Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These analyses examined the relationship between dementia and comorbid conditions with respect to degree of functional impairment and emotional impact. Analyses were conducted using National Health Interview Survey (2001 through 2005) data from a subset of individuals aged > or =60 years with activity limitations attributed to dementia, senility, or Alzheimer disease compared with those whose limitations were attributed to other conditions. The mean number of limited activities was 6.84 (95% confidence interval: 6.48-7.20) for persons with dementia-related limitations and 4.87 (95% confidence interval: 4.81-4.93) for those with limitations not dementia related. Both groups reported similar prevalence of diabetes, acute myocardial infarction, heart disease, prostate cancer, breast cancer, angina, and emphysema; respondents with dementia-related functional limitations were more likely to report diabetes, depression or anxiety, and vision problems as being related to functional limitations. Persons with dementia-related functional limitations were also more likely than persons with non-dementia-related functional limitations to report feeling sad, hopeless, worthless, nervous, and that "everything is an effort." Improving or maintaining functional independence in patients with dementia will likely require a multifaceted approach across disease states. Additional research will help define the impact of dementia on the development and progression of functional limitations related to comorbidities.
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PMID:Prevalence and impact of dementia-related functional limitations in the United States, 2001 to 2005. 1956 54

The cysteine protease inhibitor cystatin C is thought to be secreted by most cells and eliminated in the kidneys, so its concentration in plasma is diagnostic of kidney function. Low extracellular cystatin C is linked to pathologic protease activity in cancer, arthritis, atherosclerosis, aortic aneurism, and emphysema. Cystatin C forms non-inhibitory dimers and aggregates by a mechanism known as domain swapping, a property that reportedly protects against Alzheimer disease but can also cause amyloid angiopathy. Despite these clinical associations, little is known about the regulation of cystatin C production, dimerization, and secretion. We show that hematopoietic cells are major contributors to extracellular cystatin C levels in healthy mice. Among these cells, macrophages and dendritic cells (DC) are the predominant producers of cystatin C. Both cell types synthesize monomeric and dimeric cystatin C in vivo, but only secrete monomer. Dimerization occurs co-translationally in the endoplasmic reticulum and is regulated by the levels of reactive oxygen species (ROS) derived from mitochondria. Drugs or stimuli that reduce the intracellular concentration of ROS inhibit cystatin C dimerization. The extracellular concentration of inhibitory cystatin C is thus partly dependent on the abundance of macrophages and DC, and the ROS levels. These results have implications for the diagnostic use of serum cystatin C as a marker of kidney function during inflammatory processes that induce changes in DC or macrophage abundance. They also suggest an important role for macrophages, DC, and ROS in diseases associated with the protease inhibitory activity or amyloidogenic properties of cystatin C.
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PMID:Developmental regulation of synthesis and dimerization of the amyloidogenic protease inhibitor cystatin C in the hematopoietic system. 2457 4