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Robert Rejdak - One of the best experts on this subject based on the ideXlab platform.

  • A novel biomarker for retinal degeneration: vitreous body neurofilament proteins
    Journal of Neural Transmission, 2009
    Co-Authors: Axel Petzold, Sebastian Thaler, Pawel Grieb, Konrad Rejdak, Tomasz Zarnowski, Eberhart Zrenner, Anselm Junemann, Friedrich E Kruse, Robert Rejdak
    Abstract:

    Retinal degeneration leads to release of cell-type specific proteins into the Adjacent Compartment. Here we investigated whether the neurofilament heavy chain protein (NfH) could be measured from the vitreous body and anterior chamber fluid. This prospective study included 85 patients who underwent vitrectomy (44 retinal detachment, 12 macular hole, 15 epiretinal gliosis, 8 organ donors) or trabelectomy (six glaucoma). The cut-off level was calculated from the organ donors. An established enzyme-linked immunosorbent assay (ELISA, SMI35) was used for quantification of NfH (190–210 kDa). Measurable levels of NfH were detected from the vitreous body homogenate, but not from the anterior chamber fluid. The cut-off level was 0.29 ng/mL. A significant proportion of patients suffering from retinal detachment (43.2%, mean 0.74 ng/mL) had vitreous body NfH levels above cut-off when compared to organ donors (0%, 0.12 ng/mL, p  = 0.02), epiretinal sclerosis (1.6%, 0.05 ng/mL, p  = 0.01), macular hole (0%, 0.04 ng/mL, p  = 0.004). Following retinal detachment, vitreous NfH-SMI35 levels correlated with time from onset ( R  = −0.3, p  

  • a novel biomarker for retinal degeneration vitreous body neurofilament proteins
    Journal of Neural Transmission, 2009
    Co-Authors: Axel Petzold, Sebastian Thaler, Pawel Grieb, Konrad Rejdak, Tomasz Zarnowski, Eberhart Zrenner, Anselm Junemann, Robert Rejdak, Friedrich E Kruse
    Abstract:

    Retinal degeneration leads to release of cell-type specific proteins into the Adjacent Compartment. Here we investigated whether the neurofilament heavy chain protein (NfH) could be measured from the vitreous body and anterior chamber fluid. This prospective study included 85 patients who underwent vitrectomy (44 retinal detachment, 12 macular hole, 15 epiretinal gliosis, 8 organ donors) or trabelectomy (six glaucoma). The cut-off level was calculated from the organ donors. An established enzyme-linked immunosorbent assay (ELISA, SMI35) was used for quantification of NfH (190–210 kDa). Measurable levels of NfH were detected from the vitreous body homogenate, but not from the anterior chamber fluid. The cut-off level was 0.29 ng/mL. A significant proportion of patients suffering from retinal detachment (43.2%, mean 0.74 ng/mL) had vitreous body NfH levels above cut-off when compared to organ donors (0%, 0.12 ng/mL, p = 0.02), epiretinal sclerosis (1.6%, 0.05 ng/mL, p = 0.01), macular hole (0%, 0.04 ng/mL, p = 0.004). Following retinal detachment, vitreous NfH-SMI35 levels correlated with time from onset (R = −0.3, p < 0.05), persisting for up to 2 years. This study shows that NfH can be quantified from the human vitreous body and may be a useful novel biomarker for retinal degeneration. The method can be applied for investigating the dynamics of retinal degeneration and the response to neuroprotective strategies in a broad range of retinal diseases in either clinical or experimental research.

Axel Petzold - One of the best experts on this subject based on the ideXlab platform.

  • A novel biomarker for retinal degeneration: vitreous body neurofilament proteins
    Journal of Neural Transmission, 2009
    Co-Authors: Axel Petzold, Sebastian Thaler, Pawel Grieb, Konrad Rejdak, Tomasz Zarnowski, Eberhart Zrenner, Anselm Junemann, Friedrich E Kruse, Robert Rejdak
    Abstract:

    Retinal degeneration leads to release of cell-type specific proteins into the Adjacent Compartment. Here we investigated whether the neurofilament heavy chain protein (NfH) could be measured from the vitreous body and anterior chamber fluid. This prospective study included 85 patients who underwent vitrectomy (44 retinal detachment, 12 macular hole, 15 epiretinal gliosis, 8 organ donors) or trabelectomy (six glaucoma). The cut-off level was calculated from the organ donors. An established enzyme-linked immunosorbent assay (ELISA, SMI35) was used for quantification of NfH (190–210 kDa). Measurable levels of NfH were detected from the vitreous body homogenate, but not from the anterior chamber fluid. The cut-off level was 0.29 ng/mL. A significant proportion of patients suffering from retinal detachment (43.2%, mean 0.74 ng/mL) had vitreous body NfH levels above cut-off when compared to organ donors (0%, 0.12 ng/mL, p  = 0.02), epiretinal sclerosis (1.6%, 0.05 ng/mL, p  = 0.01), macular hole (0%, 0.04 ng/mL, p  = 0.004). Following retinal detachment, vitreous NfH-SMI35 levels correlated with time from onset ( R  = −0.3, p  

