The Experts below are selected from a list of 169515 Experts worldwide ranked by ideXlab platform
Paul C. Jutte - One of the best experts on this subject based on the ideXlab platform.
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The push-through total femoral prosthesis offers a Functional Alternative to total femoral replacement: a case series
International Orthopaedics, 2017Co-Authors: Jelle Gorter, Joris J. W. Ploegmakers, Bas L. E. F. Ten Have, Hendrik W. B. Schreuder, Paul C. JutteAbstract:Purpose Oncologic resections or complications of segmental femoral prostheses can result in severe bone loss of the femur for which a total femoral prosthesis (TFP) is required. This study assesses whether the loss of stability and function caused by the loss of muscle attachments can be improved by using a push-through total femoral endoprosthesis (PTTF), because it saves parts of the femur and its muscle attachments. Methods In this retrospective case series, ten patients aged 25–77 (mean 54) who received a PTTF between 2005 and 2014 were included for baseline, complications and survival analysis with a mean follow-up of 5.3 (1.1–9.6) years. Functional outcome was assessed in six patients using the Musculoskeletal Tumor Society (MSTS) score, WHO performance scale, Toronto Extremity Salvage Score (TESS), SF36, EQ-5D, NRS pain score, fatigue score and satisfaction score. Results The mean MSTS score was 64% (23–93%). Five patients had a WHO performance scale of 1, one patient of 3. Mean TESS was 69% (13–90%). SF36 was most notably limited by physical functioning (mean 48), vitality (68) and general health (67). NRS score was 1.9, 1.8 and 8.3 for pain, fatigue and satisfaction, respectively. There were four failures: two infections (one resulting in amputation and one in a minor revision) and two mechanical failures (which required one revision to a TFP and one minor revision). Patient survival was 100%, limb survival 90%, and prosthesis survival 80%. Conclusion The push-through total femoral endoprosthesis allows preservation of muscle attachments and offers a good Alternative to total femoral prostheses.
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The push-through total femoral prosthesis offers a Functional Alternative to total femoral replacement: a case series
International orthopaedics, 2017Co-Authors: Jelle Gorter, Joris J. W. Ploegmakers, Hendrik W. B. Schreuder, Bas L. E. F. Ten Have, Paul C. JutteAbstract:Purpose Oncologic resections or complications of segmental femoral prostheses can result in severe bone loss of the femur for which a total femoral prosthesis (TFP) is required. This study assesses whether the loss of stability and function caused by the loss of muscle attachments can be improved by using a push-through total femoral endoprosthesis (PTTF), because it saves parts of the femur and its muscle attachments.
Viktor Berge - One of the best experts on this subject based on the ideXlab platform.
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Interleukin-1α, interleukin 6 and tumor necrosis factor α increase the synthesis and expression of the Functional Alternative and terminal complement pathways by human umbilical vein endothelial cells in vitro
APMIS : acta pathologica microbiologica et immunologica Scandinavica, 1996Co-Authors: Viktor Berge, Egil Johnson, K. E. BergeAbstract:The proinflammatory cytokines interleukin 1 alpha (IL-1 alpha), tumor necrosis factor alpha (TNF alpha) and interleukin 6 (IL-6) modulate the synthesis of complement factors B and C3 by endothelial cells (EC), and are considered to play an important role in the development of sepsis. By using agarose beads activating the Alternative pathway of complement, we wanted to study the net effect of these cytokines on EC synthesis of the Alternative and terminal pathways, measured by binding of anti-C3c and anti-TCC (terminal complement complex) antibodies to beads kept with the EC. Addition of IL-1 alpha and TNF alpha at concentrations of 50 and 100 U/ml resulted in a significant increase in binding of these antibodies to co-incubated beads, most pronounced for anti-C3c. IL-6 from 50-200 U/ml resulted in a stronger (two to fourfold) binding for both antibodies compared to experiments with IL-1 alpha and TNF. However, increased concentrations of IL-1 alpha (200 U/ml) and IL-6 (400 U/ml) resulted in a strong reduction in binding of anti-C3c and anti-TCC antibodies to the co-cultured beads. This study indicates that proinflammatory cytokines upregulate the synthesis by EC of the Functional Alternative and terminal pathways of complement.
