The pericellular matrix (PCM) is a narrow tissue region surrounding chondrocytes in articular cartilage, which together with the enclosed cell(s) has been termed the "chondron." While the function of this region is not fully understood, it is hypothesized to have important biological and biomechanical functions. In this article, we review a number of studies that have investigated the structure, composition, mechanical properties, and biomechanical role of the chondrocyte PCM. This region has been shown to be rich in proteoglycans (e.g., aggrecan, hyaluronan, and decorin), collagen (types II, VI, and IX), and fibronectin, but is defined primarily by the presence of type VI collagen as compared to the extracellular matrix (ECM). Direct measures of PCM properties via micropipette aspiration of isolated chondrons have shown that the PCM has distinct mechanical properties as compared to the cell or ECM. A number of theoretical and experimental studies suggest that the PCM plays an important role in regulating the microenvironment of the chondrocyte. Parametric studies of cell-matrix interactions suggest that the presence of the PCM significantly affects the micromechanical environment of the chondrocyte in a zone-dependent manner. These findings provide support for a potential biomechanical function of the chondrocyte PCM, and furthermore, suggest that changes in the PCM and ECM properties that occur with osteoarthritis may significantly alter the stress-strain and fluid environments of the chondrocytes. An improved understanding of the structure and function of the PCM may provide new insights into the mechanisms that regulate chondrocyte physiology in health and disease.

The pericellular matrix (PCM) is a narrow region of tissue that completely surrounds chondrocytes in articular cartilage. Previous theoretical models of the "chondron" (the PCM with enclosed cells) suggest that the structure and properties of the PCM may significantly influence the mechanical environment of the chondrocyte. The objective of this study was to quantify changes in the three-dimensional (3D) morphology of the chondron in situ at different magnitudes of compression applied to the cartilage extracellular matrix. Fluorescence immunolabeling for type-VI collagen was used to identify the boundaries of the cell and PCM, and confocal microscopy was used to form 3D images of chondrons from superficial, middle, and deep zone cartilage in explants compressed to 0%, 10%, 30%, and 50% surface-to-surface strain. Lagrangian tissue strain, determined locally using texture correlation, was highly inhomogeneous and revealed depth-dependent compressive stiffness and Poisson's ratio of the extracellular matrix. Compression significantly decreased cell and chondron height and volume, depending on the zone and magnitude of compression. In the superficial zone, cellular-level strains were always lower than tissue-level strains. In the middle and deep zones, however, tissue strains below 25% were amplified at the cellular level, while tissue strains above 25% were decreased at the cellular level. These findings are consistent with previous theoretical models of the chondron, suggesting that the PCM can serve as either a protective layer for the chondrocyte or a transducer that amplifies strain, such that cellular-level strains are more homogenous throughout the tissue depth despite large inhomogeneities in local ECM strains.

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Fracture toughness of re-entrant foam materials with a negative Poisson's ratio is explored experimentally as a function of permanent volumetric compression ratio, a processing variable. Jic values of toughness of negative Poisson's ratio open cell copper foams are enhanced by 80percent, 130percent, and 160percent for permanent volumetric compression ratio values of 2.0, 2.5, and 3.0, respectively, compared to the Jic value of the conventional foam (with a positive Poisson's ratio). Analytical study based on idealized polyhedral cell structures, approximating the shape of the conventional and re-entrant cells, disclose for re-entrant foam, toughness increasing as Poisson's ratio becomes more negative. The increase in toughness is accompanied by an increase in compliance, a combination not seen in conventional foam, and which may be useful in some applications such as sponges.

The shape and orientation of the chondron appear to reflect the local collagen architecture of the interterritorial matrix, which varies significantly with depth. Quantitative measurements of morphology of the chondron and its variation with site, disease, or aging may provide new insights into the influence of this structure on physiology and the pathology of articular cartilage.

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Background This study aimed to evaluate the current overall preventable trauma death rate (PTDR) in Korea and identify factors associated with preventable trauma death (PTD). Methods The target sample size for review was designed to be 1,131 deaths in 60 emergency medical institutions nationwide. The panels for the review comprised trauma specialists working at the regional trauma centers (RTCs); a total of 10 teams were formed. The PTDR and factors associated with PTD were analyzed statistically. Results Of the target cases, 943 were able to undergo panel review and be analyzed statistically. The PTDR was 30.5% (6.1% preventable and 24.4% possibly preventable). Those treated at a RTC showed a significantly lower PTDR than did those who were not (21.9% vs. 33.9%; P = 0.002). The PTDR was higher when patients were transferred from other hospitals than when they directly visited the last hospital (58.9% vs. 28.4%; P = 0.058; borderline significant). The PTDR increased gradually as the time from accident to death increased; a time of more than one day had a PTDR 14.99 times higher than when transferred within one hour (95% confidence interval, 4.68 to 47.98). Conclusion Although the PTDR in Korea is still high compared to that in developed countries, it was lower when the time spent from the accident to the death was shorter and the final destined institution was the RTC. To reduce PTDR, it is necessary to make an effort to transfer trauma patients to RTCs directly within an appropriate time.

Osteopontin (OPN) is an adhesive glycoprotein linked to a variety of pathophysiological processes. We investigated whether OPN might act as an opsonin in the diseased brain by studying the postischemic expression and localization of OPN mRNA and protein in a rat model of ischemic stroke. In addition, we characterized the subcellular localization of OPN protein in the ischemic brain core. Induction of OPN mRNA occurred in activated microglia/macrophages in the ischemic core on days 3-7 after reperfusion and this was sustained up to day 28, at least. OPN protein was synthesized and secreted by brain macrophages, which first surrounded damaged striatal white matter tracts and then infiltrated into them. Punctate OPN-immunoreactive profiles were scattered throughout the infarction core except in white matter bundles. Electron microscopy showed the localization of OPN protein along the membranes lining what appeared to be the debris of dead neurons. These were located in the extracellular space and within the cytoplasm of brain macrophages, indicating that the OPN protein accumulated selectively on the surface of dead cells, most of which were phagocytosed subsequently by brain macrophages. However, no significant induction of OPN occurred in degenerating striatal white matter tracts or in brain macrophage-engulfed axonic or myelin debris. These data suggest that OPN secreted by brain macrophages in this rat model of stroke might be involved in the phagocytosis of fragmented cell debris and possibly not in the phagocytosis of axonic or myelin debris.