bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of compressive loading on chondrocyte differentiation in agarose cultures of chick limb‐bud cells
Authors: Elder S. H. , Kimura J. H. , Soslowsky L. J. , Lavagnino M. , Goldstein S. A. 
Published: February 2005

AbstractIt is well established that mechanical loading is important to homeostasis of cartilage tissue, and growing evidence suggests that it influences cartilage differentiation as well. Whereas the effect of mechanical forces on chondrocyte biosynthesis and gene expression has been vigorously investigated, the effect of the mechanical environment on chondrocyte differentiation has received little attention. The long‐term objective of this research is to investigate the regulatory role of mechanical loading in cell differentiation. The goal of this study was to determine if mechanical compression could modulate chondrocyte differentiation in vitro. Stage 23/24 chick limb‐bud cells, embedded in agarose gel, were subjected to either static (constant 4.5‐k Pa stress) or cyclic (9.0‐kPa peak stress at 0.33 Hz) loading in unconfined compression during the initial phase of commitment to a phenotypic lineage. Compared with nonloaded controls, cyclic compressive loading roughly doubled the number of cartilage nodules and the amount of sulfate incorporation on day 8, whereas static compression had little effect on these two measures. Neither compression protocol significantly affected overall cell viability or the proliferation of cells within nodules. Since limb‐bud mesenchymal cells were seeded directly into agarose, an assessment of cartilage nodules in the agarose reflects the proportion of the original cells that had given rise to chondrocytes. Thus, the results indicate that about twice as many mesenchymal cells were induced to enter the chondrogenic pathway by cyclic mechanical compression. The coincidence of the increase in sulfate incorporation and nodule density indicates that the primary effect of mechanical compression on mesenchymal cells was on cellular differentiation and not on their subsequent metabolism. Further studies are needed to identify the primary chondrogenic signal associated with cyclic compressive loading and to determine the mechanism by which it influences commitment to or progression through the chondrogenic lineage, or both.
Assessment of resorbable bioactive material for grafting of critical‐size cancellous defects
Authors: Wheeler D. L. , Eschbach E. J. , Hoellrich R. G. , Montfort M. J. , Chamberland D. L. 
Published: February 2005

AbstractBioactive glasses form a surface apatite layer in vivo that enhances the formation and attachment of bone. Sol‐gel Bioglass graft material provides greater nanoscale porosity than bioactive glass (on the order of 50–200 Å), greater particle surface area, and improved resorbability, while maintaining bioactivity. This study histologically and biomechanically evaluated, in a rabbit model, bone formed within critical‐sized distal femoral cancellous bone defects filled with 45S5 Bioglass particulates, 77S sol‐gel Bioglass, or 58S sol‐gel Bioglass and compared the bone in these defects with normal, intact, untreated cancellous bone and with unfilled defects at 4, 8, and 12 weeks. All grafted defects had more bone within the area than did unfilled controls (p < 0.05). The percentage of bone within the defect was significantly greater for the 45S5 material than for the 58S or 77S material at 4 and 8 weeks (p < 0.05), yet by 12 weeks equivalent amounts of bone were observed for all materials. By 12 weeks, all grafted defects were equivalent to the normal untreated bone. The resorption of 77S and 58S particles was significantly greater than that of 45S5 particles (p < 0.05). Mechanically, the grafted defects had compressive stiffness equivalent to that of normal bone at 4 and 8 weeks. At 12 weeks, 45S5‐grafted defects had significantly greater stiffness (p < 0.05). At 8 and 12 weeks, all grafted defects had significantly greater stifness than unfilled control defects (p < 0.05). In general, the 45S5‐filled defects exhibited greater early bone ingrowth than did those filled with 58S or 77S. However, by 12 weeks, the bone ingrowth in each defect was equivalent to each other and to normal bone. The 58S and 77S materials resorbed faster than the 45S5 materials. Mechanically, the compressive characteristics of all grafted defects were equivalent or greater than those of normal bone at all time points.
Relationship between quadriceps strength and rate of loading during gait in women
Authors: Mikesky Alan E. , Meyer Adele , Thompson Kerry L. 
Published: February 2005

