Results 181 to 190 of about 981,404 (392)

Molecular Mechanisms of Intrinsic Streptomycin Resistance in Mycobacterium abscessus

open access: yesAntimicrobial Agents and Chemotherapy, 2017
M. Dal Molin   +5 more
semanticscholar   +1 more source

Lactoferrin treatment activates acetylcholinesterase, decreasing acetylcholine levels in non‐small cell lung cancer (NSCLC) cell culture supernatants, inhibiting cell survival

open access: yesFEBS Open Bio, EarlyView.
Representation of the suggested mode of action of lactoferrin (Lf) in nonsmall cell lung cancer (NSCLC) A549 cells. Lf induces activation of caspase‐3 by activating p53 and AChE leading to decreased ACh concentrations. In turn, ACh signaling leads to activation of VEGF and AKT and blocking of caspase‐3.
Stuti Goel   +9 more
wiley   +1 more source

Thermal Degradation of Streptomycin Residues in Honey During Storage

open access: yesFood Technology and Biotechnology, 2013
In Europe there is an increasing emphasis on the quality control of honey, especially on maximum limits of veterinary drug residues (particularly antibiotics) permitted in it.
Monica Cristina Cara   +4 more
doaj  

ATG4B is required for mTORC1‐mediated anabolic activity and is associated with clinical outcomes in non‐small cell lung cancer

open access: yesFEBS Open Bio, EarlyView.
The relationship between anabolic and catabolic processes governing lung cancer cell growth is nuanced. We show that ATG4B, an autophagy regulator, is elevated in lung cancer and that high ATG4B is associated with worse patient outcomes. Targeting ATG4B in cells reduces growth, protein synthesis, and mTORC1 activity, demonstrating a new relationship ...
Patrick J. Ryan   +6 more
wiley   +1 more source

Streptomycin Poisoning in Renal Failure [PDF]

open access: green, 1959
K. D. G. Edwards, H. M. Whyte
openalex   +1 more source

Calcium‐sensing receptor induces the apoptosis of chondrocytes in cooperation with phosphate transporter

open access: yesFEBS Open Bio, EarlyView.
Excess Ca2+ ions activate the Calcium‐Sensing Receptor (CaSR), which subsequently drives the uptake of excess inorganic phosphate (Pi) via the Pi transporter (Pit−1) in chondrocytes. This mechanism causes a toxic increase in intracellular Pi concentration, ultimately leading to chondrocyte apoptosis and pathological mineralization. Excess extracellular
Sachie Nakatani   +7 more
wiley   +1 more source

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