Investigation of Head Kinematics and Brain Strain Response During Soccer Heading Using a Custom-Fit Instrumented Mouthguard.

Association football, also known as soccer in some regions, is unique in encouraging its participants to intentionally use their head to gain a competitive advantage, including scoring a goal. Repetitive head impacts are now being increasingly linked to an inflated risk of developing long-term neurodegenerative disease. This study investigated the effect of heading passes from different distances, using head acceleration data and finite element modelling to estimate brain injury risk. Seven university-level participants wore a custom-fitted instrumented mouthguard to capture linear and angular acceleration-time data. They performed 10 headers within a laboratory environment, from a combination of short, medium, and long passes. Kinematic data was then used to calculate peak linear acceleration, peak angular velocity, and peak angular acceleration as well as two brain injury metrics: head injury criterion and rotational injury criterion. Six degrees of freedom acceleration-time data were also inputted into a widely accepted finite element brain model to estimate strain-response using mean peak strain and cumulative strain damage measure values. Five headers were considered to have a 25% concussion risk. Mean peak linear acceleration equalled 26 ± 7.9 g, mean peak angular velocity 7.20 ± 2.18 rad/s, mean peak angular acceleration 1730 ± 611 rad/s2, and 95th percentile mean peak strain 0.0962 ± 0.252. Some of these data were similar to brain injury metrics reported from American football, which supports the need for further investigation into soccer heading.

Maternal dietary fat type influences the growth and fatty acid composition of newborn and weanling rats.

To determine whether the long-term consumption of different amounts or types of fat by female rats affects the growth and development of their progeny, Wistar rats were fed from weaning either a low fat diet (4.5% by weight) or one of three high fat (32%) diets containing predominantly beef tallow (high saturated fat), corn oil (high polyunsaturated fat) or equal portions of tallow and corn oil (high mixed fat). Offspring were killed at birth or weaning. Weight of newborn pups was lower with maternal consumption of high polyunsaturated fat diets. Carcass composition of newborn pups and body weight of weanling rats was unaffected by maternal diet. The percentage of carcass lipid was greater in weanling rats from all high fat-fed dams. In both newborn pups and weanling rats, percent composition in carcass lipids of 16:0, 16:1 and 18:1 fatty acids generally decreased and 18:2 increased as the high fat maternal diet became more unsaturated. The consumption of diets high in polyunsaturated fatty acids prior to and throughout gestation thus seemed to have a transitory effect on reducing fetal growth in rats.

Effect of fatty acid supplementation on cholesterol and retinol esterification in J774 macrophages.

J774 macrophages exposed to medium containing cholesterol-rich phospholipid dispersions accumulate cholesteryl ester. Supplementing this medium with 100 micrograms oleate/ml increased cellular cholesteryl ester contents 3-fold. Cell retinyl ester contents increased 8-fold when medium containing retinol dispersed in dimethyl sulfoxide was supplemented with oleate. These increases were not the result of increases in total lipid uptake by the cells but rather of redistribution of cholesterol and retinol into their respective ester pools. Effective oleate concentration of 15-30 micrograms/ml increased cellular retinyl and cholesteryl ester contents. The effective oleate concentration was reduced to 5 micrograms/ml when the fatty acid/albumin molar ratio was increased. The oleate-stimulated increase in cholesterol esterification was blocked by incubating cells with Sandoz 58-035, a specific inhibitor of acyl-CoA:cholesterol acyltransferase (ACAT), indicating that the effect of fatty acid exposure is mediated through changes in ACAT activity. When cholesterol or retinol was added to cells which had been exposed to oleate for 24 h to provide a triacylglycerol store, the cellular contents of cholesteryl or retinyl ester were also significantly increased compared to cells not previously exposed to oleate. The oleate-stimulated increase in the esterification of cholesterol and/or retinol was also observed in P388D1 macrophages, human (HepG2) and rat (Fu5AH) hepatomas, human fibroblasts, rabbit aortic smooth muscle cells and MCF-7 breast carcinoma cells. In addition to oleate, a number of other fatty acids increased retinol esterification in J774 macrophages; however, cellular cholesterol esterification in these cells was increased only by unsaturated fatty acids and was inhibited in the presence of saturated fatty acids. Although the cellular uptake of radiolabeled oleate and palmitate was similar, a significant difference in the distribution of these fatty acids among the lipid classes was observed. These data demonstrate that exogenous fatty acids are one factor that regulate cellular cholesteryl and retinyl ester contents in cultured cells.

Physical state of cholesteryl esters deposited in cultured macrophages.

J774 macrophages load with cholesteryl ester (CE) when incubated with acetylated low-density lipoprotein and cholesterol-rich liposomes; the CE accumulates as cytoplasmic inclusions 1-2 micron in diameter. The CE core of the droplet comprises about 90% of its mass; the predominant CE species present are cholesteryl palmitate (CP, 41%) and cholesteryl oleate (CO, 37%). The thermotropic properties of the inclusions, both in intact cells and after isolation, have been characterized by differential scanning calorimetry. On heating, the inclusions exhibit two endothermic transitions at about 41 and 53 degrees C with a total enthalpy of 7.7 +/- 1.2 cal/g of CE. Very similar thermal behavior is exhibited by a binary mixture containing equal weights of CO and CP; this indicates that these two species dominate the phase behavior of CE in J774 inclusions. A phase diagram for the CO/CP system has been generated, and this reflects simple eutectic behavior. The eutectic is 83% w/w CO, and it melts at 49-50 degrees C. Below this temperature, CO and CP form two immiscible crystalline phases due to the very limited ability of the unsaturated oleate and saturated palmitate acyl chains to mix in the crystal phase. On heating a 1/1 w/w CO/CP mixture, an isotropic liquid of eutectic composition forms at 49 degrees C, and the remaining crystalline cholesteryl palmitate melts over the temperature range 50-69 degrees C. The phase diagram indicates that bulk mixtures of CE molecules in J774 inclusions should be crystalline at 37 degrees C, the growth temperature of the cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Incubation of acetylated low-density lipoprotein with cholesterol-rich dispersions enhances cholesterol uptake by macrophages.

Incubation of J774 macrophages with mixtures of acetylated low-density lipoprotein (acLDL) and free cholesterol-rich phospholipid dispersions increases cellular cholesterol deposition 2-4-fold over that achieved with either acLDL or dispersions alone. Both free and esterified cholesterol accumulate in cells incubated with the mixture of acLDL and dispersions. A similar result is observed when acLDL is replaced by malondialdehyde-LDL. The enhanced deposition of cholesterol is not unique to J774 macrophages, as P388D1 macrophages also accumulate more cholesterol when incubated with the mixture of acLDL and dispersions than either particle alone. A preincubation of the particles for at least 6 h prior to incubation with cells is required in order to observe maximal cholesterol delivery. Both dispersion free cholesterol and phospholipid accumulate in J774 cells, suggesting that a complex is formed between acLDL and dispersions which results in a cholesterol-rich acLDL/dispersion particle. Partial purification of the acLDL-dispersion complex revealed increases in the size distribution of the particles compared to acLDL and increases in free cholesterol and phospholipid contents. Cholesterol uptake from the mixture of acLDL and dispersions was saturable and the enhanced cellular uptake of both cholesterol and phospholipid from the complex could be abolished by inhibitors of the scavenger receptor pathway. In addition to the receptor-mediated uptake of cholesterol from the acLDL-dispersion complex, it was observed that approx. 30% of the total cholesterol uptake from the complex was via non-specific components, including surface transfer.