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Regional Centre of Advanced Technologies and Materials
The common use of various medications can influence susceptibility to toxic chemicals mainly because many drugs bind to serum proteins and thus influence the transport, distribution or excretion rate of various toxic chemicals, or because many drugs are capable of inducing relevant detoxifying enzymes or depressing their activity (e.g., the cytochrome P450 enzymes), thus affecting the toxicity of chemicals with the same biotransformation pathway. Characteristic for either of the mechanisms is increased urinary excretion of trichloroacetic acid (the metabolite of several chlorinated hydrocarbons) when using salicylate, sulphonamide or phenylbutazone, and an increased hepato-nephrotoxicity of carbon tetrachloride when using phenobarbital. In addition, some medications contain a considerable amount of a potentially toxic chemical, for example, the aluminium-containing antacids or preparations used for therapeutic management of the hyperphosphataemia arising in chronic renal failure.
This is obviously the case regarding important antioxidants such as vitamin C and glutathione (GSH), which are essential for maintaining redox equilibrium and which have a protective role against the adverse effects of the oxygen- or xenobiotic-derived free radicals which are involved in a variety of pathological conditions (Kehrer 1993). Humans cannot auto-synthesize vitamin C, contrary to the rat, and levels as well as the turnover rate of erythrocyte GSH in humans are considerably lower than that in the rat. Humans also lack some of the protective antioxidant enzymes, compared to the rat or other mammals (e.g., GSH- peroxidase is considered to be poorly active in human sperm). These examples illustrate the potentially greater vulnerability to oxidative stress in humans (particularly in sensitive cells, e.g., apparently greater vulnerability of the human sperm to toxic influences than that of the rat), which can result in different response or greater susceptibility to the influence of various factors in humans compared to other mammals (Teliman 1995).
Researche institute in Czech Republic focuses on nanotechnology
The significance of the neurophysiological abnormalities in blast-exposed wild-type C57BL/6 mice is substantial. First, although blast exposure did not produce detectable long-term dysfunction in basal synaptic transmission, exposure to a single sublethal blast was sufficient to induce profound and persistent impairment of both activity- and cAMP-dependent LTP in hippocampal CA1 pyramidal neurons, candidate cellular mechanisms of long-term memory processing. The fact that both forms of LTP require dendritic protein synthesis (, ) and gene transcription () indicate that blast exposure may induce long-lasting damage to cellular signal transduction downstream of synaptic glutamate release. Mechanisms that may be altered by blast exposure include N-methyl-D-aspartate glutamate receptor activation, intracellular second messenger systems, gene expression, protein synthesis, and posttranslational modification. Our results also indicate that blast exposure can induce persistent axonal conduction defects that further impair cognitive processing and are consistent with recent findings from human studies (, ). These effects may be mediated by diffuse axonal injury, Wallerian degeneration, and/or differential susceptibility of larger neurons to structural or functional axotomy. Damage to these and other brain structures, systems, and mechanisms may contribute to abnormalities in neurochemical homeostasis, cerebral metabolism, and neurophysiological functions associated with blast-related TBI (). Our results suggest that blast exposure may hold comparable or even greater pathogenic potential than repetitive head injury associated with contact athletics (–).
Limitations of the human neuropathology reported here include the small number of available cases, the time interval between trauma and postmortem examination, potential contributions of confounding comorbidities and risk factors, and inherent limitations of neuropathological analysis to establish mechanistic causality. Clinicopathological correlation may be further complicated by genetic contributions [for example, APOE (apolipoprotein E) genotype ()], history of previous head trauma, innate inflammatory responsivity, neuropsychiatric comorbidity, age and gender, and other factors with potential to modulate susceptibility and pathological expression of blast-related neurotrauma and sequelae. Furthermore, emerging evidence indicates that PTSD may represent an important overlapping comorbidity with potential to synergistically affect both the incidence and the severity of blast TBI and military deployment–related cognitive dysfunction (, , –). Limitations of our animal experiments include use of adult male C57BL/6 wild-type mice subjected to a single-blast exposure with post-exposure evaluation at time points only up to 1 month. Interpretation and generalizability of our animal experiments are further constrained by interspecies differences, including the significantly greater deformability of the murine skull, the relative instability of the murine cervical spine, and differential force loading on the head and neck in mice and humans.
