991 resultados para executive dysfunction


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Bipolar disorder (BD) and alcohol use disorders (AUDs) are usually comorbid, and both have been associated with significant neurocognitive impairment. Patients with the BD-AUD comorbidity (dual diagnosis) may have more severe neurocognitive deficits than those with a single diagnosis, but there is paucity of research in this area. To explore this hypothesis more thoroughly, we carried out a systematic literature review through January 2015. Eight studies have examined the effect of AUDs on the neurocognitive functioning of BD patients. Most studies found that BD patients with current or past history of comorbid AUDs show more severe impairments, especially in verbal memory and executive cognition, than their non-dual counterparts. Greater neurocognitive dysfunction is another facet of this severe comorbid presentation. Implications for clinical practice and research are discussed. Specifically, the application of holistic approaches, such as clinical staging and systems biology, may open new avenues of discoveries related to the BD-AUD comorbidity.

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Extensive losses of coastal wetlands in the United States caused by sea-level rise, land subsidence, erosion, and coastal development have increased hterest in the creation of salt marshes within estuaries. Smooth cordgrass Spartina altemiflora is the species utilized most for salt marsh creation and restoration throughout the Atlantic and Gulf coasts of the U.S., while S. foliosa and Salicomia virginica are often used in California. Salt marshes have many valuable functions such as protecting shorelines from erosion, stabilizing deposits of dredged material, dampening flood effects, trapping water-born sediments, serving as nutrient reservoirs, acting as tertiary water treatment systems to rid coastal waters of contaminants, serving as nurseries for many juvenile fish and shellfish species, and serving as habitat for various wildlife species (Kusler and Kentula 1989). The establishment of vegetation in itself is generally sufficient to provide the functions of erosion control, substrate stabilization, and sediment trapping. The development of other salt marsh functions, however, is more difficult to assess. For example, natural estuarine salt marshes support a wide variety of fish and shellfish, and the abundance of coastal marshes has been correlated with fisheries landings (Turner 1977, Boesch and Turner 1984). Marshes function for aquatic species by providing breeding areas, refuges from predation, and rich feeding grounds (Zimmerman and Minello 1984, Boesch and Turner 1984, Kneib 1984, 1987, Minello and Zimmerman 1991). However, the relative value of created marshes versus that of natural marshes for estuarine animals has been questioned (Carnmen 1976, Race and Christie 1982, Broome 1989, Pacific Estuarine Research Laboratory 1990, LaSalle et al. 1991, Minello and Zimmerman 1992, Zedler 1993). Restoration of all salt marsh functions is necessary to prevent habitat creation and restoration activities from having a negative impact on coastal ecosystems.

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The Transboundary Diagnosis Analysis(TDA) quantifies and ranks water-related environmental transboundary issues and their causes according to the severity of environmental and/or socio-economic impacts. The three main issues in BOBLME are; overexploitation of marine living resources; degradation of mangroves, coral reefs and seagrasses; pollution and water quality.

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Mental dependence, characterized by craving and impulsive seeking behavior, is the matter of intensive study in the field of drug addiction. The mesolimbic dopamine system has been suggested to play an important role in rewarding of drugs and relapse. Although chronic drug use can induce neuroadaptations of the mesolimbic system and changes of drug reinforcement, these mechanisms cannot fully account for the craving and the compulsive drug-using behavior of addicts. Acknowledging the reinforcement effects of drugs, most previous studies have studied the impact of environmental cues and conditioned learning on addiction behavior, often using established classical or operant conditioning model. These studies, however, paid little attention to the role of cognitive control and emotion in addiction. These mental factors that are believed to have an important influence on conditioned learning. The medial prefrontal cortex (mPFC) has close anatomic and functional connections with the mesolimbic dopamine system. A number of the cognitive neurological studies demonstrate that mPFC is involved in motivation, emotional regulation, monitoring of responses and other executive functions. Thus we speculated that the function of abnormality in mPFC following chronic drug use would cause related to the abnormal behavior in addicts including impulse and emotional changes. In the present study of a series of experiments, we used functional magnetic resonance imaging to examine the hemodynamic response of the mPFC and related circuits to various cognitive and emotional stimuli in heroin addicts and to explore the underlying dopamine neuromechnism by microinjection of tool drugs into the mPFC in laboratory animals. In the first experiment, we found that heroin patients, relative to the normal controls, took a much shorter time and committed more errors in completing the more demanding of cognitive regulation in the reverse condition of the task, while the neural activity in anterior cingulate cortex (ACC) was attenuated. In the second experiment, the scores of the heroin patients in self-rating depression scale (SDS) and Self-rating anxiety scale (SAS) were significantly higher than the normal controls and they rated the negative pictures more aversive than the normal controls. Being congruent with the behavioral results, hemodynamic response to negative pictures showed significant difference between the two groups in bilateral ventral mPFC (VMPFC), amygdala, and right thalamus. The VMPFC of patients showed increased activation than normal controls, whereas activation in the amygdala of patients was weaker than that in normal subjects. Our third experiment showed that microinjection of D1 receptor agonist SKF38393 into the mPFC of rats decreased hyperactivity, which was induced by morphine injection, in contrast, D1 receptor antagonist SCH23390 increased the hyperactivity, These findings suggest: (1) The behavior and neural activity in ACC of addicts changed in chronic drug users. Their impulsive behavior might result from the abnormal neural activity in the mPFC especially the ACC. (2) Heroine patients were more depress and anxiety than normal controls. The dysfunction of the mPFC---amygdala circuit of heroine addicts might be related to the abnormal emotion response. (3) Dopamine in the mPFC has an inhibitory effect on morphine induced behavior. The hyperactivity induced by chronic morphine was reduced by dopamine increase with D1 receptor agonist, confirm the first experiment that the neuroadaption of mPFC system induced by chronic morphine administration appears to be the substrate the impulse behavior of drug users.

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McArdle disease, caused by inherited deficiency of the enzyme muscle glycogen phosphorylase (GP-MM), is arguably the paradigm of exercise intolerance. The recent knock-in (p.R50X/p.R50X) mouse disease model allows an investigation of the phenotypic consequences of muscle glycogen unavailability and the physiopathology of exercise intolerance. We analysed, in 2-month-old mice [wild-type (wt/wt), heterozygous (p.R50X/wt) and p.R50X/p.R50X)], maximal endurance exercise capacity and the molecular consequences of an absence of GP-MM in the main glycogen metabolism regulatory enzymes: glycogen synthase, glycogen branching enzyme and glycogen debranching enzyme, as well as glycogen content in slow-twitch (soleus), intermediate (gastrocnemius) and glycolytic/fast-twitch (extensor digitorum longus; EDL) muscles.

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Spink, S., Urquhart, C., Cox, A. & Higher Education Academy - Information and Computer Sciences Subject Centre. (2007). Procurement of electronic content across the UK National Health Service and Higher Education sectors. Report to JISC executive and LKDN executive. Sponsorship: JISC/LKDN