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Empowerment can be an effective strategy for changing an individual's health behaviours. However, how to empower whole families to manage their children's asthma is a challenge that requires innovative nursing intervention based on family-centred care.To evaluate the effectiveness of a family empowerment program on family function and pulmonary function of children with asthma compared to those receiving traditional self-management only.A randomized control trial.Sixty-five families were recruited from one asthma clinic in a medical centre in Taiwan. After random assignment, 34 families in the experimental group received the family empowerment program consisting of four counselling dialogues with the child and its family. We empowered the family caregiver's ability to manage their child's asthma problems through finding the problems in the family, discovery and discussion about the way to solve problems, and enabling the family's cooperation and asthma management. The other 31 families received the traditional care in asthma clinics. The Parental Stress Index and Family Environment Scale of family caregivers, and pulmonary function, and asthma signs of children with asthma were collected at pre-test, 3-month post-test, and one-year follow-up. We utilized the linear mixed model in SPSS (18.0) to analyze the effects between groups, across time, and the interaction between group and time.The family empowerment program decreased parental stress (F=13.993, p.0001) and increased family function (cohesion, expression, conflict solving, and independence) (F=19.848, p.0001). Children in the experimental group had better pulmonary expiratory flow (PEF) (F=26.483, p.0001) and forced expiratory volume in first second (FEV1) (F=7.381, p=.001) than children in the comparison group; however, no significant change in forced expiratory volume in first second (FEV1)/forced vital capacity (FVC) was found between the two groups. Sleep problems did not show significant changes but cough, wheezing, and dyspnoea were significantly reduced by family caregiver's observations.We empowered families by listening, dialogues, reflection, and taking action based on Freire's empowerment theory. Nurses could initiate the families' life changes and assist children to solve the problems by themselves, which could yield positive health outcomes.

Hsueh K-C, Lin Y-J, Lin HC, Lin C-Y. Serum leptin and adiponectin levels correlate with severity of allergic rhinitis. Pediatr Allergy Immunol 2010: 21: e155–e159. © 2009 John Wiley & Sons A/S The aim of this study was to evaluate the roles of leptin and adiponectin, which are adipokines produced by adipose tissue, in childhood allergic rhinitis (AR), and their association with severity of AR, parameters of atopy and pro-/anti-inflammatory cytokines. Serum levels of leptin, adiponectin, mite allergen-specific and total immunoglobulin E, eosinophil cationic protein (ECP), and pro- and anti-inflammatory cytokines were analysed in 97 non-asthmatic children presenting with persistent AR and in 64 controls. The nasal symptom scores and body mass index were evaluated at the time of blood collection. We found that patients had significantly higher serum levels of leptin and significantly lower serum levels of adiponectin than controls. Furthermore, multivariate logistic regression analysis revealed that leptin and adiponectin were significant predictive factors for AR. Serum levels of leptin and adiponectin were significantly correlated with nasal symptom scores. There was no correlation between levels of pro- and anti-inflammatory cytokines and level of leptin or adiponectin. A significant negative correlation was observed between serum levels of adiponectin and ECP levels in AR children. Our findings suggest that serum leptin and adiponectin levels may serve as predictors of disease severity in childhood AR and both of them appear to be attractive candidates for unmasking or modulating AR.

The butyrophilin-like 2 (BTNL2) gene is a member of the B7 receptor family that probably functions as a T cell costimulatory molecule. Because altered T cell functions are implicated in dysregulation of the immune response seen in Kawasaki disease (KD), it is reasonable to speculate that BTNL2 gene is involved in the pathophysiology of KD. The purpose of this study was to investigate whether polymorphisms of the BTNL2 gene are associated with KD and the development of coronary artery lesions (CALs) in Taiwanese children. Nine-three patients with KD and 669 ethnically matched healthy controls were genotyped for BTNL2 gene rs1555115 C/G and rs2395158 A/G polymorphisms. The frequency of GG genotype of rs 1555115 was significantly higher in KD patients compared with controls (2.2% vs 0.2%, P = 0.012). The odds ratio for developing KD in individuals with rs 1555115 GG genotype was 14.7 (95% confidence interval, 2.04-105.5, P = 0.003) compared with individuals with rs 1555115 CG and CC genotypes. No significant difference was observed in the genotype and allelic frequencies of rs 2395158 polymorphism between KD patients and controls. However, the frequency of the G allele of rs 2395158 was significantly higher in KD patients with CALs than in those without CALs (P = 0.001). No significant difference was observed in the genotype and allelic frequencies of rs 1555115 polymorphism between KD patients with and without CALs. In conclusion, our results suggest that BTNL2 gene polymorphisms might be genetic markers of KD susceptibility and risk of coronary artery complication in Taiwanese children.

