A long-standing association exists between elevated triglyceride levels and cardiovascular disease* (CVD).1,2 However, the extent to which triglycerides directly promote CVD or represent a biomarker of risk has been debated for 3 decades.3 To this end, 2 National Institutes of Health consensus conferences evaluated the evidentiary role of triglycerides in cardiovascular risk assessment and provided therapeutic recommendations for hypertriglyceridemic states.4,5 Since 1993, additional insights have been made vis-a-vis the atherogenicity of triglyceride-rich lipoproteins (TRLs; ie, chylomicrons and very low-density lipoproteins), genetic and metabolic regulators of triglyceride metabolism, and classification and treatment of hypertriglyceridemia. It is especially disconcerting that in the United States, mean triglyceride levels have risen since 1976, in concert with the growing epidemic of obesity, insulin resistance (IR), and type 2 diabetes mellitus (T2DM).6,7 In contrast, mean low-density lipoprotein cholesterol (LDL-C) levels have receded.7 Therefore, the purpose of this scientific statement is to update clinicians on the increasingly crucial role of triglycerides in the evaluation and management of CVD risk and highlight approaches aimed at minimizing the adverse public health–related consequences associated with hypertriglyceridemic states. This statement will complement recent American Heart Association scientific statements on childhood and adolescent obesity8 and dietary sugar intake9 by emphasizing effective lifestyle strategies designed to lower triglyceride levels and improve overall cardiometabolic health. It is not intended to serve as a specific guideline but will be of value to the Adult Treatment Panel IV (ATP IV) of the National Cholesterol Education Program, from which evidence-based guidelines will ensue. Topics to be addressed include epidemiology and CVD risk, ethnic and racial differences, metabolic determinants, genetic and family determinants, risk factor correlates, and effects related to nutrition, physical activity, and lipid medications.

In the United States, the National Health and …

https://www.ahajournals.org/doi/pdf/10.1161/CIR.0b013e3182160726

Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association

Copper Homeostasis and Neurodegenerative Disorders (Alzheimer's, Prion, and Parkinson's Diseases and Amyotrophic Lateral Sclerosis)

Oxidative stress is considered a major contributor to etiology of both "normal" senescence and severe pathologies with serious public health implications. Mitochondria generate reactive oxygen species (ROS) that are thought to augment intracellular oxidative stress. Mitochondria possess at least nine known sites that are capable of generating superoxide anion, a progenitor ROS. Mitochondria also possess numerous ROS defense systems that are much less studied. Studies of the last three decades shed light on many important mechanistic details of mitochondrial ROS production, but the bigger picture remains obscure. This review summarizes the current knowledge about major components involved in mitochondrial ROS metabolism and factors that regulate ROS generation and removal. An integrative, systemic approach is applied to analysis of mitochondrial ROS metabolism, which is now dissected into mitochondrial ROS production, mitochondrial ROS removal, and mitochondrial ROS emission. It is suggested that mitochondria augment intracellular oxidative stress due primarily to failure of their ROS removal systems, whereas the role of mitochondrial ROS emission is yet to be determined and a net increase in mitochondrial ROS production in situ remains to be demonstrated.

/pdf/mitochondrial-metabolism-of-reactive-oxygen-species-4bf4e010ud.pdf

Mitochondrial metabolism of reactive oxygen species.

α, α-diphenyl-β-picrylhydrazyl (DPPH) free radical scavenging method offers the first approach for evaluating the antioxidant potential of a compound, an extract or other biological sources. This is the simplest method, wherein the prospective compound or extract is mixed with DPPH solution and absorbance is recorded after a defined period. However, with the advancement and sophistication in instrumental techniques, the method has undergone various modifications to suit the requirements, even though the basic approach remains same in all of them. This article presents a critical review on various developments to the DPPH method.

