Converting of Boolean Expression to Linear Equations, Inequalities and QUBO Penalties for Cryptanalysis

There exists a wide range of constraint programming (CP) problems defined on Boolean functions depending on binary variables. One of the approaches to solving CP problems is using specific appropriate solvers, e.g., SAT solvers. An alternative is using the generic solvers for mixed-integer linear programming problems (MILP), but they require transforming expressions with Boolean functions to linear equations or inequalities. Here, we present two methods of such a transformation which applies to any Boolean function defined by explicit rules giving values of the Boolean function for all combinations of its Boolean variables. The first method represents the Boolean function as a linear equation in the original binary variables and, possibly, binary ancillaries, which become additional variables of the MILP problem being composed. The second method represents the Boolean function as a set of linear inequalities in the original binary variables and one additional continuous variable (representing the value of the function). The choice between the first or second method is a trade-off between the number of binary variables and number of linear constraints in the emerging MP problem. The advantage of the proposed approach is that both methods reduce important cryptanalysis problems, such as the preimaging of hash functions or breaking symmetric ciphers as the MILP problems, which are solved by the generic MILP solvers. Furthermore, the first method enables to reduce the binary linear equations to quadratic unconstrained binary optimization (QUBO), by the quantum annealer, e.g., D-Wave

The Loss of Myocardial Benefit following Ischemic Preconditioning Is Associated with Dysregulation of Iron Homeostasis in Diet-Induced Diabetes

<div><p>Whether the diabetic heart benefits from ischemic preconditioning (IPC), similar to the non-diabetic heart, is a subject of controversy. We recently proposed new roles for iron and ferritin in IPC-protection in Type 1-like streptozotocin-induced diabetic rat heart. Here, we investigated iron homeostasis in Cohen diabetic sensitive rat (CDs) that develop hyperglycemia when fed on a high-sucrose/low-copper diet (HSD), but maintain normoglycemia on regular-diet (RD). Control Cohen-resistant rats (CDr) maintain normoglycemia on either diet. The IPC procedure improved the post-ischemic recovery of normoglycemic hearts (CDr-RD, CDr-HSD and CDs-RD). CDs-HSD hearts failed to show IPC-associated protection. The recovery of these CDs-HSD hearts following I/R (without prior IPC) was better than their RD controls. During IPC ferritin levels increased in normoglycemic hearts, and its level was maintained nearly constant during the subsequent prolonged ischemia, but decayed to its baseline level during the reperfusion phase. In CDs-HSD hearts the baseline levels of ferritin and ferritin-saturation with iron were notably higher than in the controls, and remained unchanged during the entire experiment. This unique and abnormal pattern of post-ischemic recovery of CDs-HSD hearts is associated with marked changes in myocardial iron homeostasis, and suggests that iron and iron-proteins play a causative role/s in the etiology of diabetes-associated cardiovascular disorders.</p></div

The Bitter Fate of the Sweet Heart: Impairment of Iron Homeostasis in Diabetic Heart Leads to Failure in Myocardial Protection by Preconditioning

<div><p>Cardiovascular dysfunction is a major complication of diabetes. Examining mechanistic aspects underlying the incapacity of the diabetic heart to respond to ischemic preconditioning (IPC), we could show that the alterations in iron homeostasis can explain this phenomenon. Correlating the hemodynamic parameters with levels of ferritin, the main iron storage and detoxifying protein, without and with inhibitors of protein degradation, substantiated this explanation. Diabetic hearts were less sensitive to ischemia-reperfusion stress, as indicated by functional parameters and histology. Mechanistically, since ferritin has been shown to provide cellular protection against insults, including ischemia-reperfusion stress and as the basal ferritin level in diabetic heart was 2-fold higher than in controls, these are in accord with the greater resistance of the diabetic heart to ischemia-reperfusion. Additionally, during ischemia-reperfusion, preceded by IPC, a rapid and extensive loss in ferritin levels, during the prolonged ischemia, in diabetic heart but not in non-diabetic controls, provide additional substantiation to the explanation for loss of respond to IPC. Current research is shedding light on the mechanism behind ferritin degradation as well, suggesting a novel explanation for diabetes-induced loss of cardioprotection.</p> </div

Hemodynamic parameters of the rats' hearts before and after I/R with and without prior IPC.

<p>Hemodynamic parameters of the rats' hearts before and after I/R with and without prior IPC.</p

The levels of H-ferritin mRNA in Cohen rats subjected to IPC+I/R protocol.

<p>The levels of ferritin H-subunit mRNA (RQ) in hearts of Cohen diabetes-resistant and Cohen diabetes-sensitive rats' (A and B, respectively) when fed on HSD or RD, and subjected to IPC followed by I/R. Actin was used as a house-keeping gene. In the current experiments the measurements were performed at the end of the stabilization phase (10 min), followed by the end of IPC procedure (+15 min), completion of ischemia (+35 min) and end of reperfusion (+60 min). mRNA levels of H-subunit of ferritin were quantified by qRT-PCR. Means ± SEM are shown. *—denotes p < 0.05 <i>vs</i>. Perfusion (baseline) value of the same group.</p

The Loss of Myocardial Benefit following Ischemic Preconditioning Is Associated with Dysregulation of Iron Homeostasis in Diet-Induced Diabetes - Fig 1

