Confined-walking mode for an elliptical polarized undulator and its application.

Elliptical polarized undulators (EPUs) are broadly used in the soft X-ray energy range. They have the advantage of providing photons with both varied energy and polarization through adjustments to the value of the gap and/or shift magnet arrays in an undulator. Yet these adjustments may create a disturbance on the stability of the electron beam in a storage ring. To correct such a disturbance, it is necessary to establish a feed-forward table of key nodes in the gap-shift-defined two-dimensional parameter space. Such a table can only be scanned during machine-study time. For a free-walking mode, whereby an undulator is allowed to manoeuvre in the whole gap-shift space, all the key nodes need to be scanned at the expense of a large amount of machine-study time. This will greatly delay the employment of a full-polarization capable undulator (especially circularly polarized). By analyzing data-collecting patterns of user experiments, this paper defines a reduced set of key nodes in gap-shift parameter space, with the number of key nodes to be scanned for feed-forwarding scaled down to one-third of the original; and introduces a new walking mode for EPUs: confined-walking mode, whereby the undulator is manoeuvred only within the reduced set of key nodes. Such a mode is firstly realized on the EPUs at the DREAMLINE beamline at Shanghai Synchrotron Radiation Facility (SSRF). Under confined-walking mode, the undulator movements are stable and there is no obvious disturbance to the electron beam with the feed-forward system in operation. Successful experiments have been carried out using the circularly polarized light obtained via the new walking mode. This mode is expected to be applied to future EPUs at SSRF with the increasing requirements for various polarization modes.

Combination of targeting CD24 and inhibiting autophagy suppresses the proliferation and enhances the apoptosis of colorectal cancer cells.

CD24 can regulate angiogenesis, drug sensitivity and the progression of colorectal cancer (CRC). However, whether CD24 regulates autophagy and apoptosis in CRC cells remains to be fully elucidated. The present study investigated the functional role of the altered expression of CD24 in the autophagy and apoptosis of HCT116 and HT29 human CRC cells. The results revealed lower expression levels of CD24 in HCT116 cells but higher levels in HT29 cells. Inducing the overexpression or the knockdown of CD24 did not affect the viability or spontaneous apoptosis of HCT116 and HT29 cells, respectively. Induction of the overexpression of CD24 significantly decreased the relative expression levels of Beclin­1, autophagy­related (Atg)3 and Atg5, and the numbers of microtubule­associated protein­1 light chain­3 (LC3)­positive puncta, but increased the expression of p62 in HCT116 cells. By contrast, CD24 silencing increased the expression of Beclin­1, Atg3 and Atg5, and the numbers of LC3­positive puncta, but decreased the expression of p62 in HT29 cells. Treatment with 3­methyladenine, or the knockdown of Atg5 by specific small interfering RNA to attenuate autophagy significantly enhanced the viability of CD24­overexpressing HCT116 cells, but reduced the viability of CD24­silenced HT29 cells, relative to their controls. As a result, the attenuation of autophagy significantly decreased the frequency of apoptotic CD24­overexpressing HCT116 cells, but increased the percentages of apoptotic CD24­silenced HT29 cells. The overexpression of CD24 promoted the activation of nuclear factor (NF)­κBp65, whereas CD24 silencing attenuated its activation in CRC cells. Inhibition of the activation of NF­κB enhanced the CD24 overexpression­induced decrease in autophagy, but attenuated the CD24 silencing­induced increase in autophagy in CRC cells. Therefore, CD24 inhibited the autophagy of CRC cells, and the combination of targeting CD24 and inhibiting autophagy promoted the apoptosis of CRC cells. Conceivably, these findings may aid in the design of novel therapies for the intervention of CRC.

P-LORAKS: Low-rank modeling of local k-space neighborhoods with parallel imaging data.

PURPOSE: To propose and evaluate P-LORAKS a new calibrationless parallel imaging reconstruction framework. THEORY AND METHODS: LORAKS is a flexible and powerful framework that was recently proposed for constrained MRI reconstruction. LORAKS was based on the observation that certain matrices constructed from fully sampled k-space data should have low rank whenever the image has limited support or smooth phase, and made it possible to accurately reconstruct images from undersampled or noisy data using low-rank regularization. This paper introduces P-LORAKS, which extends LORAKS to the context of parallel imaging. This is achieved by combining the LORAKS matrices from different channels to yield a larger but more parsimonious low-rank matrix model of parallel imaging data. This new model can be used to regularize the reconstruction of undersampled parallel imaging data, and implicitly imposes phase, support, and parallel imaging constraints without needing to calibrate phase, support, or sensitivity profiles. RESULTS: The capabilities of P-LORAKS are evaluated with retrospectively undersampled data and compared against existing parallel MRI reconstruction methods. Results show that P-LORAKS can improve parallel imaging reconstruction quality, and can enable the use of new k-space trajectories that are not compatible with existing reconstruction methods. CONCLUSION: The P-LORAKS framewok provides a new and effective way to regularize parallel imaging reconstruction.

Membranous ABCG2 expression in colorectal cancer independently correlates with shortened patient survival.

BACKGROUND: ABCG2 is a member of the ATP binding cassette (ABC) transporter superfamily and identified to play an important role in multidrug resistance in many studies. But the expression of ABCG2 is controversial in many kinds of tumors including colorectal cancer (CRC). OBJECTIVE: To clarify the expression patterns of ABCG2 and elucidate the prognostic value of ABCG2 in CRC. METHODS: ABCG2 expression was analyzed in 225 primary CRC tissues using immunohistochemical assessment. Cytoplasmic and membranous immunoreactivity were semiquantitatively scored and correlated with clinicopathological variables. 69 cases were used for survival analysis. χ2 test for trends, Kaplan-Meier analysis and Cox's regression were used for statistical analysis. RESULTS: 83.1% cases showed positive cytoplasmic expression including 13.3% strongly positive. 66.2% showed positive membranous expression including 15.6% strongly positive. 50% normal mucosa exhibited a strong membranous staining on the apical membrane. The strongly membranous staining significantly correlated to lymph node and distant metastasis. While the cytoplasmic expression levels of ABCG2 protein were only correlated with tumor stage. Survival analysis showed strongly membranous ABCG2 staining correlated to shortened patient survival than negative one (HR=2.439, 95%CI 1.053-5.650, P=0.038), but not cytoplasmic ABCG2 staining. DISCUSSION: Our results showed that membranous ABCG2 expression was significantly associated with Dukes' stage, lymph node metastasis and distant metastasis. However, cytoplasmic ABCG2 expression was only significantly associated with Dukes' stage. CONCLUSIONS: Strong membranous ABCG2 staining is a potential new independent prognostic factor of CRC. Further studies are needed to clarify the role of ABCG2 in colon carcinogenesis.