New PDF release: Fetal and Neonatal Brain Injury, 4th Edition

By William E. Benitz (Editor), Philip Sunshine (Editor), Susan R. Hintz (Editor), Maurice L. Druzin (Editor) David K. Stevenson (Editor)

ISBN-10: 052188859X

ISBN-13: 9780521888592

Advancements within the detection of fetal and neonatal mind accidents, advances in our knowing of the pathophysiology, mobile and molecular bases of encephalopathy, and new treatments have all mixed to provide major alterations within the administration of neonatal mind issues some time past few years. This new version of Fetal and Neonatal mind harm brings the reader totally brand new with all advances in medical administration and end result evaluate. New fabric contains pregnancy-induced high blood pressure, HELLP syndrome and protracted high blood pressure, issues of a number of gestation, neurogenic problems of the mind, neonatal stroke and lots more and plenty extra. An multiplied, hugely illustrated bankruptcy on structural and sensible imaging of the fetal and neonatal mind can also be incorporated. a superb foreign workforce of hugely skilled neonatologists and maternal-fetal drugs clinicians have produced a realistic, authoritative scientific textual content that provides transparent administration suggestion to all clinicians interested in the remedy of those sufferers.

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Extra resources for Fetal and Neonatal Brain Injury, 4th Edition

Example text

Experiments done by us [163,168] and others [169–172] have shown that neuronal degeneration triggered by excitoxicity and HI can be apoptotic, apoptosis–necrosis hybrids, and necrotic; furthermore, entire populations of neurons in the adult CNS can indeed undergo apoptosis after injury. Rigid conceptualization regarding cellular pathology is unrealistic and misleading and can hinder our goal of the identification of relevant molecular mechanisms in complex biological 24 systems, such as the injured perinatal brain, and ultimately limit the realization of therapeutic opportunities.

The different categories of cell death are discussed below. Necrosis Cell death caused by cytoplasmic swelling, nuclear dissolution (karyolysis), and lysis has been classified traditionally as necrosis [31]. Cell necrosis (sometimes termed oncosis) [32] results from rapid and severe failure to sustain cellular homeostasis, notably cell volume control [33]. , Naþ and Ca2þ) and H2O, and rapid mitochondrial damage and energetic collapse [27,34–36]. Metabolic inhibition and oxidative stress from ROS are major culprits in triggering necrosis.

A hallmark of autophagic cell death is accumulation of autophagic vacuoles of lysosomal origin. Autophagy has been seen in developmental and pathological conditions. For example, insect metamorphosis involves autophagy [63], and developing neurons can use autophagy as a PCD mechanism [64,65]. Degeneration of Purkinje neurons in the mouse mutant Lurcher appears to be a form of autophagy, thus possibly linking excitotoxic and autophagic cell deaths to constitutive activation of the GluR2 glutamate receptor [66].

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Fetal and Neonatal Brain Injury, 4th Edition by William E. Benitz (Editor), Philip Sunshine (Editor), Susan R. Hintz (Editor), Maurice L. Druzin (Editor) David K. Stevenson (Editor)


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