Acoustic and mechanical properties of tympanic membrane transplants

BACKGROUND: The human tympanic membrane has reasonably good sound transmission properties and withstands high static pressure loads. Destruction of the tympanic membrane resulting from middle ear diseases or trauma may be repaired by different types of grafts. Middle ear surgery mostly uses autologous temporal fascia, cartilage, or cartilage perichondrium transplants which differ in their acoustical characteristics and mechanical strength. METHODS: We have investigated the acoustical and mechanical properties of these materials and compared them with human tympanic membranes by constructing an ear canal-tympanic membrane model. Fresh human tympanic membrane, fascia, perichondrium, and cartilage preparations were exposed to static pressures up to 4 kPa and white noise sound pressure levels of 70 dB. The vibrational amplitudes and displacements due to static pressure were measured by laser Doppler vibrometry. RESULTS: The temporal fascia and perichondrium show similar amplitude frequency responses compared to the tympanic membrane for dynamic excitation. The displacement of these materials at static pressures above 4 kPa indicates a higher compliance than the tympanic membrane. The acoustical and mechanical properties of cartilage transplants are determined by the thickness of the slices. Thin cartilage slices are less stable although their frequency response is comparable to the intact tympanic membrane. Layer thickness above 500 microns result in a decrease of vibration amplitudes. CONCLUSIONS: Cartilage is an excellent transplant material which provides a better prognosis than soft materials in cases of ventilation disorders with long-term middle ear pressure problems. Large cartilage slice transplants should not exceed layer thickness of 500 microns in order to minimize transmission loss.     

A high-frequency shear device for testing soft biological tissues

Accurate mechanical property data obtained at large shear deformations and high frequencies are a fundamental component of realistic numerical simulations of soft tissue injury. Although many commercial systems exist for testing shear properties of viscoelastic materials with properties similar to soft biological tissue, none are capable of determining properties at high loading rates necessary for modeling soft tissue injury. Previous custom shear testing systems, though capable of high-frequency loading, indirectly measure tissue properties by using analytical corrections for inertial effects. To address these limitations, a new custom designed oscillatory shear testing apparatus (STA) capable of testing soft biological tissues in simple shear has been constructed and validated. Through a proper selection of sample thickness, direct measurement of material properties at high frequencies is achieved mechanically without analytical inertial adjustments. The complex shear modulus of three mixtures of silicone gel with viscoelastic properties in a range similar to soft biological tissue was characterized in the STA over a dynamic frequency range of 20-200 Hz and validated with a commercially available solids rheometer. The frequency-dependent complex shear modulus measurements of the STA were within 10% of the rheometer measurements for all mixtures over the entire frequency range tested. The STA represents substantive improvement over current shear testing methods by providing direct measurement of the shear behavior of soft viscoelastic material at high frequencies. Mechanical property data gained from this device will provide a more realistic basis for numerical simulations of biological structures.     

Yttrium aluminum garnet powders by nitrate decomposition and nitrate–urea solution combustion reactions—a comparative study

