Loading…
Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland
Oral Diseases (2010) 16, 661–667 Objective: To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide‐exposed rat parotid gland. Materials and methods: Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of i...
Saved in:
Published in: | Oral diseases 2010-10, Vol.16 (7), p.661-667 |
---|---|
Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c4612-d2ea4e9c253a66868968068bda2d7d780db533e745f450ac4c1bd4df982215893 |
---|---|
cites | |
container_end_page | 667 |
container_issue | 7 |
container_start_page | 661 |
container_title | Oral diseases |
container_volume | 16 |
creator | Çevik-Aras, H Ekström, J |
description | Oral Diseases (2010) 16, 661–667
Objective: To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide‐exposed rat parotid gland.
Materials and methods: Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration.
Results: The myeloperoxidase activity of the lipopolysaccharide‐exposed gland was 10‐fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin‐8 (10 or 25 μg kg−1, given twice intraperitoneally) or melatonin (10 or 25 mg kg−1 × 2) the lipopolysaccharide‐induced response was elevated 4.6‐ and 3.5‐folds at the most. The cholecystokinin‐A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin‐8, while the melatonin 2‐preferring receptor antagonist luzindole had no effect on the melatonin‐induced inhibition. Unselective nitric oxide‐synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide‐synthase (of non‐nervous origin) halved the inflammatory response.
Conclusion: Some hormones may contribute to anti‐inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide‐synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide. |
doi_str_mv | 10.1111/j.1601-0825.2010.01672.x |
format | article |
fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_gup_ub_gu_se_139412</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>755171492</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4612-d2ea4e9c253a66868968068bda2d7d780db533e745f450ac4c1bd4df982215893</originalsourceid><addsrcrecordid>eNpFkU1v1DAQhi0Eoh_wF5BvnLL4O86BQynQVipUQkXlNnJiZ-ttEqexo-7--zpsWayRPJ55ZjyaFyFMyYrm82mzoorQgmgmV4zkKKGqZKvtK3R8SLzOPpeikIz_OUInMW4IoWXF2Vt0xIgWikp2jH6dDckXfmg70_cmhWmHTZN8GHBocXMfOtfsYgoPfvADNoPFvesytryypXuHJ5PwaKaQvMXrLiPv0JvWdNG9f7lP0e_v327PL4vrm4ur87Prosl_s8IyZ4SrGia5UUorXSlNlK6tYba0pSa2lpy7UshWSGIa0dDaCttWmjEqdcVPUbHvG5_cONcwTr430w6C8bCeR8ih9QzRAeWVoCzzH_f8OIXH2cUEvY-N6_LMLswRSilpSUW1kB9eyLnunT10_re2DHzeA0--c7tDnhJY5IENLCrAogIs8sBfeWALN1-vFu__6D4mtz3Um-kBVMlLCXc_L-CH_MLV5d0tKP4M_hySUQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>755171492</pqid></control><display><type>article</type><title>Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Çevik-Aras, H ; Ekström, J</creator><creatorcontrib>Çevik-Aras, H ; Ekström, J</creatorcontrib><description>Oral Diseases (2010) 16, 661–667
Objective: To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide‐exposed rat parotid gland.
Materials and methods: Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration.
Results: The myeloperoxidase activity of the lipopolysaccharide‐exposed gland was 10‐fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin‐8 (10 or 25 μg kg−1, given twice intraperitoneally) or melatonin (10 or 25 mg kg−1 × 2) the lipopolysaccharide‐induced response was elevated 4.6‐ and 3.5‐folds at the most. The cholecystokinin‐A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin‐8, while the melatonin 2‐preferring receptor antagonist luzindole had no effect on the melatonin‐induced inhibition. Unselective nitric oxide‐synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide‐synthase (of non‐nervous origin) halved the inflammatory response.
