The Experts below are selected from a list of 246 Experts worldwide ranked by ideXlab platform
Martin I Boyer - One of the best experts on this subject based on the ideXlab platform.
-
assessment of Epiphyseal Plate allograft viability and function after ex vivo storage in university of wisconsin solution
Journal of Pediatric Orthopaedics, 2011Co-Authors: Soumya Ravindran, Martin I Boyer, Erin Martens, Helena Ntouvali, Audrey McalindenAbstract:BACKGROUND: Compromised Epiphyseal Plate function can result in limb deformities. Microvascular transplantation of an Epiphyseal Plate allograft is a potentially effective approach to reestablish longitudinal limb growth. For this procedure to become clinically useful, the technique for temporary ex vivo storage of allografts must be reliable. The goal of this study was to determine a time frame for which proximal tibial Epiphyseal Plate allografts could be stored in University of Wisconsin Preservation Solution (UWPS) and remain functional in vivo after microvascular transplantation. METHODS: Proximal tibial Epiphyseal Plate allografts from skeletally immature female New Zealand White rabbits (10 to 12 wk of age) were used. Allografts (isolated on the popliteal arteriovenous pedicle) were stored ex vivo in cold UWPS for periods of up to 21 days. Chondrocyte viability, phenotype, and extracellular matrix composition of growth Plate cartilage was assessed. Microvascular transplantations of nonstored or prestored (3 d) allografts were performed and analysis of bromodeoxyuridine and calcein incorporation was done to determine chondrocyte proliferation and new bone growth, respectively. RESULTS: In vitro analysis showed that, compared with control tissue, Epiphyseal Plate chondrocyte viability (P>0.05), organization, and collagen extracellular matrix was preserved up to 4 days in cold UWPS. Microvascular transplantation of nonstored Epiphyseal Plate allografts was successful. Despite care being taken to ensure vascular patency during the microvascular procedure, transplantation of prestored allografts failed due to absent flow in the larger vessels and in the allograft based upon the visualization of organized thrombus within the vascular pedicle, and absent flow within the composite graft itself. However, growth Plate viability and function was detected in a peripheral region of a single allograft where partial blood flow had been maintained during the transplantation period. CONCLUSIONS: Ex vivo storage in cold UWPS for 3 days maintains growth Plate chondrocyte viability and function in vivo. However, future studies must be directed toward investigating the direct effect of ex vivo storage on the integrity and function of the vascular pedicles.
-
development and validation of new model for microvascular transplantation of Epiphyseal Plate allografts with minimal adjoining Epiphyseal and metaphyseal bone
Microsurgery, 2003Co-Authors: Peter W Bray, Martin I Boyer, Vaughan C A Bowen, Peter C Neligan, Jayne S DanskaAbstract:A model for the free allograft microvascular transplantation of rabbit proximal tibial Epiphyseal Plate allografts was developed, validated, and tested in an in vivo animal model. Transplants contained the minimum amount of adjacent Epiphyseal and metaphyseal bone compatible with preservation of the Epiphyseal-Plate vascular supply, as determined by corrosion casting. Perfusion to this graft was evaluated quantitatively using radioactive microspheres, and qualitatively using India-ink injection. Female New Zealand White rabbits at 12 weeks of age were utilized. Vascularized transplantation of Epiphyseal Plate allografts was performed either into a defect of matched size in the iliac crest or into a soft-tissue pocket without bone contact. Cyclosporine A immunosuppression (CSA) was administered daily for 6 weeks. Two control groups underwent identical surgical procedures, but had no postoperative immunosuppression. Epiphyseal Plates both with and without bone contact, in rabbits immunosuppressed postoperatively with CSA, demonstrated longitudinal growth and preserved viability as determined by positive bromodeoxyuridine uptake. Control Epiphyseal Plates transferred without postoperative immunosuppression were uniformly nonviable. This new model has value as a basis for further studies into the clinical applicability of isolated Epiphyseal-Plate transplants. © 2003 Wiley-Liss, Inc. MICROSURGERY 23:153–163 2003
-
transplantation of Epiphyseal Plate allografts between animals of different ages
Journal of Pediatric Orthopaedics, 1999Co-Authors: D G Stevens, Martin I Boyer, C V A BowenAbstract:Summary: The purpose of the experiment was to study growth of Epiphyseal Plate allografts after transplantation into subjects of a different age, thus preparing for future transplantation of Epiphyseal Plate or extremity allografts in children. Microvascular transplantation of proximal tibial Epiphyseal Plate allografts was performed in skeletally immature New Zealand White female rabbits. The growth of 9-week-old Epiphyseal Plate allografts was examined in both 9-week-old and 17-week-old recipients, as was the growth of 17-week-old Epiphyseal Plate allografts in 17-week-old recipients. Immunosuppression was with cyclosporine (Cyclosporine A). Successful transplants were confirmed with 99mTc-MDP isotope scanning, and growth was evaluated with weekly standardized radiographs until death. Growth rate was found to depend on the age of the donor Epiphyseal Plate and was independent of the age of the recipient. This has clinical implications for the procurement of donor tissue in potential transplantation of Epiphyseal Plate allografts in children.
