China 
Africa 
Explore chapters and articles related to this topic
Inorganic Chemical Pollutants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Macrophage flux involves monocyte migration across the endothelium, monocyte differentiation to macrophages, macrophage retention in the atheromata, exit, or death. The preferential accumulation of Ly-6Chigh monocytes in the growing atheromata relies on chemokine-dependent signaling through CCR2-CCL2, CX3CR1-CX3CL1, and CCR5-CCL5,252 and neutralizing these axes in mice almost abolishes atherosclerosis.253,254 Upon accumulation and lipid ingestion, macrophages release netrin-1, a guidance molecule that binds to UNC5b on the plasma membrane and blocks the directed migration of macrophages out of the lesion.255 In the absence of netrin-1, lesions are smaller. Lesions with large necrotic cores are most vulnerable. When one surveys, the peripheral blood counts differential in the chemically sensitive monocytes are usually decreased. This suggests that they are converting to macrophages in the tissue areas containing toxics.
Microfluidics in Neuroscience
Published in Tuhin S. Santra, Microfluidics and Bio-MEMS, 2020
Pallavi Gupta, Nandhini Balasubramaniam, Kiran Kaladharan, Fan-Gang Tseng, Moeto Nagai, Hwan-You Chang, Tuhin S. Santra
Local modifications at synapses play an important role in neuronal plasticity, but the complete information is still lacking due to the availability of limited techniques for exploring local processing within synaptic regions. Therefore, Taylor et al. developed a μFD or chamber to optimize synaptic cell biology [38]. This visualized and manipulated synapses and pre- and postsynaptic cell bodies in an independent manner [35, 99]. The device consisted of a compartmentalized microfluidic chamber that employed direct cortical growth and hippocampal axons across parallel microgrooves. This was the first attempt to direct the growth of dendrites through microgrooves and check whether there was any formation of functional synapses inside the microfluidic chamber. The two populations of neurons were cultured on either side of the microgrooves. Additionally, a small perfusion channel imposing local perturbations and probing synaptic regions of high spatial and temporal resolution was also implemented. As a proof of concept, this chamber can be used to study synapse-to-nucleus signaling in several ways using calcium imaging, study transcriptional response comparison to massed and spaced stimulation, and explore the variations in Arc transcription and mRNA localization; subsequent to the local introduction of the mGluR1 group I agonist, dihydroxyphenylglycine was also demonstrated. Later, in 2017, Nagendran et al. studied and assessed the progress of intrinsic events occurring in the long projection pyramidal neurons after distal axotomy, hence remodeling synapses [100]. For this study, microfluidic chambers containing microgroove-embedded barriers of ∼900 μm in length were used. The results show that axotomized pyramidal neurons undergo dendritic spine loss followed by a trans-synaptic enhancement in presynaptic excitability. They also found that directly injured neurons show excitability and loss of inhibitory inputs. Axotomy shows considerable detrimental effects on netrin-1. But the exogenous netrin-1 protein several hours after axotomy re-establishes spine density and brings presynaptic excitability and inhibitory inputs onto the injured neurons to optimal levels [100].
Potential protective roles of curcumin against cadmium-induced toxicity and oxidative stress
Published in Journal of Toxicology and Environmental Health, Part B, 2021
Jae Hyeon Park, Byung Mu Lee, Hyung Sik Kim
Previously, Lee et al. (2014) found that exposure to a high dose of Cd (25 mg/kg, oral route) markedly induced acute kidney injury (AKI) as evidenced by a rise in urinary excretion of KIM-1, NGAL, clusterin, TIMP-1, and netrin-1. In a murine model, curcumin exerted protective effects against Cd-induced renal toxicity and renal tubular injury by significantly reducing KIM-1, NGAL, and TIMP-1 levels in the urine (Lee et al. 2014). Prolonged exposure to Cd is responsible for human renal impairment by decreasing the glomerular filtration rate (GFR), potentially leading to renal failure (Blum et al. 2015; Hellström et al. 2001; Liang et al. 2012) closely associated with damage to the proximal tubules of the kidney (Thévenod 2003).