Common urological problems in children: primary nocturnal enuresis.

Enuresis is a common complaint in children, with a prevalence of around 15% at age 6 years. Evidence suggests that enuresis could affect neuropsychiatric development. The condition may represent an entire spectrum of underlying urological conditions. It is important to understand the difference between monosymptomatic and non-monosymptomatic enuresis. Primary monosymptomatic enuresis can be managed efficaciously with care in different settings, like primary care, specialist nursing, or paediatric specialists, while non-monosymptomatic enuresis requires more complex evaluation and treatment. The diagnosis, investigation, and management of the two types of enuresis are discussed in this review.

Interleukin-23 is sufficient to induce rapid de novo gut tumorigenesis, independent of carcinogens, through activation of innate lymphoid cells.

Chronic inflammation has been associated with increased risk for developing gastrointestinal cancer. Interleukin-23 (IL-23) receptor signaling has been correlated with inflammatory bowel disease pathogenesis, as well as promotion of tumor growth. However, little is known about the relative potential for IL-23-directed causality in gut tumorigenesis. We report that IL-23 transgene expression was sufficient to induce rapid (3-4 weeks) de novo development of intestinal adenomas with 100% incidence. Initiation of tumorigenesis was independent of exogenous carcinogens, Helicobacter colonization, or pre-existing tumor-suppressor gene mutations. Tumorigenesis was mediated by Thy1(+)IL-23R(+) innate lymphoid cells (ILC3), in part, through IL-17 responses as tumor development was inhibited in RAG(-/-) × IL-17(-/-) double knockout mice. Remarkably, IL-23 initiation of tumorigenesis by resident ILCs consistently occurred before recruitment of conspicuous inflammatory infiltrates. Our results reveal an explicit role for IL-23-mediated initiation of gut tumorigenesis and implicate a key role for IL-23R(+) ILC3 in the absence of overt cellular infiltrate recruitment.

Thoracoscopic resection of congenital cystic lung lesions is associated with better post-operative outcomes.

INTRODUCTION: The incidence of congenital cystic lung lesions has been increasing in recent years due to better antenatal detection. With the introduction and maturation of thoracoscopy, the operative management for these lesions has seen advancement in the last decade. In this study, we aimed to compare the post-operative outcomes of patients who had thoracoscopic resection with those who underwent open resection. METHODS: A retrospective review of all patients who underwent surgery for congenital cystic lung lesions between January 1996 and June 2012 in a tertiary referral center was conducted. Patients' demographics, operative procedures and post-operative outcomes were analyzed. RESULTS: Sixty-seven patients were identified over the past 15 years. Thirty-nine patients had thoracoscopic resections and 28 had open resections. Thirteen patients in the thoracoscopic group required conversion. Both groups had similar demographics in terms of age, body weight and laterality of lesions. The mean operative time and blood loss in the two groups were comparable. Patients in the thoracoscopic group had significantly shorter duration of chest tube drainage (4.3 vs. 6.9 days, p = 0.004), shorter intensive care unit stay (2.5 vs. 5.9 days, p = 0.003) and shorter hospital stay (6.9 vs. 12.0 days, p < 0.001). Post-operative complication rate was similar between the two groups. Patients with body weight less than 5 kg showed a significantly higher conversion to open surgery as compared to those with body weight more than 5 kg (62.5 vs. 25.8 %, p = 0.049). CONCLUSION: Successful thoracoscopic resection for congenital cystic lung lesions results in better post-operative outcomes. However, this technique remains technically challenging in patients with body weight less than 5 kg.

Laparoscopic inguinal hernia repair in premature neonates: is it safe?

