A recent study proposed a treatment algorithm for pediatric DRE, including non-pharmacological treatment options such as VNS and the KD ( Interestingly, the KD therapy has some advantages in comparison to VNS: the SFR is slightly higher for patients on the KD ( Currently, we are unable to pinpoint the mechanism(s) of action of the KD, and it is possible that dietary therapies will be classified as magic shotguns ( Primary Antiseizure Mechanisms of the Kd A high-fat low-carbohydrate KD replicates a fasting state. Subsequently, this state results in (1) fatty acid oxidation producing ketone bodies (KBs), (2) production of polyunsaturated fatty acids (PUFAs), (3) decreased activity of lactate dehydrogenase (LDH), and (4) inhibition of the mTOR pathway ( First, KBs [i.e., -hydroxybutyrate (BHB), acetone, and acetoacetate] have been considered the key effectors of the antiseizure effects of the KD by modulating neurotransmissions and altering metabolic, inflammatory, and epigenetic pathways, as reviewed elsewhere ( B activation ( ATP ( Besides replicating a fasting state, resulting in production of various effectors, the antiseizure mechanisms of the KD are also thought to result in anti-inflammatory and antioxidant activity, as reviewed by Koh et al
Occupational Safety and Health Administration (OSHA) standardized the exposure to 500 ppm TWA considering 8 h working shift
Determination of emodin in L-02 cells and cell culture media with liquid chromatography-mass spectrometry: application to a cellular toxicokinetic study
NLRP3, NOD-like receptor protein 3
