Test 1157: John Deere 2630 and 2640 Diesel

EXPLANATION OF TEST REPORT GENERAL CONDITIONS East tractor is a production model equipped for common usage. Power consuming accessories can be disconnected only when it is convenient for the operator to do so in practice. Additional weight can be added as ballast if the manufacturer regularly supplies it for sale. The static tire loads and the inflation pressures muse conform to recommendations in the Tire Standards published by the Society of Automotive Engineers. PREPARATION FOR PERFORMANCE RUNS The engine crank case is drained and refilled with a measured amount of new oil conforming to specifications in the operator’s manual. The fuel used and the maintenance operations must also conform to the published information delivered with the tractor. The tractor is then limbered-up for 1 hour on drawbar work in accordance with the manufacturers published recommendations. The manufacturer’s representative is present to make appropriate decisions regarding mechanical adjustments. The tractor is equipped with approximately the amount of added ballast that is used during maximum drawbar tests. The tire tread-bar height must be at least 65% of new tread height prior to the maximum power run. BELT OR POWER TAKE-OFF PERFORMANCE Maximum Power and Fuel Consumption. The manufacturer’s representative makes carburetor, fuel pump, ignition and governor control settings which remain unchanged throughout tall subsequent runs. The governor and the manually operated governor control lever is set to provide the high-idle speed specified by the manufacturer for maximum power. Maximum power is measured by connecting the belt pulley or the power take-off to a dynamometer. The dynamometer load is then gradually increased until the engine is operating at the rated speed specified by the manufacturer for maximum power. The corresponding fuel consumption is measured. Varying Power and Fuel Consumption. Six different horsepower levels are used to show corresponding fuel consumption rates and how the governor causes the engine to react to the following changes in dynamometer load: 85% of the dynamometer torque at maximum power; minimum dynamometer torque, ½ the 85% torque; maximum power; ¼ and ¾ of the 85% torque. Since at tractor is generally subjected to varying loads the average of the results in this test serve well for predicting the fuel consumption of a tractor in general usage. DRAWBAR PERFORMANCE All engine adjustments are the same as those used in the belt or power take-off tests. If the manufacturer specifies a different rated crankshaft speed for drawbar operations, then the position of the manually operated governor control is changed to provide the high-idle speed specified by the manufacturer in the operating instructions. Varying Power and Fuel Consumption With Ballast. The varying power runs are made to show the effect of speed-control devices (engine governor, automatic transmissions, etc.) on horsepower, speed and fuel consumption. These runs are made around the entire test course with has two 180 degree turns with a minimum radius of 50 feet. The drawbar pull is set at 3 different levels as follows: (1) as near to the pull a maximum power as possible and still have the tractor maintain the travel speed at maximum horsepower on the straight sections of the test course; (2) 75% of the pull at maximum power; and (3) 50% of the pull at maximum power. Prior to 1958, fuel consumption data (10 hour test) were shown only for the pull obtained at maximum power for tractors having torque converters and at 75% of the pull obtained at maximum power for gear-type tractors. Maximum Power With Ballast. Maximum power is measured on straight level sections of the test course. Data are shown for not more that 12 different gears or travel speeds. Some gears or travel speeds may be omitted because of high slippage of the traction members or because the travel speed may exceed the safe-limit for the test course. The maximum safe speed for the Nebraska Test course has been set at 15 miles per hour. The slippage limits have been set at 15% and 7% for pneumatic tires and steel tracks or lugs, respectively. Higher slippage gives widely varying results. Maximum Power Without Ballast. All added ballast is removed from the tractor. The maximum drawbar power of the tractor is determined by the same procedure used for getting maximum power with ballast. The gear (or travel speed) is the same as that used in the 10-hours test. Varying Power and Travel Speed With Ballast. Travel speeds corresponding to drawbar pulls beyond the maximum power range are obtained to show the “lugging ability” of the tractor. The run starts with the pull at maximum power; then additional drawbar pull is applied to cause decreasing speeds. The run is ended by one of three conditions; (1) maximum pull is obtained, (2) the maximum slippage limit is reached, or (3) some other operating limit is reached

Hypothalamic AgRP-neurons control peripheral substrate utilization and nutrient partitioning

Obesity-related diseases such as diabetes and dyslipidemia result from metabolic alterations including the defective conversion, storage and utilization of nutrients, but the central mechanisms that regulate this process of nutrient partitioning remain elusive. As positive regulators of feeding behaviour, agouti-related protein (AgRP) producing neurons are indispensible for the hypothalamic integration of energy balance. Here, we demonstrate a role for AgRP-neurons in the control of nutrient partitioning. We report that ablation of AgRP-neurons leads to a change in autonomic output onto liver, muscle and pancreas affecting the relative balance between lipids and carbohydrates metabolism. As a consequence, mice lacking AgRP-neurons become obese and hyperinsulinemic on regular chow but display reduced body weight gain and paradoxical improvement in glucose tolerance on high-fat diet. These results provide a direct demonstration of a role for AgRP-neurons in the coordination of efferent organ activity and nutrient partitioning, providing a mechanistic link between obesity and obesity-related disorders

Marseille, capitale ?

Alexandre Clapier, Marseille, son passé, son présent et son avenir, Paris, 1863, p. 81-87. … Le commerce de Marseille a prospéré tant que Marseille a tenu en ses mains son gouvernement et réglé ses intérêts. Ainsi de la chute de Carthage à la chute de l’empire romain, Marseille va grandissant sans cesse, parce qu’elle obéit à ses magistrats et à ses lois ; aux temps des croisades, elle prend un accroissement rapide, parce qu’à l’exemple des républiques italiennes, elle conquiert son indépenda..

