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Introduction: The Unified Dyskinesia Rating Scale (UDysRS) was developed to provide a comprehensive rating tool of dyskinesia in Parkinson's disease (PD). Because dyskinesia therapy trials involve multicenter studies, having a scale that is validated in multiple non-English languages is pivotal to international efforts to treat dyskinesia. The aim of the present study was to organize and perform an independent validation of the UDysRS Finnish version., Methods: The UDysRS was translated into Finnish and then back-translated into English using 2 independent teams. Cognitive pretesting was conducted on the Finnish version and required modifications to the structure or wording of the translation. The final Finnish version was administered to 250 PD patients whose native language is Finnish. The data were analyzed to assess the confirmatory factor structure to the Spanish UDysRS (the reference standard). Secondary analyses included an exploratory factor analysis (EFA), independent of the reference standard., Results: The comparative fit index (CFI), in comparison with the reference standard factor structure, was 0.963 for Finnish. In the EFA, where variability from sample to sample is expected, isolated item differences of factor structure were found between the Finnish and Reference Standard versions of the UDysRS. These subtle differences may relate to differences in sample composition or variations in disease status., Conclusion: The overall factor structure of the Finnish version was consistent with that of the reference standard, and it can be designated as the official version of the UDysRS for Finnish speaking populations., (© 2021 S. Karger AG, Basel.)

Vegetation, generally present along river margins and floodplains, governs key hydrodynamic processes in riverine systems. Despite the flow-influencing mechanisms exhibited by natural vegetation and driven by its complex morphology and flexibility, vegetation has been conventionally simulated by using rigid cylinders. This article presents a dataset obtained from hydraulic experiments performed for investigating the flow-vegetation interaction in partly vegetated channels. Vegetation was simulated by using both natural-like and rigid model plants. Specifically, two sets of experiments are described: in the first, vegetation was simulated with natural-like flexible foliated plants standing on a grassy bed; in the second, rigid cylinders were used. Experiments with rigid cylinders were designed to be compared against tests with natural-like plants, as to explore the effects of vegetation representation. The following experimental data were produced: 3D instantaneous velocity measured by acoustic Doppler velocimetry, vegetation motion video recordings, and auxiliary data including detailed vegetation characterization. These experiments are unique both for the use of natural-like flexible woody vegetation in hydraulic experiments and for the similarity achieved between the resulting observed vegetated shear layers. These data are expected to be useful in vegetated flows model development and validation, and represent a unique benchmark for the interpretation of the flow-vegetation interaction in partly vegetated channels., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships which have, or could be perceived to have, influenced the work reported in this article., (© 2020 The Authors.)

Background: Although there is a relationship between the extent of striatal dopaminergic defect and the severity of motor symptoms in Parkinson's disease (PD), studies investigating associations between dopamine and mortality in PD have been scarce. If a relationship were established, dopamine restoring neuroprotective treatments could be used to decrease mortality. The objective of this study was to determine whether the initial degree of hypodopaminergic defect, as measured by 6-[(18)F]fluoro-L-DOPA positron emission tomography (FDOPA-PET), can predict patient survival., Methods: The study population included a cohort of 88 recently diagnosed and untreated patients with PD who were clinically examined and scanned with FDOPA-PET between the years 1998 and 2000. The date of exit for the survival analysis was in April 2013 with a follow-up interval of 13-15 years. The survival model included FDOPA uptake, age, sex and symptom severity as explaining factors. Death certificates of the patients were obtained, and causes of death were analyzed., Results: Mortality rate was 56.8%. Although higher age (p < 0.001) and greater motor symptom severity (p < 0.05) were associated with increased mortality, there was no association between survival and FDOPA uptake in any striatal subregion (p > 0.48)., Conclusion: Unlike age and early motor symptom severity, dopamine synthesis capacity, as measured with PET, does not predict survival in PD., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Mobile mapping systems (MMSs) are used for mapping topographic and urban features which are difficult and time consuming to measure with other instruments. The benefits of MMSs include efficient data collection and versatile usability. This paper investigates the data processing steps and quality of a boat-based mobile mapping system (BoMMS) data for generating terrain and vegetation points in a river environment. Our aim in data processing was to filter noise points, detect shorelines as well as points below water surface and conduct ground point classification. Previous studies of BoMMS have investigated elevation accuracies and usability in detection of fluvial erosion and deposition areas. The new findings concerning BoMMS data are that the improved data processing approach allows for identification of multipath reflections and shoreline delineation. We demonstrate the possibility to measure bathymetry data in shallow (0-1 m) and clear water. Furthermore, we evaluate for the first time the accuracy of the BoMMS ground points classification compared to manually classified data. We also demonstrate the spatial variations of the ground point density and assess elevation and vertical accuracies of the BoMMS data.

