Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice
Pneumonia is usually caused by a wide variety of pathogen infection. The underlying mechanism contributing to pneumonia remains elusive. Here, the role of microRNA-497-3p (miR-497-3p) was explored in bacterial pneumonia. The expression levels of miR-497-3p and procalcitonin (PCT) in patient serum we...
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| Veröffentlicht in: | Inflammation 2020-12, Vol.43 (6), p.2119-2127 |
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| creator | Wang, Wenlong Zhu, Yitang Yin, Linlin Deng, Yaoyao Chu, Guoxian Liu, Supin |
| description | Pneumonia is usually caused by a wide variety of pathogen infection. The underlying mechanism contributing to pneumonia remains elusive. Here, the role of microRNA-497-3p (miR-497-3p) was explored in bacterial pneumonia. The expression levels of miR-497-3p and procalcitonin (PCT) in patient serum were detected by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. The interaction between miR-497-3p and PCT was further verified in A549 cell line. To further explore the role of miR-497-3p in pneumonia, mouse model of bacterial pneumonia was established
via Sp
TIGR4 strain (SpT4) infection. Subsequently, LV-miR-497-3p sponge was administrated in mice with bacterial pneumonia. The severity of pneumonia and inflammatory response were evaluated. Serum miR-497-3p and PCT levels increased in patients with bacterial pneumonia and miR-497-3p level positively corrected with the PCT level. The functional assay demonstrated that CALCA is the target of miR-497-3p in the A549 cell line. In mice with bacterial pneumonia, both miR-497-3p and PCT levels were upregulated after SpT4 infection. LV-miR-497-3p sponge administration attenuated pneumonia, accompanied with increasing gain of bodyweight and blood oxygen levels, as well as uninjured lungs. miR-497-3p inhibition attenuates the expression of C-reactive protein (CRP) and inflammatory cytokines in lung tissues of SpT4-infected mice, including nterleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). In conclusion, inhibition of miR-497-3p downregulates the expression of procalcitonin and ameliorates bacterial pneumonia in mice. |
| doi_str_mv | 10.1007/s10753-020-01279-w |
| format | Article |
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via Sp
TIGR4 strain (SpT4) infection. Subsequently, LV-miR-497-3p sponge was administrated in mice with bacterial pneumonia. The severity of pneumonia and inflammatory response were evaluated. Serum miR-497-3p and PCT levels increased in patients with bacterial pneumonia and miR-497-3p level positively corrected with the PCT level. The functional assay demonstrated that CALCA is the target of miR-497-3p in the A549 cell line. In mice with bacterial pneumonia, both miR-497-3p and PCT levels were upregulated after SpT4 infection. LV-miR-497-3p sponge administration attenuated pneumonia, accompanied with increasing gain of bodyweight and blood oxygen levels, as well as uninjured lungs. miR-497-3p inhibition attenuates the expression of C-reactive protein (CRP) and inflammatory cytokines in lung tissues of SpT4-infected mice, including nterleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). In conclusion, inhibition of miR-497-3p downregulates the expression of procalcitonin and ameliorates bacterial pneumonia in mice.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-020-01279-w</identifier><identifier>PMID: 32591941</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>A549 Cells ; Animals ; Bacteria ; Biomedical and Life Sciences ; Biomedicine ; C-reactive protein ; Calcitonin Gene-Related Peptide ; Cytokines - metabolism ; Down-Regulation ; Enzyme-linked immunosorbent assay ; Gene Expression Profiling ; Humans ; Immunology ; Infections ; Inflammation ; Interleukin 6 ; Internal Medicine ; Mice ; Mice, Inbred C57BL ; MicroRNAs - antagonists & inhibitors ; miRNA ; Original Article ; Pathology ; Pharmacology/Toxicology ; Pneumonia ; Pneumonia, Bacterial - metabolism ; Pneumonia, Bacterial - therapy ; Polymerase chain reaction ; Procalcitonin ; Procalcitonin - biosynthesis ; Rheumatology ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Up-Regulation</subject><ispartof>Inflammation, 