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Tamara Vyshkina1 and Bernadette Kalman1,2Received 12 March 2008; Revised 21 April 2008; Accepted 25 April 2008; Published online 2 June 2008.Top of pageAbstractNeurodegeneration develops in association with inflammation and demyelination in multiple sclerosis. Available data suggest that the progressive neuroaxonal loss Authenitc Kids John Abraham jersey begins in the earliest stages of the disease and Elite red Frostee Rucker jersey underlies the accumulation of clinical disability. The loss of neurons and their processes is driven by a complex molecular mechanism involving cellular and humoral immune histotoxicity, demyelination, reduced neurotrophic support, metabolic impairment, and altered intracellular processes. Here we survey available data concerning the role of autoreactive immunoglobulins in neurotoxicity. A generally accepted view of MS pathogenesis has linked the disease process to myelin specific, CD4 T lymphocytes which, upon activation by unknown factors, migrate through the blood barrier (BBB), engage CNS related antigenic Authenitc Kids Frostee Rucker jersey peptides presented by antigen presenting cells, clonally expand, and exert cytotoxic attacks on oligodendrocytes and myelin. This hypothesis has been largely driven by observations from the experimental autoimmune encephalomyelitis (EAE) model that represents a demyelinating CNS disorder mediated by myelin specific CD4 T cells.2, 3However, recent histological analyses4 and in vivo studies by magnetic resonance imaging (MRI) and spectroscopy (MRS)5, 6 emphasize that neurodegeneration develops along with inflammatory demyelination. The pathology affects the entire brain, but with different distributions of inflammation, demyelination, and neurodegeneration in the white and gray matter.7 The neuroaxonal loss is likely to be secondary to inflammation and demyelination, but it begins in the earliest stages of the disease and progresses even after the decline of inflammation. Most importantly, neuroaxonal loss represents the major pathological correlate of clinical disability.5 Further evidence to support the importance of neurodegeneration in MS is obtained from clinical data showing only a partial success of the available disease modifying drugs (interferons, glatiramer acetate, monoclonal antibodies to antigenic determinants expressed on T lymphocytes), which impede activation and migration of inflammatory cells via the BBB, but have no direct effect on the degenerative processes in CNS.8The exploration of neurodegeneration Authenitc Deone Bucannon jersey in MS received high priority in the last Youth John Abraham jersey few years. The data establish that this is a multifactorial process involving loss of myelin protection, immune mediated histotoxicity, decreased trophic support, mitochondrial damage, metabolic changes, and altered signaling.9, 10, 11, 12 We recently reviewed our and others’ published works concerning the involvement of mitochondrial mechanisms in neurodegeneration associated with inflammation.13, 14, 15 As an extension of surveys on neuroaxonal loss related to inflammatory demyelination, the present paper focuses on the involvement of humoral immune factors (Table 1). The available information allows us to generate a preliminary concept of immune mediated neuronal dysfunction and loss, and to highlight potential pathways amenable to therapeutic interventions (Figure 1; Tables 2, 3 and 4). This figure depicts the thus far identified CNS antigens targeted by humoral autoimmunity in inflammatory demyelination. Signs of autoimmunity are lacking in type III and IV lesions which appear as variants of a primary oligodendrocytopathy. However, humoral autoimmunity Womens Elite Kids Jonathan Cooper jersey Frostee Rucker jersey is not only involved in certain forms of demyelination, but also instrumental in the process of neurodegeneration but with thus far unknown relative destructivity in various disease subtypes.Immunologic and Molecular DataThe literature is markedly weighted towards characterization of the cellular arm of autoimmunity, but new data also support that B cells and humoral immunity play important roles in MS. The B cell lineage is represented by B lymphocytes (CD19 CD138 plasma blasts (CD19 CD138 and plasma cells (CD19 CD138 for brevity, altogether B cells) in CNS and cerebrospinal fluid (CSF). Most of these cells express memory (CD27 phenotypes in MS. Therapeutic observations support that B cells may both directly and indirectly contribute to the development of MS. Removal of immunoglobulins from the peripheral blood by plasmapheresis appears to be beneficial in the subgroup of patients with type II lesions59 and depletion of CD20 B cells by rituximab results in a significant reduction in the number of enhancing MRI lesions. The latter intervention, however, does not exert its beneficial effects by directly affecting the immunoglobulin pool, but by depleting memory B cells and altering antigen presentation, T cell activation, or T cell recruitment into the CNS.60Molecular data also support the involvement of B lymphocytes and their products in MS. Intrathecal production of immunoglobulins with an oligoclonal electrophoretic distribution pattern is a hallmark of the disease. These B cell clones exhibit complex molecular characteristics and intraclonal diversity.Activation of B CellsWhat drives B cell activation and clonal expansion is not fully understood. Epstein virus (EBV), a B lymphotropic microorganism, has been implicated in the development of the disease by epidemiological, immune serological, and histological studies.64, 65 MS patients have intracerebral accumulation of EBV infected B cells and plasma blasts, mostly in ectopic B cell follicles,39 and a cross reactivity of the anti EBV specific cells with CNS antigens has been noted.64, 65 Other mechanisms leading to autoimmune B cell activation may be initiated by CD4 T helper type 2 (TH2) lymphocytes and their soluble inflammatory products (eg interleukine 4, 5, and 13),66 followed by an antigen specific expansion of clones either in the peripheral circulation or in the damaged CNS Authenitc Bobby Massie jersey tissue, where intracellular proteins are released. Bystander activation describes a non antigen specific activation of T or B cells usually mediated by soluble inflammatory products of nearby immune cells.Anti Myelin AntibodiesImmunoglobulins produced by activated B cells in the CNS and CSF target numerous self antigens including components of the CNS myelin such as myelin basic protein, proteolipid protein, myelin associated glycoprotein, and myelin oligodendrocyte glycoprotein.67, 68 A great number of papers discusses the involvement of myelin specific antibodies in the development of demyelination and disease progression.69, 70 Pros and cons for the primary pathogenic significance or the reactive nature of anti myelin specific B cells have been debated.71, 72 The Authenitc Mens Jonathan Cooper jersey use of some of these antibodies as biomarkers to support the diagnosis or to monitor disease activity and course also has been proposed, but not uniformly accepted.73, 74Anti Neuronal AntibodiesAutoantibodies that target neuronal molecules and potentially exert histotoxicity have been less scrutinized. Nevertheless, growing data reveal that these antigen interactions play important roles in a number of neuroinflammatory and neurodegenerative conditions. In contrast to the usual scenario of a T lymphocyte driven autoimmunity and tissue damage, the humoral immune system appears to be more successful in breaking anti neuronal tolerance than the cellular system, and has greater pathogenic significance.43 This survey presents information that supports the involvement of the humoral immune response in Elite Kids Chandler Catanzarojersey MS related neurodegeneration.Top of Authenitc Mens Bobby Massie jersey pageANTI Elite Youth Jonathan Cooper jersey NEURONAL ANTIBODIES IN MSAntibodies Targeting Neuronal Cell Surface MoleculesNeuronal cell surface antigens Molecules in the surface membrane of myelinated axons are normally hidden from the immune system, and only become exposed after demyelination when they become antigenic and induce the Authenitc red Chandler Catanzarojersey production of neuron specific antibodies. IgG and IgM antibodies binding to the surface of a neuronal cell line were found in 70 of sera from patients with secondary progressive (SP) MS and in 25 of sera from patients with relapsing remitting (RR) MS.42 This finding may indicate the spreading of autoimmunity to neuronal antigens as a consequence of CNS tissue damage, and the expansion of pathology from moderate to marked neuroaxonal loss associated with a transition from RR to Authenitc red Frostee Rucker jersey SP MS course.Axolemma enriched fractions Antibodies to axolemma enriched fractions (AEF) of the CNS are also present in CSF and sera of MS patients.16 These antibodies damage neurites and prevent neuronal outgrowth in vitro. The production of anti axolemma and anti myelin IgGs appears to be independent. Based on these observations, the use of anti axolemma IgGs as markers of axonal damage was proposed.55Neurofascin One of the targets in antibody mediated axonal injury is a cell adhesion molecule neurofascin. The 186 neuron specific isoform of neurofascin (NF186) is required for the clustering of voltage gated Na channels