OBJECTIVE: With advances in clinical medicine, many premature babies nowadays can have excellent survival outcomes. As the incidence of inguinal hernias in this group is high and there is scarce data in the literature regarding the optimal timing for repair, this study aims to review our experience in laparoscopic repair in premature infants. METHODS: In our centre, premature neonates with inguinal hernia noted during hospitalization were offered laparoscopic repair when the body weights reached 2.5 kg unless there is contraindication for laparoscopy. A retrospective review was carried out for all premature neonates who underwent laparoscopic inguinal hernia repair from 2001 to 2011. The operative results, complications, incarceration risk and postoperative apnea risk were recorded. RESULT: A total of 79 premature neonates received laparoscopic inguinal hernia repair during this period. The mean gestational age at birth was 31.9 weeks (27-36 weeks) and the mean gestational age at operation was 46.5 weeks (33-92 weeks). One patient had incarceration and required emergency operation while waiting for the elective repair. The mean operative time was 44.9 min (25-93 min). One patient (1.3 %) had recurrence. No postoperative apnea was noted in any patient. CONCLUSION: Laparoscopic hernia repair is safe and feasible in premature neonates when they attain reasonable body size, as long as there is excellent anaesthesia support. Low risk of incarceration was noted in this study and it is worth waiting for the body weight to build up and hence facilitate laparoscopic repair.

Thoracoscopic repair of oesophageal atresia: experience of 33 patients from two tertiary referral centres.

BACKGROUND: With advances in minimally invasive surgery, thoracoscopic repair of oesophageal atresia has become popular in many centres worldwide and indeed has been described as the pinnacle of neonatal surgery. Here, we report our experience in two tertiary referral centres. METHODS: Thoracoscopic technique was introduced in 2007. Thus, a retrospective review of all patients diagnosed with oesophageal atresia was carried out. Patients who had thoracoscopic repair were included, and those who had open repair due to co-morbidities were excluded. Patient demographics, operative data, complications, and associated anomalies were noted. RESULTS: A total of thirty-three patients underwent thoracoscopic repair during the time period. Thirty-one were successfully repaired thoracoscopically. Two patients had conversions due to intra-operative instability. The mean body weight of the neonates was 2.58 kg. The mean operative time was 146 min. Three patients suffered from minor anastomotic leaks, which healed on conservative management. Seven patients had anastomotic strictures, which responded successfully to endoscopic dilatation. Two patients died in the post-operative period due to pneumonia. One patient had a recurrent fistula 3 months after the primary repair, and he subsequently underwent a successful second repair. CONCLUSIONS: In experienced hands, thoracoscopic repair of oesophageal atresia is at least as good as open surgery but with less surgical trauma. Standard of post-operative care contributes significantly to post-operative outcome. Thoracoscopic technique is now our preferred approach.

Serum small-dense LDL abnormalities in chronic renal disease patients.

Cardiovascular disease (CVD) is the principal cause of mortality in chronic kidney disease (CKD) patients. Dyslipoproteinaemia is a common metabolic derangement in CKD and a traditional risk factor for CVD. This study investigates serum lipoprotein, especially small-dense low-density lipoprotein (sd-LDL), abnormalities in CKD patients. A total of 131 CKD patients (age: 59 +/- 12 years, male = 64) diagnosed according to Kidney Disease: Improving Global Outcomes, 2004 (KDIGO) and 121 age- and gender-matched control subjects (age: 58 +/- 6 years, male = 62) were recruited from Hong Kong and Macau. Serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C) and direct LDL-C were assayed enzymatically. In addition, sd-LDL, together with very low density and intermediate-density lipoproteins (VLDL and IDL) were measured by US Food and Drug Administration (FDA)-approved polyacrylamide gradient gel electrophoresis. Compared to controls, CKD patients showed significantly decreased TC, LDL-C, normal-size LDL and HDL-C with increased TG, VLDL, IDL and sd-LDL (all P < 0.01). The increased sd-LDL and decreased normal-size LDL fractions resulted in a significantly elevated sd-LDL:LDL ratio in CKD (P < 0.005). In contrast to the low TC and LDL-C, sd-LDL and sd-LDL:LDL ratio were significantly elevated in CKD. Thus, sd-LDL will be used increasingly for CVD risk assessment in CKD and other diseases that show lipoprotein derangement.