In the postnatal rodent hippocampus status epilepticus (SE) leads to age- and region-specific excitotoxic neuronal damage, the precise mechanisms of which are still incompletely known. Recent studies suggest that the activation of inflammatory responses together with glial cell reactivity highly contribute to excitotoxic neuronal damage. However, pharmacological tools to attenuate their activation in the postnatal brain are still poorly elucidated. In this study, we investigated the role of inflammatory mediators in kainic acid (KA)-induced neuronal damage in organotypic hippocampal slice cultures (OHCs). A specific cyclooxygenase-2 (COX-2) inhibitor N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS-398) was used to study whether or not it could ameliorate neuronal death. Our results show that KA treatment (24 h) resulted in a dose-dependent degeneration of CA3a/b pyramidal neurons. Furthermore, COX-2 immunoreactivity was pronouncedly enhanced particularly in CA3c pyramidal neurons, microglial and astrocyte morphology changed from a resting to active appearance, the expression of the microglial specific protein, Iba1, increased, and prostaglandin E₂ (PGE₂) production increased. These indicated the activation of inflammatory processes. However, the expression of neither proinflammatory cytokines, i.e. tumour necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), nor the anti-inflammatory cytokine IL-10 mRNA was significantly altered by KA treatment as studied by real-time PCR. Despite activation of an array of inflammatory processes, neuronal damage could not be rescued either with the combined pre- and co-treatment with a specific COX-2 inhibitor, NS-398. Our results suggest that KA induces activation of a repertoire of inflammatory processes in immature OHCs, and that the timing of anti-inflammatory treatment to achieve neuroprotection is a challenge due to developmental properties and the complexity of inflammatory processes activated by noxious stimuli. This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Background: Status epilepticus (SE) is proposed to lead to an age-dependent acute activation of a repertoire of inflammatory processes, which may contribute to neuronal damage in the hippocampus. The extent and temporal profiles of activation of these processes are well known in the adult brain, but less so in the developing brain. We have now further elucidated to what extent inflammation is activated by SE by investigating the acute expression of several cytokines and subacute glial reactivity in the postnatal rat hippocampus., Methods: SE was induced by an intraperitoneal (i.p.) injection of kainic acid (KA) in 9- and 21-day-old (P9 and P21) rats. The mRNA expression of interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), matrix metalloproteinase-9 (MMP-9), glial-derived neurotrophic factor (GDNF), interferon gamma (IFN-γ), and transforming growth factor-beta 1 (TGF-β1) were measured from 4 h up to 3 days after KA injection with real-time quantitative PCR (qPCR). IL-1β protein expression was studied with ELISA, GFAP expression with western blotting, and microglial and astrocyte morphology with immunohistochemistry 3 days after SE., Results: SE increased mRNA expression of IL-1β, TNF-α and IL-10 mRNA in hippocampus of both P9 and P21 rats, their induction being more rapid and pronounced in P21 than in P9 rats. MMP-9 expression was augmented similarly in both age groups and GDNF expression augmented only in P21 rats, whereas neither IFN-γ nor TGF-β1 expression was induced in either age group. Microglia and astrocytes exhibited activated morphology in the hippocampus of P21 rats, but not in P9 rats 3 d after SE. Microglial activation was most pronounced in the CA1 region and also detected in the basomedial amygdala., Conclusion: Our results suggest that SE provokes an age-specific cytokine expression in the acute phase, and age-specific glial cell activation in the subacute phase as verified now in the postnatal rat hippocampus. In the juvenile hippocampus, transient increases in cytokine mRNA expression after SE, in contrast to prolonged glial reactivity and region-specific microglial activity after SE, suggest that the inflammatory response is changed from a fulminant and general initial phase to a more moderate and specific subacute response.

Purpose: Epileptic seizures lead to age-dependent neuronal damage in the developing brain, particularly in the hippocampus, but the mechanisms involved have remained poorly elucidated. In this study, we investigated the contribution of apoptosis and inflammatory processes to neuronal damage after status epilepticus (SE) in postnatal rats., Methods: SE was induced by an intraperitoneal injection of kainic acid (KA) in 21- and 9-day-old (P21 and P9) rats. The expression of Bax, Bcl-2 and caspase-3, markers for apoptosis, and cyclooxygenase-2 (COX-2), an indicator for activation of inflammatory processes, were studied from 6 h up to 1 week after SE by Western blotting and immunocytochemistry. Neuronal damage was verified by Fluoro-Jade B staining., Results: In P21 rats, SE resulted in neuronal damage in the CA1 neurons of the hippocampus. COX-2 expression was extensively, but transiently, increased and its immunoreactivity pronouncedly enhanced in several hippocampal subregions, amygdala, and piriform cortex by 24 h after SE. The expression of Bax and caspase-3 remained unchanged, whereas the antiapoptotic factor Bcl-2 transiently decreased by 24 h. Single caspase-3 positive neurons appeared in the CA1 region of both control and KA-treated rats. In P9 rats, no neuronal death was detected, and COX-2 expression and immunoreactivity remained at the control level., Discussion: Our results suggest that SE provokes age-specific effects on COX-2 expression. This together with the activation of putative inflammatory processes may contribute to neuronal cell death in the hippocampus of postnatal rats, whereas caspase-dependent apoptosis seems not to be involved in the death process.