On N = 2 Truncations of IIB on T^{1,1}

We study the N=4 gauged supergravity theory which arises from the consistent truncation of IIB supergravity on the coset T^{1,1}. We analyze three N=2 subsectors and in particular we clarify the relationship between true superpotentials for gauged supergravity and certain fake superpotentials which have been widely used in the literature. We derive a superpotential for the general reduction of type I supergravity on T^{1,1} and this together with a certain solution generating symmetry is tantamount to a superpotential for the baryonic branch of the Klebanov-Strassler solution.Comment: 32 pages, v2:references adde

Cytochrome P450 1A2 (CYP1A2) activity, mammographic density, and oxidative stress: a cross-sectional study

INTRODUCTION: Mammographically dense breast tissue is a strong predictor of breast cancer risk, and is influenced by both mitogens and mutagens. One enzyme that is able to affect both the mitogenic and mutagenic characteristics of estrogens is cytochrome P450 1A2 (CYP1A2), which is principally responsible for the metabolism of 17β-estradiol. METHODS: In a cross-sectional study of 146 premenopausal and 149 postmenopausal women, we examined the relationships between CYP1A2 activity, malondialdehyde (MDA) levels, and mammographic density. In vivo CYP1A2 activity was assessed by measuring caffeine metabolites in urine. Levels of serum and urinary MDA, and MDA–deoxyguanosine adducts in DNA were measured. Mammograms were digitized and measured using a computer-assisted method. RESULTS: CYP1A2 activity in postmenopausal women, but not in premenopausal women, was positively associated with mammographic density, suggesting that increased CYP1A2 activity after the menopause is a risk factor for breast cancer. In premenopausal women, but not in postmenopausal women, CYP1A2 activity was positively associated with serum and urinary MDA levels; there was also some evidence that CYP1A2 activity was more positively associated with percentage breast density when MDA levels were high, and more negatively associated with percentage breast density when MDA levels were low. CONCLUSION: These findings provide further evidence that variation in the activity level of enzymes involved in estrogen metabolism is related to levels of mammographic density and potentially to breast cancer risk

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Gaussian approximation for the downlink interference in heterogeneous cellular networks

This paper derives Gaussian approximation bounds for the standardized aggregate wireless interference (AWI) in the downlink of dense K-tier heterogenous cellular networks when base stations in each tier are distributed over the plane according to a (possibly non-homogeneous) Poisson process. The proposed methodology is general enough to account for general bounded path-loss models and fading statistics. The deviations of the distribution of the standardized AWI from the standard normal distribution are measured in terms of the Kolmogorov-Smirnov distance. An explicit expression bounding the Kolmogorov-Smirnov distance between these two distributions is obtained as a function of a broad range of network parameters such as per-tier transmission power levels, base station locations, fading statistics and the path-loss model. A simulation study is performed to corroborate the analytical results. In particular, a good statistical match between the standardized AWI distribution and its normal approximation occurs even for moderately dense heterogenous cellular networks. These results are expected to have important ramifications for the characterization of performance upper and lower bounds for emerging 5G network architectures

A Tractable Framework for the Analysis of Dense Heterogeneous Cellular Networks

This paper investigates the downlink performance of dense K-tier heterogeneous cellular networks (HCNs) under general settings. First, Gaussian approximation bounds for the standardized aggregate wireless interference (AWI) in dense K-tier HCNs are obtained for when base stations (BSs) in each tier are distributed over the plane according to a spatial and general Poisson point process. The Kolmogorov-Smirnov (KS) distance is used to measure deviations of the distribution of the standardized AWI from the standard normal distribution. An explicit and analytical expression bounding the KS distance between these two distributions is obtained as a function of a broad range of network parameters, such as per-tier transmission power levels, per-tier BS intensity, BS locations, general fading statistics, and general bounded path-loss models. Bounds achieve a good statistical match between the standardized AWI distribution and its normal approximation even for moderately dense HCNs. Second, various spatial performance metrics of interest, such as outage capacity, ergodic capacity, and area spectral efficiency in the downlink of K-tier HCNs for general signal propagation models are investigated by making use of the derived distribution approximation results. Considering two specific BS association policies, it is shown that the derived performance bounds track the actual performance metrics reasonably well for a wide range of BS intensities, with the gap among them becoming negligibly small for denser HCN deployments. Finally, both analytical and numerical results on the area spectral efficiency reveal a non-linear growth trend with diminishing returns of HCN performance. Hence, the SIR invariance property does not hold under bounded path-loss models, which is a critical finding from the HCN design perspective. In particular, it points out a critical BS density beyond which the HCN performance starts to decline due to excessive wireless interference

