Droplet fluid infusion into a dust layer in relation to self-cleaning

Wettability of a droplet liquid on a dusty hydrophobic plate is considered and the fluid infusion into the dust layer is studied pertinent to dust removal from the hydrophobic surfaces via rolling/sliding droplets. Influence of droplet hydrostatic pressure on the fluid infusion into dust layer is also investigated towards exploring the dust removal mechanisms. Environmental dust characteristics are evaluated and their interface with the droplet fluid is assessed. Sets of experiments are carried out to examine: (i) droplet fluid infusion into the dust layer, (ii) droplet fluid cloaking of dust, and (iii) evaluate the weight gain of the dust particles during cloaking. The findings reveal that droplet fluid (water) spreads onto the dusty surface and infuses on the dust particles. Cloaking velocity decays sharply with time and the weight gain of the dust particles is about 17% of the original dust weight after cloaking. The dust particles have a large area of nano-size open-pores-sites on the surface; however, capillary diffusion through these sites is limited with shallow depths and the weight gain of a dust particle via capillary diffusion is about 1% of the particle weight. The maximum infusion depth of the droplet fluid in the dust layer is about 74 μm, which is slightly less than the dust layer thickness on the surface. The rolling droplet picks up all the dust from the 150 μm thick dust layer on the surface.

Wettability of a droplet liquid on a dusty hydrophobic plate is considered and the fluid infusion into the dust layer is studied pertinent to dust removal from the hydrophobic surfaces via rolling/sliding droplets.     

Intraplaque Hemorrhage and the Plaque Surface in Carotid Atherosclerosis: The Plaque At RISK Study (PARISK)

BACKGROUND AND PURPOSE:An important characteristic of vulnerable plaque, intraplaque hemorrhage, may predict plaque rupture. Plaque rupture can be visible on noninvasive imaging as a disruption of the plaque surface. We investigated the association between intraplaque hemorrhage and disruption of the plaque surface.MATERIALS AND METHODS:We selected the first 100 patients of the Plaque At RISK study, an ongoing prospective noninvasive plaque imaging study in patients with mild-to-moderate atherosclerotic lesions in the carotid artery. In carotid artery plaques, disruption of the plaque surface (defined as ulcerated plaques and/or fissured fibrous cap) and intraplaque hemorrhage were assessed by using MDCTA and 3T MR imaging, respectively. We used a χ² test and multivariable logistic regression to assess the association between intraplaque hemorrhage and disrupted plaque surface.RESULTS:One hundred forty-nine carotid arteries in 78 patients could be used for the current analyses. Intraplaque hemorrhage and plaque ulcerations were more prevalent in symptomatic compared with contralateral vessels (hemorrhage, 38% versus 11%; P < .001; and ulcerations, 27% versus 7%; P = .001). Fissured fibrous cap was more prevalent in symptomatic compared with contralateral vessels (13% versus 4%; P = .06). After adjustment for age, sex, diabetes mellitus, and degree of stenosis, intraplaque hemorrhage was associated with disrupted plaque surface (OR, 3.13; 95% CI, 1.25–7.84) in all vessels.CONCLUSIONS:Intraplaque hemorrhage is associated with disruption of the plaque surface in patients with a carotid artery stenosis of <70%. Serial studies are needed to investigate whether intraplaque hemorrhage indeed increases the risk of plaque rupture and subsequent ischemic stroke during follow-up.

The need to identify patients with mild-to-moderate carotid artery stenosis and an increased stroke risk who might benefit from surgical treatment has shifted research interest from assessment of the degree of carotid stenosis to assessment of vulnerable plaque characteristics.¹ Vulnerable plaques are atherosclerotic plaques more prone to rupture and are associated with a higher risk for thromboembolism and ischemic stroke.^2,3 Intraplaque hemorrhage is an important characteristic of the vulnerable plaque.⁴ Prevalence of intraplaque hemorrhage has been shown to be higher in symptomatic than in asymptomatic lesions.⁵ Moreover, the presence of intraplaque hemorrhage in carotid artery disease is associated with an increased risk of cerebral ischemic events.^6–8The pathophysiologic mechanism leading to intraplaque hemorrhage is a topic of debate. However, a common viewpoint is that small leaky neovessels in the atherosclerotic plaques are a likely source of intraplaque hemorrhage.^5,9,10 The presence of intraplaque hemorrhage is thought to initiate several biologic processes like phagocytosis and local inflammation, leading to the release of proteolytic enzymes, deposition of free cholesterol and subsequently plaque growth, plaque destabilization, and possible plaque rupture.^5,9–12 Plaque rupture can be visible on imaging as a disruption of the atherosclerotic plaque surface (plaque ulceration and/or a fissured fibrous cap).^13,14 A previous study reported that plaque ulceration on CTA was useful for the prediction of intraplaque hemorrhage on MR imaging in a broad group of symptomatic patients referred for carotid artery imaging.¹⁵ Ulcerated plaques themselves are independently associated with an increased risk of ipsilateral ischemic events as well.^16,17The aim of the current study was to investigate the association between intraplaque hemorrhage, as assessed on MR imaging, and disruption of the plaque surface, assessed on MDCTA, in symptomatic patients with a carotid artery stenosis of <70%.     

