3,902 research outputs found
Double-diffusive transport in multicomponent vertical convection
Get PDFMotivated by the ablation of vertical ice faces in salt water, we use
three-dimensional direct numerical simulations to investigate the heat and salt
fluxes in two-scalar vertical convection. For parameters relevant to ice-ocean
interfaces in the convection-dominated regime, we observe that the salinity
field drives the convection and that heat is essentially transported as a
passive scalar. By varying the diffusivity ratio of heat and salt (i.e., the
Lewis number ), we identify how the different molecular diffusivities
affect the scalar fluxes through the system. Away from the walls, we find that
the heat transport is determined by a turbulent Prandtl number of and that double-diffusive effects are practically negligible. However, the
difference in molecular diffusivities plays an important role close to the
boundaries. In the (unrealistic) case where salt diffused faster than heat, the
ratio of salt-to-heat fluxes would scale as , consistent with
classical nested scalar boundary layers. However, in the realistic case of
faster heat diffusion (relative to salt), we observe a transition towards a
scaling of the ratio of the fluxes. This coincides with the thermal
boundary layer width growing beyond the thickness of the viscous boundary
layer. We find that this transition is not determined by a critical Lewis
number, but rather by a critical Prandtl number , slightly below
that for cold seawater where . We compare our results to similar studies
of sheared and double-diffusive flow under ice shelves, and discuss the
implications for fluxes in large-scale ice-ocean models. By coupling our
results to ice-ocean interface thermodynamics, we describe how the flux ratio
impacts the interfacial salinity, and hence the strength of solutal convection
and the ablation rate.Comment: 17 pages, 9 figure
Ice melting in salty water: layering and non-monotonic dependence on the mean salinity
Get PDFThe presence of salt in seawater strongly affects the melt rate and the shape evolution of ice, both of utmost relevance in ice–ocean interactions and thus for the climate. To get a better quantitative understanding of the physical mechanics at play in ice melting in salty water, we numerically investigate the lateral melting of an ice block in stably stratified saline water. The developing ice shape from our numerical results shows good agreement with the experiments and theory from Huppert & Turner (J. Fluid Mech., vol. 100, 1980, pp. 367–384). Furthermore, we find that the melt rate of ice depends non-monotonically on the mean ambient salinity: it first decreases for increasing salt concentration until a local minimum is attained, and then increases again. This non-monotonic behaviour of the ice melt rate is due to the competition among salinity-driven buoyancy, temperature-driven buoyancy and salinity-induced stratification. We develop a theoretical model based on the force balance which gives a prediction of the salt concentration for which the melt rate is minimal, and is consistent with our data. Our findings give insight into the interplay between phase transitions and double-diffusive convective flows
Effects of the basic multicellular unit and lamellar thickness on osteonal fatigue life
No full textA remodeling cycle sets the size of the osteon and associated lamellae in the basic multicellular unit. Treatments and aging affect these micro-structural features. We previously demonstrated decreased fatigue life with an unexplained mechanism and decreased osteon size in cortical bone treated with high-dose bisphosphonate. Here, three finite element models were examined: type-1: a single osteon, as a homogeneous unit and with heterogeneous lamellae and interlamellae, type-2: a control, interstitial-only tissue and type-3: the osteon with cement line, set within the interstitial tissue. Models were loaded in simulated, sinusoidal bending fatigue. As osteon size was decreased, lamellar number and lamellar thickness were incrementally adjusted for each model. As hypothesized, lamellae within the larger type-1 models attained greater cycles to failure and the addition of an osteon to type-2 models (generating a type-3 model set) yielded increased fatigue life. However, as the osteon size was decreased, the potential for compressive damage nucleation was increased within the lamellae of the osteons versus the interstitium. Also, osteons with fewer, thicker lamellae displayed increased fatigue life. Osteonal microstructure plays a role in damage initiation location, especially when BMU size is smaller. Previous findings by us and others could partially be explained by this further understanding of increased probability for damage nucleation in smaller osteons.Peer reviewe
Chronic High Fructose Intake Reduces Serum 1,25(OH)<sub>2</sub>D<sub>3</sub>Levels in Calcium-Sufficient Rodents
