New designs for Hybrid latch flip-flip (HLFF) and implicit-pulsed data-close-to-output (ip-DCO) flipflop circuits are proposed to improve the redundant switching activity, speed and power as these flip-flop circuits are basic building blocks of many timing elements. This paper evaluates and compares the performance of various flip-flop circuits which can reduce the effect of redundant switching...

A new flip-flop design using a double-pulsed static latch is presented. The flip-flop has only a single stage of logic in the critical path and as a result is up to three times faster than the fastest previously known flip-flops, while consuming approximately the same energy as the lowestpower flip-flops. The flip-flop has asymmetric timing properties which make it a good match to skewed logic ...

The antiapoptotic protein FLIP(S) is a key suppressor of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in human glioblastoma multiforme (GBM) cells. We previously reported that a novel phosphatase and tensin homologue (PTEN)-Akt-atrophin-interacting protein 4 (AIP4) pathway regulates FLIP(S) ubiquitination and stability, although the means by which PTEN and A...

c-FLIP is an inhibitor of apoptosis mediated by the death receptors Fas, DR4, and DR5 and is expressed as long (c-FLIP(L)) and short (c-FLIP(S)) splice forms. We found that small interfering RNA (siRNA)-mediated silencing of c-FLIP induced spontaneous apoptosis in a panel of p53 wild-type, mutant, and null colorectal cancer cell lines and that this apoptosis was mediated by caspase-8 and Fas-as...

Phosphatase and tensin homologue (PTEN) loss and activation of the Akt-mammalian target of rapamycin (mTOR) pathway increases mRNA translation, increases levels of the antiapoptotic protein FLIP(S), and confers resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in glioblastoma multiforme (GBM). In PTEN-deficient GBM cells, however, the FLIP(S) protei...

In this paper, a novel mixed selection methodology using flip-flops for scan and reset design is proposed. The method runs test generation for a sequential circuit to obtain reachable states of flip-flops and required states for hard-to-detect faults. The circuit is also explored so as to acquire the structural connection relationship among the flip-flops. By analyzing these three sets of infor...

API-1 (pyrido[2,3-d]pyrimidines) is a novel small-molecule inhibitor of Akt, which acts by binding to Akt and preventing its membrane translocation and has promising preclinical antitumor activity. In this study, we reveal a novel function of API-1 in regulation of cellular FLICE-inhibitory protein (c-FLIP) levels and TRAIL-induced apoptosis, independent of Akt inhibition. API-1 effectively ind...

Cellular FLICE-like inhibitory protein (c-FLIP, gene symbol CFLAR) was first identified as a negative regulator of death receptor-mediated apoptosis in mammals. To understand the ubiquity and diversity of the c-FLIP protein subfamily during evolution, c-FLIP orthologs were identified from a comprehensive range of vertebrates, including birds, amphibians, and fish, and were characterized by comb...

In this paper, we introduce design models for Totally Self Checking, Code Disjoint (T S C / C D) and Strongly Fault Secure, Strongly Code Disjoint (SFS/SCDJ synchronous controllers. The T S C / C D and SF / S C D models based on two new proposed low-cost, modular, Totally Self Checking (TSC), edge triggered and error propagating (code disjoint) Flip-Flops; one, a D Flip-Flop which can be used i...

FLICE-like inhibitory protein (FLIP) has been shown in both humans and mice to inhibit apoptosis and NF-kappaB activation induced by pro-inflammatory mediators. The activation of NF-kappaB and the induction of apoptosis are critical events in the pathogenesis of a variety of disease states in cattle, including mastitis. Since FLIP is known to moderate these events in other species, we mapped th...