Retrograde Inversion Stripping as a Complication of the Clarivein? Mechanochemical Venous Ablation Procedure

The endovenous revolution has accelerated the development of new techniques and devices for the treatment of varicose veins. The ClariVein^® mechanochemical ablation device offers tumescentless treatment with a rotating ablation tip that can theoretically become stuck in tissue. We present the first report of retrograde stripping of the small saphenous vein without anaesthesia following attempted use of the ClariVein^® device, without adverse sequelae.     

Increased regional and transmyocardial dispersion of ventricular repolarization in end-stage renal disease

BACKGROUND: Approximately half of patients with end-stage renal disease die because of cardiac disease, and ventricular arrhythmias are the common terminal events. Increased dispersion of the repolarization phase of the myocardial action potential can predispose patients to ventricular tachycardia and fibrillation causing cardiac death. OBJECTIVE: To determine the existence of increased regional and transmyocardial dispersion of ventricular repolarization in end-stage renal disease. STUDY DESIGN: Case-control prospective study. PATIENTS AND METHODS: The QT dispersion and the interval between the peak of the T wave (Tp) and the end of the T wave (Te) on a surface electrocardiogram represent regional and transmyocardial dispersion in ventricular repolarization, respectively. The prehemodialysis QT dispersions and Tp-Te intervals of 94 consecutive patients with end-stage renal disease were determined and compared with those of age- and sex-matched healthy controls. RESULTS: Both the QT and the QTc dispersion were significantly higher in the end-stage renal disease group than in the control group (QT dispersion 46 +/- 17 ms [mean +/- SD] versus 26 +/- 16 ms, P < 0.001; QTc dispersion 51 +/- 20 ms versus 30 +/- 20 ms, P < 0.001). Similarly, both the corrected average Tp-Te and the corrected maximum Tp-Te intervals were significantly higher in the end-stage renal disease group than in the control group (corrected average Tp-Te interval 99 +/- 19 ms versus 87 +/- 19 ms, P = 0.023; corrected maximum Tp-Te interval 114 +/- 23 ms versus 103 +/- 23 ms, P = 0.023). CONCLUSIONS: Increased regional and transmyocardial dispersion of ventricular repolarization in end-stage renal disease was demonstrated. This increased dispersion may be a contributory factor in the high cardiac mortality in patients with end-stage renal disease.     

Association of NT-ProBNP,Blood Pressure,and Cardiovascular Events: The ARIC Study

BackgroundAlthough intensive blood pressure reduction has cardiovascular benefits, the absolute benefit is greater in those at higher cardiovascular disease (CVD) risk.ObjectivesThis study examined whether N-terminal pro–B-type natriuretic peptide (NT-proBNP) helps identify subjects at higher risk for CVD events across systolic blood pressure (SBP), diastolic blood pressure (DBP), or pulse pressure (PP) categories.MethodsParticipants from the ARIC (Atherosclerosis Risk In Communities) study visit 4 (1996 to 98) were grouped according to SBP, DBP, or PP categories and further stratified by NT-proBNP categories. Cox regression models were used to estimate hazard ratios for incident CVD (coronary heart disease, ischemic stroke, or heart failure hospitalization) and mortality across combined NT-proBNP and/or BP categories, adjusting for CVD risk factors.ResultsThere were 9,309 participants (age: 62.6 ± 5.6 years; 58.3% women) with 2,416 CVD events over a median follow-up of 16.7 years. Within each SBP, DBP, or PP category, a higher category of NT-proBNP (100 to <300 or 300 pg/ml, compared with NT-proBNP <100 pg/ml) was associated with a graded increased risk for CVD events and mortality. Participants with SBP 130 to 139 mm Hg but NT-proBNP ≥300 pg/ml had a hazards ratio of 3.4 for CVD (95% confidence interval: 2.44 to 4.77) compared with a NT-proBNP of <100 pg/ml and SBP of 140 to 149 mm Hg.ConclusionsElevated NT-proBNP is independently associated with CVD and mortality across SBP, DBP, and PP categories and helps identify subjects at the highest risk. Participants with stage 1 hypertension but elevated NT-proBNP had greater cardiovascular risk compared with those with stage 2 SBP but lower NT-proBNP. Future studies are needed to evaluate use of biomarker-based strategies for CVD risk assessment to assist with initiation or intensification of BP treatment.