Cytotoxic brain edema triggered by neuronal swelling is the chief cause of mortality following brain trauma and cerebral infarct. Using fluorescence lifetime imaging to analyze contributions of intracellular ionic changes in brain slices, we find that intense Na(+) entry triggers a secondary increase in intracellular Cl(-) that is required for neuronal swelling and death. Pharmacological and siRNA-mediated knockdown screening identified the ion exchanger SLC26A11 unexpectedly acting as a voltage-gated Cl(-) channel that is activated upon neuronal depolarization to membrane potentials lower than -20 mV. Blockade of SLC26A11 activity attenuates both neuronal swelling and cell death. Therefore cytotoxic neuronal edema occurs when sufficient Na(+) influx and depolarization is followed by Cl(-) entry via SLC26A11. The resultant NaCl accumulation causes subsequent neuronal swelling leading to neuronal death. These findings shed light on unique elements of volume control in excitable cells and lay the ground for the development of specific treatments for brain edema.

Complement receptor 3 (CR3) activation in microglia is involved in neuroinflammation-related brain disorders and pruning of neuronal synapses. Hypoxia, often observed together with neuroinflammation in brain trauma, stroke, and neurodegenerative diseases, is thought to exacerbate inflammatory responses and synergistically enhance brain damage. Here we show that when hypoxia and an inflammatory stimulus (lipopolysaccharide [LPS]) are combined, they act synergistically to trigger long-term synaptic depression (LTD) that requires microglial CR3, activation of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), and GluA2-mediated A-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) internalization. Microglial CR3-triggered LTD is independent of N-methyl-D-aspartate receptors (NMDARs), metabotropic glutamate receptors (mGluRs), or patterned synaptic activity. This type of LTD may contribute to memory impairments and synaptic disruptions in neuroinflammation-related brain disorders.

One of the detailed and useful ways to develop land use classification maps is use of geospatial techniques such as remote sensing and Geographic Information System (GIS). It vastly improves the selection of areas designated as agricultural, industrial and/or urban sector of a region. In Islamabad city and its surroundings, change in land use has been observed and new developments (agriculture, commercial, industrial and urban) are emerging every day. Thus, the rationale of this study was to evaluate land use/cover changes in Islamabad from 1992 to 2012. Quantification of spatial and temporal dynamics of land use/cover changes was accomplished by using two satellite images, and classifying them via supervised classification algorithm and finally applying post-classification change detection technique in GIS. The increase was observed in agricultural area, built-up area and water body from 1992 to 2012. On the other hand forest and barren area followed a declining trend. The driving force behind this change was economic development, climate change and population growth. Rapid urbanization and deforestation resulted in a wide range of environmental impacts, including degraded habitat quality.

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