Histidine-rich Glycoprotein Could Be an Early Predictor of Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Cerebral vasospasm (CVS) is a major contributor to the high morbidity and mortality of aneurysmal subarachnoid hemorrhage (aSAH) patients. We measured histidine-rich glycoprotein (HRG), a new biomarker of aSAH, in cerebrospinal fluid (CSF) to investigate whether HRG might be an early predictor of CVS. A total of seven controls and 14 aSAH patients (8 males, 6 females aged 53.4±15.4 years) were enrolled, and serial CSF and serum samples were taken. We allocated these samples to three phases (T1-T3) and measured HRG, interleukin (IL)-6, fibrinopeptide A (FpA), and 8-hydroxy-2’-deoxyguanosine (8OHdG) in the CSF, and the HRG in serum. We also examined the release of HRG in rat blood incubated in artificial CSF. In contrast to the other biomarkers examined, the change in the CSF HRG concentration was significantly different between the nonspasm and spasm groups (p<0.01). The rat blood/CSF model revealed a time course similar to that of the human CSF samples in the non-spasm group. HRG thus appears to have the potential to become an early predictor of CVS. In addition, the interaction of HRG with IL-6, FpA, and 8OHdG may form the pathology of CVS

AN APPROACH FOR THE OPTIMUM HYDRODYNAMIC DESIGN OF HYDROKINETIC TURBINE BLADES

This work aims to develop a simple and efficient mathematical model applied to optimization of horizontal-axis hydrokinetic turbine blades considering the cavitation effect. The approach uses the pressure minimum coefficient as a criterion for the cavitation limit on the flow around the hydrokinetic blades. The methodology corrects the chord and twist angle at each blade section by a modification on the local thrust coefficient in order to takes into account the cavitation on the rotor shape. The optimization is based on the Blade Element Theory (BET), which is a well known method applied to design and performance analysis of wind and hydrokinetic turbines, which usually present good agreement with experimental data. The results are compared with data obtained from hydrokinetic turbines designed by the classical Glauert's optimization. The present method yields good behavior, and can be used as an alternative tool in efficient hydrokinetic turbine designs

Long-term cultivation of colorectal carcinoma cells with anti-cancer drugs induces drug resistance and telomere elongation: an in vitro study

BACKGROUND: The role of telomerase activation in the expression and/or maintenance of drug resistance is not clearly understood. Therefore, we investigated the relationships, among the telomerase activity, telomere length and the expression of multidrug resistance genes in colorectal cancer cell lines cultivated with anti-cancer drugs. METHODS: LoVo and DLD-1 cells were continuously grown in the presence of both CDDP and 5-FU for up to 100 days. Cell proliferation, telomerase activity, telomere length and the expression of multidrug resistance genes were serially monitored as the PDL increased. RESULTS: The expression of multidrug resistance genes tended to increase as the PDL increased. However, an abnormal aneuploid clone was not detected as far as the cells were monitored by a DNA histogram analysis. Tumor cells showing resistance to anti-cancer drugs revealed a higher cell proliferation rate. The telomere length gradually increased with a progressive PDL. The telomerase activity reached a maximum level at 15 PDL in LoVo cells and at 27 PDL in DLD-1 cells. An increase in the mRNA expression of the telomerase components, especially in hTERT and in hTR, was observed at the same PDLs. CONCLUSIONS: These results suggest that a high telomerase activity and an elongation of telomeres both appear to help maintain and/or increase drug resistance in colorectal cancer cells. Cancer cells with long telomeres and a high proliferative activity may thus be able to better survive exposure to anti-cancer drugs. This is presumably due to an increased chromosome stability and a strong expression of both mdr-1 and MRP genes

Observation of B^0 \to D^{*-} \tau^+ \nu_{\tau} decay at Belle

We report an observation of the decay $B^0\to D^{*-} \tau^+ \nu_{\tau}$ in a data sample containing $535\times10^6$ $B\bar{B}$ pairs collected with the Belle detector at the KEKB asymmetric-energy $e^+e^-$ collider. We find a signal with a significance of 5.2 standard deviations and measure the branching fraction $\mathcal{B}(B^0\to D^{*-} \tau ^+ \nu_{\tau})=(2.02 ^{+0.40}_{-0.37} (stat) \pm 0.37 (syst))$. This is the first observation of an exclusive $B$ decay with a $b \to c \tau \nu_{\tau}$ transition.Comment: 6 pages, 3 figures, submitted to Phys. Rev. Let

Search for B -> h(*) nu nubar Decays at Belle

We present a search for the rare decays B -> h(*) nu nubar, where h(*) stands for a light meson. A data sample of 535 million BBbar pairs collected with the Belle detector at the KEKB e+e- collider is used. Signal candidates are required to have an accompanying B meson fully reconstructed in a hadronic mode and signal-side particles consistent with a single h(*) meson. No significant signal is observed and we set upper limits on the branching fractions at 90% confidence level. The limits on B0 -> K*0 nu nubar and B+ -> K+ nu nubar decays are more stringent than the previous constraints, while the first searches for B0 -> K0 nu nubar, pi0 nu nubar, rho0 nu nubar, phi nu nubar and B+ -> K*+ nu nubar, rho+ nu nubar are reported.Comment: 6 pages, 2 figures, submit to PR

Improved measurement of time-dependent CP violation in B0 -> J/Psi pi0 decays

We report improved measurements of time-dependent CP violation parameters for $B^0(\bar{B}^0) \to J/\psi \pi^0$ decay. This analysis is based on 535 million $B\bar{B}$ pairs accumulated at the $\Upsilon(4S)$ resonance with the Belle detector at the KEKB asymmetric-energy e^+e^- collider. From the distribution of proper time intervals between the two B decays, we obtain the following CP violation parameters $\mathcal{S}_{J/\psi \pi^0} = -0.65\pm0.21 (\rm{stat})\pm0.05 (\rm{syst})$ and $\mathcal{A}_{J/\psi \pi^0} = +0.08\pm0.16 (\rm{stat})\pm0.05 (\rm{syst})$, which are consistent with Standard Model expectations.Comment: Resubmitted to PRD(RC), including 4 figures, 6pages Revision has been made according to communication with PRD referee