On the Exact Evaluation of Certain Instances of the Potts Partition Function by Quantum Computers

We present an efficient quantum algorithm for the exact evaluation of either the fully ferromagnetic or anti-ferromagnetic q-state Potts partition function Z for a family of graphs related to irreducible cyclic codes. This problem is related to the evaluation of the Jones and Tutte polynomials. We consider the connection between the weight enumerator polynomial from coding theory and Z and exploit the fact that there exists a quantum algorithm for efficiently estimating Gauss sums in order to obtain the weight enumerator for a certain class of linear codes. In this way we demonstrate that for a certain class of sparse graphs, which we call Irreducible Cyclic Cocycle Code (ICCC_\epsilon) graphs, quantum computers provide a polynomial speed up in the difference between the number of edges and vertices of the graph, and an exponential speed up in q, over the best classical algorithms known to date

Continuous right ventricular volumetry by fast-response thermodilution during right ventricular ischemia: head-to-head comparison with conductance catheter measurements.

Item does not contain fulltextOBJECTIVE: To evaluate the accuracy of right ventricular ejection fraction and right ventricular end-diastolic volume obtained by volumetric pulmonary artery catheter, using the conductance catheter as reference method. DESIGN: Prospective, comparative study. SETTING: Research laboratory of a university hospital. SUBJECTS: Seven young female German landrace pigs. INTERVENTIONS: Ligation of the distal right coronary artery to induce temporary acute ischemia. MEASUREMENTS AND MAIN RESULTS: Right ventricular ejection fraction and right ventricular end-diastolic volume were measured simultaneously with a volumetric pulmonary artery catheter and the conductance catheter technique (reference method), in an animal model of acute right ventricular ischemia. Measurements were performed at baseline, during ischemia, and during reperfusion. The methods were compared with Bland-Altman analyses and their diagnostic accuracy to detect ischemia was quantified by receiver operating characteristic curve analysis. For right ventricular ejection fraction measurements, Bland-Altman analysis indicated a bias of -9.9% indicating underestimation by pulmonary artery catheter with limits of agreement ranging from -26% to 6.1%. The data showed a trend for more underestimation at higher right ventricular ejection fraction values. For right ventricular end-diastolic volume, a bias of 31 mL, indicating overestimation by pulmonary artery catheter was found. Limits of agreement ranged from -25 mL to 88 mL. Ischemia induced a decrease in right ventricular ejection fraction and an increase in right ventricular end-diastolic volume, as expected, which was detected by conductance catheter with a significant higher diagnostic accuracy indicated by a receiver operating characteristic area under the curve of 0.98 (p 94 mL). However, diagnostic accuracy for right ventricular ejection fraction pulmonary artery catheter and end-diastolic volume pulmonary artery catheter to detect ischemia was limited with area under the curve 0.76 (p = .06) and 0.57 (p = .65), respectively. CONCLUSIONS: Accuracy of volumetric pulmonary artery catheter in conditions of right ventricular ischemia is low and inadequate for diagnosis of right ventricular ischemia and failure

Anti-ischemic effects of inotropic agents in experimental right ventricular infarction.

Contains fulltext : 80106.pdf (publisher's version ) (Closed access)BACKGROUND: Right ventricular (RV) function is an important determinant of survival after myocardial infarction. The efficacy of reperfusion therapy might be increased by the cardioprotective action of inotropic agents, which are used for symptomatic therapy in situations with compromised hemodynamics. Therefore, we used a porcine model of RV ischemia and reperfusion (IR) injury to study the influence of milrinone, levosimendan and dobutamine on the extent and degree of myocardial injury. METHODS: IR injury was induced by temporary ligation of the distal right coronary artery for 90 min, followed by 120 min of reperfusion. Treatment was initiated 30 min after coronary artery occlusion. A bolus of milrinone (n=12; 50 microg/kg) and levosimendan (n=10; 24 microg/kg) was applied in different groups, followed by continuous infusion of the drugs at 0.5 and 0.2 microg/kg/min, respectively. The effects on myocardial injury and inflammation were compared with a control (n=12) and a dobutamine group (n=10), where treatment was started with an infusion of 5 microg/kg/min. RESULTS: Milrinone and levosimendan reduced the resulting infarct size with respect to the area at risk (41.7+/-10.2%, 45.7+/-8.1%) when compared with the control group (58.3+/-6.1%). In contrast, dobutamine had no effect (55.8+/-7.7%). All drugs reduced the number of neutrophils infiltrating into the different myocardial regions and the circulating levels of interleukin-6. Increased levels of tumor necrosis factor alpha during reperfusion were only abated by milrinone and levosimendan. CONCLUSIONS: Cardioprotective properties of milrinone and levosimendan were demonstrated for the first time in a clinically relevant model of RV infarction

Comparison of 3 methods to induce acute pulmonary hypertension in pigs.

Large animal models for acute pulmonary hypertension (PHT) show distinct differences between species and underlying mechanisms. Two embolic procedures and continuous infusion of a stable thromboxane A(2) analogue (U46619) were explored for their ability to induce PHT and their effects on right ventricular function and pulmonary and systemic circulation in 9 pigs. Injection of small (100 to 200 microm) or large (355 to 425 microm) polystyrene beads and incremental dosage (0.2 to 0.8 microg kg(-1) min(-1)) of U46619 all induced PHT. However, infusion of U46619 resulted in stable PHT, whereas that after bead injection demonstrated a gradual continuous decline in pressure. This instability was most pronounced with small beads, due to right ventricular failure and consecutive circulatory collapse. Furthermore, cardiac output decreased during U46619 infusion but increased after embolization with no relevant differences in systemic pressure. This result was likely due to the more pronounced effect of U46619 on pulmonary resistance and impedance in combination with limited effects on pulmonary gas exchange. Coronary autoregulation and adaption of contractility to afterload increase was not impaired by U46619. All parameters returned to baseline values after infusion was discontinued. Continuous infusion of a thromboxane A2 analogue is an excellent method for induction of stable, acute PHT in large animal hemodynamic studies

Phosphodiesterase III inhibition affects platelet-monocyte aggregate formation depending on the axis of stimulation.