Performing Kasai portoenterostomy beyond 60 days of life is not necessarily associated with a worse outcome.

The introduction of Kasai portoenterostomy has dramatically improved the management and survival of children with biliary atresia. The success rate of this operation worldwide varies with different centers. In this respect, many authors have studied the correlation of a successful outcome with various factors, such as the experience and workload of the surgical center, the use of postoperative steroids, the underlying biliary anatomy, as well as the age of patients at the time of the operation. Indeed, the age of 60 days has been used by clinicians as a critical time beyond which the rate of success of the Kasai operation markedly reduces. Despite this worldwide adoption, clear evidence supporting this critical operative time is still lacking. We undertook a review of our experience in the management of children with biliary atresia and focused specifically on the issue of the timing of operation. We showed that performing the Kasai operation beyond the age of 60 days was not associated with a worse outcome and that a high percentage of patients could still achieve good bile flow with normal bilirubin postoperatively. Thus, we believe that until the age of 100 days, the age of the patients does not play a significant role in determining the success of the Kasai operation.

The first report of a single-port laparoscopic nephrectomy in a child.

There has been an exponential rise in the use of minimally invasive procedures in surgery, with obvious benefits to patients. Recently, transumbilical single-port laparoscopic surgery has been championed as the next major technical advance. In this article, we report the first case where single-port laparoscopic surgery has been used to manage a paediatric problem in the region.

Activation of peripheral Th17 lymphocytes in patients with asthma.

A recently identified interleukin (IL)-17-producing T-helper (Th) lymphocyte subset, which comprises Th17 cells producing hallmark cytokines IL-17A, IL-17F and IL-22, is involved in chronic inflammatory diseases. Elevated gene and protein expressions of IL-17 are manifested in allergic asthma. We further characterized the activation of Th17 cells in asthmatic patients. Peripheral blood mononuclear cells (PBMC) were purified from 31 asthmatic patients and 20 sex- and age-matched control subjects. The number of IL-17A secreting cells in peripheral blood was enumerated by enzyme-linked immunosorbent spot assay. Cell surface expression of Th17-related chemokine receptor CCR6, and plasma level of IL-17A, IL-17F and IL-22, and ex vivo production of IL-17A and IL-22 were measured by flow cytometry and enzyme-linked immunosorbent assay, respectively. The number of peripheral Th17 lymphocytes, expression of CCR6 on Th cells, and ex vivo IL-23, anti-CD3 and anti-CD28 induced production of IL-22 by PBMC were significantly elevated in asthmatic patients compared with control subjects (all p < 0.01). This clinical study further confirmed increased number of peripheral Th17 lymphocytes and cell surface expression of CCR6 receptors on Th cells in asthmatic patients. Pro-inflammatory cytokine IL-23 can exacerbate disease severity by activating pathogenic Th17 lymphocytes to release downstream inflammatory cytokine IL-22 in asthma.

Thyroid hormone receptor mutants implicated in human hepatocellular carcinoma display an altered target gene repertoire.

Thyroid hormone receptors (TRs) are hormone-regulated transcription factors that control multiple aspects of normal physiology and development. Mutations in TRs have been identified at high frequency in certain cancers, including human hepatocellular carcinomas (HCCs). The majority of HCC-TR mutants bear lesions within their DNA recognition domains, and we have hypothesized that these lesions change the mutant receptors' target gene repertoire in a way crucial to their function as oncoproteins. Using stable cell transformants and expression array analysis, we determined that mutant TRs isolated from two different HCCs do, as hypothesized, display a target gene repertoire distinct from that of their normal TR progenitors. Only a subset of genes regulated by wild-type TRs was regulated by the corresponding HCC-TR mutants. More surprisingly, the HCC-TR mutants also gained the ability to regulate additional target genes not recognized by the wild-type receptors, and were not simply restricted to repression, but could also activate a subset of their target genes. We conclude that the TR mutants isolated from HCC have sustained multiple alterations from their normal progenitors that include not only changes in their transcriptional outputs, but also changes in the genes they target; both are likely to contribute to neoplasia.

