Verbazingwekkende groei na spenen: studieavond 'Grote korrel voor kleine big'

Toen dr. Henry van den Brand (Wageningen University) beweerde dat grote korrels bij zogende biggen voor hogere voeropname en groei leiden, geloofde niemand hem. Inmiddels produceert Coppens diervoeding een korrel van 15 millimeter doorsnee voor jonge biggen. Resultaten van de eerste praktijkproeven tonen aan dat de groei na spenen hoog i

Biggenkorrel in paardenformaat

Varkenshouder Lei Hermans voert zijn zogende biggen geen hagelslagvoer meer, maar korrels met een doorsnee van 15 milimeter. "Het was even wenne, maar ik ga er zeker mee door. De biggen zijn gezonder en de groei na spenen is enorm gestegen.

Verbazingwekkende groei na spenen: studieavond 'Grote korrel voor kleine big'

Toen dr. Henry van den Brand (Wageningen University) beweerde dat grote korrels bij zogende biggen voor hogere voeropname en groei leiden, geloofde niemand hem. Inmiddels produceert Coppens diervoeding een korrel van 15 millimeter doorsnee voor jonge biggen. Resultaten van de eerste praktijkproeven tonen aan dat de groei na spenen hoog i

Effect of vagus nerve stimulation on tissue damage and function loss in a mouse myocardial ischemia-reperfusion model

Objectives: In cardiac ischemia, acute inflammatory responses further increase the detrimental effect on myocardial tissue. Since vagus nerve stimulation (VS) attenuates inflammatory responsiveness this study examines the effect of VS on myocardial damage development in a cardiac ischemia-reperfusion (IR) mouse model. Methods: 54 male C57Bl/6j mice were subjected to an IR procedure with or without prior VS. The effects on inflammatory responsiveness, infarct size, cardiac function, neutrophils, lymphocytes and vascular endothelial growth factor (VEGF) in the infarcted myocardium were measured at 48 h after intervention. Group results were compared with unpaired Mann-Whitney or Kruskall-Wallis test. Results: A significant decrease in inflammatory responsiveness was not verified by decreased TNFα levels in blood from VS and IR treated mice. The percentage infarct size over area at risk was smaller in the group with VS + IR compared with IR (22.4 ± 10.2% vs 37.6 ± 9.0%, p = 0.003). The degree of the reduction in cardiac function was not different between the IR groups with or without VS and no group differences were found in amounts of neutrophils, CD3+ lymphocytes and VEGF in the reperfused mouse heart. Conclusion: The present study does not provide clear evidence of a reducing role for VS on cardiac function loss. This could mean that VS has a less inhibiting effect on myocardial inflammation than may be expected from the literature

23Na chemical shift imaging and Gd enhancement of myocardial edema

Myocardial edema can arise in several disease states. MRI contrast agent can accumulate in edematous tissue, which complicates differential diagnosis with contrast-enhanced (CE)-MRI and might lead to overestimation of infarct size. Sodium Chemical Shift Imaging ((23)Na-CSI) may provide an alternative for edema imaging. We have developed a non-infarct, isolated rat heart model with two levels of edema, which was studied with (23)Na-CSI and CE-MRI. In edematous, but viable tissue the extracellular sodium (Na (e) (+)) signal is hypothesized to increase, but not the intracellular sodium (Na (i) (+)) signal. Isolated hearts were perfused at 60 (n = 6) and 140 mmHg (n = 5). Dimethyl methylphosphonate (DMMP) and phenylphosphonate (PPA) were used to follow edema formation by (31)P-MR Spectroscopy. In separate groups, Thulium(III)1,4,7,10 tetraazacyclododecane-N,N',N″,N'''-tetra(methylenephosphonate) (TmDOTP(5-)) and Gadovist were used for (23)Na-CSI (n = 8) and CE-MRI (n = 6), respectively. PPA normalized signal intensity (SI) was higher at 140 versus 60 mmHg, with a ratio of 1.27 ± 0.12 (p <0.05). The (DMMP-PPA)/dry weight ratio, as a marker of intracellular volume, remained unchanged. The mid-heart cross sectional area (CSA) of the left ventricle (LV) was significantly increased at 140 mmHg. In addition, at 140 mmHg, the LV Na (e) (+) SI increased with a 140 mmHg/60 mmHg ratio of 1.24 ± 0.18 (p <0.05). Na (i) (+) SI remained essentially unchanged. With CE-MRI, a subendocardially enhanced CSA was identified, increasing from 0.20 ± 0.02 cm(2) at 60 mmHg to 0.31 ± 0.02 cm(2) at 140 mmHg (p <0.05). Edema shows up in both CE-MRI and Na (e) (+) . High perfusion pressure causes more edema subendocardially than subepicardially. (23)Na-CSI is an attractive alternative for imaging of edema and is a promising tool to discriminate between edema, acute and chronic M

Toll-like receptor 4 mediates maladaptive left ventricular remodeling and impairs cardiac function after myocardial infarction

Left ventricular (LV) remodeling leads to congestive heart failure and is a main determinant of morbidity and mortality following myocardial infarction. Therapeutic options to prevent LV remodeling are limited, which necessitates the exploration of alternative therapeutic targets. Toll-like receptors (TLRs) serve as pattern recognition receptors within the innate immune system. Activation of TLR4 results in an inflammatory response and is involved in extracellular matrix degradation, both key processes of LV remodeling following myocardial infarction. To establish the role of TLR4 in postinfarct LV remodeling, myocardial infarction was induced in wild-type BALB/c mice and TLR4-defective C3H-Tlr4(LPS-d) mice. Without affecting infarct size, TLR4 defectiveness reduced the extent of LV remodeling (end-diastolic volume: 103.7+/-6.8 microL versus 128.5+/-5.7 microL; P <0.01) and preserved systolic function (ejection fraction: 28.2+/-3.1% versus 16.6+/-1.3%; P <0.01), as assessed by MRI. In the noninfarcted area, interstitial fibrosis, and myocardial hypertrophy were reduced in C3H-Tlr4(LPS-d) mice. In the infarcted area, however, collagen density was increased, which was accompanied by fewer macrophages, reduced inflammation regulating cytokine expression levels (interleukin [IL]-1alpha, IL-2, IL-4, IL-5, IL-6, IL-10, IL-17, tumor necrosis factor-alpha, interferon-gamma, granulocyte/macrophage colony-stimulating factor), and reduced matrix metalloproteinase-2 (4684+/-515 versus 7573+/-611; P=0.002) and matrix metalloproteinase-9 activity (76.0+/-14.3 versus 168.0+/-36.2; P=0.027). These data provide direct evidence for a causal role of TLR4 in postinfarct maladaptive LV remodeling, probably via inflammatory cytokine production and matrix degradation. TLR4 may therefore constitute a novel target in the treatment of ischemic heart failur