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The eighth season of the stop-motion television series Robot Chicken began airing in the United States on Cartoon Network's late night programming block, Adult Swim, on October 26, 2015,[a] with the episode Robot Chicken DC Comics Special III: Magical Friendship.
The Robot Chicken scientist gets his cable cut off, then reinstated as part of the show's 150th episode milestone; Mike from The Blair Witch Project is found standing in the corner to relieve himself; an old lady has trouble picking out a raccoon in a police line-up; Family Double Dare airs a special edition featuring infidelity; Gonzo and his chicken find out if they're going to be parents; Oprah Winfrey welcomes Cthulhu on an episode of her talk show; Galactus auditions new heralds; nut taps at a funeral; Robin the Boy Wonder uses the Batmobile as a Lyft vehicle; a woman goes off the wagon after tasting a Thin Mint Girl Scout cookie; a man wants to have sex with a dinosaur on an episode of Fantasy Island; a man sleeps with a Game Genie and gets caught by a classic Nintendo console; Leonidas and his Spartan Army literally dine in Hell; an awkward teenage boy looking to make his move imagines himself on a sexual version of Nickelodeon GUTS; a school assembly featuring rapping broccoli and Carrot Top; Aladdin and Jasmine have sex; a superhero team of mice get attacked by a cat.
Paul Edgecomb escorts John Coffey down the Green Mile, but has to go back when he forgets his keys (running joke throughout episode); The Dementors from Harry Potter go on strike for longer lunch hours; Kel Kimble from Kenan and Kel comforts his half-boy, half-orange soda son; two kids imagine which "Ranger" character from pop culture could win in a fight; a possessed child is given a time-out for disrupting dinner; Skylanders: Trap Team learn a different meaning of the word trap; Oskar Schindler has a grocery list and the customer behind him realizes he's in a Robot Chicken sketch; Optimus Prime goes to jury duty; Zelda from the Legend of Zelda games farts in bed; Master Splinter gives the Teenage Mutant Ninja Turtles the sex talk; a neutered dog gets a change in personality; two teens trying to cover up a crime get attacked by a haunted moped; John Coffey finally gets sent to the electric chair -- and gets a surprise when Edgecomb pulls the lever.
Abstract:Recurrent Binge Eating (BE) episodes characterize several eating disorders. Here, we attempted to reassemble a condition closer to BE disorder, and we analyzed whether recurrent episodes might evoke molecular alterations in the hypothalamus of rats. The hypothalamus is a brain region which is sensitive to stress and relevant in motivated behaviors, such as food intake. A well-characterized animal model of BE, in which a history of intermittent food restriction and stress induce binge-like palatable food consumption, was used to analyze the transcriptional regulation of the endocannabinoid system (ECS). We detected, in rats showing the BE behavior, an up-regulated gene expression of cannabinoid type-1 receptor (CB1), sn-1-specific diacylglycerol lipase, as well as fatty acid amide hydrolase (Faah) and monoacylglycerol lipase. A selective reduction in DNA methylation was also observed at the promoter of Faah, which is consistent with the changes in the gene expression. Moreover, BE behavior in rats was associated with an increase in anandamide (AEA) levels. Our findings support the relevant role of the ECS in the regulation of food intake in rats subjected to repeated BE episodes, and, in particular, on AEA signaling, acting via CB1 and FAAH modulation. Notably, the epigenetic regulation of the Faah gene might suggest this enzyme as a possible target for developing new therapeutical approaches.Keywords: binge eating; endocannabinoid system; epigenetic mechanisms; food restriction; frustration stress; gene expression
OSA is characterized by recurrent episodes of upper airway collapse during sleep [9]. This can either be partial or complete, causing hypopnea or apnea respectively. Subsequently patients can experience oxygen desaturation, blood pressure and heart rate disturbance, as well as sleep fragmentation. Symptoms of OSA include daytime sleepiness, morning headaches, nocturia, irritability, somnolence, and fatigue [4]. Consequently, patients with OSA have poorer quality of life outcomes compared to healthy individuals [10]. Prompt recognition and appropriate therapy can ameliorate the neurobehavioral consequences and may also have favorable effects on cardiovascular and cerebrovascular health in moderate-severe disease [11]. Untreated OSA is independently associated with considerable long-term health risks [12]. OSA is associated with loss of productivity in the workplace and a higher incidence of road traffic accidents [13]. Recent data also suggests that moderate-to-severe OSA is independently associated with a significant increased risk of all-cause mortality [14].
This study was able to demonstrate risk factors that had an independent association with an OSA diagnosis. Men were found to be both at higher risk of OSA, and subsequently OSA with worse severity as indicated by home CPAP use. The reason for this is likely multifactorial as women are more likely to present with non-classical symptoms of fatigue and tiredness, rather than heavy snoring with witnessed apneic episodes [32]. Male bed partners of female patients having higher thresholds for OSA symptom perception compound this, making diagnosing female patients with OSA more difficult [33]. There is also a likely biological basis for this difference in disease prevalence including anatomical differences in the upper airways between both sexes and hormonal influences [34,35,36].
Abnormalities in craniofacial anatomy have previously been demonstrated to contribute to the pathogenesis of OSA and sleep-disordered breathing. Deviations from normal anatomy of the pharynx, glottis, and bones of the head and neck can increase the susceptibility for airway collapse and subsequent apneic episodes during sleep [36]. The results from this study were unable to show any relationship between diagnosed craniofacial abnormalities. This is however accounted for by the limitations of database studies, which are reliant on correct coding. The prevalence of craniofacial abnormalities detected in the population of this study is unlikely to be a true prevalence. Contrastingly acromegaly showed a significant association with OSA. Acromegaly, characterized by excessive endogenous growth hormone, can impair maintenance of airway patency during sleep by causing changes in the size and shape of the mandible and maxilla, as well as soft tissue thickening of the soft palate, uvula, and tongue [37]. 2ff7e9595c
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