All-sky search for gravitational-wave bursts in the second joint LIGO-Virgo run

We present results from a search for gravitational-wave bursts in the data collected by the LIGO and Virgo detectors between July 7, 2009 and October 20, 2010: data are analyzed when at least two of the three LIGO-Virgo detectors are in coincident operation, with a total observation time of 207 days. The analysis searches for transients of duration < 1 s over the frequency band 64-5000 Hz, without other assumptions on the signal waveform, polarization, direction or occurrence time. All identified events are consistent with the expected accidental background. We set frequentist upper limits on the rate of gravitational-wave bursts by combining this search with the previous LIGO-Virgo search on the data collected between November 2005 and October 2007. The upper limit on the rate of strong gravitational-wave bursts at the Earth is 1.3 events per year at 90% confidence. We also present upper limits on source rate density per year and Mpc^3 for sample populations of standard-candle sources. As in the previous joint run, typical sensitivities of the search in terms of the root-sum-squared strain amplitude for these waveforms lie in the range 5 10^-22 Hz^-1/2 to 1 10^-20 Hz^-1/2. The combination of the two joint runs entails the most sensitive all-sky search for generic gravitational-wave bursts and synthesizes the results achieved by the initial generation of interferometric detectors.Comment: 15 pages, 7 figures: data for plots and archived public version at https://dcc.ligo.org/cgi-bin/DocDB/ShowDocument?docid=70814&version=19, see also the public announcement at http://www.ligo.org/science/Publication-S6BurstAllSky

A mathematical model of vascular and hemodynamics changes in early and late forms of preeclampsia

Abstract Preeclampsia–eclampsia syndrome is a leading cause of maternal mortality. The precise etiology of preeclampsia is still not well‐defined and different forms exist, including early and late forms or preeclampsia, which may arise via distinctly different mechanisms. Low‐dose aspirin administered at the end of the first trimester in women identified as high risk has been shown to reduce the incidence of early, but not late, preeclampsia; however, current risk factors show only fair predictive capability. There is a pressing need to develop accurate descriptions for the different forms of preeclampsia. This paper presents 1D fluid, solid, growth, and remodeling models for pregnancies complicated with early and late forms of preeclampsia. Simulations affirm a broad set of literature results that early forms of preeclampsia are characterized by elevated uterine artery pulsatility index (UA‐PI) and total peripheral resistance (TPR) and lower cardiac output (CO), with modestly increased mean arterial blood pressure (MAP) in the first half of pregnancy, with elevation of TPR and MAP beginning at 20 weeks. Conversely, late forms of preeclampsia are characterized by only slightly elevated UA‐PI and normal pre‐term TPR, and slightly elevated MAP and CO throughout pregnancy, with increased TPR and MAP beginning after 34 weeks. Results suggest that preexisting arterial stiffness may be elevated in women that develop both early forms and late forms of preeclampsia; however, data that verify these results are lacking in the literature. Pulse wave velocity increases in early‐ and late‐preeclampsia, coincident with increases in blood pressure; however, these increases are mainly due to the strain‐stiffening response of larger arteries, rather than arterial remodeling‐derived changes in material properties. These simulations affirm that early forms of preeclampsia may be associated with abnormal placentation, whereas late forms may be more closely associated with preexisting maternal cardiovascular factors; simulations also highlight several critical gaps in available data

Current Efavirenz (EFV) or Ritonavir-Boosted Lopinavir (LPV/r) Use Correlates with Elevate Markers of Atherosclerosis in HIV-Infected Subjects in Addis Ababa, Ethiopia

<div><p>Background</p><p>HIV patients on antiretroviral therapy have shown elevated incidence of dyslipidemia, lipodystrophy, and cardiovascular disease (CVD). Most studies, however, focus on cohorts from developed countries, with less data available for these co-morbidities in Ethiopia and sub-Saharan Africa.</p><p>Methods</p><p>Adult HIV-negative (<i>n</i> = 36), treatment naïve (<i>n</i> = 51), efavirenz (EFV)-treated (<i>n</i> = 91), nevirapine (NVP)-treated (<i>n</i> = 95), or ritonavir-boosted lopinavir (LPV/r)-treated (<i>n</i>=44) subjects were recruited from Black Lion Hospital in Addis Ababa, Ethiopia. Aortic pressure, augmentation pressure, and pulse wave velocity (PWV) were measured via applanation tonometry and carotid intima-media thickness (cIMT) and carotid arterial stiffness, and brachial artery flow-mediated dilation (FMD) were measured via non-invasive ultrasound. Body mass index, waist-to-hip circumference ratio (WHR), skinfold thickness, and self-reported fat redistribution were used to quantify lipodystrophy. CD4+ cell count, plasma HIV RNA levels, fasting glucose, total-, HDL-, and LDL-cholesterol, triglycerides, hsCRP, sVCAM-1, sICAM-1, leptin and complete blood count were measured.</p><p>Results</p><p>PWV and normalized cIMT were elevate and FMD impaired in EFV- and LPV/r-treated subjects compared to NVP-treated subjects; normalized cIMT was also elevated and FMD impaired in the EFV- and LPV/r-treated subjects compared to treatment-naïve subjects. cIMT was not statistically different across groups. Treated subjects exhibited elevated markers of dyslipidemia, inflammation, and lipodystrophy. PWV was associated with age, current EFV and LPV/r used, heart rate, blood pressure, triglycerides, LDL, and hsCRP, FMD with age, HIV duration, WHR, and glucose, and cIMT with age, current EFV use, skinfold thickness, and blood pressure.</p><p>Conclusions</p><p>Current EFV- or LPV/r-treatment, but not NVP-treatment, correlated with elevated markers of atherosclerosis, which may involve mechanisms distinct from traditional risk factors.</p></div

