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Remediation regarding zinc-contaminated groundwater by simply metal oxide throughout situ adsorption obstacles : Through lab to the area.
ntly lowering clinical mortality. Cerebral ischemia reperfusion injury (CIRI), one of the major causes of death from stroke in the world, not only causes tremendous damage to human health, but also brings heavy economic burden to society. Current available treatments for CIRI, including mechanical therapies and drug therapies, are often accompanied by significant side-effects. Therefore, it is necessary to discovery new strategies for treating CIRI. Many studies have confirmed that the herbal medicine has the advantages of abundant resources, good curative effect and little side effects, which can be used as potential drug for treatment of CIRI through multiple targets. It's known that oral administration commonly has low bioavailability, and injection administration is inconvenient and unsafe. Many drugs can't delivery to brain through routine pathways due to the blood-brain-barrier (BBB). Interestingly, increasing evidences have suggested the nasal administration is a potential direct route to transport drug into brain avoiding the BBB and has the characteristics of high bioavailability for treating brain diseases. Therefore, intranasal administration can be treated as an alternative way to treat brain diseases. In the present review, effective methods to treat CIRI by using active ingredients derived from herbal medicine through nose to brain drug delivery (NBDD) are updated and discussed, and some related pharmacological mechanisms have also been emphasized. Our present study would be beneficial for the further drug development of natural agents from herbal medicines via NBDD. Mitochondrial dysfunction has been demonstrated as one key event in arsenic-induced hepatic cell damage though the exact molecular target remains unknown. Here we examined NaAsO2-induced mitochondrial damage in the L-02 cell led to mitochondrial depolarization and cytochrome c release, mitophagy, apoptosis in a dose response manner. Mitophagy was measured by analysis of PINK1, Parkin, LC3-II and p62 protein. Apoptosis was assessed by measuring Annexin V. Using the mitophagy inhibitor cyclosporine A (CsA) or ERK inhibitor (PD98059), the balance between mitophagy and apoptosis were further explored. When CsA was used prior to cell exposure to NaAsO2, it was found that the levels of mitophagy were decreased as expected and apoptosis was increased in response. CsA alone had no effect on the apoptosis rate. When the ERK signaling inhibitor PD98095 was used, there was a similar result that mitophagy was reduced though in contrast with CsA the apoptosis rate was also decreased compared with NaAsO2 alone. This result, along with the increased levels of ERK measured here in response to NaAsO2, indicates that ERK activation is a second key molecular response to NaAsO2 through the activation of both apoptosis and mitophagy. Sodium L-lactate mw Thus the results with CsA indicate that the likely key biological event in NaAsO2 toxicity is at the level of the mitochondria leading to cytochrome c release and apoptosis. Mitophagy is increased in response to a secondary effect of NaAsO2 on ERK signaling that activates both mitophagy and apoptosis. The activation of mitophagy allows the cell to avoid some apoptosis. When ERK signaling is inhibited by PD98095 both the levels of apoptosis and mitophagy are decreased compared with the response produced by NaAsO2 alone in comparison to the inhibition of mitophagy by CsA that reduced mitophagy but dramatically increased apoptosis in response. Advancements in measurement and modeling capabilities are providing unprecedented access to estimates of chemical exposure and bioactivity. With this influx of new data, there is a need for frameworks that help organize and disseminate information on chemical hazard and exposure in a manner that is accessible and transparent. A case study approach was used to demonstrate integration of the Adverse Outcome Pathway (AOP) and Aggregate Exposure Pathway (AEP) frameworks to support cumulative risk assessment of co-exposure to two phthalate esters that are ubiquitous in the environment and that are associated with disruption of male sexual development in the rat di(2-ethylhexyl) phthalate (DEHP) and di-n-butyl phthalate (DnBP). A putative AOP was developed to guide selection of an in vitro assay for derivation of bioactivity values for DEHP and DnBP and their metabolites. AEPs for DEHP and DnBP were used to extract key exposure data as inputs for a physiologically based pharmacokinetic (PBPK) model to predict internal metabolite concentrations. These metabolite concentrations were then combined using in vitro-based relative potency factors for comparison with an internal dose metric, resulting in an estimated margin of safety of ~13,000. This case study provides an adaptable workflow for integrating exposure and toxicity data by coupling AEP and AOP frameworks and using in vitro and in silico methodologies for cumulative risk assessment. The OECD QSAR-Toolbox can be considered a milestone in predictive toxicology. Because of the reliability of its supporting institutions (OECD and ECHA), its broadness in terms of feeder databases, and its predictive capacity, the QSAR-Toolbox is called to have a major role in regulatory toxicology. Recently, a novel functionality was built for the QSAR-Toolbox the alert performance (AP). This prompted us to analyze the strengths, potentialities, and limitations of this new functionality, especially in the light of a pivotal framework recently discussed in the literature for the predictive use of nonclinical screening and testing. After meticulous analysis, and through some worked examples, a high predictive capability and applicability was found for the AP in both predictive and regulatory toxicology. For a specified chemical, the AP is useful in (a) anticipating its overall results in a given nonclinical test; (b) predicting its overall results regarding a selected toxicological endpoint in humans, and (c) facilitating post- to pre-test probabilities approaches that may support regulatory authorization for the waiving of selected tests in laboratory animals. Furthermore, if a QSAR-Toolbox initiative is developed in or extended to pharmacology (e.g., safety pharmacology, drug abuse potential), it could represent another milestone, in that case, one that would give rise to the field of predictive pharmacology.
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