-
Short-term response of Epiphyseal Plate cell populations following selective devascularization and microsurgical revascularization.
Microsurgery, 1994Co-Authors: C V A Bowen, Martin I Boyer, Peter W Bray, J. D. Fowler, L. NolanAbstract:The distal femoral Epiphyseal Plates of 21 8-week-old New Zealand white rabbits were totally or partially (nutrient artery only) devascularized, or devascularized and then microsurgically revascularized. Sacrifice was at 24, 48 or 72 hours postoperatively. The heights of the proliferative and hypertrophic zones of the Epiphyseal Plates operated upon were compared with the contralateral control Epiphyseal Plates for both the central and the peripheral regions of the Epiphyseal Plate. Neither extent of devascularization nor revascularization had a significant effect on the height of the proliferative zone of chondrocytes at any of the follow-up intervals. Selective devascularization of the nutrient artery led to a significant increase in height of the central region of the hypertrophic zone of chondrocytes at 48 and 72 hours. Microsurgical revascularization did not lead to a significant change in the height of either the central or the peripheral regions of the hypertrophic zone of chondrocytes at any of the follow-up intervals. This study is another ‘building block’ experiment toward vascularized Epiphyseal Plate transplantation in humans. © 1994 Wiley-Liss, Inc.
-
Epiphyseal Plate transplantation an historical review
British Journal of Plastic Surgery, 1994Co-Authors: Martin I Boyer, Peter W Bray, Vaughan C A BowenAbstract:Abstract Non-vascularized and vascularized transplantation of Epiphyseal Plate autografts have been performed both clinically and experimentally for over 100 years. However, the ultimate clinical goal of vascularized transplantation of Epiphyseal Plate allografts for paediatric extremity reconstruction remains elusive, due primarily to the lack of suitably nontoxic techniques to prevent graft rejection. We have summarized the published clinical and experimental investigations of vascularized Epiphyseal Plate transplantation, and organized the experiments and clinical operations into four main groups: (1) local vascular studies on unmanipulated Epiphyseal Plates, (2) studies of Epiphyseal Plate behaviour after orthotopic replantation, (3) studies of Epiphyseal Plate behaviour after heterotopic transplantation, and (4) studies of Epiphyseal Plate behaviour after allograft transplantation. Prior investigations into the non-vascularized transplantation of Epiphyseal Plate autografts and allografts are presented as background. These groups of studies serve as the building blocks for the more clinically applicable experimental investigations outlined in the final section of this review.
Shemin Lu - One of the best experts on this subject based on the ideXlab platform.
-
t 2 toxin induces Epiphyseal Plate lesions via decreased secisbp2 mediated selenoprotein expression in da rats exacerbated by selenium deficiency
Cartilage, 2018Co-Authors: Wenxiang Zhao, Safdar Hussain, Yitong Zhao, Fujun Zhang, Huang Huang, Nannan Zhong, Peng Xu, Shemin LuAbstract:ObjectiveBoth selenium (Se) deficiency and mycotoxin T2 lead to Epiphyseal Plate lesions, similar to Kashin-Beck disease (KBD). However, regulation of selenoproteins synthesis mediated by SECISBP2,...
