Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnetic resonance (MR) has begun to play an important role in neonatal neurology. Several MRI techniques have been applied to the diagnosis of hypoxic ischemic encephalopathy. Cerebral perfusion examined by intravoxel incoherent motion, a non-invasive tool, seems to be opening new inroads for detecting variations (neurophysiological modifications) in cerebral flows during hypoxic ischemic encephalopathy. MR spectroscopy allows identification of specific biochemical alteration of spectra patterns at various moments of hypoxic ischemic distress, including: (1) primary expression of metabolic disorders induced by the lack of blood and O2, revealed by a peak of the water-suppressed H1 spectrum, the earliest and most persistent-marker; (2) a secondary marker for the establishment of permanent lesions of anoxic-ischemic origin revealed that variations of the phosphocreatine/inorganic phosphorous index in the P31 spectrum are of diagnostic and prognostic significance in this phase. In relation to different neuropathological, structural lesions, MRI becomes particularly important in diagnosing the acute phase of cerebral edema and the different types of infarct. MRI is especially fruitful in monitoring the evolution of the lesion, providing an evaluation of myelinization, and defining the neuropathological outlook. Spectroscopic studies on human neonates have helped establish the therapeutic effects of mannitol in cerebral metabolism. MR studies on neonate animals seem to open new therapeutic prospect for CA antagonists.
 ...
PMID:State of the art of magnetic resonance (MR) in neonatal hypoxic-ischemic encephalopathy. 269 12

Complement is an essential component of inflammation that plays a role in ischemic brain injury. Recent reports demonstrate novel functions of complement in normal and diseased CNS, such as regulation of neurogenesis and synapse elimination. Here, we examined the role of complement-derived peptide C3a in unilateral hypoxia-ischemia (HI), a model of neonatal HI encephalopathy. HI injury was induced at postnatal day 9 (P9), and loss of hippocampal tissue was determined on P31. We compared WT mice with transgenic mice expressing C3a under the control of glial fibrillary acidic protein promoter, which express biologically active C3a only in CNS and without the requirement of a priori complement activation. Further, we injected C3a peptide into the lateral cerebral ventricle of mice lacking the C3a receptor (C3aR) and WT mice and assessed HI-induced memory impairment 41 d later. We found that HI-induced tissue loss in C3a overexpressing mice was reduced by 50% compared with WT mice. C3a peptide injected 1 h after HI protected WT but not C3aR-deficient mice against HI-induced memory impairment. Thus, C3a acting through its canonical receptor ameliorates behavioral deficits after HI injury, and C3aR is a novel therapeutic target for the treatment of neonatal HI encephalopathy.
 ...
PMID:Receptor for complement peptide C3a: a therapeutic target for neonatal hypoxic-ischemic brain injury. 2373 50