Adaptive Disorder Control in Data Stream Processing

Out-of-order tuples in continuous data streams may cause inaccurate query results since conventional window operators generally discard those tuples. Existing approaches use a buffer to fix disorder in stream tuples and estimate its size based on the maximum network delay seen in the streams. However, they do not provide a method to control the amount of tuples that are not saved and discarded from the buffer, although users may want to keep it within a predefined error bound according to application requirements. In this paper, we propose a method to estimate the buffer size while keeping the percentage of tuple drops within a user-specified bound. The proposed method utilizes tuples' interarrival times and their network delays for estimation, whose parameters reflect real-time stream characteristics properly. Based on two parameters, our method controls the amount of tuple drops adaptively in accordance with fluctuated stream characteristics and keeps their percentage within a given bound, which we observed through our experiments

Regulation of HuR by DNA Damage Response Kinases

As many DNA-damaging conditions repress transcription, posttranscriptional processes critically influence gene expression during the genotoxic stress response. The RNA-binding protein HuR robustly influences gene expression following DNA damage. HuR function is controlled in two principal ways: (1) by mobilizing HuR from the nucleus to the cytoplasm, where it modulates the stability and translation of target mRNAs and (2) by altering its association with target mRNAs. Here, we review evidence that two main effectors of ataxia-telangiectasia-mutated/ATM- and Rad3-related (ATM/ATR), the checkpoint kinases Chk1 and Chk2, jointly influence HuR function. Chk1 affects HuR localization by phosphorylating (hence inactivating) Cdk1, a kinase that phosphorylates HuR and thereby blocks HuR's cytoplasmic export. Chk2 modulates HuR binding to target mRNAs by phosphorylating HuR's RNA-recognition motifs (RRM1 and RRM2). We discuss how HuR phosphorylation by kinases including Chk1/Cdk1 and Chk2 impacts upon gene expression patterns, cell proliferation, and survival following genotoxic injury

The Interaction of Phospholipase C-{beta}3 with Shank2 Regulates mGluR-mediated Calcium Signal

Phospholipase C-{beta} isozymes that are activated by G protein-coupled receptors (GPCR) and heterotrimeric G proteins carry a PSD-95/Dlg/ZO-1 (PDZ) domain binding motif at their C terminus. Through interactions with PDZ domains, this motif may endow the PLC-{beta} isozyme with specific roles in GPCR signaling events that occur in compartmentalized regions of the plasma membrane. In this study, we identified the interaction of PLC-{beta}3 with Shank2, a PDZ domain-containing multimodular scaffold in the postsynaptic density (PSD). The C terminus of PLC-{beta}3, but not other PLC-{beta} isotypes, specifically interacts with the PDZ domain of Shank2. Homer 1b, a Shank-interacting protein that is linked to group I metabotropic glutamate receptors and IP3 receptors, forms a multiple complex with Shank2 and PLC-{beta}3. Importantly, microinjection of a synthetic peptide specifically mimicking the C terminus of PLC-{beta}3 markedly reduces the mGluR-mediated intracellular calcium response. These results demonstrate that Shank2 brings PLC-{beta}3 closer to Homer 1b and constitutes an efficient mGluR-coupled signaling pathway in the PSD region of neuronal synapses

On the origin of the hump structure in the in-plane optical conductivity of high Tc cuprates based on a SU(2) slave-boson theory

An improved version of SU(2) slave-boson approach is applied to study the in-plane optical conductivity of the two dimensional systems of high Tc cuprates. We investigate the role of fluctuations of both the phase and amplitude of order parameters on the (Drude) peak-dip-hump structure in the in-plane conductivity as a function of hole doping concentration and temperature. The mid-infrared(MIR) hump in the in-plane optical conductivity is shown to originate from the antiferromagnetic spin fluctuations of short range(the amplitude fluctuations of spin singlet pairing order parameters), which is consistent with our previous U(1) study. However the inclusion of both the phase and amplitude fluctuations is shown to substantially improve the qualitative feature of the optical conductivity by showing substantially reduced Drude peak widths for entire doping range. Both the shift of the hump position to lower frequency and the growth of the hump peak height with increasing hole concentration is shown to be consistent with observations.Comment: 7 pages, 6 figure