Contains fulltext : 50956.pdf (publisher's version ) (Closed access)OBJECTIVE: The purpose of this study was to investigate the effect of the phosphodiesterase (PDE) type 3 inhibitor milrinone on the adhesion of platelets to monocytes in vitro. DESIGN: Prospective study. SETTING: University experimental laboratory. PARTICIPANTS: Ten healthy volunteers. INTERVENTIONS: Whole blood was incubated with 1, 10, or 100 micromol/L of milrinone. After stimulation with N-formyl-methionyl-leucyl-phenylalanine (FMLP) or adenosine-5-diphosphate (ADP), platelet-monocyte adhesion and CD11b, PSGL-1, GPIIb/IIIa, and P-selectin expression were measured by flow cytometry. MEASUREMENTS AND RESULTS: The formation of platelet-monocyte conjugates after PDE3 inhibition depended on the type of stimulation. In unstimulated and FMLP-stimulated blood platelet monocytes, aggregation was enhanced by increasing concentrations of milrinone. This augmentation was accompanied by a rise in P-selectin expression in platelets. In ADP-stimulated blood the number of platelet-monocyte aggregates decreased with increasing concentrations of milrinone. Concurrent with the reported antiinflammatory properties of PDE-inhibition, an inhibition of CD11b expression was found in monocytes after stimulation with FMLP. In contrast, in unstimulated samples lower concentrations of milrinone caused an increase in CD11b. CONCLUSIONS: These findings suggest that the effects of PDE3 inhibition on platelets and monocytes are modified by the type of stimulation and only partially suppress the inflammatory response of platelets and monocytes. The increase in platelet-monocyte conjugates in unstimulated and FMLP-stimulated blood suggested that PDE3 inhibition may also trigger proinflammatory reactions

The effect of xenon on isoflurane protection against experimental myocardial infarction.

Contains fulltext : 81312.pdf (publisher's version ) (Closed access)OBJECTIVES: To investigate if the protective effects of xenon and isoflurane against myocardial ischemia-reperfusion damage would be additive. DESIGN: A prospective, randomized laboratory investigation. SETTING: An animal laboratory of a university hospital. PARTICIPANTS: Thirty-six pigs (female German landrace). INTERVENTIONS: In an open-chest preparation with thiopental anesthesia, the left anterior descending artery was occluded to produce ischemia for 60 minutes. One hour previously, ischemic preconditioning, isoflurane (0.55 minimum alveolar concentration [MAC]) alone, or isoflurane together with xenon (0.55 MAC each) were started in the respective groups. A fourth (control) group received no protective intervention. Myocardial ischemia was followed by 2 hours of reperfusion. MEASUREMENTS AND MAIN RESULTS: Hearts were excised and stained (Evans Blue/TTC) to measure infarct size as related to the area at risk. Myocardial infarct size was reduced (means +/- standard deviation) from 64% +/- 9% of the area at risk in the control group to 19% +/- 12% with ischemic preconditioning to 46% +/- 12% with isoflurane and to 39% +/- 13% with isoflurane and xenon. All intervention groups were significantly different from the control (p < 0.05), and both anesthetic groups were significantly different from ischemic preconditioning (p < 0.05). CONCLUSION: Combined isoflurane/xenon anesthesia reduced infarct size but not more than isoflurane alone. Ischemic preconditioning was more effective than the anesthetics

Xenon and isoflurane improved biventricular function during right ventricular ischemia and reperfusion.

Contains fulltext : 87447.pdf (publisher's version ) (Closed access)BACKGROUND: Although anesthetics have some cardioprotective properties, these benefits are often counterbalanced by their negative inotropic effects. Xenon, on the other hand, does not influence myocardial contractility. Thus, xenon may be a superior treatment for the maintenance of global hemodynamics, especially during right ventricular ischemia, which is generally characterized by a high acute complication rate. METHODS: The effects of 70 vol% xenon and 0.9 vol% isoflurane on biventricular function were assessed in a porcine model (n=36) using the conductance catheter technique, and the expression of the type B natriuretic peptide (BNP) gene was measured. The animals underwent 90 min of right ventricular ischemia followed by 120 min of reperfusion. A barbiturate-anesthetized group was included as a control. RESULTS: Cardiac output was compromised in unprotected animals during ischemia by 33+/-18% and during reperfusion by 53+/-17%. This was mainly due to impaired contractility in the left ventricle (LV) and increased stiffness. Isoflurane attenuated the increase in stiffness and resulted in a higher preload. In contrast, xenon increased the right ventricular afterload, which was compensated by an increase in contractility. Its effects on diastolic function were less pronounced. Upregulation of BNP mRNA expression was impeded in the remote area of the LV by both isoflurane and xenon. CONCLUSIONS: Xenon and isoflurane demonstrated equipotent effects in preventing the hemodynamic compromise that is induced by right ventricular ischemia and reperfusion, although they acted through somewhat differential inotropic and vasodilatory effects.1 april 201