Underneath the cerclage: an ex vivo study on the cerclage-bone interface mechanics

Cerclages regain interest due to a rising number of periprosthetic fractures. The contact distribution at the circumferential cerclage-bone interface is still unknown. Local interface pressure depends on the amount of contact area. Cortical damage at the interface would provoke cerclage loosening. Therefore, the contact area, the bone pressure along the interface and the cortical resistance underneath loaded cerclages were determined in an ex vivo model.

A novel interface for hybrid mock circulations to evaluate ventricular assist devices

This paper presents a novel mock circulation for the evaluation of ventricular assist devices (VADs), which is based on a hardware-in-the-loop concept. A numerical model of the human blood circulation runs in real time and computes instantaneous pressure, volume, and flow rate values. The VAD to be tested is connected to a numerical-hydraulic interface, which allows the interaction between the VAD and the numerical model of the circulation. The numerical-hydraulic interface consists of two pressure-controlled reservoirs, which apply the computed pressure values from the model to the VAD, and a flow probe to feed the resulting VAD flow rate back to the model. Experimental results are provided to show the proper interaction between a numerical model of the circulation and a mixed-flow blood pump.

Microscopic and Spectroscopic Methods for Probing the Clay Water Interface

Clay minerals have a fundamental importance in many processes in soils and sediments such as the bioavailability of nutrients, water retention, the adsorption of common pollutants, and the formation of an impermeable barrier upon swelling. Many of the properties of clay minerals are due to the unique environment present at the clay mineral/water interface. Traditional techniques such as X-ray diffraction (XRD) and absorption isotherms have provided a wealth of information about this interface but have suffered from limitations. The methods and results presented herein are designed to yield new experimental information about the clay mineral/water interface.A new method of studying the swelling dynamics of clay minerals was developed using in situ atomic force microscopy (AFM). The preliminary results presented here demonstrate that this technique allows one to study individual clay mineral unit layers, explore the natural heterogeneities of samples, and monitor swelling dynamics of clay minerals in real time. Cation exchange experiments were conducted monitoring the swelling change of individual nontronite quasi-crystals as the chemical composition of the surrounding environment was manipulated several times. A proof of concept study has shown that the changes in swelling are from the exchange of interlayer cations and not from the mechanical force of replacing the solution in the fluid cell. A series of attenuated total internal reflection Fourier transform infrared spectroscopy (ATR-FTIR) experiments were performed to gain a better understanding of the organization of water within the interlayer region of two Fe-bearing clay minerals. These experiments made use of the Subtractive Kramers-Kronig (SKK) Transform and the calculation of difference spectra to obtain information about interfacial water hidden within the absorption bands of bulk water. The results indicate that the reduction of structural iron disrupts the organization of water around a strongly hydrated cation such as sodium as the cation transitions from an outer-sphere complex with the mineral surface to an inner-sphere complex. In the case of a less strongly hydrated cation such as potassium, reduction of structural iron actually increases the ordering of water molecules at the mineral surface. These effects were only noticed with the reduction of iron in the tetrahedral sheet close to the basal surface where the increased charge density is localized closer to the cations in the interlayer.

Translocation and potential neurological effects of fine and ultrafine particles a critical update

ABSTRACT: Particulate air pollution has been associated with respiratory and cardiovascular disease. Evidence for cardiovascular and neurodegenerative effects of ambient particles was reviewed as part of a workshop. The purpose of this critical update is to summarize the evidence presented for the mechanisms involved in the translocation of particles from the lung to other organs and to highlight the potential of particles to cause neurodegenerative effects.Fine and ultrafine particles, after deposition on the surfactant film at the air-liquid interface, are displaced by surface forces exerted on them by surfactant film and may then interact with primary target cells upon this displacement. Ultrafine and fine particles can then penetrate through the different tissue compartments of the lungs and eventually reach the capillaries and circulating cells or constituents, e.g. erythrocytes. These particles are then translocated by the circulation to other organs including the liver, the spleen, the kidneys, the heart and the brain, where they may be deposited. It remains to be shown by which mechanisms ultrafine particles penetrate through pulmonary tissue and enter capillaries. In addition to translocation of ultrafine particles through the tissue, fine and coarse particles may be phagocytized by macrophages and dendritic cells which may carry the particles to lymph nodes in the lung or to those closely associated with the lungs. There is the potential for neurodegenerative consequence of particle entry to the brain. Histological evidence of neurodegeneration has been reported in both canine and human brains exposed to high ambient PM levels, suggesting the potential for neurotoxic consequences of PM-CNS entry. PM mediated damage may be caused by the oxidative stress pathway. Thus, oxidative stress due to nutrition, age, genetics among others may increase the susceptibility for neurodegenerative diseases. The relationship between PM exposure and CNS degeneration can also be detected under controlled experimental conditions. Transgenic mice (Apo E -/-), known to have high base line levels of oxidative stress, were exposed by inhalation to well characterized, concentrated ambient air pollution. Morphometric analysis of the CNS indicated unequivocally that the brain is a critical target for PM exposure and implicated oxidative stress as a predisposing factor that links PM exposure and susceptibility to neurodegeneration.Together, these data present evidence for potential translocation of ambient particles on organs distant from the lung and the neurodegenerative consequences of exposure to air pollutants.

Peri-implant inflammation defined by the implant-abutment interface

An implant-abutment interface at the alveolar bone crest is associated with sustained peri-implant inflammation; however, whether magnitude of inflammation is proportionally dependent upon interface position remains unknown. This study compared the distribution and density of inflammatory cells surrounding implants with a supracrestal, crestal, or subcrestal implant-abutment interface. All implants developed a similar pattern of peri-implant inflammation: neutrophilic polymorphonuclear leukocytes (neutrophils) maximally accumulated at or immediately coronal to the interface. However, peri-implant neutrophil accrual increased progressively as the implant-abutment interface depth increased, i.e., subcrestal interfaces promoted a significantly greater maximum density of neutrophils than did supracrestal interfaces (10,512 +/- 691 vs. 2398 +/- 1077 neutrophils/mm(2)). Moreover, inflammatory cell accumulation below the original bone crest was significantly correlated with bone loss. Thus, the implant-abutment interface dictates the intensity and location of peri-implant inflammatory cell accumulation, a potential contributing component in the extent of implant-associated alveolar bone loss.