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A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/pr.2017.290 http://scihub22266oqcxt.onion/10.1038/pr.2017.290 C5902650!5902650 !29166383     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29166383 &cmd=llinks): Failed to open stream: HTTP request failed! 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Prematurity disrupts glomeruli development, whereas prematurity and hyperglycemia lead to altered nephron maturation and increased oxidative stress in newborn baboons |pdf=|usr=}}{{29166383 }} gab.com Text Prematurity disrupts glomeruli development, whereas prematurity and hyperglycemia lead to altered nephron maturation and increased oxidative stress in newborn baboons JO: Pediatr Res http://www.kidney.de/pget.php?&tw=1&pmid=29166383 #FOAvip BackgroundPremature birth occurs when nephrogenesis is incomplete and has been linked to increased renal pathologies in the adult. Metabolic factors complicating preterm birth may have additional consequences for kidney development. Here, we evaluated the effects of prematurity and hyperglycemia on nephrogenesis in premature baboons when compared with those in term animals.MethodsBaboons were delivered prematurely (67% gestation; n=9) or at term (n=7) and survived for 2-4 weeks. Preterm animals were classified by glucose control during the first 5 days of life: normoglycemic (PtN; serum glucose 50-100?mg/dl, n=6) and hyperglycemic (PtH; serum glucose 150-250?mg/dl, n=3). Kidneys were assessed histologically for glomeruli relative area, maturity, size, and overall morphology. Kidney lysates were evaluated for oxidative damage with 4-hydroxynonenal (4-HNE) antibody.ResultsHistological examination revealed decreased glomeruli relative area (P<0.05), fewer glomerular generations (P<0.01), and increased renal corpuscle area (P<0.001) in preterm compared with those in term animals. Numbers of apoptotic glomeruli were similar between groups. PtH kidneys exhibited reduced nephrogenic zone width (P<0.0001), increased numbers of mature glomeruli (P<0.05), and increased 4-HNE staining compared with those in PtN kidneys.ConclusionPrematurity interrupts normal kidney development, independent of glomerular cell apoptosis. When prematurity is complicated by hyperglycemia; kidney development shifts toward accelerated maturation and increased oxidative stress. Twit Text FOAVip Prematurity disrupts glomeruli development, whereas prematurity and hyperglycemia lead to altered nephron maturation and increased oxidative stress in newborn baboons ????Pediatr Res http://www.kidney.de/pget.php?&tw=1&pmid=29166383 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29166383 #FOAvip English Wikipedia <ref>{{Cite pmid|29166383 }}</ref> Prematurity disrupts glomeruli development, whereas prematurity and hyperglycemia lead to altered nephron maturation and increased oxidative stress in newborn baboons #MMPMID29166383 Callaway DA ; McGill-Vargas LL ; Quinn A ; Jordan JL ; Winter LA ; Anzueto D ; Dick EJ Jr ; Blanco CL Pediatr Res 2018[Mar]; 83 (3 ): 702-711 PMID29166383 show ga BackgroundPremature birth occurs when nephrogenesis is incomplete and has been linked to increased renal pathologies in the adult. Metabolic factors complicating preterm birth may have additional consequences for kidney development. Here, we evaluated the effects of prematurity and hyperglycemia on nephrogenesis in premature baboons when compared with those in term animals.MethodsBaboons were delivered prematurely (67% gestation; n=9) or at term (n=7) and survived for 2-4 weeks. Preterm animals were classified by glucose control during the first 5 days of life: normoglycemic (PtN; serum glucose 50-100?mg/dl, n=6) and hyperglycemic (PtH; serum glucose 150-250?mg/dl, n=3). Kidneys were assessed histologically for glomeruli relative area, maturity, size, and overall morphology. Kidney lysates were evaluated for oxidative damage with 4-hydroxynonenal (4-HNE) antibody.ResultsHistological examination revealed decreased glomeruli relative area (P<0.05), fewer glomerular generations (P<0.01), and increased renal corpuscle area (P<0.001) in preterm compared with those in term animals. Numbers of apoptotic glomeruli were similar between groups. PtH kidneys exhibited reduced nephrogenic zone width (P<0.0001), increased numbers of mature glomeruli (P<0.05), and increased 4-HNE staining compared with those in PtN kidneys.ConclusionPrematurity interrupts normal kidney development, independent of glomerular cell apoptosis. When prematurity is complicated by hyperglycemia; kidney development shifts toward accelerated maturation and increased oxidative stress. |*Oxidative Stress [MESH] |*Premature Birth [MESH] |Aldehydes/chemistry [MESH] |Animals [MESH] |Animals, Newborn [MESH] |Apoptosis [MESH] |Blood Glucose/analysis [MESH] |Female [MESH] |Hyperglycemia/*complications [MESH] |Immunohistochemistry [MESH] |Kidney Glomerulus/growth & development [MESH] |Kidney/growth & development/*pathology [MESH] |Male [MESH] |Nephrons/*growth & development [MESH] |Organogenesis [MESH] |Papio [MESH]Prematurity disrupts glomeruli development, whereas prematurity and hy(epmc).pdf DeepDyve Pubget Overpricing