> library(httr)

> baseurl=https://eutils.ncbi.nlm.nih.gov/

> pubmedaction=list(base="entrez/eutils/index.fcgi",search="entrez/eutils/esearch.fcgi",fetch="entrez/eutils/efetch.fcgi",summary="entrez/eutils/esummary.fcgi")

> searcharticleparam=list(retstart=0,retmax=20,usehistory="Y",querykey="",webenv="",term="(cell[TA] AND 2017[DP])",total_num=0,total_page=1,page_size=20,current_page=1)

postsearchurl=paste(baseurl,pubmedaction$search,sep="")

> r<-POST(postsearchurl,body=list(db="pubmed",term=searcharticleparam$term,retmode="json",retstart=searcharticleparam$retstart,retmax=searcharticleparam$retmax,usehistory=searcharticleparam$usehistory,rettype="uilist"))

> stop_for_status(r)

data=content(r,"parsed","application/json")

> esearchresult=data$esearchresult

> count=esearchresult$count

> print(esearchresult)

> print(count)

[1] "563"

> searcharticleparam$total_num=esearchresult$count

> searcharticleparam$querykey=esearchresult$querykey

> searcharticleparam$webenv=esearchresult$webenv

> pubmedidstr="29275861,29275860,29275859"

> postfetchurl=paste(baseurl,pubmedaction$fetch,sep="")

> r2<-POST(postfetchurl,body=list(db="pubmed",id=pubmedidstr,retmode="xml",usehistory=searcharticleparam$usehistory,querykey=searcharticleparam$querykey,webenv=searcharticleparam$webenv))

> stop_for_status(r2)

> library(xml2)

> data2=content(r2,"parsed","application/xml")

> article=xml_children(data2)

> count=length(article)

> cnt=1

while(cnt<=count) {

title=xml_find_first(article[cnt], ".//ArticleTitle") 

abstract=xml_find_first(article[cnt],".//AbstractText") 

print(xml_text(title)) 

print(xml_text(abstract)) 

cnt=cnt+1

}

[1] "Natural Killer Cells Control Tumor Growth by Sensing a Growth Factor."

[1] "Many tumors produce platelet-derived growth factor (PDGF)-DD, which promotes cellular proliferation, epithelial-mesenchymal transition, stromal reaction, and angiogenesis through autocrine and paracrine PDGFRβ signaling. By screening a secretome library, we found that the human immunoreceptor NKp44, encoded by NCR2 and expressed on natural killer (NK) cells and innate lymphoid cells, recognizes PDGF-DD. PDGF-DD engagement of NKp44 triggered NK cell secretion of interferon gamma (IFN)-γ and tumor necrosis factor alpha (TNF-α) that induced tumor cell growth arrest. A distinctive transcriptional signature of PDGF-DD-induced cytokines and the downregulation of tumor cell-cycle genes correlated with NCR2 expression and greater survival in glioblastoma. NKp44 expression in mouse NK cells controlled the dissemination of tumors expressing PDGF-DD more effectively than control mice, an effect enhanced by blockade of the inhibitory receptor CD96 or CpG-oligonucleotide treatment. Thus, while cancer cell production of PDGF-DD supports tumor growth and stromal reaction, it concomitantly activates innate immune responses to tumor expansion."

[1] "Antigen Identification for Orphan T Cell Receptors Expressed on Tumor-Infiltrating Lymphocytes."

[1] "The immune system can mount T cell responses against tumors; however, the antigen specificities of tumor-infiltrating lymphocytes (TILs) are not well understood. We used yeast-display libraries of peptide-human leukocyte antigen (pHLA) to screen for antigens of \"orphan\" T cell receptors (TCRs) expressed on TILs from human colorectal adenocarcinoma. Four TIL-derived TCRs exhibited strong selection for peptides presented in a highly diverse pHLA-A∗02:01 library. Three of the TIL TCRs were specific for non-mutated self-antigens, two of which were present in separate patient tumors, and shared specificity for a non-mutated self-antigen derived from U2AF2. These results show that the exposed recognition surface of MHC-bound peptides accessible to the TCR contains sufficient structural information to enable the reconstruction of sequences of peptide targets for pathogenic TCRs of unknown specificity. This finding underscores the surprising specificity of TCRs for their cognate antigens and enables the facile indentification of tumor antigens through unbiased screening."

[1] "Microbiome Influences Prenatal and Adult Microglia in a Sex-Specific Manner."

[1] "Microglia are embryonically seeded macrophages that contribute to brain development, homeostasis, and pathologies. It is thus essential to decipher how microglial properties are temporally regulated by intrinsic and extrinsic factors, such as sexual identity and the microbiome. Here, we found that microglia undergo differentiation phases, discernable by transcriptomic signatures and chromatin accessibility landscapes, which can diverge in adult males and females. Remarkably, the absence of microbiome in germ-free mice had a time and sexually dimorphic impact both prenatally and postnatally: microglia were more profoundly perturbed in male embryos and female adults. Antibiotic treatment of adult mice triggered sexually biased microglial responses revealing both acute and long-term effects of microbiota depletion. Finally, human fetal microglia exhibited significant overlap with the murine transcriptomic signature. Our study shows that microglia respond to environmental challenges in a sex- and time-dependent manner from prenatal stages, with major implications for our understanding of microglial contributions to health and disease."

install.packages("RISmed")

> library(RISmed)

> cell2017<-EUtilsSummary("cell[TA] AND 2017[DP]")

> View(cell2017)

> summary(cell2017)

Query:

"Cell"[Journal] AND 2017[DP] 

Result count:  563

> QueryId(cell2017)

  [1] "29336887" "29290469" "29290468" "29290467"

  [5] "29290466" "29290465" "29275861" "29275860"

  [9] "29275859" "29275858" "29249361" "29249360"

> records<-EUtilsGet(29336887)

> pubmed_data <- data.frame('Title'=ArticleTitle(records),'Abstract'=AbstractText(records),'ID'= ArticleId(records))

> pubmed_data

Title

1 GroEL Ring Separation and Exchange in the Chaperonin Reaction.                                                                                                                                                                                                                                                                                                Abstract

1 The bacterial chaperonin GroEL and its cofactor, GroES, form a nano-cage for a single molecule of substrate protein (SP) to fold in isolation. GroEL and GroES undergo an ATP-regulated interaction cycle to close and open the folding cage. GroEL consists of two heptameric rings stacked back to back. Here, we show that GroEL undergoes transient ring separation, resulting in ring exchange between complexes. Ring separation occurs upon ATP-binding to the trans ring of the asymmetric GroEL:7ADP:GroES complex in the presence or absence of SP and is a<U+00A0>consequence of inter-ring negative allostery. We find that a GroEL mutant unable to perform ring separation is folding active but populates symmetric GroEL:GroES2 complexes, where both GroEL rings function simultaneously rather than sequentially. As a consequence, SP binding and release from the folding chamber is inefficient, and E.<U+00A0>coli growth is impaired. We suggest that transient ring separation is an integral part of the chaperonin mechanism.

        ID

1 29336887