A strong approximation of the shortt process

A shortt of a one dimensional probability distribution is defined to be an interval which has at least probability t and minimal length. The length of a shortt, U(t), and its obvious estimator, U_n(t), are significant measures of scale of a probability distribution and the corresponding random sample, respectively. The shortt process is defined to be $\sqrt{n}(U_n(t)-U(t)) / U'(t)$, similarly to the definition of the quantile process. It is known that this process converges weakly, under natural regularity conditions, to a Brownian bridge. In this note a strong approximation of the shortt process by a Kiefer process is established, which yields the weak convergence as a corollary. Applications of the result to the global and local strong limiting behaviour of the shortt process are also presented

Worst-case throughput analysis for parametric rate and parametric actor execution time scenario-aware dataflow graphs

Scenario-aware dataflow (SADF) is a prominent tool for modeling and analysis of dynamic embedded dataflow applications. In SADF the application is represented as a finite collection of synchronous dataflow (SDF) graphs, each of which represents one possible application behaviour or scenario. A finite state machine (FSM) specifies the possible orders of scenario occurrences. The SADF model renders the tightest possible performance guarantees, but is limited by its finiteness. This means that from a practical point of view, it can only handle dynamic dataflow applications that are characterized by a reasonably sized set of possible behaviours or scenarios. In this paper we remove this limitation for a class of SADF graphs by means of SADF model parametrization in terms of graph port rates and actor execution times. First, we formally define the semantics of the model relevant for throughput analysis based on (max,+) linear system theory and (max,+) automata. Second, by generalizing some of the existing results, we give the algorithms for worst-case throughput analysis of parametric rate and parametric actor execution time acyclic SADF graphs with a fully connected, possibly infinite state transition system. Third, we demonstrate our approach on a few realistic applications from digital signal processing (DSP) domain mapped onto an embedded multi-processor architecture

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Selective Induction of Apoptosis in Melanoma Cells by Tyrosinase Promoter-Controlled CD95 Ligand Overexpression

Induction of apoptosis has been demonstrated previously by overexpression of CD95 ligand (CD95L) in cultured human melanoma cells. For in vivo approaches based on CD95L, however, targeted expression is a prerequisite and tyrosinase promoters have been considered for selection. Luciferase reporter gene assays performed for a representative panel of melanoma cell lines characterized by strong (SK-Mel-19), moderate (SK-Mel-13, MeWo), weak (A-375), and missing expression (M-5) of endogenous tyrosinase revealed high tyrosinase promoter activities in SK-Mel-19, SK-Mel-13, and MeWo, but only weak activities in A-375 and M-5 as well as in non-melanoma cell lines. After transfection of a CMV promoter CD95L expression construct, melanoma cells were found highly sensitive, as compared with non-melanoma cells. By applying a tyrosinase promoter CD95L construct, apoptosis was selectively induced in SK-Mel-19, SK-Mel-13, MeWo as well as in A-375, which was characterized by high CD95 surface expression and high sensitivity to agonistic CD95 activation. M5 and non-melanoma cell lines remained uninfluenced. Also, resistance to agonistic CD95 activation seen in MeWo characterized by weak CD95 surface expression was overcome by overexpression of CD95L. Our investigations provide evidence that tyrosinase promoter CD95L constructs may be of value for selective induction of apoptosis in therapeutic strategies for melanoma

On the implementation and execution of adaptive streaming applications modeled as MADF

Computer Systems, Imagery and Medi

The Bax/Bcl-2 Ratio Determines the Susceptibility of Human Melanoma Cells to CD95/Fas-Mediated Apoptosis

Defective cytochrome c release and the resulting loss of caspase-3 activation was recently shown to be essential for the susceptibility of human melanoma cells to CD95/Fas-induced apoptosis. Cytochrome c release from mitochondria is regulated by the relative amounts of apoptosis-promoting and apoptosis-inhibiting Bcl-2 proteins in the outer membrane of these organelles. The assignment of Bax/Bcl-2 ratios by quantitative Western blotting in 11 melanoma cell populations revealed a relation to the susceptibility to CD95-mediated apoptosis. We could show that a low Bax/Bcl-2 ratio was characteristic for resistant cells and a high Bax/Bcl-2 ratio was characteristic for sensitive cells. Low Bax expression was not a consequence of mutations in the p53 coding sequence. The Bax/Bcl-2 ratio was also in clear correlation with sensitivity to another cell death inducer, N-acetylsphingosine. Furthermore, Bcl-2 overexpression abolished apoptosis triggered by both apoptotic stimuli, confirming the critical role of the Bax/Bcl-2 ratio as a rheostat that determines the susceptibility to apoptosis in melanoma cells by regulating mitochondrial function. Interestingly, some chemotherapeutics lead to the activation of death pathways by CD95L upregulation, ceramide generation, direct activation of upstream caspases, or upregulation of proapoptotic genes. Taken together, these signals enter the apoptotic pathway upstream of mitochondria, resulting in activation of this central checkpoint. We therefore assumed that apoptosis deficiency of malignant melanoma can be circumvented by drugs directly influencing mitochondrial functions. For this purpose we used betulinic acid, a cytotoxic agent selective for melanoma, straightly perturbing mitochondrial functions. In fact, betulinic acid induced mitochondrial cytochrome c release and DNA fragmentation in both CD95-resistant and CD95-sensitive melanoma cell populations, independent of the Bax/Bcl-2 ratio