AbstractOne function of skeletal muscle is to serve as the body's shock absorbers and thus dampen rates of loading during activity. The aim of this cross‐sectional study was to determine the significance of muscle strength on rates of loading during gait. Thirty‐seven women (mean age: 34.5 ± 8.2 years) were solicited by advertisement and placed into one of two groups—strength‐trained or sedentary—on the basis of training history. They walked (10 trials) over a 10‐m walkway at a controlled speed of 1.22–1.35 m/s while the rate of loading was sampled with a 1.000‐Hz force platform. Quadriceps and hamstring strength was measured at 90%/s with an isokinetic dynamometer. Statistical analyses (p <0.05) included descriptive statistics and unpaired / tests for comparison between groups. The women in the sedentary group weighed more and had significantly less concentric and eccentric strength of the quadriceps and hamstrings relative to body weight than did those in the strength‐trained group. In addition, they demonstrated significantly higher rates of loading (2.21 ± 0.15 compared with 1.75 ± 0.08%wt/ms) than those in the strength‐trained group.
Characterization of hamstring reflexes during anterior cruciate ligament disruption: In vivo results from a goat model
Authors: Fujita Ikuo , Nishikawa Tetsuo , Kambic Helen E. , Andrish Jack T. , Grabiner Mark D. 
Published: February 2005

AbstractThe existence of an anterior cruciate ligament‐hamstring reflex arc, the extent to which these reflexes can protect the knee, and the extent to which they are affected by rupture of the anterior cruciate ligament remain controversial. We evaluated the temporal components of the anterior cruciate ligament‐hamstring synergy by simulating an injury to the ligament in a goat model. Reflexive hamstring activation in anesthetized goats was evaluated when the anterior cruciate ligament was loaded with static subfailure, dynamic subfailure, and dynamic failure loads. Reflexive hamstring activation was not found in response to static subfailure loading but was observed in response to dynamic subfailure and failure loading. The latency of the reflex evoked by dynamic failure loading was shorter than that evoked by dynamic subfailure loading. The findings suggest that the extent to which the hamstring reflexes can protect the knee may be bounded by the ability of these muscles to generate force rapidly and the amplitude and time‐course of the loads applied to the knee joint. The present data present a framework for further investigation of the contribution of anterior cruciate ligament‐hamstring reflexes to the stability of the knee joint under high loads and loading rates.
Assessment of elbow joint kinematics in passive motion by electromagnetic motion tracking
Authors: Bottlang M. , Madey S. M. , Steyers C. M. , Marsh J. L. , Brown T. D. 
Published: February 2005

AbstractThis research provides a detailed analysis of the kinematics of passive elbow motion. It quantifies how closely humeroulnar kinematics approximates rotation around a fixed axis. The results are clinically relevant for emerging treatment modalities that impose an artificial hinge to the elbow joint, such as total elbow arthroplasty and articulated external fixation. In a cadaveric study of seven specimens, we quantified ulnar rotation around the humerus in terms of instantaneous screw displacement axes calculated from electromagnetic motion‐tracking source data. This methodology enabled description of the complex excursion of the elbow axis in terms of translation and orientation changes of the screw displacement axes over the range of motion. Furthermore, we analyzed the envelope of joint laxity for elbow motion under applied small varus and valgus moments. In addition, radiographic landmarks of clinical utility for axis location were evaluated by visualizing the elbow's radiographic appearance when viewed from along the calculated best‐fit (average) rotation axis. Over the normal range of elbow motion, the screw displacement axis varied 2.6–5.7° in orientation and 1.4–2.0 mm in translation. All instantaneous rotation axes nearly intersected on the medial facet of the trochlea. The breadth of the envelope of varus‐valgus joint laxity was greatest within the initial 40° of flexion and decreased by a factor of approximately two for flexion angles exceeding 100°.
Time‐dependent increases in type‐III collagen gene expression in medial collateral ligament fibroblasts under cyclic strains
Authors: Hsieh Adam H. , Tsai Cliff M‐H. , Ma Qing‐Jun , Lin Tong , Banes Albert J. , Villarreal Francisco J. , Akeson Wayne H. , Paul Sung K‐L. 
Published: February 2005

