326 research outputs found

    Quantum Circuits for General Multiqubit Gates

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    We consider a generic elementary gate sequence which is needed to implement a general quantum gate acting on n qubits -- a unitary transformation with 4^n degrees of freedom. For synthesizing the gate sequence, a method based on the so-called cosine-sine matrix decomposition is presented. The result is optimal in the number of elementary one-qubit gates, 4^n, and scales more favorably than the previously reported decompositions requiring 4^n-2^n+1 controlled NOT gates.Comment: 4 pages, 3 figure

    Quantum circuits with uniformly controlled one-qubit gates

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    Uniformly controlled one-qubit gates are quantum gates which can be represented as direct sums of two-dimensional unitary operators acting on a single qubit. We present a quantum gate array which implements any n-qubit gate of this type using at most 2^{n-1} - 1 controlled-NOT gates, 2^{n-1} one-qubit gates and a single diagonal n-qubit gate. The circuit is based on the so-called quantum multiplexor, for which we provide a modified construction. We illustrate the versatility of these gates by applying them to the decomposition of a general n-qubit gate and a local state preparation procedure. Moreover, we study their implementation using only nearest-neighbor gates. We give upper bounds for the one-qubit and controlled-NOT gate counts for all the aforementioned applications. In all four cases, the proposed circuit topologies either improve on or achieve the previously reported upper bounds for the gate counts. Thus, they provide the most efficient method for general gate decompositions currently known.Comment: 8 pages, 10 figures. v2 has simpler notation and sharpens some result

    Genetic support for the causal role of insulin in coronary heart disease

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    Epidemiological studies have identified several traits associated with CHD, but few of these have been shown to be causal risk factors and thus suitable targets for treatment. Our aim was to evaluate the causal role of a large set of known CHD risk factors using single-nucleotide polymorphisms (SNPs) as instrumental variables.Peer reviewe

    Slow-Release Urea as a Sustainable Alternative to Soybean Meal in Ruminant Nutrition

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    Three experiments were conducted to evaluate the feasibility of using a commercial slow-release urea product (SRU; Optigen®, Alltech Inc., Nicholasville, KY, USA) as a partial replacement for vegetable protein sources in cattle diets. The first experiment was an in vitro rumen fermentation that evaluated the effect of replacing soybean meal (SBM) nitrogen with nitrogen from either SRU or free urea in diets varying in forage:concentrate ratios. The second experiment examined the effect of replacing SBM with SRU on in situ dry matter and nitrogen degradability in the rumen. In the third experiment, a feeding trial was conducted to evaluate the effect of replacing SBM (0% as-fed SRU) with 1% or 3% as-fed SRU on feed carbon footprint (CFP; total greenhouse gas emissions associated with the life cycle of feed raw materials) and the toxicity potential of SRU in growing beef cattle. Results showed that replacing SBM with SRU up to 1.3% did not negatively affect in vitro rumen fermentation parameters. Supplementing SRU favourably decreased ruminal accumulation of ammonia and lactic acid when compared to free urea. There was no significant effect on effective rumen degradability of dry matter and nitrogen when one-third of SBM was replaced by SRU in the in situ study. Compared with the 0% SRU diet, feed CFP decreased by 18% and 54% in 1% SRU and 3% SRU diets, respectively. Additionally, feeding up to 3% SRU diet to beef cattle did not affect health and intake, and blood hematological and biochemical indices were within the physiological range for healthy bulls, suggesting no indication of ammonia toxicity. Overall, these results indicate that SRU can be used as a sustainable alternative to partially replace vegetable protein sources in ruminant diets without compromising rumen function and health of ruminants.info:eu-repo/semantics/publishedVersio

    Endotoxemia is associated with an adverse metabolic profile

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    Our aim was to analyze whether endotoxemia, i.e. translocation of LPS to circulation, is reflected in the serum metabolic profile in a general population and in participants with cardiometabolic disorders. We investigated three Finnish cohorts separately and in a meta-analysis (n = 7178), namely population-based FINRISK97, FinnTwin16 consisting of young adult twins, and Parogene, a random cohort of cardiac patients. Endotoxemia was determined as serum LPS activity and metabolome by an NMR platform. Potential effects of body mass index (BMI), smoking, metabolic syndrome (MetS), and coronary heart disease (CHD) status were considered. Endotoxemia was directly associated with concentrations of VLDL, IDL, LDL, and small HDL lipoproteins, VLDL particle diameter, total fatty acids (FA), glycoprotein acetyls (GlycA), aromatic and branched-chain amino acids, and Glc, and inversely associated with concentration of large HDL, diameters of LDL and HDL, as well as unsaturation degree of FAs. Some of these disadvantageous associations were significantly stronger in smokers and subjects with high BMI, but did not differ between participants with different CHD status. In participants with MetS, however, the associations of endotoxemia with FA parameters and GlycA were particularly strong. The metabolic profile in endotoxemia appears highly adverse, involving several inflammatory characters and risk factors for cardiometabolic disorders.Peer reviewe