Tumour necrosis factor-α (TNF-α), an important proinflammatory cytokine, exerts a variety of physiological and pathogenic effects that lead to tissue destruction. Studies on the association of TNF-α genetic polymorphisms with systemic lupus erythematosus (SLE) have yielded inconclusive results. We investigated the association of TNF-α genetic polymorphisms (−1031T/C, −863C/A, −857T/C, −308A/G and +489A/G) with SLE in Taiwanese patients and controls. Our results indicate that 1) the frequency of the A-allele at −863 position was significantly higher in SLE patients (odds ratio = 1.46; 95% CI = 1.02–2.08); 2) the frequency of the A-allele at +489 position was significantly higher in SLE patients (odds ratio = 1.79; 95% CI = 1.21–2.65); 3) the AA or GA genotype frequencies at +489 position were significantly increased in SLE patients (AA genotype: odds ratio = 11.20; 95% CI = 1.36–92.55; GA genotype: odds ratio = 1.63; 95% CI = 1.03–2.58); 4) no significant association of TNF-α haplotypic distributions was observed, except for the haplotypes TCCGA, CACGA and CCCGG; and 5) the genotype frequency of the polymorphisms at −1031 was significantly different in patients with antinuclear antibodies ( P = 0.022). The allele and genotype frequencies of the polymorphisms at −863 were not significantly different. The genotype frequency of the polymorphisms at −857 was significantly different in patients with haematological disorder ( P = 0.025). The frequency of A allele of the polymorphisms at −308 was significantly increased in patients with malar rash ( P = 0.033), discoid rash ( P = 0.023), photosensitivity ( P = 0.037), oral ulcers ( P = 0.002) and serositis ( P = 0.029). The genotype frequency of the polymorphisms at +489 was significantly different in patients with discoid rash and photosensitivity (data not shown; discoid rash, P = 0.031; photosensitivity, P = 0.044). These results suggest that TNF-α genetic polymorphisms contribute to SLE susceptibility in the Taiwanese population.

Background Resistin, a recently discovered adipokine, has been shown to have proinflammatory properties in humans. The purpose of this study was to evaluate serum resistin levels in children with allergic rhinitis (AR) and to investigate its association with clinical disease severity, parameters of atopy and pro-/anti-inflammatory cytokines. Methods A case-controlled study was performed on 50 pediatric patients with persistent AR and 30 healthy controls with similar age, sex, and body mass index. Serum levels of resistin, parameters of atopy, and cytokines were analyzed. The nasal symptom scores were evaluated and patients were classified into mild (n = 20) and moderate-severe (n = 30) persistent AR. Results Serum levels of resistin were significantly increased in children with AR compared with controls (p < 0.001). Serum levels of resistin went hand in hand with disease severity as they were significantly higher in moderate-severe than mild persistent AR. In addition, they correlated positively with nasal symptom scores (r = 0.74; p < 0.001). A significant positive correlation was observed between serum levels of resistin and IL-6 (r = 0.358; p = 0.011). Conclusion Patients with persistent AR were found to have higher serum levels of resistin, and resistin levels increased with the progress of disease severity. Resistin may represent a novel link between inflammation and AR.

Elevated serum levels of interleukin-10 (IL-10) have been reported in patients with Kawasaki disease (KD). IL-10 reduces the inflammatory actions of macrophages and T cells and it may play a significant role in the regulation of inflammatory vascular damage associated with systemic vasculitis. The aim of this study was to examine whether -592 IL-10 promoter polymorphism is a susceptibility or severity marker of KD in Chinese patients in Taiwan. The study included 105 KD patients and 100 normal controls. Genotype and allelic frequencies for the IL-10 gene polymorphism in both groups were compared. There were no significant between-group differences in the genotype distribution of IL-10 A-592C gene polymorphism (P=0.08). However, the frequency of the -592*A allele was significantly increased in the patients with KD compared with controls (71.9% vs. 61.0%, P=0.019). The odds ratio for developing KD in individuals with IL-10-592*A allele was 1.64 (95% confidence interval, 1.06-2.52) compared to individuals with the IL-10-592*C allele. No significant difference was observed in the genotype and allelic frequencies for the IL-10 A-592C polymorphism between patients with and without coronary artery lesions. The IL-10-592*A allele may be involved in the development of KD in Taiwanese children.

