Редактирование: SELE

E-selectin precursor (CD62 antigen-like family member E) (Endothelial leukocyte adhesion molecule 1) (ELAM-1) (Leukocyte-endothelial cell adhesion molecule 2) (LECAM2) (CD62E antigen) [ELAM1]

==Publications==

{{medline-entry
|title=Experience of aging in patients with rheumatic disease: a comparison with the general population.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22360140
|abstract=Self-perceptions of aging have been shown to predict mental and physical health and even longevity. This study examined the aging perceptions of patients with rheumatic disease and compared them with the general Dutch population. Consecutive patients visiting a rheumatology clinic completed the Personal Experience of Aging Scale (PEAS) subscales: physical decline, social loss, continuous growth, and two sentence stems from the [[SELE]] instrument (What I like/do not like about getting older ...) as qualitative measures of the subjective experience of aging. A representative sample from the general Dutch population between 40 and 85 years was used as a comparison group. Participants included in this study were 208 patients with a rheumatic disease and 975 persons from the Dutch Aging Survey (DAS). Both quantitative and qualitative data showed that patients perceived aging more strongly as physical decline. These negative experiences did not extend to social and psychological domains of aging. Age-group comparisons revealed that patients in middle adulthood experienced physical aging similar to older people without a rheumatic disease. The negative experience of aging in patients is limited to the physical domain and does not extend to other domains of life. The negative experience of physical aging even in middle-aged groups warrants further studies on its effects on mental and physical health outcomes and health behavior in patients with rheumatic disease.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Aging
* Data Collection
* Female
* Health Status
* Humans
* Male
* Middle Aged
* Netherlands
* Rheumatic Diseases
* Self Concept

|full-text-url=https://sci-hub.do/10.1080/13607863.2011.651438
}}
{{medline-entry
|title=Genetic influences on lipid metabolism trait variability within the Stanislas Cohort.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/11714857
|abstract=The contribution of 17 polymorphisms within 13 candidate genes on lipid trait variability was investigated by a multiplex assay in 772 men and 780 women coming for a health checkup examination. The studied genes were [[APOE]], [[APOB]], [[APOC3]], [[CETP]], [[LPL]], PON, [[MTHFR]], [[FGB]], GpIIIa, [[SELE]], [[ACE]], and [[AGT]]. We found that [[APOB]]-Thr71Ile, [[APOE]]-(112/158), [[APOC3]]-1100C/T, and [[SELE]]-98G/T polymorphisms had a significant effect on lipid traits (P < or = 0.001 to P < or = 0.01). Genetic effects accounted for 3.5-5.7% of variation in apolipoprotein B (apoB)-related traits among men, and for 5.7-9.0% among women. The contribution of [[APOE]] polymorphism on apoB-related traits variability was two to three times more important in women than in men. We found suggestive evidence for interactive effects between genetics and age, smoking status, and oral contraceptives. Increase of LDL-cholesterol and apoB concentrations with age was stronger among the epsilon4 carriers in women, and apolipoprotein A-I (apoA-I) concentration decreased with age in epsilon4 male carriers. The effect of epsilon2 allele on LDL-cholesterol was more important in the oral contraceptive users. In nonsmokers only, the [[APOC3]]-1100C allele in women was related to lower apoB-related traits concentrations, and in men to higher apoA-I and HDL-cholesterol concentrations. In conclusion, this work, in addition to the reinforcement of the already known associations between [[APOB]], [[APOE]], and [[APOC3]] genes and lipids, leads to new perspectives in the complex relationships among genes and environmental factors. The newly observed relationships between E-selectine gene and lipid concentrations support the hypotheses of multiple metabolic pathways contributing to the complexity of lipids variability.
|mesh-terms=* Adult
* Aging
* Alleles
* Apolipoprotein A-I
* Apolipoprotein C-III
* Apolipoproteins B
* Apolipoproteins C
* Apolipoproteins E
* Cholesterol, LDL
* Codon
* Cohort Studies
* Contraceptives, Oral
* Female
* Genetic Variation
* Humans
* Lipid Metabolism
* Lipids
* Male
* Middle Aged
* Polymorphism, Genetic
* Sex Characteristics
* Smoking


}}