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51.
2015年中华医学会感染病学分会艾滋病学组发布了第三版《艾滋病诊疗指南》。新版指南强调抗病毒治疗时点前移:一旦成人确诊感染人类免疫缺陷病毒(HIV), 若无禁忌宜尽早启动抗HIV治疗。对于合并机会性感染的HIV感染者, 在感染控制、病情稳定后也应及早开始抗病毒治疗。尤其强调HIV合并结核患者在CD4阳性淋巴细胞数少于200/μL的情况下, 建议抗结核两周内即开始抗病毒治疗。在抗HIV治疗用药中, 淘汰了一些毒副作用大、依从性较差的药物, 如司他夫定、去羟肌苷、茚地那韦等, 优选抗病毒效力强、服药方便的组合, 如拉米夫定、替诺福韦、依非韦伦组合。对于HIV感染的婴幼儿, 亦主张及早抗HIV治疗。对于五岁以内的幼儿, 主张确诊后即启动抗病毒治疗。对于HIV感染的孕产妇, 建议尽快予以全程、联合抗HIV治疗, 寓防于治。 相似文献
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Benyam Kinde Harrison W. Gabel Caitlin S. Gilbert Eric C. Griffith Michael E. Greenberg 《Proceedings of the National Academy of Sciences of the United States of America》2015,112(22):6800-6806
DNA methylation at CpG dinucleotides is an important epigenetic regulator common to virtually all mammalian cell types, but recent evidence indicates that during early postnatal development neuronal genomes also accumulate uniquely high levels of two alternative forms of methylation, non-CpG methylation and hydroxymethylation. Here we discuss the distinct landscape of DNA methylation in neurons, how it is established, and how it might affect the binding and function of protein readers of DNA methylation. We review studies of one critical reader of DNA methylation in the brain, the Rett syndrome protein methyl CpG-binding protein 2 (MeCP2), and discuss how differential binding affinity of MeCP2 for non-CpG and hydroxymethylation may affect the function of this methyl-binding protein in the nervous system. 相似文献
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《Journal of vascular surgery》2020,71(1):149-157
ObjectiveVascular Ehlers-Danlos syndrome (vEDS) is a rare disorder and 1 of 13 types of EDS. The syndrome results in aortic and arterial aneurysms and dissections at a young age. Diagnosis is confirmed with molecular testing via skin biopsy or genetic testing for COL3A1 pathogenic variants. We describe a multi-institutional experience in the diagnosis of vEDS from 2000 to 2015.MethodsThis is a multi-institutional cross-sectional retrospective study of individuals with vEDS. The institutions were recruited through the Vascular Low Frequency Disease Consortium. Individuals were identified using the International Classification of Diseases-9 and 10-CM codes for EDS (756.83 and Q79.6). A review of records was then performed to select individuals with vEDS. Data abstraction included demographics, family history, clinical features, major and minor diagnostic criteria, and molecular testing results. Individuals were classified into two cohorts and then compared: those with pathogenic COL3A1 variants and those diagnosed by clinical criteria alone without molecular confirmation.ResultsEleven institutions identified 173 individuals (35.3% male, 56.6% Caucasian) with vEDS. Of those, 11 (9.8%) had nonpathogenic alterations in COL3A1 and were excluded from the analysis. Among the remaining individuals, 86 (47.7% male, 68% Caucasian, 48.8% positive family history) had pathogenic COL3A1 variants and 76 (19.7% male, 19.7% Caucasian, 43.4% positive family history) were diagnosed by clinical criteria alone without molecular confirmation. Compared with the cohort with pathogenic COL3A1 variants, the clinical diagnosis only cohort had a higher number of females (80.3% vs 52.3%; P < .001), mitral valve prolapse (10.5% vs 1.2%; P = .009), and joint hypermobility (68.4% vs 40.7%; P < .001). Additionally, they had a lower frequency of easy bruising (23.7% vs 64%; P < .001), thin translucent skin (17.1% vs 48.8%; P < .001), intestinal perforation (3.9% vs 16.3%; P = .01), spontaneous pneumothorax/hemothorax (3.9% vs 14%, P.03), and arterial rupture (9.2% vs 17.4%; P = .13). There were no differences in mortality or age of mortality between the two cohorts.ConclusionsThis study highlights the importance of confirming vEDS diagnosis by testing for pathogenic COL3A1 variants rather than relying on clinical diagnostic criteria alone given the high degree of overlap with other forms genetically triggered arteriopathies. Because not all COL3A1 variants are pathogenic, the interpretation of the genetic testing results by an individual trained in variant assessment is essential to confirm the diagnosis. An accurate diagnosis is critical and has serious implications for lifelong screening and treatment strategies for the affected individual and family members. 相似文献
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《Sleep medicine》2021
BackgroundTheoretical models argue that coping reduces stress responses, yet no studies have tested whether coping moderates the prospective stress effects on sleep in daily life.PurposeThis study tested if coping moderates the stress-sleep association using a daily, intensive longitudinal design across 7–12 days.Methods326 young adults (Mage = 23.24 ± 5.46) reported perceived stress and coping (problem-focused, emotional-approach, and avoidance) every evening between 20:00–02:00, providing over 2400 nights of sleep data and 3000 stress surveys from all participants. Actigraphy and sleep diaries measured total-sleep-time and sleep efficiency. Multilevel models tested the interaction effects of within- and between-person stress and coping on sleep.ResultsWithin-person problem-focused and emotional-approach coping moderated the within-person stress effects on actigraphic total-sleep-time (both p = 0.02); higher stress predicted shorter total-sleep-time only during high use of problem-focused or emotional-approach coping (both p = 0.01). Between-person avoidance moderated the between-person stress effect on actigraphic total-sleep-time (p = 0.04); higher stress predicted shorter total-sleep-time for high avoidance coping (p = 0.02). Within-person emotional-approach coping buffered the between-person stress effect on actigraphic sleep efficiency (p = 0.02); higher stress predicted higher sleep efficiency for high emotional-approach coping (p = 0.04).ConclusionsThis study showed that daily coping moderates the effects of evening stress on sleep that night. More efforts to cope with stress before bedtime had a short-term cost of shorter sleep that night. However, high use of emotional-approach coping buffered the impact of stress to promote sleep efficiency. 相似文献
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