No full textExcessive fructose consumption inhibits adaptive increases in intestinal Ca2+transport in lactating and weanling rats with increased Ca2+requirements by preventing the increase in serum levels of 1,25(OH)2D3. Here we tested the hypothesis that chronic fructose intake decreases 1,25(OH)2D3 levels independent of increases in Ca2+ requirements. Adult mice fed for five wk a high glucose-low Ca2+ diet displayed expected compensatory increases in intestinal and renal Ca2+ transporter expression and activity, in renal CYP27B1 (coding for 1α-hydroxylase) expression as well as in serum 1,25(OH)2D3 levels, compared with mice fed isocaloric glucose- or fructose-normal Ca2+ diets. Replacing glucose with fructose prevented these increases in Ca2+ transporter, CYP27B1, and 1,25(OH)2D3 levels induced by a low Ca2+ diet. In adult mice fed for three mo a normal Ca2+ diet, renal expression of CYP27B1 and of CYP24A1 (24-hydroxylase) decreased and increased, respectively, when the carbohydrate source was fructose instead of glucose or starch. Intestinal and renal Ca2+ transporter activity and expression did not vary with dietary carbohydrate. To determine the time course of fructose effects, a high fructose or glucose diet with normal Ca2+ levels was fed to adult rats for three mo. Serum levels of 1,25(OH)2 D3 decreased and of FGF23 increased significantly over time. Renal expression of CYP27B1 and serum levels of 1,25(OH)2D3 still decreased in fructose- compared to those in glucose-fed rats after three mo. Serum parathyroid hormone, Ca2+ and phosphate levels were normal and independent of dietary sugar as well as time of feeding. Thus, chronically high fructose intakes can decrease serum levels of 1,25(OH)2D3 in adult rodents experiencing no Ca2+ stress and fed sufficient levels of dietary Ca2+. This finding is highly significant because fructose constitutes a substantial portion of the average diet of Americans already deficient in vitamin D.Peer reviewe
Pannexin-1 and P2X7-Receptor Are Required for Apoptotic Osteocytes in Fatigued Bone to Trigger RANKL Production in Neighboring Bystander Osteocytes
No full textOsteocyte apoptosis is required to induce intracortical bone remodeling after microdamage in animal models, but how apoptotic osteocytes signal neighboring “bystander” cells to initiate the remodeling process is unknown. Apoptosis has been shown to open pannexin-1 (Panx1) channels to release adenosine diphosphate (ATP) as a “find me” signal for phagocytic cells. To address whether apoptotic osteocytes use this signaling mechanism, we adapted the rat ulnar fatigue-loading model to reproducibly introduce microdamage into mouse cortical bone and measured subsequent changes in osteocyte apoptosis, receptor activator of NF-kB ligand (RANKL) expression and osteoclastic bone resorption in wild-type (WT; C57Bl/6) mice and in mice genetically deficient in Panx1 (Panx1KO). Mouse ulnar loading produced linear microcracks comparable in number and location to the rat model. WT mice showed increased osteocyte apoptosis and RANKL expression at microdamage sites at 3 days after loading and increased intracortical remodeling and endocortical tunneling at day 14. With fatigue, Panx1KO mice exhibited levels of microdamage and osteocyte apoptosis identical to WT mice. However, they did not upregulate RANKL in bystander osteocytes or initiate resorption. Panx1 interacts with P2X7R in ATP release; thus, we examined P2X7R-deficient mice and WT mice treated with P2X7R antagonist Brilliant Blue G (BBG) to test the possible role of ATP as a find-me signal. P2X7RKO mice failed to upregulate RANKL in osteocytes or induce resorption despite normally elevated osteocyte apoptosis after fatigue loading. Similarly, treatment of fatigued C57Bl/6 mice with BBG mimicked behavior of both Panx1 KO and P2X7RKO mice; BBG had no effect on osteocyte apoptosis in fatigued bone but completely prevented increases in bystander osteocyte RANKL expression and attenuated activation of resorption by more than 50%. These results indicate that activation of Panx1 and P2X7R are required for apoptotic osteocytes in fatigued bone to trigger RANKL production in neighboring bystander osteocytes and implicate ATP as an essential signal mediating this process.Peer reviewe
Bistability in Radiatively Heated Melt Ponds
No full textMelting and solidification processes, intertwined with convective flows, play a fundamental role in geophysical contexts. One of these processes is the formation of melt ponds on glaciers, ice shelves, and sea ice. It is driven by solar radiation and is of great significance for Earth’s heat balance, as it significantly lowers the albedo. Through direct numerical simulations and theoretical analysis, we unveil a bistability phenomenon in the melt pond dynamics. As solar radiation intensity and the melt pond’s initial depth vary, an abrupt transition occurs: this tipping point transforms the system from a stable fully frozen state to another stable equilibrium state, characterized by a distinct melt pond depth. The physics of this transition can be understood within a heat flux balance model, which exhibits excellent agreement with our numerical results. Together with the Grossmann-Lohse theory for internally heated convection, the model correctly predicts the bulk temperature and the flow strength within the melt ponds, offering insight into the coupling of phase transitions with adjacent turbulent flows and the interplay between convective melting and radiation-driven processes
Data for Thermodynamics of proton insertion across the perovskite-brownmillerite transition in La0.5Sr0.5CoO3-δ
