SPT of the pancreas is a rare indolent neoplasm that typically occurs in young females. It is a low-grade malignancy and can be cured with extended resection. The prognosis of such patients is good although the tumor may recur and metastasize.

The role of leaf water relations in controlling cell expansion in leaves of water-stressed maize and barley depends on time scale. Sudden changes in leaf water status, induced by sudden changes in humidity, light and soil salinity, greatly affect leaf elongation rate, but often only transiently. With sufficiently large changes in salinity, leaf elongation rates are persistently reduced. When plants are kept fully turgid throughout such sudden environmental changes, by placing their roots in a pressure chamber and raising the pressure so that the leaf xylem sap is maintained at atmospheric pressure, both the transient and persistent changes in leaf elongation rate disappear. All these responses show that water relations are responsible for the sudden changes in leaf elongation rate resulting from sudden changes in water stress and putative root signals play no part. However, at a time scale of days, pressurization fails to maintain high rates of leaf elongation of plants in either saline or drying soil, indicating that root signals are overriding water relations effects. In both saline and drying soil, pressurization does raise the growth rate during the light period, but a subsequent decrease during the dark results in no net effect on leaf growth over a 24 h period. When transpirational demand is very high, however, growth-promoting effects of pressurization during the light period outweigh any reductions in the dark, resulting in a net increase in growth of pressurized plants over 24 h. Thus leaf water status can limit leaf expansion rates during periods of high transpiration despite the control exercised by hormonal effects on a 24 h basis.

Recent studies have shown that the photochemical reflectance index (PRI), derived from narrow waveband reflectance at 531 and 570 nm, can be used as a remote measure of photosynthetic light-use efficiency (LUE). However, uncertainty remains as to the consistency of the relationship between PRI and LUE across species. In this study we examined the relationship between the PRI and various photosynthetic parameters for a group of species with varying photosynthetic capacity. At constant irradiance, for the species group as a whole, the PRI was well correlated with LUE ( r 2 =0.58) and with several other photosynthetic parameters, but best correlated with the ratio of carotenoids to chlorophylls contents (Caro/Chl). Despite the interspecific trends observed, determination of light response functions for the PRI in relation to photosynthetic parameters revealed that species-specific relationships were clearly stronger. For example, r 2 >0.90 for species-level PRI/LUE relationships. Also, the species-specific light-response data show that the magnitude of the PRI can be related to the magnitude of the saturated irradiance and the rate of CO 2 uptake. As demonstrated here, a light response function provides a simple yet precise approach for characterising the relationship between the PRI and photosynthetic parameters, which should assist with improved evaluation of the usefulness of the PRI as a generalised measure of LUE.

Attention-based sequence-to-sequence models for speech recognition jointly train an acoustic model, language model (LM), and alignment mechanism using a single neural network and require only parallel audio-text pairs. Thus, the language model component of the end-to-end model is only trained on transcribed audio-text pairs, which leads to performance degradation especially on rare words. While there have been a variety of work that look at incorporating an external LM trained on text-only data into the end-to-end framework, none of them have taken into account the characteristic error distribution made by the model. In this paper, we propose a novel approach to utilizing text-only data, by training a spelling correction (SC) model to explicitly correct those errors. On the LibriSpeech dataset, we demonstrate that the proposed model results in an 18.6% relative improvement in WER over the baseline model when directly correcting top ASR hypothesis, and a 29.0% relative improvement when further rescoring an expanded n-best list using an external LM.

Purpose: The purpose of this systematic review and meta-analysis was to evaluate the effects of massage on alleviating delayed onset of muscle soreness (DOMS) and muscle performance after strenuous exercise.Method: Seven databases consisting of PubMed, Embase, EBSCO, Cochrane Library, Web of Science, CNKI and Wanfang were searched up to December 2016. Randomized controlled trials (RCTs) were eligible and the outcomes of muscle soreness, performance (including muscle maximal isometric force (MIF) and peak torque) and creatine kinase (CK) were used to assess the effectiveness of massage intervention on DOMS.Results: Eleven articles with a total of 23 data points (involving 504 participants) satisfied the inclusion criteria and were pooled in the meta-analysis. The findings demonstrated that muscle soreness rating decreased significantly when the participants received massage intervention compared with no intervention at 24 h (SMD: –0.61, 95% CI: –1.17 to –0.05, P = 0.03), 48 h (SMD: –1.51, 95% CI: –2.24 to –0.77, P < 0.001), 72 h (SMD: –1.46, 95% CI: –2.59 to –0.33, P = 0.01) and in total (SMD: –1.16, 95% CI: –1.60 to –0.72, P < 0.001) after intense exercise. Additionally, massage therapy improved MIF (SMD: 0.56, 95% CI: 0.21–0.90, P = 0.002) and peak torque (SMD: 0.38, 95% CI: 0.04–0.71, P = 0.03) as total effects. Furthermore, the serum CK level was reduced when participants received massage intervention (SMD: –0.64, 95% CI: –1.04 to –0.25, P = 0.001).Conclusion: The current evidence suggests that massage therapy after strenuous exercise could be effective for alleviating DOMS and improving muscle performance.