Life-threatening Torsades de Pointes resulting from "natural" cancer treatment.

INTRODUCTION: Nonradioactive cesium chloride (CsCl) is used by some alternative medicine advocates as a treatment for cancer. The therapy was proven to be neither safe nor effective. Chronic use of CsCl has resulted in cases with severe cardiotoxicity. CASE REPORT: A 65-year-old lady presented to our hospital's accident and emergency department with recurrent syncope attacks. Electrocardiogram monitoring showed QT prolongation and transient Torsades de Pointes (TDP) ventricular tachycardia. She was taking anticancer naturopathic drugs for 6 weeks before admission. One of her naturopathic drugs was subsequently confirmed containing 89% CsCl by weight. Besides conventional treatment of QT prolongation and TDP, the patient was given a 4-week course of oral Prussian blue to enhance gastrointestinal elimination of cesium. The serum half-life of cesium was reduced from 61.7 to 29.4 days after the use of Prussian blue. QT prolongation was normalized in 27 days. DISCUSSION: To our knowledge, this is the first published case of nonradioactive cesium poisoning treated with Prussian blue. A transient rise in serum cesium level was observed during Prussian blue therapy. Possible explanations for this observation include poor drug compliance during outpatient treatment and redistribution of cesium from body stores. CONCLUSION: Nonradioactive CsCl poisoning can result in severe cardiotoxicity with QT prolongation and TDP ventricular tachycardia. The key points in the management of nonradioactive cesium poisoning include cessation of cesium exposure, vigorous electrolytes replacement, and oral Prussian blue therapy.

Asthma and atopy are associated with chromosome 17q21 markers in Chinese children.

BACKGROUND: Single-nucleotide polymorphism (SNP)-based genome-wide association study revealed that markers on chromosome 17q21 were linked to childhood asthma but not atopy in Caucasians, with the strongest signal being detected for the SNP rs7216389 in the ORMDL3 gene. Such association was unknown in Chinese. This study delineated the allele and genotype frequencies of 10 SNPs at chromosome 17q21, and investigated the relationship between these SNPs and asthma and plasma IgE in southern Chinese children. METHODS: Asthmatic children and non-allergic controls were recruited from pediatric clinics. Their plasma total and aeroallergen-specific IgE concentrations were measured by immunoassay. Ten SNPs on 17q21 region were genotyped by multiplex SNaPshot, and their genotype associations with asthma traits analyzed using multivariate regression. RESULTS: 315 patients and 192 controls were enrolled. The allele frequency for C allele of rs7216389 varied significantly from 0.232 in our controls, 0.389 in Han Chinese to 0.536 in Caucasians. Asthma diagnosis was associated with rs11650680 and five other SNPs including rs7216389 (P = 0.019-0.034), whereas atopy was associated only with rs11650680 (P = 0.0004). Linear regression revealed the covariates for plasma total IgE to be significant for rs11650680 (P = 0.008-0.0002). Haplotypic associations were found with atopy and increased plasma total IgE, with the respective odds ratios and 95% confidence intervals for TTTCCGTT haplotype to be 0.21 and 0.09-0.52 (P = 0.0002) and 0.41 and 0.18-0.90 (P = 0.025). CONCLUSION: Childhood asthma and atopy are associated with chromosome 17q21 in Chinese, but such association may involve genes other than ORMDL3 in this region.

Study of gene-gene interactions for endophenotypic quantitative traits in Chinese asthmatic children.

