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Articles by J Dong
Total Records ( 2 ) for J Dong
  J Dong , Y Li , Z Yang and J. Luo
 

Background and objectives: To explore the correlation between dietary sodium intake and cardiovascular and overall mortality, and then determine whether this correlation can be explained by protein and energy intake paralleled with sodium intake in dialysis patients.

Design, setting, participants, & measurements: This single-center retrospective cohort study enrolled 305 incident patients who started peritoneal dialysis in our unit from July 2002 to February 2007. All patients were followed until death or until being censored in February 2008. Demographic data were collected at baseline. Biochemical, dietary, and nutrition data were examined at baseline and thereafter at regular intervals to calculate the average values throughout the study.

Results: Participants with the highest average sodium intake were more likely to be younger, male, and overweight. Patients in the high tertile of average sodium intake had higher albumin, prealbumin, and lean body mass levels, and more nutrient intakes paralleling with sodium intake. Low average sodium intake independently predicted the increased risk for overall and cardiovascular death after adjusting for recognized confounders. Further adjustment for dietary protein, energy, and other nutrient intakes individually had minimal impact on the association between average sodium intake and overall death, with hazard ratios varying between 0.35 and 0.44, and cardiovascular death, with hazard ratios varying between 0.06 and 0.11.

Conclusions: This study revealed that low dietary sodium intake independently predicts the high overall and cardiovascular mortality in dialysis patients. This correlation could not be entirely explained by deficient protein and energy intake.

  J Dong , E Jimi , C Zeiss , M. S Hayden and S. Ghosh
 

NF-B is well established as a key component of the inflammatory response. However, the precise mechanisms through which NF-B activation contributes to inflammatory disease states remain poorly defined. To test the role of NF-B in inflammation, we created a knock-in mouse that expresses a constitutively active form of NF-B p65 dimers. These mice are born at normal Mendelian ratios, but display a progressive, systemic hyperinflammatory condition that results in severe runting and, typically, death 8–20 d after birth. Examination of homozygous knock-in mice demonstrates significant increases in proinflammatory cytokines and chemokines. Remarkably, crossing this strain with mice lacking TNF receptor 1 (TNFR1) leads to a complete rescue of the hyperinflammatory phenotype. However, upon aging, these rescued mice begin to display chronic keratitis accompanied by increased corneal expression of TNF, IL-1β, and MMP-9, similar to that seen in human keratoconjunctivitis sicca (KCS) or "dry eyes." Therefore, our results show that, while constitutively active NF-B can trigger systemic inflammation, it does so indirectly, through increased TNF production. However, certain inflammatory disease states, such as keratitis or KCS, a condition that is seen in Sjogren's syndrome, are dependent on NF-B, but are independent of TNFR1 signaling.

 
 
 
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