Gaussian quantum computation with oracle-decision problems

We study a simple-harmonic-oscillator quantum computer solving oracle decision problems. We show that such computers can perform better by using nonorthogonal Gaussian wave functions rather than orthogonal top-hat wave functions as input to the information encoding process. Using the Deutsch-Jozsa problem as an example, we demonstrate that Gaussian modulation with optimized width parameter results in a lower error rate than for the top-hat encoding. We conclude that Gaussian modulation can allow for an improved trade-off between encoding, processing and measurement of the information.Comment: RevTeX4, 10 pages with 4 figure

Identification of a new promoter in the early region of the human papillomavirus type 16 genome

Transcription of the human papillomavirus type 16 (HPV-16) genome is controlled by several promoters; the P97 promoter is considered to be the main one. An additional promoter has been identified within the E7 ORF as well as an antisense promoter just upstream of the L2 ORF. The significance of these promoters for early and late gene expression and their activity related to cell differentiation is not known in detail. Identification of two new, previously undescribed transcription start sites at nt 542 just upstream of the E7 ORF and at nt 611 within the E7 ORF is reported. The promoter responsible for the start site at nt 542 (P542) was active in SiHa, HeLa and C33A cells. Very low promoter activity was found upstream of the nt 611 start site. The E7 protein has previously been shown to be synthesized from a polycistronic mRNA encoding both the E6 and E7 proteins under the control of the P97 promoter. The data reported in the present paper suggest that promoter P542 may control synthesis of the E7 oncoprotein from a monocistronic mRNA

Supplementary Material for: Endothelial Nitric Oxide Synthase Phosphorylation at Threonine 495 and Mitochondrial Reactive Oxygen Species Formation in Response to a High H₂O₂ Concentration

<b><i>Background:</i></b> Hydrogen peroxide (H₂O₂) is produced in vessels during ischemia/reperfusion and during inflammation, both leading to vascular dysfunction. We investigated cellular pathways involved in endothelial nitric oxide synthase (eNOS) phosphorylation at Threonine 495 (Thr⁴⁹⁵) in human umbilical vein endothelial cells (HUVECs) exposed to H₂O₂. <b><i>Methods:</i></b> HUVECs were exposed to 400 μM H₂O₂ for 30 min. Phosphorylation at Thr⁴⁹⁵ was assessed by Western blotting and reactive oxygen species (ROS) monitored by flow cytometry. Protein kinase C (PKC) pathways were investigated by pretreatment with PKC-β inhibitor ruboxistaurin or pan-PKC inhibitor GF109203X. In addition, we investigated ROCK and ERK pathways by MEKK1/2 inhibitor U0126 and ROCK inhibitor Y27632. <b><i>Results:</i></b> H₂O₂ increased eNOS phosphorylation at Thr⁴⁹⁵ (to 176% vs. control (100%), p < 0.001) along with increased mitochondrial ROS formation (from 19.7 to 45.3%, p < 0.01). This rise in phosphorylation could be prevented by U0126 and Y27632 in a dose-dependent manner, but did not result in lowered mitochondrial ROS formation. Conversely, addition of the antioxidant N-acetyl-L-cysteine only prevented mitochondrial ROS formation but did not prevent phosphorylation of eNOS Thr⁴⁹⁵. <b><i>Conclusion:</i></b> H₂O₂-mediated phosphorylation of eNOS Thr⁴⁹⁵ is mediated by ROCK and ERK activity, but not by PKC, and is uncoupled from mitochondrial ROS signaling. Furthermore, ERK inhibition increased mitochondrial ROS formation

Ordered Nucleation and Spreading of Silenced Chromatin in Saccharomyces cerevisiae

In Saccharomyces cerevisiae, silencing at the HM loci depends on Sir proteins, which are structural components of silenced chromatin. To explore the structure and assembly of silenced chromatin, the associations of Sir proteins with sequences across the HMR locus were examined by chromatin immunoprecipitation. In wild-type cells, Sir2p, Sir3p, and Sir4p were spread throughout and coincident with the silenced region at HMR. Sir1p, in contrast, associated only with the HMR-E silencer, consistent with its role in establishment but not maintenance of silencing. Sir4p was required for the association of other Sir proteins with silencers. In contrast, in the absence of Sir2p or Sir3p, partial assemblies of Sir proteins could form at silencers, where Sir protein assembly began. Spreading across HMR required Sir2p and Sir3p, as well as the deacetylase activity of Sir2p. These data support a model for the spreading of silenced chromatin involving cycles of nucleosome deacetylation by Sir2p followed by recruitment of additional Sir2p, Sir3p, and Sir4p to the newly deacetylated nucleosome. This model suggests mechanisms for boundary formation, and for maintenance and inheritance of silenced chromatin. The principles are generalizable to other types of heritable chromatin states