Super-refractory status epilepticus is defined as status epilepticus that continues or recurs 24 h or more after the onset of anaesthetic therapy, including those cases where status epilepticus recurs on the reduction or withdrawal of anaesthesia. It is an uncommon but important clinical problem with high mortality and morbidity rates. This article reviews the treatment approaches. There are no controlled or randomized studies, and so therapy has to be based on clinical reports and opinion. The published world literature on the following treatments was critically evaluated: anaesthetic agents, anti-epileptic drugs, magnesium infusion, pyridoxine, steroids and immunotherapy, ketogenic diet, hypothermia, emergency resective neurosurgery and multiple subpial transection, transcranial magnetic stimulation, vagal nerve stimulation, deep brain stimulation, electroconvulsive therapy, drainage of the cerebrospinal fluid and other older drug therapies. The importance of treating the identifying cause is stressed. A protocol and flowchart for managing super-refractory status epilepticus is suggested. In view of the small number of published reports, there is an urgent need for the establishment of a database of outcomes of individual therapies.

The treatment of super-refractory status epilepticus: a critical review of available therapies and a clinical treatment protocol

Preclinical models of non-alcoholic fatty liver disease.

In a complex system of interrelated reactions, the heart converts chemical energy to mechanical energy. Energy transfer is achieved through coordinated activation of enzymes, ion channels, and contractile elements, as well as structural and membrane proteins. The heart’s needs for energy are difficult to overestimate. At a time when the cardiovascular research community is discovering a plethora of new molecular methods to assess cardiac metabolism, the methods remain scattered in the literature. The present statement on “Assessing Cardiac Metabolism” seeks to provide a collective and curated resource on methods and models used to investigate established and emerging aspects of cardiac metabolism. Some of those methods are refinements of classic biochemical tools, whereas most others are recent additions from the powerful tools of molecular biology. The aim of this statement is to be useful to many and to do justice to a dynamic field of great complexity.

Assessing Cardiac Metabolism

Ageing causes loss of function in tissues and organs, is accompanied by a chronic inflammatory process and affects life- and healthspan. Calorie restriction (CR) is a non-genetic intervention that prevents age-associated diseases and extends longevity in most of the animal models studied so far. CR produces a pleiotropic effect and improves multiple metabolic pathways, generating benefits to the whole organism. Among the effects of CR, modulation of mitochondrial activity and a decrease in oxidative damage are two of the hallmarks. Oxidative damage is reduced by the induction of endogenous antioxidant systems and modulation of the peroxidability index in cell membranes. Mitochondrial activity changes are regulated by inhibition of IGF-1 and Target of Rapamycin (TOR)-dependent activities and activation of AMP-dependent kinase (AMPK) and the sirtuin family of proteins. The activity of PGC-1α and FoxO is regulated by these systems and is involved in mitochondria biogenesis, oxidative metabolism activity and mitochondrial turnover. The use of mimetics and the regulation of common factors have demonstrated that these molecular pathways are essential to explain the effect of CR in the organism. Finally, the anti-inflammatory effect of CR is an interesting emerging factor to be taken into consideration. In the present revision we focus on the general effect of CR and other mimetics in longevity, focusing especially on the cardiovascular system and skeletal muscle.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/JP270543

Calorie restriction as an intervention in ageing

Herbal medicines for the prevention of alcoholic liver disease: a review

Betaine modulates oxidative stress, inflammation, apoptosis, autophagy, and Akt/mTOR signaling in methionine-choline deficiency-induced fatty liver disease.

Iron-based nanoparticles and their potential toxicity: Focus on oxidative stress and apoptosis

