40 research outputs found
The Cox-Voinov law for traveling waves in the partial wetting regime
Get PDFWe consider the thin-film equation in with partial-wetting boundary
conditions and inhomogeneous mobility of the form , where is the film height, is the
slip length, denotes the lateral variable, and is the
mobility exponent parameterizing the nonlinear slip condition. The
partial-wetting regime implies the boundary condition at the triple junction (nonzero
microscopic contact angle). Existence and uniqueness of traveling-wave
solutions to this problem under the constraint as have been proved in previous work by Chiricotto and Giacomelli in
[Commun. Appl. Ind. Math., 2(2):e-388, 16, 2011]. We are interested in the
asymptotics as and . By reformulating the
problem as as a dynamical system for the difference between
the solution and the microscopic contact angle, values for are found for
which linear as well as nonlinear resonances occur. These resonances lead to a
different asymptotic behavior of the solution as depending on
.
Together with the asymptotics as characterizing the Cox-Voinov
law for the velocity-dependent macroscopic contact angle as found by
Giacomelli, the first author of this work, and Otto in [Nonlinearity,
29(9):2497-2536, 2016], the rigorous asymptotics of traveling-wave solutions to
the thin-film equation in partial wetting can be characterized. Furthermore,
our approach enables us to analyze the relation between the microscopic and
macroscopic contact angle. It is found that the Cox-Voinov law for the
macroscopic contact angle depends continuously differentiably on the
microscopic contact angle.Comment: 24 pages, 3 figures, revised version; changed title, extended
introductio
Classical solutions to the thin-film equation with general mobility in the perfect-wetting regime
Get PDFWe prove well-posedness, partial regularity, and stability of a thin-film
equation with general mobility and
mobility exponent in the regime of
perfect wetting (zero contact angle). After a suitable coordinate
transformation to fix the free boundary (the contact line where liquid, air,
and solid coalesce), the thin-film equation is rewritten as an abstract Cauchy
problem and we obtain maximal -regularity for the linearized
evolution. Partial regularity close to the free boundary is obtained by
studying the elliptic regularity of the spatial part of the linearization. This
yields solutions that are non-smooth in the distance to the free boundary, in
line with previous findings for source-type self-similar solutions. In a
scaling-wise quasi-minimal norm for the initial data, we obtain a
well-posedness and asymptotic stability result for perturbations of traveling
waves. The novelty of this work lies in the usage of estimates in time,
where , while the existing literature mostly deals with
at least for nonlinear mobilities. This turns out to be essential to obtain for
the first time a well-posedness result in the perfect-wetting regime for all
physical nonlinear slip conditions except for a strongly degenerate case at and the well-understood perfect-slip case . Furthermore,
compared to [J. Differential Equations, 257(1):15-81, 2014] by Giacomelli, the
first author of this paper, Kn\"upfer, and Otto, where a PDE-approach yields
-estimates, well-posedness, and stability for ,
our functional-analytic approach is significantly shorter while at the same
time giving a more general result.Comment: 40 pages, 4 figure
Fish consumption, does it beneficially affect markers of colorectal carcinogenesis?
No full textBackground: Fish consumption is possibly associated with a decreased risk of colorectal cancer, as has been shown in several observational studies. However, most of these studies did not discriminate between the effects of oil-rich and lean fish. To date, no randomized controlled trials (RCTs) have examined the possible beneficial effects of fish intake on colorectal cancer risk. Aim: The aim of this thesis was to investigate whether fish consumption beneficially affects markers of colorectal carcinogenesis. Methods and Results: In a case control study (363 cases, 498 controls), we studied the association of serum n 3 polyunsaturated fatty acid (PUFA) levels as a marker of oil rich fish intake with colorectal adenomas, a precursor lesion of colorectal cancer. We found that individuals with high serum long chain n 3 PUFA levels had a decreased risk of colorectal adenomas (odds ratio (OR) 0.67, 95% confidence interval (CI) 0.46; 0.96), whereas individuals with high serum n 6 PUFA levels had an increased risk of colorectal adenomas (OR 1.68, 95% CI 1.17; 2.42). In an RCT, we studied the effects of 3.5g/d fish oil (~1.5g/d n 3 PUFA) for 12 weeks on 19 serum inflammation markers in 77 healthy subjects and found that serum levels of these cytokines and chemokines were not changed. Finally, we studied the effects of increasing fish consumption compared with no additional fish, on markers of colorectal carcinogenesis in an RCT. Subjects (n=242), at an increased risk of colorectal cancer and those with no macroscopic signs of disease, were randomly allocated to receive dietary advice (DA) plus either two additional weekly portions of oil rich fish (salmon, ~1.4g/d n 3 PUFA) or lean fish (cod, ~0.09 g/d n 3 PUFA), or only DA for six months. We observed no change in apoptotic and mitotic cell numbers after the 6 months intervention with either salmon or cod compared with DA. Furthermore, colorectal genotoxicity, levels of cytokines and chemokines in colonic biopsies and feces, and fecal calprotectin were also not markedly changed after fish consumption. Only serum C reactive protein (CRP) levels were statistically significantly decreased after consumption of salmon ( 0.5 mg/l, 95% CI 0.9; 0.2) and cod ( 0.4 mg/l, 95% CI 0.7; 0.0) compared with DA. Conclusion: The results of this thesis do not provide strong evidence for beneficial effects of fish consumption on markers of colorectal carcinogenesis. <br/
