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At least 19 recordsLinked to original sources
PubMed2006

Detection of chronic kidney disease in patients with or at increased risk of cardiovascular disease: a science advisory from the American Heart Association Kidney And Cardiovascular Disease Council; the Councils on High Blood Pressure Research, Cardiovascular Disease in the Young, and Epidemiology and Prevention; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: developed in collaboration with the National Kidney Foundation.

Chronic kidney disease (CKD) occurs commonly in patients with cardiovascular disease. In addition, CKD is a risk factor for the development and progression of cardiovascular disease. In this advisory, we present recommendations for the detection of CKD in patients with cardiovascular disease. CKD can be reliably detected with the combined use of the Modification of Diet in Renal Disease equation to estimate glomerular filtration rate and a sensitive test to detect microalbuminuria. All patients with cardiovascular disease should be screened for evidence of kidney disease with these two determinations.

American Hospital Association↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMed2001

Morality is not a curable disease: probing the history of venereal diseases, morality and prostitution. [Review of: Spongberg, M. Feminizing venereal disease: the body of the prostitute in nineteenth-century discourse, 1997; Fisher, T. Prostitution and the Victorians, 1997; Mooij, A. Out of otherness: characters and narrators in the Dutch venereal disease debates 1850-1990, 1998; Merians, LE. The secret malady: venereal disease in eighteenth century Britain and France, 1996; Brandt, A; Rozin P. Morality and health, 1997; Lewis, M. Thorns on the rose: the history of sexually transmitted diseases in Australia in international perspective, 1998; Lundberg, A. Care and coercion: medical knowledge, social policy and patients with venereal disease in Sweden, 1999].

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Historiography↗
PubMed2003

Prevalence of left main coronary artery disease, of three- or four-vessel coronary artery disease, and of obstructive coronary artery disease in patients with and without peripheral arterial disease undergoing coronary angiography for suspected coronary artery disease.

Data from the present investigation showed that the prevalence of current cigarette smoking, current or ex-cigarette smoking, systemic hypertension, diabetes mellitus, and dyslipidemia was significantly higher in patients with peripheral arterial disease (PAD) than in patients without PAD. The present report also showed that compared with patients without PAD undergoing coronary angiography for suspected coronary artery disease (CAD), patients with PAD undergoing coronary angiography for suspected CAD had a higher prevalence of left main CAD (18% vs <1%), a higher prevalence of 3- or 4-vessel CAD (63% vs 11%), and a higher prevalence of obstructive CAD (98% vs 81%).

Adult↗
PubMedDate not supplied

Chronic kidney disease and cardiovascular disease--using the ANNA Standards and Practice Guidelines to improve care. Part 1: the epidemiology of chronic kidney disease: the risk factors and complications that contribute to cardiovascular disease.

Recent National Kidney Foundation Kidney Disease Outcome Quality Initiative Guidelines for cardiovascular disease recommend that patients with chronic kidney disease be considered at highest risk for development of cardiovascular disease and that cardiac risk factor reduction begin with diagnosis of chronic kidney disease. Risk factors for cardiovascular disease in patients with chronic kidney disease include both traditional and nontraditional renal-related cardiac risk factors. The ANNA Nephrology Nursing Standards of Practice and Guidelines for Care can provide the foundation for planning care to patients with CKD and not only slow the progression of CKD but reduce exposure to cardiac risk factors. This article, on the epidemiology of chronic kidney disease and the risk factors and complications that contribute to cardiovascular disease, is the first in a series of three articles on the risk factors and complications related to chronic kidney disease and its impact on cardiovascular disease.

Adult↗
PubMed2003

Association of plasma homocysteine in elderly persons with atherosclerotic vascular disease and dementia, atherosclerotic vascular disease without dementia, dementia without atherosclerotic vascular disease, and no dementia or atherosclerotic vascular disease.

BACKGROUND: Increased plasma homocysteine has been associated with atherosclerotic vascular disease in elderly persons. The Framingham Study found that plasma homocysteine was a risk factor for dementia and Alzheimer's disease. METHODS: We investigated in an academic nursing home the association of plasma homocysteine with atherosclerotic vascular disease plus dementia (group 1), atherosclerotic vascular disease without dementia (group 2), dementia without atherosclerotic vascular disease (group 3), and no dementia or atherosclerotic vascular disease (group 4). RESULTS: The mean plasma homocysteine level was 15.3 +/- 3.0 micromol/L in 50 group 1 patients, 15.1 +/- 2.7 micromol/L in 50 group 2 patients, 14.4 +/- 2.7 micromol/L in 50 group 3 patients, and 10.6 +/- 3.2 micromol/L in 50 group 4 patients (p <.0001 for group 1 vs group 4, for group 2 vs group 4, and for group 3 vs group 4). CONCLUSIONS: The mean plasma homocysteine level was significantly higher in elderly patients with atherosclerotic vascular disease plus dementia, atherosclerotic vascular disease without dementia, and dementia without atherosclerotic vascular disease than in patients with no dementia or atherosclerotic vascular disease.

