Harmonic analysis of lossy piezoelectric composite transducers using the plane wave expansion method

Periodic composite ultrasonic transducers oer many advantages but the periodic pillar architecture can give rise to unwanted modes of vibration which interfere with the piston like motion of the fundamental thickness mode. In this paper, viscoelastic loss is incorporated into a three dimensional plane wave expansion model (PWE) of these transducers. A comparison with experimental and nite element data is conducted and a design to damp out these lateral modes is investigated. Scaling and regularisation techniques are introduced to the PWE method to reduceill-conditioning in the large matrices which can arise. The identication of the modes of vibration is aided by examining proles of the displacements, electrical potentialand Poynting vector. The dispersive behaviour of a 2-2 composite transducer with high shear attenuation in the passive phase is examined. The model shows thatthe use of a high shear attenuation ller material improves the frequency band gap surrounding the fundamental thickness mode

Analysis of ultrasonic transducers with fractal architecture

Ultrasonic transducers composed of a periodic piezoelectric composite are generally accepted as the design of choice in many applications. Their architecture is normally very regular and this is due to manufacturing constraints rather than performance optimisation. Many of these manufacturing restrictions no longer hold due to new production methods such as computer controlled, laser cutting, and so there is now freedom to investigate new types of geometry. In this paper, the plane wave expansion model is utilised to investigate the behaviour of a transducer with a self-similar architecture. The Cantor set is utilised to design a 2-2 conguration, and a 1-3 conguration is investigated with a Sierpinski Carpet geometry

In Situ Type I Oligomeric Collagen Macroencapsulation Promotes Islet Longevity and Function in Vitro and in Vivo

Widespread use of pancreatic islet transplantation for treatment of type 1 diabetes (T1D) is currently limited by requirements for long-term immunosuppression, limited donor supply, and poor long-term engraftment and function. Upon isolation from their native microenvironment, islets undergo rapid apoptosis, which is further exacerbated by poor oxygen and nutrient supply following infusion into the portal vein. Identifying alternative strategies to restore critical microenvironmental cues, while maximizing islet health and function, is needed to advance this cellular therapy. We hypothesized that biophysical properties provided through type I oligomeric collagen macroencapsulation are important considerations when designing strategies to improve islet survival, phenotype, and function. Mouse islets were encapsulated at various Oligomer concentrations (0.5–3.0 mg/ml) or suspended in media and cultured for 14 days, after which viability, protein expression, and function were assessed. Oligomer-encapsulated islets showed a density-dependent improvement in in vitro viability, cytoarchitecture, and insulin secretion, with 3 mg/ml yielding values comparable to freshly isolated islets. For transplantation into streptozotocin-induced diabetic mice, 500 islets were mixed in Oligomer and injected subcutaneously, where rapid in situ macroencapsulation occurred, or injected with saline. Mice treated with Oligomer-encapsulated islets exhibited rapid (within 24 h) diabetes reversal and maintenance of normoglycemia for 14 (immunocompromised), 90 (syngeneic), and 40 days (allogeneic). Histological analysis showed Oligomer-islet engraftment with maintenance of islet cytoarchitecture, revascularization, and no foreign body response. Oligomer-islet macroencapsulation may provide a useful strategy for prolonging the health and function of cultured islets and has potential as a subcutaneous injectable islet transplantation strategy for treatment of T1D

Cardiac-Specific Inactivation of LPP3 in Mice Leads to Myocardial Dysfunction and Heart Failure

Lipid Phosphate phosphatase 3 (LPP3), encoded by the Plpp3 gene, is an enzyme that dephosphorylates the bioactive lipid mediator lysophosphatidic acid (LPA). To study the role of LPP3 in the myocardium, we generated a cardiac specific Plpp3 deficient mouse strain. Although these mice were viable at birth in contrast to global Plpp3 knockout mice, they showed increased mortality ~ 8 months. LPP3 deficient mice had enlarged hearts with reduced left ventricular performance as seen by echocardiography. Cardiac specific Plpp3 deficient mice had longer ventricular effective refractory periods compared to their Plpp3 littermates. We observed that lack of Lpp3 enhanced cardiomyocyte hypertrophy based on analysis of cell surface area. We found that lack of Lpp3 signaling was mediated through the activation of Rho and phospho-ERK pathways. There are increased levels of fetal genes Natriuretic Peptide A and B (Nppa and Nppb) expression indicating myocardial dysfunction. These mice also demonstrate mitochondrial dysfunction as evidenced by a significant decrease (P \u3c 0.001) in the basal oxygen consumption rate, mitochondrial ATP production, and spare respiratory capacity as measured through mitochondrial bioenergetics. Histology and transmission electron microscopy of these hearts showed disrupted sarcomere organization and intercalated disc, with a prominent disruption of the cristae and vacuole formation in the mitochondria. Our findings suggest that LPA/LPP3-signaling nexus plays an important role in normal function of cardiomyocytes

The critical fugacity for surface adsorption of self-avoiding walks on the honeycomb lattice is 1+21+\sqrt{2}