A Tractable Framework for the Analysis of Dense Heterogeneous Cellular Networks

This paper investigates the downlink performance of dense K-tier heterogeneous cellular networks (HCNs) under general settings. First, Gaussian approximation bounds for the standardized aggregate wireless interference (AWI) in dense K-tier HCNs are obtained for when base stations (BSs) in each tier are distributed over the plane according to a spatial and general Poisson point process. The Kolmogorov-Smirnov (KS) distance is used to measure deviations of the distribution of the standardized AWI from the standard normal distribution. An explicit and analytical expression bounding the KS distance between these two distributions is obtained as a function of a broad range of network parameters, such as per-tier transmission power levels, per-tier BS intensity, BS locations, general fading statistics, and general bounded path-loss models. Bounds achieve a good statistical match between the standardized AWI distribution and its normal approximation even for moderately dense HCNs. Second, various spatial performance metrics of interest, such as outage capacity, ergodic capacity, and area spectral efficiency in the downlink of K-tier HCNs for general signal propagation models are investigated by making use of the derived distribution approximation results. Considering two specific BS association policies, it is shown that the derived performance bounds track the actual performance metrics reasonably well for a wide range of BS intensities, with the gap among them becoming negligibly small for denser HCN deployments. Finally, both analytical and numerical results on the area spectral efficiency reveal a non-linear growth trend with diminishing returns of HCN performance. Hence, the SIR invariance property does not hold under bounded path-loss models, which is a critical finding from the HCN design perspective. In particular, it points out a critical BS density beyond which the HCN performance starts to decline due to excessive wireless interference

Low BMD is less predictive than reported falls for future limb fractures in women across Europe: results from the European Prospective Osteoporosis Study.

We have previously shown that center- and sex-specific fall rates explained one-third of between-center variation in upper limb fractures across Europe. In this current analysis, our aim was to determine how much of the between-center variation in fractures could be attributed to repeated falling, bone mineral density (BMD), and other risk factors in individuals, and to compare the relative contributions of center-specific BMD vs. center-specific fall rates. A clinical history of fracture was assessed prospectively in 2451 men and 2919 women aged 50-80 from 20 centers participating in the European Prospective Osteoporosis Study (EPOS) using standardized questionnaires (mean follow-up = 3 years). Bone mineral density (BMD, femoral neck, trochanter, and/or spine) was measured in 2103 men and 2565 women at these centers. Cox regression was used to model the risk of incident fracture as a function of the person-specific covariates: age, BMD, personal fracture history (PFH), family hip fracture history (FAMHIP), time spent walking/cycling, number of 'all falls' and falls not causing fracture ('fracture-free') during follow-up, alcohol consumption, and body mass index. Center effects were modeled by inclusion of multiplicative gamma-distributed random effects, termed center-shared frailty (CSF), with mean 1 and finite variance theta (theta) acting on the hazard rate. The relative contributions of center-specific fall risk and center-specific BMD on the incidence of limb fractures were evaluated as components of CSF. In women, the risk of any incident nonspine fracture (n = 190) increased with age, PFH, FAMHIP, > or =1 h/day walking/cycling, and number of 'all falls' during follow-up (all P < 0.074). 'Fracture-free' falls (P = 0.726) and femoral neck BMD did not have a significant effect at the individual level, but there was a significant center-shared frailty effect (theta = 0.271, P = 0.001) that was reduced by 4% after adjusting for mean center BMD and reduced by 19% when adjusted for mean center fall rate. Femoral trochanter BMD was a significant determinant of lower limb fractures (n = 53, P = 0.014) and the center-shared frailty effect was significant for upper limb fractures (theta = 0.271, P = 0.011). This upper limb fracture center effect was unchanged after adjusting for mean center BMD but was reduced by 36% after adjusting for center mean fall rates. In men, risk of any nonspine fracture (n = 75) increased with PFH, fall during follow-up (P < 0.026), and with a decrease in trochanteric BMD [RR 1.38 (1.08, 1.79) per 1 SD decrease]. There was no center effect evident (theta = 0.081, P = 0.096). We conclude that BMD alone cannot be validly used to discriminate between the risk of upper limb fractures across populations without taking account of population-specific variations in fall risk and other factors. These variations might reflect shared environmental or possibly genetic factors that contribute quite substantially to the risk of upper limb fractures in women