AbstractNumerous studies have demonstrated the capacity of mechanical strains to modulate cell behavior through several different signaling pathways. Understanding the response of ligament fibroblasts to mechanically induced strains may provide useful knowledge for treating ligament injury and improving rehabilitation regimens. Biomechanical studies that quantify strains in the anterior cruciate and medial collateral ligaments have shown that these ligaments are subjected to 4–5% strains during normal activities and can be strained to 7.7% during external application of loads to the knee joint. The objective of this study was to characterize the expression of types I and III collagen in fibroblast monolayers of anterior cruciate and medial collateral ligaments subjected to equibiaxial strains on flexible growth surfaces (0.05 and 0.075 strains) by quantifying levels of mRNA encoding these two proteins. Both cyclic strain magnitudes were studied under a frequency of 1 Hz. The results indicated marked differences in responses to strain regimens not only between types I and III collagen mRNA expression within each cell type but also in patterns of expression between anterior cruciate and medial collateral ligament cells. Whereas anterior cruciate ligament fibroblasts responded to cyclic strains by expression of higher levels of type‐I collagen message with almost no significant increases in type‐III collagen, medial collateral ligament fibroblasts exhibited statistically significant increases in type‐III collagen mRNA at all time points atter initiation of strain with almost no significant increases in type‐I collagen. Furthermore, differences in responses by fibroblasts from the two ligaments were detected between the two strain magnitudes. In particular, 0.075 strains induced a time‐dependent increase in type‐III collagen mRNA levels in medial collateral ligament fibroblasts whereas 0.05 strains did not. The strain‐induced changes in gene expression of these two collagens may have implications for the healing processes in ligament tissue. The differences may explain, in part, the healing differential between the anterior cruciate and medial collateral ligaments in vivo.
Mechanical compression of the lumbar nerve root alters pain‐related behaviors induced by the nucleus pulposus in the rat
Authors: Kawakami Mamoru , Tamaki Tetsuya , Hayashi Nobuhiro , Hashizume Hiroshi , Matsumoto Takuji , Minamide Akihito , Kihira Tameko 
Published: February 2005

AbstractThe purpose of this study was to refine a method of nerve‐root injury in the rat to produce hyperalgesia, a pain‐related behavior, and to determine if there were any relationships between the histological extent of nerve‐root injury and the magnitude of hyperalgesia. Three methods were used to produce hyperalgesia: irritation of a nerve root by ectopic nucleus pulposus, silk loop alone, or both silk loop and ectopic nucleus pulposus. Autologous nucleus pulposus obtained from coccygeal intervertebral discs was relocated on the lumbar nerve roots after laminectomy. Two loops of 4‐0 silk were placed around the exposed nerve roots. Hyperalgesia was measured preoperatively and postoperatively. The distribution of myelinated axons in the dorsal nerve roots was evaluated histologically. Mechanical hyperalgesia was detected in rats in which autologous nucleus pulposus was applied to the nerve root but not in those in which silk loops were used. Silk loops around the nerve root resulted in thermal hyperalgesia only in rats in which autologous nucleus pulposus was applied to the nerve root. Fewer large myelinated fibers were seen in the rats in which silk loops were used. Although a silk loop around the nerve root was not sufficient to produce hyperalgesia, supplemental application of autologous nucleus pulposus to the nerve root produced thermal hyperalgesia. It is possible that mechanical constriction of the nerve root alters the pain‐related behavior elicited by chemical factors from the nucleus pulposus.
Evaluation of recombinant human bone morphogenetic protein‐2 as a bone‐graft substitute in a canine segmental defect model
Authors: Sciadini Marcus F. , Johnson Kenneth D. 
Published: February 2005

