In situ accretion of gaseous envelopes on to planetary cores embedded in evolving protoplanetary discs

The core accretion hypothesis posits that planets with significant gaseous envelopes accreted them from their protoplanetary discs after the formation of rocky/icy cores. Observations indicate that such exoplanets exist at a broad range of orbital radii, but it is not known whether they accreted their envelopes in situ, or originated elsewhere and migrated to their current locations. We consider the evolution of solid cores embedded in evolving viscous discs that undergo gaseous envelope accretion in situ with orbital radii in the range 0.1–10 au. Additionally, we determine the long-term evolution of the planets that had no runaway gas accretion phase after disc dispersal. We find the following. (i) Planets with 5 M⊕ cores never undergo runaway accretion. The most massive envelope contained 2.8 M⊕ with the planet orbiting at 10 au. (ii) Accretion is more efficient on to 10 M⊕ and 15 M⊕ cores. For orbital radii ap ≥ 0.5 au, 15 M⊕ cores always experienced runaway gas accretion. For ap ≥ 5 au, all but one of the 10 M⊕ cores experienced runaway gas accretion. No planets experienced runaway growth at ap = 0.1 au. (iii) We find that, after disc dispersal, planets with significant gaseous envelopes cool and contract on Gyr time-scales, the contraction time being sensitive to the opacity assumed. Our results indicate that Hot Jupiters with core masses ≲15 M⊕ at ≲0.1 au likely accreted their gaseous envelopes at larger distances and migrated inwards. Consistently with the known exoplanet population, super-Earths and mini-Neptunes at small radii during the disc lifetime, accrete only modest gaseous envelopes.The simulations presented in this paper utilized Queen Mary's MidPlus computational facilities, supported by QMUL Research-IT and funded by EPSRC grant EP/K000128/1. This research was supported in part by the National Science Foundation under Grant No. NSF PHY-1125915. We acknowledge the referee, Kaitlin Kratter, whose comments helped to improve this paper

Full-scale fatigue testing of a wind turbine blade in flapwise direction and examining the effect of crack propagation on the blade performance

In this paper, the sensitivity of the structural integrity of wind turbine blades to debonding of the shear web from the spar cap was investigated. In this regard, modal analysis, static and fatigue testing were performed on a 45.7 m blade for three states of the blade: (i) as received blade (ii) when a crack of 200 mm was introduced between the web and the spar cap and (iii) when the crack was extended to 1000 mm. Calibration pull-tests for all three states of the blade were performed to obtain the strain-bending moment relationship of the blade according to the estimated target bending moment (BM) which the blade is expected to experience in its service life. The resultant data was used to apply appropriate load in the fatigue tests. The blade natural frequencies in flapwise and edgewise directions over a range of frequency domain were found by modal testing for all three states of the blade. The blade first natural frequency for each state was used for the flapwise fatigue tests. These were performed in accordance with technical specification IEC TS 61400-23. The fatigue results showed that, for a 200 mm crack between the web and spar cap at 9 m from the blade root, the crack did not propagate at 50% of the target BM up to 62,110 cycles. However, when the load was increased to 70% of target BM, some damages were detected on the pressure side of the blade. When the 200 mm crack was extended to 1000 mm, the crack began to propagate when the applied load exceeded 100% of target BM and the blade experienced delaminations, adhesive joint failure, compression failure and sandwich core failure

Composition profiles of InAs–GaAs quantum dots determined by medium-energy ion scattering

The composition profile along the [001] growth direction of low-growth-rate InAs–GaAs quantum dots (QDs) has been determined using medium-energy ion scattering (MEIS). A linear profile of In concentration from 100% In at the top of the QDs to 20% at their base provides the best fit to MEIS energy spectra

Cerebrospinal fluid changes in the renin-angiotensin system in Alzheimer's disease

Observations in autopsied brain tissue indicate that overactivation of the classical renin-angiotensin system (cRAS) and underactivity within regulatory RAS pathways (rRAS) are associated with pathology in Alzheimer’s disease (AD). The primary aim of this study was to investigate whether cerebrospinal fluid (CSF) markers of RAS are altered in AD in relation to established CSF markers of disease pathology (lower Aβ42 and elevated tau) and CSF markers of capillary dysfunction. We studied 40 controls and 40 AD cases grouped according to a biomarker profile (i.e., AD cases t-tau>400 pg/mL, pTau >60 pg/mL, and Aβ42 <550 pg/mL). Angiotensin-II converting enyme-1 (ACE1) and ACE2 enzyme activity was measured using fluorogenic peptide substrates; sPDGFRβ and albumin level by sandwich ELISA; and angiotensin-I (Ang-I), Ang-II, and Ang-(1-7) by direct ELISA. CSF Aβ42, total, and phosphorylated tau levels were previously measured by INNOTEST sandwich ELISA. CSF ACE1 activity was significantly elevated in AD (p = 0.008) and positively correlated with ACE2 in AD (r = 0.420, p = 0.007). CSF ACE1 weakly correlated with t-tau (r = 0.294, p = 0.066) and p-tau (r = 0.329, p = 0.038) but not with Aβ42 in the controls but not in AD. ACE1 correlated positively with sPDGFRβ (r = 0.426, p = 0.007), a marker of pericyte injury, and ACE2 correlated positively with albumin (r = 0.422, p = 0.008), a marker of blood-brain barrier integrity. CSF Ang-I, Ang-II, and Ang-(1-7) levels were unchanged in AD. This cross-sectional CSF study indicates RAS dysfunction in relation to capillary damage in