Preclinical markers of atherosclerosis are elevated in EFV-treated and LPV/r-treated subjects compared to HAART-naïve and NVP-treated.

<p>Wilcoxon rank sum test <i>p</i>-values are shown. *Note: Although the pairwise Wilcoxon rank sum test showed differences in cIMT between EFV- and LPV/r-treated and NVP-treated subject, ANOVA yielded a <i>p</i> = 0.12, which is above the defined criteria of <i>p</i><0.05 for statistical significance. When normalized to carotid artery diameter (cIMT-norm = cIMT/(<i>D</i>/2), where <i>D</i> = carotid diameter), EFV- and LPV/r-treated subjects exhibited significantly increased values compared to NVP-treated and HAART-naïve subject.</p

Baseline characteristics, body composition.

<p>Continuous variables are reported as median (interquartile range). BMI = body mass index, and WHR = waist-to-hip ratio, mm = millimeters.</p><p>A, a = p<0.005 or p<0.05 versus HIV-negative controls, respectively;</p><p>B, b = p<0.005 or p<0.05 versus HAART-naive, respectively;</p><p>D, d = p<0.005 or p<0.05 versus EFV, respectively;</p><p>E, e = p<0.005 or p<0.05 versus NVP, respectively.</p><p>Baseline characteristics, body composition.</p

Cardiovascular metrics.

<p>Continuous variables are reported as median (interquartile range). bpm = beats per minute, mmHg = millimeters of mergury, SBP = systolic blood pressure, DBP = diastolic blood pressure, MP = mean preasure, PP = pulse pressure, AP = augmentation pressure, AIx = augmentation index, AIx = 75 = augmentation index, normalize to a heart rate of 75 bpm, mm = millimeters, kPa = kiloPascals, TC = total cholesterol, TG = triglycerides, HDL = high density lipoprotein cholesterol, LDL = low density lipoprotein cholesterol, hs-CRP = high sensitivity C-reactive protein, sICAM = soluble intercellular adhesion molecule-1, sVCAM = soluble vascular cell adhesion molecule-1, mg = milligrams, ug = micrograms, ng = nanograms, dL = deciliter, mL = milliliters.</p><p>A, a = p<0.005 or p<0.05 versus HIV-negative controls, respectively;</p><p>B, b = p<0.005 or p<0.05 versus HAART-naive, respectively;</p><p>D, d = p<0.005 or p<0.05 versus EFV, respectively;</p><p>E, e = p<0.005 or p<0.05 versus NVP, respectively.</p><p>Cardiovascular metrics.</p

Inhibition of the angiotensin type 1 receptor equalizes aortic contractile force and cross sectional area in pendrin null and wild type mice.

<p>Aortic rings from candesartan-treated wild type and pendrin null mice were isometrically mounted and maximum force generated/cross sectional area was measured in response to the cumulative addition of KCl (Panel A) and PE (Panel B) (n = 5–6). Cross sectional area of the aorta wall was measured in each of the vessels studied (Panel C). Aorta thickness (intima and media, Panel D) was measured by morphometry in separate candesartan-treated wild type (n = 6) and pendrin null (n = 6) mice. Body weights for the aorta thickness measurements were the following: wild type 24.4±0.9 g versus 21.4±1.0 g for pendrin null mice.</p

Pendrin gene ablation does not affect steady state catecholamine production.

<p>24 hour urinary epinephrine and norepinephrine excretion of pendrin null and wild type mice are shown.</p

Angiotensin receptor type 1 inhibition eliminates the increase in MLC20 protein abundance observed in aortas from pendrin null mice.

<p>Pendrin null and wild type mice were given candesartan for 14 days and then sacrificed. Contractile protein abundance (α actin and MLC 20) and a “housekeeping gene” (cdk4) were quantified by immunoblot in lysates of aortas taken from mice in each group. Representative immunoblots (Left Panel) and band density normalized to wild type mice (Right Panel) are shown.</p