2020-12, Vol.43 (6), p.2119-2127</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-f89a3d90cce4351010451a61a7d63935dabbe5fbed725cfbc29a0c5e5f2ae8d83</citedby><cites>FETCH-LOGICAL-c375t-f89a3d90cce4351010451a61a7d63935dabbe5fbed725cfbc29a0c5e5f2ae8d83</cites><orcidid>0000-0003-2122-3628</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-020-01279-w$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-020-01279-w$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32591941$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Wenlong</creatorcontrib><creatorcontrib>Zhu, Yitang</creatorcontrib><creatorcontrib>Yin, Linlin</creatorcontrib><creatorcontrib>Deng, Yaoyao</creatorcontrib><creatorcontrib>Chu, Guoxian</creatorcontrib><creatorcontrib>Liu, Supin</creatorcontrib><title>Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Pneumonia is usually caused by a wide variety of pathogen infection. The underlying mechanism contributing to pneumonia remains elusive. Here, the role of microRNA-497-3p (miR-497-3p) was explored in bacterial pneumonia. The expression levels of miR-497-3p and procalcitonin (PCT) in patient serum were detected by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. The interaction between miR-497-3p and PCT was further verified in A549 cell line. To further explore the role of miR-497-3p in pneumonia, mouse model of bacterial pneumonia was established
via Sp
TIGR4 strain (SpT4) infection. Subsequently, LV-miR-497-3p sponge was administrated in mice with bacterial pneumonia. The severity of pneumonia and inflammatory response were evaluated. Serum miR-497-3p and PCT levels increased in patients with bacterial pneumonia and miR-497-3p level positively corrected with the PCT level. The functional assay demonstrated that CALCA is the target of miR-497-3p in the A549 cell line. In mice with bacterial pneumonia, both miR-497-3p and PCT levels were upregulated after SpT4 infection. LV-miR-497-3p sponge administration attenuated pneumonia, accompanied with increasing gain of bodyweight and blood oxygen levels, as well as uninjured lungs. miR-497-3p inhibition attenuates the expression of C-reactive protein (CRP) and inflammatory cytokines in lung tissues of SpT4-infected mice, including nterleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). In conclusion, inhibition of miR-497-3p downregulates the expression of procalcitonin and ameliorates bacterial pneumonia in mice.</description><subject>A549 Cells</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>C-reactive protein</subject><subject>Calcitonin Gene-Related Peptide</subject><subject>Cytokines - metabolism</subject><subject>Down-Regulation</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Gene Expression Profiling</subject><subject>Humans</subject><subject>Immunology</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Internal Medicine</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>miRNA</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Pneumonia</subject><subject>Pneumonia, Bacterial - metabolism</subject><subject>Pneumonia, Bacterial - therapy</subject><subject>Polymerase chain reaction</subject><subject>Procalcitonin</subject><subject>Procalcitonin - biosynthesis</subject><subject>Rheumatology</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Up-Regulation</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp90cFuFSEUBmBiNPZafQEXhsSNG_QAwzAsa221SY2N0TVhmDMtzQxcYSZX376096qJC9mQwHd-SH5CXnJ4ywH0u8JBK8lAAAMutGG7R2TDlZZMKN0-JhuQLTBpjD4iz0q5BYDOdPIpOZJCGW4aviH5It6EPiwhRZpGOoevrDGayS39kHYx4_U6uQULXW6Qnv3cZizlQK9y8m7yYUkxROriQE9mnELKD_698wvm4CZ6FXGdq3G0ss_B43PyZHRTwReH_Zh8Pz_7dvqJXX75eHF6csm81GphY2ecHAx4j41UHDg0iruWOz200kg1uL5HNfY4aKH82HthHHhVj4TDbujkMXmzz93m9GPFstg5FI_T5CKmtVjR8I4L2bSi0tf_0Nu05lh_V5Xmqq7mXom98jmVknG02xxml39ZDva-EbtvxNZG7EMjdleHXh2i137G4c_I7woqkHtQ6lW8xvz37f_E3gGlC5d4</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Wang, Wenlong</creator><creator>Zhu, Yitang</creator><creator>Yin, Linlin</creator><creator>Deng, Yaoyao</creator><creator>Chu, Guoxian</creator><creator>Liu, Supin</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2122-3628</orcidid></search><sort><creationdate>20201201</creationdate><title>Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice</title><author>Wang, Wenlong ; Zhu, Yitang ; Yin, Linlin ; Deng, Yaoyao ; Chu, Guoxian ; Liu, Supin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-f89a3d90cce4351010451a61a7d63935dabbe5fbed725cfbc29a0c5e5f2ae8d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>A549 Cells</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>C-reactive protein</topic><topic>Calcitonin Gene-Related Peptide</topic><topic>Cytokines - metabolism</topic><topic>Down-Regulation</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Gene Expression Profiling</topic><topic>Humans</topic><topic>Immunology</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Internal Medicine</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>miRNA</topic><topic>Original Article</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Pneumonia</topic><topic>Pneumonia, Bacterial - metabolism</topic><topic>Pneumonia, Bacterial - therapy</topic><topic>Polymerase chain reaction</topic><topic>Procalcitonin</topic><topic>Procalcitonin - biosynthesis</topic><topic>Rheumatology</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Wenlong</creatorcontrib><creatorcontrib>Zhu, Yitang</creatorcontrib><creatorcontrib>Yin, Linlin</creatorcontrib><creatorcontrib>Deng, Yaoyao</creatorcontrib><creatorcontrib>Chu, Guoxian</creatorcontrib><creatorcontrib>Liu, Supin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Wenlong</au><au>Zhu, Yitang</au><au>Yin, Linlin</au><au>Deng, Yaoyao</au><au>Chu, Guoxian</au><au>Liu, Supin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>43</volume><issue>6</issue><spage>2119</spage><epage>2127</epage><pages>2119-2127</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>Pneumonia is usually caused by a wide variety of pathogen infection. The underlying mechanism contributing to pneumonia remains elusive. Here, the role of microRNA-497-3p (miR-497-3p) was explored in bacterial pneumonia. The expression levels of miR-497-3p and procalcitonin (PCT) in patient serum were detected by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. The interaction between miR-497-3p and PCT was further verified in A549 cell line. To further explore the role of miR-497-3p in pneumonia, mouse model of bacterial pneumonia was established
via Sp
TIGR4 strain (SpT4) infection. Subsequently, LV-miR-497-3p sponge was administrated in mice with bacterial pneumonia. The severity of pneumonia and inflammatory response were evaluated. Serum miR-497-3p and PCT levels increased in patients with bacterial pneumonia and miR-497-3p level positively corrected with the PCT level. The functional assay demonstrated that CALCA is the target of miR-497-3p in the A549 cell line. In mice with bacterial pneumonia, both miR-497-3p and PCT levels were upregulated after SpT4 infection. LV-miR-497-3p sponge administration attenuated pneumonia, accompanied with increasing gain of bodyweight and blood oxygen levels, as well as uninjured lungs. miR-497-3p inhibition attenuates the expression of C-reactive protein (CRP) and inflammatory cytokines in lung tissues of SpT4-infected mice, including nterleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). In conclusion, inhibition of miR-497-3p downregulates the expression of procalcitonin and ameliorates bacterial pneumonia in mice.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32591941</pmid><doi>10.1007/s10753-020-01279-w</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-2122-3628</orcidid></addata></record> |
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| subjects | A549 Cells Animals Bacteria Biomedical and Life Sciences Biomedicine C-reactive protein Calcitonin Gene-Related Peptide Cytokines - metabolism Down-Regulation Enzyme-linked immunosorbent assay Gene Expression Profiling Humans Immunology Infections Inflammation Interleukin 6 Internal Medicine Mice Mice, Inbred C57BL MicroRNAs - antagonists & inhibitors miRNA Original Article Pathology Pharmacology/Toxicology Pneumonia Pneumonia, Bacterial - metabolism Pneumonia, Bacterial - therapy Polymerase chain reaction Procalcitonin Procalcitonin - biosynthesis Rheumatology Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α Up-Regulation |
| title | Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice |
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