This paper is concerned with the event-triggered sliding mode control (SMC) strategy for the discrete-time two-dimensional (2-D) systems represented by Roesser model with time delays. Firstly, the linear sliding surface functions combined with the event-triggered scheme are constructed for the 2-D Roesser model. Then sufficient conditions are established for the asymptotic stability of the reduced-order sliding mode dynamics and the existence of linear sliding surface functions in terms of linear matrix inequality. Subsequently, the event-triggered sliding mode control law is designed by the Lyapunov function approach to drive the state trajectories of the resultant closed-loop system into a bounded region and maintain there for subsequent time. Finally, a numerical example is given to illustrate the effectiveness of the proposed SMC design method.
Contrast-induced neurotoxicity (CIN) is a rare complication of neurointerventional procedures and its understanding remains limited. We evaluated the association of CIN with systemic hemodynamics in patients undergoing neuroendovascular interventions.
We conducted a 12 matched case-control study from a prospectively collected database of 2510 neurointerventional patients. We defined CIN as new neurological deficits presented ≤24h post-operation after excluding other possible etiologies. We obtained demographic, clinical and imaging data, and baseline and intraprocedural blood pressures (BP) from medical records. The area between baseline and intraprocedural BP was used to measure sustained variability of BP over time. A generalized linear mixed model and generalized estimating equation were used to analyze the BP difference between groups over time.
We evaluated 11 CIN cases and 22 controls. 2746 and 5837min of continued BP data were analyzed for cases and controls, respectively. CIN cases had higher measurements and greater variability for Systolic BP (SBP) [median 125 (IQR121-147) vs. 114 (IQR107-124) mmHg], median area above baseline [median 350 (IQR25-1328) vs. 52 (IQR0-293) mmHg*minutes] and mean arterial pressure (MAP) [median 85 (IQR79-98) vs. 80 (IQR74-89) mmHg]. CIN cases demonstrated a significant mean increase in SBP and MAP of 23.41mmHg (p<0.01) and 13.79mmHg (p<0.01) when compared to controls, respectively, over the perioperative time.
Sustained hypertension and high BP variability may contribute to the pathophysiology of CIN. Acute hypertension can increase blood-brain barrier permeability and potentially allow contrast to leak into the brain parenchyma causing direct toxicity and CIN symptoms.
Sustained hypertension and high BP variability may contribute to the pathophysiology of CIN. CVT-313 mw Acute hypertension can increase blood-brain barrier permeability and potentially allow contrast to leak into the brain parenchyma causing direct toxicity and CIN symptoms.Seminal plasma (SP) antioxidants are considered biomarkers of sperm function and fertility for AI-boars. The current protocol for their measurement implies the SP was harvested immediately after ejaculation and prompt stored at -80 °C until analysis. Such protocol may be impractical for AI-centers. This study evaluated how SP levels of antioxidants were influenced by delays in (1) SP-harvesting (0 [control], 2 or 24 h at 17 °C after ejaculate collection), in (2) SP-freezing (0 [control] or 24 h at 17 °C after SP-harvesting) or (3) the temperature of storage (-80 °C [control] or - 20 °C). The SP-antioxidants evaluated were glutathione peroxidase [GPx], superoxide dismutase [SOD], paraoxonase-1 [PON-1], trolox equivalent antioxidant capacity [TEAC] and oxidative stress index [OSI]. A total of 120 aliquots from 10 entire ejaculates were handled in three trials. They were centrifuged (1500 g, 10 min) for harvesting SP and antioxidants were measured with an Automatic Chemistry Analyzer. A 24 h-delay in harvesting the SP led to an increase (p˂0.001) in TEAC and SOD SP-levels, and a decrease (p˂0.05) of OSI and PON-1. Similarly, a 24 h-delay to freeze the SP increased (p˂0.01) TEAC values and decreased (p˂0.01) PON-1 and GPx activity levels. Finally, storing the SP at -20 °C decreased (p˂0.001) SP-levels of TEAC, PON-1 and GPx, and increased (p˂0.01) OSI values. Strong positive relationships (p˂0.001) were found between antioxidant SP-levels in processed samples and their respective controls. In sum, handling and SP storage influence antioxidant measurements in AI-boars. Reliable levels of SP-antioxidants can only be warranted if a strict protocol for harvesting and SP storage is followed.Canine degenerative myelopathy (DM) is an adult-onset fatal disease characterized by progressive degeneration of the spinal cord. Affected dogs have homozygous mutations in superoxide dismutase 1, and thus DM is a potential spontaneous animal model of human familial amyotrophic lateral sclerosis (ALS). Neuroinflammation is the pathological hallmark of ALS, whereby proinflammatory cytokines and chemokines are overproduced by activated glial cells such as astrocytes and microglia. However, the detailed pathogenesis of spinal cord degeneration in DM remains unknown. To further characterize the pathological mechanism of DM, we analyzed the caudal cervical cords of ten Pembroke Welsh Corgis pathologically diagnosed with DM by quantitative real-time reverse transcription polymerase chain reaction, immunohistochemistry (IHC), and double immunofluorescence. Compared to control spinal cord tissues, we found significantly enhanced transcriptions of interleukin-1β, tumor necrosis factor-α, CC motif chemokine ligand (CCL) 2 and vascular cell adhesion molecule -1 mRNA in the spinal cords of DM dogs. Moreover, IHC for the class II major histocompatibility complex molecules HLA-DR and CCL2 indicated that the immunopositive areas of activated macrophages/microglia and CCL2 protein were significantly increased in DM, and CCL2 protein was mainly overproduced by astrocytes. Our results suggest a proinflammatory state of the microenvironment in the DM spinal cord in which activated microglia and astrocytes play important roles by secreting a set of cytokines, chemokines, and expressing adhesion molecules.CVT-313 mw
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