Precursors for yttrium aluminum garnet (Y₃Al₅O₁₂—YAG) were synthesized by simple decomposition of concentrated aqueous solution of nitrates and combustion of concentrated aqueous solution of nitrates with urea on a heater. The precursor formed by the former reaction was granules of agglomerated powder while that from the latter reaction was a voluminous and porous sponge-like mass. Both precursors were ground to powders and subjected to detailed thermogravimetric–differential thermal analysis and X-ray diffraction studies. The precursor from the simple decomposition of nitrates exhibited a total loss in weight of about 18% in stages (25 to 300 °C and 300 to 600 °C) accompanied by endotherms—characterized as processes of dehydration of absorbed moisture and decomposition of residual nitrates, respectively. The as formed precursor and that heated to 820 °C were amorphous. Crystallization to YAG phase occurred from an amorphous oxide characterized by an exotherm above 820 °C with no loss of weight. The precursor from nitrate–urea combustion reaction was found to exhibit a weight loss of 2.5% accompanied by a shallow endotherm in the range of 25 to 300 °C—characterized as the process of dehydration of absorbed moisture. No further weight loss or heat effect was noticed, confirming it to be chemically pure YAG. This as formed precursor was found to be crystalline YAG. The difference in chemical composition of the precursors formed by these two reactions is attributed to the difference in the actual reaction temperatures during their formation—lower reaction temperature for the endothermic decomposition of nitrates and higher reaction temperature for the exothermic combustion associated with the formation of a bright flame. The morphology of the precursor powder formed by the former reaction exhibited only cracks while that of the precursor from the latter reaction exhibited pores and voids. The precursor from the former reaction was calcined at 1100 °C to form into chemically pure YAG. Zeta potential variation with pH for the aqueous suspensions of the crystalline YAG powders from both the reactions exhibited a maximum value in the range of 40 to 50 mV around a pH of 4, indicating stability of these dispersions towards coagulation at this pH. Particle size distribution of wet ground powders (slurries with 20%, v/v, solid at a pH of 4) showed that the powder from combustion reaction could be formed into a finer size than that from simple nitrate decomposition, indicating the agglomerates of combustion reaction were softer.     

Detecting vascular access dysfunction

Access flow (QACC) is a major determinant of patency. Access recirculation (AR > 2%), normalized venous intra-access pressure (vPIA/MAP), and QACC are used to detect access dysfunction. We compared these three measures of access function (ultrasound dilution to measure AR and QACC). A total of 779 measurements were performed on 58 arteriovenous fistulas (AVFs) and 114 polytetrafluoroethylene (PTFE) grafts (1-8/access) over 13 months, and the access parameters at the beginning of each period were related to access events within that period. Pump blood flow averaged > 420 ml/min. AR occurred uncommonly (3.8%), and in half the cases, resulted from technical error by staff. In accesses that thrombosed or underwent intervention for stenosis, AR was present in only 3 of 11 AVFs and 8 of 57 PTFE accesses. When AR was present in grafts, QACC averaged 270 +/- 23, and access thrombosis followed unless intervention occurred. In grafts, vPIA/MAP averaged 0.34 +/- 0.01 in those remaining patent, 0.52 +/- 0.08 in those that had undergone intervention, and 0.54 +/- 0.04 in those that had thrombosed. QACC averaged 1,121 +/- 26, 605 +/- 45, and 550 +/- 65 ml/min, respectively, in the three groups. By contrast, QACC differed significantly in patent AVFs (1,053 +/- 35) compared with failing AVFs (363 +/- 48), but vPIA/MAP did not. AR is thus a late manifestation of access failure. QACC is the best diagnostic test of access dysfunction in AVFs. Interpretation of vPIA/MAP in grafts is enhanced by periodic QACC measurements.     

Selection of timed token protocol parameters to guarantee messagedeadlines

Networks that use the timed token protocol (such as the 100 Mbit/s FDDI network) are well suited for real-time applications because they guarantee, to each node, an average bandwidth and a bounded access time to the communication network. This guarantee is necessary but not sufficient for the timely delivery of deadline-constrained messages; protocol parameters must be carefully selected to ensure that these messages meet their deadlines. This paper addresses the issue of selecting the protocol parameters TTRT (target token rotation time) and the synchronous capacities assigned to each node. The objective is to guarantee that each synchronous message is transmitted before its deadline. An upper bound is derived on the worst case achievable utilization (WCAU) of any parameter selection scheme. The WCAU of a scheme is defined as the maximum utilization U such that the scheme guarantees all synchronous messages as long as their utilization is less than U. An algorithm for selecting the above parameters is proposed, The algorithm is shown to have a WCAU that is very close to the upper bound     

G-protein-mediated signaling in cholesterol-enriched arterial smooth muscle cells. 2. Role of protein kinase C-delta in the regulation of eicosanoid production

