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Kenneth S Kornman

Publications and source records attributed to Kenneth S Kornman.

9 recordsLinked to original sources
PubMed2006

Relationship of IgG and IgM autoantibodies to oxidized low density lipoprotein with coronary artery disease and cardiovascular events.

The relationship between autoantibodies to oxidized low density lipoprotein (OxLDL) and coronary artery disease (CAD) remains controversial. IgM and IgG OxLDL autoantibodies to malondialdehyde (MDA)-modified LDL, copper oxidized low density lipoprotein (CuOxLDL), and oxidized cholesterol linoleate (OxCL), as well as apolipoprotein B-100 immune complexes (apoB-ICs), were measured in 504 patients undergoing clinically indicated coronary angiography. Patients were followed for cardiovascular events for a median of 4 years. In univariate analysis, IgM OxLDL autoantibodies and IgM apoB-ICs were inversely associated with the presence of angiographically determined CAD, whereas IgG OxLDL autoantibodies and IgG apoB-ICs were positively associated. In logistic regression analysis, compared with the first quartile, patients in the fourth quartile of IgM OxLDL autoantibodies and apoB-ICs showed a lower probability of angiographically determined CAD (>50% diameter stenosis). Odds ratios and (95% confidence intervals) were as follows: MDA-LDL, 0.51 (0.32-0.82; P = 0.005); CuOxLDL, 0.63 (0.39-1.01; P = 0.05); OxCL, 0.63 (0.39-1.01; P = 0.05); and apoB-IC, 0.55 (0.34-0.88; P = 0.013). These relationships were accentuated in the setting of hypercholesterolemia, with the highest IgM levels showing the lowest risk of CAD for the same level of hypercholesterolemia. Multivariable analysis revealed that neither IgM or IgG OxLDL autoantibodies nor apoB-ICs were independently associated with angiographically determined CAD or cardiovascular events. In conclusion, IgG and IgM OxLDL biomarkers have divergent associations with CAD in univariate analysis but are not independent predictors of CAD or clinical events.

Adult↗
PubMed2006

Single nucleotide polymorphisms in the human interleukin-1B gene affect transcription according to haplotype context.

We questioned the significance of haplotype structure in gene regulation by testing whether individual single nucleotide polymorphisms (SNPs) within a gene promoter region [interleukin-1-beta (IL1B)] might affect promoter function and, if so, whether function was dependent on haplotype context. We sequenced genomic DNA from 25 individuals of diverse ethnicity, focusing on exons and upstream flanking regions of genes of the cluster. We identified four IL1B promoter region SNPs that were active in transient transfection reporter gene assays. To substantiate allelic differences found in reporter gene assays, we also examined nuclear protein binding to promoter sequence oligonucleotides containing different alleles of the SNPs. The effect of individual SNPs on reporter gene transcription varied according to which alleles of the three other SNPs were present in the promoter construct. The SNP patterns that influenced function reflected common haplotypes that occur in the population, suggesting functionally significant interactions between SNPs according to haplotype context. Of the haplotypes that include the four functional IL1B promoter SNPs (-3737, -1464, -511, -31), the four haplotypes that showed different contextual effects on SNP function accounted for >98% of the estimated haplotypes in Caucasian and African-American populations. This finding underlines the importance of understanding the haplotype structure of populations used for genetic studies and may be especially important in the functional analysis of genetic variation across gene regulatory regions.

Black or African American↗
PubMed2006

Interleukin 1 genetics, inflammatory mechanisms, and nutrigenetic opportunities to modulate diseases of aging.

Inflammation plays a central role in many diseases of aging, and genetic differences in the inflammatory response appear to influence different disease courses among individuals. Variations in the genes for the family of interleukin 1 (IL-1) proteins are inherited together in a small set of patterns and provide an example of the role of inflammatory genetics as a modifier of diseases of aging. The IL-1 genetic variations are associated with variation in both the inflammatory response and the clinical presentation of a range of diseases, including coronary artery disease, Alzheimer disease, gastric cancer, and periodontitis. This growing understanding of the role of genetic variation in inflammation and chronic disease presents opportunities to identify healthy persons who are at increased risk of disease and to potentially modify the trajectory of disease to prolong healthy aging. Nutrition represents one of the promising approaches to modulation of the risk of diseases of aging because of the effects of certain nutrients on gene expression. One of the most practical applications of nutritional modulation of chronic disease may be nutrients that regulate the expression of key inflammatory genes.

