bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of injurious compression on matrix turnover around individual cells in calf articular cartilage explants
Authors: Quinn Thomas M. , Grodzinsky Alan J. , Hunziker Ernst B. , Sandy John D. 
Published: February 2005

AbstractThe effects of mechanical injury on the metabolism of cartilage matrix are of interest for understanding the pathogenesis of osteoarthrosis and the development of strategies for cartilage repair. The purpose of the present study was to examine the effects of injury on matrix turnover in a calf articular cartilage explant system for which the effects of mechanical loading on cell activity and the cell‐mediated pathways of matrix metabolism are already well characterized. New methods of quantitative autoradiography were used in combination with established biochemical and biomechanical techniques for the analysis of cell and matrix responses to acute mechanical injury, with particular attention to the processes of localized matrix turnover in the cell‐associated matrices of individual chondrocytes. Matrix deposition and turnover around cells in control explants was spatially dependent, with the highest rates of proteoglycan deposition and tunrtover arid the lowest rates of collagen deposition (as indicated by [3H]proline autoradiography) occurring in the pericellular matrix. Injurious compression was associated with (a) an abrupt decrease in the tensile load‐carrying capacity of the collagen matrix, apparently associated with mechanical failure of the tissue, (b) a considerable but subtotal decrease in cell viability, marked by the emergence of an apparently inactive cell population interspersed within catabolically active but abnormally large cells, and (c) sustained, elevated rates of protcoglycan turnover, particularly in the cell‐associated matrices of apparently viable cells, which involved the increased release of aggregating species in addition to a spectrum of degradation fragments that were also in controls. These results may represent an in vitro model for the responses of chondrocytes and the cartilage extracellular matrix to mechanical injury.
Effect of ciprofloxacin on the proliferation of osteoblast‐like MG‐63 human osteosarcoma cells in vitro
Authors: Miclau Theodore , Edin Matthew L. , Lester Gayle E. , Lindsey Ronald W. , Dahners Laurence E. 
Published: February 2005

AbstractLocally applied antibiotic therapy is gaining popularity for the treatment of infections associated with open fractures and posttraumatic osteomyelitis. With use of local techniques, ciprofloxacin levels as high as 1,300 μg/ml. or over 200 times the bone levels achieved with intravenous administration, have been reported. To study the possible effects of ciprofloxacin on bone, osteoblast‐like cells from the MG‐63 human osteosarcoma cell line were studied. The cells were grown in antibiotic‐free media and exposed to concentrations of ciprofloxacin at 0, 10, 100, 200, and 1,000 μg/ml to establish an initial dose‐response curve. Media containing the appropriate dose of ciprofloxacin were changed every 24 hours. Cell number and [3H]thymidine incorporation per cell were determined at 0, 24 and 72 hours. A second dose‐response curve was performed at concentrations of 0, 10, 20, 40, and 80 μg/ ml. Three experiments, each with four observations, were performed. The results of this study demonstrated that ciprofloxacin caused significant decreases (p < 0.05) in cell number at 40 μg/ml at 24 hours and 20 μg/ml at 72 hours. [3H]thymidine incorporation per cell decreased significantly at levels of 80 μg/ml at 24 hours and 20 μg/ml at 72 hours. The authors conclude that reported local levels of ciprofloxacin seen in vivo inhibit the proliferation of human osteoblast‐like cells in vitro.
Expression of cartilage extracellular matrix and potential regulatory genes in a new human chondrosarcoma cell line
Authors: Chansky Howard , Robbins James R. , Cha Steven , Raskind Wendy H. , Conrad Ernest U. , Sandell Linda J. 
Published: February 2005