PGI2 generation by the vessel wall is an agonist for cyclic-AMP-dependent cholesteryl ester hydrolysis. The process of enhanced PGI2 synthesis is stimulated, in part, by G-protein-coupled receptor ligands. Cellular cholesterol enrichment has been hypothesized to alter G-protein-mediated PGI2 synthesis. In the studies reported herein, cells generated PGI2 in response to AlF4-, GTPgammaS, and ATP in a dose-dependent manner. G-protein agonists stimulated eicosanoid production principally by activating phospholipase A2, but not phospholipase C. This is in contrast to PDGF, which stimulated phospholipase A2 and PLCgamma activities. Galphai subunits mediate G-protein agonist-induced PGI2 synthesis, since ATP- and PDGF-induced PGI2 synthesis was inhibited by pertussis toxin. Although cholesterol enrichment reduced arachidonic acid- and PDGF-induced PGI2 synthesis, cholesterol enrichment enhanced PGI2 release in response to AlF4-, GTPgammaS, and ATP. The enhancement of PGI2 release in cholesterol-enriched cells was augmented by mevalonate, which inhibits the ability of cholesterol enrichment to reduce membrane-associated G-protein subunits. Since cholesterol enrichment inhibited PDGF and AlF4--induced MAP kinase activity [Pomerantz, K., Lander, H. M., Summers, B., Robishaw, J. D., Balcueva, E. A., & Hajjar, D. P. (1997) Biochemistry 36, 9523-9531] (the major mechanism by which phospholipase A2 is activated), these results suggest that cholesterol enrichment induces other alternative signaling pathways leading to phospholipase A2 activation. A PKC-dependent pathway is described herein that is involved in enhanced eicosanoid production in cholesterol-enriched cells. This conclusion is supported by two observations: (1) G-protein-linked PGI2 production is inhibited by calphostin, and (2) cholesterol enrichment augments the specific translocation of the delta-isoform of PKC from the cytosol to the plasma membrane following treatment of cells with phorbol ester. These data support the concept that, in cells possessing normal levels of cholesterol, MAP-kinase-dependent pathways mediate eicosanoid synthesis in response to G-protein activation; however, under conditions of high cellular cholesterol levels, augmented G-protein-linked eicosanoid production results from enhanced PKCdelta activity.     

Twenty-four-hour pharmacokinetics of rectal acetaminophen in children: an old drug with new recommendations

Oxidized low density lipoprotein (LDL) and acetyl LDL are recognized by the scavenger receptor class A type I/II (SR-AI/II) on macrophages and liver endothelial cells. Several investigators have suggested that there are additional receptors specific for oxidized LDL, but characterization of these alternate receptors for oxidized LDL and evaluation of their quantitative importance in uptake of oxidized LDL has been difficult because of overlapping ligand specificity with SR-AI/II. The purpose of this study was to determine the importance of SR-AI/II in the removal of modified LDL from the bloodstream in vivo. The clearance rate of oxidized LDL from plasma in normal mice was very rapid, and > 90% of injected dose was removed from the blood within 5 min. Clearance rates of oxidized LDL were equally high in SR-AI/II knockout mice, indicating that this receptor is not required for removal of oxidized LDL from plasma. Surprisingly, there was no difference in the clearance rate of acetyl LDL in wild-type and SR-AI/II knockout animals. The plasma clearance of radioiodinated acetyl LDL was almost fully blocked by a 50-fold excess of unlabeled acetyl LDL, but the latter only inhibited oxidized LDL clearance by approximately 5%. Both modified LDLs were cleared mostly by the liver, and there was no difference in the tissue distribution of modified LDL in control and knockout mice. Studies in isolated nonparenchymal liver cells showed that Kupffer cells accounted for most of the uptake of oxidized LDL. Extensively oxidized LDL and LDL modified by exposure to fatty acid peroxidation products were efficient competitors for the uptake of labeled oxidized LDL by SR-AI/II-deficient Kupffer cells, while acetyl LDL and malondialdehyde-modified LDL were relatively poor competitors.