We found that some common respiratory viruses, such as adenoviruses, enteroviruses, rhinoviruses, and coronaviruses, were associated with KD cases.

WHAT'S KNOWN ON THIS SUBJECT: Sleep disturbance affects 47% to 60% of children with atopic dermatitis and is a leading cause of impaired quality of life for the patients and their family. WHAT THIS STUDY ADDS:Sleep disturbance in children with atopic dermatitis can be predicted by a Scoring Atopic Dermatitis index of $48.7, and lower nocturnal melatonin secretion might play a role in the pathophysiology. abstract BACKGROUND AND OBJECTIVES: Sleep disturbance is common in patients with atopic dermatitis (AD). However, studies have largely been questionnaire-based, and the pathophysiology remains unclear. The aims of this study were to determine objective characteristics of sleep disturbance in children with AD and explore contributing factors and clinical predictors.METHODS: Sleep parameters were measured by actigraphy and polysomnography in 72 patients with AD and 32 controls ages 1 to 18 years. Urinary 6-sulfatoxymelatonin levels, serum cytokines, and total and allergen-specific immunoglobulin E (IgE) levels were also measured. RESULTS:The patients with AD had significantly reduced sleep efficiency, longer sleep onset latency, more sleep fragmentation, and less nonrapid eye movement sleep. Results from actigraphy correlated well with those from polysomnography. The AD disease severity was associated with sleep disturbance (r = 0.5520.7), and a Scoring Atopic Dermatitis index of $48.7 predicted poor sleep efficiency with a sensitivity of 83.3% and a specificity of 75% (area under the curve = 0.81, P = .001). Lower nocturnal melatonin secretion was significantly associated with sleep disturbance in the patients with AD. Other correlates of sleep disturbance included pruritus, scratching movements, higher total serum IgE levels, and allergic sensitization to dust mite and staphylococcal enterotoxins. CONCLUSIONS:Poor sleep efficiency is common in children with AD and can be predicted by the Scoring Atopic Dermatitis index. Melatonin and IgE might play a role in the sleep disturbance. Further studies are required to explore the mechanisms and clinical implications, and actigraphy could serve as a useful evaluating tool. Atopic dermatitis (AD) is a common chronically relapsing pruritic inflammatory skin disease. 1 Disturbed sleep is frequently reported by the patients and their family and is a major factor leading to an impaired quality of life. [2][3][4] Sleep disturbance can have many negative consequences, including impaired neurocognitive function, higher rates of behavioral problems, and changes in mood. 5,6 Therefore, the recognition and proper management of sleep disturbance should be an important issue in AD.The sleep disturbance in AD might be due to the pruritus and scratching movements during sleep, 7-10 but it is likely that other factors are involved. 11 Melatonin is a hormone secreted by the pineal gland that is essential for regulating the circadian rhythm. 12 Dysfunction in the diurnal secretion of melatonin in patients with AD has been reported, 13 but its association with their sleep disturbance has...

The overall incidence of Kawasaki disease was 69 in 100000 children <5 years of age between 2003 and 2006 in Taiwan, comparable with the incidence of 66 in 100000 children between 1996 and 2002. Taiwan has the third highest incidence of Kawasaki disease in the world, after Japan and Korea. In Taiwan, it occurs more frequently during the summer.

HMW-HA may have a structure-modifying effect for OA by down-regulation of aggrecanase-2 in FLS. HMW-HA also has an anti-inflammatory effect by down-regulation of TNF-alpha, IL-8, and iNOS in FLS. These effects may be mediated through the interaction of CD44 and HMW-HA.

A notable proportion of fully vaccinated adolescents had lost immune memory conferred by a plasma-derived HB vaccine 15-18 years later. This decay of immune memory may raise concerns about the need for a booster vaccine for high-risk groups in the long run.

No abstract

SummaryOur purpose was to determine whether numbers of CD4 + CD25 + T [T regulatory (Treg)] cells and mRNA expression of functional molecules of Treg are related to airway allergy and disease severity in 51 paediatric patients with allergic rhinitis or bronchial asthma and 47 healthy controls. Surface markers were evaluated with flow cytometry, and mRNA was determined with realtime polymerase chain reaction. Children with allergic disease had fewer CD4 + CD25 + T cells (8·49% Ϯ 2·41% versus 9·58% Ϯ 2·43%, P < 0·05) and CD4 + CD25 hi T cells (1·32% Ϯ 0·68% versus 1·70% Ϯ 0·68%, P < 0·01) than control subjects. Numbers of CD4 + CD25 + and CD4 + CD25 hi T lymphocytes were higher in children with persistent allergic rhinitis and/or moderatesevere bronchial asthma than in those with respective milder disease. The number of Treg cells was correlated positively with total immunoglobulin E level. The mRNA expression of forkhead box P3 (FoxP3) was increased in moderate-severe versus mild asthma (2·93 Ϯ 0·38 versus 1·60 Ϯ 0·31, P < 0·01). Patients with moderate-severe bronchial asthma also had increased mRNA expression of interleukin (IL)-10 compared with patients with mild asthma (15·24 Ϯ 4·07 versus 3·77 Ϯ 2·18, P < 0·01). The suppressive function of Treg cells from patients with more severe asthma was competent in vitro. On average, decreased numbers of Treg cells in children with allergic airway disease might represent a defect of the Treg population. With increased expression of FoxP3 and IL-10 in Treg from patients with relatively severe allergic disease, adaptive and functional Treg might be generated in response to aggravated atopy and disease severity.

Betel quid (BQ) chewing is an etiologic factor of oral cancer and submucus fibrosis (OSF). Keratinocyte inflammation is crucial for the pathogenesis of cancer and tissue fibrosis. We found that areca nut (AN) extract (100-400 micro g/ml) induced PGE2 production by KB cells by 2.34- to 23.1-fold and also TNF-alpha production by gingival keratinocytes (GK). Arecoline (0.2-1.2 mM) elevated PGE2 production by KB cells by 2.5- to 6.1-fold. AN extract (200-400 micro g/ml) also induced IL-6 production by GK (7.5- to 8.4-fold) and KB cells. In contrast, arecoline (0.1-1.2 mM) suppressed IL-6 production by GK and KB cells, with 42-81 and 41-63% inhibition, respectively. A 48 h exposure of GK to 800-1200 micro g/ml AN extract led to 37-69% cell death. Arecoline cytotoxicity to GK was noted at concentrations of 0.8-1.2 mM, which led to 28-38% cell death. AN extract (400-800 micro g/ml) induced Cox-2 and IL-6 mRNA expression and also COX-2 protein production by KB cells. IL-6 (5-100 ng/ml) suppressed GK growth by 20-33%, but enhanced oral fibroblast (OMF) and KB cell growth. PGE2 (0.05-5 micro g/ml) and anti-IL-6 antibody (ab) (50-1000 ng/ml) showed little effect on GK and KB cell growth. Incubation of GK and KB cells with aspirin, anti-IL-6 ab and anti-TNF-alpha ab showed little effect on arecoline- and AN-induced cytotoxicity, cell cycle arrest and apoptosis. Exposure to anti-TNF-alpha ab slightly affected arecoline- and AN-modulated PGE2 and IL-6 production by GK and KB cells. Arecoline- and AN-conditioned medium decreased phytohemagglutinin-mediated CD4+ and CD8+ T cell activation. These results indicate that BQ chewing contributes to the pathogenesis of cancer and OSF by impairing T cell activation and by induction of PGE2, TNF-alpha and IL-6 production, which affect oral mucosal inflammation and growth of OMF and oral epithelial cells.