AbstractA human chondrosarcoma cell line has been established from an aggressive chondrosarcoma. The cells grow in a monolayer culture (doubling time: 2 days) and form aggregates. The aggregates consist of a rim of cells surrounding a hollow core. The cell line exhibits a unique pattern of mRNA expression with several molecules characteristic of the chondrocyte phenotype. Consistent with the chondrocyte phenotype, mRNAsencoding types IX and XI collagens were present along with an abundant expression of mRNAsencoding the core protein of the cartilage proteoglycans biglycan and aggrecan. No expression of mRNAs encoding types I or II fibrillar collagens or the proteoglycan decorin was observed. Sodium dodecyl sulfate‐polyacrylamide gel electrophoretic analysis of [35S]sulfate‐radiolabeled material confirmed the translation of proteoglycans containing glycosaminoglycan chains. The expression of molecules that contribute to cartilage development and tumorigenesis was examined. The cell line produces abundant mRNA that encodes transforming growth factor‐β1, a member of a family of cartilage and bone inductive proteins. The expression of mRNA encoding two proteins associated specifically with chondrogenesis was detected: Cart‐1, a homeobox protein involved in cartilage differentiation, and CD‐RAP, a secreted molecule restricted under normal conditions to differentiating chondrocytes and cartilage. Overexpression of p53, a tumor‐suppressor gene, was detected. DNA analysis revealed a loss of heterozygosity at the chromosomal locus encoding p53, with the deletion of one p53 allele and the mutation of the remaining allele in both the parent tumor and the cell line. The malignant chondrosarcoma phenotype may be related to the unique gene expression pattern that is characteristic in many ways of differentiating chondroblasts, as well as to the inactivation of the p53 function that could contribute to the proliferative capacity of the cell line. This cell line may serve as a biological model for further investigation of the etiology of human chondrosarcomas and for the synthesis and regulation of cartilage‐specific genes.
Deformation of femoral nails with intramedullary insertion
Authors: Krettek Christian , Mannß Jürgen , Miclau Theodore , Schandelmaier Peter , Linnemann Ina , Tscherne Harald 
Published: February 2005

AbstractCurrent methods of distal interlocking of intramedullary femoral nails are dependent on image intensification. However, radiation exposure to the patient, the operating room staff, and the surgeon remains a concern. Proximally mounted, radiation‐free aiming systems for distal interlocking of femoral nails have reportedly failed because of nail deformation with insertion. To better understand this deformation, a threedimensional magnetic motion tracking system was used to determine the position of the distal interlocking hole following nail insertion. The amount and direction of deformation of commercially available smalldiameter implants (unslotted 9‐mm nails inserted without reaming) and large‐diameter implants (slotted 13‐mm nails inserted with reaming) from a single manufacturer were analyzed. Measurements of deformation (three translations and three angles), based on the center of the distal transverse locking hole, were performed on 10 paired intact human cadaveric femora before and after insertion. The technique produced the following results for the small and large‐diameter nails, respectively: lateral translations of 18.1 ± 10.0 mm (mean ± SD, range: 47.8 mm) and 21.5 ± 7.9 mm (range: 26.4 mm), dorsal translations of ‐3.1 ± 4.3 mm (range: 15.2 mm) and 0.4 ± 9.8 mm (range: 30.1 mm), and rotation about the longitudinal axes of −0.1 ± 0.2° (range: 0.7°) and 10.0 ±3.1° (range: 7.8°). This technique is useful for measuring insertion‐related femoral nail deformation. The data for the nails tested suggest that a simple aiming arm, mounted on the proximal end of the femoral nail alone, will not sufficiently provide accurate distal aiming.
Quadriceps load aggravates and roofplasty mitigates active impingement of anterior cruciate ligament grafts against the intercondylar roof
Authors: Goss Ben C. , Howell Stephen M. , Hull M. L. 
Published: February 2005

AbstractBecause of the complications of impingement of anterior cruciate ligament grafts on the intercondylar roof and because current surgical procedures locate the tibial tunnel such that impingement is avoided during passive but not active extension, the objectives of this study were to determine if (a) active extension precipitates and aggravates roof impingement, and (b) a roofplasty mitigates the effects of impingement. The tibial translation, flexion angle defining the onset of roof impingement, graft‐roof contact pressure, and graft tension were measured for six cadaveric specimens. In each specimen, two tibial tunnel positions were studied: one customized for the slope of the intercondylar roof, and the other translated 6 mm anteriorly from the customized position. For a quadriceps load of 1,500 N, the flexion angle defining the onset of impingement, the peak contact pressure, and the graft tension increased significantly for both tunnel positions. The increases occurred because of the anterior tibial translation caused by the active load. Although a roofplasty decreased the onset of the angle of impingement, the graft tension remained unaffected. Thus, to mitigate the effect of impingement during active rehabilitative knee extension exercises, the position of the tibial tunnel must be customized to the angle of the intercondylar roof and a roofplasty must be performed. The extent of bone removed must be customized as well and can be determined by removing bone from the intercondylar roof in excess of that required to freely pass a rod. the same diameter of the graft, through the tibial tunnel into the intercondylar notch with the knee in full passive extension.
Increased substance P in subacromial bursa and shoulder pain in rotator cuff diseases
Authors: Gotoh Masafumi , Hamada Kazutoshi , Yamakawa Hideyuki , Inoue Akio , Fukuda Hiroaki 
Published: February 2005

