Effects of Violent Video Game Exposure on Aggressive Behavior, Aggressive thought Accessibility, and Aggressive Affect among Adults with and without Autism Spectrum Disorder

Recent mass shootings have prompted the idea among some members of the public that exposure to violent video games can have a pronounced effect on individuals with autism spectrum disorder (ASD). Empirical evidence for or against this claim currently is absent. To address this issue, adults with and without ASD were assigned to play a violent or nonviolent version of a customized first-person shooter video game, after which responses on three aggression-related outcome variables (aggressive behavior, aggressive thought accessibility, and aggressive affect) were assessed. Results showed strong evidence that adults with ASD are not differentially affected by acute exposure to violent video games compared to typically developing adults. Moreover, model comparisons showed modest evidence against any effect of violent game content whatsoever. Findings from the current experiment suggest that societal concerns over whether violent game exposure has a unique effect on adults with autism are not supported by evidence

Functional Importance of Oxidative Post-Translational Modifications of Ryanodine Receptor in Cardiac Sarcoplasmic Reticulum Ca2+ Handling During Oxidative Stress

Free ionic calcium (Ca2+) plays an essential role as a second messenger that initiates muscle contraction in the heart. Ryanodine receptor (RyR2) acts as the primary Sarcoplasmic Reticulum (SR) Ca2+ release channel in the heart. In the event that intracellular SR Ca2+ handling is compromised, both the contractility and electrical excitability of the heart can be altered. As a consequence, heart function may not be able to maintain the necessary cardiac output to meet the metabolic demand of the body. Increased oxidation of RyR2 has been implicated in abnormal Ca2+ handling that promotes the onset and progression of cardiovascular disease. However, little has been done to specifically characterize oxidative post-translational modifications (PTMs) of RyR2 as a result of oxidative stress within the ischemic or failing myocardium. Commonly observed in many disease phenotypes, including cardiovascular disease, is the prominence of glutathione mixed-disulfides as a result of oxidative stress. This work tests the hypothesis: Increased glutathione mixed-disulfides will promote oxidation of RyR2, promoting augmentation of SR Ca2+ fractional release and SR Ca2+ will leak. Oxidative PTMs of RyR2, observed as a result of experimentally induced oxidative stress, will manifest in models of disease. To test these hypotheses, changes in SR Ca2+ cycling parameters were measured in isolated ventricular myocytes from rabbit. RyR2 oxidation was determined by measuring relative free thiol content and western blot analysis. In the first part, the cellular redox environment is manipulated experimentally. With increased intracellular glutathione-mixed disulfides, RyR2-mediated SR Ca2+ release and RyR2 intersubunit disulfide formation (cross-linking) was increased. Moreover, RyR2 intersubunit cross-linking was strongly associated with depleting steady state SR Ca2+. The second part defines RyR2 oxidation in ischemia-reperfused (I/R) and failing myocardium (HF). Increased RyR2 oxidation and RyR2-mediated SR Ca2+ release manifested in both I/R and HF. RyR2 intersubunit cross-linking was observable in I/R whole tissue preparations. These findings implicate intersubunit cross-linking as an important mechanism for the regulation of RyR2 channel activity in disease

Use of sweeteners in osmotic pretreatment before freeze-drying of pear and pineapple

The aim of the study was to analyse the influence of the type of osmotic substance (sucrose, glucose, xylitol, trehalose, and sorbitol) on the physicochemical properties of freeze-dried fruit (pear and pineapple). Controlling the functional properties of freeze-dried fruit after osmotic dehydration with aqueous solutions at water activity of a w=0.90 is presented. Decrease in the water adsorption index (WAI) was recorded for all dehydrated samples. The largest decrease (for pears and pineapples by 25 and 65%, respectively) was observed in osmoactive solutions containing trehalose. Considerable increase in the FAI was recorded in samples of dehydrated pineapple. In osmoactive trehalose solutions that increase hardly reached 46%, whereas in sorbitol and xylitol its value elevated to 39% and 13%, respectively. Regardless of the osmoactive sweetener applied prior to freeze-drying, an increase in specific surface area (SBET) of dried materials was observed. For dehydrated pears, SBET ranged from 96 to 697 m2 g−1, and for pineapple, from 115 to 938 m2 g−1. Osmotic dehydration before lyophilisation of fruit samples weakened rehydration relative to the control. The dehydration carried out with osmoactive sweeteners, that is, sorbitol, xylitol, and trehalose, allows obtaining a product with good functional properties that can be successfully used for supplementation of dietary products, in particular for diabetics

Increased Energy Demand during Adrenergic Receptor Stimulation Contributes to Ca2+ Wave Generation

