Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Complement Factor I (CFI) and the CD46 complement regulator (CD46) play an important role in the complement activation pathways, which is known to affect the development of uveitis. The present study was performed to investigate the association of the CFI and CD46 genes with acute anterior uveitis (AAU).', 'A total of 600 subjects (300 patients with AAU and 300 healthy controls) were recruited for this case-control study. Six CFI single nucleotide polymorphisms (SNP) (rs7356506, rs10029485, rs11726949, rs12512308, rs7438961, rs998538) and four CD46 SNPs (rs12138764, rs2466571, rs2796278, rs7545126) were genotyped using Sequenom MassARRAY technology. Allele and genotype frequencies were compared between patients and controls using the χ(2) test. Analyses were stratified for gender, human leukocyte antigen (HLA)-B27, and ankylosing spondylitis status.', 'Rs7356506 in the CFI gene was found to be protective against AAU. There was a significant increase in the frequency of the A allele (p=0.003, pc=0.03, OR=0.684, CI 0.534 to 0.876) and AA homozygosity (p=0.004, pc=0.04, OR=0.624, CI 0.452 to 0.862) in AAU patients as compared to controls. Stratified analysis, according to gender and HLA-B27 status for AAU, also revealed the association with CFI-rs7356506. None of the tested SNPs of CD46 were associated with AAU.
Is cFI-rs7356506 a genetic protective factor for acute anterior uveitis in Chinese patients?

Cardiovascular device-centered infections are a major cause of hospital morbidity, mortality, and expense. Caused by opportunistic bacteria, this phenomenon is thought to arise because of a defect in neutrophil bacterial killing. We have shown that neutrophils that adhere to polystyrene remain viable, whereas neutrophils that adhere to the vascular biomaterials expanded polytetrafluoroethylene (ePTFE) and Dacron undergo a rapid nonapoptotic death. This study was designed to test the hypothesis that surface topography is a determinant of the nonapoptotic death response of neutrophils to biomaterials.', 'We took advantage of the ease with which a polystyrene surface can be manipulated to examine the effect of surface topography on neutrophil viability. Neutrophils were exposed to smooth or roughened polystyrene surfaces both in vivo and in vitro. Changes in cell membrane permeability and production of reactive oxygen species by individual cells were monitored with fluorescent dyes.', 'Host cells and isolated human neutrophils died rapidly after adhesion to roughened polystyrene. Neutrophils adherent to roughened surfaces produced more reactive oxygen intermediates than those adherent to smooth surfaces and were first to die. The cell death response precipitated by expanded polytetrafluoroethylene, Dacron, or the roughened surfaces was significantly reduced with treatment of the neutrophils with catalase, diphenylene iodonium, or the src kinase inhibitor PP2 before adhesion.
Is neutrophil survival on biomaterials determined by surface topography?

Ovarian cancer is the most lethal gynecologic malignancy, and there is an unmet clinical need to develop new therapies. Although showing promising anticancer activity, Niclosamide may not be used as a monotherapy. We seek to investigate whether inhibiting IGF signaling potentiates Niclosamide's anticancer efficacy in human ovarian cancer cells.", 'Cell proliferation and migration are assessed. Cell cycle progression and apoptosis are analyzed by flow cytometry. Inhibition of IGF signaling is accomplished by adenovirus-mediated expression of siRNAs targeting IGF-1R. Cancer-associated pathways are assessed using pathway-specific reporters. Subcutaneous xenograft model is used to determine anticancer activity.', "We find that Niclosamide is highly effective on inhibiting cell proliferation, cell migration, and cell cycle progression, and inducing apoptosis in human ovarian cancer cells, possibly by targeting multiple signaling pathways involved in ELK1/SRF, AP-1, MYC/MAX and NFkB. Silencing IGF-1R exert a similar but weaker effect than that of Niclosamide's. However, silencing IGF-1R significantly sensitizes ovarian cancer cells to Niclosamide-induced anti-proliferative and anticancer activities both in vitro and in vivo.

Does a Blockade of IGF Signaling sensitize Human Ovarian Cancer Cells to the Anthelmintic Niclosamide-Induced Anti-Proliferative and Anticancer Activities?