  • a novel biomarker for retinal degeneration vitreous body neurofilament proteins
    Journal of Neural Transmission, 2009
    Co-Authors: Axel Petzold, Sebastian Thaler, Pawel Grieb, Konrad Rejdak, Tomasz Zarnowski, Eberhart Zrenner, Anselm Junemann, Robert Rejdak, Friedrich E Kruse
    Abstract:

    Retinal degeneration leads to release of cell-type specific proteins into the Adjacent Compartment. Here we investigated whether the neurofilament heavy chain protein (NfH) could be measured from the vitreous body and anterior chamber fluid. This prospective study included 85 patients who underwent vitrectomy (44 retinal detachment, 12 macular hole, 15 epiretinal gliosis, 8 organ donors) or trabelectomy (six glaucoma). The cut-off level was calculated from the organ donors. An established enzyme-linked immunosorbent assay (ELISA, SMI35) was used for quantification of NfH (190–210 kDa). Measurable levels of NfH were detected from the vitreous body homogenate, but not from the anterior chamber fluid. The cut-off level was 0.29 ng/mL. A significant proportion of patients suffering from retinal detachment (43.2%, mean 0.74 ng/mL) had vitreous body NfH levels above cut-off when compared to organ donors (0%, 0.12 ng/mL, p = 0.02), epiretinal sclerosis (1.6%, 0.05 ng/mL, p = 0.01), macular hole (0%, 0.04 ng/mL, p = 0.004). Following retinal detachment, vitreous NfH-SMI35 levels correlated with time from onset (R = −0.3, p < 0.05), persisting for up to 2 years. This study shows that NfH can be quantified from the human vitreous body and may be a useful novel biomarker for retinal degeneration. The method can be applied for investigating the dynamics of retinal degeneration and the response to neuroprotective strategies in a broad range of retinal diseases in either clinical or experimental research.

Kevin C. Baker - One of the best experts on this subject based on the ideXlab platform.

  • Analysis of Retrieved UniCompartmental Knee Implants and Tissue: Third-Body Wear as a Potential Contributor to Progression of Arthritis to Adjacent Compartments
    Orthopedics, 2019
    Co-Authors: Lige M Kaplan, Matthew P. Siljander, James J. Verner, Kevin C. Baker, Corinn K. Gehrke, Meagan R. Salisbury, Erin A. Baker
    Abstract:

    UniCompartmental knee arthroplasty (UKA) for the treatment of single-Compartment osteoarthritis has been associated with polyethylene wear and progression of osteoarthritis into Adjacent Compartments, leading to revision. In this study, damage and clinical failure modes of retrieved UKA implants were investigated and protein expression profiles between articular cartilage Adjacent to UKA and primary osteoarthritic cartilage were compared. Fifty retrieved UKA implants were analyzed for various damage. Records review and radiographic analysis were performed to collect clinical data and implant characteristics. Cartilage harvested from revision UKA and primary total knee arthroplasty surgeries was characterized with a proteome profiling array detecting levels of 36 different cytokines, chemokines, and acute phase inflammatory proteins. Progression of osteoarthritis (n=18, 36%) and component loosening (n=17, 34%) were the most common reasons for revision. Liners exhibited the highest frequency of damage modes. Progression of arthritis positively correlated with radiographic presence of extruded bone cement and burnishing of liner components. A protein-level profile between revision UKA and primary total knee arthroplasty cartilage showed 12 differentially expressed cytokines. Failure of UKA may be secondary to the effects of wear debris particulate migration into the Adjacent Compartment, suggesting an additional pathway of cartilage damage manifesting as traditional clinical symptoms. [Orthopedics. 2019; 42(3):149-157.].