-
abnormality of Epiphyseal Plate induced by selenium deficiency diet in two generation da rats
Apmis, 2015Co-Authors: Wenxiang Zhao, Fujun Zhang, Nannan Zhong, Quancheng Wang, Rui Zhang, Lifang Tian, Qilan Ning, Liesu Meng, Shemin LuAbstract:Abstract This study aimed to observe the effects of Se deficiency on Epiphyseal Plates of two generation DA rats fed with artificial total synthetic low Se diet. All F0 and F1 DA rats were fed with synthetic low Se diet (SeD group) and low Se diet supplied with Se (SeS group). The levels of selenium and enzyme activities of GPx were detected in plasma of the rats. General growth of bone and articular cartilage was measured macroscopically and microscopically. The Epiphyseal Plate of femur heads or tibia were obtained to histological and immunohistochemical examinations. The cartilage from left knee joints and femur heads was used to detect the gene expression of collagens, ADAMTSs and several selenoproteins by RT-qPCR. Two generation SeD rats showed Se insufficiency status. The thicknesses of the femur and tibial Epiphyseal Plates in both F0 and F1 SeD rats were significantly less than that of SeS rats. In F1 generation, SeD rats showed much fewer proliferative chondrocyte layers than SeS ones. Importantly, two generation SeD rats both showed significantly more serious pathological changes of Epiphyseal Plates. In two generation rats, gene expressions of COL II, GPx1 and GPx4 were significantly down-regulated in SeD rats than SeS ones; meanwhile ADAMTS-4 showed an up-regulated expression in cartilage. Dietary Se deficiency can apparently cause Epiphyseal Plate lesion and decrease cartilage type II collagen production and GPx1 activity in two generation DA rats fed with the artificial total synthesis low Se diet.
Peter W Bray - One of the best experts on this subject based on the ideXlab platform.
-
development and validation of new model for microvascular transplantation of Epiphyseal Plate allografts with minimal adjoining Epiphyseal and metaphyseal bone
Microsurgery, 2003Co-Authors: Peter W Bray, Martin I Boyer, Vaughan C A Bowen, Peter C Neligan, Jayne S DanskaAbstract:A model for the free allograft microvascular transplantation of rabbit proximal tibial Epiphyseal Plate allografts was developed, validated, and tested in an in vivo animal model. Transplants contained the minimum amount of adjacent Epiphyseal and metaphyseal bone compatible with preservation of the Epiphyseal-Plate vascular supply, as determined by corrosion casting. Perfusion to this graft was evaluated quantitatively using radioactive microspheres, and qualitatively using India-ink injection. Female New Zealand White rabbits at 12 weeks of age were utilized. Vascularized transplantation of Epiphyseal Plate allografts was performed either into a defect of matched size in the iliac crest or into a soft-tissue pocket without bone contact. Cyclosporine A immunosuppression (CSA) was administered daily for 6 weeks. Two control groups underwent identical surgical procedures, but had no postoperative immunosuppression. Epiphyseal Plates both with and without bone contact, in rabbits immunosuppressed postoperatively with CSA, demonstrated longitudinal growth and preserved viability as determined by positive bromodeoxyuridine uptake. Control Epiphyseal Plates transferred without postoperative immunosuppression were uniformly nonviable. This new model has value as a basis for further studies into the clinical applicability of isolated Epiphyseal-Plate transplants. © 2003 Wiley-Liss, Inc. MICROSURGERY 23:153–163 2003
-
Short-term response of Epiphyseal Plate cell populations following selective devascularization and microsurgical revascularization.
Microsurgery, 1994Co-Authors: C V A Bowen, Martin I Boyer, Peter W Bray, J. D. Fowler, L. NolanAbstract:The distal femoral Epiphyseal Plates of 21 8-week-old New Zealand white rabbits were totally or partially (nutrient artery only) devascularized, or devascularized and then microsurgically revascularized. Sacrifice was at 24, 48 or 72 hours postoperatively. The heights of the proliferative and hypertrophic zones of the Epiphyseal Plates operated upon were compared with the contralateral control Epiphyseal Plates for both the central and the peripheral regions of the Epiphyseal Plate. Neither extent of devascularization nor revascularization had a significant effect on the height of the proliferative zone of chondrocytes at any of the follow-up intervals. Selective devascularization of the nutrient artery led to a significant increase in height of the central region of the hypertrophic zone of chondrocytes at 48 and 72 hours. Microsurgical revascularization did not lead to a significant change in the height of either the central or the peripheral regions of the hypertrophic zone of chondrocytes at any of the follow-up intervals. This study is another ‘building block’ experiment toward vascularized Epiphyseal Plate transplantation in humans. © 1994 Wiley-Liss, Inc.
