{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,9,15]],"date-time":"2023-09-15T05:44:43Z","timestamp":1694756683663},"reference-count":41,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2017,1,24]],"date-time":"2017-01-24T00:00:00Z","timestamp":1485216000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001700","name":"Ministry of Education, Culture, Sports, Science and Technology","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001700","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pediatrics International"],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Glycine protected adult brains against injury in an experimental model of stroke, but, because the ischemic response of neonatal brains differs from that of adult brains, we examined the neuroprotective efficacy of glycine and associated mechanisms in an experimental model of neonatal hypoxic\u2013ischemic (<jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content>) encephalopathy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Neonatal (postnatal day 7) Wistar rats were randomly divided into an untreated group (non\u2010<jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content>) and two <jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content> groups that were treated with left common carotid artery ligation and saline control or glycine. After recovery, pups that received surgery were injected i.p. with saline or glycine (800 mg\/kg; optimal dose determined in pilot experiments) and were placed in a controlled 8% O<jats:sub>2<\/jats:sub> chamber for 120 min. Brains were harvested at various times after return to normoxia (several hours\u2013days after <jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content>) for analysis of infarct area, glial activation, cell apoptosis, and tumor necrosis factor\u2010\u03b1 (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1) expression on histology and reverse transcription\u2013polymerase chain reaction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Glycine injections induced large (approx. 15\u2010fold) but brief (approx. 2 h) increases in cerebrospinal fluid concentrations. In particular, the glycine group had a &gt;70% decrease in infarct areas compared with controls at 7 days after <jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content>. Glycine also significantly reduced astrocyte reactive transformation, microglia activation, and terminal deoxynucleotidyl transferase <jats:styled-content style=\"fixed-case\">dUTP<\/jats:styled-content> nick end labeling\u2010positive (apoptotic) cell numbers in peri\u2010lesional areas at 3 days after <jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content>, and <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1 <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> expression in the injured hemisphere at 12 and 24 h after HI.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Glycine protected neonatal rat brains against <jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content>, in part by inhibiting <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1\u2010induced inflammation and gliosis. Hence, systemic glycine infusions may have clinical utility for the treatment of <jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content> injury in human newborns.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ped.13164","type":"journal-article","created":{"date-parts":[[2016,9,10]],"date-time":"2016-09-10T09:36:44Z","timestamp":1473500204000},"page":"321-327","source":"Crossref","is-referenced-by-count":4,"title":["Amelioration by glycine of brain damage in neonatal rat brain following hypoxia\u2013ischemia"],"prefix":"10.1111","volume":"59","author":[{"given":"Hiroko","family":"Mori","sequence":"first","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ken","family":"Momosaki","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jun","family":"Kido","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tetsuo","family":"Naramura","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kenichi","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shirou","family":"Matsumoto","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kimitoshi","family":"Nakamura","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroshi","family":"Mitsubuchi","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fumio","family":"Endo","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masanori","family":"Iwai","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Graduate School of Medical Science Kumamoto University Kumamoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2017,1,24]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1097\/00019052-200204000-00005"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra041996"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)17946-X"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMcps050929"},{"key":"e_1_2_8_6_1","first-page":"18","article-title":"Lysine and arginine reduce the effects of cerebral ischemic insults and inhibit glutamate\u2010induced neuronal activity in rats","volume":"4","author":"Kondoh T","year":"2010","journal-title":"Front. 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