The purpose of this study was to determine whether the hyperbolic relationship between power output and time to exhaustion (work -time and power -[1/time] models) could be estimated from a modified version of a three-minute all-out rowing test (3-min RT), and to investigate the test-retest reliability of the 3-min RT. Eighteen male rowers volunteered to participate in this study and underwent an incremental exercise test (IRT), three constant-work rate tests to establish the critical power (CP) and the curvature constant (W 0 ), and two 3-min RTs against a fixed resistance to estimate the end-test power (EP) and work-done-above-EP (WEP) on a rowing ergometer. Peak _ VO 2peak À Á and maximal _ VO 2 max À Á oxygen uptakes were calculated as the highest 30 s average achieved during the 3-min RT and IRT tests. The results showed that EP and WEP determinations, based on the 3-min RT, have moderate reproducibility (P = 0.002). EP (269 ± 39 W) was significantly correlated with CP (work -time, 272 ± 30 W; power -[1/time], 276 ± 32 W) (P = 0.000), with no significant differences observed between the EP and CP values (P = 0.474). However, WEP did not significantly correlate with W 0 (P = 0.254), and was significantly higher than the W 0 values. There was a significant correlation between the _ VO 2peak (60 ± 3 ml kg -1 min -1 ) and _ VO 2 max (61 ± 4 ml kg -1 min -1 ) (P = 0.003). These results indicate that the 3-min RT has moderate reliability, and is able to appropriately estimate the aerobic capacity in rowers, particularly for the CP and _ VO 2 max parameters.

Background and AimLynch syndrome, caused by germline mutations in mismatch repair genes, is a predisposing factor for colorectal cancer (CRC). This retrospective cohort study investigated the risk factors associated with the development of CRC in patients with MLH1 and MSH2 germline mutations.MethodsIn total, 301 MLH1 and MSH2 germline mutation carriers were identified from the Amsterdam criteria family registry provided by the Taiwan Hereditary Nonpolyposis Colorectal Cancer Consortium. A Cox proportional hazard model was used to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) to determine the association between the risk factors and CRC development. A robust sandwich covariance estimation model was used to evaluate family dependence.ResultsAmong the total cohort, subjects of the Hakka ethnicity exhibited an increased CRC risk (HR = 1.62, 95% CI = 1.09–2.34); however, those who performed regular physical activity exhibited a decreased CRC risk (HR = 0.62, 95% CI = 0.41–0.88). The CRC risk was enhanced in MLH1 germline mutation carriers, with corresponding HRs of 1.72 (95% CI = 1.16–2.55) and 0.54 (95% CI = 0.34–0.83) among subjects of the Hakka ethnicity and those who performed regular physical activity, respectively. In addition, the total cohort with a manual occupation had a 1.56 times higher CRC risk (95% CI = 1.07–2.27) than did that with a skilled occupation. Moreover, MSH2 germline mutation carriers with blood group type B exhibited an increased risk of CRC development (HR = 2.64, 95% CI = 1.06–6.58) compared with those with blood group type O.ConclusionThe present study revealed that Hakka ethnicity, manual occupation, and blood group type B were associated with an increased CRC risk, whereas regular physical activity was associated with a decreased CRC risk in MLH1 and MSH2 germline mutation carriers.

CIP2A is an oncoprotein that upregulates p-Akt and promotes cancer cell proliferation and survival. The proteasome inhibitor bortezomib has been shown to reduce CIP2A and lead to cell apoptosis. Here; we modified the functional group of bortezomib to generate a series of novel compounds and conducted a structure-activity relationship (SAR) study. The results showed that compound 1 was able to repress CIP2A expression and cell apoptosis in the same manner as bortezomib, but with less potency in inhibition of proteasome activity. This finding provides a new direction for the design of CIP2A inhibitors.

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In this paper, we aim to detect distributed denial of service (DDoS) attacks, and receive a notification of destination service, changing immediately, without the additional efforts of other modules. We designed a kernel-based mechanism to build a new Transmission Control Protocol/Internet Protocol (TCP/IP) connection smartly by the host while the users or clients not knowing the location of the next host. Moreover, we built a lightweight flooding attack detection mechanism in the user mode of an operating system. Given that reinstalling a modified operating system on each client is not realistic, we managed to replace the entry of the system call table with a customized sys_connect. An effective defense depends on fine detection and defensive procedures. In according with our experiments, this novel mechanism can detect flooding DDoS successfully, including SYN flood and ICMP flood. Furthermore, through cooperating with a specific low cost network architecture, the mechanism can help to defend DDoS attacks effectively.