AbstractA study was performed in dogs to evaluate the dose‐response characteristics and effectiveness of recombinant human bone morphogenetic protein‐2 with a collagen sponge carrier in a segmental defect model. Twenty‐seven dogs underwent bilateral radial osteotomies with creation of a 2.5‐cm diaphyseal defect. All received autogenous cancellous bone graft in one defect and a collagen implant in the other. These implants contained recombinant human bone morphogenetic protein‐2 at the following doses: group 1 at 0 μg (three dogs, 0 μg/ml total implant volume), group 2 at 150 μg (three dogs, 50 μg/ml), group 3 at 600 μg (three dogs, 200 μg/ml), group 4 at 2,400 μg (three dogs, 800 μg/ml), group 5 at 0 μg (five dogs, 0 μg/ml), group 6 at 150 μg (five dogs, 200 μg/ml), and group 7 at 600 μg (five dogs, 50 μg/ml). The defects were stabilized with external fixators. The dogs in group 1–4 were killed at 12 weeks postoperatively, and those in groups 5–7 were killed at 24 weeks postoperatively except for one dog in group 7, which was killed at 48 weeks. Evaluation included monthly radiographs, biomechanical testing, and nondemineralized histology. All 27 radii with autogenous cancellous bone graft and all 19 implants treated with recombinant human bone morphogenetic protein‐2 achieved radiographic and histologic union and gross stability. The eight radii treated with collagen carrier alone went on to radiographic and histologic nonunion and were grossly unstable at death. A dose‐dependent occurrence of cyst‐like bone voids was noted radiographically and histologically. Biomechanical performance tended to be better at the lowest dose studied at 12 weeks, and all three doses performed better than the placebo (p < 0.05) at 12 and 24 weeks. By 24 weeks, radiolucent areas corresponding to histologic bone voids persisted radiographically, although there was evidence of early bone remodeling. This remodeling progressed to 48 weeks in the single animal followed to this time point, although bone voids remained. These radiologic findings were confirmed histologically. Recombinant human bone morphogenetic protein‐2 in a collagen sponge carrier has significant osteoinductive activity in this canine segmental defect model. A dose‐response relationship is evident, with heterotopic bone and cyst‐like void formation at higher doses and a minimum effective dose of 0‐150 μg. At 12 and 24 weeks postoperatively, biomechanical parameters achieved by defects treated with recombinant human bone morphogenetic protein‐2 were comparable with those of autograft controls and were significantly stronger than those of the placebo (p < 0.05).
Experimental model for allograft incorporation and allograft fracture repair
Authors: Lee Francis Young‐In , Hazan Eric J. , Gebhardt Mark C. , Mankin Henry J. 
Published: February 2005

AbstractThis study describes a rat model of allograft osteotomy healing. An intercalary skeletal defect was created in adult Lewis rats by resecting a 2‐cm segment of the femur in the diaphysis, including the periosteum and the cuff of muscle layers. The skeletal defects were replaced with fresh‐frozen devascularized intercalary allografts from Sprague‐Dawley rats. A transverse osteotomy was made in the middle of the allograft. The osteolomized segments were stabilized with an intramedullary threaded Kirschner wire, which allowed immediate ambulation. Radiographic and histological examination at 4 and 8 weeks revealed a charactcristic healing process at three different interfaces. Radiographically, the distal metaphyseal host‐donor junction healed faster than the proximal diaphyscal host‐donor interface. The osteotomy site did not have evidence of an intramembranous or endochondral repair process. This model can serve as a baseline for assessing allograft incorporation and fracture repair.
Sequential labelling of microdamage in bone using chelating agents
Authors: Lee T. C. , Arthur T. L. , Gibson L. J. , Hayes W. C. 
Published: February 2005

AbstractBasic fuchsin labels microcracks, but a series of stains is required to differentiate between preexisting and test‐induced microcracks and to label their growth in vitro. Basic fuchsin and five chelating agents—alizarin complexone, calcein, calcein blue, oxytetracycline, and xylenol orange—were randomly assigned to label microcracks in sequential rib sections from 10 donors. The density, length, and location of the microcracks did not differ significantly between he six stains, suggesting that each was equally effective in detecting microcracks. Paired specimens of trabecular bone were machined from bovine tibiae, stained with oxytetracycline, and fatigued in compression. One specimen from each pair was then stained with xylenol orange. Preexisting microdamage was stained with oxytetracycline, propagating microcracks with both stains and new, test‐initiated damage with xylenol orange. Chelating agents are site‐specific markers of the initiation and growth of microcracks.
Localization of dominantly inherited isolated triphalangeal thumb to chromosomal region 7q36
Authors: Dobbs Matthew B. , Dietz Frederick R. , Gurnett Christina A. , Morcuende Jose A. , Steyers Curtis M. , Murray Jeffrey C. 
Published: February 2005

