Birth asphyxia can cause moderate to severe brain injury. It is unclear to what degree apoptotic or necrotic mechanisms of cell death account for damage after neonatal hypoxia-ischemia (HI). In a 7-d-old rat HI model, we determined the contributions of apoptosis and necrosis to neuronal injury in adjacent Nisslstained, hematoxylin and eosin-stained, and terminal deoxynucleotidyl transferase-mediated UTP nick end-labeled sections. We found an apoptotic-necrotic continuum in the morphology of injured neurons in all regions examined. Eosinophilic necrotic neurons, typical in adult models, were rarely observed in neonatal HI. Electron microscopic analysis showed "classic" apoptotic and necrotic neurons and "hybrid" cells with intermediate characteristics. The time course of apoptotic injury varied regionally. In CA3, dentate gyrus, medial habenula, and laterodorsal thalamus, the density of apoptotic cells was highest at 24-72 hr after HI and then declined. In contrast, densities remained elevated from 12 hr to 7 d after HI in most cortical areas and in the basal ganglia. Temporal and regional patterns of neuronal death were compared with expression of caspase-3, a cysteine protease involved in the execution phase of apoptosis. Immunocytochemical and Western blot analyses showed increased caspase-3 expression in damaged hemispheres 24 hr to 7 d after HI. A p17 peptide fragment, which results from the proteolytic activation of the caspase-3 precursor, was detected in hippocampus, thalamus, and striatum but not in cerebral cortex. The continued expression of activated caspase-3 and the persistence of cells with an apoptotic morphology for days after HI suggests a prolonged role for apoptosis in neonatal hypoxic ischemic brain injury. Key words: apoptosis; necrosis; hypoxia-ischemia; cysteine proteases; caspase-3 cleavage; cell death continuum; cerebral palsy; newborn brain injury; developmental brainBirth asphyxia can cause cerebral hypoxic ischemic injury, resulting in severe neurological sequelae and death. Survivors of perinatal asphyxia frequently have moderate to severe brain injury for which there currently is no promising therapy (Johnston, 1997). The results of morphological, histochemical, and molecular studies indicate that apoptotic and necrotic mechanisms account for neuronal death after cerebral hypoxia-ischemia (HI) in different neonatal animal models (Mehmet et al., 1994; Charriaut-Marlangue et al., 1996a,b;Chopp and Li, 1996;Macaya, 1996;Yue et al., 1997;Banasiak and Haddad, 1998;Pulera et al., 1998;Renolleau et al., 1998). For example, a neonatal ischemia-reperfusion model showed terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL)-positive nuclei from 4 hr to 30 d after reperfusion (Renolleau et al., 1998). A human study demonstrated apoptotic and necrotic forms of cell death after hypoxic injury, whereas in some brains from stillbirths, only apoptotic figures were observed (Scott and Hegyi, 1997). The form of cell death also may depend on the severity of ischemic injury (Kerr...

The scaling of respiratory metabolism with body mass is one of the most pervasive phenomena in biology. Using a single allometric equation to characterize empirical scaling relationships and to evaluate alternative hypotheses about mechanisms has been controversial. We developed a method to directly measure respiration of 271 whole plants, spanning nine orders of magnitude in body mass, from small seedlings to large trees, and from tropical to boreal ecosystems. Our measurements include the roots, which have often been ignored. Rather than a single power-law relationship, our data are fit by a biphasic, mixed-power function. The allometric exponent varies continuously from 1 in the smallest plants to 3/4 in larger saplings and trees. The transition from linear to 3/4-power scaling may indicate fundamental physical and physiological constraints on the allocation of plant biomass between photosynthetic and nonphotosynthetic organs over the course of ontogenetic plant growth.allometry | metabolic scaling | mixed-power function | whole-plant respiration | simple-power function F rom the smallest seedlings to giant trees, the masses of vascular plants span 12 orders of magnitude in mass (1). The growth rates of most plants, which are generally presented in terms of net assimilation rates of CO 2 , are believed to be controlled by respiration (2, 3). Furthermore, many of the CO 2 -budget models of plant growth and carbon dynamics in terrestrial ecosystems are based on whole-plant respiration rates in relation to plant size (2, 4-7). Thus far, however, there have been few studies of wholeplant respiration over the entire range of plant size from tiny seedlings to large trees. The purpose of the present study was to quantify the allometric scaling of metabolism by directly measuring whole-plant respiration over a representative range of sizes.For the past century, the scaling of metabolic rate with body size has usually been described using an allometric equation, or simple power function, for the form (8-17)where Y is the respiratory metabolic rate (μmol s −1 ), F is a constant (μmol s −1 kg -f ), M is the body mass (kg), and f is the scaling exponent. The exponent f has been controversial, and various values have been reported based on studies of both animals and plants (15). Recently, it was suggested that f = 1 for relatively small plants, based on data for a 10 6 -fold range of body mass (16), including measurements using a whole-plant chamber (18,19). If f = 1, this means that whole-plant respiration scales isometrically with body mass, which may be reasonable in the case of herbaceous plants and small trees because nearly all of their cells, even those in the stems, should be active in respiration. However, it was suggested that f = 3/4 based originally on empirical studies of animal metabolism (8). This idea is consistent with the mechanistic models of resource distribution in vascular systems (10, 11), including the pipe model (20, 21) and models based on space-filling, hierarchical, fractal-like networks of br...

