Volume,
Issue = fetch@Issue,
ISOAbbreviation = fetch@ISOAbbreviation,
MedlinePgn = fetch@MedlinePgn
#CopyrightInformation = fetch@CopyrightInformation,
#Country = fetch@Country,
#GrantID = fetch@GrantID,
#Acronym = fetch@Acronym,
#RegistryNumber = fetch@RegistryNumber,
#RefSource = fetch@RefSource,
#Affiliation = as.character(fetch@Affiliation),
#CollectiveName = fetch@CollectiveName,
#PublicationType = as.character(fetch@PublicationType)
)
#}
dim(abstracts)
## [1] 39 12
head(abstracts,3)
## Query
## 1 nerve[TIAB] OR neuro[TIAB] OR nervous[TIAB] AND TCDD[TIAB] AND 2010[PDAT] : 2020[PDAT]
## 2 nerve[TIAB] OR neuro[TIAB] OR nervous[TIAB] AND TCDD[TIAB] AND 2010[PDAT] : 2020[PDAT]
## 3 nerve[TIAB] OR neuro[TIAB] OR nervous[TIAB] AND TCDD[TIAB] AND 2010[PDAT] : 2020[PDAT]
## PMID YearReceived
## 1 31775093 2019
## 2 31217064 2018
## 3 31152735 2019
## Author
## 1 list(LastName = c("Chen", "Xie", "Sha", "Xu", "Zhang", "Fu", "Xia", "Liu", "Xu", "Zhao"), ForeName = c("Yangsheng", "Heidi Qunhui", "Rui", "Tuan", "Songyan", "Hualing", "Yingjie", "Yiyun", "Li", "Bin"), Initials = c("Y", "HQ", "R", "T", "S", "H", "Y", "Y", "L", "B"), order = 1:10)
## 2 list(LastName = c("Wu", "Yin", "Zhang", "Jiao", "Zhao", "Wu"), ForeName = c("Chang Yue", "Kai Zhi", "Yan", "Man", "Xin Yuan", "Qi Yun"), Initials = c("CY", "KZ", "Y", "M", "XY", "QY"), order = 1:6)
## 3 list(LastName = c("Sha", "Chen", "Luo", "Liu", "Xu", "Xie", "Zhao"), ForeName = c("Rui", "Yangsheng", "Yali", "Yiyun", "Li", "Heidi Qunhui", "Bin"), Initials = c("R", "Y", "Y", "Y", "L", "HQ", "B"), order = 1:7)
## ISSN
## 1 1873-6750
## 2 2214-0190
## 3 1872-7786
## ArticleTitle
## 1 2,3,7,8-Tetrachlorodibenzo-p-dioxin and up-regulation of neurofilament expression in neuronal cells: Evaluation of AhR and MAPK pathways.
## 2 2,3,7,8-Tetrachlorodibenzo-p-dioxin Promotes Proliferation of Astrocyte Cells via the Akt/STAT3/Cyclin D1 Pathway.
## 3 Effects of astrocyte conditioned medium on neuronal AChE expression upon 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure.
## ELocationID
## 1 S0160-4120(19)31290-5
## 2 10.3967/bes2019.038
## 3 S0009-2797(19)30356-4
## AbstractText
## 1 Dioxin exposure is reported to affect nervous system development and increase the risk of neurodegenerative diseases. Generally, dioxin exerts its neurotoxicity via aryl hydrocarbon receptor (AhR). Neurofilament (NF) light (NFL) protein is a biomarker for both neuronal differentiation and neurodegeneration and its expression is controlled by the mitogen-activated protein kinase (MAPK) pathway. However, the effects of dioxin on NFL expression and involved mechanisms are incompletely understood. We aimed to investigate the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on NFL expression and elucidate the underlining signaling pathways and their potential crosstalk, specifically between MAPK and AhR pathway. We employed primary cultured rat cortical neurons to evaluate the effect of TCDD exposure on NFL expression. We also used nerve growth factor (NGF)-treated PC12 cells with specific inhibitors to investigate the involvement of and potential crosstalk between the MAPK pathway and the AhR pathway in mediating the effects of TCDD on NFL expression. After TCDD exposure, NFL mRNA and protein levels were upregulated in cultured neurons. NFL protein was preferentially found in the cell body compared with neurites of the cultured neurons. In PC12 cells, TCDD enhanced both NGF-induced NFL expression and phosphorylation of ERK1/2 and p38. The addition of MAPK-pathway inhibitors (PD98059 and SB230580) partially blocked the TCDD-induced NFL upregulation. CH223191, an AhR antagonist, reversed the upregulation of NFL and phosphorylation of ERK1/2 and p38 induced by TCDD. This study demonstrated TCDD-induced upregulation of NFL in cultured neurons, with protein retained in the cell body. TCDD action was dependent on activation of AhR and MAPK, while crosstalk was found between these two signaling pathways.
## 2 OBJECTIVE: The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a persistent organic pollutant, is harmful to the nervous system, but its effects on the brain are still unclear. This study aimed to investigate the effects of TCDD on astrocytes proliferation and underlying molecular mechanism.METHODS: The cell proliferation was measured by EdU-based proliferation assay and PI staining by flow cytometry. Protein expression levels were detected by Western blotting. Immunofluorescence, cytoplasmic and nuclear fractions separation were used to assess the distribution of signal transducer and activator of transcription 3 (STAT3).RESULTS: C6 cells treated with 10 and 50 nmol/L TCDD for 24 h showed significant promotion of the proliferation of. The exposure to TCDD resulted in the upregulation in the expression levels of phosphorylated protein kinase B (p-Akt), phosphorylated STAT3, and cyclin D1 in a dose- and time-dependent manner. The inhibition of Akt expression with LY294002 or STAT3 expression with AG490 abolished the TCDD-induced cyclin D1 upregulation and cell proliferation. Furthermore, LY294002 suppressed the activation of STAT3. Finally, TCDD promoted the translocation of STAT3 from the cytoplasm to the nucleus, and LY294002 treatment blocked this effect.CONCLUSION: TCDD exposure promotes the proliferation of astrocyte cells via the Akt/STAT3/cyclin D1 pathway, leading to astrogliosis.
## 3
## Volume Issue ISOAbbreviation MedlinePgn
## 1 134 <NA> Environ Int 105193
## 2 32 4 Biomed. Environ. Sci. 281-290
## 3 309 <NA> Chem. Biol. Interact. 108686
write.csv(abstracts,paste0(Sys.Date(),"-",i,'-literature_info.csv'),na = "", row.names = F)