at the nodes of Ranvier. The 155 glial specific isoform (NF155) is required for the proper assembly of paranodal junction, Kids Deone Bucannon jersey an important site of interactions between the myelin and axon. Early changes in the distribution of NF155 were observed in MS lesions preceding demyelination.44 Maier et al45 showed that the NF155 levels were reduced and a 40 NF155 fragment increased in plaques, suggesting that NF155 is subject to protein degradation in the lesions.Levels of antibodies to NF155 and NF186 were significantly higher in sera of patients with chronic progressive forms of MS compared to that of patients with other inflammatory neurological diseases.17 In vitro studies showed that antibodies to neurofascin inhibit axonal conduction. In vivo experiments revealed that antibodies to neurofascin and complement can selectively target nodes of Ranvier, cause axonal injury, and trigger disease exacerbation in EAE. Mathey et al17 also showed that Kareem Martin jersey NF155 specific antibodies cross react with NF186 transfected cells. The recognition of NF186 at the nodes of Ranvier by these antibodies may initiate axonal Authenitc Kids John Abraham Chandler Catanzarojersey jersey injury and Mens Bobby Massie jersey accelerate disease progression. Neurofascin specific antibodies can also inhibit remyelination by binding to NF155 expressed on the surface of oligodendrocytes.Gangliosides Another group of neuronal antigens includes the gangliosides, which are glycolipids with sialic residues in the outer layer of cell membranes. Gangliosides are particularly enriched in the membranes of neuron. To generate antibody responses, gangliosides do not require major histocompatibility complex (MHC) molecules and T cell help.75 Although it is unclear whether anti ganglioside antibodies can cause or result from axonal damage,18 they may certainly serve as a marker of this process. Experimental data reveal that anti ganglioside antibodies can disrupt the BBB,19 create neuromuscular block by binding to neuronal gangliosides in the neuromuscular junction,56 and inhibit axonal regeneration after peripheral nerve injury in mice.20 Complexes of anti ganglioside antibodies and complement destroy Schwann cells and myelin membranes in demyelinating neuropathies, and contribute to axonal degeneration in acute motor axonal neuropathy.41 Increased levels of anti GM3 (monosialo ganglioside) antibodies can be found in sera of a great proportion of patients with progressive forms of MS (56.3 in primary progressive (PP) MS and 42.9 in SP MS vs 2.9 in RR MS and 14.6 in OND).18 Anti GD2 (disialo ganglioside) like IgM autoantibodies were detected in sera of 30 of MS patients, and a positive correlation of anti GD2 like IgM reactivity with neurological disability was observed.21 The increased prevalence of GD2 specific IgM antibodies in SP MS (47.8 compared to RR MS (24.2 and PP MS (26.7 also suggests the involvement of these antibodies in inflammation induced neurodegeneration.In summary, these data suggest that antibodies specific to neuronal cell surface molecules are produced during demyelination and may themselves contribute to axonal injury in MS. These antibodies can activate complement and exert cytotoxicity, provide binding sites for the Fc receptors on macrophages and microglial cells, interrupt axon interaction, inhibit axonal conduction and outgrowth, disrupt the BBB, and alter oligodendrocyte functioning. Correlation of the antibody titers Authenitc red Deone Bucannon jersey with the severity of disability offers an opportunity of using these neuronal cell surface antibodies as biomarkers.Antibodies to Cytoskeletal ProteinsNeurofilaments Neurofilaments are a group of cytoskeletal proteins expressed in neuronal cells and axons. A variety of neurodegenerative disorders like Alzheimer’s disease, Parkinson’s disease, and dementia with Lewy bodies are characterized by accumulation of NF proteins signifying abnormalities in the axonal transport and an impending neuronal loss.76, 77Antibodies to axonal cytoskeletal proteins may be markers of axonal damage, as well as important contributors to neurodegeneration and clinical disability in MS. CSF levels of antibodies against the light subunit of neurofilaments (NFL) correlate with the disease duration, clinical disability, IgG index, and the degree of cerebral atrophy measured by MRI.22, 23 Although elevated levels of NFL specific antibodies are present in sera of patients with PP MS,24 these antibodies are also increased in sera of patients with OND.22Tamara Vyshkina1 and Bernadette Kalman1,2Received 12 March 2008; Revised 21 April 2008; Accepted 25 April 2008; Published online 2 June 2008.Top of pageAbstractNeurodegeneration develops in association with inflammation and demyelination in multiple sclerosis. Available data suggest that the progressive neuroaxonal loss begins in the earliest stages of the disease and underlies the accumulation of clinical disability. The loss of neurons and Elite red John Abraham jersey their processes is driven by a complex molecular mechanism involving cellular and humoral immune histotoxicity, demyelination, reduced neurotrophic support, metabolic impairment, and altered intracellular processes. Here we survey available data concerning the role of autoreactive immunoglobulins in neurotoxicity. A generally accepted view of MS pathogenesis has linked the disease process to myelin specific, CD4 T lymphocytes which, upon activation by unknown factors, migrate through the blood barrier (BBB), engage CNS related antigenic peptides presented by antigen presenting cells, clonally expand, and exert cytotoxic attacks on oligodendrocytes and myelin. This hypothesis has been largely driven by observations from the experimental autoimmune encephalomyelitis (EAE) model that represents a demyelinating CNS disorder Elite Kids John Abraham jersey mediated by myelin specific CD4 T cells.2, 3However, recent histological analyses4 and in vivo studies by magnetic resonance imaging (MRI) and spectroscopy (MRS)5, 6 emphasize that neurodegeneration develops along with inflammatory demyelination. The pathology affects the entire brain, but with Elite Mens Jonathan Cooper jersey different distributions of inflammation, demyelination, and neurodegeneration in the white and gray matter.7 The Authenitc Youth Bobby Massie jersey neuroaxonal loss is likely to be secondary to inflammation and demyelination, but it begins in the earliest stages of the disease and progresses even after the decline of inflammation. Most importantly, neuroaxonal loss represents the major pathological correlate of clinical disability.5 Elite Womens John Abraham jersey Further evidence to support the importance of neurodegeneration in MS is obtained from clinical data showing only a partial success of the available disease modifying drugs (interferons, glatiramer acetate, monoclonal antibodies to antigenic determinants Elite Authenitc Mens Bobby Massie jersey Womens John Abraham jersey expressed on T lymphocytes), which impede activation and migration of inflammatory cells Authenitc Womens John Abraham jersey via the BBB, but have no direct effect on the degenerative processes in CNS.8The exploration of neurodegeneration in MS received high priority in the last few years. The data establish that this is a multifactorial process involving loss of myelin protection, immune mediated histotoxicity, decreased trophic support, mitochondrial damage, metabolic changes, and altered signaling.9, 10, 11, 12 We recently reviewed Womens Frostee Rucker jersey our and others’ published Elite Womens Deone Bucannon jersey works concerning the involvement of mitochondrial mechanisms in neurodegeneration associated with inflammation.13, 14, 15 As an extension of surveys on neuroaxonal loss related to inflammatory demyelination, the present paper focuses on the involvement of humoral immune factors (Table 1). The available information allows us to generate a preliminary concept of immune Frostee Rucker jersey mediated neuronal dysfunction and loss, and to highlight potential pathways amenable to therapeutic interventions (Figure 1; Tables 2, 3 and 4). This figure depicts the thus far identified CNS antigens targeted by humoral autoimmunity in inflammatory demyelination. Signs of autoimmunity are lacking in type III and IV lesions which appear as variants of a primary oligodendrocytopathy. However, humoral autoimmunity is not only involved in certain forms of demyelination, but also instrumental in the process of neurodegeneration but with thus far unknown relative destructivity in various disease subtypes.Immunologic and Molecular DataThe literature is markedly weighted towards characterization of the Elite Womens Bobby Massie jersey cellular arm of autoimmunity, but new data also support that B cells and humoral immunity play important roles in MS. The B cell lineage is represented by B lymphocytes (CD19 CD138 plasma blasts (CD19 CD138 and plasma cells (CD19 CD138 for brevity, altogether B cells) in CNS and cerebrospinal fluid (CSF). Most of these cells express memory (CD27 phenotypes in MS. Therapeutic observations support that B cells may both directly and indirectly contribute to the development of MS. Removal of immunoglobulins from the peripheral blood by plasmapheresis appears to be beneficial in the subgroup of patients with type II lesions59 and depletion of CD20 B cells by rituximab results in