Distributed Hypothesis Testing with Privacy Constraints

We revisit the distributed hypothesis testing (or hypothesis testing with communication constraints) problem from the viewpoint of privacy. Instead of observing the raw data directly, the transmitter observes a sanitized or randomized version of it. We impose an upper bound on the mutual information between the raw and randomized data. Under this scenario, the receiver, which is also provided with side information, is required to make a decision on whether the null or alternative hypothesis is in effect. We first provide a general lower bound on the type-II exponent for an arbitrary pair of hypotheses. Next, we show that if the distribution under the alternative hypothesis is the product of the marginals of the distribution under the null (i.e., testing against independence), then the exponent is known exactly. Moreover, we show that the strong converse property holds. Using ideas from Euclidean information theory, we also provide an approximate expression for the exponent when the communication rate is low and the privacy level is high. Finally, we illustrate our results with a binary and a Gaussian example

An Alphabet of Leakage Measures

We introduce a family of information leakage measures called maximal $\alpha,\beta$-leakage, parameterized by real numbers $\alpha$ and $\beta$. The measure is formalized via an operational definition involving an adversary guessing an unknown function of the data given the released data. We obtain a simple, computable expression for the measure and show that it satisfies several basic properties such as monotonicity in $\beta$ for a fixed $\alpha$, non-negativity, data processing inequalities, and additivity over independent releases. Finally, we highlight the relevance of this family by showing that it bridges several known leakage measures, including maximal $\alpha$-leakage $(\beta=1)$, maximal leakage $(\alpha=\infty,\beta=1)$, local differential privacy $(\alpha=\infty,\beta=\infty)$, and local Renyi differential privacy $(\alpha=\beta)$

Investigating possible effects of aryl hydrocarbon receptor G1661A polymorphism on asthma severity in adults

311-319Aryl hydrocarbon Receptor (AhR) is a ligand-activated transcription factor with an important role in lung health. The association of AhR polymorphisms with asthma severity has not been yet investigated. We analyzed the association of G1661A, the most prevalent polymorphism of AhR, with the asthma stages in a population-based study including 555 asthmatics (Intermittent: 93, Mild: 240, Moderate: 158, and Severe: 64). The SNP was genotyped using allele-specific PCR. Obtained data were analyzed using the Generalized-Ordered Logit Estimates. Genotypes GA (OR: 0.53, CI: 0.32-0.90, P=0.019) and AA (OR: 0.22, CI: 0.06-0.76, P=0.017) were associated with decreased risk of Severe, Moderate, Mild vs. Intermittent stage; and Severe, Moderate, vs. Mild, Intermittent stages respectively. However, Genotype GA (OR: 1.90, CI: 1.05-3.44, P=0.033), dominant model GA+AA (OR: 2.04, CI: 1.17-3.57, P=0.012), and allele A (OR: 1.68, CI: 1.06-2.66, P=0.027) were associated with increased risk of Severe stage vs. Moderate, Mild, Intermittent stages. Also, male sex and higher age were associated with an increased odds ratio for severe asthma. Furthermore, significant associations with asthma stages were found for the interactions of the SNP and sex, smoking, and alcohol consumption. In conclusion, we revealed that the mutant allele of AhR-G1661A may interact with independent variables and act as a protective factor against lower stages of asthma but it may increase the risk of severe asthma

Liquid Phase Equilibria of Aqueous Mixtures of Carboxylic Acids (C₁–C₄) with Ethylbenzene: Thermodynamic and Mathematical Modeling

Liquid–liquid equilibrium (LLE) data were experimentally determined and correlated for the aqueous solutions of a series of carboxylic acids (i.e., formic, acetic, propionic, and butyric acids) with ethylbenzene at a temperature of 298.15 K and <i>p</i> = 101.32 kPa. The ternary mixtures containing of the acids exhibit type-1 LLE behavior. The quality of the observed tie-lines was checked using the Othmer–Tobias equation. The correlations were carried out using the thermodynamic and statistical modeling. The activity coefficient models of UNIQUAC and NRTL were applied to fit the tie lines and values of the binary interaction parameters between each pair of components were obtained. The correlation of the tie lines was also carried out by a GMDH type-NN, which are in agreement with those obtained experimentally. In this work, experimental distribution coefficients and separation factors were estimated. Moreover, the Kamlet–Taft LSER model was employed to correlate these quantities and was interpreted in terms of intermolecular interactions

Evaluation of intracellular anion superoxide level, heat shock protein A2 and protamine positive spermatozoa percentages in teratoasthenozoospermia

Background: Teratoasthenozoospermia (TA) is a severe form of male infertility with no clear etiology. Objective: To compare the level of intracellular anion superoxide (O2–), heat shock protein A2 (HSPA2) and protamine deficiencies in ejaculated spermatozoa between teratoasthenozoospermic and normozoospermic men. Materials and Methods: In this case- control study, semen samples of 20 infertile men, with TA (with normal morphology lower than 4%_ and total motility lower than 40% ) as the case group and 20 normozoospermic fertile men as the control group were evaluated for intracellular O2 – and HSPA2 by flow cytometry and protamine deficiency by Chromomycin A3 (CMA3) test. Results: The rate of CMA3+ spermatozoa in the case group was higher than controls (p=0.001). The percentages of HSPA2+ spermatozoa in the cases were significantly lower than controls (p=0.001). Also, intracellular O2 – levels in the case group were significantly higher than controls (p=0.001) and had positive correlations with sperm apoptosis (r=0.79, p=0.01) and CMA3 positive sperm (r=0.76, p=0.01), but negative correlations with normal morphology (r=-0.81, p=0.01) and motility (r=-0.81, p=0.01). There was no significant correlation between intracellular O2 – and HSPA2 in the case group (r=0.041, p=0.79). Conclusion: We suggest that the increase in intracellular O2 –, decrease in spermatozoa HSPA2+, and high percentages of spermatozoa with immature chromatin might be considered as etiologies of infertility in TA patient

Investigating possible effects of aryl hydrocarbon receptor G1661A polymorphism on asthma severity in adults

Aryl hydrocarbon Receptor (AhR) is a ligand-activated transcription factor with an important role in lung health. The association of AhR polymorphisms with asthma severity has not been yet investigated. We analyzed the association of G1661A, the most prevalent polymorphism of AhR, with the asthma stages in a population-based study including 555 asthmatics (Intermittent: 93, Mild: 240, Moderate: 158, and Severe: 64). The SNP was genotyped using allele-specific PCR. Obtained data were analyzed using the Generalized-Ordered Logit Estimates. Genotypes GA (OR: 0.53, CI: 0.32-0.90, P=0.019) and AA (OR: 0.22, CI: 0.06-0.76, P=0.017) were associated with decreased risk of Severe, Moderate, Mild vs. Intermittent stage; and Severe, Moderate, vs. Mild, Intermittent stages respectively. However, Genotype GA (OR: 1.90, CI: 1.05-3.44, P=0.033), dominant model GA+AA (OR: 2.04, CI: 1.17-3.57, P=0.012), and allele A (OR: 1.68, CI: 1.06-2.66, P=0.027) were associated with increased risk of Severe stage vs. Moderate, Mild, Intermittent stages. Also, male sex and higher age were associated with an increased odds ratio for severe asthma. Furthermore, significant associations with asthma stages were found for the interactions of the SNP and sex, smoking, and alcohol consumption. In conclusion, we revealed that the mutant allele of AhR-G1661A may interact with independent variables and act as a protective factor against lower stages of asthma but it may increase the risk of severe asthma