No full textThe `protonation-of-lsco` zip includes the plots which appear in our manuscript, along with the data and scripts used to generate them. In addition to the structures, energies, and other data related to host, oxygen vacancy, and hydrogen interstitial structures of La0.5Sr0.5CoO3-δ (and SrCoO2.5), metadata (e.g., INCAR settings) related to the first-principle calculations is included in the data files. Each subfolder (`scripts`, `figures`, `dos_data`, and `data`) contains a detailed README.md file that provides additional information related to the files contained within.This repository exists to share the data and scripts used in the paper "Thermodynamics of proton insertion across the perovskite-brownmillerite transition in La0.5Sr0.5CoO3-δ" by Armand J. Lannerd, Nathan J. Szymanski, and Christopher J. Bartel. The files are contained in the folder `protonation-of-lsco` with additional detailed information presented in the `README.md` files of each subfolder (`scripts`, `figures`, `dos_data`, and `data`).This work was supported primarily by the National Science Foundation through the University of Minnesota MRSEC under Award Number DMR-2011401. This material is based upon work partially supported by the National Science Foundation Graduate Research Fellowship Program under Grant No. 2237827. Any opinions, findings, and conclusions or recommendations expressed in this material are those of the author(s) and do not necessarily reflect the views of the National Science Foundation. The authors acknowledge the Minnesota Supercomputing Institute (MSI) at the University of Minnesota for providing resources that contributed to the research results reported within this paper.Lannerd, Armand J; Szymanski, Nathan J; Bartel, Christopher J. (2026). Data for Thermodynamics of proton insertion across the perovskite-brownmillerite transition in La0.5Sr0.5CoO3-δ. Retrieved from the Data Repository for the University of Minnesota (DRUM), https://doi.org/10.13020/5etj-a120
The effects of estrogen deficiency on cortical bone microporosity and mineralization
No full textRecent studies have demonstrated matrix-mineral alterations in bone tissue surrounding osteocytes in estrogen-deficient animals.While cortical bone porosity has been shown to be a contributor to the mechanical properties of bone tissue, little analysis has been done to investigate the effects of estrogen deficiency on bone's microporosities, including the vascular and osteocyte lacunar porosities. In this study we examined alterations in cortical bone microporosity, mineralization, and cancellous bone architecture due to estrogen deficiency in the ovariectomized rat model of postmenopausal osteoporosis. Twenty-week-old female Sprague–Dawley rats were subjected to either ovariectomy or sham surgery. Six weeks post-surgery tibiae were analyzed using high-resolution micro-CT, backscattered electron imaging, nanoindentation, and dynamic histomorphometry. Estrogen deficiency caused an increase in cortical bone vascular porosity, with enlarged vascular pores and little change in tissue mineral density in the proximal tibial metaphysis. Measurements of cancellous architecture corresponded to previous studies reporting a decrease in bone volume fraction, an increase in trabecular separation, and a decrease in trabecular number in the proximal tibia due to estrogen deficiency. Nanoindentation results showed no differences in matrix stiffness in osteocyte-rich areas of the proximal tibia of estrogen-deficient rats, and bone labeling and backscattered electron imaging showed no significant changes in mineralization around the vascular pores. The findings demonstrate local surface alterations of vascular pores due to estrogen deficiency. An increase in cortical vascular porosity may diminish bone strength as well as alter bone mechanotransduction via interstitial fluid flow, both of which could contribute to bone fragility during postmenopausal osteoporosis.Peer reviewe
American Society of Biomechanics Journal of Biomechanics Award 2013: Cortical bone tissue mechanical quality and biological mechanisms possibly underlying atypical fractures
No full textThe biomechanics literature contains many well-understood mechanisms behind typical fracture types that have important roles in treatment planning. The recent association of "atypical" fractures with long-term use of drugs designed to prevent osteoporosis has renewed interest in the effects of agents on bone tissue-level quality. While this class of fracture was recognized prior to the introduction of the anti-resorptive bisphosphonate drugs and recently likened to stress fractures, the mechanism(s) that lead to atypical fractures have not been definitively identified. Thus, a causal relationship between these drugs and atypical fracture has not been established. Physicians, bioengineers and others interested in the biomechanics of bone are working to improve fracture-prevention diagnostics, and the design of treatments to avoid this serious side-effect in the future. This review examines the mechanisms behind the bone tissue damage that may produce the atypical fracture pattern observed increasingly with long-term bisphosphonate use. Our recent findings and those of others reviewed support that the mechanisms behind normal, healthy excavation and tunnel filling by bone remodeling units within cortical tissue strengthen mechanical integrity. The ability of cortical bone to resist the damage induced during cyclic loading may be altered by the reduced remodeling and increased tissue age resulting from long-term bisphosphonate treatment. Development of assessments for such potential fractures would restore confidence in pharmaceutical treatments that have the potential to spare millions in our aging population from the morbidity and death that often follow bone fracture.Peer reviewe
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