AbstractThe subacromial bursa is recognized as a site associated with the shoulder pain caused by rotator cuff disease in the middle‐aged and elderly. Substance P is contained in primary afferent nerves, and its quantity increases during chronic pain. The amount of substance P in the subacromial bursa of patients with rotator cuff disease was examined. Radioimmunoassay and immunohistochemistry were employed to quantify and localize substance P. The preoperative pain level was measured with a visual analogue scale with 0 as no pain. 5 as moderate, and 10 as severe. Thirty‐seven patients that had undergone operation were divided into two groups: one composed of 19 patients with subacromial bursitis and a partial‐thickness tear of the rotator cuff (nonperforated cuff) and the other composed of 18 patients with a full‐thickness tear (perforated cuff). Subacromial bursae obtained from seven fresh cadavers with no shoulder pain before death were used as controls. The visual analogue scale showed significantly greater pain in the group with the nonperforated rotator cuff than in the group with the perforated cuff. Consistent with these results, the amount of substance P in the subacromial bursa was significantly greater in the former group than in the latter. Nerve fibers immunoreactive to substance P were localized around the vessels, with a larger number of fibers in the group with the nonperforated rotator cuff. Therefore, an increased amount of substance P in the subacromial bursa appears to correlate with the pain caused by rotator cuff disease.
Osteoclasts are required for bone tumors to grow and destroy bone
Authors: Clohisy Denis R. , Ramnaraine Margaret L. 
Published: February 2005

AbstractIt has been hypothesized that bone resorption during tumor osteolysis is performed by osteoclasts. Data supporting this hypothesis have been provided from analysis of human biopsy specimens obtained from sites of tumor osteolysis, as well as from experimentation with in vivo animal models. Experiments in this report take this concept one step further by testing the hypothesis that osteoclasts are required for bone tumors to grow and destroy bone. To test this hypothesis, the influence of an osteolytic sarcoma tumor, NCTC clone 2472 (2472). on bone was studied in animals that are osteoclast deficient (microphthalmic, strain B6C3Fe‐a/a‐Mitfmi) but whose osteoclast deficiency can be reversed following bone marrow transplantation. Femora of these mice and unaffected wild‐type siblings were injected with 105 2472 cells, and after 14 days the femora were analyzed by radiographic and histomorphometric analysis. Macroscopic tumor, tumor‐induced osteolysis, and increased osteoclast number were noted in femora of normal mice but not in femora of osteoclast‐deficient mice (p < 0.001). Bone marrow transplantation converted osteoclast‐deficient mice to mice with femora that contained osteoclasts in 4 weeks. Femora of these mice were then injected with 105 2472 tumor cells; after 14 days, in contrast to the findings in the original osteoclast‐deficient mice, macroscopic tumor was present, tumor‐induced osteolysis was noted on roentgenograms, and osteoclast number was increased when tumor‐bearing limbs were compared with sham‐injected limbs (p < 0.001). These data prove the hypothesis that osteoclasts are required for 2472 tumor‐induced osteolysis, and they introduce the exciting possibility that osteoclasts are also required for tumors to grow in bone.
Up‐regulation of inducible nitric oxide synthase and production of nitric oxide by the swarm rat and human chondrosarcoma
Authors: Cesare Paul E. Di , Carlson Cathy S. , Attur Mukundan , Kale Ashay A. , Abramson Steven B. , Valle Craig Delia , Steiner German , Amin Ashok R. 
Published: February 2005

