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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Injuries to the immature optic radiation (OR) are associated with thinning of the retinal nerve fiber layer and corresponding visual field (VF) defects. The aim of the current study was to seek evidence for causal retrograde trans-synaptic degeneration by exploring the correspondence between the localization and extension of the injury to the OR and the structure of the macular ganglion cell complex, and the relation to VF function. Seven adults (age range 18-35) with visual dysfunction secondary to white-matter damage of immaturity and six healthy adults (age range 22-33) underwent magnetic resonance imaging (MRI). Fiber tractography was used to generate the geniculate projections to the dorsal and ventral striate cortex, delineated by retinotopic functional MRI mapping. The structure of the macular ganglion cell complex was measured with optical coherence tomography. The tractography showed overlaps between the dorsal and ventral geniculo-striate projections. However, in four patients with inferior VF defects, the dorsal projections were to a large extent traversing the space normally solely occupied by ventral projections. This is consistent with structural changes to the OR and suggests of re-organization upon injury. Diffusion parameters were significantly different between patients and controls, and most pronounced in the dorsal geniculo-striate projections, with a pattern indicating primary injury. The macular ganglion cell complex was significantly thinner in the patients and most pronounced in the superior sectors; a pattern particularly evident in the four patients with inferior VF defects. The ratio of the mean thickness of the macular ganglion cell complex in the superior and inferior sectors significantly correlated with the axial and mean diffusivities in the contra- and ipsilateral dorsal striate projections. The results suggest a causal link between injuries to the superior portion of the immature OR and secondary thinning in the macular ganglion cell complex, resulting in inferior VF defects.
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PMID:Injuries to the Immature Optic Radiation Show Correlated Thinning of the Macular Ganglion Cell Layer. 2986 30

Brain injury in the perinatal period occurs in many clinical settings, e.g. hypoxic-ischemic encephalopathy (HIE) in term infants, neonatal stroke, encephalopathy of prematurity, and infections. These insults often result in life-long disabilities including cerebral palsy, cognitive deficits, visual dysfunction, hearing impairments, and epilepsy. However, the success of clinical implementation of a broad array of potential neuroprotective strategies tested experimentally has been limited with the exception of therapeutic hypothermia (TH) used within hours of birth in term human babies with mild to moderate HIE. There is an extensive search for adjuvant therapeutic approaches to enhance the outcomes. One strategy is to modify susceptibility in the developing CNS by means of preconditioning or postconditioning using sublethal stress. The pre-clinical and clinical literature has shown that CNS immaturity at the time of ischemic insult plays a central role in the response to injury. Thus, better understanding of the molecular regulation of the endogenous vulnerability of the immature brain is needed. Further, the use of sublethal stressors of different origin may help shed light on mechanistic similarities and distinctions beween conditioning strategies. In this review we discuss the mechanisms of protection that are achieved by an interplay of changes on the systemic level and brain level, and via changes of intracellular and mitochondrial signaling. We also discuss the barriers to improving our understanding of how brain immaturity and the type of insult-hypoxic, ischemic or inflammatory-affect the efficacy of conditioning efforts in the immature brain.
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PMID:Positive and negative conditioning in the neonatal brain. 3121 66