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The green leaves of plants are optimised for carbon fixation and the production of sugars, which are used as central units of carbon and energy throughout the plant. However, there are physical limits to this optimisation that remain insufficiently understood. Here, quantitative anatomical analysis combined with mathematical modelling and sugar transport rate measurements were used to determine how effectively sugars are exported from the needle-shaped leaves of conifers in relation to leaf length. Mathematical modelling indicated that phloem anatomy constrains sugar export in long needles. However, we identified two mechanisms by which this constraint is overcome, even in needles longer than 20 cm (1) the grouping of transport conduits, and (2) a shift in the diurnal rhythm of sugar metabolism and export in needle tips. The efficiency of sugar transport in the phloem can have a significant influence on leaf function. The constraints on sugar export described here for conifer needles are likely to also be relevant in other groups of plants, such as grasses and angiosperm trees.MECP2 duplication syndrome (MDS), a rare X-linked genomic disorder affecting predominantly males, is caused by duplication of the chromosomal region containing the methyl CpG binding protein-2 (MECP2) gene, which encodes methyl-CpG-binding protein 2 (MECP2), a multi-functional protein required for proper brain development and maintenance of brain function during adulthood. Disease symptoms include severe motor and cognitive impairment, delayed or absent speech development, autistic features, seizures, ataxia, recurrent respiratory infections, and shortened lifespan. The cellular and molecular mechanisms by which a relatively modest increase in MECP2 protein causes such severe disease symptoms are poorly understood and consequently there are no treatments available for this fatal disorder. This review summarizes what is known to date about the structure and zcomplex regulation of MECP2 and its many functions in the developing and adult brain. Additionally, recent experimental findings on the cellular and molecular underpinnings of MDS based on cell culture and mouse models of the disorder are reviewed. The emerging picture from these studies is that MDS is a neurodegenerative disorder in which neurons die in specific parts of the central nervous system, including the cortex, hippocampus, cerebellum, and spinal cord. Neuronal death likely results from astrocytic dysfunction, including a breakdown of glutamate homeostatic mechanisms. The role of elevations in the expression of glial acidic fibrillary protein (GFAP) in astrocytes and the microtubule-associated protein, Tau, in neurons to the pathogenesis of MDS is discussed. Lastly, potential therapeutic strategies to potentially treat MDS are discussed.

To examine interrater agreement and validity of the Functional Communication Classification System (FCCS) for young children with cerebral palsy (CP) aged 2 or 3 years.

Speech-language pathologist (SLP) and parent FCCS ratings for 31 children with CP (aged 2y, n=16; aged 3y, n=15; 18 males, 13 females) were examined for interrater agreement using a weighted Cohen's kappa statistic. Relationships between FCCS (SLP) ratings and (1) concurrent validity with the Language Use Inventory, a standardized pragmatic assessment for children aged 18 to 47 months, (2) gross motor and fine motor function, (3) associated impairments (visual and intellectual), and (4) primary expressive communication mode were examined using Spearman's correlation coefficients.

Almost perfect interrater agreement between SLP and parent FCCS ratings were found (k

=0.94). Correlations with FCCS (SLP) were excellent for pragmatic function (r

=-0.83,p<0.001), intellectual function (r

=0.89, p<0.001), and primary expressive commxist when compared to older children with CP.

The FCCS has excellent interrater agreement and validity for communication classification of children with CP aged 2 or 3 years and is highly suitable for surveillance and research purposes. What this paper adds The Functional Communication Classification System (FCCS) is a valid instrument for children with cerebral palsy (CP) aged 2 or 3 years. Excellent agreement exists between speech-language pathologist and parent FCCS ratings. The FCCS has excellent correlation with intelligence, pragmatic function, and primary expressive mode. Stronger correlations with the Gross Motor Function Classification System and vision exist for children aged 2 or 3 years. Weaker correlations with manual ability exist when compared to older children with CP.Zinc has been suggested to act as an intracellular signaling molecule due to its regulatory effects on numerous protein targets including enzymes, transcription factors, ion channels, neurotrophic factors, and postsynaptic scaffolding proteins. However, intracellular zinc concentration is tightly maintained at steady levels under natural physiological conditions. Dynamic changes in intracellular zinc concentration have only been detected in certain types of cells that are exposed to pathologic stimuli or upon receptor ligand binding. Unlike calcium, the ubiquitous signaling metal ion that can oscillate periodically and spontaneously in various cells, spontaneous zinc oscillations have never been reported. In this work, we made the novel observation that the developing neurons generated spontaneous and synchronous zinc spikes in primary hippocampal cultures using a fluorescent zinc sensor, FluoZin-3. Blocking of glutamate receptor-dependent calcium influx depleted the zinc spikes, suggesting that these zinc spikes were driven by the glutamate-mediated spontaneous neural excitability and calcium spikes that have been characterized in early developing neurons. Simultaneous imaging of calcium or pH together with zinc, we uncovered that a downward pH spike was evoked with each zinc spike and this transient cellular acidification occurred downstream of calcium spikes but upstream of zinc spikes. Our results suggest that spontaneous, synchronous zinc spikes were generated through calcium influx-induced cellular acidification, which liberates zinc from intracellular zinc binding ligands. Monocrotaline Given that changes in zinc concentration can modulate activities of proteins essential for synapse maturation and neuronal differentiation, these zinc spikes might act as important signaling roles in neuronal development.

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