Fragmentation function of g→QQˉ(3S1[8])g\to Q\bar{Q}(^3S_1^{[8]}) in soft gluon factorization and threshold resummation

We study the fragmentation function of the gluon to color-octet $^3S_1$ heavy quark-antiquark pair using the soft gluon factorization (SGF) approach, which expresses the fragmentation function in a form of perturbative short-distance hard part convoluted with one-dimensional color-octet $^3S_1$ soft gluon distribution (SGD). The short distance hard part is calculated to next-to-leading order in $\alpha_s$ and a renormalization group equation for the SGD is derived. By solving the renormalization group equation, threshold logarithms are resummed to all orders in perturbation theory. The comparison with gluon fragmentation function calculated in NRQCD factorization approach indicates that the SGF formula resums a series of velocity corrections in NRQCD which are important for phenomenological study.Comment: 38 pages, 8 figure

Quasi-two-body decays Bc→D∗h→DπhB_c\to D^*h\to D\pi h in the perturbative QCD

In this work, we investigate the quasi-two-body decays $B_c\to D^*h\to D\pi h$ with $h = (K^0,\pi^0,\eta,\eta^{\prime})$ using the perturbative QCD(PQCD) approach. The description of final state interactions between the $D\pi$ pair is achieved through the two-meson distribution amplitudes(DAs), which are normalized to the time-like form factor. The PQCD predictions on the branching ratios of the quasi-two-body decays $B_c\to D^*h\to D\pi h$ show an obvious hierarchy: $Br(B_{c}^+ \to D^{*+} K^{0}\to D^0\pi^+K^{0})=({5.22}_{-0.74}^{+0.86})\times{10}^{-6}, Br(B_{c}^+ \to D^{*+} \pi^{0}\to D^0\pi^+\pi^{0})=(0.93\pm0.26)\times{10}^{-7}, Br(B_{c}^+ \to D^{*+} \eta\to D^0\pi^+\eta) =({2.83}_{-0.52}^{+0.59})\times{10}^{-8}$ and $Br(B_{c}^+ \to D^{*+} \eta^\prime\to D^0\pi^+\eta^\prime)=({1.89}_{-0.36}^{+0.40})\times{10}^{-8}$. From the invariant mass $m_{D\pi}$-dependence of the decay spectrum for each channel, one can find that the branching fraction is concentrated in a narrow region around the $D^{*}$ pole mass. So one can obtain the branching ratios for the corresponding two-body decays $B_c\to D^{*+}h$ under the narrow width approximation. We find that the branching ratios of the decays $B_c\to D^{*+}h$ are consistent well with the previous PQCD calculations within errors. These predictions will be tested by the future experiments.Comment: 12 pages, 3 figures, accepted for publication in Chin. Phys.

Phosphocreatine Preconditioning Attenuates Apoptosis in Ischemia-Reperfusion Injury of Rat Brain

Phosphocreatine (PCr) is an endogenous compound containing high-energy phosphate bonds. It has been confirmed that PCr is effective in preventing and treating cardiac and renal ischemia-reperfusion injury. In this study, rat cerebral ischemia-reperfusion injury models were constructed. Apoptotic cells in the cortex region were measured by TUNEL method. Malondialdehyde (MDA) content was detected by chromatometry, and calmodulin (CaM) activity was detected by ELISA. Compared with sham-operated group (sham group), TUNEL-positive cells, MDA, and level of CaM activity increased in ischemia-reperfusion group (I/R group) and PCr preconditioning group (PCr group); compared with I/R group, TUNEL-positive cells, MDA content, and level of CaM activity decreased in PCr group. This study indicated that PCr can decrease the morphological damage and the neuron apoptosis of the ischemia-reperfusion injury brain through attenuating abnormalities of calcium balance and production of oxygen free radicals

High reward enhances perceptual learning.

Studies of perceptual learning have revealed a great deal of plasticity in adult humans. In this study, we systematically investigated the effects and mechanisms of several forms (trial-by-trial, block, and session rewards) and levels (no, low, high, subliminal) of monetary reward on the rate, magnitude, and generalizability of perceptual learning. We found that high monetary reward can greatly promote the rate and boost the magnitude of learning and enhance performance in untrained spatial frequencies and eye without changing interocular, interlocation, and interdirection transfer indices. High reward per se made unique contributions to the enhanced learning through improved internal noise reduction. Furthermore, the effects of high reward on perceptual learning occurred in a range of perceptual tasks. The results may have major implications for the understanding of the nature of the learning rule in perceptual learning and for the use of reward to enhance perceptual learning in practical applications

Gemcitabine enhances cell invasion via activating HAb18G/CD147-EGFR-pSTAT3 signaling

Pancreatic cancer, one of the most lethal cancers, has very poor 5-year survival partly due to gemcitabine resistance. Recently, it was reported that chemotherapeutic agents may act as stressors to induce adaptive responses and to promote chemoresistance in cancer cells. During long-term drug treatment, the minority of cancer cells survive and acquire an epithelial-mesenchymal transition phenotype with increased chemo-resistance and metastasis. However, the short-term response of most cancer cells remains unclear. This study aimed to investigate the short-term response of pancreatic cancer cells to gemcitabine stress and to explore the corresponding mechanism. Our results showed that gemcitabine treatment for 24 hours enhanced pancreatic cancer cell invasion. In gemcitabine-treated cells, HAb18G/CD147 was up-regulated; and HAb18G/CD147 down-regulation or inhibition attenuated gemcitabine-enhanced invasion. Mechanistically, HAb18G/CD147 promoted gemcitabine-enhanced invasion by activating the EGFR (epidermal growth factor receptor)-STAT3 (signal transducer and activator of transcription 3) signaling pathway. Inhibition of EGFR-STAT3 signaling counteracted gemcitabine-enhanced invasion, and which relied on HAb18G/CD147 levels. In pancreatic cancer tissues, EGFR was highly expressed and positively correlated with HAb18G/CD147. These data indicate that pancreatic cancer cells enhance cell invasion via activating HAb18G/CD147-EGFR-pSTAT3 signaling. Our findings suggest that inhibiting HAb18G/CD147 is a potential strategy for overcoming drug stress-associated resistance in pancreatic cancer

Effect of supercritical CO2 on the copolymerization behavior of cyclohexene oxide/CO2 and copolymer properties with DMC/salen-Co(III) catalyst system

The copolymerization of cyclohexene oxide (CHO) and carbon dioxide (CO2) was carried out under supercritical CO2 (scCO2) conditions to afford poly (cyclohexene carbonate)(PCHC) in high yield. The scCO2 provided not only the C1 feedstock but also proved to be a very efficient solvent and processing aid for this copolymerization system. Double metal cyanide (DMC) and salen-Co(III) catalysts were employed, demonstrating excellent CO2/CHO copolymerization with high yield and high selectivity. Surprisingly, our use of scCO2 was found to significantly enhance the copolymerization efficiency and the quality of the final polymer product. Thermally stable and high molecular weight (MW) copolymers were successfully obtained. Optimization led to excellent catalyst yield (656 wt/wt, polymer/catalyst) and selectivity (over 96% toward polycarbonate) that were significantly beyond what could be achieved in conventional solvents. Moreover, detailed thermal analyses demonstrated that the PCHC copolymer produced in scCO2 exhibited higher glass transition temperatures (Tg ~114 8C) compared to polymer formed in dense phase CO2 (Tg~77 8C), and hence good thermal stability. Additionally, residual catalyst could be removed from the final polymer using scCO2, pointing toward a green method that avoids the use of conventional volatile organic based solvents for both synthesis and work-up