Conclusion: Some hormones may contribute to anti‐inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide‐synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide.</description><identifier>ISSN: 1354-523X</identifier><identifier>EISSN: 1601-0825</identifier><identifier>DOI: 10.1111/j.1601-0825.2010.01672.x</identifier><identifier>PMID: 20846152</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject><![CDATA[Animals ; anti-inflammatory ; Anti-Inflammatory Agents - administration & dosage ; Anti-Inflammatory Agents - therapeutic use ; cholecystokinin ; Dentistry ; dysfunction ; Escherichia coli ; Hormone Antagonists - pharmacology ; inflammation ; Injections, Intraperitoneal ; lipopolysaccharide ; lipopolysaccharide-induced salivary gland inflammation ; Lipopolysaccharides - adverse effects ; Lysine - analogs & derivatives ; Lysine - pharmacology ; melatonin ; Melatonin - administration & dosage ; Melatonin - antagonists & inhibitors ; Melatonin - therapeutic use ; myeloperoxidase ; myeloperoxidase activity ; neutrophil content ; Neutrophil Infiltration - drug effects ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase Type I - antagonists & inhibitors ; Nitric Oxide Synthase Type II - antagonists & inhibitors ; nitric oxide-synthase inhibitors ; nitric-oxide ; Odontologi ; Organ Size ; oxidative stress ; Parasympathectomy ; Parotid Gland - drug effects ; Parotid Gland - enzymology ; Parotid Gland - innervation ; Parotitis - chemically induced ; Parotitis - enzymology ; Parotitis - prevention & control ; Peroxidase - analysis ; Proglumide - analogs & derivatives ; Proglumide - pharmacology ; prostaglandins ; Rats ; Rats, Sprague-Dawley ; Receptor, Cholecystokinin A - antagonists & inhibitors ; Receptor, Melatonin, MT2 - antagonists & inhibitors ; salivary ; secretion ; Sincalide - administration & dosage ; Sincalide - antagonists & inhibitors ; Sincalide - therapeutic use ; Sympathectomy ; Tryptamines - pharmacology]]></subject><ispartof>Oral diseases, 2010-10, Vol.16 (7), p.661-667</ispartof><rights>2010 John Wiley & Sons A/S</rights><rights>2010 John Wiley & Sons A/S.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4612-d2ea4e9c253a66868968068bda2d7d780db533e745f450ac4c1bd4df982215893</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20846152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/139412$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Çevik-Aras, H</creatorcontrib><creatorcontrib>Ekström, J</creatorcontrib><title>Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland</title><title>Oral diseases</title><addtitle>Oral Dis</addtitle><description>Oral Diseases (2010) 16, 661–667
Objective: To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide‐exposed rat parotid gland.
Materials and methods: Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration.
Results: The myeloperoxidase activity of the lipopolysaccharide‐exposed gland was 10‐fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin‐8 (10 or 25 μg kg−1, given twice intraperitoneally) or melatonin (10 or 25 mg kg−1 × 2) the lipopolysaccharide‐induced response was elevated 4.6‐ and 3.5‐folds at the most. The cholecystokinin‐A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin‐8, while the melatonin 2‐preferring receptor antagonist luzindole had no effect on the melatonin‐induced inhibition. Unselective nitric oxide‐synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide‐synthase (of non‐nervous origin) halved the inflammatory response.
Conclusion: Some hormones may contribute to anti‐inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide‐synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide.</description><subject>Animals</subject><subject>anti-inflammatory</subject><subject>Anti-Inflammatory Agents - administration & dosage</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>cholecystokinin</subject><subject>Dentistry</subject><subject>dysfunction</subject><subject>Escherichia coli</subject><subject>Hormone Antagonists - pharmacology</subject><subject>inflammation</subject><subject>Injections, Intraperitoneal</subject><subject>lipopolysaccharide</subject><subject>lipopolysaccharide-induced salivary gland inflammation</subject><subject>Lipopolysaccharides - adverse effects</subject><subject>Lysine - analogs & derivatives</subject><subject>Lysine - pharmacology</subject><subject>melatonin</subject><subject>Melatonin - administration & dosage</subject><subject>Melatonin - antagonists & inhibitors</subject><subject>Melatonin - therapeutic use</subject><subject>myeloperoxidase</subject><subject>myeloperoxidase activity</subject><subject>neutrophil content</subject><subject>Neutrophil Infiltration - drug effects</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase Type I - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase Type II - antagonists & inhibitors</subject><subject>nitric oxide-synthase