Aged↗
PubMed2005

Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

BACKGROUND: Lp(a) lipoprotein binds proinflammatory oxidized phospholipids. We investigated whether levels of oxidized low-density lipoprotein (LDL) measured with use of monoclonal antibody E06 reflect the presence and extent of obstructive coronary artery disease, defined as a stenosis of more than 50 percent of the luminal diameter. METHODS: Levels of oxidized LDL and Lp(a) lipoprotein were measured in a total of 504 patients immediately before coronary angiography. Levels of oxidized LDL are reported as the oxidized phospholipid content per particle of apolipoprotein B-100 (oxidized phospholipid:apo B-100 ratio). RESULTS: Measurements of the oxidized phospholipid:apo B-100 ratio and Lp(a) lipoprotein levels were skewed toward lower values, and the values for the oxidized phospholipid:apo B-100 ratio correlated strongly with those for Lp(a) lipoprotein (r=0.83, P<0.001). In the entire cohort, the oxidized phospholipid:apo B-100 ratio and Lp(a) lipoprotein levels showed a strong and graded association with the presence and extent of coronary artery disease (i.e., the number of vessels with a stenosis of more than 50 percent of the luminal diameter) (P<0.001). Among patients 60 years of age or younger, those in the highest quartiles for the oxidized phospholipid:apo B-100 ratio and Lp(a) lipoprotein levels had odds ratios for coronary artery disease of 3.12 (P<0.001) and 3.64 (P<0.001), respectively, as compared with patients in the lowest quartile. The combined effect of hypercholesterolemia and being in the highest quartiles of the oxidized phospholipid:apo B-100 ratio (odds ratio, 16.8; P<0.001) and Lp(a) lipoprotein levels (odds ratio, 14.2; P<0.001) significantly increased the probability of coronary artery disease among patients 60 years of age or younger. In the entire study group, the association of the oxidized phospholipid:apo B-100 ratio with obstructive coronary artery disease was independent of all clinical and lipid measures except one, Lp(a) lipoprotein. However, among patients 60 years of age or younger, the oxidized phospholipid:apo B-100 ratio remained an independent predictor of coronary artery disease. CONCLUSIONS: Circulating levels of oxidized LDL are strongly associated with angiographically documented coronary artery disease, particularly in patients 60 years of age or younger. These data suggest that the atherogenicity of Lp(a) lipoprotein may be mediated in part by associated proinflammatory oxidized phospholipids.

Adult↗
PubMed2005

Nutritional genomics in practice: where do we begin?

Nutritional genomics, which studies the genome-wide influences of nutrition, has far-reaching potential in the prevention of diet-related disease. It is highly likely that during the next decade the nutritional supplement and functional food industries will continue robust growth in response to advances in nutritional genomics research and its applications. Parallel to this growth will be impressive progress in understanding the specific influence of certain food components on metabolic pathways and on long-term risk for disease. As genetic information about individuals becomes available, such data are likely to redefine the current concept of preventive medicine. Dietetics professionals have the potential to harness this information and influence health promotion and disease prevention on a global scale. For these reasons, the dietetics profession has an exciting opportunity that, if seized and properly executed, could enhance the scientific foundation of clinical practice, improve therapeutic outcomes, and significantly expand career and economic opportunities for practitioners. The future of dietetics is unquestionably intertwined with nutritional genomics.

Biomarkers↗
PubMed2005

Diagnostic and prognostic tests for oral diseases: practical applications.