AbstractProduction of nitric oxide by solid tumors may have important ramifications regarding tumor growth and potential metastasis. This study demonstrated that the chondrosarcoma of the Swarm rat has upregulated mRNA for inducible nitric oxide synthase and produces nitric oxide. These results were confirmed by (a) the, presence of a 4.4‐kb band of mRNA detected by Northern blot using a probe for inducible nitric oxide synthase, (b) a 133‐kDa band of prothein that was detected with either a polyclonal or monoclonal antibody to the inducible nitric oxide synthase of the murine macrophage. and (c) the detection of nitrites from the culture medium of freshly cultured, isolated chondrosarcoma cells. This study showed that the expression of inducible nitric oxide synthase and the production of nitric oxide by the tumor can be increased by stimulation with endotoxin lipopolysaccharide and can be inhibited by inducible nitric oxide synthase inhibitors (L‐N(g)‐monomethyl arginine and aminoguanidine). Immunostaining confirmed the presence of inducible nitric oxide synthase within the tumor cells and appeared to localize the enzyme to the cytoplasm of the cells. A human chondrosarcoma was also shown to have an upregulated inducible nitric oxide synthase by both the detection of mRNA for inducible nitric oxide synthase and the presence of nitrites from the culture medium of the tumor in organ culture. Because the chondrosarcoma of the Swarm rat is a well differentiated solid tumor that rarely metas‐tasizes, nitric oxide may be produced by the tumor to promote local growth by effects on vascular supply.
Fibroblast distribution in the anteromedial bundle of the human anterior cruciate ligament: The presence of α‐smooth muscle actin‐positive cells
Authors: Murray M. M. , Spector M. 
Published: February 2005

AbstractThe anterior cruciate ligament is a complex tissue composed of structural proteins, proteoglycans, and cells. The histology of the human anterior cruciate ligament is characterized by the specific distribution and density of the fibroblast phenotype as well as by the unique organization of the structural proteins. A notable finding of this study was the identification of three histologically different zones along the anteromedial bundle as it coursed from the femoral to the tibial attachment. Two of the zones, the fusiform and ovoid, were located in the proximal one‐quarter of the bundle; the third zone, the spheroid, occupied the distal three quarters of the bundle fascicles. The fusiform cell zone was characterized by a high number density of longitudinally oriented cells with a fusiform‐shaped nucleus, longitudinal blood vessels, and high crimp length. The cytoplasm of the cells in this zone appeared to be intimately attached to the extracellular collagen and followed the crimp waveform of the fibers. Fusiform cells were noted to stain positively for the α‐smooth muscle actin isoform in this region, particularly at areas of crimp disruption. The ovoid cell zone was characterized by a high number density of cells with an ovoid‐shaped nucleus, longitudinal vessels, and a high crimp length. In this zone as well, the cytoplasm of the cells appeared to follow the waveform of the adjacent collagen. Ovoid cells were noted to stain positively for the α‐smooth muscle actin isoform in this region. The spheroid cell zone was characterized by a low density of spheroid cells, few blood vessels, and short crimp length. Cells were noted within and among fascicles, as well as within lacunae. In selected areas, as many as 50% of the cells in this region stained positively for the α‐smooth muscle actin isoform. This is also the first report of cells expressing the α‐smooth muscle actin isoform in the intact human anterior cruciate ligament. This specific type of contractile actin, initially identified only in smooth‐muscle cells, pericytes, and myofibroblasts, was seen in cells with various morphologies and predominantly in cells located at areas of crimp disruption. Further work is necessary to elucidate the role of the various fibroblast phenotypes in the maintenance of the human anterior cruciate ligament.
Early expression of marker genes in the rabbit medial collateral and anterior cruciate ligaments: The use of different viral vectors and the effects of injury
Authors: Hildebrand Kevin A. , Deie Masataka , Allen Christina R. , Smith David W. , Georgescu Helga I. , Evans Christopher H. , Robbins Paul D. , Woo Savio L‐Y. 
Published: February 2005