Aged↗
PubMed2003

Association of abnormal serum lipids in elderly persons with atherosclerotic vascular disease and dementia, atherosclerotic vascular disease without dementia, dementia without atherosclerotic vascular disease, and no dementia or atherosclerotic vascular disease.

BACKGROUND: Observational data have shown that the use of statins was associated with a lower prevalence of vascular dementia and of Alzheimer's disease. METHODS: We investigated in an academic nursing home the association of dyslipidemia with atherosclerotic vascular disease (group 1), atherosclerotic vascular disease without dementia (group 2), dementia without atherosclerotic vascular disease (group 3), and no dementia or atherosclerotic vascular disease (group 4). RESULTS: Increased serum low-density lipoprotein (LDL) cholesterol was present in 36 of 50 group 1 patients (72%), in 34 of 50 group 2 patients (68%), in 34 of 50 group 3 patients (68%), and in 18 of 50 group 4 patients (36%) (p =.0003 for 1 versus 4; p = 0.001 for 2 versus 4 and 3 versus 4). Decreased serum high-density lipoprotein (HDL) cholesterol was present in 34 of 50 group 1 patients (68%), in 35 of 50 group 2 patients (70%), in 32 of 50 group 3 patients (64%), and in 16 of 50 group 4 patients (32%) (p =.0003 for 1 versus 4; p =.0001 for 2 versus 4; p =.001 for 3 versus 4). Hypertriglyceridemia was not significantly different in the 4 groups. CONCLUSIONS: The prevalence of increased serum LDL cholesterol and decreased serum HDL cholesterol were significantly higher in elderly patients with atherosclerotic vascular disease plus dementia, atherosclerotic vascular disease without dementia, and dementia without atherosclerotic vascular disease than in patients with no dementia or atherosclerotic vascular disease.

Age Distribution↗
PubMed1989

[123I-IMP-SPECT finding of a case of presenile dementia with motor neuron disease--comparison between Alzheimer's disease, Pick's disease and presenile dementia with motor neuron disease].

Cross-sectional X-CT and 123I-IMP-SPECT studies comparing patients with presenile dementia with motor neuron disease (52-year-old, female), with Alzheimer's disease (51-year-old, male) and Pick's disease (49-year-old, male), have found a pattern of reductions in regional cerebral blood flow; the most severe reductions have been in fronto-temporal regions in cases of Pick's disease and presenile dementia with motor neuron disease. 123I-IMP-SPECT in a patient with presenile dementia with motor neuron disease differed significantly from uptake in a case with Alzheimer's disease. Although these findings should be evaluated as part of a prospective longitudinal study with X-CT and 123I-IMP-SPECT, it could be suggested that the development of these diseases has different pathophysiologies.

Alzheimer Disease↗
PubMed1988

Ubiquitin is a common factor in intermediate filament inclusion bodies of diverse type in man, including those of Parkinson's disease, Pick's disease, and Alzheimer's disease, as well as Rosenthal fibres in cerebellar astrocytomas, cytoplasmic bodies in muscle, and mallory bodies in alcoholic liver disease.

Polyclonal antibodies were raised which have a high affinity for conjugated ubiquitin. Immunocytochemistry was performed on paraffin sections of tissues showing well-characterized inclusion bodies. Ubiquitin was found as a component of the intermediate filament inclusion bodies characteristic of several major diseases including Lewy bodies of Parkinson's disease, Pick bodies of Pick's disease, Mallory bodies of alcoholic liver disease, cytoplasmic bodies of a specific myopathy, and Rosenthal fibres within astrocytes. Ubiquitin was also present in the three histological lesions characteristic of Alzheimer's disease. These observations suggest a fundamental role for ubiquitin in the formation of intermediate filament inclusion bodies in man, and have implications regarding the pathogenesis of these important diseases.

Alzheimer Disease↗
PubMed2005

Protein microarray analysis of disease activity in pediatric inflammatory bowel disease demonstrates elevated serum PLGF, IL-7, TGF-beta1, and IL-12p40 levels in Crohn's disease and ulcerative colitis patients in remission versus active disease.

