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Investigating atom–surface interactions is the key to an in-depth understanding of chemical processes at interfaces, which are of central importance in many fields – from heterogeneous catalysis to corrosion. In this work, we present a joint experimental and theoretical effort to gain insights into the atomistic details of hydrogen atom scattering at the α-Al2O3(0001) surface. Surprisingly, this system has been hardly studied to date, although hydrogen atoms as well as α-Al2O3 are omnipresent in catalysis as reactive species and support oxide, respectively. We address this system by performing hydrogen atom beam scattering experiments and molecular dynamics (MD) simulations based on a high-dimensional machine learning potential trained to density functional theory data. Using this combination of methods we are able to probe the properties of the multidimensional potential energy surface governing the scattering process. Specifically, we compare the angular distribution and the kinetic energy loss of the scattered atoms obtained in experiment with a large number of MD trajectories, which, moreover, allow to identify the underlying impact sites at the surface. [ABSTRACT FROM AUTHOR]

Abstract Background The diagnostic and pathophysiological relevance of antibodies to aquaporin-4 (AQP4-Ab) in patients with neuromyelitis optica spectrum disorders (NMOSD) has been intensively studied. However, little is known so far about the clinical impact of AQP4-Ab seropositivity. Objective To analyse systematically the clinical and paraclinical features associated with NMO spectrum disorders in Caucasians in a stratified fashion according to the patients' AQP4-Ab serostatus. Methods Retrospective study of 175 Caucasian patients (AQP4-Ab positive in 78.3%). Results Seropositive patients were found to be predominantly female (p < 0.0003), to more often have signs of co-existing autoimmunity (p < 0.00001), and to experience more severe clinical attacks. A visual acuity of ≤ 0.1 during acute optic neuritis (ON) attacks was more frequent among seropositives (p < 0.002). Similarly, motor symptoms were more common in seropositive patients, the median Medical Research Council scale (MRC) grade worse, and MRC grades ≤ 2 more frequent, in particular if patients met the 2006 revised criteria (p < 0.005, p < 0.006 and p < 0.01, respectively), the total spinal cord lesion load was higher (p < 0.006), and lesions ≥ 6 vertebral segments as well as entire spinal cord involvement more frequent (p < 0.003 and p < 0.043). By contrast, bilateral ON at onset was more common in seronegatives (p < 0.007), as was simultaneous ON and myelitis (p < 0.001); accordingly, the time to diagnosis of NMO was shorter in the seronegative group (p < 0.029). The course of disease was more often monophasic in seronegatives (p < 0.008). Seropositives and seronegatives did not differ significantly with regard to age at onset, time to relapse, annualized relapse rates, outcome from relapse (complete, partial, no recovery), annualized EDSS increase, mortality rate, supratentorial brain lesions, brainstem lesions, history of carcinoma, frequency of preceding infections, oligoclonal bands, or CSF pleocytosis. Both the time to relapse and the time to diagnosis was longer if the disease started with ON (p < 0.002 and p < 0.013). Motor symptoms or tetraparesis at first myelitis and > 1 myelitis attacks in the first year were identified as possible predictors of a worse outcome. Conclusion This study provides an overview of the clinical and paraclinical features of NMOSD in Caucasians and demonstrates a number of distinct disease characteristics in seropositive and seronegative patients.

Abstract Background Microvascular alterations contribute to the development of stroke and vascular dementia. The goal of this study was to evaluate age and hypertension related changes of the basal lamina in cerebral microvessels of individuals, who died from non-cerebral causes. Results We examined 27 human brains: 11 young and 16 old patients. Old patients were divided into two subgroups, those with hypertension (n = 8) and those without hypertension (n = 8). Basal lamina changes of the cerebral microvessels were determined in the putamen using antibodies against collagen type IV and by quantitative analysis of vessel number, total stained area of collagen, thickness of the vessel wall and lumen, and relative staining intensity using immunofluorescence. The total number of collagen positive vessels per microscopic field was reduced in old compared to young subjects (12.0+/-0.6 vs. 15.1+/-1.2, p = 0.02). The relative collagen content per vessel (1.01+/-0.06 vs. 0.76+/-0.05, p = 0.01) and the relative collagen intensity (233.1+/-4.5 vs. 167.8+/-10.6, p < 0.0001) shown by immunofluorescence were higher in the older compared to the younger patients with a consecutive reduction of the lumen / wall ratio (1.29+/-0.05 vs. 3.29+/-0.15, p < 0.0001). No differences were observed for these parameters between old hypertensive and non-hypertensive patients. Conclusions The present data show age-related changes of the cerebral microvessels in sections of human putamen for the first time. Due to the accumulation of collagen, microvessels thicken and show a reduction in their lumen. Besides this, the number of vessels decreases. These findings might represent a precondition for the development of vascular cognitive impairment. However, hypertension was not proven to modulate these changes.