The ingestion of foreign bodies such as coins, fish bones, plastic toy parts, batteries, and needles is common in children. Although the majority of ingested foreign bodies pass through the gastrointestinal tract unaided, some children require either nonsurgical or surgical intervention. The medical records of children who presented to the pediatric emergency department of a single tertiary referral center between December 2001 and May 2006 were reviewed. A total of 87 patients underwent an endoscopic procedure because of suspected foreign body ingestion and foreign bodies were identified by endoscopy in 74 patients (85.1%). The mean age of these 74 patients was 3.4 years (range, 6 months to 13 years). The most common site of foreign body lodgement was the esophagus (n = 38, 51.4%); other sites included the stomach (n = 33, 44.6%) and duodenum (n = 3, 4.0%). The types of foreign bodies included coins (n = 42, 56.8%), button batteries (n = 16, 21.6%), sharp objects (n = 9, 12.2%), chicken bones (n = 2, 2.7%) and others (n = 5, 6.7%). Only two foreign bodies (button batteries) in the duodenum could not be removed successfully by endoscopy. Instead, they were moved into the intestine and then eliminated spontaneously the following day. There were no major complications caused by foreign body ingestion or endoscopic procedures. The outcome of all patients was uneventful without morbidity or mortality. In our experience, endoscopic removal of foreign bodies under general anesthesia is an effective and safe method in children; the method also prevents erosion and perforation of the gastrointestinal tract.

Kawasaki disease (KD) is an acute, inflammatory and self-limited vasculitis affecting infants and young children. Coronary artery aneurysm (CAA) formation is the major complication of KD and the leading cause of acquired cardiovascular disease among children. To identify susceptible loci that might predispose patients with KD to CAA formation, a genome-wide association screen was performed in a Taiwanese KD cohort. Patients with both KD and CAA had longer fever duration and delayed intravenous immunoglobulin treatment time. After adjusting for these factors, 100 susceptibility loci were identified. Four genes were identified from a single cluster of 35 using the Ingenuity Pathway Analysis (IPA) Knowledge Base. Silencing KCNQ5, PLCB1, PLCB4 and PLCL1 inhibited the effect of lipopolysaccharide-induced endothelial cell inflammation with varying degrees of proinflammatory cytokine expression. PLCB1 showed the most significant inhibition. Endothelial cell inflammation was also inhibited by using a phospholipase C (PLC) inhibitor. The single nucleotide polymorphism rs6140791 was identified between PLCB4 and PLCB1. Plasma PLC levels were higher in patients with KD and CC+CG rs6140791genotypes and these genotypes were more prevalent in patients with KD who also had CAA. Our results suggest that polymorphism of the PLCB4/B1 genes might be involved in the CAA pathogenesis of KD.

Flavonoids are associated with multiple biological and pharmacological activities, including anti-enterovirus activity. An internal ribosomal entry site (IRES) required for viral protein translation is a potential drug target for enterovirus 71 (EV71). Regulation translation initiation requires the interaction of IRES specific trans-acting host factors with viral IRES element. By evaluation of 12 flavonoids against EV71 infection, we found that (a) 7,8-dihydroxyflavone, kaempferol, quercetin, hesperetin and hesperidin exhibited more than 80% of cell survival and inhibition of EV71 infection; however, no anti-oxidative effects were noted from these flavonoids; (b) among them, only 7,8-dihydroxyflavone, kaempferol and hesperetin showed 40% of viral IRES activity; (c) kaempferol interfered with EV71 virus replication and pseudotyped virus production; and (d) FUBP1, FUBP3, HNRPD, HNRH1 and HNRPF proteins are associated with EV71 5'-UTR as shown using RNA affinity pull-down assay coupled with LC-MS/MS analysis. We firstly found that kaempferol may change the composition of these IRES associated trans-acting factors, and affect IRES function and EV71 virus replication. These studies help not only to understand the IRES function but also the mechanism by which drug induced cellular proteins are acting against EV71 infection.