AbstractWhile β-adrenergic receptor (β-AR) stimulation ensures adequate cardiac output during stress, it can also trigger life-threatening cardiac arrhythmias. We have previously shown that proarrhythmic Ca2+ waves during β-AR stimulation temporally coincide with augmentation of reactive oxygen species (ROS) production. In this study, we tested the hypothesis that increased energy demand during β-AR stimulation plays an important role in mitochondrial ROS production and Ca2+-wave generation in rabbit ventricular myocytes. We found that β-AR stimulation with isoproterenol (0.1 μM) decreased the mitochondrial redox potential and the ratio of reduced to oxidated glutathione. As a result, β-AR stimulation increased mitochondrial ROS production. These metabolic changes induced by isoproterenol were associated with increased sarcoplasmic reticulum (SR) Ca2+ leak and frequent diastolic Ca2+ waves. Inhibition of cell contraction with the myosin ATPase inhibitor blebbistatin attenuated oxidative stress as well as spontaneous SR Ca2+ release events during β-AR stimulation. Furthermore, we found that oxidative stress induced by β-AR stimulation caused the formation of disulfide bonds between two ryanodine receptor (RyR) subunits, referred to as intersubunit cross-linking. Preventing RyR cross-linking with N-ethylmaleimide decreased the propensity of Ca2+ waves induced by β-AR stimulation. These data suggest that increased energy demand during sustained β-AR stimulation weakens mitochondrial antioxidant defense, causing ROS release into the cytosol. By inducing RyR intersubunit cross-linking, ROS can increase SR Ca2+ leak to the critical level that can trigger proarrhythmic Ca2+ waves

Mathematical modeling of atmospheric fine particle-associated primary organic compound concentrations

An atmospheric transport model has been used to explore the relationship between source emissions and ambient air quality for individual particle phase organic compounds present in primary aerosol source emissions. An inventory of fine particulate organic compound emissions was assembled for the Los Angeles area in the year 1982. Sources characterized included noncatalyst- and catalyst-equipped autos, diesel trucks, paved road dust, tire wear, brake lining dust, meat cooking operations, industrial oil-fired boilers, roofing tar pots, natural gas combustion in residential homes, cigarette smoke, fireplaces burning oak and pine wood, and plant leaf abrasion products. These primary fine particle source emissions were supplied to a computer-based model that simulates atmospheric transport, dispersion, and dry deposition based on the time series of hourly wind observations and mixing depths. Monthly average fine particle organic compound concentrations that would prevail if the primary organic aerosol were transported without chemical reaction were computed for more than 100 organic compounds within an 80 km × 80 km modeling area centered over Los Angeles. The monthly average compound concentrations predicted by the transport model were compared to atmospheric measurements made at monitoring sites within the study area during 1982. The predicted seasonal variation and absolute values of the concentrations of the more stable compounds are found to be in reasonable agreement with the ambient observations. While model predictions for the higher molecular weight polycyclic aromatic hydrocarbons (PAH) are in agreement with ambient observations, lower molecular weight PAH show much higher predicted than measured atmospheric concentrations in the particle phase, indicating atmospheric decay by chemical reactions or evaporation from the particle phase. The atmospheric concentrations of dicarboxylic acids and aromatic polycarboxylic acids greatly exceed the contributions that are due to direct emissions from primary sources, confirming that these compounds are principally formed by atmospheric chemical reactions

Molecular Marker Analysis as a Guide to the Sources of Fine Organic Aerosols

The molecular composition of fine particulate (D_p ≥ 2 µm) organic aerosol emissions from the most important sources in the Los Angeles area has been determined. Likewise, ambient concentration patterns for more than 80 single organic compounds have been measured at four urban sites (West Los Angeles, Downtown Los Angeles, Pasadena, and Rubidoux) and at one remote offshore site (San Nicolas Island). It has been found that cholesterol serves as a marker compound for emissions from charbroilers and other meat cooking operations. Vehicular exhaust being emitted from diesel and gasoline powered engines can be traced in the Los Angeles atmosphere using fossil petroleum marker compounds such as steranes and pentacyclic triterpanes (e.g., hopanes). Biogenic fine particle emission sources such as plant fragments abraded from leaf surfaces by wind and weather can be traced in the urban atmosphere. Using distinct and specific source organic tracers or assemblages of organic compounds characteristic for the sources considered it is possible to estimate the influence of different source types at any urban site where atmospheric data are available