a Elite Mens Chandler Catanzarojersey significant reduction in the number of enhancing MRI lesions. The latter intervention, however, does not exert its beneficial effects by directly affecting the immunoglobulin pool, but by depleting memory Authenitc Mens Bobby Massie jersey B cells and altering antigen presentation, T cell activation, or T cell recruitment into the CNS.60Molecular data also support the involvement of B lymphocytes and their products in MS. Intrathecal production of immunoglobulins with an oligoclonal electrophoretic distribution pattern is a hallmark of the disease. These B cell clones exhibit complex molecular characteristics and intraclonal diversity.Activation of B CellsWhat drives B cell activation and clonal expansion is not Elite red Bobby Massie jersey fully understood. Epstein virus (EBV), a B lymphotropic microorganism, has been implicated in the development of the disease by epidemiological, immune serological, and histological studies.64, 65 MS patients have intracerebral accumulation of EBV infected B cells and plasma blasts, mostly in ectopic B cell follicles,39 and a cross reactivity of the anti EBV specific cells with CNS antigens has been noted.64, 65 Other mechanisms leading to autoimmune B cell activation may be initiated by CD4 T helper type 2 (TH2) lymphocytes and their soluble inflammatory products (eg interleukine 4, 5, and 13),66 followed by an antigen specific expansion of clones either in the peripheral circulation or in the damaged CNS tissue, where intracellular proteins are released. Bystander activation describes a non antigen specific activation of T or B cells usually mediated by Authenitc Mens Jonathan Cooper jersey soluble inflammatory products of nearby immune cells.Anti Myelin AntibodiesImmunoglobulins produced by activated B cells in the CNS and CSF target numerous self antigens including components of the CNS myelin such as myelin basic protein, proteolipid protein, myelin associated glycoprotein, and myelin oligodendrocyte glycoprotein.67, 68 A great number of papers discusses the involvement of myelin specific antibodies in the development of demyelination and disease progression.69, 70 Pros and cons for the primary pathogenic significance or the reactive nature of anti myelin specific B cells have been debated.71, 72 The use of some of these antibodies as biomarkers to support the diagnosis or to monitor disease activity and course also has been proposed, but not uniformly accepted.73, 74Anti Neuronal AntibodiesAutoantibodies that target neuronal molecules and potentially exert histotoxicity have been less scrutinized. Nevertheless, growing data reveal that these antigen interactions play important roles in a number of neuroinflammatory and neurodegenerative conditions. In contrast to the usual scenario of a T lymphocyte driven autoimmunity and tissue damage, the humoral immune system appears to be more successful in breaking anti neuronal tolerance than the cellular system, and has greater pathogenic significance.43 This survey presents information that supports the involvement of the humoral immune response in MS related neurodegeneration.Top of pageANTI NEURONAL ANTIBODIES IN MSAntibodies Targeting Neuronal Cell Surface MoleculesNeuronal cell surface antigens Molecules in the surface membrane of myelinated axons are normally hidden from the immune system, and only become exposed after demyelination when they become antigenic and induce the production of neuron specific antibodies. IgG and IgM antibodies binding to the surface of a neuronal cell line were found in 70 of sera from patients with secondary progressive (SP) MS and in 25 of sera from patients with relapsing remitting (RR) MS.42 This finding may indicate the spreading of autoimmunity to neuronal antigens as a consequence of CNS tissue damage, and the expansion of pathology from moderate to marked neuroaxonal loss associated with a transition from RR to SP MS course.Axolemma enriched fractions Antibodies to axolemma enriched fractions (AEF) of the CNS are also present in CSF and sera of MS patients.16 These antibodies damage neurites and prevent neuronal outgrowth in vitro. The production of anti axolemma and anti myelin IgGs appears to be independent. Based on these observations, the use of anti axolemma IgGs as markers of axonal damage was proposed.55Neurofascin One of the targets in antibody mediated axonal injury is a cell adhesion molecule neurofascin. The 186 neuron specific isoform of neurofascin (NF186) is required for the clustering of voltage gated Na channels at the nodes of Ranvier. The 155 glial specific isoform (NF155) is required for the proper assembly of paranodal junction, an important site of interactions between the myelin and axon. Early changes in the distribution of NF155 were observed in MS lesions preceding demyelination.44 Maier et al45 showed that the NF155 levels were reduced and a 40 NF155 fragment increased in plaques, suggesting that NF155 is subject to protein degradation in the lesions.Levels of antibodies to NF155 and NF186 were significantly higher in sera of patients with chronic progressive forms of MS compared to that of patients with other inflammatory neurological diseases.17 In vitro studies showed that antibodies to neurofascin inhibit axonal conduction. In vivo experiments revealed that antibodies to neurofascin and complement can selectively target nodes of Ranvier, cause axonal injury, and trigger disease exacerbation in EAE. Mathey et al17 also showed that NF155 specific antibodies cross react with NF186 transfected cells. The recognition of NF186 at Elite Frostee Rucker jersey the nodes of Ranvier by these antibodies may initiate axonal injury and accelerate disease progression. Neurofascin specific antibodies can also inhibit remyelination by binding to NF155 expressed on the surface Authenitc Bobby Massie jersey of oligodendrocytes.Gangliosides Another group of neuronal antigens includes the gangliosides, which are glycolipids with sialic residues in the outer layer of cell membranes. Gangliosides are particularly enriched in the membranes of neuron. To generate Kareem Martin jersey antibody responses, gangliosides do not require Elite Youth John Abraham jersey major histocompatibility complex (MHC) molecules and T cell help.75 Although it is unclear whether anti ganglioside antibodies can cause or result from axonal damage,18 they may certainly serve as a marker of this process. Experimental data reveal that anti ganglioside antibodies can disrupt the BBB,19 create neuromuscular block by binding to neuronal gangliosides in the neuromuscular junction,56 and inhibit axonal regeneration after peripheral nerve injury in mice.20 Complexes of anti ganglioside antibodies and complement destroy Schwann cells and myelin membranes in demyelinating neuropathies, and contribute to axonal degeneration in acute motor axonal neuropathy.41 Increased levels of anti GM3 (monosialo ganglioside) antibodies can be found in sera of a great proportion of patients with progressive forms of MS (56.3 in primary progressive (PP) MS and 42.9 in SP MS vs 2.9 in RR MS and 14.6 in OND).18 Anti GD2 (disialo ganglioside) like IgM autoantibodies were detected in sera of 30 of MS patients, and a positive correlation of anti GD2 like IgM reactivity with neurological disability was observed.21 The increased prevalence of GD2 specific IgM antibodies in SP MS (47.8 compared to RR MS (24.2 and PP MS (26.7 also suggests the involvement of these antibodies in inflammation induced neurodegeneration.In summary, these data suggest that antibodies specific to neuronal cell surface molecules are produced during demyelination and may themselves contribute to axonal injury in MS. These antibodies can activate complement and exert cytotoxicity, provide binding sites for the Fc receptors on macrophages and microglial cells, interrupt axon interaction, inhibit axonal conduction and outgrowth, disrupt the BBB, and alter oligodendrocyte functioning. Correlation of the antibody titers with the severity of disability offers an opportunity of using these neuronal cell surface antibodies as biomarkers.Antibodies to Cytoskeletal ProteinsNeurofilaments Neurofilaments are a group of cytoskeletal proteins expressed in neuronal cells and axons. A variety of neurodegenerative disorders like Alzheimer’s disease, Parkinson’s disease, and dementia with Lewy bodies are characterized by accumulation of NF proteins signifying abnormalities in the axonal transport and an impending neuronal loss.76, 77Antibodies to axonal cytoskeletal proteins may be markers of axonal damage, as well as important contributors to neurodegeneration and clinical disability in MS. CSF levels of antibodies against the light subunit of neurofilaments (NFL) correlate with the disease duration, clinical disability, IgG index, and the degree of cerebral atrophy measured by MRI.22, 23 Although elevated levels of NFL specific antibodies are present in sera of patients with PP MS,24 these antibodies are also increased in sera of patients with OND.22
A single trained observer using the GDx nerve fibre layer analyser (LDT) performed pre and post operative measurements of nerve fibre layer thickness (NFLT). NFLT parameters, best corrected LogMAR visual acuity, and automated visual fields were assessed before and after Kids Jonathan Cooper jersey phacoemulsification cataract extraction with implantation of an acrylic intraocular lens.