Low BMD is less predictive than reported falls for future limb fractures in women across Europe: results from the European Prospective Osteoporosis Study.

We have previously shown that center- and sex-specific fall rates explained one-third of between-center variation in upper limb fractures across Europe. In this current analysis, our aim was to determine how much of the between-center variation in fractures could be attributed to repeated falling, bone mineral density (BMD), and other risk factors in individuals, and to compare the relative contributions of center-specific BMD vs. center-specific fall rates. A clinical history of fracture was assessed prospectively in 2451 men and 2919 women aged 50-80 from 20 centers participating in the European Prospective Osteoporosis Study (EPOS) using standardized questionnaires (mean follow-up = 3 years). Bone mineral density (BMD, femoral neck, trochanter, and/or spine) was measured in 2103 men and 2565 women at these centers. Cox regression was used to model the risk of incident fracture as a function of the person-specific covariates: age, BMD, personal fracture history (PFH), family hip fracture history (FAMHIP), time spent walking/cycling, number of 'all falls' and falls not causing fracture ('fracture-free') during follow-up, alcohol consumption, and body mass index. Center effects were modeled by inclusion of multiplicative gamma-distributed random effects, termed center-shared frailty (CSF), with mean 1 and finite variance theta (theta) acting on the hazard rate. The relative contributions of center-specific fall risk and center-specific BMD on the incidence of limb fractures were evaluated as components of CSF. In women, the risk of any incident nonspine fracture (n = 190) increased with age, PFH, FAMHIP, &gt; or =1 h/day walking/cycling, and number of 'all falls' during follow-up (all P &lt; 0.074). 'Fracture-free' falls (P = 0.726) and femoral neck BMD did not have a significant effect at the individual level, but there was a significant center-shared frailty effect (theta = 0.271, P = 0.001) that was reduced by 4% after adjusting for mean center BMD and reduced by 19% when adjusted for mean center fall rate. Femoral trochanter BMD was a significant determinant of lower limb fractures (n = 53, P = 0.014) and the center-shared frailty effect was significant for upper limb fractures (theta = 0.271, P = 0.011). This upper limb fracture center effect was unchanged after adjusting for mean center BMD but was reduced by 36% after adjusting for center mean fall rates. In men, risk of any nonspine fracture (n = 75) increased with PFH, fall during follow-up (P &lt; 0.026), and with a decrease in trochanteric BMD [RR 1.38 (1.08, 1.79) per 1 SD decrease]. There was no center effect evident (theta = 0.081, P = 0.096). We conclude that BMD alone cannot be validly used to discriminate between the risk of upper limb fractures across populations without taking account of population-specific variations in fall risk and other factors. These variations might reflect shared environmental or possibly genetic factors that contribute quite substantially to the risk of upper limb fractures in women