The new simulation of Martian general circulation based on CCSR/NIES AGCM has been performed and the numerical results analyzed. We attempt to reproduce the atmospheric states of Mars which have been observed by the Mars Global Surveyor, and Viking by introducing three kinds of time-and latitudedependent dust opacity scenarios which are made to be consistent with the past observational results, as the observed dust distribution during spring and summer in south hemisphere varies largely at each year and so does observed atmospheric conditions. The model with TES2 dust scenario, which is the dust distribution based on the observation by the Mars Global Surveyor in 1999, generally reproduces distributions of temperature and zonal wind observed by the Mars Global Surveyor in 1999, though the temperature tends to be lower at high altitude. The maximum value of CO 2 ice thickness at polar regions relatively reproduces the observation, but the edge of the northern and southern seasonal caps are outside of the observational results during spring, which results in lower surface pressure especially in northern spring. Annual variations of the amplitudes of the diurnal and semidiurnal tide are qualitatively comparable between our model with VIK1 dust scenario, which is the dust distribution based on the observation by Viking Orbiter in 1977, and observation by Viking Lander 1 in 1977. The baroclinic waves with consistent periods, wavenumbers and phase speeds with observational results by Viking Lander 2 in 1977 are reproduced in the autumn, though in the winter, during the second dust storm, and in the spring, the phase speeds are faster than observation.
The cell of origin of tumors and the the factors determining the cell of origin remain unclear. In this study, a mouse model of precursor-B acute lymphoblastic leukemia/lymphoma (pre-B ALL/LBL) was established by retroviral transduction of Myc genes (N-Myc or c-Myc) into mouse bone marrow cells. Hematopoietic stem cells (HSCs) exhibited the highest susceptibility to N-Myc-induced pre-B ALL/LBL versus lymphoid progenitors, myeloid progenitors and committed progenitor B cells. N-Myc was able to induce pre-B ALL/LBL directly from progenitor B cells in the absence of Ink4a and Arf. Arf was expressed higher in progenitor B cells than Ink4a. In addition, N-Myc induced pre-B ALL/LBL from Arf−/− progenitor B cells, suggesting that Arf plays a predominant role in determining the cell of origin of pre-B ALL/LBL. Tumor cells derived from Ink4a/Arf−/− progenitor B cells exhibited a higher rate of proliferation and were more chemoresistant than those derived from wild-type HSCs. Furthermore, the Mdm2 inhibitor Nutlin-3 restored p53 and induced massive apoptosis in mouse pre-B ALL/LBL cells derived from Ink4a/Arf−/− cells and human B-ALL cell lines lacking Ink4a and Arf expression, suggesting that Mdm2 inhibition may be a novel therapeutic approach to the treatment of Ink4a/Arf−/− B-ALL/LBL, such as is frequently found in Ph+ ALL and relapsed ALL. Collectively, these findings indicate that Ink4a and Arf are critical determining factors of the cell of origin and the therapeutic sensitivity of Myc-induced lymphoid tumors.
a b s t r a c tThe classification of the bio-signal has been used for various purposes in the literature as they are versatile in diagnosis of anomalies, improvement of overall health and sport performance and creating intuitive human computer interfaces. However, automatic identification of the signal patterns on a streaming real-time signal requires a series of complex procedures. A plethora of heuristic methods, such as neural networks and fuzzy systems, have been proposed as a solution. These methods stipulate certain conditions, such as preconditioning the signals, manual feature selection and large number of training samples.In this study, we introduce a novel variant and application of the Collaborative Representation based Classification (CRC) in spectral domain for recognition of hand gestures using raw surface electromyography (EMG) signals. The CRC based methods do not require large number of training samples for an efficient pattern classification. Additionally, we present a training procedure in which a high end subspace clustering method is employed for clustering the representative samples into their corresponding class labels. Thereby, the need for feature extraction and spotting patterns manually on the training samples is obviated.We presented the intuitive use of spectral features via circulant matrices. The proposed Spectral Collaborative Representation based Classification (SCRC) is able to recognize gestures with higher levels of accuracy for a fairly rich gesture set compared to the available methods. The worst recognition result which is the best in the literature is obtained as 97.3% among the four sets of the experiments for each hand gestures. The recognition results are reported with a substantial number of experiments and labeling computation.
The Sparse Representation based Classification (SRC) method has been utilized for various pattern recognition problems, especially for face recognition. Upon its success, the SRC method is extended by introducing Block Sparsity (BS) for the signal to be recovered and much better results are reported in the related literature. In this study, we test three block sparsity approach:Block Sparse Bayesian Learning, Dynamic Group Sparsity and Block Sparse Convex Programming frameworks for the previously introduced SRC based gesture recognition algorithm. The results show that it yields faster and more accurate results than the SRC based gesture recognition algorithm and is suitable for real-time applications such as for commanding a robotic wheelchair.
Death receptor Fas-mediated apoptosis not only eliminates nonspecific and autoreactive B cells but also plays a major role in antitumor immunity. However, the possible mechanisms underlying impairment of Fas-mediated induction of apoptosis during lymphomagenesis remain unknown. In this study, we employed our developed syngeneic lymphoma model to demonstrate that downregulation of Fas is required for both lymphoma development and lymphoma cell survival to evade immune cytotoxicity. CD40 signal activation significantly restored Fas expression and thereby induced apoptosis after Fas ligand treatment in both mouse and human lymphoma cells. Nevertheless, certain human lymphoma cell lines were found to be resistant to Fas-mediated apoptosis, with Livin (melanoma inhibitor of apoptosis protein; ML-IAP) identified as a driver of such resistance. High expression of Livin and low expression of Fas were associated with poor prognosis in patients with aggressive non-Hodgkin's lymphoma. Livin expression was tightly driven by bromodomain and extraterminal (BET) proteins BRD4 and BRD2, suggesting that Livin expression is epigenetically regulated in refractory lymphoma cells to protect them from Fas-mediated apoptosis. Accordingly, the combination of CD40-mediated Fas restoration with targeting of the BET proteins-Livin axis may serve as a promising immunotherapeutic strategy for refractory B-cell lymphoma.
FZR1 (fizzy-related protein homolog; also known as CDH1 [cell division cycle 20 related 1]) functions in the cell cycle as a specific activator of anaphase-promoting complex or cyclosome ubiquitin ligase, regulating late mitosis, G phase, and activation of the G-M checkpoint. FZR1 has been implicated as both a tumor suppressor and oncoprotein, and its precise contribution to carcinogenesis remains unclear. Here, we examined the role of FZR1 in tumorigenesis and cancer therapy by analyzing tumor models and patient specimens. In an gene-trap mouse model of B-cell acute lymphoblastic leukemia (B-ALL), mice with-deficient B-ALL survived longer than those with -intact disease, and sensitivity of-deficient B-ALL cells to DNA damage appeared increased. Consistently, conditional knockdown of FZR1 sensitized human B-ALL cell lines to DNA damage-induced cell death. Moreover, multivariate analyses of reverse-phase protein array of B-ALL specimens from newly diagnosed B-ALL patients determined that a low FZR1 protein expression level was an independent predictor of a longer remission duration. The clinical benefit of a low FZR1 expression level at diagnosis was no longer apparent in patients with relapsed B-ALL. Consistent with this result, secondary and tertiary mouse recipients of -deficient B-ALL cells developed more progressive and radiation-resistant disease than those receiving-intact B-ALL cells, indicating that prolonged inactivation of promotes the development of resistant clones. Our results suggest that reduction of FZR1 increases therapeutic sensitivity of B-ALL and that transient rather than tonic inhibition of FZR1 may be a therapeutic strategy.
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