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BACKGROUND: Severe acute respiratory syndrome (SARS) became a worldwide outbreak with a mortality of 9.2%. This new human emergent infectious disease is dominated by severe lower respiratory illness and is aetiologically linked to a new coronavirus (SARS-CoV). METHODS: Pulmonary pathology and clinical correlates were investigated in seven patients who died of SARS in whom there was a strong epidemiological link. Investigations include a review of clinical features, morphological assessment, histochemical and immunohistochemical stainings, ultrastructural study, and virological investigations in postmortem tissue. RESULTS: Positive viral culture for coronavirus was detected in most premortem nasopharyngeal aspirate specimens (five of six) and postmortem lung tissues (two of seven). Viral particles, consistent with coronavirus, could be detected in lung pneumocytes in most of the patients. These features suggested that pneumocytes are probably the primary target of infection. The pathological features were dominated by diffuse alveolar damage, with the presence of multinucleated pneumocytes. Fibrogranulation tissue proliferation in small airways and airspaces (bronchiolitis obliterans organising pneumonia-like lesions) in subpleural locations was also seen in some patients. CONCLUSIONS: Viable SARS-CoV could be isolated from postmortem tissues. Postmortem examination allows tissue to be sampled for virological investigations and ultrastructural examination, and when coupled with the appropriate lung morphological changes, is valuable to confirm the diagnosis of SARS-CoV, particularly in clinically unapparent or suspicious but unconfirmed cases.  相似文献   
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TNF is a potent proinflammatory cytokine important for the development of arthritis in human and animals. We have investigated the roles of TNF receptor-1 (TNFR1) and TNF receptor-2 (TNFR2) in collagen-induced arthritis (CIA) by inducing CIA in mice genetically deficient in TNFR1. TNFR1-/- mice developed arthritis with similar incidence and severity as TNFR1+/- littermates, indicating that TNFR1 is redundant for the development of CIA. Anti-type II collagen (CII) antibody levels and T cell responses to CII did not differ between TNFR1-/- mice and controls. Neutralization of TNF with soluble TNF binding protein suppressed the development of arthritis in TNFR1+/- mice but not in TNFR1-/- mice, indicating that TNFR2 cannot substitute for TNFR1 for the proinflammatory function. To further investigate the functions of TNFR2, TNFR1-/- mice were injected with murine TNF-alpha at different stages during the course of CIA. Repeated TNF-alpha injection during the early induction phase enhanced the development of arthritis, but inhibited arthritis when administered during the late progression phase. These results show that the engagement of TNFR2 by TNF is involved in the development of CIA in the absence of TNFR1 and that opposing signals can be transduced by TNFR2.  相似文献   
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Transgenic Mice as an in vivo Model for Self-Reactivity   总被引:1,自引:0,他引:1  
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A commercial line blot using recombinant antigens was compared with a commercial ELISA and 'in-house' IFA (reference test). Two panels were evaluated: Panel A was selected to distinguish between primary infections (89), past infections (20) and seronegatives (8) in immunocompetent individuals. In panel B, patients with a high number of reactivations were included: immunosuppressed patients (37), lymphoma (19), nasopharyngeal carcinoma (10), chronic fatigue syndrome (14). Blood donors (43) and cross-reactive sera (29) were added as controls. Line blot and IFA were concordant in 94% of primary infections, 100% of seronegatives and 100% of past infections, similar to ELISA. Results differed significantly with regard to reactivations. When compared with IFA, the incidence of reactivations was overestimated by the blot, 24 and 58% in blood donors and cross-reactive sera, respectively. ELISA showed a similar problems with 21 and 34% indeterminate results, respectively. The line blot is easy to carry out, has a good concordance with the reference IFA for primary infections, and is, therefore, a sufficient choice for distinguishing primary infection from seronegative and past infection. EBV reactivation assessment will require other methods such as EBV viral load.  相似文献   
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Advances in Health Sciences Education - Professional identity is believed to foster self-confidence and resilience in health care professionals. While literature exists describing professional...  相似文献   
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BackgroundSocial media has become a ubiquitous part of daily life during the COVID-19 pandemic isolation. However, the role of social media use in depression and suicidal ideation of the general public remains unclear. Related empirical studies were limited and reported inconsistent findings. Little is known about the potential underlying mechanisms that may illustrate the relationship between social media use and depression and suicidal ideation during the COVID-19 pandemic.ObjectiveThis study tested the mediation effects of social loneliness and posttraumatic stress disorder (PTSD) symptoms on the relationship between social media use and depressive symptoms and suicidal ideation, as well as the moderation effect of age on the mediation models.MethodsWe administered a population-based random telephone survey in May and June 2020, when infection control measures were being vigorously implemented in Hong Kong. A total of 1070 adults (658 social media users and 412 nonusers) completed the survey. Structural equation modeling (SEM) and multigroup SEM were conducted to test the mediation and moderation effects.ResultsThe weighted prevalence of probable depression was 11.6%; 1.6% had suicidal ideation in the past 2 weeks. Both moderated mediation models of depressive symptoms (χ262=335.3; P<.05; comparative fit index [CFI]=0.94; nonnormed fit index [NNFI]=0.92; root mean square error of approximation [RMSEA]=0.06) and suicidal ideation (χ234=50.8; P<.05; CFI=0.99; NNFI=0.99; RMSEA=0.02) showed acceptable model fit. There was a significantly negative direct effect of social media use on depressive symptoms among older people (β=–.07; P=.04) but not among younger people (β=.04; P=.55). The indirect effect via PTSD symptoms was significantly positive among both younger people (β=.09; P=.02) and older people (β=.10; P=.01). The indirect effect via social loneliness was significant among older people (β=–.01; P=.04) but not among younger people (β=.01; P=.31). The direct effect of social media use on suicidal ideation was not statistically significant in either age group (P>.05). The indirect effects via PTSD symptoms were statistically significant among younger people (β=.02; P=.04) and older people (β=.03; P=.01). Social loneliness was not a significant mediator between social media use and suicidal ideation among either age group (P>.05).ConclusionsSocial media may be a “double-edged sword” for psychosocial well-being during the COVID-19 pandemic, and its roles vary across age groups. The mediators identified in this study can be addressed by psychological interventions to prevent severe mental health problems during and after the COVID-19 pandemic.  相似文献   
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