22 research outputs found
Polymorphisms at microRNA binding sites of Ara-C and anthracyclines-metabolic pathway genes are associated with outcome of acute myeloid leukemia patients
Estimating the Effects of Government Size, Interventions, and Other Regulations on Labor Productivity
Tissue-Nonspecific Alkaline Phosphatase Is Required for MC3T3 Osteoblast–Mediated Protection of Acute Myeloid Leukemia Cells from Apoptosis
Studies on Transport of Vanadium (V) and Nickel (II) from Wastewater Using Activated Composite Membranes
Characterization of fibrous polymer silver/cobalt nanocomposite with enhanced bactericide activity
This manuscript describes the synthesis (based on the intermatrix
synthesis (IMS) method), optimization, and application to bacterial
disinfection of Ag@Co polymer metal nanocomposite materials with magnetic
and bactericidal properties. This material showed ideal bactericide
features for being applied to bacterial disinfection of water, particularly (1)
an enhanced bactericidal activity (when compared with other nanocomposites
only containing Ag or Co nanoparticles), with a cell viability close to 0% for
bacterial suspensions with an initial concentration below 105 colony forming
units per milliliter (CFU/mL) after a single pass through the material, (2)
capacity of killing a wide range of bacterial types (from coliforms to Grampositive
bacteria), and (3) a long performance-time, with an efficiency of
100% (0% viability) up to 1 h of operation and higher than 90% during the first
24 h of continuous operation. The nanocomposite also showed a good
performance when applied to water samples from natural sources with more complex matrices with efficiencies always higher
than 80%.Peer Reviewe
Characterization of Fibrous Polymer Silver/Cobalt Nanocomposite with Enhanced Bactericide Activity
Ferroptosis is Involved in Acetaminophen Induced Cell Death.
The recently described form of programmed cell death, ferroptosis can be induced by agents causing GSH depletion or the inhibition of GPX4. Ferroptosis clearly shows distinct morphologic, biochemical and genetic features from apoptosis, necrosis and autophagy. Since NAPQI the highly reactive metabolite of the widely applied analgesic and antipyretic, acetaminophen induces a cell death which can be characterized by GSH depletion, GPX inhibition and caspase independency the involvement of ferroptosis in acetaminophen induced cell death has been investigated. The specific ferroptosis inhibitor ferrostatin-1 failed to elevate the viability of acetaminophen treated HepG2 cells. It should be noticed that these cells do not form NAPQI due to the lack of phase I enzyme expression therefore GSH depletion cannot be observed. However in the case of acetaminophen treated primary mouse hepatocytes the significant elevation of cell viability could be observed upon ferrostatin-1 treatment. Similar to ferrostatin-1 treatment, the addition of the RIP1 kinase inhibitor necrostatin-1 could also elevate the viability of acetaminophen treated primary hepatocytes. Ferrostatin-1 has no influence on the expression of CYP2E1 or on the cellular GSH level which suggest that the protective effect of ferrostatin-1 in APAP induced cell death is not based on the reduced metabolism of APAP to NAPQI or on altered NAPQI conjugation by cellular GSH. Our results suggest that beyond necroptosis and apoptosis a third programmed cell death, ferroptosis is also involved in acetaminophen induced cell death in primary hepatocytes