/pdf/genesis-and-development-of-dpph-method-of-antioxidant-assay-vb625t39xs.pdf

Genesis and development of DPPH method of antioxidant assay

/pdf/triglycerides-and-cardiovascular-disease-a-scientific-25jmfgszcb.pdf

Triglycerides and Cardiovascular Disease : A Scientific Statement From the

Serum and plasma gave different electrophoretic patterns when enolase isoenzymes were evaluated by electrophoresis on cellulose acetate. Plasma isoenzyme bands were more intense, and there was an additional one (band P) that was not present in serum. We show that, under the conditions of electrophoresis, some of the residual platelets in the plasma are ruptured, releasing intracellular enolases and consequently leading to intensification of the isoenzyme bands. The band P originated from the remaining unruptured platelets. Thus plasma samples must be platelet-free for determination of enolase isoenzyme to be reliable.

Interference by platelets in the electrophoretic determination of enolase isoenzymes in plasma.

Translation of brain messenger ribonucleic acids in homologous, heterologous and mixed cell free systems.

A simple and rapid method, using only two chromatographic steps, is described for the purification and preparation of γγ enolase isoenzymes from human and beef brain extracts. In the first step, a crude γγ enolase was obtained by chromatography on Q-Sepharose Fast Flow column. The crude fraction was then purified by high performance anion exchange chromatography on a Mono-Q column. γγ enolase obtained in this manner was shown to be homogeneous by two dimensional polyacrylamide gel electrophoresis and by high performance gel permeation chromatography. The yield of γγ enolase by this method was 7–8 mg of pure enzyme per 100 g of brain.

Preparation and purification of gamma gamma enolase (neuron-specific enolase) using high performance anion exchange chromatography.

Conditioning studies involving administration of biochemical or pharmacological agents are often stressful to experimental animals. Some of these stressful manipulations were examined for their effect on the avoidance conditioning of the budgerigar to sound stimuli. There were individual variations in the capacity of the birds to accommodate to these stresses, but generally the stress factors had negative effects on their subsequent conditioning, the degree of this effect depending upon the type and severity of stress. Simple anesthesia with ether had the least effect, intravenous injection being next in severity, while intracerebral injection was most inhibitory. The effects due to anesthesia and intravenous injection could be decreased by delaying the conditioning procedure for 1 to 2 hours following the treatment, but the effect of intracerebral injection was more prolonged. The retrieval of temporarily lost conditioned response through brief reconditioning was not affected by intracerebral injection, indicating that, once a memory trace was formed, subsequent emotional and physical stresses did not obliterate it irreversibly.

Memory formation in birds: 2. Effects of stress due to experimental procedures on the conditioning of the budgerigar (Melopsittacus undulatus) to sound stimuli.

Publisher Summary This chapter describes the novel method for the fractionation of polysomes and mRNA that combines the resolving capacity of SDG centrifugation with the analytical versatility of a gel medium. In principle, the gradient in which polysomes are fractionated by centrifugation contains, in addition to the usual ingredients, other components that, by themselves, have no effect on the sedimentation of polysomes, but are able to solidify the gradient when an appropriate signal is given at the desired time. This is achieved by including in the medium a mixture of acrylamide, bisacrylamide (cross-linker), N,N,N',N'-tetramethylethylenediamine (TEMED; polymerization accelerator), and riboflavin (polymerization catalyst). The separation and entrapment of polysomes of different size, classes in a gel matrix in the above fashion, opens the way for the potential fine analysis of polysomes and their constituents (mRNA, rRNA, proteins) by the highly versatile techniques of polyacrylamide gel systems. This chapter concludes with scanning and quantitation of polysome bands.

[18] Characterization of polysomes and polysomal mRNAs by sucrose density gradient centrifugation followed by immobilization in polyacrylamide gel matrix

M.R. Ven Murthy

Papers

Interference by platelets in the electrophoretic determination of enolase isoenzymes in plasma.

Translation of brain messenger ribonucleic acids in homologous, heterologous and mixed cell free systems.

Preparation and purification of gamma gamma enolase (neuron-specific enolase) using high performance anion exchange chromatography.

Memory formation in birds: 2. Effects of stress due to experimental procedures on the conditioning of the budgerigar (Melopsittacus undulatus) to sound stimuli.

[18] Characterization of polysomes and polysomal mRNAs by sucrose density gradient centrifugation followed by immobilization in polyacrylamide gel matrix