Time filter

Source Type

Menlo Park, CA, United States

The use of metallic materials for implantable medical devices has prompted numerous studies aimed at characterizing the corrosion susceptibility of these materials and understanding their electrochemical behavior in simulated and actual physiological liquids. This review focuses on the forms of corrosion that are of principal interest for Ti and its alloys in vivo: general corrosion, pitting corrosion, crevice corrosion, galvanic corrosion, and fretting corrosion. It also addresses environmentally assisted cracking in the form of hydrogen embrittlement. Of particular interest is the susceptibility of Ti and its alloys to the different forms of corrosion with regard to both solution chemistry, especially the effect of organic species, and surface characteristics such as oxide composition, surface inclusions, and wear/fretting. Source

Pound B.G.,Exponent, Inc.
Journal of Biomedical Materials Research - Part A | Year: 2014

The metallic materials used for implantable medical devices are predominantly stainless steels, Ti and its alloys, and Co-Cr alloys. The corrosion resistance of each of these materials is associated with a passive oxide film on its surface. Since corrosion resistance is crucial to implant performance, considerable effort has been focused on understanding the nature of the passive film present under physiological conditions. Surface analytical techniques and electrochemical impedance spectroscopy have been used in a number of studies to investigate the passive film formed on metallic biomaterials in simulated physiological solutions. This review focuses on the surface characteristics of these materials with regard to composition, thickness, and impedance of the passive films. Of particular interest are changes in the films with surface treatment and the nature of the films developed over time in the simulated solutions. © 2013 Wiley Periodicals, Inc. Source

Lovald S.,Exponent, Inc.
Journal of surgical orthopaedic advances | Year: 2014

The purpose of the current study is to identify patients who are at high risk for rehospitalization, revision, complications, and mortality after outpatient and short-stay total knee arthroplasty (TKA). The Medicare 5% limited data set sample was used to identify patients with a TKA procedure who were treated in an outpatient setting or who were discharged within 1 or 2 days in the hospital setting. Rehospitalization risk increased with higher Charlson score (i.e., poorer health status), older patients, inpatients (vs. outpatients), patients not receiving a femoral nerve block, earlier (vs. recent) year of surgery, and those with a recent history of heart failure. The findings of this study suggest that existing comorbidities, particularly heart failure, have the greatest effect on event risk after outpatient and short-stay TKA. The information obtained from this study should assist with patient selection for TKA performed on an outpatient basis. Source

Seven current contending cancer theories consider different sets of critical events as sufficient for tumorigenesis. These theories, most recently the microRNA dysregulation (MRD) theory, have overlapping attributes and extensive empirical support, but also some discrepancies, and some do not address both benign and malignant tumorigenesis. By definition, the most efficient tumorigenic pathways will dominate under conditions that selectively activate those pathways. The MRD theory provides a mechanistic basis to combine elements of the current theories into a new hypothesis that: (i) tumors arise most efficiently under stress that induces and sustains either protective or regenerative states of adaptive hyperplasia (AH) that normally are epigenetically maintained unless terminated; and (ii) if dysregulated by a somatic mutation that prevents normal termination, these two AH states can generate benign and malignant tumors, respectively. This hypothesis, but not multistage cancer theory, predicts that key participating AH-stem-cell populations expand markedly when triggered by stress, particularly chronic metabolic or oxidative stress, mechanical irritation, toxic exposure, wounding, inflammation, and/or infection. This hypothesis predicts that microRNA expression patterns in benign vs. malignant tumor tissue will correlate best with those governing protective vs. regenerative AH in that tissue, and that tumors arise most efficiently inmutagen-exposed stem cells that either happen to be in, or incidentally later become recruited into, an AH state. © 2012 Elsevier Ltd. Source

O'Reilly K.T.,Exponent, Inc.
Integrated environmental assessment and management | Year: 2014

A realistic understanding of contaminant sources is required to set appropriate control policy. Forensic chemical methods can be powerful tools in source characterization and identification, but they require a multiple-lines-of-evidence approach. Atmospheric receptor models, such as the US Environmental Protection Agency (USEPA)'s chemical mass balance (CMB), are increasingly being used to evaluate sources of pyrogenic polycyclic aromatic hydrocarbons (PAHs) in sediments. This paper describes the assumptions underlying receptor models and discusses challenges in complying with these assumptions in practice. Given the variability within, and the similarity among, pyrogenic PAH source types, model outputs are sensitive to specific inputs, and parsing among some source types may not be possible. Although still useful for identifying potential sources, the technical specialist applying these methods must describe both the results and their inherent uncertainties in a way that is understandable to nontechnical policy makers. The authors present an example case study concerning an investigation of a class of parking-lot sealers as a significant source of PAHs in urban sediment. Principal component analysis is used to evaluate published CMB model inputs and outputs. Targeted analyses of 2 areas where bans have been implemented are included. The results do not support the claim that parking-lot sealers are a significant source of PAHs in urban sediments. © 2013 SETAC. Source

Discover hidden collaborations