Background The national hepatitis B (HB) vaccination program in Taiwan that began in 1984 has resulted in a significant reduction in the carrier rate among children. However, a significant proportion of Taiwanese neonatal HB immunization recipients have exhibited low anti-HBs titers that fall to non-protective or undetectable levels. Methods We recruited 1677 entering freshman and graduate student participants at a Taiwanese university health center, grouped them into three age groups representing three stages of Taiwan's HB vaccination program, then conducted hepatitis B surface antigen (HBsAg) and antibodies to HBsAg (anti-HBs) serological surveillances for each individual. Univariate and multivariate regression analyses of clinical characteristics and Interleukin-10 (IL-10) genetic variations were also conducted. Results A trend toward a decreasing HBsAg carrier rate was observed over the starting dates of the vaccination program (11.7%, 1.6% and 1.7% for age groups 1, 2 and 3, respectively), but we also observed an increasing rate of non-protective anti-HBs titers (15%, 26% and 50.3% for cohorts 1–3, respectively). The percentage of students with non-protective anti-HBs titers increased from 23.1% for students born in 1984, to 25.2% for those born in 1985, to 39.4% for birth-year 1986 students, to 45.7% for birth-year 1987 students, and to 56.5% for birth-year 1988 students. The risk for low anti-HBs titers increased concurrently with increases in systolic blood pressure (BP), the IL-10 ATA/ACC haplotype, and the IL-10 ATA present haplotype. Risk for low anti-HBs titers decreased with concurrent decreases in glucose ante cibum (AC, before meals) and the IL-10 ACC/ACC haplotype. Conclusions These results suggest that the genetic determinants may also contribute to variations in anti-HBs titers in immune responses to HB vaccination.

Aims and objectives. To evaluate the effectiveness of a nurse-led patient-centred asthma education programme on home environmental control behaviours of parents of children with moderate or severe asthma. Background. Reducing allergic triggers is important self-management behaviour for preventing asthma attacks and patientcentred asthma education has been shown to effectively manage chronic disease. Design. A preliminary quasi-experimental, non-equivalent control group design was used. Method. Dyads (n = 75) of parents and their children with moderate or severe asthma (ages 6–14 years) were purposively recruited from the asthma clinics of two hospitals in central Taiwan. The experimental group of 38 children/parents from one hospital received patient-centred asthma education. The comparison group of 37 children/parents from the other hospital received routine individual education. At pretest and at the end of the three-month patient-centred asthma education programme, we measured parents’ control of home environmental triggers, children’s asthma signs/symptoms and children’s pulmonary function. Data were analysed by the general linear model for repeat measures. Results. The level of improvement in dust and cleaning methods was significantly greater among parents in the experimental group than among those in the comparison group (p < 0AE05). Children with moderate or severe asthma in the experimental group had fewer signs/symptoms of asthma and better lung function than children in the comparison group. Conclusions. Our patient-centred asthma education programme improved parents’ home environmental control and children’s asthma sign/symptoms and lung function. Relevance to clinical practice. Nurses can play primary roles as patient educators in asthma clinics. Well-trained patient educators can continuously monitor self-management behaviours to improve patients’ compliance with home environmental control, thus leading to better physical outcomes in children with asthma than routine individual asthma education alone.

Systemic lupus erythematosus (SLE), a multisystemic autoimmune disease, is characterized by the production of a range of autoantibodies against nuclear constituents and other self-antigens. The studies in DNA repair deficiencies in SLE patients have been recently investigated.Few studies have been conducted on DNA repair gene polymorphisms and their role in autoimmune diseases. Our study purpose was to examine and compare NBS1 genotype distributions in a group of Taiwanese SLE patients and controls in Taiwan.Participants were Taiwanese SLE patients and healthy controls. We studied associations among NBS1 polymorphisms--rs1061302, rs709816, and rs1805794--considering clinical features for the entire group and stratified subgroups. No statistically significant differences between the patients and controls were noted. However, we observed significant decreases in Ht1-GGG, Ht2-AAC, and Ht3-AGC in the SLE patients (Ht1-GGG, OR = 0.26, 95% CI: 0.16-0.41; Ht2-AAC, OR = 0.30, 95% CI: 0.17-0.53; Ht3-AGC, OR = 0.35, 95% CI: 0.19-0.71) and significant increases in Ht4-AAG, Ht5-AGG, and Ht8-GGC among the SLE patients. Combined, these results suggest an association between NBS1 genetic polymorphisms and Taiwanese SLE patients.

Background Emotional stress triggers and exacerbates asthma in children. Reducing anxiety in adults by relaxation-breathing techniques has been shown in clinical trials to produce good asthma outcomes. However, more evidence is needed on using this intervention with asthmatic children. Objective To evaluate the effectiveness of combined self-management and relaxation-breathing training for children with moderate-to-severe asthma compared to self-management-only training. Design Two-group experimental design. Setting and participants Pediatric outpatient clinic of a medical center in central Taiwan. Participants were 48 children, ages 6–14 years, with moderate-to-severe asthma and their parents. Methods Participants were randomly assigned to an experimental or comparison group and matched by gender, age, and asthma severity. Both groups participated in an asthma self-management program. Children in the experimental group were also given 30 min of training in a relaxation-breathing technique and a CD for home practice. Data on anxiety levels, self-perceived health status, asthma signs/symptoms, peak expiratory flow rate, and medication use were collected at baseline and at the end of the 12-week intervention. Effects of group, time, and group–time interaction were analyzed using the Mixed Model in SPSS (12.0). Results Anxiety (especially state anxiety) was significantly lower for children in the experimental group than in the comparison group. Differences in the other four physiological variables were also noted between pre- and post-intervention, but these changes did not differ significantly between groups. Conclusions A combination of self-management and relaxation-breathing training can reduce anxiety, thus improving asthmatic children's health. These results can serve as an evidence base for psychological nursing practice with asthmatic children.

