12.07.2015 Views

Ştiinţe Medicale - Academia de Ştiinţe a Moldovei

Ştiinţe Medicale - Academia de Ştiinţe a Moldovei

Ştiinţe Medicale - Academia de Ştiinţe a Moldovei

SHOW MORE
SHOW LESS

Create successful ePaper yourself

Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.

194tube <strong>de</strong>velopment by BDNF. Trk-B Development. 1997; 124(10):1877–185.15. Kidane A. H. et al. Differential NeuroendocrineExpression of Multiple Brain-Derived Neurotrophic FactorTranscripts. Endocrinology, 2008; 13 Nov.16. Kokaia Z. et al. Regional brain-<strong>de</strong>rived neurotrophicfactor in RNA and protein levels following transientforebrain ischemia in the rat. Molecular Brain Research,1996; 38 (1):139-144.17. Korhonen et al. Brain <strong>de</strong>rived neurotrophic factoris increased in cerebrospinal fluid of children suffering fromasphixia. Neuroscience Letters, 1998; 240 (3): 151-154.18. Li Z. K. et al. Effects of androgen on the expressionof brain aromatase cytopigment and nerve growth factor inneonatal rats with hypoxic-ischemic brain damage. ZhongguoDang Dai Er Ke Za Zhi, 2008;10(4):441-446.19. Mattson M.P. Glutamate and neurotrophic factorsin neuronal plasticity and disease. Ann N.Y., Acad Sci.,2008:97-112.20. McDonald D.G., Kelehan P., McMenamin J.B. etal. Placental fetal thrombotic vasculopathy is associated withneonatal encephalopathy. Hum. Pathol., 2004; p. 35.21. Mureșanu D.F. Factorii neurotrofici. București: Libripress,2001, p.22. Novicov L. et al. Brain-<strong>de</strong>rived neurotrophic factorpromoted axonal regeneration and long-term survival ofadult rat spinal motoneurons in vivo. Neuroscience, 1997;79 (3): 765-774.23. Popescu V. Neurologie pediatrică. București, 2004,p. 445-498.24. Redline R.W. Severe fetal placental vascular lesionsin term infants with neurologic impairment. Am. J. Obstet.Gynecol.; 2005; 192:452.25. Reyes J. H. et al. Glutamatergic neuronal differentiationof mouse embryonic stem cells after transient expressionof neurogenin 1 and treatment with BDNF and GDNF: invitro and in vivo studies. J. Neurosci., 2008; 28(48):12622-12631.26. Samsonava Т., Bobrova E. et al. Dinamica producţiineirotroficeskih faktorov u <strong>de</strong>iei v rannem vostanoviteinomperio<strong>de</strong> perinatainâh ghipoxiceskih porajenii golovnogomozga. Iaroslavl; 2006; p. 212-215.27. Scbwab M. Physiological effect and brain protectionby hypothermia and cerebrolysin after mo<strong>de</strong>rate forebrainischemia in rats. Txicol. Pathol., 1997; 49: 105-106.28. Sugita V. The protective effect of FPF 1070 (cerebrolysin)on <strong>de</strong>layed neuronal <strong>de</strong>ath in the gerbil – <strong>de</strong>tection ofhydroxyl radicals with sallicylic acid. Brain and Nerve, 1993;45:325-601.29. Tang S., Machaalani R., Waters K.A. Brain-<strong>de</strong>rivedneurotrophic factor (BDNF) and TrkB in the piglet brainstemafter post-natal nicotine and intermittent hypercapnic hypoxia.Brain Res., 2008; 1232:195-205.30. Tsukahara T. et al. Increases in levels of brain-<strong>de</strong>rivedneurotrophic factor m RNA and its promoted after transientferebrain ischemia in the rat brain. NeurochemistryInternational, 1998; 33 (2): 201-207.31. Volpe M.D. Neurology of the Newborn. Secon<strong>de</strong>dition; W.B.Saun<strong>de</strong>rs Company, Phila<strong>de</strong>lphia, London,Buletinul AŞMToronto, MexicoCity, Rio <strong>de</strong> Janetro, Sydney, Tokyo, HongKong, 1987, vol. 22, p.159-236.32. Wu Y.W., Backstrand K.H., Zhao S. et al. Decliningdiagnosis of birth asphyxia in California: 1991-2000. Pediatrics,2004; 114:1584.33. Yamashita K. et al. Post-occlusion treatment withBDNF reduced infarct size in a mo<strong>de</strong>l of permanent occlisionin the middle cerebral artery in rat. Metabolic Brain Disease,1997; 12 (4):271-280.34. Yan Q. et al. Expression of brain-<strong>de</strong>rived neurotrophicfactor protein in the adult rat central nervous system.Neiroscience, 1997; 78 (2):431-448.35. Yoshimura R., Ito K., Endo Y. Differentiation/maturationof neuropepti<strong>de</strong> Y neurons in the corpus callosumis promoted by brain-<strong>de</strong>rived neurotrophic factor in mousebrain slice cultures. Neuros. Lett, 2008; 16 Dec.RezumatÎn studiul prezent au fost apreciate nivelele plasmaticeale factorului neurotrofic BDNF la copiii cu leziuni hipoxicoischemiceperinatale (EHIP) <strong>de</strong> diferit grad, în perioadaacută și în cea <strong>de</strong> recuperare. Nivele foarte scăzute <strong>de</strong> BDNFse apreciau la copiii cu leziuni grave ale SNC. S-a presupus,că BDNF este o neurotrofină responsabilă <strong>de</strong> neuro<strong>de</strong>zvoltarela naștere și în perioada <strong>de</strong> creștere. S-a constatat, căvalorile înalte <strong>de</strong> BDNF (la copiii cu grad ușor și mediu <strong>de</strong>afectare a SNC) ameliorează procesele neurometabolice șineuroplastice la copilul în creștere, protejează creierul <strong>de</strong>distrucţie, susţin supraveţuirea și diferenţierea neuronilor.Valorile scăzute <strong>de</strong> BDNF constituie un criteriu obiectiv <strong>de</strong>prognostic al dizabilităţilor neuropsihice și motorii la nounăscut.În EHIP <strong>de</strong> grad sever procesele <strong>de</strong> neurogenezăse <strong>de</strong>compensează și neuronii corticali nu sunt protejaţi<strong>de</strong> <strong>de</strong>strucţiune. Nivelul scăzut al factorului neurotrofic,în acest caz, nu este suficient pentru a menţine la nivelulcuvenit procesele <strong>de</strong> neurotroficitate și neuroregenerare.Administrarea unui exces <strong>de</strong> factori neurotrofici ar protejaţesuturile cerebrale sensibile contra leziunilor hipoxicoischemiceși ar conduce la ameliorarea neuro<strong>de</strong>zvoltării și lască<strong>de</strong>rea gradului <strong>de</strong> invaliditate.SummaryIn this study we appreciated the brain-<strong>de</strong>rived neurotrophicfactor (BDNF) in the serum of children with diversegra<strong>de</strong> perinatal hypoxic-ischemic injuries (PHIE) in acuteand retrieval periods. A higher level of BDNF is associatedto a better protection of brain against <strong>de</strong>struction, maintainsthe neuronal survival and differentiation. The lowBDNF level in serum of newborns with PHIE constitutesan objective criterion in prognostic of neuropsychical andmotor disabilities. In severe PHIE the processes of neurogenesisare <strong>de</strong>compensated and the cortical neurons are notprotected against <strong>de</strong>struction. In this case, the low BDNFlevel is not sufficient to maintain efficiently the processes ofneurotrophicity and neuroregeneration. Administration ofneurotrophic factor excess protects sensible cerebral tissuesagainst hypoxic-ischemic injuries.

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!