Sentinel surveillance for influenza among severe acute respiratory infection and acute febrile illness inpatients at three hospitals in Ghana.

BACKGROUND: Influenza epidemiology in Africa is generally not well understood. Using syndrome definitions to screen patients for laboratory confirmation of infection is an established means to effectively conduct influenza surveillance. METHODS: To compare influenza-related epidemiologic data, from October 2010 through March 2013, we enrolled hospitalized severe acute respiratory infection (SARI; fever with respiratory symptoms) and acute febrile illness (AFI; fever without respiratory or other localizing symptoms) patients from three referral hospitals in Ghana. Demographic and epidemiologic data were obtained from enrolled patients after which nasopharyngeal and oropharyngeal swabs were collected, and processed by molecular methods for the presence of influenza viruses. RESULTS: Of 730 SARI patients, 59 (8%) were influenza positive; of 543 AFI patients, 34 (6%) were positive for influenza. Both SARI and AFI surveillance yielded influenza A(H3N2) (3% versus 1%), A(H1N1)pdm09 (2% versus 1%), and influenza B (3% versus 4%) in similar proportions. Data from both syndromes show year-round influenza transmission but with increased caseloads associated with the rainy seasons. CONCLUSIONS: As an appreciable percentage of influenza cases (37%) presented without defined respiratory symptoms, and thus met the AFI but not the SARI definition, it is important to consider broader screening criteria (i.e., AFI) to identify all laboratory-confirmed influenza. The identified influenza transmission seasonality has important implications for the timing of related public health interventions.

Down-regulation of ANXA7 decreases metastatic potential of human hepatocellular carcinoma cells in vitro.

We report for the first time the influence of ANXA7 gene on human hepatocellular carcinoma cells (HCC). We down-regulated ANXA7 in human HCC cell line (HepG2) using siRNA method. By Western Blot analysis, we confirmed about 70% down-regulation of the gene in the shRNA-ANXA7 transfected cells (shRNA-ANXA7-HepG2) compared to the non-specific sequence shRNA transfected cells (control-shRNA-HepG2) and the un-manipulated-HepG2 cells. We used CCK-8 cell proliferation kit and observed about 65% reduction in the shRNA-ANXA7-HepG2 cells where the two controls exhibited comparable cell proliferation rates. Also, by using PI staining followed by flow cytometry, we noticed a cell cycle arrest at G0/G1 with more than one fold reduction of shRNA-ANXA7-HepG2 cell population in the S-phase of the cell cycle. Also of particular note was a significant aneuploidy in the controls compared to zero aneuploidy in the ANXA7 down-regulated cells. Migration of the cells was detected using Boyden's transwell chamber and scratch wound healing assay which showed 50% and 30% respective reductions in shRNA-ANXA7-HepG2 cells migration. Furthermore, the control-shRNA-HepG2 cells and the un-manipulated-HepG2 cells invaded through the ECM-coated transwell plates two times more than the shRNA-ANXA7-HepG2 cells. We have found ANXA7 to be functioning like a tumour promoter in HepG2 human hepatocellular carcinoma cells and could have a potential as a therapeutic window into the management of liver cancer.