Effects of macronutrient intake in obesity: A meta-analysis of low-carbohydrate and low-fat diets on markers of the metabolic syndrome
Get PDFThe metabolic syndrome (MetS) comprises cardiometabolic risk factors frequently found in individuals with obesity. Guidelines to prevent or reverse MetS suggest limiting fat intake, however, lowering carbohydrate intake has gained attention too. The aim for this review was to determine to what extent either weight loss, reduction in caloric intake, or changes in macronutrient intake contribute to improvement in markers of MetS in persons with obesity without cardiometabolic disease. A meta-analysis was performed across a spectrum of studies applying low-carbohydrate (LC) and low-fat (LF) diets. PubMed searches yielded 17 articles describing 12 separate intervention studies assessing changes in MetS markers of persons with obesity assigned to LC (<40% energy from carbohydrates) or LF (<30% energy from fat) diets. Both diets could lead to weight loss and improve markers of MetS. Meta-regression revealed that weight loss most efficaciously reduced fasting glucose levels independent of macronutrient intake at the end of the study. Actual carbohydrate intake and actual fat intake at the end of the study, but not the percent changes in intake of these macronutrients, improved diastolic blood pressure and circulating triglyceride levels, without an effect of weight loss. The homeostatic model assessment of insulin resistance improved with both diets, whereas high-density lipoprotein cholesterol only improved in the LC diet, both irrespective of aforementioned factors. Remarkably, changes in caloric intake did not play a primary role in altering MetS markers. Taken together, these data suggest that, beyond the general effects of the LC and LF diet categories to improve MetS markers, there are also specific roles for weight loss, LC and HF intake, but not reduced caloric intake, that improve markers of MetS irrespective of diet categorization. On the basis of the results from this meta-analysis, guidelines to prevent MetS may need to be re-evaluated
Self-initiated dietary changes reduce general somatic and mental symptoms in a relatively healthy Dutch population
Get PDFThe risk for development of non-communicable diseases (NCDs) can be predicted by somatic or mental symptoms and dietary alterations aimed at improvement of those symptoms could potentially delay development of NCDs. The goal of this study was to identify whether self-initiated dietary changes could reduce mental and somatic symptoms in relatively healthy individuals. Participants (n = 494) recruited from the Dutch population filled out weekly questionnaires on dietary intake, somatic and mental symptoms and physical activity at baseline and during dieting for four weeks. There was a significant reduction in mental and somatic symptoms, body weight, and waist circumference at four weeks, whereas physical activity remained unchanged. Five dietary patterns were identified by principal component analysis labelled “Processed foods”, “Animal source foods”, “Wheel of Five”, “Traditional Dutch”, and “Party”. Reduction in mental symptoms was correlated to increased physical activity and increased intake of Wheel of Five foods. Reduction in somatic symptoms was correlated to body weight loss and less Processed foods, more Wheel of Five foods, and lower intake of fat and protein. Higher intake of protein and fat and lower intake of carbohydrates, however, were correlated to body weight loss. In conclusion this research showed that a self-initiated dietary change can lead to a significant reduction of mental and somatic symptoms
Chlorophylls and carotenoids of kiwifruit puree are affected similarly or less by microwave than by conventional heat processing and storage
Get PDF[EN] The impact of microwave (1000 W – 340 s) and conventional heat (97 C – 30 s) pasteurisation and storage
(4, 10, 22 C for up to 63 d) on total and individual carotenoids and chlorophylls in kiwifruit puree
was evaluated. Bioaccessibility of carotenoids, before and after pasteurisation and storage, was also studied.
Microwaves and conventional heating led to marked changes in the chlorophyll (42–100% losses) and
carotenoid (62–91% losses) content. First- and second-order kinetics appropriately explained the
degradation of total carotenoids and chlorophylls over time, respectively. Pasteurised samples
showed significantly (p < 0.05) enhanced stability of these pigments, with microwaves (k = 0.007–
0.031 100 g mg1 day1 at 4–22 C) promoting chlorophyll stability to a greater extent than conventional
heating (k = 0.0015–0.034 100 g mg1 day1 at 4–22 C). Bioaccessibility of carotenoids remained
(p < 0.05) unaffected by processing and storage. These results highlighted that the pigment composition
of microwaved kiwifruit was more similar to that of the fresh fruit and better preserved during storage.