In 2010, Duminil-Copin and Smirnov proved a long-standing conjecture of Nienhuis, made in 1982, that the growth constant of self-avoiding walks on the hexagonal (a.k.a. honeycomb) lattice is $\mu=\sqrt{2+\sqrt{2}}.$ A key identity used in that proof was later generalised by Smirnov so as to apply to a general O(n) loop model with $n\in [-2,2]$ (the case $n=0$ corresponding to SAWs). We modify this model by restricting to a half-plane and introducing a surface fugacity $y$ associated with boundary sites (also called surface sites), and obtain a generalisation of Smirnov's identity. The critical value of the surface fugacity was conjectured by Batchelor and Yung in 1995 to be $y_{\rm c}=1+2/\sqrt{2-n}.$ This value plays a crucial role in our generalized identity, just as the value of growth constant did in Smirnov's identity. For the case $n=0$, corresponding to \saws\ interacting with a surface, we prove the conjectured value of the critical surface fugacity. A crucial part of the proof involves demonstrating that the generating function of self-avoiding bridges of height $T$, taken at its critical point $1/\mu$, tends to 0 as $T$ increases, as predicted from SLE theory.Comment: Major revision, references updated, 25 pages, 13 figure

A kinetic study of the CH₂OO Criegee intermediate self-reaction, reaction with SO₂ and unimolecular reaction using cavity ring-down spectroscopy

A rate coefficient is reported for the CH2OO self-reaction and evidence presented for SO2-catalysed CH2OO isomerization or intersystem crossing.</p

Nitrogen fertilizer rate but not form affects the severity of Fusarium wilt in banana

Nitrogen (N) fertilizers are routinely applied to bananas (Musa spp.) to increase production but may exacerbate plant diseases like Fusarium wilt of banana (FWB), which is the most economically important disease. Here, we characterized the effects of N rate and form on banana plant growth, root proteome, bacterial and fungal diversity in the rhizosphere, the concentration of Fusarium oxysporum f.sp. cubense (Foc) in the soil, and the FWB severity. Banana plants (Musa subgroup ABB) were grown under greenhouse conditions in soil with ammonium or nitrate supplemented at five N rates, and with or without inoculation with Foc. The growth of non-inoculated plants was positively correlated with the N rate. In bananas inoculated with Foc, disease severity increased with the N rate, resulting in the Foc-inoculated plant growth being greatest at intermediate N rates. The abundance of Foc in the soil was weakly related to the treatment conditions and was a poor predictor of disease severity. Fungal diversity was consistently affected by Foc inoculation, while bacterial diversity was associated with changes in soil pH resulting from N addition, in particular ammonium. N rate altered the expression of host metabolic pathways associated with carbon fixation, energy usage, amino acid metabolism, and importantly stress response signaling, irrespective of inoculation or N form. Furthermore, in diseased plants, Pathogenesis-related protein 1, a key endpoint for biotic stress response and the salicylic acid defense response to biotrophic pathogens, was negatively correlated with the rate of ammonium fertilizer but not nitrate. As expected, inoculation with Foc altered the expression of a wide range of processes in the banana plant including those of defense and growth. In summary, our results indicate that the severity of FWB was negatively associated with host defenses, which was influenced by N application (particularly ammonium), and shifts in microbial communities associated with ammonium-induced acidification. Copyright © 2022 Orr, Dennis, Wong, Browne, Cooper, Birt, Lapis-Gaza, Pattison and Nelson

The impact of seawater saturation state and bicarbonate ion concentration on calcification by new recruits of two Atlantic corals

Author Posting. © The Author(s), 2010. This is the author's version of the work. It is posted here by permission of Springer for personal use, not for redistribution. The definitive version was published in Coral Reefs 30 (2011): 321-328, doi:10.1007/s00338-010-0697-z.Rising concentrations of atmospheric CO2 are changing the carbonate chemistry of the oceans, a process known as ocean acidification (OA). Absorption of this CO2 by the surface oceans is increasing the amount of total dissolved inorganic carbon (DIC) and bicarbonate ion (HCO3 -) available for marine calcification, yet is simultaneously lowering the seawater pH and carbonate ion concentration ([CO3 2-]), and thus the saturation state of seawater with respect to aragonite (Ωar). We investigated the relative importance of [HCO3 -] versus [CO3 2-] for early calcification by new recruits (primary polyps settled from zooxanthellate larvae) of two tropical coral species, Favia fragum and Porites astreoides. The polyps were reared over a range of Ωar values, which were manipulated by both acid-addition at constant pCO2 (decreased total [HCO3 -] and [CO3 2-]) and by pCO2 elevation at constant alkalinity (increased [HCO3 -], decreased [CO3 2-]). Calcification after two weeks was quantified by weighing the complete skeleton (corallite) accreted by each polyp over the course of the experiment. Both species exhibited the same negative response to decreasing [CO3 2-] whether Ωar was lowered by acid-addition or by pCO2 elevation - calcification did not follow total DIC or [HCO3 -]. Nevertheless, the calcification response to decreasing [CO3 2-] was non-linear. A statistically significant decrease in calcification was only detected between Ωar = < 2.5 and Ωar = 1.1 – 1.5, where calcification of new recruits was reduced by 22 – 37 % per 1.0 decrease in Ωar. Our results differ from many previous studies that report a linear coral calcification response to OA, and from those showing that calcification increases with increasing [HCO3 -]. Clearly, the coral calcification response to OA is variable and complex. A deeper understanding of the biomineralization mechanisms and environmental conditions underlying these 3 variable responses is needed to support informed predictions about future OA impacts on corals and coral reefs.This study was supported by NSF award 0648157 (Cohen and McCorkle), NSF 1041106 (Cohen, McCorkle), NSF 1041052 (de Putron), the VITA foundation (de Putron), WHOI Ocean Life Institute (Cohen), PEI and EEB Departments at Princeton University, Bill and Anne Charrier, and the Anthony B. Evnin, Dean’s Roundtable, and Edmund Hayes Sr. senior thesis funds (Dillon)