Bischofia javanica Blume, an exotic tree, dominates many forest areas of the Bonin Islands in the western Pacific of Japan. The aim of this study was to test the hypothesis that the success of B. javanica (a mid-successional plant species) is related to its high acclimation capacity to sudden light increase due to canopy gap formation. We compared its ecophysiological response to simulated canopy opening with those of native species of different successional status: Trema orientalis Blume, Schima mertensiana (Sieb, et Zucc.) Koidz, Elaeocarpus photiniaefolius Hook.Et Arn. and Ardisia sieboldii Miquel. In all species, transfer of leaves developed in shade (5.3% of full sun) to full sun resulted in a substantial initial reduction in the dark-adapted quantum yield of photosystem II (Fv/Fm). T. orientalis, a pioneer plant species, showed the least reduction (38%), whereas E. photiniaefolius and A. sieboldii, both late-successional plant species, demonstrated large reductions (about 80%). In all four native species, Fv/Fm in shade leaves gradually recovered following transfer, but B. javanica recovered more fully and rapidly than the other species. Unlike Fv/Fm, the chlorophyll content in all species did not recover following the initial decline. This indicates that the recovery of quantum yield (Fv/Fm) was independent of the reduction in chlorophyll. Among all the species, B. javanica showed the highest (1) increase in maximum photosynthetic rate of shade leaves after transfer, (2) production of newly formed sun leaves, and (3) increase in relative growth rate. Ecophysiological characters of B. javanica in simulated canopy openings indicated rapid photosynthetic acclimation in existing shade leaves by minimizing photoinhibition and a rapid deployment of new sun leaves with high photosynthetic capacity. Because its habitats on these Pacific Islands are prone to typhoon disturbance, the successful invasion of B. javanica may lie in the congruence of its acclimation potential and the frequent gap events.

The child's brain is more malleable or plastic than that of adults and this accounts for the ability of children to learn new skills quickly or recovery from brain injuries. Several mechanisms contribute to this ability including overproduction and deletion of neurons and synapses, and activity-dependent stabilization of synapses. The molecular mechanisms for activity dependent synaptic plasticity are being discovered and this is leading to a better understanding of the pathogenesis of several disorders including neurofibromatosis, tuberous sclerosis, Fragile X syndrome and Rett syndrome. Many of the same pathways involved in synaptic plasticity, such as glutamate-mediated excitation, can also mediate brain injury when the brain is exposed to stress or energy failure such as hypoxia-ischemia. Recent evidence indicates that cell death pathways activated by injury differ between males and females. This new information about the molecular pathways involved in brain plasticity and injury are leading to insights that will provide better therapies for pediatric neurological disorders. KeywordsPlasticity; Injury; Fragile X Syndrome; Rett Syndrome; Hypoxia-Ischemia; NMDA; AMPA; Periventricular Leukomalacia Many disorders and injuries of the developing brain affect the basic mechanisms that allow the nervous system to be shaped by experience during childhood. These mechanisms provide the substrate for brain plasticity (kasosei in Japanese), which is much more active in children than in adults. Plasticity in the child's brain is enhanced because the organization of networks of *Correspondence: 707 North Broadway, Baltimore, MD 21205, Fax: 443-923-9317 Phone: 443-923-9315, Johnston@kennedykrieger.org. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. neuronal synapses as well as white matter pathways remain "under construction" well into adolescence and even later(1). Accordingly, the effects of intensive learning in school, exposure to a second language or practice in athletics has a much greater impact on children than adults. Several neurobiological mechanism contribute to brain plasticity, including an over-production of neurons in early development, apoptosis or programmed cell death of excessive neurons, overproduction and elimination of immature synapses in childhood, and continuous stabilization and strengthening of synaptic connections later in life(2). In this review we focus on some mechanisms for synaptic plasticity, and emerging evidence that these processes are disrupted in several pediatric neurological disorders. NIH Public Access Synaptic PlasticitySynaptic p...