2015 Elsevier Ltd. All rights reserved.The authors thank the Ministerio de Educacion y Ciencia for the financial support given through the Projects AGL 2010-22176 and AGL 2013-48993-C2-2-R and the Generalitat Valenciana for the Grant awarded to the author Maria Benlloch-Tinoco. The authors also thank the Luxembourg Institute of Science and Technology for access to their materials, methods and laboratories.Benlloch Tinoco, M.; Kaulmann, A.; Corte-Real, J.; Rodrigo Aliaga, MD.; Martínez Navarrete, N.; Bohn, T. (2015). Chlorophylls and carotenoids of kiwifruit puree are affected similarly or less by microwave than by conventional heat processing and storage. Food Chemistry. 187:254-262. https://doi.org/10.1016/j.foodchem.2015.04.052S25426218
Author Correction: Heritability estimates for 361 blood metabolites across 40 genome-wide association studies (Nature Communications, (2020), 11, 1, (39), 10.1038/s41467-019-13770-6)
No full textThe original version of the Supplementary Information associated with this Article included an incorrect Supplementary Data 1 file, in which additional delimiters were included in the first column for a number of rows, resulting in column shifts for some of these rows. The HTML has been updated to include a corrected version of Supplementary Data 1; the original incorrect version of Supplementary Data 1 can be found as Supplementary Information associated with this Correction. In addition, the original version of this Article contained an error in the author affiliations. An affiliation of Abdel Abdellaoui with Department of Psychiatry, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands was inadvertently omitted. This has now been corrected in both the PDF and HTML versions of the Article
Decreased agonist-stimulated mitochondrial ATP production caused by a pathological reduction in endoplasmic reticulum calcium content in human complex I deficiency.
No full textContains fulltext :
48077.pdf (Publisher’s version ) (Open Access)Although a large number of mutations causing malfunction of complex I (NADH:ubiquinone oxidoreductase) of the OXPHOS system is now known, their cell biological consequences remain obscure. We previously showed that the bradykinin (Bk)-induced increase in mitochondrial [ATP] ([ATP](M)) is significantly reduced in primary skin fibroblasts from a patient with an isolated complex I deficiency. The present work addresses the mechanism(s) underlying this impaired response. Luminometry of fibroblasts from 6 healthy subjects and 14 genetically characterized patients expressing mitochondria targeted luciferase revealed that the Bk-induced increase in [ATP](M) was significantly, but to a variable degree, decreased in 10 patients. The same variation was observed for the increases in mitochondrial [Ca(2+)] ([Ca(2+)](M)), measured with mitochondria targeted aequorin, and cytosolic [Ca(2+)] ([Ca(2+)](C)), measured with fura-2, and for the Ca(2+) content of the endoplasmic reticulum (ER), calculated from the increase in [Ca(2+)](C) evoked by thapsigargin, an inhibitor of the ER Ca(2+) ATPase. Regression analysis revealed that the increase in [ATP](M) was directly proportional to the increases in [Ca(2+)](C) and [Ca(2+)](M) and to the ER Ca(2+) content. Our findings provide evidence that a pathological reduction in ER Ca(2+) content is the direct cause of the impaired Bk-induced increase in [ATP](M) in human complex I deficiency
The future of burn care from a complexity science perspective
Get PDFHealth care is undergoing a profound technological and digital transformation and has become increasingly complex. It is important for burns professionals and researchers to adapt to these developments which may require new ways of thinking and subsequent new strategies. As Einstein has put it: "We must learn to see the world anew." The relatively new scientific discipline "Complexity science" can give more direction to this and is the metaphorical open door that should not go unnoticed in view of the burn care of the future. Complexity science studies "why the whole is more than the sum of the parts." It studies how multiple separate components interact with each other and their environment and how these interactions lead to "behavior of the system." Biological systems are always part of smaller and larger systems and exhibit the behavior of adaptivity, hence the name complex adaptive systems. From the perspective of complexity science, a severe burn injury is an extreme disruption of the "human body system." But this disruption also applies to the systems at the organ and cellular levels. All these systems follow the principles of complex systems. Awareness of the scaling process at multilevel helps to understand and manage the complex situation when dealing with severe burn cases. This paper aims to create awareness of the concept of complexity and to demonstrate the value and possibilities of complexity science methods and tools for the future of burn care through examples from preclinical, clinical, and organizational perspectives in burn care
