McMaster University

About: McMaster University is a education organization based out in Hamilton, Ontario, Canada. It is known for research contribution in the topics: Population & Health care. The organization has 41361 authors who have published 101269 publications receiving 4251422 citations.

Optimal search strategies for retrieving scientifically strong studies of diagnosis from Medline: analytical survey

Abstract: Objective To develop and test optimal Medline search strategies for retrieving sound clinical studies on prevention or treatment of health disorders. Design Analytical survey. Data sources 161 clinical journals indexed in Medline for the year 2000. Main outcome measures Sensitivity, specificity, precision, and accuracy of 4862 unique terms in 18 404 combinations. Results Only 1587 (24.2%) of 6568 articles on treatment met criteria for testing clinical interventions. Combinations of search terms reached peak sensitivities of 99.3% (95% confidence interval 98.7% to 99.8%) at a specificity of 70.4% (69.8% to 70.9%). Compared with best single terms, best multiple terms increased sensitivity for sound studies by 4.1% (absolute increase), but with substantial loss of specificity (absolute difference 23.7%) when sensitivity was maximised. When terms were combined to maximise specificity, 97.4% (97.3% to 97.6%) was achieved, about the same as that achieved by the best single term (97.6%, 97.4% to 97.7%). The strategies newly reported in this paper outperformed other validated search strategies except for two strategies that had slightly higher specificity (98.1% and 97.6% v 97.4%) but lower sensitivity (42.0% and 92.8% v 93.1%). Conclusion New empirical search strategies have been validated to optimise retrieval from Medline of articles reporting high quality clinical studies on prevention or treatment of health disorders.

Consensus guidelines for the definition, detection and interpretation of immunogenic cell death

Abstract: Cells succumbing to stress via regulated cell death (RCD) can initiate an adaptive immune response associated with immunological memory, provided they display sufficient antigenicity and adjuvanticity. Moreover, multiple intracellular and microenvironmental features determine the propensity of RCD to drive adaptive immunity. Here, we provide an updated operational definition of immunogenic cell death (ICD), discuss the key factors that dictate the ability of dying cells to drive an adaptive immune response, summarize experimental assays that are currently available for the assessment of ICD in vitro and in vivo, and formulate guidelines for their interpretation.

A herpes simplex virus mutant in which glycoprotein D sequences are replaced by beta-galactosidase sequences binds to but is unable to penetrate into cells.

Abstract: Herpes simplex virus (HSV) glycoprotein gD is a major component of the virion envelope and is thought to play an important role in the initial stages of viral infection and stimulates the production of high titers of neutralizing antibodies. We assumed that gD plays an essential role in virus replication, and so to complement viruses with mutations in the gD gene we constructed a cell line, denoted VD60, which is capable of expressing high levels of gD after infection with HSV. A recombinant virus, designated F-gD beta, in which sequences encoding gD and a nonessential glycoprotein, gI, were replaced by Escherichia coli beta-galactosidase sequences, was selected on the basis that it produced blue plaques on VD60 cell monolayers under agarose overlays containing 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside (X-Gal). F-gD beta was able to replicate normally on complementing VD60 cells. However, F-gD beta was unable to form plaques on noncomplementing Vero cells. Virions lacking gD were produced in normal amounts by Vero cells infected with F-gD beta, and the virus particles were distributed throughout the cytoplasm and on the cell surface, suggesting that gD is not essential for HSV envelopment and egress. Virions lacking gD were able to bind to cells, but were unable to initiate synthesis of viral early polypeptides. Plaque production of F-gD beta particles lacking gD was enhanced by polyethylene glycol treatment, suggesting that gD is essential for penetration of HSV into cells. Other HSV glycoproteins have been implicated in the entry of virus into cells, and thus this process appears to involve multiple interactions at the cell surface.