Objective-Generalized social phobia involves fear/avoidance, specifically of social situations, whereas generalized anxiety disorder involves intrusive worry about diverse circumstances. It remains unclear the degree to which these two, often comorbid, conditions represent distinct disorders or alternative presentations of a single, core underlying pathology. Functional magnetic resonance imaging assessed the neural response to facial expressions in generalized social phobia and generalized anxiety disorder.Method-Individuals matched on age, IQ, and gender with generalized social phobia without generalized anxiety disorder (N=17), generalized anxiety disorder (N= 17), or no psychopathology (N=17) viewed neutral, fearful, and angry expressions while ostensibly making a simple gender judgment.Results-The patients with generalized social phobia without generalized anxiety disorder showed increased activation to fearful relative to neutral expressions in several regions, including the amygdala, compared to healthy individuals. This increased amygdala response related to selfreported anxiety in patients with generalized social phobia without generalized anxiety disorder. In contrast, patients with generalized anxiety disorder showed significantly less activation to fearful relative to neutral faces compared to the healthy individuals. They did show significantly increased response to angry expressions relative to healthy individuals in a lateral region of the middle frontal gyrus. This increased lateral frontal response related to self-reported anxiety in patients with generalized anxiety disorder.Conclusions-These results suggest that neural circuitry dysfunctions differ in generalized social phobia and generalized anxiety disorder.Generalized social phobia and generalized anxiety disorder are two highly prevalent, chronic, and disabling anxiety disorders (1,2) that are sometimes comorbid. Generalized social phobia involves fear/avoidance, specifically of social situations, whereas generalized anxiety disorder involves intrusive worry about a broader array of everyday life circumstances. Although both have considerable social and economic costs, disagreement exists concerning the degree to which the conditions result from a shared or unique pathophysiology. For example, high rates of comorbidity in cross-sectional and longitudinal studies suggest that the distinction between the two conditions may be relatively subtle at the descriptive level (3,4). On the other hand, data from family-based and therapeutic research suggest the two conditions can be dissociated. Specifically, such dissociation is reflected in patterns of disorder aggregation within families (5), as well as by the fact that generalized anxiety disorder, but not social phobia, responds to most tricyclic antidepressants and to buspirone (6-8). Because no brain-imaging study has directly compared the two conditions, it remains unclear whether the two disorders have dissociable neural correlates.The principal goal of the current study was to inves...
Amyloidosis is a rare systemic disease caused by extracellular deposition of an insoluble protein. Although it is usually seen in a systemic form, 1O%-20% of cases can be localized. Systemic amyloidosis is subclassified into an idiopathic primary form and a secondary or reactive form. Patients with primary amyloidosis have no underlying condition or disease. Men are affected more than women, and the mean age at
Mitochondrial oxidative damage is thought to contribute to a wide range of human diseases; therefore, the development of approaches to decrease this damage may have therapeutic potential. Mitochondria-targeted antioxidants that selectively block mitochondrial oxidative damage and prevent some types of cell death have been developed. These compounds contain antioxidant moieties, such as ubiquinone, tocopherol, or nitroxide, that are targeted to mitochondria by covalent attachment to a lipophilic triphenylphosphonium cation. Because of the large mitochondrial membrane potential, the cations are accumulated within the mitochondria inside cells. There, the conjugated antioxidant moiety protects mitochondria from oxidative damage. Here, we outline some of the work done to date on these compounds and how they may be developed as therapies.
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