Dental caries and periodontitis are initiated by specific bacteria and modified by host and environmental factors. Individuals have great differences in their rates of disease progression, but a small set of risk factors, such as smoking and diabetes, can distinguish patients at high risk for more severe disease. The application of information about factors that influence disease can be used to improve disease prevention and management. Knowledge of when specific information may be valuable should lead to the optimal management of individual patients. The use of diagnostic and prognostic tests and their application to the assessment and management of dental caries and periodontitis are the focus of this review.

Dental Caries↗
PubMed2003

IL-1 gene polymorphism and smoking as risk factors for peri-implant bone loss in a well-maintained population.

The aim of the present study was (i) to investigate the relation between specific interleukin-1 (IL-1) gene polymorphisms and peri-implant bone loss at osseointegrated ITI(R) dental implants and (ii) to explore the association between these allelic variants of the IL-1 gene complex and peri-implant mucosal inflammation, in both smoking and non-smoking individuals. A sample of 90 consecutive Caucasian patients (aged 33-88 years), treated with at least one ITI-implant participated in this retrospective investigation. Standardized periapical radiographs were taken after prosthetic rehabilitation (133.6 days, SD 136.9 days) and at the time of the re-examination, on average 5.6 years (SD 2.5 years) thereafter. The radiographs were analyzed by a calibrated examiner for changes in peri-implant bone levels. The examiner was blind with respect to clinical parameters and IL-1 status. The distance between the implant shoulder and the first visible bone-implant contact (DIB) at the respective time points were measured using a computerized method. The absolute bone level difference during the years of service (ABL) and the annual bone loss (DeltaBL/year) were calculated for all the implants. Percentages of full mouth bleeding on probing (BOP), as well as of BOP calculated separately for teeth and implants, were determined for all visits and averaged for the entire observation period. Out of the total patient sample, there were 14 heavy smokers (= 20 cigarettes/day), 14 moderate smokers (5-19 cigarettes/day), 23 previous smokers (smoking cessation > 5 years) and 39 non-smokers. Twenty-eight (31.11%) patients were IL-1 genotype positive. Upon stratification for smoking status, significant differences were found for the variables ABL (P < 0.04, U-test) and DeltaBL/year (P < 0.04, U-test) between non-smokers and heavy smokers for the IL-1 genotype positive group but not for the IL-1 genotype negative group. Moreover, significant differences in ABL (P < 0.04, U-test) and DeltaBL/year (P < 0.04, U-test) were identified between former smokers and heavy smokers for the IL-1 genotype positive group. The differences in inflammatory parameters (BOP) did not reach statistical significance. This study suggests that in heavy cigarette smokers, carriage of a functionally significant IL-1 gene complex polymorphism is associated with an increased risk for peri-implant bone loss following prosthetic reconstruction and during the supportive periodontal care phase of the treatment.

Adult↗
PubMed2002

C-reactive protein levels are influenced by common IL-1 gene variations.

Elevated markers of systemic inflammation are associated with the development of acute coronary syndromes, but there is no current explanation for increased inflammation in overtly healthy individuals. The influence of genetic control of the inflammatory response on the observed variability is unknown. We studied the frequency of four polymorphisms in interleukin (IL) 1 genes, known to modulate inflammation, in 454 individuals undergoing coronary angiography and analysed their influence on plasma C-reactive protein (CRP) and fibrinogen levels. Females and smokers had higher levels of CRP than males (Pi = 0.001) and non-smokers (Pi = 0.001). Patients with genotype 2.2 for the IL-1B(+3954) polymorphism had twice the median CRP levels of patients who were genotype 1.1 (4.33 vs 2.01 mg/l; P = 0.001). Patients with genotype 1.2 or 2.2 at the IL-1A(+4845) polymorphism also had higher median CRP (2.92 vs 2.05 mg/l, Pi = 0.023). In multivariate analyses, CRP levels remained significantly associated with IL-1 polymorphisms after adjustment for smoking, gender and age. Fibrinogen levels had similar associations with the IL-1 genotypes. These data indicate that IL-1 gene polymorphisms known to affect the inflammatory response are highly related to plasma levels of CRP and fibrinogen in patients referred for coronary angiography.

Adult↗