Determination of Organic Compounds Present in Airborne Particulate Matter

Fine organic aerosol samples (d_p ≤ 2.1 µm) were collected systematically during the entire year 1982 at four urban sites in the greater Los Angeles area and at one remote station: West Los Angeles, Downtown Los Angeles, Pasadena, Rubidoux, and San Nicolas Island. Samples were taken at 6-day intervals and composited to form monthly sample sets. The aerosol sample composites were subjected to high resolution gas chromatography (HRGC) and gas chromatography/rnass spectrometry (GC/MS). The objective is to quantify the abundance and seasonal variation of individual organic compounds that may be diagnostic for the contribution of particular emission sources to the ambient organic complex. More than 80 organic compounds are quantified, including the series of a-alkanes, g-alkanoic acids, n-alkenoic acids, n-alkanals, and aliphatic dicarboxylic acids, as well as aromatic polycarboxylic acids, diterpenoids, polycyclic aromatic hydrocarbons, polycyclic aromatic ketones and quinones, nitrogen-containing organic compounds, and other organics. Primary organic aerosol constituents are readily identified, revealing an annual pattern with high winter concentrations and low summer concentrations in the Los Angeles area. In contrast, dicarboxylic acids of likely secondary origin show a reverse pattern, with high concentration in late spring/early summer. The total ambient annual average dicarboxylic acids concentration shows a steady increase when moving in the prevailing summer downwind direction from the most western urban sampling site (West Los Angeles) to the farthest eastern sampling location (Rubidoux), with an increase from 199 ng m^(-3) at West Los Angeles to 312 ng m^(-3) at Rubidoux. The occurrence of aromatic polycarboxylic acids in the fine particulate matter is discussed in detail in this study, including possible sources and formation pathways. The total aromatic polycarboxylic acid concentration reveals elevated summer concentrations when compared to the annual concentration cycle, indicating increased formation or/and emissions in summertime. Polycyclic aromatic hydrocarbons (PAH's), without exception, show low summer and high winter concentrations; whereas, polycyclic aromatic ketones (PAK's) and quinones (PAQ's) show slightly increased input/formation during early summer, indicating possible atmospheric chemical reactions involving PAH's as precursor compounds. Molecular markers characteristic of wood smoke are identified, and their concentrations change by season in close agreement with prior estimates of the seasonal use of wood as a fuel. The total mass concentration of identified aerosol organic compounds ranges from about 650 ng m^(-3) (West LA) to about 760 ng m^(-3) (Downtown LA) on an annual basis. Subdividing the total identified masses into their single compound classes reveals that n-alkanoic acids and aliphatic dicarboxylic acids make up the main portions quantified, followed by aromatic polycarboxylic acids, n-alkanes, diterpenoid acids, and polycyclic aromatic hydrocarbons. This compilation of fine organic aerosol data on a molecular level provides an extensive catalog of the organic compounds quantified, covering an entire year. Further research is underway to characterize the organic aerosol released by primary emission sources in the Los Angeles area. That study will not only provide complete characterizations of these emissions sources on a molecular basis, but in addition will enable the identification and quantification of additional organic compounds in the same airborne particle samples which otherwise would have gone unidentified in the complexity of the organic matrix inherent in fine airborne particle samples. In the future, these data from the monitoring network can be used to evaluate the predictions of mathematical models for the atmospheric transport and reaction of organic aerosol constituents defined at a molecular level

Endothelin 1-induced retinal ganglion cell death is largely mediated by JUN activation.

Glaucoma is a neurodegenerative disease characterized by loss of retinal ganglion cells (RGCs), the output neurons of the retina. Multiple lines of evidence show the endothelin (EDN, also known as ET) system is important in glaucomatous neurodegeneration. To date, the molecular mechanisms within RGCs driving EDN-induced RGC death have not been clarified. The pro-apoptotic transcription factor JUN (the canonical target of JNK signaling) and the endoplasmic reticulum stress effector and transcription factor DNA damage inducible transcript 3 (DDIT3, also known as CHOP) have been shown to act downstream of EDN receptors. Previous studies demonstrated that JUN and DDIT3 were important regulators of RGC death after glaucoma-relevant injures. Here, we characterized EDN insult in vivo and investigated the role of JUN and DDIT3 in EDN-induced RGC death. To accomplish this, EDN1 ligand was intravitreally injected into the eyes of wildtype, Six3-cre+Junfl/fl (Jun-/-), Ddit3 null (Ddit3-/-), and Ddit3-/-Jun-/- mice. Intravitreal EDN1 was sufficient to drive RGC death in vivo. EDN1 insult caused JUN activation in RGCs, and deletion of Jun from the neural retina attenuated RGC death after EDN insult. However, deletion of Ddit3 did not confer significant protection to RGCs after EDN1 insult. These results indicate that EDN caused RGC death via a JUN-dependent mechanism. In addition, EDN signaling is known to elicit potent vasoconstriction. JUN signaling was shown to drive neuronal death after ischemic insult. Therefore, the effects of intravitreal EDN1 on retinal vessel diameter and hypoxia were explored. Intravitreal EDN1 caused transient retinal vasoconstriction and regions of RGC and Müller glia hypoxia. Thus, it remains a possibility that EDN elicits a hypoxic insult to RGCs, causing apoptosis via JNK-JUN signaling. The importance of EDN-induced vasoconstriction and hypoxia in causing RGC death after EDN insult and in models of glaucoma requires further investigation