Objectives: Focal cerebral ischemia is responsible for alterations of vascular permeability, and the loss of microvascular integrity is a primary source of subsequent hemorrhages. We evaluated the influence of different durations of ischemia and reperfusion on infarction size and microvascular damage after focal cerebral ischemia in the mouse. Methods: C57BL/6 mice (n = 39) were subjected to focal cerebral ischemia (I) and reperfusion (R). Consecutive brain sections were analysed for infarction volumes (Nissl-staining) and for collagen type IV (immunohistochemistry and western blot). Results: Infarction size (percentage of the infarction volume versus ipsilateral hemisphere) increased with total time of ischemia and reperfusion: 19 ± 2% (I3R0), 30 ± 2% (I3R3), 36 ± 4% (I3R12), 41 ± 4% (I1R24), 45 ± 6% (I2R24) and 58 ± 2% (I3R24). The ischemic hemispheres showed a significant progressive reduction of collagen type IV positive vessels (ischemic versus non-ischemic contralateral area): 90 ± 3% (I3R0), 88 ± 1% (I3R3), 82 ± 3% (I3R12), 85 ± 3% (I1R24), 79 ± 3% (I2R24), 72 ± 2% (I3R24). Conclusions: Both prolonged ischemia and reperfusion lead to an increased infarction volume, as well as progressive microvascular damage. [ABSTRACT FROM AUTHOR]

Abstract: The spontaneously hypertensive stroke-prone rat (SHR-SP) is an experimental model of malignant hypertension which lead to secondary alterations of the extracellular matrix. Our aim was to determine ACE-inhibitor related changes of proteases involved in the reconstruction of the extracellular matrix in the brain. Twelve SHR-SP rats were randomized into two groups. Each group was treated with either an antihypertensive dose of ramipril or placebo for 6 months. Brain tissue plasminogen activator (t-PA) and urokinase (u-PA) were quantified by using casein-dependent plasminogen zymography, matrix metalloproteinase (MMP)-2 and MMP-9, by MMP-zymography, and tissue inhibitor of MMP (TIMP)-1 and -2, by reverse zymography. The amounts of u-PA, t-PA, and MMPs were significantly reduced in animals treated with ACE inhibitor. Plasminogen zymography showed a 39% reduction of u-PA in the basal ganglia (p &#60;0.0001); t-PA expression was reduced by 26% in the cortex and by 33% in the basal ganglia (p &#60;0.0001). MMP-2 expression was reduced by 15% in the cortex (p &#60;0.05) and by 10% in the basal ganglia (p &#60;0.05); MMP-9 expression significantly decreased by 37% in the cortex and by 25% in the basal ganglia (p &#60;0.0001 each). No differences were observed in the amount of TIMP-1 or TIMP-2. These findings provide new insights into the biochemical mechanisms underlying extracellular matrix proliferation and its modulation by ACE inhibitors. Therapeutic alterations that influence the proteolytic systems might prove important in the prevention of extracellular matrix accumulation and secondary microvascular vessel wall changes. [Copyright &y& Elsevier]

Investigating atom-surface interactions is the key to an in-depth understanding of chemical processes at interfaces, which are of central importance in many fields - from heterogeneous catalysis to corrosion. In this work, we present a joint experimental and theoretical effort to gain insights into the atomistic details of hydrogen atom scattering at the α-Al 2 O 3 (0001) surface. Surprisingly, this system has been hardly studied to date, although hydrogen atoms as well as α-Al 2 O 3 are omnipresent in catalysis as reactive species and support oxide, respectively. We address this system by performing hydrogen atom beam scattering experiments and molecular dynamics (MD) simulations based on a high-dimensional machine learning potential trained to density functional theory data. Using this combination of methods we are able to probe the properties of the multidimensional potential energy surface governing the scattering process. Specifically, we compare the angular distribution and the kinetic energy loss of the scattered atoms obtained in experiment with a large number of MD trajectories, which, moreover, allow to identify the underlying impact sites at the surface.