Efficient universal quantum computation with auxiliary Hilbert space

We propose a scheme to construct the efficient universal quantum circuit for qubit systems with the assistance of possibly available auxiliary Hilbert spaces. An elementary two-ququart gate, termed the controlled-double-NOT gate, is proposed first in ququart (four-level) systems, and its physical implementation is illustrated in the four-dimensional Hilbert spaces built by the path and polarization states of photons. Then an efficient universal quantum circuit for ququart systems is constructed using the gate and the quantum Shannon decomposition method. By introducing auxiliary two-dimensional Hilbert spaces, the universal quantum circuit for qubit systems is finally achieved using the result obtained in ququart systems with the lowest complexity

Functional role of the spatial proximity of Asp114(2.50) in TMH 2 and Asn332(7.49) in TMH 7 of the μ opioid receptor

AbstractWe examined whether a proposed spatial proximity between Asp114(2.50) and Asn332(7.49) affected the functional properties of the μ opioid receptor. The D114(2.50)N mutant had reduced binding affinities for morphine, DAMGO and CTAP, but not for naloxone and [3H]diprenorphine; this mutation also abolished agonist-induced increase in [35S]GTPγS binding. The N332(7.49)D mutation eliminated detectable binding of either [3H]diprenorphine or [3H]DAMGO. The combined D114(2.50)N-N332(7.49)D mutation restored high affinity binding for [3H]diprenorphine, CTAP and naloxone, and restored partially the binding affinities, potencies and efficacies of morphine and DAMGO. Thus, reciprocal mutations of Asp114(2.50) and Asn332(7.49) compensate for the detrimental effects of the single mutations, indicating that the residues are adjacent in space and that their chemical functionalities are important for ligand binding and receptor activation

Lepton Flavor Violating Muon Decays in a Model of Electroweak-Scale Right-Handed Neutrinos

The small neutrino mass observed in neutrino oscillations is nicely explained by the seesaw mechanism. Rich phenomenology is generally expected if the heavy neutrinos are not much heavier than the electroweak scale. A model with this feature built in has been suggested recently by Hung. The model keeps the standard gauge group but introduces chirality-flipped partners for the fermions. In particular, a right-handed neutrino forms a weak doublet with a charged heavy lepton, and is thus active. We analyze the lepton flavor structure in gauge interactions. The mixing matrices in charged currents (CC) are generally non-unitary, and their deviation from unitarity induces flavor changing neutral currents (FCNC). We calculate the branching ratios for the rare decays \mu\to e\gamma and \mu\to ee\bar e due to the gauge interactions. Although the former is generally smaller than the latter by three orders of magnitude, parameter regions exist in which \mu\to e\gamma is reachable in the next generation of experiments even if the current stringent bound on \mu\to ee\bar e is taken into account. If light neutrinos dominate for \mu\to e\gamma, the latter cannot set a meaningful bound on unitarity violation in the mixing matrix of light leptons due to significant cancelation between CC and FCNC contributions. Instead, the role is taken over by the decay \mu\to ee\bar e.Comment: 11 pages, 2 figures. v2: added 2 refs and improved a comment on previous work; no other changes. v3: proofread version for PLB; added a few clarifying sentences in paragraph before eq (17) plus minor editting change

Identification and Characterization of \u3cem\u3eOGG1\u3c/em\u3e Mutations in Patients with Alzheimer\u27s Disease

Patients with Alzheimer\u27s disease (AD) exhibit higher levels of 8-oxo-guanine (8-oxoG) DNA lesions in their brain, suggesting a reduced or defective 8-oxoG repair. To test this hypothesis, this study investigated 14 AD patients and 10 age-matched controls for mutations of the major 8-oxoG removal gene OGG1. Whereas no alterations were detected in any control samples, four AD patients exhibited mutations in OGG1, two carried a common single base (C796) deletion that alters the carboxyl terminal sequence of OGG1, and the other two had nucleotide alterations leading to single amino acid substitutions. In vitro biochemical assays revealed that the protein encoded by the C796-deleted OGG1 completely lost its 8-oxoG glycosylase activity, and that the two single residue-substituted OGG1 proteins showed a significant reduction in the glycosylase activity. These results were consistent with the fact that nuclear extracts derived from a limited number of AD patients with OGG1 mutations exhibited greatly reduced 8-oxoG glycosylase activity compared with age-matched controls and AD patients without OGG1 alterations. Our findings suggest that defects in OGG1 may be important in the pathogenesis of AD in a significant fraction of AD patients and provide new insight into the molecular basis for the disease