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Effect of gamma‐interferon on the synthesis of the Functional Alternative and terminal comdement pathways by human umbilical vein endothelial cells in vitro
APMIS : acta pathologica microbiologica et immunologica Scandinavica, 1994Co-Authors: Viktor Berge, Egil Johnson, M. NazirAbstract:The cytokine gamma-interferon (gIFN) has been reported to modulate synthesis by endothelial cells (EC) of Alternative pathway complement factors (H, I, and B). However, the net effect of gIFN on the synthesis and expression of the Functional Alternative and terminal pathways has not yet been reported. EC cultured under serum-free conditions were treated with different concentrations of gIFN and simultaneously co-incubated with agarose beads, which activate the Alternative pathway. C3b and the terminal complement complex (TCC) bound to co-incubated beads were measured by radioimmunoassay using anti-human C3c and TCC antibodies. gIFN in concentrations 500-4000 U/ml increasingly reduced the amount of C3b and TCC detected on the beads. The down-regulating effect of gIFN on EC complement biosynthesis may be physiologically relevant by locally controlling complement activation.
Iris Leinhase - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of the Alternative complement activation pathway in traumatic brain injury by a monoclonal anti-factor B antibody: a randomized placebo-controlled study in mice
Journal of Neuroinflammation, 2007Co-Authors: Iris Leinhase, Joshua M. Thurman, Denise Harhausen, Oliver I. Schmidt, Mohy E Taha, Daniel Rittirsch, Michal Rozanski, Amir M Hossini, Peter A Ward, V. Michael HolersAbstract:Background The posttraumatic response to traumatic brain injury (TBI) is characterized, in part, by activation of the innate immune response, including the complement system. We have recently shown that mice devoid of a Functional Alternative pathway of complement activation (factor B-/- mice) are protected from complement-mediated neuroinflammation and neuropathology after TBI. In the present study, we extrapolated this knowledge from studies in genetically engineered mice to a pharmacological approach using a monoclonal anti-factor B antibody. This neutralizing antibody represents a specific and potent inhibitor of the Alternative complement pathway in mice. Methods A focal trauma was applied to the left hemisphere of C57BL/6 mice ( n = 89) using a standardized electric weight-drop model. Animals were randomly assigned to two treatment groups: (1) Systemic injection of 1 mg monoclonal anti-factor B antibody ( mAb 1379 ) in 400 μl phosphate-buffered saline (PBS) at 1 hour and 24 hours after trauma; (2) Systemic injection of vehicle only (400 μl PBS), as placebo control, at identical time-points after trauma. Sham-operated and untreated mice served as additional negative controls. Evaluation of neurological scores and analysis of brain tissue specimens and serum samples was performed at defined time-points for up to 1 week. Complement activation in serum was assessed by zymosan assay and by murine C5a ELISA. Brain samples were analyzed by immunohistochemistry, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) histochemistry, and real-time RT-PCR. Results The mAb 1379 leads to a significant inhibition of Alternative pathway complement activity and to significantly attenuated C5a levels in serum, as compared to head-injured placebo-treated control mice. TBI induced histomorphological signs of neuroinflammation and neuronal apoptosis in the injured brain hemisphere of placebo-treated control mice for up to 7 days. In contrast, the systemic administration of an inhibitory anti-factor B antibody led to a substantial attenuation of cerebral tissue damage and neuronal cell death. In addition, the posttraumatic administration of the mAb 1379 induced a neuroprotective pattern of intracerebral gene expression. Conclusion Inhibition of the Alternative complement pathway by posttraumatic administration of a neutralizing anti-factor B antibody appears to represent a new promising avenue for pharmacological attenuation of the complement-mediated neuroinflammatory response after head injury.
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inhibition of the Alternative complement activation pathway in traumatic brain injury by a monoclonal anti factor b antibody a randomized placebo controlled study in mice
Journal of Neuroinflammation, 2007Co-Authors: Iris Leinhase, Joshua M. Thurman, Denise Harhausen, Oliver I. Schmidt, Mohy E Taha, Daniel Rittirsch, Michal Rozanski, Amir M Hossini, Peter A Ward, Michael V HolersAbstract:Background The posttraumatic response to traumatic brain injury (TBI) is characterized, in part, by activation of the innate immune response, including the complement system. We have recently shown that mice devoid of a Functional Alternative pathway of complement activation (factor B-/- mice) are protected from complement-mediated neuroinflammation and neuropathology after TBI. In the present study, we extrapolated this knowledge from studies in genetically engineered mice to a pharmacological approach using a monoclonal anti-factor B antibody. This neutralizing antibody represents a specific and potent inhibitor of the Alternative complement pathway in mice.