Endoplasmic reticulum stress induces cardiac dysfunction through architectural modifications and alteration of mitochondrial function in cardiomyocytes

International audienceAims: Endoplasmic reticulum (ER) stress has recently emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases. However, the molecular mechanisms by which ER stress leads to cardiac dysfunction remain poorly understood. Methods and results: In the present study, we evaluated the early cardiac effects of ER stress induced by tunicamycin (TN) in mice. Echocardiographic analysis indicated that TN-induced ER stress led to a significant impairment of the cardiac function. Electron microscopic observations revealed that ultrastructural changes of cardiomyocytes in response to ER stress manifested extensively at the level of the reticular membrane system. Smooth tubules of sarcoplasmic reticulum in connection with short sections of rough endoplasmic reticulum were observed. The presence of rough instead of smooth reticulum was increased at the interfibrillar space, at the level of dyads and in the vicinity of mitochondria. At the transcriptional level, ER stress resulted in a substantial decrease in the expression of the major regulator of mitochondrial biogenesis PGC-1α and of its targets NRF1, Tfam, CS and COXIV. At the functional level, ER stress also induced an impairment of mitochondrial Ca 2+ uptake, an alteration of mitochondrial oxidative phosphorylation and a metabolic remodeling characterized by a shift from fatty acid to glycolytic substrate consumption. Conclusion: Our findings show that ER stress induces cytoarchitectural and metabolic alterations in cardiomyocytes and provide evidences that ER stress could represent a primary mechanism that contributes to the impairment of energy metabolism reported in most cardiac diseases

: OPA1 deficit and cardiac mitochondria

International audienceAIMS: The optic atrophy 1 (OPA1) protein is an essential protein involved in the fusion of the mitochondrial inner membrane. Despite its high level of expression, the role of OPA1 in the heart is largely unknown. We investigated the role of this protein in Opa1(+/-) mice, having a 50% reduction in OPA1 protein expression in cardiac tissue. METHODS AND RESULTS: In mutant mice, cardiac function assessed by echocardiography was not significantly different from that of the Opa1(+/+). Electron and fluorescence microscopy revealed altered morphology of the Opa1(+/-) mice mitochondrial network; unexpectedly, mitochondria were larger with the presence of clusters of fused mitochondria and altered cristae. In permeabilized mutant ventricular fibres, mitochondrial functional properties were maintained, but direct energy channelling between mitochondria and myofilaments was weakened. Importantly, the mitochondrial permeability transition pore (PTP) opening in isolated permeabilized cardiomyocytes and in isolated mitochondria was significantly less sensitive to mitochondrial calcium accumulation. Finally, 6 weeks after transversal aortic constriction, Opa1(+/-) hearts demonstrated hypertrophy almost two-fold higher (P< 0.01) than in wild-type mice with altered ejection fraction (decrease in 43 vs. 22% in Opa1(+/+) mice, P< 0.05). CONCLUSIONS: These results suggest that, in adult cardiomyocytes, OPA1 plays an important role in mitochondrial morphology and PTP functioning. These properties may be critical for cardiac function under conditions of chronic pressure overload

Hypothalamic AgRP-neurons control peripheral substrate utilization and nutrient partitioning

International audienceObesity-related diseases such as diabetes and dyslipidemia result from metabolic alterations including the defective conversion, storage and utilization of nutrients, but the central mechanisms that regulate this process of nutrient partitioning remain elusive. As positive regulators of feeding behaviour, agouti-related protein (AgRP) producing neurons are indispensible for the hypothalamic integration of energy balance. Here, we demonstrate a role for AgRP-neurons in the control of nutrient partitioning. We report that ablation of AgRP-neurons leads to a change in autonomic output onto liver, muscle and pancreas affecting the relative balance between lipids and carbohydrates metabolism. As a consequence, mice lacking AgRP-neurons become obese and hyperinsulinemic on regular chow but display reduced body weight gain and paradoxical improvement in glucose tolerance on high-fat diet. These results provide a direct demonstration of a role for AgRP-neurons in the coordination of efferent organ activity and nutrient partitioning, providing a mechanistic link between obesity and obesity-related disorders

SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation

Over the past decade, endoplasmic reticulum (ER) stress has emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases including heart failure. Cardiac therapy based on ER stress modulation is viewed as a promising avenue toward effective therapies for the diseased heart. Here, we tested whether sirtuin-1 (SIRT1), a NAD(+)-dependent deacetylase, participates in modulating ER stress response in the heart. Using cardiomyocytes and adult-inducible SIRT1 knockout mice, we demonstrate that SIRT1 inhibition or deficiency increases ER stress-induced cardiac injury, whereas activation of SIRT1 by the SIRT1-activating compound STAC-3 is protective. Analysis of the expression of markers of the three main branches of the unfolded protein response (i.e., PERK/eIF2α, ATF6 and IRE1) showed that SIRT1 protects cardiomyocytes from ER stress-induced apoptosis by attenuating PERK/eIF2α pathway activation. We also present evidence that SIRT1 physically interacts with and deacetylates eIF2α. Mass spectrometry analysis identified lysines K141 and K143 as the acetylation sites on eIF2α targeted by SIRT1. Furthermore, mutation of K143 to arginine to mimic eIF2α deacetylation confers protection against ER stress-induced apoptosis. Collectively, our findings indicate that eIF2α deacetylation on lysine K143 by SIRT1 is a novel regulatory mechanism for protecting cardiac cells from ER stress and suggest that activation of SIRT1 has potential as a therapeutic approach to protect the heart against ER stress-induced injury