Boron- and Nitrogen-Doped Graphene Quantum …
We analyzed a case series of postmortem human brains from U.S. military veterans with blast exposure and/or concussive injury and compared them to brains from young-adult athletes with histories of concussive injury and from normal controls of comparable ages without histories of blast exposure, concussive injury, or neurological disease. We uncovered evidence of CTE-linked tau neuropathology, including multifocal perivascular foci of neurofibrillary and glial tangles immunoreactive for phosphorylation-independent (Tau-46) and phosphorylation-dependent (CP-13) tau epitopes (, ), in the brains of blast-exposed and/or concussive-injured veterans. This blast-associated CTE-linked tau neuropathology was indistinguishable from the tau neuropathology, neuroinflammation, and neurodegeneration observed in the brains of young-adult athletes with histories of repeat concussive injury. Examination of brains from wild-type C57BL/6 mice 2 weeks after exposure to a single controlled blast also revealed histopathological, ultrastructural, and biochemical evidence of CTE-linked neuropathology, including tau protein–linked immunoreactivity, persistent perivascular pathology, cortical and hippocampal neurodegeneration, myelinated axonopathy, chronic neuroinflammation with widespread astrocytosis and microgliosis, and phosphorylated tau proteinopathy. Overall, our findings of persistent CTE-linked neuropathology in the brains of military veterans with blast exposure and/or concussive injury and young athletes with repeat concussive injury suggest that TBI induced by different insults under different conditions can trigger common pathogenic mechanisms leading to similar neuropathology and sequelae. Notably, within this small controlled case series, the effects of blast exposure, concussive injury, and mixed trauma (blast exposure and concussive injury) were indistinguishable.
Basically the skin consists of three layers: epidermis, true skin (dermis) and subcutaneous tissue (hypodermis). From the toxicological point of view the epidermis is of most interest here. It is built of many layers of cells. A horny surface of flattened, dead cells (stratum corneum) is the top layer, under which a continuous layer of living cells (stratum corneum compactum) is located, followed by a typical lipid membrane, and then by stratum lucidum, stratum gramulosum and stratum mucosum. The lipid membrane represents a protective barrier, but in hairy parts of the skin, both hair follicles and sweat gland channels penetrate through it. Therefore, dermal absorption can occur by the following mechanisms:
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Staff Profile - City University of Hong Kong
Animal studies have revealed that after penetration into the cell, some metal ions are bound to a specific protein, metallothionein. This low molecular weight protein is present in the cells of liver, kidney and other organs and tissues. Its sulphydryl groups can bind six ions per molecule. Increased presence of metal ions induces the biosynthesis of this protein. Ions of cadmium are the most potent inducer. Metallothionein serves also to maintain homeostasis of vital copper and zinc ions. Metallothionein can bind zinc, copper, cadmium, mercury, bismuth, gold, cobalt and other cations.
General & Introductory Chemistry
The theory of the process giving rise to detonation nanodiamond (DND) particles is still a matter of discussion and, in our opinion, there is no adequate physicochemical model of detonation synthesis. Nevertheless, the data obtained by ourselves and other scientists during the experiments involving the blasting of a TNT–hexogen compound (about 50/50) and hydrogenfree benzotrifuroxane enable one to come to a better understanding of the mechanism of DND formation.
In their Communication on page 5447 ff., S
Meanwhile, the QD also functions as signal transducer that reports information regarding molecular structure, conformation, and interaction through the QD-FRET mechanism.Proteases were one of the earliest enzymes studied by QD-FRET nanosensors.
Using Stand-off LIBS to Detect Explosive Residues | Andor
According to the stage at which these factors act (absorption, distribution, biotransformation or excretion of a particular chemical), the mechanisms can be roughly categorized according to two basic consequences of interaction: (1) a change in the quantity of the chemical in a target organ, that is, at the site(s) of its effect in the organism (toxicokinetic interactions), or (2) a change in the intensity of a specific response to the quantity of the chemical in a target organ (toxicodynamic interactions). The most common mechanisms of either type of interaction are related to competition with other chemical(s) for binding to the same compounds involved in their transport in the organism (e.g., specific serum proteins) and/or for the same biotransformation pathway (e.g., specific enzymes) resulting in a change in the speed or sequence between initial reaction and final adverse health effect. However, both toxicokinetic and toxicodynamic interactions may influence individual susceptibility to a particular chemical. The influence of several concomitant factors can result in either: (a) additive effectsthe intensity of the combined effect is equal to the sum of the effects produced by each factor separately, (b) synergistic effectsthe intensity of the combined effect is greater than the sum of the effects produced by each factor separately, or (c) antagonistic effectsthe intensity of the combined effect is smaller than the sum of the effects produced by each factor separately.
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