High spectral resolution Fabry-Perot interferometer measurements of comet Halley at H-alpha and 6300 A

A 40.6 cm Newtonian telescope has been interfaced to the Fabry-Perot interferometer at the Arecibo Observatory to make high spectral resolution measurements of Comet Halley emissions at 6562.72 A (H-alpha) and 6300.3 A (OI). In March 1986 the H-alpha surface brightness for a 5'.9 field of view centered on the comet nucleus decreased from 39+/-7.8 rayleighs on 12 March to 16+/-3.8 rayleighs on 23 March. The atomic hydrogen production rate on 12 March 1986 was 1.62+/-0.5 x 1030 s-1, and on 23 March 1986 it was 6.76+/-2.3 x 1029 s-1. Using spectral resolution of 0.196 A, we found the atomic hydrogen outflow velocity to be approximately 7.9+/-1.0 km s-1. In general, the H-alpha spectra are highly structured, and indicative of a multiple component atomic hydrogen velocity distribution. An isotropic outflow of atomic hydrogen at various velocities is not adequate to explain the spectra measured at H-alpha. The 6300.3 A emission of O(1D) had a surface brightness of 81+/-16 rayleighs on 15 March 1986, and 95+/-11 rayleighs on 17 March 1986. After adjustment for atmospheric extinction, the implied O(1D) production rate on 15 March is 6.44+/-3.0 x 1028 s-1, and the production rate on 17 March is 5.66+/-2.7 x 1028 s-1. These spectra included a feature at 6300.8 A that we attribute to NH2. The brightness of this emission feature was 37+/-11 rayleighs on 15 March.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25881/1/0000444.pd

Post-stimulus fMRI and EEG responses: evidence for a neuronal origin hypothesised to be inhibitory

Post-stimulus undershoots, negative responses following cessation of stimulation, are widely observed in functional magnetic resonance (fMRI) blood oxygenation level dependent (BOLD) data. However, the debate surrounding whether the origin of this response phase is neuronal or vascular, and whether it provides functionally relevant information, that is additional to what is contained in primary response, means that undershoots are widely overlooked. We simultaneously recorded electroencephalography (EEG), BOLD and cerebral blood-flow (CBF) [obtained from arterial spin labelled (ASL) fMRI] fMRI responses to hemifield checkerboard stimulation to test the potential neural origin of the fMRI post-stimulus undershoot. The post-stimulus BOLD and CBF signal amplitudes in both contralateral and ipsilateral visual cortex depended on the post-stimulus power of the 8-13 Hz (alpha) EEG neuronal activity, such that trials with highest EEG power showed largest fMRI undershoots in contralateral visual cortex. This correlation in post-stimulus EEG-fMRI responses was not predicted by the primary response amplitude. In the contralateral visual cortex we observed a decrease in both cerebral rate of oxygen metabolism (CMRO2) and CBF during the post-stimulus phase. In addition, the coupling ratio (n) between CMRO2 and CBF was significantly lower during the positive contralateral primary response phase compared with the post-stimulus phase and we propose that this reflects an altered balance of excitatory and inhibitory neuronal activity. Together our data provide strong evidence that the post-stimulus phase of the BOLD response has a neural origin which reflects, at least partially, an uncoupling of the neuronal responses driving the primary and post-stimulus responses, explaining the uncoupling of the signals measured in the two response phases. We suggest our results are consistent with inhibitory processes driving the post-stimulus EEG and fMRI responses. We therefore propose that new methods are required to model the post-stimulus and primary responses independently, enabling separate investigation of response phases in cognitive function and neurological disease

Rock Varnish on Hualalai and Mauna Kea Volcanoes, Hawai'i

Tropical rock varnishes found on Hualalai and Mauna Kea Volcanoes, Hawai'i, vary systematically with time and environment. Radiocarbon dating of encapsulated organic matter, (K+ + Ca2+)/Ti4+ ratios, and Zn, Cu, and Ni trace element concentrations in rock varnish are consistent with lava flowages established by K-Ar and 14C dating, where samples are collected from arid microsites well away from the soil surface. However, inaccurate ages are obtained from rock varnish in subsurface locations and from sites with abundant lichens, cyanobacteria, and fungi that chemically erode varnish. In contrast with continental deserts, Hawaiian varnishes commonly interfinger with and are less common than rock coatings of amorphous silica. Laboratory experiments on Hawaiian rock varnishes indicate that K and Ca are preferentially leached relative to Ti over time and at higher temperatures. The location of in situ leaching has been identified in Hawaiian varnishes as porous textures without abundant detrital grains