Angiotensin-converting enzyme 2 is reduced in Alzheimer's disease in association with increasing amyloid-β and tau pathology

BACKGROUND: Hyperactivity of the classical axis of the renin-angiotensin system (RAS), mediated by angiotensin II (Ang II) activation of the angiotensin II type 1 receptor (AT1R), is implicated in the pathogenesis of Alzheimer’s disease (AD). Angiotensin-converting enzyme-2 (ACE-2) degrades Ang II to angiotensin 1–7 (Ang (1-7)) and counter-regulates the classical axis of RAS. We have investigated the expression and distribution of ACE-2 in post-mortem human brain tissue in relation to AD pathology and classical RAS axis activity. METHODS: We measured ACE-2 activity by fluorogenic peptide substrate assay in mid-frontal cortex (Brodmann area 9) in a cohort of AD (n = 90) and age-matched non-demented controls (n = 59) for which we have previous data on ACE-1 activity, amyloid β (Aβ) level and tau pathology, as well as known ACE1 (rs1799752) indel polymorphism, apolipoprotein E (APOE) genotype, and cerebral amyloid angiopathy severity scores. RESULTS: ACE-2 activity was significantly reduced in AD compared with age-matched controls (P < 0.0001) and correlated inversely with levels of Aβ (r = −0.267, P < 0.001) and phosphorylated tau (p-tau) pathology (r = −0.327, P < 0.01). ACE-2 was reduced in individuals possessing an APOE ε4 allele (P < 0.05) and was associated with ACE1 indel polymorphism (P < 0.05), with lower ACE-2 activity in individuals homozygous for the ACE1 insertion AD risk allele. ACE-2 activity correlated inversely with ACE-1 activity (r = −0.453, P < 0.0001), and the ratio of ACE-1 to ACE-2 was significantly elevated in AD (P < 0.0001). Finally, we show that the ratio of Ang II to Ang (1–7) (a proxy measure of ACE-2 activity indicating  conversion of Ang II to Ang (1–7)) is reduced in AD. CONCLUSIONS: Together, our findings indicate that ACE-2 activity is reduced in AD and is an important regulator of the central classical ACE-1/Ang II/AT1R axis of RAS, and also that dysregulation of this pathway likely plays a significant role in the pathogenesis of AD. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13195-016-0217-7) contains supplementary material, which is available to authorized users

Walking on common ground: a cross-disciplinary scoping review on the clinical utility of digital mobility outcomes

Physical mobility is essential to health, and patients often rate it as a high-priority clinical outcome. Digital mobility outcomes (DMOs), such as real-world gait speed or step count, show promise as clinical measures in many medical conditions. However, current research is nascent and fragmented by discipline. This scoping review maps existing evidence on the clinical utility of DMOs, identifying commonalities across traditional disciplinary divides. In November 2019, 11 databases were searched for records investigating the validity and responsiveness of 34 DMOs in four diverse medical conditions (Parkinson's disease, multiple sclerosis, chronic obstructive pulmonary disease, hip fracture). Searches yielded 19,672 unique records. After screening, 855 records representing 775 studies were included and charted in systematic maps. Studies frequently investigated gait speed (70.4% of studies), step length (30.7%), cadence (21.4%), and daily step count (20.7%). They studied differences between healthy and pathological gait (36.4%), associations between DMOs and clinical measures (48.8%) or outcomes (4.3%), and responsiveness to interventions (26.8%). Gait speed, step length, cadence, step time and step count exhibited consistent evidence of validity and responsiveness in multiple conditions, although the evidence was inconsistent or lacking for other DMOs. If DMOs are to be adopted as mainstream tools, further work is needed to establish their predictive validity, responsiveness, and ecological validity. Cross-disciplinary efforts to align methodology and validate DMOs may facilitate their adoption into clinical practice

Looking For Disoriented Chiral Condensates From Pion Distributions

We suggest two methods for the detection of the formation of disoriented chiral condensates in heavy ion collisions. We show that the variance in the number of charged pions (in a suitable range of momentum space) provides a signature for the observation of a disoriented chiral condensate. The signal should be observable even if multiple domains of D$\chi$C form provided the average number of pions per domain is significantly larger than unity. The variance of the number charged pions alone provides a signal which can be used even if the number of neutral pions cannot be measured in a given detector. On the other hand, the probability distribution in $R$, the proportion of neutral pions to all pions emitted in heavy ion collisions in certain kinematic regions, has been suggested as a signal of a disoriented chiral condensate. Here we note that the signature can be greatly enhanced by making suitable cuts in the data. In particular, we consider reducing the data set such that the $k$ pions with lowest $p_T$ are all neutral. We find that, given such cuts, can be substantially different from 1/3. For example, for a single D$\chi$C domain without contamination due to incoherently emitted pions, is 3/5 given the pion with lowest $p_T$ is neutral, and 5/7 given the two pions with lowest $p_T$ are both neutral, {\it etc.}. The effects of multi-domain D$\chi$C formation and noise due to incoherent pion emission can be systematically incorporated. Potential applications to experiments and their limitations are briefly discussed.Comment: 16 pages in REVTeX, 7 figures. Combined and updated version of nucl-th/9903029 and nucl-th/9904074. Accepted by Phys. Rev.