AbstractTriphalangeal thumb is an autosomal dominantly inherited form of abnormal preaxial skeletal development. In most families, however, the triphalangeal thumb phenotype coexists with a spectrum of limb deformities, including polydactyly and syndactyly. We describe two Iowa kindreds with triphalangeal thumb. In one family, with nine affected members, triphalangeal thumb was the only manifestation of limb deformity. We performed linkage analysis on both pedigrees, demonstrating a maximum LOD score of 6.23 with marker D7S559 on chromosome 7q36. This corresponds to a previous study of a candidate region of 450 kb in which data from several families with preaxial polydactyly were employed. Further analysis of the unique family with isolated triphalangeal thumb in the current study may demonstrate allelic variability of the gene involved in these disorders.
Inhibition of caspase‐3‐like activity prevents apoptosis while retaining functionality of human chondrocytes in vitro
Authors: Nuttall Mark E. , Nadeau Daniel P. , Fisher Paul W. , Wang Feilan , Keller Paul M. , Dewolf Walter E. , Goldring Mary B. , Badger Alison M. , Lee Dennis , Levy Mark A. , Gowen Maxine , Lark Michael W. 
Published: February 2005

AbstractApoptosis was induced in a human chondrocyte cell line, T/C 28a4, by treatment with various stimuli, including camptothecin, tumor necrosis factor‐α, staurosporine, okadaic acid, and reduced serum conditions. All stimuli induced a cytosolic DEVDase activity, coincident with apoptosis. Caspase activities in the lysates were characterized and quantitated with peptide cleavage profiles. To confirm that the results were not related to the immortalized nature of the cell line, primary human chondrocytes also were shown to undergo apoptosis under similar conditions, which resulted in increased cytosolic DEVDase activity. There was little or no caspase‐1 (interleukin‐1β‐converting enzyme) or caspase‐8‐like activity in the apoptotic cells. In all cases, the irreversible nonselective caspase inhibitor, Z‐VAD‐FMK, and the caspase‐3‐selective inhibitor, Ac‐DMQD‐CHO, inhibited DEVDase activity and apoptosis, whereas the caspase‐1‐selective inhibitor, Ac‐YVAD‐CHO, had no effect. Human chondrocytes were stably and transiently transfected with a type‐II collagen gene (COL2A1) regulatory sequence driving a luciferase reporter as a specific marker of chondrocyte gene expression. Treatment of the cells with camptothecin or tumor necrosis factor‐α plus cycloheximide significantly inhibited COL2A1 transcriptional activity. Significantly, cotreatment with Z‐VAD‐FMK or Ac‐DMQD‐CHO maintained COL2A1‐reporter gene activity, indicating that the prevention of apoptosis by caspase‐3 inhibition was sufficient to maintain cell functionality as assessed by the retention of type‐II collagen promoter activity.
Alterations in cartilage type‐ii procollagen and aggrecan contents in synovial fluid in equine osteochondrosis
Authors: Laverty S. , Ionescu M. , Marcoux M. , Bouré L. , Doizé B. , Poole A. R. 
Published: February 2005

AbstractThe etiology and pathophysiology of osteochondrosis remain poorly understood because it is difficult to obtain material from lesions in the early stage of this disease and because there is no satisfactory experimental animal model. We wished to determine whether there are changes in articular cartilage turnover in equine osteochondrosis, which closely resembles the human disease, by assaying cartilage matrix molecules in synovial fluids. We used immunoassays that measure a keratan sulfate epitope and the epitope 846 on the cartilage proteoglycan aggrecan and the C‐propeptide of cartilage type‐II procollagen, which is released following the synthesis of this molecule, to analyse synovial fluids from equine tarsocrural joints with and without osteochondrosis. In young horses with osteochondrosis, there was a significant increase of C‐propeptide of type‐II procollagen accompanied by a decrease in the 846 and keratan sulfate epitopes. The results identify differential alterations in aggrecan and type‐II collagen turnover in the cartilage matrix in young animals with osteochondrosis that may contribute to the pathological degeneration of articular cartilage in this disease.