BACKGROUND: Asthma is a complex disease resulting from interactions between multiple genes and environmental factors. Study of gene-gene interactions could provide insight into the pathophysiology of asthma. METHODS: We investigated the interactions among 18 single-nucleotide polymorphisms in eight candidate genes for plasma total immunoglobulin E (IgE) concentration and peripheral blood (PB) eosinophil count in 298 Chinese asthmatic children and 175 controls. Generalized multifactor dimensionality reduction and generalized linear model were used to analyze gene-gene interactions for the quantitative traits. RESULTS: A significant interaction was found between R130Q in IL13 and I50V in IL4RA for plasma total IgE concentration, with a cross-validation (CV) consistency of nine of 10 and a prediction error of 41.1% (P = 0.013). Plasma total IgE concentration was significantly higher in the high-risk than the low-risk groups (P < 0.0001). For PB eosinophil count, significant interaction was found between C-431T in TARC and RsaI_in2 in FCERIB, with a CV consistency of nine of 10 and a prediction error of 40.2% (P = 0.009). PB eosinophil count was significantly higher in the high-risk group than the low-risk groups (P < 0.0001). Generalized linear model also revealed significant gene-gene interaction for the above two endophenotypes with P = 0.013 for plasma total IgE concentration and P = 0.029 for PB eosinophil count respectively. CONCLUSIONS: Our data suggest significant interactions between IL13 and IL4RA for plasma total IgE concentration, and this is the first report to show significant interaction between TARC and FCERIB for PB eosinophil count in Chinese asthmatic children.

Suppression and recovery of the hypothalamic function after high-dose corticosteroid treatment in preterm infants.

BACKGROUND: High-dose systemic dexamethasone is effective in facilitating extubation of ventilated infants with bronchopulmonary dysplasia. Although the suppression and recovery of pituitary-adrenal response had been assessed after corticosteroid treatment in very low birth weight infants, its effect on hypothalamic function has not been longitudinally monitored. AIMS: This study was designed to assess the longitudinal hypothalamic response before, during and 4 weeks after a 3-week dose-tapering course of systemic dexamethasone treatment. PATIENTS AND METHODS: Twenty very low birth weight infants had blood collected for corticotropin-releasing hormone, ACTH and cortisol measurements immediately before starting dexamethasone (week 0), after receiving the maximum dose of treatment (week 1), at the end of the 3-week course (week 3) and 4 weeks after stopping corticosteroids (week 7). RESULTS: All circulating hormone concentrations were significantly suppressed during the treatment period at week 1 and week 3 compared with pretreatment concentrations at week 0 (p < 0.001). The recovery of pituitary function started early soon after week 1, whereas that of hypothalamus and adrenal functions started after the end of the dexamethasone course. Plasma ACTH concentration at week 7 had returned to the pretreatment level, but plasma corticotropin-releasing hormone (p < 0.05) and serum cortisol (p < 0.001) concentrations remained significantly suppressed. Partial recovery of hypothalamic and adrenal function was observed at week 7 (62 vs. 36% of their pretreatment levels, respectively). CONCLUSION: Our findings suggest that the hypothalamic function is suppressed during systemic corticosteroid treatment but partial recovery occurs 4 weeks after stopping therapy. Even in preterm infants, the hypothalamic-pituitary-adrenal axis behaves in a similar manner as in adult subjects and the pituitary function recovers earlier than that of hypothalamus and adrenals.

Association between candidate genes and lung function growth in Chinese asthmatic children.

