[Genetic characterization of influenza A virus and assessment of vaccine efficacy in Yantai from 2014 to 2017].

In this study, the swabs were collected among patients with an influenza-like illness (ILI) admitted to 2 sentinel surveillance hospitals of Yantai from April 2014 to August 2017. All specimen were cultured and identified by hemagglutination inhibition assay. Complete sequences of Hemagglutinin (HA) of influenza A were amplified, sequenced and analyzed using molecular and phylogenetic methods. The potential vaccine efficacy were calculated using Pepitope model. The results showed that the antigenicity of A (H3N2) had changed greatly. 8 strains of influenza A (H1N1) pdm09 belonged to subclade 6B.1 and 14 strains clustered in 6B.2. 12 strains of influenza A (H3N2) fell into subgroup 3C.3a and 33 strains clustered in 3C.2a. Several residues at antigen sites and potential glycosylation sites had changed in influenza A strains. Vaccine efficacy of influenza A (H1N1) pdm09 in 2015/2016 and 2016/2017 seasons were 77.29% and 79.11% of that of a perfect match with vaccine strain, meanwhile vaccine efficacy of influenza A (H3N2) in 2014/2015, 2015/2016 and 2016/2017 were-5.18%, 16.97% and 42.05% separately. In conclusion, the influenza A virus circulated in Yantai from 2014 to 2017 presented continual genetic variation. The recommended vaccine strains still afforded protection against influenza A (H1N1) pdm09 strains and provided suboptimal protection against influenza A (H3N2) strains.

Nox1 promotes colon cancer cell metastasis via activation of the ADAM17 pathway.

OBJECTIVE: Reactive oxygen species (ROS) generated by endogenous metabolic enzymes are involved in a variety of pathology processes, including cancer. In particular, superoxide-generating NADPH oxidase 1 (Nox1), a member of Nox enzyme family, is highly expressed in the colon tissue and has been implicated in physiological and pathophysiological states of colon cancer. However, the underlying molecular mechanism of Nox1 in the regulation of colon cancer progression remains largely unknown. MATERIALS AND METHODS: In vitro scratch wound healing and invasion assays were used to compare the migration and invasion abilities of HT29 cells in which Nox1 protein levels were manipulated. Western blot assay was performed to detect the expression of key proteins of the EGFR-PI3K-AKT signaling pathway. Immunoprecipitation assay was performed to detect the interaction between Nox1 and ADAM17. RESULTS: Nox1 overexpression promoted colon cancer cell growth, migration, and invasion through the EGFR-PI3K-AKT signaling pathway. At the molecular level, Nox1 regulated the expression of tumor necrosis factor-α (TNF-α) converting enzyme (TACE)/a disintegrin and metalloprotease domain 17 (ADAM17). Furthermore, Nox1 interacted with and stabilized ADAM17 from ubiquitin-mediated degradation, leading to the activation of the ADAM17 signaling pathway. CONCLUSIONS: This study suggests that Nox1 promotes colorectal cancer metastasis by modulating the stability of ADAM17.

[Epidemiologic characteristics and risk factors for congenital hypothyroidism from 1989 to 2014 in Beijing].

OBJECTIVE: To investigate the epidemiologic characteristics and risk factors for congenital hypothyroidism (CH) in Beijing between the years 1989 and 2014. METHODS: Information on neonatal screening, and diagnoses and treatment of CH from 1989 to 2014 were obtained from the database of the Beijing Neonatal Screening Center. The screening parameter was thyroid-stimulating hormone (thyrotropin; TSH), which was measured by radioimmunoassay (RIA) from 1989 to 1995, enzyme-linked immunosorbent assay (ELISA) from 1996 to 2003, and time-resolved fluorescence immunoassay (DELFIA(®)) from 2004 to 2014. The cutoff value of each screening method was set as the international standard for the corresponding years (20 mIU/L from 1989 to 1995 and 10 mIU/L from 1996 to 2014). CH was diagnosed using "The Technical Specification of Diagnosis and Treatment of Phenylketonuria and Congenital Hypothyroidism" , published in 2010 by the Ministry of Health of the People's Republic of China. Data on live birth infants were obtained from Beijing obstetric quality reports. The incidence of CH using different screening methods was compared, and trends in annual incidence were analyzed. To exclude the influence of different screening methods, data from the years 2004 to 2014 were used to identify the risk factors for CH. RESULTS: Between 1989 and 2014, the incidence of CH in Beijing was 36.7 per 100 000 individuals, with permanent CH (PCH) and transient CH (TCH) having incidences of 16.4 per 100 000 and 15.9 per 100 000, respectively. The annual incidence of CH increased from 11.2 per 100 000 in 1989 to 51.0 per 100 000 in 2014 (χ(2)=119.02, P<0.001), with PCH increasing from 5.6 to 16.0 per 100 000 (χ(2)=34.38, P<0.001) and TCH increasing from 5.6 to 13.0 per 100 000 (χ(2)=26.93, P<0.001). Among the PCH cases, 70.44% (255/362) were thyroid dysgenesis or ectopic glands, while the other 29.56% (107/362) were dyshormonogenesis. Between 2004 and 2014, the incidence of CH in females (51.7/100 000) was higher than in males (37.0/100 000), and it was higher in post-term (334.5/100 000) and preterm births (77.8/100 000) than that in term births (41.4/100 000). It was also higher in the low birth weight (87.7/100 000) than the normal (42.4/100 000) and high birth weight (42.6/100 000) populations. CONCLUSIONS: Between 1989 and 2014, there was a tendency towards an increase in the overall incidence of CH, and the incidence of both PCH and TCH in Beijing. Female sex, preterm birth, older gestational age, low birth weight, and preterm birth were risk factors affecting the incidence of CH in Beijing.