OBJECTIVES: Cytokines and growth factors play a major role in the dysregulated immune response in inflammatory bowel disease (IBD). We hypothesized that significant differences exist between the serum cytokine and growth factor profiles of pediatric IBD patients with active disease (AD) and those in remission, and that levels of some of these soluble mediators may be used to define regulators in IBD and determine disease activity. METHODS: Eighty-eight consecutive patients with confirmed Crohn's disease (CD) and ulcerative colitis (UC) seen at the Duke Children's Hospital were prospectively enrolled and a serum sample was obtained. Data were recorded at the time of serum collection to calculate disease activity indices. The relative expression of 78 cytokines, growth factors, and soluble receptors was determined using proprietary antibody-based protein microarrays amplified by rolling circle amplification. SPSS 8 (SPSS Inc., Chicago, IL) was used to compare protein profiles for CD and UC patients in clinical remission (CR) versus AD. RESULTS: Sixty-five CD patients and 23 UC patients were enrolled. Forty-one CD patients had available samples and PCDAI results. Twenty-two patients were in remission PCDAI < or = 12.5 (median 5), 19 patients had disease activity >15 (median 30). Univariate analysis revealed that PLGF, IL-7, IL-12p40, and TGF-beta1 cytokine levels were significantly elevated for patients in CR versus AD (p < 0.01). Twelve UC serum samples had Seo/Truelove Witt AI for analysis. Five patients were in remission by TW AI and Seo AI < or =110 and 7 patients had active mild-to-severe disease by TW and Seo AI >110. Only one cytokine, IL12p40, showed significance between CR versus AD (p < 0.02). CONCLUSIONS: Surprisingly, we found no differences in circulating levels of proinflammatory cytokines but found that pediatric IBD patients in remission compared to those with AD had higher levels of specific circulating cytokines, including the regulatory cytokines IL-12p40 and TGF-beta1. It may be that these cytokines directly regulate intestinal inflammation in IBD or reflect the activity of T regulatory cells in negatively regulating the inflammatory response. Further studies will be needed to validate our results to define the molecular pathways involved in the intestinal immune response in man.

Adolescent↗
PubMed2000

Short-term treatment with proton pump inhibitors, H2-receptor antagonists and prokinetics for gastro-oesophageal reflux disease-like symptoms and endoscopy negative reflux disease.

BACKGROUND: Heartburn affects 25% of the adult population on a monthly basis and represents the core symptom of gastro-oesophageal reflux disease (GORD). Treatment is readily available and puts a large demand on healthcare budgets. Research in the past has focused largely on the treatment of oesophagitis. A majority of GORD patients show no endoscopic abnormalities and in daily practice most patients are treated empirically. OBJECTIVES: Summarise, quantify and compare the efficacy of the short-term use of proton pump inhibitors (PPI), H2-receptor antagonists (H2RA) and prokinetics in the empirical treatment of GORD and the treatment of endoscopy negative reflux disease (ENRD). SEARCH STRATEGY: Electronic searches were performed of the Cochrane Controlled Trials Register, MEDLINE and EMBASE. Bibliographies were screened. SELECTION CRITERIA: Included were randomised controlled trials focussing on symptomatic outcome after short-term treatment for GORD using proton pump inhibitors, H2-receptor antagonists or prokinetic agents. Participants had to be classifiable in the empirical treatment group (no endoscopy used in treatment allocation) or in the endoscopy negative reflux disease group (no endoscopic signs of erosive oesophagitis). DATA COLLECTION AND ANALYSIS: Data from included trials were extracted by two reviewers independently. The impact of interventions was expressed as relative risks (RR) together with 95% confidence intervals (95% CI). Meta-analysis was only performed if there were sufficient trials of similar comparisons reporting the same outcomes. Relative risks were combined for binary outcomes. MAIN RESULTS: Twenty-one trials were included: eleven in the empirical treatment group, seven in the ENRD group and three in both. In empirical treatment of GORD the RR for heartburn remission in placebo-controlled trials for PPI was 0.35 (1 trial, 95% CI 0.26 to 0.46), for H2RAs 0.77 (2 trials, 95% CI 0.60 to 0.99) and for prokinetics 0.86 (1 trial, 95% CI 0.73 to 1.01). In direct comparison PPIs were significantly (p<0.05) more effective than H2RAs (3 trials, RR 0.67, 95% CI 0.57 to 0.80) and prokinetic's (2 trials, RR 0.53, 95% CI 0.32 to 0.87). In treatment of ENRD, RR for heartburn remission for PPI versus placebo was 0.68 (4 trials, 95% CI 0.53 to 0.88) and for H2RA versus placebo was 0.84 (2 trials, 95% CI 0.74 to 0.95). The RR for PPI versus H2RA was 0.69 (2 trials, 95% CI 0.39 to 1.20) and versus prokinetic 0.72 (1 trial, 95% CI 0.56 to 0.92). REVIEWER'S CONCLUSIONS: The findings in this review suggest that antisecretory drugs are effective in the empirical treatment of complaints likely to originate from GORD and in treatment of ENRD and furthermore that PPIs are superior to H2RAs in empirical treatment of typical GORD symptoms.

