In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

[Q]: Context: To assess the effect of six different enteral diets on the gut barrier.', 'Laboratory study.', 'University hospital, Germany.', '70 Specific pathogen free female Crl:CDR BR rats.', 'For 7 days, 6 groups of rats were fed orally with standard chow (n = 15); total parenteral nutrition solution (oral TPN, n = 15); elemental diet (ED, n = 10); nutrient-defined diet (NDD, n = 10); or the NDD supplemented with uracil (NDD+uracil, n = 10), or fibre (NDD+fibre, n = 10).', 'Bacterial translocation to mesenteric lymph nodes, numbers of Gram negative enterobacteria and total aerobic bacteria in the caecum, and intestinal concentrations of secretory IgA.', 'The incidence of bacterial translocation was significantly increased in the groups given oral TPN, ED, NDD, and NDD+uracil compared with the group given chow. Only NDD+fibre resulted in a similar degree of translocation to that in the chow group. All groups in which there was increased translocation had a highly significant overgrowth of aerobic bacteria in the caecum, mainly by Gram negative enteric organisms. The secretory IgA concentration was reduced in the group that had been given oral TPN, and that in the ED and NDD+uracil groups was similar to that in the chow group. NDD and NDD+fibre were associated with higher intestinal concentrations of secretory IgA than chow.\Question: Is fibre an essential ingredient of enteral diets to limit bacterial translocation in rats?
[A]: Fibre-free enteral diets do not protect the gut antimicrobial barrier whatever else is in them. The superiority of early enteral as opposed to parenteral nutrition after injury may, therefore, not be the result of a specific protective effect on the gut barrier. The supplementation of commercial enteral diets with bulk fibre should be tested in clinical trials.


[Q]: Context: Inflammation has been implicated in the initiation, progression and manifestation of hypertensive heart disease. We sought to determine the role of monocytes/macrophages in hypertension and pressure overload induced left ventricular (LV) remodeling.', 'We used two models of LV hypertrophy (LVH). First, to induce hypertension and LVH, we fed Sabra salt-sensitive rats with a high-salt diet. The number of macrophages increased in the hypertensive hearts, peaking at 10 weeks after a high-salt diet. Surprisingly, macrophage depletion, by IV clodronate (CL) liposomes, inhibited the development of hypertension. Moreover, macrophage depletion reduced LVH by 17% (p<0.05), and reduced cardiac fibrosis by 75%, compared with controls (p=0.001). Second, to determine the role of macrophages in the development and progression of LVH, independent of high-salt diet, we depleted macrophages in mice subjected to transverse aortic constriction and pressure overload. Significantly, macrophage depletion, for 3 weeks, attenuated LVH: a 12% decrease in diastolic and 20% in systolic wall thickness (p<0.05), and a 13% in LV mass (p=0.04), compared with controls. Additionally, macrophage depletion reduced cardiac fibrosis by 80% (p=0.006). Finally, macrophage depletion down-regulated the expression of genes associated with cardiac remodeling and fibrosis: transforming growth factor beta-1 (by 80%) collagen type III alpha-1 (by 71%) and atrial natriuretic factor (by 86%).\Question: Do macrophages dictate the progression and manifestation of hypertensive heart disease?
[A]: Macrophages mediate the development of hypertension, LVH, adverse cardiac remodeling, and fibrosis. Macrophages, therefore, should be considered as a therapeutic target to reduce the adverse consequences of hypertensive heart disease.


[Q]: Context: Hydrogen peroxide is enzymatically processed by catalase, and catalase deficiency in blood is known as acatalasemia. We examined whether low catalase activity is a risk factor for diabetes mellitus.', 'Blood glucose, insulin and glucose tolerance test were examined in acatalasemic and normal mice under non-stress and oxidative stress conditions. Alloxan administration was used as oxidative stress.', 'Alloxan, which was a drug that caused diabetes mellitus, mostly generated hydrogen peroxide by the reaction of alloxan and reduced glutathione, in vitro. Incidence of hyperglycemia in alloxan-untreated acatalasemic mice was as low as that in the normal mice. However, the incidence of acatalasemia mice treated with alloxan was higher than that in normal mice, and the number of pancreatic beta-cells in the acatalasemic mice was less than that in normal mice.\Question: Is low catalase activity in blood associated with the diabetes caused by alloxan?
[A]:
These results indicate that low catalase activity in the blood is associated with the diabetes mellitus caused by alloxan administration.