The state of the Martian climate

60°N was +2.0°C, relative to the 1981–2010 average value (Fig. 5.1). This marks a new high for the record. The average annual surface air temperature (SAT) anomaly for 2016 for land stations north of starting in 1900, and is a significant increase over the previous highest value of +1.2°C, which was observed in 2007, 2011, and 2015. Average global annual temperatures also showed record values in 2015 and 2016. Currently, the Arctic is warming at more than twice the rate of lower latitudes

Successful Aging And Your Brain

The Dana Foundation, a national brain research organization, teamed up with the University of New England to host a program for the public about aging and the brain. Erica Robertson, M.P.H.(c), fitness director for UNE’s U-ExCEL program, provided opening exercises to get the group warmed up and brains stimulated. The session then provided information on three topic areas: normal brain function and normal age-related changes; brain diseases and disorders; and successful aging. Panelists included Geoff Ganter, Ph.D., professor of Biology in the UNE College of Arts and Sciences; Rob Anderson, M.D., Emergency medicine and geriatrics, Maine Medical Center, assistant professor with Tufts Medical School and visiting lecturer with the UNE College of Osteopathic Medicine (UNE COM); and Stacey Thieme, D.O., director of UNE COM’s preceptor program. The moderator was Marilyn R., Gugliucci, Ph.D., professor and director of Geriatrics Education and Research at UNE COM. The event was sponsored by the Dana Foundation - Dana Alliance for Brain Initiatives, Maine AARP, and University of New England and was organized by Edward Bilsky, Ph.D., and Danielle Deason, B.A., M.B.A. of the UNE Office of Research and Scholarship and Center for Excellence in the Neurosciences.https://dune.une.edu/cen_events/1000/thumbnail.jp

Steroid Receptor Isoform Expression in <i>Drosophila</i> Nociceptor Neurons Is Required for Normal Dendritic Arbor and Sensitivity

<div><p>Steroid hormones organize many aspects of development, including that of the nervous system. Steroids also play neuromodulatory and other activational roles, including regulation of sensitivity to painful stimuli in mammals. In <i>Drosophila</i>, ecdysteroids are the only steroid hormones, and therefore the fly represents a simplified model system in which to explore mechanisms of steroid neuromodulation of nociception. In this report, we present evidence that ecdysteroids, acting through two isoforms of their nuclear ecdysone receptor (EcR), modulate sensitivity to noxious thermal and mechanical stimuli in the fly larva. We show that EcRA and EcRB1 are expressed by third instar larvae in the primary nociceptor neurons, known as the class IV multidendritic neurons. Suppression of EcRA by RNA interference in these cells leads to hyposensitivity to noxious stimulation. Suppression of EcRB1 leads to reduction of dendritic branching and length of nociceptor neurons. We show that specific isoforms of the ecdysone receptor play critical cell autonomous roles in modulating the sensitivity of nociceptor neurons and may indicate human orthologs that represent targets for novel analgesic drugs.</p></div

Ecdysone receptor mutants are less sensitive to noxious mechanical stimulation.

<p>Foraging third instar larvae were stimulated on their dorsal surface with a von Frey filament calibrated to deliver 45 mN. Larvae responding with a nocifensive roll were classified as responders. Distributions were compared with Fisher’s exact test. Asterisks indicate statistically different groups (* is p<0.05, *** is p<0.001). N > 90. (A) Mutants bearing one null allele of EcR (EcR^M554fs) and one temperature sensitive allele (EcR^A483T) were significantly less sensitive than controls comprising the genetic backgrounds of each mutation (+ = Canton-S). (B) EcR RNAi is driven by the mifepristone-inducible neuron-specific elav-Geneswitch. (C-F) Various EcR and a USP RNAi are driven by ppk1.9-Gal4, specific to the nociceptive class IV multidendritic neurons.</p

Summary of consequences of nociceptor-specific RNAi suppression of EcR isoforms and USP.