inhibitors</subject><subject>nitric-oxide</subject><subject>Odontologi</subject><subject>Organ Size</subject><subject>oxidative stress</subject><subject>Parasympathectomy</subject><subject>Parotid Gland - drug effects</subject><subject>Parotid Gland - enzymology</subject><subject>Parotid Gland - innervation</subject><subject>Parotitis - chemically induced</subject><subject>Parotitis - enzymology</subject><subject>Parotitis - prevention & control</subject><subject>Peroxidase - analysis</subject><subject>Proglumide - analogs & derivatives</subject><subject>Proglumide - pharmacology</subject><subject>prostaglandins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Cholecystokinin A - antagonists & inhibitors</subject><subject>Receptor, Melatonin, MT2 - antagonists & inhibitors</subject><subject>salivary</subject><subject>secretion</subject><subject>Sincalide - administration & dosage</subject><subject>Sincalide - antagonists & inhibitors</subject><subject>Sincalide - therapeutic use</subject><subject>Sympathectomy</subject><subject>Tryptamines - pharmacology</subject><issn>1354-523X</issn><issn>1601-0825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNpFkU1v1DAQhi0Eoh_wF5BvnLL4O86BQynQVipUQkXlNnJiZ-ttEqexo-7--zpsWayRPJ55ZjyaFyFMyYrm82mzoorQgmgmV4zkKKGqZKvtK3R8SLzOPpeikIz_OUInMW4IoWXF2Vt0xIgWikp2jH6dDckXfmg70_cmhWmHTZN8GHBocXMfOtfsYgoPfvADNoPFvesytryypXuHJ5PwaKaQvMXrLiPv0JvWdNG9f7lP0e_v327PL4vrm4ur87Prosl_s8IyZ4SrGia5UUorXSlNlK6tYba0pSa2lpy7UshWSGIa0dDaCttWmjEqdcVPUbHvG5_cONcwTr430w6C8bCeR8ih9QzRAeWVoCzzH_f8OIXH2cUEvY-N6_LMLswRSilpSUW1kB9eyLnunT10_re2DHzeA0--c7tDnhJY5IENLCrAogIs8sBfeWALN1-vFu__6D4mtz3Um-kBVMlLCXc_L-CH_MLV5d0tKP4M_hySUQ</recordid><startdate>201010</startdate><enddate>201010</enddate><creator>Çevik-Aras, H</creator><creator>Ekström, J</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>F1U</scope></search><sort><creationdate>201010</creationdate><title>Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland</title><author>Çevik-Aras, H ; Ekström, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4612-d2ea4e9c253a66868968068bda2d7d780db533e745f450ac4c1bd4df982215893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>anti-inflammatory</topic><topic>Anti-Inflammatory Agents - administration & dosage</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>cholecystokinin</topic><topic>Dentistry</topic><topic>dysfunction</topic><topic>Escherichia coli</topic><topic>Hormone Antagonists - pharmacology</topic><topic>inflammation</topic><topic>Injections, Intraperitoneal</topic><topic>lipopolysaccharide</topic><topic>lipopolysaccharide-induced salivary gland inflammation</topic><topic>Lipopolysaccharides - adverse effects</topic><topic>Lysine - analogs & derivatives</topic><topic>Lysine - pharmacology</topic><topic>melatonin</topic><topic>Melatonin - administration & dosage</topic><topic>Melatonin - antagonists & inhibitors</topic><topic>Melatonin - therapeutic use</topic><topic>myeloperoxidase</topic><topic>myeloperoxidase activity</topic><topic>neutrophil content</topic><topic>Neutrophil Infiltration - drug effects</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase Type I - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase Type II - antagonists & inhibitors</topic><topic>nitric oxide-synthase inhibitors</topic><topic>nitric-oxide</topic><topic>Odontologi</topic><topic>Organ Size</topic><topic>oxidative stress</topic><topic>Parasympathectomy</topic><topic>Parotid Gland - drug effects</topic><topic>Parotid Gland - enzymology</topic><topic>Parotid Gland - innervation</topic><topic>Parotitis - chemically induced</topic><topic>Parotitis - enzymology</topic><topic>Parotitis - prevention & control</topic><topic>Peroxidase - analysis</topic><topic>Proglumide - analogs & derivatives</topic><topic>Proglumide - pharmacology</topic><topic>prostaglandins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Cholecystokinin A - antagonists & inhibitors</topic><topic>Receptor, Melatonin, MT2 - antagonists & inhibitors</topic><topic>salivary</topic><topic>secretion</topic><topic>Sincalide - administration & dosage</topic><topic>Sincalide - antagonists & inhibitors</topic><topic>Sincalide - therapeutic use</topic><topic>Sympathectomy</topic><topic>Tryptamines - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Çevik-Aras, H</creatorcontrib><creatorcontrib>Ekström, J</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>Oral diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Çevik-Aras, H</au><au>Ekström, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland</atitle><jtitle>Oral diseases</jtitle><addtitle>Oral Dis</addtitle><date>2010-10</date><risdate>2010</risdate><volume>16</volume><issue>7</issue><spage>661</spage><epage>667</epage><pages>661-667</pages><issn>1354-523X</issn><eissn>1601-0825</eissn><abstract>Oral Diseases (2010) 16, 661–667
Objective: To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide‐exposed rat parotid gland.