Moderate caloric restriction prolongs lifespan Changes in oxidative stress and hormesis may be involved in this process The aim of this study is to examine the effects of different levels of chronic caloric restriction (CR) and acute fasting on stress response and oxidative stress parameters in rat liver and plasma Forty-two rats were divided into groups: control group, calorie-restricted groups with intake of 80-90%, 60-70%, 40-50%, 20-30% of daily caloric needs and acute fasting group To determine alanine aminotransferase (ALT), aspartate aminotransferase (AST) and superoxide dismutase (SOD) activity, concentration of corticosterone, nitrites and nitrates (NOx), malondialdehyde (MDA) and glutathione (GSH), liver samples and blood were collected Increase in plasma corticosterone concentration and AST and ALT activity was found in severe CR Ingestion 40-50% daily caloric needs or less increased liver MDA and NOx concentration and decreased SOD activity Ingestion 60-70% daily caloric needs increased Mn-SOD activity, GSH and NOx In acute fasting group and group taking 20-30% daily caloric needs, GSH was significantly lower than in control group Severe CR and acute fasting increase oxidative damage and decrease antioxidative capacity of hepatocytes Moderate CR increases antioxidative capacity of hepatocytes due to increase in Mn-SOD activity and GSH concentration, which might have a role in anti-aging and hormetic mechanism of CR

/pdf/effects-of-caloric-restriction-on-oxidative-stress-3iu36qjgr0.pdf

Effects of caloric restriction on oxidative stress parameters

Introduction. Oxidative stress plays an important role in pathogenesis of alcoholic liver injury. The main source of free oxygen species is cytochrome P450-dependent monooxygenase, which can be induced by ethanol. Role of cytochrome P4502E1 in ethanol-induced oxidative stress. Reactive oxygen species produced by this enzyme are more important in intracellular oxidative damage compared to species derived from activated phagocytes. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in alcohol-induced oxidative stress. Production of mitochondrial reactive oxygen species is increased, and glutathione content is decreased in chronically ethanolfed animals. Oxidative stress in mitochondria leads to mitochondrial DNA damage and has a dual effect on apoptosis. Role of Kupffer cells in alcohol-induced liver injury. Chronic ethanol consumption is associated with increased release of endotoxin from gut lumen into portal circulation. Endotoxin activates Kupffer cells, which then release proinflammatory cytokines and oxidants. Role of neutrophils in alcohol-induced liver injury. Alcoholic liver injury leads to the accumulation of neutrophils, which release reactive oxygen species and lysosomal enzymes and contribute to hepatocyte damage and necrosis. Role of nitric oxide in alcohol-induced oxidative stress. High amounts of nitric oxide contribute to the oxidative damage, mainly by generating peroxynitrites. Role of antioxidants in ethanol-induced oxidative stress. Chronic ethanol consumption is associated with reduced liver glutathione and α-tocopherol level and with reduced superoxide dismutase, catalase and glutathione peroxidase activity. Conclusion. Oxidative stress in alcoholic liver disease is a consequence of increased production of oxidants and decreased antioxidant defense in the liver.

/pdf/the-role-of-oxidative-stress-in-alcoholic-liver-injury-632k24714v.pdf

The role of oxidative stress in alcoholic liver injury

We report a study on the relation between open-field behavior and electroencephalographic (EEG) changes during lindane-induced seizures in 2-month-old adult male Wistar rats. For chronic EEG recordings and power spectra analysis, 3 electrodes were implanted into the skull. Three groups of animals, (i) saline-injected control (n = 6), (ii) DMSO-treated (n = 6), and (iii) lindane intraperitoneally administered: L4 (4 mg/kg, n = 10), L6 (6 mg/kg, n = 11), and L8 (8 mg/kg, n = 11), were observed for 30 min for the occurrence of convulsive behavior. It was assessed by incidence of motor seizures, and seizure severity grade was determined by a descriptive rating scale (0, no response; 1, head nodding, lower jaw twitching; 2, myoclonic body jerks, bilateral forelimb clonus with full rearing; 3, progression to generalized clonic convulsions followed by tonic extension of fore and hind limbs and tail; 4, status epilepticus). EEG signal and spectral analyses were suitable to describe the dynamics of complex behavio...

Danijela Vucevic

Papers

Betaine modulates oxidative stress, inflammation, apoptosis, autophagy, and Akt/mTOR signaling in methionine-choline deficiency-induced fatty liver disease.

Iron-based nanoparticles and their potential toxicity: Focus on oxidative stress and apoptosis

Effects of caloric restriction on oxidative stress parameters

The role of oxidative stress in alcoholic liver injury

Correlation between electrocorticographic and motor phenomena in lindane-induced experimental epilepsy in rats.