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We study the semiclassical limit of the least energy solutions to the nonlinear Dirac equation
for x ∈ ℝ3. We prove that the equation has least energy solutions for all ħ > 0 small, and, in addition, that the solutions converge in a certain sense to the least energy solution of the associated limit problem as ħ → 0.
Patients with major depressive disorder (MDD) show deficits in processing of facial emotions that persist beyond recovery and cessation of treatment. Abnormalities in neural areas supporting attentional control and emotion processing in remitted depressed (rMDD) patients suggests that there may be enduring, trait-like abnormalities in key neural circuits at the interface of cognition and emotion, but this issue has not been studied systematically.
Nineteen euthymic, medication-free rMDD patients (mean age 33.6 years; mean duration of illness 34 months) and 20 age- and gender-matched healthy controls (HC; mean age 35.8 years) performed the Emotional Face N-Back (EFNBACK) task, a working memory task with emotional distracter stimuli. We used blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) to measure neural activity in the dorsolateral (DLPFC) and ventrolateral prefrontal cortex (VLPFC), orbitofrontal cortex (OFC), ventral striatum and amygdala, using a region of interest (ROI) approach in SPM2.
rMDD patients exhibited significantly greater activity relative to HC in the left DLPFC [Brodmann area (BA) 9/46] in response to negative emotional distracters during high working memory load. By contrast, rMDD patients exhibited significantly lower activity in the right DLPFC and left VLPFC compared to HC in response to positive emotional distracters during high working memory load. These effects occurred during accurate task performance.
Remitted depressed patients may continue to exhibit attentional biases toward negative emotional information, reflected by greater recruitment of prefrontal regions implicated in attentional control in the context of negative emotional information.
Nanoscale silver crystals at the interface of silver thick film contacts on n-type silicon carry the current across the contact and therefore control the contact resistance, which is a main performance limiting parameter for semiconductor devices. The silver crystals are located in pits at the silicon surface. The shape of the pits is different on Si-(111) and Si-(100). During contact formation, these pits form before the silver crystals. Hence they determine the crystal size and shape. Consequently, the pits with the crystals influence the contact resistance. We investigate these pits experimentally by scanning electron microscopy. We are the first to simulate the mechanism of pit formation at a contact interface by considering a model that is based on the removal probability of silicon surface atoms. This model leads to good agreement between experimental and simulated data. It enables the prediction of pit formation for arbitrary process parameters like temperature and duration for silver thick film contact formation on silicon.
New defects were revealed in PECVD SiOxNyHz thin layers upon VUV-illuminations with a deuterium (De) lamp. The ESR signal measured after a 8-hour illumination reached a saturated amplitude one or two decades higher than the dark ESR signal. The dark ESR signal level was recovered after a 3-hour anneal at 380°C. In addition to the silicon dangling bonds already identified in the dark ESR, the bridging nitrogen dangling bonds and over-coordinated nitrogen were identified after VUV-radiations. The relative densities of the various kinds of defect are given as a function of the O/O+N oxynitride composition.
From January 1983 until December 1985, 35 cases of sporadic nosocomial legionella pneumonia, all caused by Legionella pneumophila, were diagnosed in a university hospital. L. pneumophila serogroup (SG) 1 was cultured from 12 of the 35 cases and compared to corresponding L. pneumophila SG 1 isolates from water outlets in the patients' immediate environment by subtyping with monoclonal antibodies. The corresponding environmental isolates were identical to 9 out of 12 (75%) of those from the cases. However, even in the remaining three cases identical subtypes were found distributed throughout the hospital water supply. From the hospital water supply four different subtypes of L. pneumophila SG 1 were isolated, three of which were implicated in legionella pneumonia. Of 453 water samples taken during the study 298 (65.8%) were positive for legionellae. Species of Legionella other than L. pneumophila have not been isolated. This may explain the exclusiveness of L. pneumophila as the legionella pneumonia-causing agent. Our results suggest that the water supply system was the source of infection.
Infections caused by mycobacteria other than Mycobacterium tuberculosis (MOTT) have often been described as common in AIDS patients. To evaluate whether infections with MOTT are specific for HIV related immunosuppression or are also frequent in patients with immunosuppression of different aetiology, data on the frequency of isolation from immunosuppressed patients with HIV infection are important. Blood, stool and urine specimens from 134 patients with non-HIV related immunosuppression, and from 55 immunocompetent subjects were examined for mycobacteria. MOTT have been isolated from one immunocompetent person but from none of the immunosuppressed patients. Since in AIDS patients an initial colonization of the gastrointestinal tract (GI-tract) with MOTT is common, GI-tract biopsy specimens from an additional 80 patients were examined microscopically and histologically for mycobacteria. Mycobacteria were not isolated from these specimens.
In the same period of time 72 AIDS patients have been examined: 7 (10%) had infections with M. tuberculosis whereas MOTT have been isolated from 16 (22%) of these patients. Mycobacteria have been found only rarely in immunocompetent patients and have not been isolated from patients with non-HIV related immunosuppression. The isolation of MOTT is highly correlated with an HIV-related immunosuppression.
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