Although our review suggests that interventions aimed at facilitating, supporting, and sustaining self-managment in people with COPD and delivered via smart technology significantly improved HRQoL and levels of activity up to six months compared with interventions given through face-to-face/digital and/or written support, no firm conclusions can be drawn. This improvement may not be sustained over a long duration. The only included study that measured outcomes up to 12 months highlighted the need to ensure sustained engagement with the technology over time. Limited evidence suggests that using computer and mobile technology for self-management for people with COPD is not harmful and may be more beneficial for some people than for others, for example, those with an interest in using technology may derive greater benefit.The evidence, provided by three studies at high risk of bias, is of poor quality and is insufficient for advising healthcare professionals, service providers, and members of the public with COPD about the health benefits of using smart technology as an effective means of supporting, encouraging, and sustaining self-management. Further research that focuses on outcomes relevant to different stages of COPD is needed. Researchers should provide clear information on how self-management is assessed and should include longitudinal measures that allow comment on behavioural change.
Dopaminergic transmission in the nucleus accumbens has been proposed to modulate the effects of converging excitatory inputs from the cortex, hippocampus, and amygdala. Here, we used in vivo intracellular recording in anesthetized rats to examine the response of nucleus accumbens neurons to stimulation of the prefrontal cortex (PFC) and the ventral tegmental area (VTA). The EPSP elicited in accumbens neurons by PFC stimulation was attenuated by VTA train stimulation in a pattern mimicking dopamine cell burst firing. PFC-elicited EPSPs were smaller in amplitude and faster to decay after VTA stimulation. These changes could not be explained by membrane depolarization alone, because EPSPs evoked during the sustained depolarization after VTA stimulation were significantly smaller than EPSPs evoked during spontaneously occurring up states. Furthermore, no attenuation of PFC-elicited responses was observed during depolarization produced by positive current injection through the recording electrode. Administration of a D 1 antagonist (SCH 23390; 0.5 mg/kg, i.p.) had no effect on the VTA reduction of PFC-elicited responses, whereas administration of a D 2 antagonist (eticlopride; 0.5 mg/kg, i.p.) reversed the reduction of PFC inputs when the analysis was limited to comparisons with spontaneous up states. These results suggest that the ability of PFC inputs to drive accumbens neurons is dampened by dopamine acting primarily at D 2 receptors. Along with previous reports of dopaminergic attenuation of limbic afferents to the accumbens, these findings support the hypothesis that dopamine mediates the selection and integration of excitatory inputs and thus shapes information processing in accumbens output neurons.
Executive functions consist of multiple high-level cognitive processes that drive rule generation and behavioral selection. An emergent property of these processes is the ability to adjust behavior in response to changes in one's environment (i.e., behavioral flexibility). These processes are essential to normal human behavior, and may be disrupted in diverse neuropsychiatric conditions, including schizophrenia, alcoholism, depression, stroke, and Alzheimer's disease. Understanding of the neurobiology of executive functions has been greatly advanced by the availability of animal tasks for assessing discrete components of behavioral flexibility, particularly strategy shifting and reversal learning. While several types of tasks have been developed, most are non-automated, labor intensive, and allow testing of only one animal at a time. The recent development of automated, operant-based tasks for assessing behavioral flexibility streamlines testing, standardizes stimulus presentation and data recording, and dramatically improves throughput. Here, we describe automated strategy shifting and reversal tasks, using operant chambers controlled by custom written software programs. Using these tasks, we have shown that the medial prefrontal cortex governs strategy shifting but not reversal learning in the rat, similar to the dissociation observed in humans. Moreover, animals with a neonatal hippocampal lesion, a neurodevelopmental model of schizophrenia, are selectively impaired on the strategy shifting task but not the reversal task. The strategy shifting task also allows the identification of separate types of performance errors, each of which is attributable to distinct neural substrates. The availability of these automated tasks, and the evidence supporting the dissociable contributions of separate prefrontal areas, makes them particularly well-suited assays for the investigation of basic neurobiological processes as well as drug discovery and screening in disease models.
The aim ofthis study was to determine the outcome of chromosomally normal livebirths with increased fetal nuchal translucency at 10-14 weeks' gestation. Clinical follow up of 89 chromosomally normal livebirths that in fetal life had a miniimum nuchal translucency thickness of 3.5 mm and a comparison group of 302 infants whose fetal nuchal translucency thickness at 10-14 weeks of gestation was less than 3.5 mm was performed. Major abnormalities, mainly structural defects of the cardiovascular or skeletal systems, were found in 10.1% (nine of 89) of the group with increased translucency, compared to 2% (five of 302) in those with translucency of less than 3.5 mm (X2=11.9, p<0.001).Delay in achievement of developmental milestones was observed in one of the infants with increased translucency and in one ofthe comparison group. The findings of this study show that in chromosomally normal fetuses increased nuchal translucency thickness at 10-14 weeks of gestation is a marker for fetal abnormalities including structural defects and genetic syndromes. (J Med Genet 1998;35:222-224)
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