BACKGROUND: Asthma is caused by a complex interaction between multiple candidate genes and environmental factors. The Childhood Asthma Management Program reported lung function decline in a significant proportion of Caucasian asthmatic children, but such a relation has not been studied in other populations. Our group recently reported that interleukin-13 (IL13), interleukin-4 receptor-alpha and thymus and the activation-regulated chemokine interacted to influence asthma and raised plasma total IgE. However, there has not been any study that has addressed the genetic influences for longitudinal lung function growth. OBJECTIVE: We studied the longitudinal changes in spirometric variables in Chinese asthmatic children, and investigated the influence and interactions between eight different loci in six candidate genes as well as environmental factors affecting lung function growth in these children. METHODS: Spirometry was performed at baseline and study completion. Genotyping was performed by restriction fragment length polymorphism. Multi-factor dimensionality reduction (MDR) was used to detect any gene-gene or gene-environment interaction. RESULTS: We prospectively followed 131 Chinese children, aged 9.9 (3.0) years, for 4.5 (0.8) years. Their mean (standard deviation) baseline forced expiratory volume in 1 s (FEV1) was 98.6 (20.6)% of predicted, and FEV1 to forced vital capacity (FVC) ratio was 77.8 (11.3)%. FEV1 and FVC increased by 210 (115) and 248 (148) mL/year during this study, and these changes were significantly larger among males (P<0.0001). Univariate analysis revealed a significant association between annual FEV1 change and C1570T of signal transducer and activator of transcription 6 gene (STAT6; P=0.009). Linear regression confirmed this finding (P=0.041). Using MDR, we detected a significant 3-locus interaction between IL13 R130Q, ADRB2 R16G and STAT6 C1570T for determining change in FVC (P=0.045). CONCLUSION: Our data suggest that STAT6 may influence lung function growth in asthmatic children. We also found significant interactions among several atopy-related genetic polymorphisms for influencing FVC change.

Association of prostaglandin-endoperoxide synthase 2 gene polymorphisms with asthma and atopy in Chinese children.

BACKGROUND: Cyclooxygenase-2 (COX-2) plays essential roles in inflammation. Previous studies have suggested associations between prostaglandin-endoperoxide synthase 2 (PTGS2) polymorphisms and prostaglandins production in asthma. OBJECTIVE: We have investigated the effects of Chinese tagging single nucleotide polymorphisms (SNPs) of PTGS2 on asthma traits in 299 Chinese asthmatic children and 175 controls. METHODS: Plasma total and allergen-specific IgE were measured by enzyme immunoassay. PTGS2.8473T-->C in the 3'-untranslated region of exon 10 and three tag SNPs covering most of the variations in PTGS2 haplotypes in Chinese were genotyped by restriction fragment length polymorphism. RESULTS: Among the four SNPs, only PTGS2.8473 showed significant association with asthma (P = 0.034) and atopy (P = 0.005 when compared with non-atopic controls; P = 0.023 with all controls). Carriers of the C allele had a 1.5-fold (95% confidence interval: 1.01-2.30) risk of developing asthma than those homozygous for the T allele. Multivariate regression revealed significant correlations between PTGS2.8473 and forced expiratory volume in 1 s (FEV(1); P = 0.002) and peak expiratory flow rate (PEFR; P = 0.001) with age and gender adjusted. Patients with the C allele of PTGS2.8473 had significantly lower FEV(1) (median: 90.0%vs 98.0%; P = 0.0047) and PEFR (70.0%vs 73.5%; P = 0.0065) than those homozygous for the T allele. No significant association between plasma total and allergen-specific IgE and these SNPs or with their haplotypes was found. CONCLUSIONS: PTGS2.8473 polymorphism is associated with asthma, atopy and lung function but not plasma IgE in Chinese children. This may help to explore the pharmacogenetics of COX-2 inhibitors.

Troponin T, left ventricular mass, and function are excellent predictors of cardiovascular congestion in peritoneal dialysis.