-
Epiphyseal Plate transplantation an historical review
British Journal of Plastic Surgery, 1994Co-Authors: Martin I Boyer, Peter W Bray, Vaughan C A BowenAbstract:Abstract Non-vascularized and vascularized transplantation of Epiphyseal Plate autografts have been performed both clinically and experimentally for over 100 years. However, the ultimate clinical goal of vascularized transplantation of Epiphyseal Plate allografts for paediatric extremity reconstruction remains elusive, due primarily to the lack of suitably nontoxic techniques to prevent graft rejection. We have summarized the published clinical and experimental investigations of vascularized Epiphyseal Plate transplantation, and organized the experiments and clinical operations into four main groups: (1) local vascular studies on unmanipulated Epiphyseal Plates, (2) studies of Epiphyseal Plate behaviour after orthotopic replantation, (3) studies of Epiphyseal Plate behaviour after heterotopic transplantation, and (4) studies of Epiphyseal Plate behaviour after allograft transplantation. Prior investigations into the non-vascularized transplantation of Epiphyseal Plate autografts and allografts are presented as background. These groups of studies serve as the building blocks for the more clinically applicable experimental investigations outlined in the final section of this review.
Zongke Zhou - One of the best experts on this subject based on the ideXlab platform.
-
magnetic resonance imaging at 7 0 t for evaluation of early lesions of Epiphyseal Plate and Epiphyseal end in a rat model of kashin beck disease
BMC Musculoskeletal Disorders, 2020Co-Authors: Pengde Kang, Zongke Zhou, Yong Li, Qing He, Dike RuanAbstract:Kashin–Beck disease (KBD) is a disabling osteoarticular disease involving growth and joint cartilage. Early diagnosis can effectively prevent the progress of the disease. However, the early diagnosis of it is still very difficult. Our aim was to study the knee joint lesions of a rat KBD model using ultra-high field magnetic resonance imaging (MRI) and compare it with X-ray imaging to analyze the possible MRI manifestations of KBD, and to further explore ways to determine the pathological damage of KBD in the early stage. A total of 96 Wistar rats were selected and randomly divided into 4 groups: normal diet (Group A), KBD-affected diet (Group B), normal diet+T-2 toxin (Group C), and KBD-affected diet+T-2 toxin (Group D). T-2 toxin was administered at a dose of 0.1 mg/kg/day. In the 4th week, 8th week, and 12th week, eight rats randomly selected in each group were sacrificed by cervical dislocation after undergoing X-ray and 7.0 T MRI imaging, and then knee joints were harvested, sliced, and subjected to hematoxylin-eosin (H&E) staining. Characteristic image changes including of continuity interruption and early closure and fusion of Epiphyseal Plates were observed on T1WI in rat model of KBD. The total necrosis rates in the H&E stain of group A to group D were 4.35, 52.38, 33.3, and 73.68%, respectively. The positive rate of image change under 7.0 T MRI was 0.833 VS. that under X-ray was 0.33 (P = 0.001). MRI at 7.0 T is highly sensitive to the early pathological changes of the epiphysis, Epiphyseal Plate, and metaphyseal end, which can improve imaging positive rate of KBD and decrease the rate of missed diagnosis. This imaging modality can be used for research on early joint lesions and for early diagnosis of KBD.
-
study on the effect of t 2 toxin combined with low nutrition diet on rat Epiphyseal Plate growth and development
International Orthopaedics, 2010Co-Authors: Pengde Kang, Xingbo Li, Jing Yang, Bing Shen, Zongke ZhouAbstract:The purpose of this study was to observe early lesions of rat Epiphyseal Plates and metaphysis caused by T-2 toxin and T-2 toxin combined with a low nutrition diet to determine possible pathogenic factors of Kashin-Beck disease (KBD). Ninety Wistar rats were divided into three groups. Group A was fed with a normal diet as control; group B was fed with a normal diet and T-2 toxin; and group C was fed with a low nutrition diet and T-2 toxin. The left knee specimens were collected, fixed in formaldehyde solution, stained by hematoxylin and eosin and Masson. After two weeks, the Epiphyseal Plate showed necrosis of chondrocytes in groups B and C. After four weeks, more obvious chondrocyte necrosis appeared. The positive rate of Lamellar necrosis in group C was significantly higher than that in groups B and A (P < 0.01). Metaphyseal trabecular bone showed sparse disorder and disruption in group C. T-2 toxin combined with a low nutrition diet could lead to more serious chondrocyte necrosis in the Epiphyseal Plate and disturb metaphyseal trabecular bone formation.