Results A total of 49 subjects were assessed: 22 (45%) had POAG and 29 (55%) PACG; all were Asian (36 (73%) were Chinese), with mean age 67.1 (7.6 SD) and mean ‘LOCS III’ lens opacity grading 11.4 (3.1 SD). Visual acuity significantly improved (mean LogMAR 0.5 vs0.15, Pvs6.4, P=0.2) and mean deviation ( 17.7 dB vs 17.0 P=0.91) were little changed after cataract removal. Pseudo phakic measurements of NFLT were significantly different from pre op values. Measures of absolute thickness (including the average thickness, ellipse, ellipse average, superior and inferior averages, superior integral) were significantly greater than preoperative values (all PP>0.1) and ‘the number’ was smaller (P=0.04). Differences in measured NFLT were most strongly correlated with posterior subcapsular cataract (average thickness, P=0.01).

Top of pageIntroductionGlaucomatous optic neuropathy is characterised by the progressive loss of ganglion cells and accompanying optic disc and retinal nerve fibre layer (NFL) changes. Alterations in visual field sensitivity Elite Kids Bobby Authenitc Mens Chandler Catanzarojersey Massie jersey are the corresponding functional measure of ganglion cell function but there Elite red Jonathan Cooper jersey may be a substantial loss of axons before visual field changes develop.1

