This paper describes spectrum occupancy measurements performed in Chicago, IL in November 2005 and proposes long-term studies in multiple locations. The Chicago project consisted of deploying a high dynamic range spectrum measurement system, a data collection and processing system and conducting spectrum occupancy measurements in all bands between 30 MHz and 3,000 MHz (see Figure 1). These measurements were taken over a two-day period and are added to an existing body of data compiled in other cities and regions including Washington, D.C., and New York City. While these studies are critical in determining what bands have low utilization, longer-term studies are crucial in developing new spectrum access technologies such as cognitive radio algorithms related to Dynamic Spectrum Sharing (DSS). The observed low spectrum occupancy in a business center like Chicago indicates that a DSS radio system could access a huge amount of "prime" spectrum. The unoccupied, large contiguous spectrum blocks show that DSS radios can use conventional contiguous waveforms and that high temporal agility may not be required to significantly expand the data capacity of an accessible section of spectrum. From both short-term and long-term spectrum occupancy studies, candidate bands for spectrum sharing can be readily identified along with unique signal characteristics within these bands. The most important use of the data will be to support senior U.S. (and non-U.S.) government officials in taking action to enhance the use of the currently under utilized RF spectrum resources and to make the R&D investments and policy changes needed to support the development of dynamic spectrum sharing radios. Figure 1: Antenna Array with Chicago Loop IntroductionAs the popularity of new wireless applications and devices continues to grow, the demand for spectral capacity is becoming insatiable. Over the past few years such applications as data centric smart phones, Bluetooth headsets, keyboards and mice, broadband WiFi internet connections, satellite radios, and GPS navigation systems (to name only a few) have moved from obscure gadgets for the wealthy to standard devices and capabilities used by the masses. Demand for spectral capacity is fundamentally experiencing a "Quadruple Whammy" composed of the dramatic increase in the number of discrete applications, the rapid rise in the deployment of these applications, the growth in the amount of time each application is utilized, and the radical growth in the data rates used when these applications are operating. These trends are placing enormous demands on the finite spectral capacity. At the same time, it is observed in this, and related studies, that most of the spectrum, in most of the places, most of the time is completely unused. These observations scream for an enhancement to the current block auction system to fundamentally include the time domain in the allocation and command and control regulatory systems to facilitate new dynamic spectrum sharing (DSS) technologies to be developed and deployed ...
Abnormal immune responses have been reported to be associated with autism. A number of studies showed that cytokines were increased in the blood, brain, and cerebrospinal fluid of autistic subjects. Elevated IL-6 in autistic brain has been a consistent finding. However, the mechanisms by which IL-6 may be involved in the pathogenesis of autism are not well understood. Here we show that mice with elevated IL-6 in the brain display many autistic features, including impaired cognitive abilities, deficits in learning, abnormal anxiety traits and habituations, as well as decreased social interactions. IL-6 elevation caused alterations in excitatory and inhibitory synaptic formations and disrupted the balance of excitatory/inhibitory synaptic transmissions. IL-6 elevation also resulted in an abnormal change in the shape, length and distributing pattern of dendritic spines. These findings suggest that IL-6 elevation in the brain could mediate autistic-like behaviors, possibly through the imbalances of neural circuitry and impairments of synaptic plasticity.
Following status epilepticus in the rat, dentate granule cell neurogenesis increases greatly, and many of the new neurons appear to develop ectopically, in the hilar region of the hippocampal formation. It has been suggested that the ectopic hilar granule cells could contribute to the spontaneous seizures that ultimately develop after status epilepticus. However, the population has never been quantified, so it is unclear whether it is substantial enough to have a strong influence on epileptogenesis. To quantify this population, the total number of ectopic hilar granule cells was estimated using unbiased stereology at different times after pilocarpine-induced status epilepticus. The number of hilar neurons immunoreactive for Prox-1, a granule-cell-specific marker, was estimated using the optical fractionator method. The results indicate that the size of the hilar ectopic granule cell population after status epilepticus is substantial, and stable over time. Interestingly, the size of the population appears to be correlated with the frequency of behavioral seizures, because animals with more ectopic granule cells in the hilus have more frequent behavioral seizures. The hilar ectopic granule cell population does not appear to vary systematically across the septotemporal axis, although it is associated with an increase in volume of the hilus. The results provide new insight into the potential role of ectopic hilar granule cells in the pilocarpine model of temporal lobe epilepsy.
Vascular endothelial growth factor (VEGF) is a protein factor which has been found to play a significant role in both normal and pathological states. Its role as an angiogenic factor is well-established. More recently, VEGF has been shown to protect neurons from cell death both in vivo and in vitro. While VEGF's potential as a protective factor has been demonstrated in hypoxia-ischemia, in vitro excitotoxicity, and motor neuron degeneration, its role in seizure-induced cell loss has received little attention. A potential role in seizures is suggested by Newton et al.'s [Newton SS, Collier EF, Hunsberger J, Adams D, Terwilliger R, Selvanayagam E, Duman RS (2003) Gene profile of electroconvulsive seizures: Induction of neurotrophic and angiogenic factors. J Neurosci 23:10841-10851] finding that VEGF mRNA increases in areas of the brain that are susceptible to cell loss after electroconvulsive-shock induced seizures. Because a linear relationship does not always exist between expression of mRNA and protein, we investigated whether VEGF protein expression increased after pilocarpine-induced status epilepticus. In addition, we administered exogenous VEGF in one experiment and blocked endogenous VEGF in another to determine whether VEGF exerts a neuroprotective effect against status epilepticus-induced cell loss in one vulnerable brain region, the rat hippocampus. Our data revealed that VEGF is dramatically up-regulated in neurons and glia in hippocampus, thalamus, amygdala, and neocortex 24 h after status epilepticus. VEGF induced significant preservation of hippocampal neurons, suggesting that VEGF may play a neuroprotective role following status epilepticus.
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