EBV infection induces p53 expression without causing mutations to TP53 (39). EBV-transformed cells are sensitive to p53-mediated apoptosis, and overexpression of p53 induces apoptosis (39). EBV infection of primary cells activates a DNA damage response (DDR) signaling pathway and inhibits cellular proliferation (40). At the same time, EBV has multiple means to counteract deleterious p53 effects. Most notably, LMP1 blocks p53-mediated apoptosis (13, 41), and EBNA3C downregulates the expression of p53 and regulates the DDR responses initiated by primary infection (40, 42, 43).

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The decision to screen for prostate cancer can be very confusing, given the various, conflicting media reports. 

LMP1 inhibits IRF5-mediated apoptosis.IRF5 is predominantly considered a tumor suppressor that potentiates apoptosis in a p53-independent manner (65), whereas LMP1 is a well-known viral oncogene that blocks apoptosis. Therefore, we suspected that LMP1 may repress apoptosis mediated by IRF5. The two isogeneic cell lines (293EBVwt and 293EBVΔLMP1) were used to examine if LMP1 affects IRF5-mediated apoptosis. Cells were transfected with IRF5 expression plasmid, and apoptosis was examined by the monitoring of the cleavage products of PARP (59). The cleavage of PARP was greatly enhanced in the 293EBVΔLMP1 line, suggesting that IRF5 was able to potentiate apoptosis in EBV-infected cells (Fig. 6A). IRF5 stimulated the expression of LMP1 in those cells, as expected (Fig. 6B). Therefore, endogenous LMP1 was capable of blocking IRF5-mediated apoptosis.

But it needs to be recognize that benefits and cost savings are estimated. The authors acknowledged that literature estimates for clinical benefits may not be applicable for the general population and the actual cost savings are uncertain because commercial payment rates are unknown.

|| Jerry Hirsch: Certainly the Arab conquest of Palestine in the seventh century had all the qualities you now criticize the Jews for. … ||

In an accompanying editorial, Andrew Vickers, PhD, Memorial Sloan Kettering Cancer Center, New York City, comments that this cost-analysis study moves the debate over PSA screening away from whether or not to use the test toward the question, "How can we get physicians to follow best practice?"

It is the quality of England’s kicking game which really makes them tick, and without it their attacking play seldom scales great heights.

The authors are grateful to Universiti Kebangsaan Malaysia Medical Centre (FF–200–2012), Ministry of Higher Education Malaysia (UKM OUP-TKP–20–97/2010) for funding this project. Special thanks to Prof. Dr. Srijit Das, Assoc. Prof Dr. Azarisman Shah Mohd. Shah and Prof.Dr. Pakeer Oothuman for editing the manuscript, and the technical staffs of Physiology and Anatomy Department of UKM for their endless support.

Thuny, F. et al. Post-Conditioning Reduces Infarct Size and Edema in Patients With ST-Segment Elevation Myocardial Infarction. J Am Coll Cardiol. 59, 2175–2181 (2012).

The effect of VB on the TXNIP/NF-кB pathway (A) and MAPK/NF-кB pathway (B). The expressions of related proteins from the TXNIP/NF-кB pathway and MAPK/NF-кB pathway were studied by Western blot analysis in VB-treated (400 mg/kg) rats. The quantification was performed based on the data of three separated experiments. All values given are the mean ± SD. #p < 0.05, ##p < 0.01, and ###p < 0.001 vs. control group (n = 3).

Wells, T. N. Natural products as starting points for future anti-malarial therapies: going back to our roots? Malar J 10 Suppl 1, S3 (2011).