Endoscopy, Digestive System↗
PubMed1995

Dendritic reorganisation in the basal forebrain under degenerative conditions and its defects in Alzheimer's disease. II. Ageing, Korsakoff's disease, Parkinson's disease, and Alzheimer's disease.

Changes in the dendritic arborisation of Golgi-impregnated basal forebrain neurones with respect to size, shape, orientation, and topology of branching were quantitatively investigated in ageing, Alzheimer's disease (AD), Korsakoff's disease (KD), and Parkinson's disease (PD). A reorganisation of the whole dendritic tree characterized by an increase in both the total dendritic length and the degree of dendritic arborisation as well as by changes in the shape of the dendritic field was found during ageing, in KD, PD, and AD. Dendritic growth under these conditions was related to the extent of cell loss in basal forebrain nuclei. There appeared to be major differences, however, with respect to the overall pattern of dendritic reorganisation between AD on one side and ageing, KD, and PD on the other side. In both ageing and KD, dendritic growth was largely restricted to the terminal dendritic segments, resulting in an increase of the size of the dendritic field (pattern of "extensive growth") In AD, however, dendritic growth mainly resulted in an increase of the dendritic density within the dendritic field without being accompanied by an increase in the size of the volume occupied by the dendritic tree (pattern of "intensive growth"). In AD, aberrant growth processes were frequently observed in the perisomatic area or on distal dendritic segments of basal forebrain neurones of the reticular type. Neurones with aberrant growth profiles were typically located in the direct vicinity of deposits of beta/A4 amyloid. Perisomatic growth profiles were covered by the low-affinity receptor of nerve growth factor p75NGFR. Aberrant growth processes were not present in ageing, KD, and PD. On the basis of the present study, it is concluded that under certain degenerative conditions, reticular basal forebrain neurones undergo a compensatory reorganisation of their dendritic arborisation, a process that has become defective in AD, thereby converting a physiological signal into a cascade of events contributing to the pathology of the disease.

Adult↗
PubMed2002

Disease and diversity in history. (Reviews of: Cartwright, FF, Biddiss, M. Disease and history. Gloucestershire: Sutton Publishing Limited, 2000; Rotberg RI, ed. Health and disease in human history. Cambridge, MA: MIT Press, 2000; Cliff, A., Haggett, P., Smallman-Raynor, M. Deciphering global epidemics: analytical approaches to the disease records of world cities, 1888-1912. Cambridge: Cambridge University Press, 1998; Riley, JC. Rising life expectancy: a global history. Cambridge: Cambridge University Press, 2001; McMichael, T. Human frontiers, environments and disease: past patterns, uncertain futures. Cambridge: Cambridge University Press, 2001).

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Disease↗
PubMed2002

Hepatic manifestations of gastrointestinal diseases. Inflammatory bowel disease, celiac disease, and Whipple's disease.

The gastrointestinal tract and the liver are closely related anatomically, physiologically, and pathologically. Some disease associations are well documented, such as PSC in association with IBD, whereas others are less well defined. A heightened clinical suspicion is required in these patients who do not present with the classical disease associations. The underlying causes of their diseases are the subject of much debate and research, and their diagnosis and management remain challenging.

Animals↗
PubMed1996

Isolated polycystic liver disease as a distinct genetic disease, unlinked to polycystic kidney disease 1 and polycystic kidney disease 2.

Polycystic liver disease (PLD) is proven to occur either sporadically or in association with autosomal dominant polycystic kidney disease (ADPKD), whereas the existence of an isolated (i.e., without any kidney cyst) familial form is disputed. We describe a family with definitely isolated PLD transmitted through three generations and exclude the linkage of the disease to the genetic markers of PKD1 and PKD2, the two main loci responsible for ADPKD. These findings strongly support the existence of PLD as a genetic disease distinct from the known forms of ADPKD.

Cysts↗