Materials and methods: Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration.
Results: The myeloperoxidase activity of the lipopolysaccharide‐exposed gland was 10‐fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin‐8 (10 or 25 μg kg−1, given twice intraperitoneally) or melatonin (10 or 25 mg kg−1 × 2) the lipopolysaccharide‐induced response was elevated 4.6‐ and 3.5‐folds at the most. The cholecystokinin‐A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin‐8, while the melatonin 2‐preferring receptor antagonist luzindole had no effect on the melatonin‐induced inhibition. Unselective nitric oxide‐synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide‐synthase (of non‐nervous origin) halved the inflammatory response.
Conclusion: Some hormones may contribute to anti‐inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide‐synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20846152</pmid><doi>10.1111/j.1601-0825.2010.01672.x</doi><tpages>7</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1354-523X |
ispartof | Oral diseases, 2010-10, Vol.16 (7), p.661-667 |
issn | 1354-523X 1601-0825 |
language | eng |
recordid | cdi_swepub_primary_oai_gup_ub_gu_se_139412 |
source | Wiley-Blackwell Read & Publish Collection |
subjects | Animals anti-inflammatory Anti-Inflammatory Agents - administration & dosage Anti-Inflammatory Agents - therapeutic use cholecystokinin Dentistry dysfunction Escherichia coli Hormone Antagonists - pharmacology inflammation Injections, Intraperitoneal lipopolysaccharide lipopolysaccharide-induced salivary gland inflammation Lipopolysaccharides - adverse effects Lysine - analogs & derivatives Lysine - pharmacology melatonin Melatonin - administration & dosage Melatonin - antagonists & inhibitors Melatonin - therapeutic use myeloperoxidase myeloperoxidase activity neutrophil content Neutrophil Infiltration - drug effects NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase Type I - antagonists & inhibitors Nitric Oxide Synthase Type II - antagonists & inhibitors nitric oxide-synthase inhibitors nitric-oxide Odontologi Organ Size oxidative stress Parasympathectomy Parotid Gland - drug effects Parotid Gland - enzymology Parotid Gland - innervation Parotitis - chemically induced Parotitis - enzymology Parotitis - prevention & control Peroxidase - analysis Proglumide - analogs & derivatives Proglumide - pharmacology prostaglandins Rats Rats, Sprague-Dawley Receptor, Cholecystokinin A - antagonists & inhibitors Receptor, Melatonin, MT2 - antagonists & inhibitors salivary secretion Sincalide - administration & dosage Sincalide - antagonists & inhibitors Sincalide - therapeutic use Sympathectomy Tryptamines - pharmacology |
title | Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T17%3A30%3A58IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_swepu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Anti-inflammatory%20action%20of%20cholecystokinin%20and%20melatonin%20in%20the%20rat%20parotid%20gland&rft.jtitle=Oral%20diseases&rft.au=%C3%87evik-Aras,%20H&rft.date=2010-10&rft.volume=16&rft.issue=7&rft.spage=661&rft.epage=667&rft.pages=661-667&rft.issn=1354-523X&rft.eissn=1601-0825&rft_id=info:doi/10.1111/j.1601-0825.2010.01672.x&rft_dat=%3Cproquest_swepu%3E755171492%3C/proquest_swepu%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4612-d2ea4e9c253a66868968068bda2d7d780db533e745f450ac4c1bd4df982215893%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=755171492&rft_id=info:pmid/20846152&rfr_iscdi=true |