The Visual Object Tracking challenge VOT2019 is the seventh annual tracker benchmarking activity organized by the VOT initiative. Results of 81 trackers are presented; many are state-of-the-art trackers published at major computer vision conferences or in journals in the recent years. The evaluation included the standard VOT and other popular methodologies for short-term tracking analysis as well as the standard VOT methodology for long-term tracking analysis. The VOT2019 challenge was composed of five challenges focusing on different tracking domains: (i) VOT-ST2019 challenge focused on short-term tracking in RGB, (ii) VOT-RT2019 challenge focused on "real-time" shortterm tracking in RGB, (iii) VOT-LT2019 focused on longterm tracking namely coping with target disappearance and reappearance. Two new challenges have been introduced: (iv) VOT-RGBT2019 challenge focused on short-term tracking in RGB and thermal imagery and (v) VOT-RGBD2019 challenge focused on long-term tracking in RGB and depth imagery. The VOT-ST2019, VOT-RT2019 and VOT-LT2019 datasets were refreshed while new datasets were introduced for VOT-RGBT2019 and VOT-RGBD2019. The VOT toolkit has been updated to support both standard shortterm, long-term tracking and tracking with multi-channel imagery. Performance of the tested trackers typically by far exceeds standard baselines. The source code for most of the trackers is publicly available from the VOT page. The dataset, the evaluation kit and the results are publicly available at the challenge website 1 .

macromolecular complex which allows transcription factors to interact with the class II MHC promoter in a spatially and helically constrained fashion.The major histocompatibility complex (MHC) class II proteins play a central role in the immune response. Extensive analysis has underscored that much of the fluctuation in class II MHC antigen expression can be attributed to changes at the transcriptional level (46,47). In addition to the class II MHC molecules themselves, associative accessory molecules that are necessary for class II antigen MHC function appear to be controlled in a similar fashion. These associative molecules include the MHC class II-associated invariant chain (Ii) and the more recently described DM heterodimer. All class II MHC, Ii, and DM promoters share the unique presence of three DNA elements, called W, X, and Y, which are highly conserved and critical for promoter function (2, 15). The W-X-Y elements are not only important for constitutive gene expression in B cells but also critical for inducible gene expression. In addition to the conservation in sequence, the spacing between the X and Y elements is highly conserved at approximately two helical turns. Increasing the number of helical turns between these two elements preserves function, while disrupting this orientation destroys promoter activation. Our group previously hypothesized that this restrictive spacing may be required to align the X and Y elements on the same side of the DNA helix, thus allowing transcription factors which can bind these elements to directly interact or to participate in the assembly of a larger promoter complex (48,49).The Y box is a CCAAT motif, and it interacts with NF-Y/ CBF (also known as YEBP/CP-1). NF-Y/CBF is composed of A, B, and C subunits (26,27,57), with the conserved core sequences of NF-YC (CBF-C) and NF-YB (CBF-A) forming a histone fold motif similar to the nucleosome subunits H2A and H2B (1). NF-Y/CBF plays a critical role in opening chromatin because mutation of the NF-Y/CBF-binding sites in both the DRA and Ii promoters results in the loss of protein binding across these promoters in intact cells (24,54). NF-Y/CBF can preset chromatin for other transcriptional coactivators, such as the histone acetylase GCN5, p300, and pCAF (10,19,23). The X box is a bipartite sequence. X1 is bound by the trimeric transcription factor, RFX, formed by RFX5, RFXAP, and RFXANK/RFXB (12,28,45). The lack of RFX results in several subclasses of bare lymphocyte syndrome (BLS), a severe immunodeficiency attributed to the lack of class II MHC expression. RFX is required for both the constitutive and gamma interferon (IFN-␥) induction of class II MHC expression (5). The X2 element binds a protein complex, X2BP, which has been recently identified as the CREB protein (29).Despite the extensive demonstration that X and Y boxbinding proteins are important for class II MHC regulation, these proteins are constitutively expressed and cannot explain the cell-, tissue-, developmentally, and cytokine-inducible expression of class ...

NF‐Y binds a CCAAT motif found in many eukaryotic polymerase II‐dependent promoters. In the HLA‐DRA promoter it has been demonstrated that stereo‐specific alignment between this motif and the upstream elements X1 and X2 is required for activation. To study the underlying mechanism for this requirement, a panel of transfected cell lines that maintained integrated, wild‐type and mutant promoters were analyzed by in vivo genomic footprinting. Cell lines harboring a mutated CCAAT element exhibited a loss of interactions at the CCAAT site, as expected, and no transcriptional activity. Most importantly, mutation of the CCAAT sequence nearly abolished in vivo binding at the X1 and X2 sites, while mutations of X1 and X2 had little effect on CCAAT box binding. However, X1 and X2 binding was interdependent. In vitro, X1 binding activities are known to be stabilized by NF‐Y binding. Interaction between NF‐Y and X box binding proteins was demonstrated by reciprocal co‐immunoprecipitation in the absence of DNA and co‐affinity purification in the presence of DNA. Collectively, these studies indicate that occupancy of the CCAAT element represents an early event affecting other protein‐DNA interactions and suggest that NF‐Y stabilizes and interacts with X box factors to mediate this function. These findings may represent a common theme among promoters containing a CCAAT element.

Paclitaxel (Taxol) is a new generation of chemotherapeutic drug that is effective against malignant non-small cell lung (1, 2), prostate (3, 4), and breast cancer (5), with the most encouraging effects observed in cancer chemotherapy-refractory ovarian cancer (6). Paclitaxel exhibited significant antitumor activity against human ovarian cancer in a nude mouse model (6). Furthermore, paclitaxel significantly inhibited the angiogenic response induced by tumor cell supernatant in mice (7,8). The primary mechanism of action of paclitaxel is attributed to its ability to bind microtubules and to prevent their disassembly. However, the effect of paclitaxel exceeds that of conventional microtubule-disrupting agents, and there is increasing evidence that paclitaxel has multiple cellular effects in addition to the blockage of mitosis (9 -15).One of the effects of paclitaxel is to alter gene expression. In murine macrophages, paclitaxel can induce the expression of a series of lipopolysaccharide-inducible cytokines, such as IL 1