Methodological quality assessment based on the NOS.^a

a<p>Assessed with the 9-star Newcastle-Ottawa Scale(NOS).</p>b<p>Adequate definition of cases(0,1star).</p>c<p>Consecutive or obviously representative series of cases (0,1).</p>d<p>Selection of controls: Community controls (0,1).</p>e<p>Definition of controls: No history of disease (endpoint) (0,1).</p>f<p>Study controls for the most important factor or any additional factor(0,1,2).</p>g<p>Secure record (eg surgical records) (0,1).</p>h<p>Same method of ascertainment for cases and controls(0,1).</p>i<p>Same non-response rate for both groups(0,1).</p>j<p>Total: minimum equals 1; maximum equals 9 stars.</p

Characteristics of prospective studies on blood α- and γ-tocopherol levels and risk of prostate cancer.

<p>Abbreviations: BMI: body mass index, T:tertile, Q:quartile/quintile, SD: standard deviation. * Derived from the slogan of a campaign, “Give us a CLUE to cancer.”</p

Dose–response relationship between blood α-tocopherol levels and relative risk of prostate cancer.

<p>Blood α-tocopherol levels were modeled with a linear trend in a random-effects meta-regression model. The solid line represents point estimates of association between blood α-tocopherol levels and prostate cancer risk; dashed lines are 95% confidence intervals (CIs).</p

Blood α-Tocopherol, γ-Tocopherol Levels and Risk of Prostate Cancer: A Meta-Analysis of Prospective Studies

<div><p>Background</p><p>Epidemiological studies that have examined the association of blood α-tocopherol and γ-tocopherol (the principal bioactive form of vitamin E) levels with the risk of prostate cancer have yielded inconsistent results. In addition, a quantitative assessment of published studies is not available.</p><p>Methods and Findings</p><p>In this meta-analysis, relevant studies were sought by a search of the PubMed and Embase databases for articles published up to October 2013, with no restrictions. Bibliographies from retrieved articles also were scoured to find further eligible studies. Prospective studies that reported adjusted relative risk (RR) estimates with 95% confidence intervals (CIs) for the association between blood tocopherol levels and the risk of prostate cancer were included. Nine nested case–control studies involving approximately 370,000 participants from several countries were eligible. The pooled RRs of prostate cancer for the highest versus lowest category of blood α-tocopherol levels were 0.79 (95% CI: 0.68–0.91), and those for γ-tocopherol levels were 0.89 (95% CI: 0.71–1.12), respectively. Significant heterogeneity was present among the studies in terms of blood γ-tocopherol levels (<i>p</i> = 0.008) but not in terms of blood α-tocopherol levels (<i>p</i> = 0.33). The risk of prostate cancer decreased by 21% for every 25-mg/L increase in blood α-tocopherol levels (RR: 0.79; 95% CI: 0.69–0.91).</p><p>Conclusions</p><p>Blood α-tocopherol levels, but not γ-tocopherol levels, were inversely associated with the risk of prostate cancer in this meta-analysis.</p></div

Adjusted relative risks of prostate cancer for the highest vs. lowest categories of blood α- and γ-tocopherol levels.

<p>Adjusted relative risks of prostate cancer for the highest vs. lowest categories of blood α- and γ-tocopherol levels.</p

Effect of Carotene and Lycopene on the Risk of Prostate Cancer: A Systematic Review and Dose-Response Meta-Analysis of Observational Studies

<div><p>Background</p><p>Many epidemiologic studies have investigated the association between carotenoids intake and risk of Prostate cancer (PCa). However, results have been inconclusive.</p><p>Methods</p><p>We conducted a systematic review and dose-response meta-analysis of dietary intake or blood concentrations of carotenoids in relation to PCa risk. We summarized the data from 34 eligible studies (10 cohort, 11 nested case-control and 13 case-control studies) and estimated summary Risk Ratios (RRs) and 95% confidence intervals (CIs) using random-effects models.</p><p>Results</p><p>Neither dietary β-carotene intake nor its blood levels was associated with reduced PCa risk. Dietary α-carotene intake and lycopene consumption (both dietary intake and its blood levels) were all associated with reduced risk of PCa (RR for dietary α-carotene intake: 0.87, 95%CI: 0.76–0.99; RR for dietary lycopene intake: 0.86, 95%CI: 0.75–0.98; RR for blood lycopene levels: 0.81, 95%CI: 0.69–0.96). However, neither blood α-carotene levels nor blood lycopene levels could reduce the risk of advanced PCa. Dose-response analysis indicated that risk of PCa was reduced by 2% per 0.2mg/day (95%CI: 0.96–0.99) increment of dietary α-carotene intake or 3% per 1mg/day (95%CI: 0.94–0.99) increment of dietary lycopene intake.</p><p>Conclusions</p><p>α-carotene and lycopene, but not β-carotene, were inversely associated with the risk of PCa. However, both α-carotene and lycopene could not lower the risk of advanced PCa.</p></div

Pooled risks according to dietary carotenoids intake and its blood levels.

<p>Dietary intake of α-carotene, β-carotene, lycopene and PCa risk(left), blood levels of α-carotene, β-carotene, lycopene and PCa risk(right).</p

Characteristics of included studies.

<p>Abbreviations: NCCS, nested case-control study; CCS, case-control study; SD, standard deviation; T, tertile; Q, quartile/quintile; BMI, body mass index; NSAIDs, non-steroidal anti-inflammatory drugs; FHPC, family history of prostate cancer; NR, not reported; NA, not accessible.</p><p>^aDerived from the slogan of a campaign, “Give us a CLUE to cancer.”</p><p>^bIndicated interquartile range(IQR).</p><p>Characteristics of included studies.</p

Dose-response relation plots between carotenoids consumption and risk of PCa.

<p>(A) Dietary lycopene intake(mg/day) and risk of PCa; (B) Blood lycopene levels (ug/dl) and risk of PCa; (C) Dietary α-carotene intake(mg/day) and risk of PCa. These relationships were estimated by using random-effects metaregression. Dotted lines represent the 95% CIs for the fitted trend.</p

Fluorescence Detection of H5N1 Virus Gene Sequences Based on Optical Tweezers with Two-Photon Excitation Using a Single Near Infrared Nanosecond Pulse Laser

We present an analytical platform by combining near-infrared optical tweezers with two-photon excitation for fluorescence detection of H5N1 virus gene sequences. A heterogeneous enrichment strategy, which involved polystyrene (PS) microsphere and quantum dots (QDs), was adopted. The final hybrid-conjugate microspheres were prepared by a facile one-step hybridization procedure by using PS microspheres capturing target DNA and QDs tagging, respectively. Quantitative detection was achieved by the optical tweezers setup with a low-cost 1064 nm nanosecond pulse laser for both optical trapping and two-photon excitation for the same hybrid-conjugate microsphere. The detection limits for both neuraminidase (NA) gene sequences and hemagglutinin (HA) gene sequences are 16–19 pM with good selectivity for one-base mismatch, which is approximately 1 order of magnitude lower than the most existing fluorescence-based analysis method. Besides, because of the fact that only signal from the trapped particle is detected upon two-photon excitation, this approach showed extremely low background in fluorescence detection and was successfully applied to directly detect target DNA in human whole serum without any separation steps and the corresponding results are very close to that in buffer solution, indicating the strong anti-interference ability of this method. Therefore, it can be expected to be an emerging alternative for straightforward detecting target species in complex samples with a simple procedure and high-throughput