  • in vitro chondrocyte viability in response to exposure of metallic wear debris particulate
    Journal of Bone and Joint Surgery-british Volume, 2013
    Co-Authors: Michael D Kurdziel, Lige M Kaplan, Meagan R. Salisbury, Erin A. Baker, Tristan Maerz, Kevin C. Baker
    Abstract:

    Introduction: UniCompartmental knee arthroplasty (UKA) has been used in the past decades to treat progressive cartilage degeneration in a single Compartment. Concern has been raised over the rate of revision procedures for polyethylene wear and osteoarthritic progression into the Adjacent Compartment. Few studies have examined the pathology of cartilage degeneration in the setting of UKA. This study aims to investigate the viability of knee chondrocytes introduced to high and low concentrations of orthopaedic wear debris particulate. Methods: Normal human articular chondrocytes (nHAC-Kn) were expanded in DMEM/F12 containing 10% FBS, 1% Penicillin/Streptomycin (Pen/Strp), and 50 μg/mL ascorbic acid (Asc). 24 hours prior to the start of the experiment, cells were seeded on 96-well plates at a density of 3500 cells/cm 2 and exposed to DMEM/F12 containing 5% FBS, 1% Pen/Strp, and 50 μg/mL Asc. Particles (equivalent circle diameter range: 0.2–7 μm) at a low dose of 100: 1 (particles: cells) and high dose 1000: 1 (particles: cells) were introduced to treatment wells (n = 6). Control wells (n = 6) contained particles with no cells. Treatment groups included high and low doses of TiAl 6 V 4 alloy, 316L Stainless Steel, and Co-Cr-Mo alloy. At days 1, 3, 5, and 7, cells were assayed with a 3-(4,5-Dimethylthiazol-2-yl)-2,5-dyphenyltetrazolium bromide (MTT) assay for determination of cell viability. Light microscopy was performed at each timepoint to assess change in cell morphology. Results: All groups displayed a minor decrease in cell viability after 24 hours of exposure to particles. Similarly, a second distinct decrease in viability occurred at the day 3 timepoint. Days 5 and 7 yielded little change in cell viability. Results are displayed in Figure 1. Observations of light microscopy revealed cells may actively engulf particles over time. Images show particle concentrations at the same locations as chondrocytes with few particles present between cells. Conclusions: Wear debris has been implicated as a contributing source to osteolysis and component loosening. A potential effect on the cellular level can ultimate lead to effects on the entire tissue and complications on the clinical level. A decrease in chondrocyte viability has been shown in response to the presence of particulate wear debris. Our results showed decreases in cell viability were most noticeable between 24 and 72 hours after introduction to particles. Chondrocyte death may contribute to progression of cartilage degeneration into healthy Compartments of the knee. Continued experiments are underway further characterizing chondrocyte response to wear debris particulate with respect to protein and gene expression in an extended 7 day in vitro culture.

Sebastian Thaler - One of the best experts on this subject based on the ideXlab platform.

  • A novel biomarker for retinal degeneration: vitreous body neurofilament proteins
    Journal of Neural Transmission, 2009
    Co-Authors: Axel Petzold, Sebastian Thaler, Pawel Grieb, Konrad Rejdak, Tomasz Zarnowski, Eberhart Zrenner, Anselm Junemann, Friedrich E Kruse, Robert Rejdak
    Abstract:

    Retinal degeneration leads to release of cell-type specific proteins into the Adjacent Compartment. Here we investigated whether the neurofilament heavy chain protein (NfH) could be measured from the vitreous body and anterior chamber fluid. This prospective study included 85 patients who underwent vitrectomy (44 retinal detachment, 12 macular hole, 15 epiretinal gliosis, 8 organ donors) or trabelectomy (six glaucoma). The cut-off level was calculated from the organ donors. An established enzyme-linked immunosorbent assay (ELISA, SMI35) was used for quantification of NfH (190–210 kDa). Measurable levels of NfH were detected from the vitreous body homogenate, but not from the anterior chamber fluid. The cut-off level was 0.29 ng/mL. A significant proportion of patients suffering from retinal detachment (43.2%, mean 0.74 ng/mL) had vitreous body NfH levels above cut-off when compared to organ donors (0%, 0.12 ng/mL, p  = 0.02), epiretinal sclerosis (1.6%, 0.05 ng/mL, p  = 0.01), macular hole (0%, 0.04 ng/mL, p  = 0.004). Following retinal detachment, vitreous NfH-SMI35 levels correlated with time from onset ( R  = −0.3, p  

  • a novel biomarker for retinal degeneration vitreous body neurofilament proteins
    Journal of Neural Transmission, 2009
    Co-Authors: Axel Petzold, Sebastian Thaler, Pawel Grieb, Konrad Rejdak, Tomasz Zarnowski, Eberhart Zrenner, Anselm Junemann, Robert Rejdak, Friedrich E Kruse
    Abstract:

