Shown above is a mixture of liquid O2 and O3 (ozone). O3 condenses to a dark blue fluid (bottom layer) at −112 °C, and O2 to a lighter blue liquid at −183 °C. Both liquids are powerful oxidizers. Liquid O2 has applications in aerospace propellants and explosives, but liquid O3 is less useful because it can easily detonate when it reaches its boiling point. On an open lab bench, a flask like this is a safety hazard.
Philadelphia, PA, December 1, 2014 - Panic disorder is a severe form of anxiety in which the affected individual feels an abrupt onset of fear, often accompanied by profound physical symptoms of discomfort. Scientists have known from studying twins that genes contribute to the risk of panic disorder, but very little is known about which specific genes are involved.
Two of the most common and terrifying symptoms of this severe anxiety are a sense of shortness of breath and feelings of suffocation. Studies have shown that breathing air that has increased levels of carbon dioxide can trigger panic attacks in most people with panic disorder as opposed to people without the disorder.
The mechanisms through which carbon dioxide inhalation produces anxiety are also not well understood. One theory is that panic disorder involves an overly sensitive “suffocation alarm system” in the brain that evolved to protect us from suffocating, and that panic attacks result when this alarm gets triggered by signals of impending suffocation like rising carbon dioxide levels.
Previous research in mice showed that a protein called ASIC1a acts, indirectly, as a carbon dioxide sensor in the amygdala, a region in the brain key to the perception of danger and fear, and that the ASIC1a gene regulates carbon-dioxide induced anxiety.
A collaborative group of international researchers has now studied the human version of the ASIC1a gene, ACCN2, and report their findings in the current issue of Biological Psychiatry.