N Balmain - One of the best experts on this subject based on the ideXlab platform.
-
expression of bcl 2 protein in the Epiphyseal Plate cartilage and trabecular bone of growing rats
Histochemistry and Cell Biology, 1997Co-Authors: Ying Wang, R Toury, Michelle Hauchecorne, N BalmainAbstract:The protooncogene protein, Bcl-2, protects cells from apoptosis and ensures their survival in vitro by inhibiting the action of the apoptosis-inducer, Bax. Its expression in proliferative and long-lived cells in vivo also indicates that it protects against cell death. The chondrocytes of the Epiphyseal Plate cartilage undergo a series of maturation steps and deposit mineral in the cartilage matrix before dying. The possibility that Bcl-2 helps protect chondrocytes until mineral deposition is completed was investigated by determining the distribution of Bcl-2 immunoreactivity in the Epiphyseal Plate cartilage of growing rats and its subcellular localization, using a specific antibody. The involvement of Bax in the triggering of chondrocyte death was checked by immunocytochemistry. Bcl-2 expression in the osteoblasts and the final result of their evolution, the osteocytes, was also examined in trabecular bone. Bcl-2 immunoreactivity was non-uniformly distributed throughout the Epiphyseal cartilage. It was maximal in proliferative chondrocytes, decreased in mature chondrocytes, and low in hypertrophic chondrocytes, whereas there was Bax immunoreactivity in all chondrocytes examined. Immunolabeling was intense in osteoblasts but considerably lower in fully differentiated osteocytes. Bcl-2 immunoreactivity was mainly in the cytoplasm of chondrocytes, osteoblasts, and early osteocytes; the nuclei appeared clear. The subcellular distribution of Bcl-2 immunolabeling in chondrocytes, revealed by gold particles in the electron microscope, showed that gold particles were frequently concentrated in the mitochondria in all the cartilage zones and lay mainly within the organelles, not at their periphery. The endoplasmic reticulum contained moderate immunoreactivity and there were few gold particles in the cytoplasm and nuclei. The number of gold particles decreased in all the subcellular compartments from proliferative to hypertrophic chondrocytes. In contrast, Bax immunoreactivity changed little during chondrocyte terminal evolution, and its subcellular distribution mirrored that of Bcl-2. These immunocytochemical data indicate that Bcl-2 helps maintain chondrocytes and osteoblasts until their terminal maturation.
-
expression and subcellular localization of the myc superfamily proteins c myc max mad1 and mxi1 in the Epiphyseal Plate cartilage chondrocytes of growing rats
Cellular and Molecular Biology, 1997Co-Authors: Ying Wang, R Toury, Michelle Hauchecorne, N BalmainAbstract:The changes in the expressions of the protooncogene protein c-Myc, its dimerization partner Max and the competitive inhibitors Mad1 and Mxi1 during the terminal differentiation of chondrocytes in vivo were investigated by immunocytochemistry. The four immunoreactivity patterns in the Epiphyseal Plate cartilage of growing rats, as they appeared under the light microscope, showed differences in protein expression level and intracellular distribution, with the chondrocyte developmental stage. c-Myc immunoreactivity was intense and mainly in the nuclei of proliferative chondrocytes. It decreased in the nuclei of mature chondrocytes and appeared in the cytoplasm. c-Myc immunoreactivity increased in the fully-differentiated hypertrophic chondrocytes. Immunoreactivity of the c-Myc dimerization partner Max was mainly in the nucleus of proliferative chondrocytes and decreased as the chondrocytes matured. Mad1 immunoreactivity was also concentrated in the nucleus of proliferative chondrocytes, but was mainly in the cytoplasm of mature chondrocytes and almost lost from the hypertrophic chondrocytes. Lastly, there was Mxi1 immunoreactivity in the nucleus and cytoplasm of proliferative, mature and early hypertrophic chondrocytes and the cytoplasm staining was more sustained than in the nucleus. There was little labeling in late hypertrophic chondrocytes. The electron microscope pictures corroborated these findings and showed the subcellular distributions of the immunolabelings. The gold particles reflecting Mad1 frequently formed patches and those for Mxi1 appeared to accumulate within the mitochondria of all chondrocytes. The variations in immuno-patterns and intracellular distributions suggest that each protooncogene protein has specific roles in the functional changes in the chondrocytes at each step of their terminal differentiation.