    ANGPTL8 protein-truncating variant associated with lower serum triglycerides and risk of coronary disease

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    Protein-truncating variants (PTVs) affecting dyslipidemia risk may point to therapeutic targets for cardiometabolic disease. Our objective was to identify PTVs that were associated with both lipid levels and the risk of coronary artery disease (CAD) or type 2 diabetes (T2D) and assess their possible associations with risks of other diseases. To achieve this aim, we leveraged the enrichment of PTVs in the Finnish population and tested the association of low-frequency PTVs in 1,209 genes with serum lipid levels in the Finrisk Study (n = 23,435). We then tested which of the lipid-associated PTVs were also associated with the risks of T2D or CAD, as well as 2,683 disease endpoints curated in the FinnGen Study (n = 218,792). Two PTVs were associated with both lipid levels and the risk of CAD or T2D: triglyceride-lowering variants in ANGPTL8 (-24.0[-30.4 to -16.9] mg/dL per rs760351239-T allele, P = 3.4 x 10(-9)) and ANGPTL4 (-14.4[-18.6 to -9.8] mg/dL per rs746226153-G allele, P = 4.3 x 10(-9)). The risk of T2D was lower in carriers of the ANGPTL4 PTV (OR = 0.70[0.60-0.81], P = 2.2 x 10(-6)) than noncarriers. The odds of CAD were 47% lower in carriers of a PTV in ANGPTL8 (OR = 0.53[0.37-0.76], P = 4.5 x 10(-4)) than noncarriers. Finally, the phenome-wide scan of the ANGPTL8 PTV showed that the ANGPTL8 PTV carriers were less likely to use statin therapy (68,782 cases, OR = 0.52[0.40-0.68], P = 1.7 x 10(-6)) compared to noncarriers. Our findings provide genetic evidence of potential long-term efficacy and safety of therapeutic targeting of dyslipidemias. Author summary Studying the health impacts of protein-truncating variants (PTVs) enables detecting the health impact of drugs that inhibit these same genes. Our study aimed to expand our knowledge of genes associated with cardiometabolic disease, along with the side effects of these genes. To detect PTVs associated with cardiometabolic disease, we first performed a genome-wide scan of PTVs associated with serum lipid levels in Finns. We found PTVs in two genes highly enriched in Finns, which were associated with both serum lipid levels and a lower risk of type 2 diabetes or coronary artery disease: ANGPTL4 and ANGPTL8. To evaluate the other health effects of these PTVs, we performed an association scan between the PTVs and 2,683 disease endpoints curated in the FinnGen Study (n = 218,792). We demonstrate that using human populations with PTV-enrichment, such as Finns, offers considerable boosts in statistical power to detect potential long-term efficacy and safety of pharmacologically targeting genes.Peer reviewe

    Low MMP-8/TIMP-1 reflects left ventricle impairment in takotsubo cardiomyopathy and high TIM P-1 may help to differentiate it from acute coronary syndrome

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    Background Matrix metalloproteinase 8 (MMP-8) is the most potent type-I collagen protease. Such collagen mainly constitutes the transient fibrosis in takotsubo cardiomyopathy (TTC) endomyocardial biopsies. High MMP-8 and tissue-inhibitor of matrix metalloproteinase-1 (TIMP-1) levels are implicated in acute coronary syndrome (ACS). We compared MMP-8 and TIM P-1 levels in consecutive TTC and ACS patients, and their association to TTC severity. Methods and results In 45 acute serum samples of TTC, 2072 ACS and 1000 controls, TI MP-1 differed between ACS 146.7ng/mL (115.0-186.3) (median (interquartile range)), TTC 115.7 (94.3-137.7) and controls 80.9 (73.2-90.4), (p Conclusions Even with other differing factors considered, TIMP-1 differentiated TTC from ACS better than TnT. In TTC, the low MMP-8/TIM P-1 molar ratio may reflect decreased proteolysis and increased transient fibrosis, perhaps in part explaining the left-ventricle impairment.Peer reviewe
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