The detection of changes over time Youth Authenitc Womens John Abraham jersey Deone Bucannon jersey in visual function or in anatomy is the mainstay of the follow up and treatment of glaucoma. However, the inherent test variability of a psychophysical measure such as visual field testing makes the reliable detection of change in even established scotomata2,3 difficult and is highly patient dependent.4 Examination of the optic disc and NFL by careful stereoscopic biomicroscopy permits the detection of morphological changes in anatomy before perimetry shows changes in visual function.5,6 Quantification of objective measurements of these structural alterations Kids Chandler Catanzaro jersey may allow even greater sensitivity in the detection of progressive glaucomatous loss.7,8 Scanning laser polarimetry (SLP) gives a reproducible,9,10,11 objective in vivo measurement of the thickness of the NFL, based on the alteration it causes in the polarisation of light passed through it (retardation).12 It is thought that neuronal microtubules act as naturally polarising, birefringent structures, and the degree of retardation is proportional to the NFL thickness (NFLT).

Longitudinal assessments of the stability of NFLT must account for both age related ganglion cell loss12,13,14,15 and the alteration of polarising structures in the path of the SLP.16,17,18 The crystalline Elite red Deone Bucannon jersey lens is a weakly polarising structure and Elite Womens John Abraham jersey many patients with glaucoma will develop cataract following glaucoma surgery or with increasing age. Previous studies have looked at the effects of cataract extraction on the measurement of the NFL with conflicting results.19,20,21,22,23 Both Kremmer et al22 and Chiba et al19,20 found that dense cataract led to an underestimation of NFLT, whereas Park et al23 found unpredictable changes with intraocular lens (IOL) implantation and Collur et al24 suggested that there was no change after cataract extraction.

