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High Resolution Diffuse Optical Tomography of the Human Brain
Published in Francesco S. Pavone, Shy Shoham, Handbook of Neurophotonics, 2020
Muriah D. Wheelock, Adam T. Eggebrecht
Mapping spatially distributed brain activity has revolutionized our understanding of brain function (Corbetta and Shulman, 2002; Zhang and Raichle, 2010; Power et al., 2011; Yeo et al., 2011). Brain imaging via positron emission tomography (PET), functional magnetic resonance imaging (fMRI), and, more recently, diffuse optical tomography (DOT) have illuminated many aspects of the biological basis of human behavior. Brain systems that support all aspects of cognition – from sensing the visual world, to generating language, to interacting socially, to daydreaming or sleeping – are accessible to quantitative investigation because of these techniques (Petersen et al., 1988; Corbetta and Shulman, 2002; Raichle, 2010). Further, brain imaging has proven useful in clinical investigations of brain function. Specifically, several neurological disorders manifest as measurable alterations in distributed brain networks, including degenerative diseases such as Alzheimer’s disease (Buckner et al., 2009), neurodevelopmental disorders such as autism spectrum disorder (ASD) (Kennedy and Courchesne, 2008; Eggebrecht et al., 2017; Marrus et al., 2017), or disorders due to an insult such as ischemic stroke (Carter et al., 2012; Baldassarre et al., 2016). While many clinical disorders are known to manifest in the brain, optimizing neuroimaging technologies as tools for understanding these disorders and tracking their progression presents significant challenges.
The Diagnosis Of Epilepsy
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
Certain factors had a large effect on recurrence rates so that seizures associated with a neurological deficit present at birth had a 100 per cent relapse within the first 12 months, whilst seizures occurring within the context of an acute insult or precipitant had only a 40 per cent relapse over the same time period. The difference in the risk of recurrent seizures between acute symptomatic (defined as a seizure in close temporal association with a transient central nervous system insult, taken as within one week of the insult) and unprovoked seizures in the context of similar insults (traumatic brain injury, stroke or infection involving the central nervous system) has recently been addressed (Hesdorffer et al., 2009). The first unprovoked seizure group had a significantly higher risk of subsequent unprovoked seizure within ten years (65 per cent) compared with the first acute symptomatic seizure group (19 per cent), regardless of aetiology, and, as in most studies, most of this risk was within the first one to two years.
Intracellular Redox Status and Disease Development: An Overview of the Dynamics of Metabolic Orchestra
Published in Jyoti Ranjan Rout, Rout George Kerry, Abinash Dutta, Biotechnological Advances for Microbiology, Molecular Biology, and Nanotechnology, 2022
Sharmi Mukherjee, Anindita Chakraborty
In the prognosis and progression of acute diseases, oxidative stress constitutes an essential regulatory factor. In extreme cases of cardiovascular diseases (CVD) where lack of blood supply in heart muscles initiates myocardial infarction (MI), the generation of ROS and RNS is triggered, which is again responsible for some MI associated extracellular injuries. The increased ROS generation under hypoxic conditions is related to hypoxia-inducible factor 1 (HIF 1) transcription factor stabilization at low pressures of oxygen that elevate superoxide and hydrogen peroxide release (Chandel et al., 1998; Guzy and Schumacker, 2006; Sena and Chandel, 2012). ROS induced increased Nox-2 (nicotinamide adenine dinucleotide phosphate oxidase) expression in cardiomyocytes is responsible for post-MI cardiac remodeling by myocardial apoptosis, necrosis, or hypertrophy (Krijnen et al., 2003). Reperfusion of damaged myocardium also triggers oxidative stress by stimulating the peroxidation of lipids (Palace et al., 1999; Dhalla et al., 2000). This situation is more prominent in patients with diabetes mellitus (DM), where MI induces severe atherosclerosis, frequent infarcts, and worse outcomes than nondiabetic patients (Di Filippo et al., 2006). During cardiopulmonary bypass, oxidative stress activates proapoptotic and proinflammatory signaling pathways (Zakkar et al., 2015). The inflammatory cycle generated due to sepsis induces oxidative stress