This study aims to explore the mechanism of Circular RNA CDR1as implicating in regulating 5‐fluorouracil (5‐FU) chemosensitivity in breast cancer (BC) by competitively inhibiting miR‐7 to regulate CCNE1. Expressions of CDR1as and miR‐7 in 5‐FU‐resistant BC cells were determined by RT‐PCR. CCK‐8, colony formation assay and flow cytometry were applied to measure half maximal inhibitory concentration (IC50), 5‐Fu chemosensitivity and cell apoptosis. Western blot was used to detect the expressions of apoptosis‐related factors. CDR1as was elevated while miR‐7 was inhibited in 5‐FU‐resistant BC cells. Cells transfected with si‐CDR1as or miR‐7 mimic had decreased IC50 and colony formation rate, increased expressions of Bax/Bcl2 and cleaved‐Caspase‐3/Caspase‐3, indicating inhibition of CDR1as and overexpression of miR‐7 enhances the chemosensitity of 5‐FU‐resistant BC cells. Targetscan software indicates a binding site of CDR1as and miR‐7 and that CCNE1 is a target gene of miR‐7. miR‐7 can gather CDR1as in BC cells and can inhibit CCNE1. In comparison to si‐CDR1as group, CCNE1 was increased and chemosensitivity to 5‐Fu was suppressed in si‐CDR1as + miR‐7 inhibitor group. When compared with miR‐7 mimic group, CDR1as + miR‐7 mimic group had increased CCNE1 and decreased chemosensitivity to 5‐Fu. Nude mouse model of BC demonstrated that the growth of xenotransplanted tumour in si‐CDR1as + miR‐7 inhibitor group was faster than that in si‐CDR1as group. The tumour growth in CDR1as + miR‐7 mimic group was faster than that in miR‐7 mimic group. CDR1as may regulate chemosensitivity of 5‐FU‐resistant BC cells by inhibiting miR‐7 to regulate CCNE1.

Barley plants were grown in pots that would fit inside a pressure chamber, so that their shoots could be kept fully turgid by applying pressure in the chamber to bring the xylem sap of the shoot to the point of bleeding. Pressurisation increased the growth rate of NaCl-treated plants in the light period but not in the dark. The promotive effect on growth was greatest in the light period of the first day of pressurisation, but disappeared during the first night. Pressurisation promoted growth the next day during the light period, but on the second night the elongation rate was significantly lower than that of unpressurised NaCl-treated plants. This pattern of high day-time and low night-time growth then continued indefinitely. The lower night-time growth counteracted the higher day-time growth, with the result that total growth over 24 h was the same as in NaCl-treated plants that were not pressurised. Levels of total reserve carbohydrates were unaffected by pressurisation, indicating that the slower growth of the pres-surised plants during the night was not due to depletion of assimilates. These results are interpreted in the context of hormonal signals controlling growth on a 24-h basis, such that any short-term stimulation of growth arising from unusually high water status during the light period is counterbalanced by slower growth during the night.

In our study, we aimed to investigate the role of CDR1as during competitive inhibition of miR‐7 in the regulation of cisplatin chemosensitivity in breast cancer via regulating REGγ. RT‐qPCR was applied to detect the expression of CDR1as and miR‐7 in breast cancer tissues, breast cancer cell lines and corresponding drug‐resistant cell lines. The correlation between CDR1as and miR‐7 and between miR‐7 and REGγ was evaluated. MCF‐7‐R and MDA‐MB‐231‐R cells were selected followed by transfection of a series of mimics, inhibitors or siRNA. The effect of CDR1as on the half maximal inhibitor concentration (IC50), cisplatin sensitivity and cell apoptosis was also analysed. Furthermore, a subcutaneous xenograft nude mouse model was established to further confirm the effect of CDR1as on the chemosensitivity of breast cancer to cisplatin in vivo. Immunohistochemical staining was conducted to test the Ki‐67 expression in nude mice. A positive correlation was found between the drug resistance and CDR1as expression in breast cancer. CDR1as could increase the resistance of breast cancer cells to cisplatin. miR‐7 expression was low, while REGγ was highly expressed in MCF‐7‐R and MDA‐MB‐231‐R cells. CDR1as competitively inhibited miR‐7 and up‐regulated REGγ. Overexpression of miR‐7 could reverse the enhanced sensitivity of silenced CDR1as to drug‐resistant breast cancer cells. Additionally, in vivo experiments demonstrated that CDR1as mediated breast cancer occurrence and its sensitivity to cisplatin. Silencing CDR1as decreased Ki‐67 expression. Silencing CDR1as may inhibit the expression of REGγ by removing the competitive inhibitory effect on miR‐7 and thus enhancing the sensitivity of drug‐resistant breast cancer cells.