The aim of this study was to evaluate the effects of cataract extraction on the measurement of NFLT in a population of moderate to severe glaucomatous Authenitc red Chandler Catanzarojersey subjects using SLP (GDx, Laser Diagnostic Technologies, San Diego, CA, USA).

Top of pageMethodsSubjects enrolled in a prospective, randomised, placebo controlled trial of the use of intraoperative 5 fluorouracil in glaucoma filtering surgery in South East Asia were included. This study was granted ethical approval by The Ethical Review Committee of Singapore National Eye Centre, Elite Mens Frostee Rucker jersey acting for The Ministry of Health of The Republic of Singapore. Written informed consent was obtained from all participants in their own language with an interpreter where necessary.

The inclusion criteria were as follows: intraocular pressure (IOP) greater than 21 mmHg on at least one occasion, reduction of the neuroretinal rim width to less than or equal to 0.1 of the cup : disc ratio or a glaucomatous optic disc in the opinion of a fellowship trained glaucoma specialist on clinical disc assessment, and a visual field defect consisting of at least two points reduced by >5 dB or one point reduced by >10 dB below Authenitc Kids Bobby Massie jersey age specific threshold.

Exclusion criteria were: age less than 30 years, previous intraocular or conjunctival surgery, any nonlenticular axial media opacity, corneal oedema, and other ocular or systemic pathology, which might result in a visual field defect (including diabetic retinopathy or age related macular degeneration).

Data were collected regarding one eye only of each subject. During preoperative work up, a full ophthalmic examination was carried out. The degree of lens opacity (nuclear opacity and colour, cortical and posterior subcapsular opacities) was graded by clinical observation at a slit lamp using standard photographs Elite red John Abraham jersey of the LOCS III Authenitc Womens Bobby Massie jersey scheme.25

NFL measurements were performed by scanning laser polarimeter (“GDx”; Laser Diagnostic Technologies, San Diego, CA, USA; GDx software version 2.0.09) by a single experienced individual under ambient room lighting. All GDx measurements were taken within 8 weeks of surgery on each occasion; specifically, postoperative measurements were made at least 4 weeks after cataract surgery any postoperative corneal oedema, Elite Mens Chandler Catanzarojersey if any, had settled. The principles are well described elsewhere.26 Standard 15 15 measurements, which passed the internal software quality control, were made at each visit through an undilated pupil and a mean image used for analysis. The measurement ellipse was positioned at the same position at the second examination by reference to the retinal landmarks in the initial image. Image analysis was carried out using the GDx software. We compared the pre and post operative output values derived from the GDx software, as our aim was to establish the impact of cataract extraction on the use of GDx in a clinical setting.

Phacoemulsification cataract extraction was performed by one of two Elite Kids Bobby Massie jersey senior consultant surgeons via a temporal or superior clear corneal incision, as dictated by the orientation of existing astigmatism and/or the position and extent of trabeculectomy bleb. All eyes underwent in the bag implantation of a single type of foldable acrylic lens (“AcrySof”, MA60 BD, Alcon).

Visual field examination was carried out using a static automated perimeter (Model 750, Zeiss Humphrey, San Leandro, CA, Womens Deone Bucannon jersey USA). A minimum of two visual field tests were carried out on different days using the 24 2 program, requiring that the test was completed with

Differences in mean values of parametric data between individuals before and after intervention were examined using a paired sample t test. For nonparametric data, a Mann U test was used to compare means and the Wilcoxon sign rank test for the distribution of two Authenitc Mens Bobby Massie jersey related variables. 2 was used for the analysis of categorical variables. A value of P

Top of pageResultsA total of 64 cases were eligible, of which 15 cases had cataract that prevented GDx imaging. A total of 49 subjects were therefore analysed, 22 with POAG and 29 with PACG; 23 were left eyes and 26 right. Table 1 summarises the demographic and ophthalmological characteristics of the Elite Mens Chandler Catanzarojersey subjects for whom data are presented. After standard phacoemulsification and insertion of an acrylic IOL, visual acuity improved (mean LogMAR 0.5 vs 0.15, Pvs 6.38, P=0.2) and MD ( 17.7 vs 17.0 dB, P=0.9) were unchanged (Table 2). IOP was not significantly different postoperationally, (13.2 (SD 3.2) vs 14.1 mmHg (SD 3.4), P=0.4). Many, but not all, parameters of pseudophakic NFLT measurements were significantly different from phakic measurements (Table 3). Differences between SLP measures of NFLT before and after cataract extraction were correlated with the grade of posterior subcapsular cataract (Spearman correlation, rS), but not with nuclear colour, nuclear opalescence or cortical cataract (eg for PSCLO LOCS score and average thickness, rS=0.35, P=0.006; superior average, rS=0.34, P=0.008; inferior average, rS=0.32, P=0.01; ellipse average, rS=0.38, P=0.004). This was true for ‘absolute values’ of NFLT but not ratio measures (eg for PSCLO LOCS score and superior ratio, rS=0.14, Womens Frostee Rucker jersey P=0.16; inferior ratio, rS=0.14, P=0.16). There was a wide range of changes in the different parameters, and the change in one parameter did not necessarily predict the behaviour of another. A comparison of the PACG and POAG eyes (excluding two non POAG/PACG cases) showed no significant difference in the change in postoperative measurement between the two diagnoses.

