Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS

Introduction Hepatic macrophages (Kupffer cells) undergo inflammatory activation during the development of portal hypertension in experimental cirrhosis; this activation may play a pathogenic role or be an epiphenomenon. Our objective was to study serum soluble CD163 (sCD163), a sensitive marker of macrophage activation, before and after reduction of portal venous pressure gradient by insertion of a transjugular intrahepatic portosystemic shunt (TIPS) in patients with cirrhosis. Methods sCD163 was measured in 11 controls and 36 patients before and 1, 4 and 26 weeks after TIPS. We used lipopolysaccharide binding protein (LBP) levels as a marker of endotoxinaemia. Liver function and clinical status of the patients were assessed by galactose elimination capacity and Model for End Stage Liver Disease score. Results The sCD163 concentration was more than threefold higher in the patients than in the controls (median 5.22 mg/l vs 1.45 mg/l, p<0.001). The sCD163 was linearly related to the portal venous pressure gradient (r(2)=0.24, p<0.001), also after adjustment for cirrhosis status. The sCD163 concentration was 12% higher in the hepatic than in the portal vein (p<0.02). The LBP level was 70% higher in the patients (52.2 vs 30.4 mu g/l, p<0.001). During follow-up after TIPS, the sCD163 concentration did not change while LBP almost normalised. Conclusion Kupffer cells were activated in patients with liver cirrhosis in parallel with their portal hypertension. The activation was not alleviated by the mechanical reduction of portal hypertension and the decreasing signs of endotoxinaemia. The findings suggest that Kupffer cell activation is a constitutive event that may play a pathogenic role for portal hypertension

Can Aerobic Training Improve Muscle Strength and Power in Older Men?

This study examined the effect of aerobic training on leg strength, power, and muscle mass in previously sedentary, healthy older men (70-80 yr). Training consisted of 30-45 min of cycle ergometry at 50-70... maximal oxygen consumption (VO2max), 3 times weekly for 16 wk, then 4 wk detraining, or assignment to a nontraining control group (n...12 both groups). Training increased leg strength, leg power, upper leg muscle mass, and VO2max above pretraining values (21..., 12..., 4..., and 15..., respectively; p....05). However, all gains were lost after detraining, except for some gain in VO2max. This suggests that cycle ergometry is sufficient stimulus to improve neuromuscular function in older men, but gains are quickly lost with detraining. For the older population cycle ergometry provides the means to not only increase aerobic fitness but also increase leg strength and power and upper leg muscle mass. However, during periods of inactivity neuromuscular gains are quickly lost

Dynamics of the coastal zone

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