Abstract:
In his famous theorem (1982), Douglas Leonard characterized the $q$-Racah polynomials and their relatives in the Askey scheme from the duality property of $Q$-polynomial distance-regular graphs. In this paper we consider a nonsymmetric (or Laurent) version of the $q$-Racah polynomials in the above situation. Let $\Gamma$ denote a $Q$-polynomial distance-regular graph that contains a Delsarte clique $C$. Assume that $\Gamma$ has $q$-Racah type. Fix a vertex $x \in C$. We partition the vertex set of $\Gamma$ according to the path-length distance to both $x$ and $C$. The linear span of the characteristic vectors corresponding to the cells in this partition has an irreducible module structure for the universal double affine Hecke algebra $\hat{H}_q$ of type $(C^{\vee}_1, C_1)$. From this module, we naturally obtain a finite sequence of orthogonal Laurent polynomials. We prove the orthogonality relations for these polynomials, using the $\hat{H}_q$-module and the theory of Leonard systems. Changing $\hat{H}_q$ by $\hat{H}_{q^{-1}}$ we show how our Laurent polynomials are related to the nonsymmetric Askey-Wilson polynomials, and therefore how our Laurent polynomials can be viewed as nonsymmetric $q$-Racah polynomials.

Abstract:
We study a relationship between $Q$-polynomial distance-regular graphs and the double affine Hecke algebra of type $(C^{\vee}_1,C_1)$. Let $\Ga$ denote a $Q$-polynomial distance-regular graph with vertex set $X$. We assume that $\Ga$ has $q$-Racah type and contains a Delsarte clique $C$. Fix a vertex $x\in C$. We partition $X$ according to the path-length distance to both $x$ and $C$. This is an equitable partition. For each cell in this partition, consider the corresponding characteristic vector. These characteristic vectors form a basis for a $\C$-vector space $\W$. The universal double affine Hecke algebra of type $(C^{\vee}_1,C_1)$ is the $\C$-algebra $\H$ defined by generators $\{t^{\pm1}_n\}^3_{n=0}$ and relations (i) $t_nt_n^{-1}=t_n^{-1}t_n=1$; (ii) $t_n+t_n^{-1}$ is central; (iii) $t_0t_1t_2t_3 = q^{-1/2}$. In this paper, we display an $\H$-module structure for $\W$. For this module and up to affine transformation, \begin{itemize} \item $t_0t_1+(t_0t_1)^{-1}$ acts as the adjacency matrix of $\Ga$; \item $t_3t_0+(t_3t_0)^{-1}$ acts as the dual adjacency matrix of $\Ga$ with respect to $C$; \item $t_1t_2+(t_1t_2)^{-1}$ acts as the dual adjacency matrix of $\Ga$ with respect to $x$. \end{itemize} To obtain our results we use the theory of Leonard systems.

Abstract:
Variations in the upper limbs are common and are the main causes for iatrogenic injury during invasive procedures. A rare division of the axillary artery was found on the left side of a Korean cadaver during an educational dissection. The subscapular artery originated from the second part of the axillary artery. And then it gave off an aberrant branch to the pectoralis major muscle, as pectoral branch. The author describes this previously unreported case and discusses its prevalence and the clinical implications.

Abstract:
An improved assay to determine helicase directionality was developed that uses a substrate containing biotinylated oligonucleotides. As a proof of concept, it was shown that the substrates substantially improve helicase activity and directionality determination for several DNA helicases in comparison to more traditional substrates. In addition, a universal substrate that can be used to determine the directionality of both 3'→ 5' and 5'→ 3' helicases was developed.It is shown here that the use of a biotin-streptavidin complex as a helicase substrate improves helicase activity and the determination of helicase directionality. The method described is simpler that the currently available techniques.Helicases play important roles in DNA and RNA metabolic processes such as replication, recombination, repair, transcription and translation [1]. The enzyme catalyzes the unwinding of duplex nucleic acid, utilizing the energy derived from nucleoside triphosphate hydrolysis to translocate along one strand of the duplex and to displace the complementary strand. Thus, most helicases have a specific polarity. They move along the strand either in the 3'→ 5' or 5'→ 3' direction. Some helicases, however, are bipolar and can move in either direction (e.g. [2]). Thus, one of the first properties to be determined for a new helicase is its directionality.To date, several different substrates have been used to determine helicase directionality. One such substrate is schematically shown in Figure 1A[3]. It is made by annealing a 5' 32P-labled complementary strand to a blunt end restriction enzyme site on a single-stranded plasmid DNA (e.g. M13 or φX174), followed by 32P labeling of the 3' end using 32P-labled dNTP and DNA polymerase. The labeled substrate is then digested with the restriction enzyme. The result is a linear molecule with a large internal region of ssDNA where a helicase can assemble, and two 32P-labled duplex regions of different lengths. Depending on enzyme polarity, only

Abstract:
Gantzer’s muscle is an additional muscle in the forearm. We studied the incidence and the morphology of Gantzer’s muscle and its relation with neurovascular structures. However, unlike the previous suggestion by Eid et al., there is no significant difference in the frequency of the variations of these nerves whether Gantzer’s muscle is present or not.