Top of pageDiscussionMeasures of absolute thickness (including the superior and inferior deviation, average thickness, ellipse average, superior and inferior averages) were significantly greater after cataract extraction and implantation of an IOL (P26 for use in glaucoma detection, was lower after cataract extraction.A single trained observer using the GDx nerve fibre layer analyser (LDT) performed pre and post operative measurements of nerve fibre layer thickness (NFLT). NFLT parameters, best corrected LogMAR visual acuity, and automated visual fields were assessed before and after phacoemulsification cataract extraction with implantation of an acrylic intraocular lens.

Results A total of 49 subjects were assessed: 22 (45%) had POAG and 29 (55%) PACG; all were Asian (36 (73%) were Chinese), with mean age 67.1 (7.6 SD) and mean ‘LOCS III’ lens opacity grading 11.4 (3.1 SD). Visual acuity significantly improved (mean LogMAR 0.5 vs0.15, Pvs6.4, P=0.2) and mean deviation ( 17.7 dB vs 17.0 P=0.91) were little changed after cataract removal. Pseudo phakic measurements of NFLT were significantly different from pre op values. Measures of absolute thickness (including the average thickness, ellipse, ellipse average, superior and inferior averages, superior integral) were significantly greater than preoperative values (all PP>0.1) and ‘the number’ was smaller (P=0.04). Differences in measured NFLT were most strongly correlated with posterior subcapsular cataract (average thickness, P=0.01).

Top of pageIntroductionGlaucomatous optic neuropathy is characterised by the progressive loss of ganglion cells and accompanying optic disc and retinal nerve fibre layer (NFL) changes. Alterations in visual field sensitivity are the corresponding functional measure of ganglion cell function Elite red Frostee Rucker jersey but there may be a substantial loss of axons before visual field changes develop.1

The detection of changes over time in visual function or in anatomy is the mainstay Mens John Abraham jersey of the follow up and treatment of glaucoma. However, the inherent test variability of a psychophysical measure such as visual field testing makes the reliable detection of change in even established scotomata2,3 difficult and is highly patient dependent.4 Examination of the optic disc and NFL by careful stereoscopic biomicroscopy permits the detection of morphological changes in anatomy before perimetry shows changes in visual Authenitc Authenitc Deone Bucannon jersey Jonathan Cooper jersey function.5,6 Quantification of objective measurements of these structural alterations may allow even greater sensitivity in the detection of progressive glaucomatous loss.7,8 Scanning laser polarimetry (SLP) gives a reproducible,9,10,11 objective in vivo measurement of the thickness of the NFL, based on the alteration it causes in the polarisation of light passed through it (retardation).12 It is thought that neuronal microtubules act as naturally polarising, birefringent structures, and the degree of retardation is proportional to Elite Mens Deone Bucannon jersey Authenitc Kids Jonathan Cooper jersey the NFL thickness (NFLT).

Longitudinal assessments of the stability of NFLT must account for both age related ganglion cell loss12,13,14,15 and the alteration of polarising structures in the path of the SLP.16,17,18 The crystalline lens is a weakly polarising structure and many patients with glaucoma will develop cataract following glaucoma surgery or with increasing age. Previous studies have looked at the effects of cataract extraction on the measurement of the NFL with conflicting results.19,20,21,22,23 Both Kremmer et al22 and Chiba et al19,20 found that dense cataract led to an underestimation of NFLT, whereas Park et al23 found unpredictable changes with intraocular lens (IOL) implantation and Collur et al24 suggested that there was no change after cataract extraction.

The aim of this Mens Frostee Rucker jersey study was to evaluate the Elite Kids Frostee Rucker jersey effects of cataract extraction on the measurement of NFLT in a population of moderate to severe glaucomatous subjects using SLP (GDx, Laser Diagnostic Technologies, San Diego, CA, USA).

Top of pageMethodsSubjects enrolled in a prospective, randomised, placebo controlled trial of the use of intraoperative 5 fluorouracil in glaucoma filtering surgery in South East Mens Bobby Massie jersey Asia were included. This study was granted ethical approval by Jonathan Cooper jersey The Ethical Review Committee of Singapore National Eye Centre, acting for The Ministry of Health of The Republic of Singapore. Written informed consent was obtained from all participants in their own language with an interpreter where necessary.

The inclusion criteria were as follows: Authenitc John Abraham jersey intraocular pressure (IOP) greater than 21 mmHg on at least one occasion, reduction of the neuroretinal rim width to less than or equal to 0.1 of the cup : disc ratio or a glaucomatous optic disc in the opinion of a fellowship trained glaucoma specialist on clinical disc assessment, and a visual field defect consisting of at least two points reduced by >5 dB Elite Mens John Abraham jersey or one point reduced by >10 dB below age specific threshold.

