85 results on '"McCombe, P.A"'
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2. Cloning of a new form of EAAT2/GLT-1 from human and rodent brains
3. The relationship between Bayesian motor unit number estimation and histological measurements of motor neurons in wild-type and SOD1G93A mice
4. Reduced levels of interleukin 33 and increased levels of soluble ST2 in subjects with amyotrophic lateral sclerosis
5. Levels of phosphorylated axonal neurofilament subunit H (pNfH) are increased in acute ischemic stroke
6. Monocyte CD14 and HLA-DR expression increases with disease duration and severity in amyotrophic lateral sclerosis
7. Monocyte CD14 and HLA-DR expression increases with disease duration and severity in amyotrophic lateral sclerosis.
8. Antibody responses to peptides of peripheral nerve myelin proteins P0 and P2 in patients with inflammatory demyelinating neuropathy
9. T cell reactivity to P0, P2, PMP-22, and myelin basic protein in patients with Guillain-Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy
10. Biological basis for motor unit number estimation through Bayesian statistical analysis of the stimulus–response curve
11. Bayesian analysis of the stimulus–response curve
12. Results of Bayesian statistical analysis in normal and ALS subjects
13. Effects of cyclosporin A treatment on clinical course and inflammatory cell apoptosis in experimental autoimmune encephalomyelitis induced in Lewis rats by inoculation with myelin basic protein
14. Predictions of resting energy expenditure in amyotrophic lateral sclerosis are greatly impacted by reductions in fat free mass
15. Altered expression of metabolic proteins and adipokines in patients with amyotrophic lateral sclerosis
16. Serial measurements of phosphorylated neurofilament-heavy in the serum of subjects with amyotrophic lateral sclerosis
17. Gender differences in autoimmune disease
18. Body mass index and dietary intervention: Implications for prognosis of amyotrophic lateral sclerosis
19. Chapter 3 - Biological basis for motor unit number estimation through Bayesian statistical analysis of the stimulus–response curve
20. Chapter 5 - Results of Bayesian statistical analysis in normal and ALS subjects
21. Chapter 4 - Bayesian analysis of the stimulus–response curve
22. P02-53 Growth Hormone: a potential biomarker for disease progression in Amyotrophic Lateral Sclerosis (ALS)
23. P7-22 Novel upper and lower motor neuron markers in amyotrophic lateral sclerosis
24. T cells from patients with Guillain-Barré syndrome produce interferon-gamma in response to stimulation with the ganglioside GM1
25. Increased levels of activated T-cells and reduced levels of CD4/CD25+ cells in peripheral blood of Guillain-Barré syndrome patients compared to controls
26. The Effects of Pregnancy on Myelin Basic Protein-induced Experimental Autoimmune Encephalomyelitis in Lewis Rats: Suppression of Clinical Disease, Modulation of Cytokine Expression in the Spinal Cord Inflammatory Infiltrate and Suppression of Lymphocyte P
27. Results of testing for anti-GM1 antibodies
28. Chronic inflammatory demyelinating polyradiculoneuropathy and severe peripheral oedema: a renal explanation
29. Cytokine expression by inflammatory cells obtained from the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis induced by inoculation with myelin basic protein and adjuvants
30. Corticosteroid treatment of experimental autoimmune encephalomyelitis in the Lewis rat results in loss of Vβ8.2+ and myelin basic protein-reactive cells from the spinal cord, with increased total T-cell apoptosis but reduced apoptosis of Vβ8.2+ cells
31. A study of human T-cell lines generated from multiple sclerosis patients and controls by stimulation with peptides of myelin basic protein
32. Apoptosis of Vβ8.2+ T lymphocytes in the spinal cord during recovery from experimental autoimmune encephalomyelitis induced in Lewis rats by inoculation with myelin basic protein
33. Demyelination and nerve conduction abnormalities are restricted to the CNS in PLP-EAE but not in MBP-EAE
34. Inflammatory cells, microglia and MHC class II antigen-positive cells in the spinal cord of Lewis rats with acute and chronic relapsing experimental autoimmune encephalomyelitis
35. Expression of CD45RC and Ia antigen in the spinal cord in acute experimental allergic encephalomyelitis: An immunocytochemical and flow cytometric study
36. Apoptosis in the nervous system in experimental allergic encephalomyelitis
37. Cronkhite-Canada syndrome associated with peripheral neuropathy
38. Cell death by apoptosis in experimental autoimmune encephalomyelitis (EAE) — its possible implications
39. Familial occurrence of multiple sclerosis with thyroid disease and systemic lupus erythematosus
40. The effects of prophylactic cyclosporin A on experimental allergic neuritis (EAN) in the Lewis rat. Induction of relapsing EAN using low dose cyclosporin A
41. Corticosteroid treatment of experimental autoimmune encephalomyelitis in the Lewis rat results in loss of Vβ8.2+and myelin basic protein-reactive cells from the spinal cord, with increased total T-cell apoptosis but reduced apoptosis of Vβ8.2+cells
42. Class II antigen expression and T lymphocyte subsets in chronic inflammatory demyelinating polyneuropathy
43. The peripheral neuropathy of vitamin B12 deficiency
44. Corticosteroid treatment of experimental autoimmune encephalomyelitis in the Lewis rat results in loss of Vβ8.2 + and myelin basic protein-reactive cells from the spinal cord, with increased total T-cell apoptosis but reduced apoptosis of Vβ8.2 + cells
45. The peripheral neuropathy of vitamin B 12 deficiency
46. Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology
47. Disability outcomes of early cerebellar and brainstem symptoms in multiple sclerosis
48. The relationship between Bayesian motor unit number estimation and histological measurements of motor neurons in wild-type and SOD1G93A mice
49. Comparison of fingolimod, dimethyl fumarate and teriflunomide for multiple sclerosis
50. The frequency of circulating T cells reactive to PLP184-209 increases prior to MS relapse and development of new MR1 lesions
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