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Pulsed dye laser (PDL) therapy can be effective in treating psoriasis, with a long duration of remission. Although PDL therapy, albeit on a modest scale, is being used for decades now, the underlying mechanisms responsible for the long‐term remission of psoriasis remain poorly understood. The selective and rapid absorption of energy by the blood causes heating of the vascular wall and surrounding structures, like perivascular nerves. Several studies indicate the importance of nerves in psoriatic inflammation. Interestingly, denervation leads to a spontaneous remission of the psoriatic lesion. Among all dermal nerves, the perivascular nerves are the most likely to be affected during PDL treatment, possibly impairing the neuro‐inflammatory processes that promote T‐cell activation, expression of adhesion molecules, leukocyte infiltration and cytokine production. Repeated PDL therapy could cause a prolonged loss of innervation through nerve damage, or result in a 'reset' of neurogenic inflammation after temporary denervation. The current hypothesis provides strong arguments that PDL treatment affects nerve fibres in the skin and thereby abrogates the persistent and exaggerated inflammatory process underlying psoriasis, causing a long‐term remission of psoriasis. [ABSTRACT FROM AUTHOR]

Background: Damping of heartbeat‐induced pressure pulsations occurs in large arteries such as the aorta and extends to the small arteries and microcirculation. Since recently, 7 T MRI enables investigation of damping in the small cerebral arteries. Purpose: To investigate flow pulsatility damping between the first segment of the middle cerebral artery (M1) and the small perforating arteries using magnetic resonance imaging. Study Type: Retrospective. Subjects: Thirty‐eight participants (45% female) aged above 50 without history of heart failure, carotid occlusive disease, or cognitive impairment. Field Strength/Sequence: 3 T gradient echo (GE) T1‐weighted images, spin‐echo fluid‐attenuated inversion recovery images, GE two‐dimensional (2D) phase‐contrast, and GE cine steady‐state free precession images were acquired. At 7 T, T1‐weighted images, GE quantitative‐flow, and GE 2D phase‐contrast images were acquired. Assessment: Velocity pulsatilities of the M1 and perforating arteries in the basal ganglia (BG) and semi‐oval center (CSO) were measured. We used the damping index between the M1 and perforating arteries as a damping indicator (velocity pulsatilityM1/velocity pulsatilityCSO/BG). Left ventricular stroke volume (LVSV), mean arterial pressure (MAP), pulse pressure (PP), and aortic pulse wave velocity (PWV) were correlated with velocity pulsatility in the M1 and in perforating arteries, and with the damping index of the CSO and BG. Statistical Tests: Correlations of LVSV, MAP, PP, and PWV with velocity pulsatility in the M1 and small perforating arteries, and correlations with the damping indices were evaluated with linear regression analyses. Results: PP and PWV were significantly positively correlated to M1 velocity pulsatility. PWV was significantly negatively correlated to CSO velocity pulsatility, and PP was unrelated to CSO velocity pulsatility (P = 0.28). PP and PWV were uncorrelated to BG velocity pulsatility (P = 0.25; P = 0.68). PWV and PP were significantly positively correlated with the CSO damping index. Data Conclusion: Our study demonstrated a dynamic damping of velocity pulsatility between the M1 and small cerebral perforating arteries in relation to proximal stress. Level of Evidence: 4 Technical Efficacy: Stage 1 [ABSTRACT FROM AUTHOR]

Background: Hypertension is a major risk factor for dementia. Hypertension is associated with neuroinflammation and neurodegeneration, however, the exact link is unclear. Microglia can undergo senescence, resulting in primed and dystrophic cells that can contribute to the development of Alzheimer's disease. We hypothesized that microglia are affected by cumulative hypertensive brain injury and reflect an ongoing inflammatory and neurodegenerative pathology. Method: An in‐depth immunohistochemical analysis of microglia was done on the brains of Spontaneously Hypertensive Rats (SHR) and their genetic controls, Wistar Kyoto rats (WKY); n=5 each. The number of cells and morphological features, such as size, number of branches, and branch length, were measured. We qualitatively assessed microglia for the presence of characteristic dystrophic cells then performed fractal analysis on individual cells to quantitate their morphologies. Result: SHR microglia were more numerous and exhibited signs consistent with senescence and priming, with shorter, fewer branches and the sizes of their cell bodies were larger and more heterogeneous (p<0.05). In SHR, 2.91% of microglia were dystrophic as compared to 0.32% in WKY (p=0.01). Using fractal analysis, we confirmed the presence of dystrophic cells and distinctly characterized them against ramified cells based on 3 main characteristics: complexity, shape, and branching. Conclusion: Microglial senescence, an indicator of neuroinflammation and neurodegenerative pathology, is associated with hypertension. It could thus serve as a therapeutic target and may help identify novel biomarkers. Moreover, fractal analysis is a useful tool to quantify meaningful subtleties. [ABSTRACT FROM AUTHOR]