AbstractGene therapy is a technique that may offer advantages over current methods of cytokine delivery to ligaments. To determine if implanted genes could be expressed in normal and injured knee ligaments, the medial collateral ligament and anterior cruciate ligament were studied in 18 rabbits. A retroviral ex vivo technique using allograft medial collateral ligament and anterior cruciate ligament fibroblasts and an adenoviral in vivo technique were compared as methods for delivering the LacZ marker gene to knee ligaments. Bilateral knee surgeries were performed, and the rabbits were equally divided into three groups. Group 1 received the retrovirus and the medial collateral ligament was ruptured, Group 2 received the adenovirus and the medial collateral ligament was ruptured, and Group 3 received the adenovirus and the medial collateral ligament was not injured. The anterior cruciate ligament was not injured in any group. The medial collateral and anterior cruciate ligaments of the right knees received 106 allografted, transduced ligament fibroblasts or 109 adenovirus particles, whereas the ligaments of the left knee received a similar volume of saline solution only. Equal numbers of rabbits were killed at 10 days. 3 weeks, and 6 weeks following the procedure. Ligament samples were stained with X‐gal to detect the expression of the LacZ gene product, β‐galactosidase. LacZ gene expression was evident in ruptured and uninjured medial collateral ligaments as well as in the anterior cruciate ligament. The expression lasted between 10 days and 3 weeks in the medial collateral and anterior cruciate ligaments with use of the retrovirus and between 3 and 6 weeks in the medial collateral ligament and at least 6 weeks in the anterior cruciate ligament with the adenovirus. The length of gene expression in the ruptured and uninjured medial collateral ligaments did not differ. These preliminary studies indicate that gene transfer to normal and injured knee ligaments is possible.
Gene therapy: Adenovirus‐mediated human bone morphogenetic protein‐2 gene transfer induces mesenchymal progenitor cell proliferation and differentiation in vitro and bone formation in vivo
Authors: Lou Jueren , Xu Fang , Merkel Kurt , Manske Paul 
Published: February 2005

AbstractThis study reports that recombinant adenovirus‐mediated human bone morphogenetic protein‐2 gene transfer can induce mesenchymal progenitor cell differentiation and bone formation. The recombinant adenovirus with the human bone morphogenetic protein‐2 gene was constructed, and mature human bone morphogenetic protein‐2 expression mediated by adenovirus gene transfer was detected by specific antibody. Under adenovirus‐mediated bone morphogenetic‐protein gene transfer, mesenchymal progenitor cell line C3H/10T 1/2 showed cell proliferation dependent on adenovirus bone morphogenetic‐protein dose. The C3H/10T 1/2 cells transduced by adenovirus bone morphogenetic protein also exhibited differentiation to osteoblast phenotype, which indicates alkaline phosphatase activity. Injection of the C3H/10T 1/2 cells into the thigh muscles of nude mice led to ossicle development detectable on radiographs. Histological analysis indicated that the new ossicles that developed in the thigh muscles of the mice had different osseous components including bone trabeculae, bone marrow, and chondrified tissue. The results of this study demonstrate the potential for gene therapy by adenovirus‐mediated bone morphogenetic‐protein gene transfer.
Intravertebral body reconstruction with an injectable in situ‐setting carbonated apatite: Biomechanical evaluation of a minimally invasive technique
Authors: Schildhauer T. A. , Bennett A. P. , Wright T. M. , Lane J. M. , O'Leary P. F. 
Published: February 2005

AbstractThe ability to mechanically reinforce an osteoporotic vertebral body could impede spinal compression fracture and the associated pain and complications. Previous studies have shown that reinforcement of fractured vertebrae with conventional acrylic cement can relieve symptoms and avoid further collapse. In this study, we explored the use of a carbonated apatite cement combined with a minimally invasive injection technique to improve the compressive mechanical properties of cadaveric vertebral bodies. After establishing the biomechanical characteristics of cement formulations intended to have appropriate viscosities, we evaluated the infiltration of the cements into thoracic vertebral bodies using a combined suction‐injection technique. The energy‐absorption capabilities of the reinforced vertebral bodies were then measured during axial compressive tests and compared with those of nonreinforced vertebrae. The ultimate compressive strength of the cement formulations averaged from 11.6 to 17.7 MPa, depending on curing conditions. The suction‐injection technique allowed from one‐half to two‐thirds of each vertebral body to be infiltrated with cement. Energy absorption was significantly higher (p < 0.05) between 25 and 70% collapse of the vertebral body in the specimens that received the apatite injection as compared with the controls. These results suggest that osteoporotic vertebral‐body augmentation with the injection of apatite cement could prevent further collapse after initial failure has occurred. The osteoconductive nature of the cement and its ability to be remodeled by bone, together with its compressive strength, which is higher than that of cancellous bone, could provide better clinical results than those of current treatments with acrylic cement.