| 1. |
- Alwall, J., et al.
(author)
-
A standard format for Les Houches Event Files
- 2007
-
In: Computer Physics Communications. - : Elsevier BV. - 0010-4655. ; 176:4, s. 300-304
-
Journal article (peer-reviewed)abstract
- A standard file format is proposed to store process and event information, primarily output from partoti-level event generators for further use by general-purpose ones. The information content is identical with what was already defined by the Les Houches Accord five years ago, but then in terms of Fortran commonblocks. This information is embedded in a minimal XML-style structure, for clarity and to simplify parsing.
|
|
| 2. |
- Gruden, Marina A., et al.
(author)
-
Immunoprotection against toxic biomarkers is retained during Parkinson's disease progression
- 2011
-
In: Journal of Neuroimmunology. - : Elsevier. - 0165-5728 .- 1872-8421. ; 233:1-2, s. 221-227
-
Journal article (peer-reviewed)abstract
- The aim was to ascertain any possible linkage between humoral immune responses to principal biomarkers (α-synuclein monomers, its toxic oligomers or fibrils, dopamine and S100B) and cellular immunity in Parkinson's disease development. There were elevated autoantibody titers to α-synuclein monomers, oligomers plus fibrils in 72%, 56%, and 17% of Parkinsonian patients respectively with a 5-year disease duration. Additionally, there were increased titers to dopamine and S100B (96% and 89%) in the 5-year patient group. All of these values subsided in 10-year sufferers. Furthermore, CD3+, CD4+, CD8+ T-lymphocyte and B-lymphocyte subsets declined in the patient cohort during Parkinsonism indicating disease associated reductions in these lymphocyte subsets.
|
|
| 3. |
|
|
| 4. |
- Gruden, Marina A., et al.
(author)
-
Correlation between Protective Immunity to alpha-Synuclein Aggregates, Oxidative Stress and Inflammation
- 2012
-
In: Neuroimmunomodulation. - : S. Karger AG. - 1021-7401 .- 1423-0216. ; 19:6, s. 334-342
-
Journal article (peer-reviewed)abstract
- Objective: Protein aggregation leading to central amyloid deposition is implicated in Parkinson's disease (PD). During disease progression, inflammation and oxidative stress may well invoke humoral immunity against pathological aggregates of PD-associated alpha-synuclein. The aim was to investigate any possible concurrence between autoimnnune responses to alpha-synuclein monomers, oligomers or fibrils with oxidative stress and inflammation.Methods: The formation of alpha-synuclein amyloid species was assessed by thioflavin-T assay and atomic force microscopy was employed to confirm their morphology. Serum autoantibody titers to alpha-synuclein conformations were determined by ELISA. Enzyme activity and concentrations of oxidative stress/inflammatory indicators were evaluated by enzyme and ELISA protocols.Results: In PD patient sera, a differential increase in autoantibody titers to alpha-synuclein monomers, toxic oligomers or fibrils was associated with boosted levels of the pro-inflammatory cytokine interleukin-6 and tumour necrosis factor-alpha, but a decrease in interferon-gamma concentration. In addition, levels of malondialdehyde were elevated whilst those of glutathione were reduced along with decrements in the activity of the antioxidants: superoxide dismutase, catalase and glutathione transferase.Conclusions: It is hypothesized that the generation of alpha-synuclein amyloid aggregates allied with oxidative stress and inflammatory reactions may invoke humoral immunity protecting against dopaminergic neuronal death. Hence, humoral immunity is a common integrative factor throughout PD progression which is directed towards prevention of further neurodegeneration, so potential treatment strategies should attempt to maintain PD patient immune status. Copyright (c) 2012 S. Karger AG, Basel
|
|
| 5. |
- Gruden, Marina A., et al.
(author)
-
Nasal inoculation with a-synuclein aggregates evokes rigidity, locomotor deficits and immunity to such misfolded species as well as dopamine
- 2013
-
In: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 243, s. 205-212
-
Journal article (peer-reviewed)abstract
- Animal models of Parkinson's disease (PD) have been widely used to investigate the pathogenesis of this neurodegenerative disorder which is typically associated with the specific and largely disordered protein alpha-synuclein (alpha-syn). In the current study, the nasal vector was used to deliver alpha-syn aggregates to the brain. Both alpha-syn oligomers and its fibrils were firstly characterized using atomic force microscopy and the thioflavin T binding assay. The toxic oligomers alone (0.48 mg/kg) or their 50:50 combination with fibrils (in a total dose of 0.48 mg/kg) were then given intranasally for ten days in mice and PD-mimetic symptoms as well as humoral immunity to these species and dopamine (DA) were evaluated simultaneously. Open-field behavioral deficits indicated by rigidity and reduced locomotor activity were induced by the dual administration of alpha-syn oligomers plus fibrils but not the oligomers by themselves under the 10-day dosing regimen. In contrast, using ELISA, high levels of serum autoantibodies to alpha-syn monomeric, oligomeric and fibrillar conformers as well as DA were observed in both treatment groups reflecting immune system activation and this substantiates previous clinical studies in Parkinson's disease patients. Thus, nasal administration of alpha-syn amyloidogenic species may be a potential experimental PD model which results not only in motor deficits but also incitement of humoral protection to mimic the disease. Such a paradigm may be exploitable in the quest for potential therapeutic strategies and further studies are warranted.
|
|