Patients on maintenance peritoneal dialysis (PD) are frequently complicated with volume overload. In this study, we sought to evaluate troponin T testing alone or in combination with echocardiographic measures in predicting cardiovascular congestion in PD patients. This was a prospective study of 222 chronic PD patients with echocardiography and measurement of serum troponin T carried out at baseline. Patients were followed for 3 years or until death. The end point was first episode of cardiovascular congestion. Troponin T emerged as an independent predictor of cardiovascular congestion (hazard ratio, 2.98, 95% confidence intervals (CI), 1.19-7.42) in a multivariable Cox regression model, including also left ventricular mass index (LVMi) and ejection fraction (EF). Patients with troponin T>median (0.06 microg/l) and EFmedian but EF>50% had a 3.10-fold (95% CI, 1.71-5.63) and 1.88-fold (95% CI, 1.05-3.38) adjusted risk of cardiovascular congestion, respectively, than those with troponin T50%. Patients with troponin T>median and LVMi>or=median (96.23 g/m2.7) had a 2.68-fold (95% CI, 1.39-5.19) adjusted risk of cardiovascular congestion than those with troponin T

Thyroid hormone receptors mutated in liver cancer function as distorted antimorphs.

Aberrant thyroid hormone receptors (TRs) are found in over 70% of the human hepatocellular carcinomas (HCCs) analysed. To better understand the role(s) of these TR mutants in this neoplasia, we analysed a panel of HCC mutant receptors for their molecular properties. Virtually all HCC-associated TR mutants tested retained the ability to repress target genes in the absence of T3, yet were impaired in T3-driven gene activation and functioned as dominant-negative inhibitors of wild-type TR activity. Intriguingly, the HCC TRalpha1 mutants exerted dominant-negative interference at all T3 concentrations tested, whereas the HCC TRbeta1 mutants were dominant-negatives only at low and intermediate T3 concentrations, reverting to transcriptional activators at higher hormone levels. The relative affinity for the SMRT versus N-CoR corepressors was detectably altered for several of the HCC mutant TRs, suggesting changes in corepressor preference and recruitment compared to wild type. Several of the TRalpha HCC mutations also altered the DNA recognition properties of the encoded receptors, indicating that these HCC TR mutants may regulate a distinct set of target genes from those regulated by wild-type TRs. Finally, whereas wild-type TRs interfere with c-Jun/AP-1 function in a T3-dependent fashion and suppress anchorage-independent growth when ectopically expressed in HepG2 cells, at least certain of the HCC mutants did not exert these inhibitory properties. These alterations in transcriptional regulation and DNA recognition appear likely to contribute to oncogenesis by reprogramming the differentiation and proliferative properties of the hepatocytes in which the mutant TRs are expressed.

Asthma and atopy are associated with DEFB1 polymorphisms in Chinese children.

Human beta-defensin (HBD)-1 is constitutively expressed in the airway, and hBD-1 plays crucial roles in innate immunity against respiratory pathogens. Asthma was associated with DEFB1 polymorphisms in Caucasians. This study investigates whether three single nucleotide polymorphisms (SNPs) in 5'-untranslated region of DEFB1 are associated with asthma phenotypes in Chinese children. Subjects aged 5-18 years were recruited from general pediatric clinics. Plasma IgE concentrations were measured by immunoassays. DEFB1 SNPs were characterized by restriction fragment length polymorphism. In all, 305 asthmatics and 156 controls were recruited. For asthma diagnosis, atopy and plasma total IgE, higher percentages of subjects with these outcomes had the minor alleles -20A and -52G (P = 0.041-0.0002). For log-transformed total IgE, the covariate was positive and significant for G-20A under recessive model (P = 0.001) and for G-52A under both recessive and codominant models (P = 0.008 and 0.035). The recessive model covariate was also positive and significant (P = 0.020) for C-44G on peripheral blood eosinophil count. The GCA haplotype of DEFB1 was significantly associated with asthma (odds ratio (95% confidence interval): 1.64 (1.05-2.57); P = 0.029). These results suggest that DEFB1 is a candidate gene for asthma and atopy in children.

Chemokine response in children with SARS.

The chemokine response of eight children with serologically confirmed severe acute respiratory syndrome (SARS) was longitudinally monitored. All had raised plasma interferon gamma inducible protein (IP-10) concentrations, which suggested an active type 1 T-helper lymphocyte mediated immune response. High circulating IP-10 levels could facilitate viral clearance and might play a role in assisting the recovery of the patients.