Exclusion criteria were: age less than 30 years, previous intraocular or conjunctival surgery, any nonlenticular axial media opacity, corneal oedema, and other ocular or systemic pathology, which might result in a visual field defect (including diabetic retinopathy or age related macular degeneration).

Data were collected regarding one eye only of each subject. During preoperative work up, a full ophthalmic examination was carried out. The degree of lens opacity (nuclear opacity and colour, cortical and posterior subcapsular opacities) was graded by clinical observation at a slit Elite Youth Frostee Rucker jersey lamp using standard photographs of the LOCS III scheme.25

NFL measurements were performed by scanning laser polarimeter (“GDx”; Laser Diagnostic Technologies, San Diego, CA, USA; GDx software version 2.0.09) by a single experienced individual under ambient room lighting. All GDx measurements were taken within 8 weeks of surgery Authenitc Kids Frostee Rucker jersey on each occasion; specifically, Elite red Bobby Massie jersey postoperative measurements were made at least 4 weeks after cataract surgery any postoperative corneal oedema, if any, had settled. The principles are well described elsewhere.26 Standard 15 15 measurements, which passed the internal software quality control, were made at each visit through an undilated pupil and a mean image used for analysis. The measurement ellipse was positioned at the same position at the second examination by reference to the Authenitc Youth Bobby Massie jersey retinal landmarks in the initial image. Image analysis Authenitc Youth Deone Bucannon jersey was carried out using the GDx software. We compared the pre and post operative output values derived from the GDx software, as our aim was to establish the impact of cataract extraction on the use of GDx in a clinical setting.

Phacoemulsification cataract extraction was performed by one of two senior consultant surgeons via a temporal or superior clear corneal incision, as dictated by the orientation of existing astigmatism and/or the position and extent of trabeculectomy bleb. All eyes underwent in the bag implantation of a single type of foldable acrylic lens (“AcrySof”, MA60 BD, Alcon).

Visual field examination was carried out using a static automated Elite Youth Bobby Massie jersey perimeter (Model 750, Zeiss Humphrey, San Leandro, CA, USA). A minimum of two visual field tests were carried out on different days using the 24 2 program, requiring that the test was completed with

Differences in mean values of parametric data between individuals before and after intervention were examined using a paired sample t test. For nonparametric data, a Mann U test was used to compare means and the Wilcoxon sign rank test for the distribution of two related variables. 2 was used for the analysis of categorical variables. A value of P

Top of pageResultsA total of 64 cases were eligible, of which 15 cases had cataract that prevented GDx imaging. A total of 49 subjects were therefore analysed, 22 with POAG and 29 with PACG; 23 were left eyes and 26 right. Table 1 summarises the demographic and ophthalmological characteristics of the subjects for whom data are presented. After standard phacoemulsification and insertion of an acrylic IOL, visual acuity improved (mean LogMAR 0.5 vs 0.15, Pvs 6.38, P=0.2) and MD ( 17.7 vs 17.0 dB, P=0.9) were unchanged (Table 2). IOP was not significantly different postoperationally, (13.2 (SD 3.2) vs 14.1 mmHg (SD 3.4), P=0.4). Many, but not all, parameters of pseudophakic NFLT measurements were significantly different from phakic measurements (Table 3). Differences between SLP measures of NFLT before and after cataract extraction were correlated with the grade of posterior subcapsular cataract (Spearman correlation, rS), but not with nuclear colour, nuclear opalescence or cortical cataract (eg for PSCLO LOCS score and average thickness, rS=0.35, P=0.006; Authenitc Youth Frostee Rucker jersey superior average, rS=0.34, P=0.008; inferior average, rS=0.32, P=0.01; ellipse average, rS=0.38, P=0.004). This was true for ‘absolute Authenitc Mens Deone Bucannon jersey values’ of NFLT but not ratio measures (eg for PSCLO LOCS score and superior ratio, rS=0.14, P=0.16; inferior ratio, rS=0.14, P=0.16). There was a wide range of changes in the different parameters, and the change in one parameter did not necessarily predict the behaviour of another. A comparison of the PACG and POAG eyes (excluding two non POAG/PACG cases) showed no significant difference in the change in postoperative measurement between the two diagnoses.

Top of pageDiscussionMeasures of absolute thickness (including the superior and inferior deviation, average thickness, ellipse average, superior and inferior averages) were significantly greater after cataract extraction and implantation of an IOL (P26 for use in glaucoma detection, was lower after cataract extraction.

But cheerleading in the NFL actually sounds like a living hell. Women in America’s elite cheer squads have to work within a labyrinth of (ironically) inflexible , which cover Youth Mason Raymond Jersey everything from their weight to their social lives. One former cheerleader has sent Deadspin a copy of the and regulations she was expected to follow as a member of the in 2009. She says Authenitc Johnny Gaudreau Jersey the have hardly changed since then, so it’s a fairly accurate guide to how the squad works today. When Deadspin’s source was on Women Kris Russell Jersey the team,were paid $100 per game, and captains Elite White Kris Russell Jersey got another $25 to sweeten the deal. Cheerleaders also earned about $50 for appearances off the field. You can decide whether that sort of money, plus the occasional brush with fame, is Authenitc Mason Raymond Jersey worth more than the joy of a life without these suffocating . "There shall Elite White Devin Setoguchi Jersey be Authenitc Red Devin Setoguchi Jersey absolutely no contact with the players outside the scope of your job," thesay. "Cheerleaders are not permitted to socialise Kid Jarome Iginla Jersey with the players during off hours. Dating of Ravens players,
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