The Effect of Smart Device Usage Among the Undergraduate’s Towards Academic Performance

Almost all students at higher education institutions are now inseparably linked to their smart devices and have become increasingly reliant on them. So, the question of whether these devices can assist them to improve their academic performance or at least gain various benefits that improve the quality of learning through it arises. Therefore, the purpose of this study was to examine if there a relationship between smart device usage and academic performance among undergraduates’ in Universiti Utara Malaysia. The study employed quantitative method with a cross sectional time horizon and online survey with Google forms. A total of 473 students involved in the study, and the data was analysed using statistical software. The findings reveal there was a relationship between students' use of smart gadgets and their academic performance. Among the examples of such relationships are, addiction to using smart devices causes academic performance can decline. While the sharing of information and communication among students through the utilization of smart devices on the other hand can improve academic performance. Consequently, there are still negative matters related to these smart devices if they are obsessed with it without advisable self-control. So, there may be programs that can be organized by the university to manage this so as not to harm students’ health, social relationships, and weakening their academic achievement

Mitochondrial DNA Copy Number Is Associated with Breast Cancer Risk

Mitochondrial DNA (mtDNA) copy number in peripheral blood is associated with increased risk of several cancers. However, data from prospective studies on mtDNA copy number and breast cancer risk are lacking. We evaluated the association between mtDNA copy number in peripheral blood and breast cancer risk in a nested case-control study of 183 breast cancer cases with pre-diagnostic blood samples and 529 individually matched controls among participants of the Singapore Chinese Health Study. The mtDNA copy number was measured using real time PCR. Conditional logistic regression analyses showed that there was an overall positive association between mtDNA copy number and breast cancer risk (Ptrend = 0.01). The elevated risk for higher mtDNA copy numbers was primarily seen for women with <3 years between blood draw and cancer diagnosis; ORs (95% CIs) for 2nd, 3rd, 4th, and 5th quintile of mtDNA copy number were 1.52 (0.61, 3.82), 2.52 (1.03, 6.12), 3.12 (1.31, 7.43), and 3.06 (1.25, 7.47), respectively, compared with the 1st quintile (Ptrend = 0.004). There was no association between mtDNA copy number and breast cancer risk among women who donated a blood sample ≥3 years before breast cancer diagnosis (Ptrend = 0.41). This study supports a prospective association between increased mtDNA copy number and breast cancer risk that is dependent on the time interval between blood collection and breast cancer diagnosis. Future studies are warranted to confirm these findings and to elucidate the biological role of mtDNA copy number in breast cancer risk. © 2013 Thyagarajan et al

The liver-enriched transcription factor CREB-H is a growth suppressor protein underexpressed in hepatocellular carcinoma

We have previously characterized transcription factor LZIP to be a growth suppressor targeted by hepatitis C virus oncoprotein. In search of proteins closely related to LZIP, we have identified a liver-enriched transcription factor CREB-H. LZIP and CREB-H represent a new subfamily of bZIP factors. CREB-H activates transcription by binding to cAMP responsive element, box B, and ATF6-binding element. Interestingly, CREB-H has a putative transmembrane (TM) domain and it localizes ambiently to the endoplasmic reticulum. Proteolytic cleavage that removes the TM domain leads to nuclear translocation and activation of CREB-H. CREB-H activates the promoter of hepatic gluconeogenic enzyme phosphoenolpyruvate carboxykinase. This activation can be further stimulated by cAMP and protein kinase A. CREB-H transcript is exclusively abundant in adult liver. In contrast, the expression of CREB-H mRNA is aberrantly reduced in hepatoma tissues and cells. The enforced expression of CREB-H suppresses the proliferation of cultured hepatoma cells. Taken together, our findings suggest that the liver-enriched bZIP transcription factor CREB-H is a growth suppressor that plays a role in hepatic physiology and pathology