Pioglitazone rapidly reduces neuropathic pain through astrocyte and nongenomic PPARgamma mechanisms

Repeated administration of peroxisome proliferator-activated receptor gamma (PPARγ) agonists reduces neuropathic pain-like behavior and associated changes in glial activation in the spinal cord dorsal horn. As PPARγ is a nuclear receptor, sustained changes in gene expression are widely believed to be the mechanism of pain reduction. However, we recently reported that a single intrathecal (i.t.) injection of pioglitazone, a PPARγ agonist, reduced hyperalgesia within 30 minutes, a time frame that is typically less than that required for genomic mechanisms. To determine the very rapid antihyperalgesic actions of PPARγ activation, we administered pioglitazone to rats with spared nerve injury and evaluated hyperalgesia. Pioglitazone inhibited hyperalgesia within 5 minutes of injection, consistent with a nongenomic mechanism. Systemic or i.t. administration of GW9662, a PPARγ antagonist, inhibited the antihyperalgesic actions of intraperitoneal or i.t. pioglitazone, suggesting a spinal PPARγ-dependent mechanism. To further address the contribution of nongenomic mechanisms, we blocked new protein synthesis in the spinal cord with anisomycin. When coadministered intrathecally, anisomycin did not change pioglitazone antihyperalgesia at an early 7.5-minute time point, further supporting a rapid nongenomic mechanism. At later time points, anisomycin reduced pioglitazone antihyperalgesia, suggesting delayed recruitment of genomic mechanisms. Pioglitazone reduction of spared nerve injury-induced increases in GFAP expression occurred more rapidly than expected, within 60 minutes. We are the first to show that activation of spinal PPARγ rapidly reduces neuropathic pain independent of canonical genomic activity. We conclude that acute pioglitazone inhibits neuropathic pain in part by reducing astrocyte activation and through both genomic and nongenomic PPARγ mechanisms.Ryan B. Griggs, Renee R. Donahue, Jenny Morgenweck, Peter M. Grace, Amanda Sutton, Linda R. Watkins, Bradley K. Taylo

Methylglyoxal and a spinal TRPA1-AC1-Epac cascade facilitate pain in the db/db mouse model of type 2 diabetes.

Painful diabetic neuropathy (PDN) is a devastating neurological complication of diabetes. Methylglyoxal (MG) is a reactive metabolite whose elevation in the plasma corresponds to PDN in patients and pain-like behavior in rodent models of type 1 and type 2 diabetes. Here, we addressed the MG-related spinal mechanisms of PDN in type 2 diabetes using db/db mice, an established model of type 2 diabetes, and intrathecal injection of MG in conventional C57BL/6J mice. Administration of either a MG scavenger (GERP10) or a vector overexpressing glyoxalase 1, the catabolic enzyme for MG, attenuated heat hypersensitivity in db/db mice. In C57BL/6J mice, intrathecal administration of MG produced signs of both evoked (heat and mechanical hypersensitivity) and affective (conditioned place avoidance) pain. MG-induced Ca2+ mobilization in lamina II dorsal horn neurons of C57BL/6J mice was exacerbated in db/db, suggestive of MG-evoked central sensitization. Pharmacological and/or genetic inhibition of transient receptor potential ankyrin subtype 1 (TRPA1), adenylyl cyclase type 1 (AC1), protein kinase A (PKA), or exchange protein directly activated by cyclic adenosine monophosphate (Epac) blocked MG-evoked hypersensitivity in C57BL/6J mice. Similarly, intrathecal administration of GERP10, or inhibitors of TRPA1 (HC030031), AC1 (NB001), or Epac (HJC-0197) attenuated hypersensitivity in db/db mice. We conclude that MG and sensitization of a spinal TRPAl-AC1-Epac signaling cascade facilitate PDN in db/db mice. Our results warrant clinical investigation of MG scavengers, glyoxalase inducers, and spinally-directed pharmacological inhibitors of a MG-TRPAl-AC1-Epac pathway for the treatment of PDN in type 2 diabetes