Epidemiological Correlation between Fecal Adenovirus Subgroups and Pediatric Intussusception in Korea.

We investigated the adenoviral etiology and seasonal epidemic trends in intussusception and each adenoviral subgroup. Also we confirmed whether we can use the adenovirus data of Acute Infectious Agents Laboratory Surveillance Report (AIALSR) as an epidemic predictor of intussusception. Patients with intussusception (n = 126), < 5 years old, were enrolled and matched by age and sex with controls suffering acute gastroenteritis without intussusception (n = 106), all recruited at 8 centers. All fecal specimens were assayed for adenovirus, including subgroups A, B, C, E, and F, with reverse transcriptase-polymerase chain reaction (RT-PCR). Adenovirus was detected in 53 cases and 13 controls (P < 0.001). Nonenteric adenoviruses (NEAds) were detected in 51 cases and four controls (P < 0.001). We used Spearman's correlation analysis to analyze the incidence of intussusception and adenoviral epidemic trends, and compared them with fecal and respiratory adenoviral epidemic trends in the AIALSR. The trend of intussusception correlated with total NEAds (r = 0.635; P = 0.011), as did the fecal AIALSR adenovirus trends (r = 0.572; P = 0.026). Among the NEAd subgroups, subgroup C was dominant (P < 0.001), but subgroups B (P = 0.007) and E (P = 0.013) were also significant to intussusception. However, only subgroup C showed a significant epidemic correlation (r = 0.776; P = 0.001) with intussusception. Not respiratory but fecal AIALSR adenovirus trends correlated with the incidence of NEAds and intussusception. We suggest the possibility of using fecal AIALSR adenovirus data as an approximate epidemic predictor of intussusception.

Cholangiographic characteristics of common bile duct dilatation in children.

AIM: To investigate whether children with congenital common bile duct dilatation (CBDD) differ from children with obstructive CBDD in cholangiographic characteristics. METHODS: In this retrospective cohort study, the baseline data and the results of imaging analyses were reviewed among children who had endoscopic retrograde cholangiopancreatography (ERCP) due to CBDD. ERCP was performed on all pediatric patients by experienced pediatric endoscopists. The maximal transverse diameter of the common bile duct (CBD) was measured on ERCP. To assess whether age-adjusted CBDD could be used for differential diagnosis, a CBDD severity index (SI) was calculated by dividing the measured CBD diameter by the age-corrected maximal diameter of a normal CBD. RESULTS: A retrospective medical chart review revealed that 85 consecutive children under 16 years of age with hepatobiliary disease and CBDD were referred to Seoul Asan Medical Center. Fifty-five (64.7%) children had congenital CBDD and 30 (35.3%) had obstructive CBDD. The two groups did not differ significantly in terms of clinical characteristics except for sex. The congenital and obstructive CBDD groups did not differ significantly in terms of mean CBD diameter (19.3 ± 9.6 mm vs 12.2 ± 4.1 mm, P > 0.05). However, congenital CBDD cases had a significantly higher mean SI than obstructive CBDD cases (3.62 ± 1.64 vs 1.98 ± 0.71, P = 0.01). In multivariate analysis, an SI value ≥ 2.32 and comorbidity with anomalous union of pancreaticobiliary duct (APBDU) in ERCP independently predicted congenital CBDD. CONCLUSION: Measuring the CBD may aid the differential diagnosis of both CBDD and APBDU in children.

Pak regulates calpain-dependent degradation of E3b1.

E3b1, a binding partner of Eps8, plays a critical role in receptor tyrosine kinase (RTK)-mediated Rac activation by facilitating the interaction of Eps8 with Sos-1 and the consequent activation of the Rac-specific guanine nucleotide exchange factor activity of Sos-1. Here we present evidence that E3b1 levels are regulated by the Ca(2+)-activated protease calpain, and also by Pak, a downstream target of Rac signaling. Serum starvation of Rat2 or COS7 cells resulted in rapid loss of E3b1 that was reversed by calpain inhibitors. Loss was also prevented by expressing the constitutively active Pak1 mutant, Pak1(H83,86L). Activation of endogenous Pak by platelet-derived growth factor or the constitutively active Rac1 mutant, Rac1(G12V), also inhibited degradation. In contrast, inhibition of endogenous Pak activity by expressing the Pak auto-inhibitory domain caused degradation of over-expressed E3b1 even in the presence of serum. Taken together, these findings indicate that E3b1 is down-regulated by calpain activation and stabilized by Pak activation. They also suggest that RTK-mediated Rac activation can be modulated by changes in the level of E3b1 in response to signals that affect the activity of calpain or Pak.