    Retinal degeneration leads to release of cell-type specific proteins into the Adjacent Compartment. Here we investigated whether the neurofilament heavy chain protein (NfH) could be measured from the vitreous body and anterior chamber fluid. This prospective study included 85 patients who underwent vitrectomy (44 retinal detachment, 12 macular hole, 15 epiretinal gliosis, 8 organ donors) or trabelectomy (six glaucoma). The cut-off level was calculated from the organ donors. An established enzyme-linked immunosorbent assay (ELISA, SMI35) was used for quantification of NfH (190–210 kDa). Measurable levels of NfH were detected from the vitreous body homogenate, but not from the anterior chamber fluid. The cut-off level was 0.29 ng/mL. A significant proportion of patients suffering from retinal detachment (43.2%, mean 0.74 ng/mL) had vitreous body NfH levels above cut-off when compared to organ donors (0%, 0.12 ng/mL, p = 0.02), epiretinal sclerosis (1.6%, 0.05 ng/mL, p = 0.01), macular hole (0%, 0.04 ng/mL, p = 0.004). Following retinal detachment, vitreous NfH-SMI35 levels correlated with time from onset (R = −0.3, p < 0.05), persisting for up to 2 years. This study shows that NfH can be quantified from the human vitreous body and may be a useful novel biomarker for retinal degeneration. The method can be applied for investigating the dynamics of retinal degeneration and the response to neuroprotective strategies in a broad range of retinal diseases in either clinical or experimental research.

Pawel Grieb - One of the best experts on this subject based on the ideXlab platform.

  • A novel biomarker for retinal degeneration: vitreous body neurofilament proteins
    Journal of Neural Transmission, 2009
    Co-Authors: Axel Petzold, Sebastian Thaler, Pawel Grieb, Konrad Rejdak, Tomasz Zarnowski, Eberhart Zrenner, Anselm Junemann, Friedrich E Kruse, Robert Rejdak
    Abstract:

    Retinal degeneration leads to release of cell-type specific proteins into the Adjacent Compartment. Here we investigated whether the neurofilament heavy chain protein (NfH) could be measured from the vitreous body and anterior chamber fluid. This prospective study included 85 patients who underwent vitrectomy (44 retinal detachment, 12 macular hole, 15 epiretinal gliosis, 8 organ donors) or trabelectomy (six glaucoma). The cut-off level was calculated from the organ donors. An established enzyme-linked immunosorbent assay (ELISA, SMI35) was used for quantification of NfH (190–210 kDa). Measurable levels of NfH were detected from the vitreous body homogenate, but not from the anterior chamber fluid. The cut-off level was 0.29 ng/mL. A significant proportion of patients suffering from retinal detachment (43.2%, mean 0.74 ng/mL) had vitreous body NfH levels above cut-off when compared to organ donors (0%, 0.12 ng/mL, p  = 0.02), epiretinal sclerosis (1.6%, 0.05 ng/mL, p  = 0.01), macular hole (0%, 0.04 ng/mL, p  = 0.004). Following retinal detachment, vitreous NfH-SMI35 levels correlated with time from onset ( R  = −0.3, p  

  • a novel biomarker for retinal degeneration vitreous body neurofilament proteins
    Journal of Neural Transmission, 2009
    Co-Authors: Axel Petzold, Sebastian Thaler, Pawel Grieb, Konrad Rejdak, Tomasz Zarnowski, Eberhart Zrenner, Anselm Junemann, Robert Rejdak, Friedrich E Kruse
    Abstract:

    Retinal degeneration leads to release of cell-type specific proteins into the Adjacent Compartment. Here we investigated whether the neurofilament heavy chain protein (NfH) could be measured from the vitreous body and anterior chamber fluid. This prospective study included 85 patients who underwent vitrectomy (44 retinal detachment, 12 macular hole, 15 epiretinal gliosis, 8 organ donors) or trabelectomy (six glaucoma). The cut-off level was calculated from the organ donors. An established enzyme-linked immunosorbent assay (ELISA, SMI35) was used for quantification of NfH (190–210 kDa). Measurable levels of NfH were detected from the vitreous body homogenate, but not from the anterior chamber fluid. The cut-off level was 0.29 ng/mL. A significant proportion of patients suffering from retinal detachment (43.2%, mean 0.74 ng/mL) had vitreous body NfH levels above cut-off when compared to organ donors (0%, 0.12 ng/mL, p = 0.02), epiretinal sclerosis (1.6%, 0.05 ng/mL, p = 0.01), macular hole (0%, 0.04 ng/mL, p = 0.004). Following retinal detachment, vitreous NfH-SMI35 levels correlated with time from onset (R = −0.3, p < 0.05), persisting for up to 2 years. This study shows that NfH can be quantified from the human vitreous body and may be a useful novel biomarker for retinal degeneration. The method can be applied for investigating the dynamics of retinal degeneration and the response to neuroprotective strategies in a broad range of retinal diseases in either clinical or experimental research.