Abstract:
MDR variants, CEM/VLB10-2, CEM/VLB55-8 and CEM/VLB100 cells, with gradually increased levels of P-gp derived from human lymphoblastic leukemia CEM cells, were gradually more susceptible to TRAIL-induced apoptosis and cytotoxicity than parental CEM cells. The P-gp level of MDR variants was positively correlated with the levels of DNA-PKcs, pAkt, pGSK-3β and c-Myc as well as DR5 and negatively correlated with the level of c-FLIPs. Hypersensitivity of CEM/VLB100 cells to TRAIL was accompanied by the activation of mitochondrial apoptotic pathway as well as the activation of initiator caspases. In addition, TRAIL-induced down-regulation of DNA-PKcs/Akt/GSK-3β pathway and c-FLIP and up-regulation of cell surface expression of death receptors were associated with the increased susceptibility to TRAIL of MDR cells. Moreover, TRAIL inhibited P-gp efflux function via caspase-3-dependent degradation of P-gp as well as DNA-PKcs and subsequently sensitized MDR cells to MDR-related drugs such as vinblastine and doxorubicin. We also found that suppression of DNA-PKcs by siRNA enhanced the susceptibility of MDR cells to vincristine as well as TRAIL via down-regulation of c-FLIP and P-gp expression and up-regulation of DR5.This study showed for the first time that the MDR variant of CEM cells was hypersensitive to TRAIL due to up-regulation of DR5 and concomitant down-regulation of c-FLIP, and degradation of P-gp and DNA-PKcs by activation of caspase-3 might be important determinants of TRAIL-induced sensitization of MDR cells to MDR-related drugs. Therefore, combination of TRAIL and chemotherapeutic drugs may be a good strategy for treatment of cancer with multidrug resistance.Acquired resistance to chemotherapeutic agents remains a major obstacle for the effective treatment of many advanced and metastatic cancers. Several mechanisms are thought to be involved in the development of multidrug resistance (MDR), defined by simultaneous cross-resistance to a variety of anticancer drugs

Abstract:
PC3-MM2 and KM12L4A cells with high level of c-Myc and DNA-PKcs were more susceptible to TRAIL than their poorly metastatic primary PC3 and KM12 cells, which was associated with down-regulation of c-FLIPL/S and Mcl-1 and up-regulation of the TRAIL receptor DR5 but not DR4 in both metastatic cells. Moreover, high susceptibility of these metastatic cells to TRAIL was resulted from TRAIL-induced potent activation of caspase-8, -9, and -3 in comparison with their primary cells, which led to cleavage and down-regulation of DNA-PKcs. Knockdown of c-Myc gene in TRAIL-treated PC3-MM2 cells prevented the increase of DR5 cell surface expression, caspase activation and DNA-PKcs cleavage and attenuated the apoptotic effects of TRAIL. Moreover, the suppression of DNA-PKcs level with siRNA in the cells induced the up-regulation of DR5 and active caspase-8, -9, and -3. We also found that 4,5-dimethoxy-2-nitrobenzaldehyde (DMNB), a specific inhibitor of DNA-PK, potentiated TRAIL-induced cytotoxicity and apoptosis in relatively TRAIL-insensitive PC3 and KM12 cells and therefore functioned as a TRAIL sensitizer.This study showed the positive relationship between c-Myc expression in highly metastatic human prostate and colon cancer cells and susceptibility to TRAIL-induced apoptosis and therefore indicated that TRAIL might be used as an effective therapeutic modality for advanced metastatic cancers overexpressing c-Myc and combination of TRAIL therapy with agent that inhibits the DNA-PKcs/Akt signaling pathway might be clinically useful for the treatment of relatively TRAIL-insensitive human cancers.Despite the improvement of therapeutic strategies against cancer, the acquisition of invasive/metastatic capabilities and the development of resistance to therapy in cancer cells are still critical problems for successful cancer therapy because recurrent or metastatic cancers that appear after the initial radiotherapy or chemotherapy are generally refractory to secondary therapies [1]. Som