<p>Summary of consequences of nociceptor-specific RNAi suppression of EcR isoforms and USP.</p

Morphometric analysis of class IV neurons in EcR, EcRA, EcRB1 and USP mutant flies.

<p>All neurons in the analysis were class IV ddaC neurons from third instar larvae. Experimental animals were compared to control animals for number of dendritic terminals (left), total dendritic length (center) and the ratio of dendritic terminals/total dendritic length as a measure of complexity (right). (A) <i>EcR</i> mutants have significantly fewer dendritic terminals and a reduced dendritic length, but maintain the same complexity. Control n = 20, <i>EcR</i> mutant n = 19. (B) <i>EcRA</i> mutants show reduced dendritic length, but both the number of dendritic terminals and complexity remain the same. Control n = 18, <i>EcRA</i> mutant n = 19. (C) <i>EcRB1</i> mutants show a reduced number of dendritic terminals and reduced dendritic length, but are similar in complexity. Control n = 18, <i>EcRB1</i> mutant n = 17. (D) <i>USP</i> mutant animals show no difference in number of dendritic terminals, total dendritic length or complexity. Control n = 18 <i>USP</i> mutant n = 16. *** indicates p < 0.001.</p

Analysis of ecdysone receptor mutant locomotion.

<p>Third instar larvae were assayed for spontaneous locomotor activity using the <i>Drosophila</i> activity monitor (DAM). Data were collected as moves per minute for each larva and averaged over a twenty-minute period. A Students t-test was used to determine statistical significance (** indicates p<0.01, *** indicates p<0.001), n = 32 per genotype. (A) Mutants bearing one null allele of <i>EcR</i> (<i>EcR</i>^{<i>M554fs</i>}) and one temperature sensitive allele (<i>EcR</i>^<i>A483T</i>) were significantly less motile (p<0.011) than controls comprising the genetic backgrounds of each mutation (+ = Canton-S). (B) Locomotor activity was increased in larvae in which all EcR isoforms were suppressed specifically in nociceptor neurons. (C-E) The spontaneous locomotion of various other EcR and a USP RNAi driven by <i>ppk-Gal4</i> were not significantly different from both controls.</p

EcRA and EcRB1 are expressed in the class IV primary nociceptor neurons.

<p>(A) <i>ppk-eGFP</i> larva stained with anti-EcRA. (B) The class IV neuron is identified by eGFP expression in <i>ppk-eGFP</i>. (C) Merge of (A and B) indicates the presence of EcRA in the nociceptor neurons. (D) Sensory cluster of <i>ppk-eGFP</i> larva stained with anti-EcRB1. (E) Nociceptor neuron of same cluster is identified by eGFP expression in <i>ppk-eGFP</i>. (F) Merge of (D and E) indicates the presence of EcRB1 in the class IV nociceptor neurons.</p

Ecdysone receptor mutants are less sensitive to noxious thermal stimulation.

<p>Foraging third instar larvae were gently touched on their dorsal surface with a probe at 45°C. Larvae responding with a nocifensive roll were classified as fast (<6 seconds) or slow (between 6 and 20 seconds), or nonresponders if they did not respond within 20 seconds. Distributions were compared using Fisher’s exact test. Asterisks indicate statistically different results (* is p<0.05, *** is p<0.001). N > 90. (A) Mutants bearing one null allele (<i>EcR</i>^{<i>M554fs</i>}) and one temperature sensitive allele (<i>EcR</i>^<i>A483T</i>) were significantly less sensitive than controls (+ = Canton-S) comprising the genetic backgrounds of each mutation. (B) <i>EcR</i> RNAi was driven by the mifepristone-inducible neuron-specific <i>elav-Geneswitch</i>. (C-F) Various <i>EcR</i> and a <i>USP</i> RNAi were driven by <i>ppk1</i>.<i>9-Gal4</i>, specific to the nociceptive class IV multidendritic neurons.</p