with elevated lipid and protein oxidized products (Goode et al., 1995). ROS-induced mitochondrial respiratory impairment, reduced vascular tone, increased vascular permeability, vasodilation, and decreased cardiac output are responsible for multiorgan failure and mortality in septic patients (Mantzarlis et al., 2017; Prauchner, 2017). Studies have shown that postischemic stroke, increased ROS levels induce brain cell apoptosis, disruption of the blood–brain barrier, vasoconstriction, microvascular constriction which enhance the ischemic insult (Atochin et al., 2007; Crack and Taylor, 2005; Neumann-Haefelin et al., 2000; Shirley et al., 2014; Sandoval and Witt, 2008; Szczepańska-Szerej et al., 2011; Tsai et al., 2014). Traumatic brain injury is characterized by an immediate increase in ROS generation resulting in elevated lipid peroxidation, peroxy-nitrite production, reduction in antioxidant reserve, and development of secondary brain injury (Abou-El-Hassan et al., 2017; Bayir et al., 2002; Hall et al., 1993; Smith et al., 1994; Wang et al., 2016). In severe brain injury scenarios, elevated levels of nitro-tyrosine characterize the cerebrospinal fluid (Bar-Or et al., 2015; Darwish et al., 2007). In other cases of trauma like burns, ROS, and NO generation trigger systemic inflammatory reactions and the development of lipid peroxidation (Parihar et al., 2008; Wagener et al., 2013). The accumulation of polymorphonuclear leukocytes at trauma sites affects the recovery of different organs and regulates clinical outcomes (Henrich et al., 2011; Pepper et al., 1994; Zakkar et al., 2015).
Fabrication of a curcumin encapsulated bioengineered nano-cocktail formulation for stimuli-responsive targeted therapeutic delivery to enhance anti-inflammatory, anti-oxidant, and anti-bacterial properties in sepsis management
Published in Journal of Biomaterials Science, Polymer Edition, 2023
Li Teng, Yiliang Zhang, Li Chen, Ge Shi
In summary, our results suggest that functionalized CS nanoformulations loaded with CeO2 NPs and Cur is greatly associated with developments of bacterial infection control, animal survival, reduced hepatic damages and specifically decreased systemic inflammatory response after a severe septic insult in sepsis treatment. Additionally, the developed nanoformulations showed favorable drug entrapment efficiency, in vitro biocompatibility on human umbilical endothelial cells, in vitro cellular uptake, and reduced hemolysis ratios. The combination of Cur and Ce nanoformulation have provided efficient anti-bacterial efficiency against clinically approved pathogenic bacterial cells (S. aureus and P. aeruginosa), which was confirmed by in vitro and in vivo methods. Consequently, in vivo observations established that the number of leukocytes and inflammatory cytokines were significantly reduced with developed nanoformulations. Specifically, pH-responsive nanoformulations have effectively targeted to infected lungs and reduced peritoneal infection, which led to decreased activity of inflammatory transcription factors. Altogether, our results would strongly recommend developed nanoformulation using functionalized CS nanoformulation for the treatment of sepsis.
Repeated remote ischaemic preconditioning can prevent acute mountain sickness after rapid ascent to a high altitude
Published in European Journal of Sport Science, 2022
Zhen Wang, Bo Lv, Lin Zhang, Ran Gao, Wenbo Zhao, Lin Wang, Zhaojun Min, Zhen Mi, Yang Song, Jing Zhang, Yabin Yu, Xunming Ji, Junjie Li, Liyong Wu
Remote ischaemic preconditioning (RIPC) is a procedure involving transient noninvasive artificial ischaemic insult to the limbs that has been shown in several experimental and clinical studies to confer protection against many neurological diseases, including ischaemic stroke, intracranial atherosclerotic stenosis and others (Hess et al., 2015; Zhou et al., 2018). The mechanisms underlying RIPC remain unclear. It is believed that reduced levels of free radicals, increased levels of nitric oxide synthase and adenosine, downregulation of proinflammatory cytokines, and increased cerebral blood flow in response to a preconditioning stimulus may be involved (Hess et al., 2015; Zhou et al., 2018). The same target pathways are also thought to play important roles in AMS (Berger et al., 2017; Wilson et al., 2009). In addition, increased HVR has been observed after RIPC treatment at high altitudes (Rieger et al., 2017). Together, these observations provide a theoretical basis for the application of RIPC in the prevention of AMS.