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Reduced neuronal cell death after experimental brain injury in mice lacking a Functional Alternative pathway of complement activation
BMC neuroscience, 2006Co-Authors: Iris Leinhase, Joshua M. Thurman, V. Michael Holers, Denise Harhausen, Oliver I. Schmidt, Malte Pietzcker, Mohy E Taha, Daniel Rittirsch, Markus Huber-lang, Wade R. SmithAbstract:Background Neuroprotective strategies for prevention of the neuropathological sequelae of traumatic brain injury (TBI) have largely failed in translation to clinical treatment. Thus, there is a substantial need for further understanding the molecular mechanisms and pathways which lead to secondary neuronal cell death in the injured brain. The intracerebral activation of the complement cascade was shown to mediate inflammation and tissue destruction after TBI. However, the exact pathways of complement activation involved in the induction of posttraumatic neurodegeneration have not yet been assessed. In the present study, we investigated the role of the Alternative complement activation pathway in contributing to neuronal cell death, based on a standardized TBI model in mice with targeted deletion of the factor B gene (fB-/-), a "key" component required for activation of the Alternative complement pathway.
M. Nazir - One of the best experts on this subject based on the ideXlab platform.
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Effect of gamma‐interferon on the synthesis of the Functional Alternative and terminal comdement pathways by human umbilical vein endothelial cells in vitro
APMIS : acta pathologica microbiologica et immunologica Scandinavica, 1994Co-Authors: Viktor Berge, Egil Johnson, M. NazirAbstract:The cytokine gamma-interferon (gIFN) has been reported to modulate synthesis by endothelial cells (EC) of Alternative pathway complement factors (H, I, and B). However, the net effect of gIFN on the synthesis and expression of the Functional Alternative and terminal pathways has not yet been reported. EC cultured under serum-free conditions were treated with different concentrations of gIFN and simultaneously co-incubated with agarose beads, which activate the Alternative pathway. C3b and the terminal complement complex (TCC) bound to co-incubated beads were measured by radioimmunoassay using anti-human C3c and TCC antibodies. gIFN in concentrations 500-4000 U/ml increasingly reduced the amount of C3b and TCC detected on the beads. The down-regulating effect of gIFN on EC complement biosynthesis may be physiologically relevant by locally controlling complement activation.
Egil Johnson - One of the best experts on this subject based on the ideXlab platform.
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Interleukin-1α, interleukin 6 and tumor necrosis factor α increase the synthesis and expression of the Functional Alternative and terminal complement pathways by human umbilical vein endothelial cells in vitro
APMIS : acta pathologica microbiologica et immunologica Scandinavica, 1996Co-Authors: Viktor Berge, Egil Johnson, K. E. BergeAbstract:The proinflammatory cytokines interleukin 1 alpha (IL-1 alpha), tumor necrosis factor alpha (TNF alpha) and interleukin 6 (IL-6) modulate the synthesis of complement factors B and C3 by endothelial cells (EC), and are considered to play an important role in the development of sepsis. By using agarose beads activating the Alternative pathway of complement, we wanted to study the net effect of these cytokines on EC synthesis of the Alternative and terminal pathways, measured by binding of anti-C3c and anti-TCC (terminal complement complex) antibodies to beads kept with the EC. Addition of IL-1 alpha and TNF alpha at concentrations of 50 and 100 U/ml resulted in a significant increase in binding of these antibodies to co-incubated beads, most pronounced for anti-C3c. IL-6 from 50-200 U/ml resulted in a stronger (two to fourfold) binding for both antibodies compared to experiments with IL-1 alpha and TNF. However, increased concentrations of IL-1 alpha (200 U/ml) and IL-6 (400 U/ml) resulted in a strong reduction in binding of anti-C3c and anti-TCC antibodies to the co-cultured beads. This study indicates that proinflammatory cytokines upregulate the synthesis by EC of the Functional Alternative and terminal pathways of complement.
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Effect of gamma‐interferon on the synthesis of the Functional Alternative and terminal comdement pathways by human umbilical vein endothelial cells in vitro
APMIS : acta pathologica microbiologica et immunologica Scandinavica, 1994Co-Authors: Viktor Berge, Egil Johnson, M. NazirAbstract:The cytokine gamma-interferon (gIFN) has been reported to modulate synthesis by endothelial cells (EC) of Alternative pathway complement factors (H, I, and B). However, the net effect of gIFN on the synthesis and expression of the Functional Alternative and terminal pathways has not yet been reported. EC cultured under serum-free conditions were treated with different concentrations of gIFN and simultaneously co-incubated with agarose beads, which activate the Alternative pathway. C3b and the terminal complement complex (TCC) bound to co-incubated beads were measured by radioimmunoassay using anti-human C3c and TCC antibodies. gIFN in concentrations 500-4000 U/ml increasingly reduced the amount of C3b and TCC detected on the beads. The down-regulating effect of gIFN on EC complement biosynthesis may be physiologically relevant by locally controlling complement activation.