<p><b>Three basic experimental protocols (A) and post-ischemic recovery of the WI (B and C).</b> (A) (i) IPC followed by I/R (upper bar); ii) I/R (middle bar); and (iii) continuous perfusion (lower bar). (B and C) Post-ischemic recovery of WI for hearts from Cohen diabetes-resistant (CDr) rats (Panel 1B) and Cohen diabetes-sensitive rats (CDs) (Panel 1C), subjected to I/R without and with prior IPC. Animals were fed on either high sucrose/low copper diet (HSD) or regular (RD) diets. WI was calculated as the product of the Developed Pressure x Heart Rate (DP*HR). The degree of cardioprotection was expressed by as percent (%) ratio of two values: WI at the 120^th minute (completion of the reperfusion phase) and WI at 10^th minute (the last minute of the stabilization phase). Mean ± SEM values are shown; <b>*</b>—p<0.05 in IPC+I/R <i>versus</i> I/R in CDs-RD; ^<b>#</b>—p<0.05 in IPC+I/R <i>versus</i> I/R in CDr-HSD; ^<b>‡</b>—p<0.05 in IPC+I/R <i>versus</i> I/R in CDr-RD.</p

Ferritin levels in hearts of Cohen rats.

<p>Ferritin levels in hearts from Cohen diabetes-resistant rats (CDr) (Panel A) and Cohen diabetes-sensitive (CDs) (Panel B), fed on either high sucrose diet (HSD) or regular diet (RD) and subjected to IPC+I/R protocol. In these experiments hearts were stabilized (10 min), followed by the IPC procedure (15 min), ischemia (35 min) and reperfusion (60 min). Ferritin concentration was measured using ELISA. Means ± SEM are shown. <b>*</b>—denotes p < 0.05 <i>versus</i> Perfusion for the same subgroup.</p

Resonant Oscillations of Josephson Current in Nb-Bi2Te2.3Se0.7-Nb Junctions

Josephson proximity junctions and devices employing topological insulators are promising candidates for realizing topological superconductivity and topologically protected quantum circuits. Here, the new type of oscillations of the critical Josephson current in the ballistic Nb-Bi2Te2.3Se0.7-Nb junctions subject to the magnetic fields is reported. The oscillations appear below ≈400 mK and have a very unusual sharp-peaked shape. Their ultra-short period ≈1 Oe, by orders of magnitude shorter than the expected periodicity due to fluxoid quantization in the device, corresponds to the extremely low energy scale ≈1 (Formula presented.) eV. It is established that the observed effect is due to the resonant transmission of Andreev quasiparticles via the peculiar energy levels forming near the S-TI interfaces

Zn/Ga−DFO iron–chelating complex attenuates the inflammatory process in a mouse model of asthma

Background: Redox-active iron, a catalyst in the production of hydroxyl radicals via the Fenton reaction, is one of the key participants in ROS-induced tissue injury and general inflammation. According to our recent findings, an excess of tissue iron is involved in several airway-related pathologies such as nasal polyposis and asthma. Objective: To examine the anti-inflammatory properties of a newly developed specific iron–chelating complex, Zn/Ga−DFO, in a mouse model of asthma. Materials and methods: Asthma was induced in BALBc mice by ovalbumin, using aluminum hydroxide as an adjuvant. Mice were divided into four groups: (i) control, (ii) asthmatic and sham-treated, (iii) asthmatic treated with Zn/Ga−DFO [intra-peritoneally (i/p) and intra-nasally (i/n)], and (iv) asthmatic treated with Zn/Ga−DFO, i/n only. Lung histology and cytology were examined. Biochemical analysis of pulmonary levels of ferritin and iron-saturated ferritin was conducted. Results: The amount of neutrophils and eosinophils in bronchoalveolar lavage fluid, goblet cell hyperplasia, mucus secretion, and peri-bronchial edema, showed markedly better values in both asthmatic-treated groups compared to the asthmatic non-treated group. The non-treated asthmatic group showed elevated ferritin levels, while in the two treated groups it returned to baseline levels. Interestingly, i/n-treatment demonstrated a more profound effect alone than in a combination with i/p injections. Conclusion: In this mouse model of allergic asthma, Zn/Ga−DFO attenuated allergic airway inflammation. The beneficial effects of treatment were in accord with iron overload abatement in asthmatic lungs by Zn/Ga−DFO. The findings in both cellular and tissue levels supported the existence of a significant anti-inflammatory effect of Zn/Ga−DFO

Crescimento de diamante dopado com Boro para eletrodos de uso em eletroquímica

<abstract language="eng">Boron-doped polycrystalline diamond films have been deposited over silicon substrate by hot-filament chemical-vapor-deposition process. A gas mixture of 0,5 vol. % methane and 1 vol. % methanol on hydrogen at a pressure of 50 Torr, have been used. Boric oxide dissolved in methanol have been used as the boron doping source during the diamond growth process. Raman spectroscopy and Scanning Electron Microscopy (SEM) have been performed on the samples. A change of Raman spectra with film doping was observed. The diamond characteristic line at 1333 cm-1 down shifted and its intensity decreased as the film resistivity decreased. On the other hand, a broad peak around 1220 cm-1 appeared and its intensity increased with decreasing film resistivity. No modifications on films morphology have been observed with different boron doping level. The grains were well-faceted with 2 <FONT FACE="Symbol">m</font>m average siz