Proinflammatory cytokines such as interferon-gamma (IFN-gamma) play an important role in the pathogenesis of Kawasaki disease (KD). Interleukin 18 (IL-18) plays a pivotal role in the T helper 1 (Th1)-type response, principally owing to its ability to induce IFN-gamma production. We assessed potential associations between functional IL-18 gene promoter polymorphisms and susceptibility to KD, in addition to clinical features of KD in individuals from Taiwan.One hundred forty-six patients with KD and 136 ethnically matched controls from the same geographic area were genotyped for IL-18 -656T/G, -607A/C, and -137C/G promoter polymorphisms.No significant differences in allele and genotype frequencies were found between KD patients and controls for any of the IL-18 polymorphisms investigated. When we compared the overall distribution of haplotype frequencies between KD patients and controls, a significant difference was observed (p0.0001). In addition, the frequency of the GCG haplotype was significantly higher (p = 0.00001, pc = 0.00004; OR 20.8, 95% CI 3.05-142.3), whereas the frequency of the TAG haplotype was significantly lower in KD patients compared with controls (p = 0.0001, pc = 0.0004; OR 0.35, 95% CI 0.19-0.61). No significant associations were found for comparisons of KD patients to those with and without coronary artery lesions.Our results suggest a potential implication of IL-18 promoter polymorphisms in susceptibility to KD in Taiwan.

The International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire was distributed through 14 schools and was completed by 11,874 students out of which are parents of 4,167 children aged between 10 and 12 years old and 7,677 older children aged between 13 and 15 years in central Taiwan. The overall cumulative and 12-month prevalence of wheezing, rhinitis, and eczema were 7.4%, 43.0%, and 7.2%, respectively. It was shown that boys had significantly higher prevalence of wheezing and rhinitis (p0.001 and p = 0.001) when compared to girls in central Taiwan. The study also found that prevalence rates among younger children with symptoms of wheezing, rhinitis, and recurrent itchy rash in the past 12-month (8.2%, 44.4%, and 8.8%) were higher than that among older children (6.9%, 42.2%, and 6.3%, respectively). In conclusion, boys had significantly higher prevalence of wheezing and rhinitis than girls while younger children tend to have higher prevalence of the disorders than those that are older in age.

Transient hypogammaglobulinemia of infancy (THI) is characterized by a prolongation and accentuation of the physiologic hypogammaglobulinemia normally occurring during the first 3 to 6 months of life and recovers spontaneously between 18 and 36 months of age. Infants with THI may remain asymptomatic or develop recurrent sinopulmonary infections, but severe or life-threatening infections are rare. We report a case of THI in a previously healthy 1-year-old girl with Staphylococcus aureus sepsis who subsequently developed deep neck infection confirmed by magnetic resonance imaging. Intravenous oxacillin was administered for 21 days and she recovered completely. Immunologic studies were normal except for decreased immunoglobulin G levels. Under the impression of hypogammaglobulinemia with severe infection she received regular intravenous immunoglobulins (IVIG) replacement therapy every 4 weeks. One year later, the immunoglobulin concentrations had returned to the normal range even though IVIG had been discontinued for 4 months. This case report highlights the possibility of severe infection in THI, a disease which usually has a benign clinical course. As the diagnosis of THI can only be made with certainty in retrospect, long-term follow-up of clinical and immune system status is necessary.

Ophthalmoplegia, ataxia, and areflexia were first described in 1956 by Miller Fisher and later were referred to as symptoms of Miller Fisher syndrome (MFS). This syndrome shares certain features with the Guillain-Barré syndrome (GBS), including areflexia, cerebrospinal fluid findings and often a postinfectious presentation. It was believed to be a variant of GBS, but Miller Fisher syndrome has several key clinical features which differ from GBS. The anatomic location and pathogenesis of MFS continue to be a matter of debate. Our report focuses on a 6-year-old female patient who developed MFS following a respiratory tract infection with a serologically proven Mycoplasma pneumoniae infection. Although several neurological complications after Mycoplasma pneumoniae infection have been reported, subsequent MFS development has rarely been reported previously.