Редактирование: SRR

Serine racemase (EC 5.1.1.18) (D-serine ammonia-lyase) (D-serine dehydratase) (EC 4.3.1.18) (L-serine ammonia-lyase) (L-serine dehydratase) (EC 4.3.1.17)

==Publications==

{{medline-entry
|title=Mediterranean diet and its components in relation to all-cause mortality: meta-analysis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30401007
|abstract=The beneficial association of the Mediterranean diet (MedDiet) with longevity has been consistently demonstrated, but the associations of MedDiet components have not been accordingly evaluated. We performed an updated meta-analysis of prospective cohort studies published up to 31 December 2017, to quantify the association of adherence to MedDiet, expressed as an index/score (MDS) and of its components with all-cause mortality. We estimated summary relative risks ([[SRR]]) and 95 % CI using random effects models. On the basis of thirty studies (225 600 deaths), [[SRR]] for the study-specific highest/lowest and per 1sd MDS increment were 0·79 (95 % CI 0·77, 0·81, Ι 2=42 %, P-heterogeneity 0·02) and 0·92 (95 % CI 0·90, 0·94, Ι 2 56 %, P-heterogeneity <0·01), respectively. Inversely, statistically significant associations were evident in stratified analyses by country, MDS range and publication year, with some evidence for heterogeneity across countries overall (P-heterogeneity 0·011), as well as across European countries (P=0·018). Regarding MDS components, relatively stronger and statistically significant inverse associations were highlighted for moderate/none-excessive alcohol consumption (0·86, 95 % CI 0·77, 0·97) and for above/below-the-median consumptions of fruit (0·88, 95 % CI 0·83, 0·94) and vegetables (0·94, 95 % CI 0·89, 0·98), whereas a positive association was apparent for above/below-the-median intake of meat (1·07, 95 % CI 1·01, 1·13). Our meta-analyses confirm the inverse association of MedDiet with mortality and highlight the dietary components that influence mostly this association. Our results are important for better understanding the role of MedDiet in health and proposing dietary changes to effectively increase adherence to this healthy dietary pattern.
|mesh-terms=* Aged
* Aged, 80 and over
* Diet, Mediterranean
* Europe
* Female
* Fruit
* Humans
* Longevity
* Male
* Meat
* Middle Aged
* Mortality
* Proportional Hazards Models
* Prospective Studies
* Risk
* Vegetables
|keywords=*  HR hazard ratio
*  MDS Mediterranean diet score
*  MedDiet Mediterranean diet
*  RR relative risk.
* Mediterranean diet
* Meta-analyses
* Mortality
* Reviews
|full-text-url=https://sci-hub.do/10.1017/S0007114518002593
}}
{{medline-entry
|title=Genetic Biomarkers on Age-Related Cognitive Decline.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29209239
|abstract=With ever-increasing elder populations, age-related cognitive decline, which is characterized as a gradual decline in cognitive capacity in the aging process, has turned out to be a mammoth public health concern. Since genetic information has become increasingly important to explore the biological mechanisms of cognitive decline, the search for genetic biomarkers of cognitive aging has received much attention. There is growing evidence that single-nucleotide polymorphisms (SNPs) within the [i]ADAMTS9, [[BDNF]], [[CASS4]], [[COMT]], [[CR1]], [[DNMT3A]], [[DTNBP1]], [[REST]], [[SRR]], TOMM40[/i], circadian clock, and Alzheimer's diseases-associated genes may contribute to susceptibility to cognitive aging. In this review, we first illustrated evidence of the genetic contribution to disease susceptibility to age-related cognitive decline in recent studies ranging from approaches of candidate genes to genome-wide association studies. We then surveyed a variety of association studies regarding age-related cognitive decline with consideration of gene-gene and gene-environment interactions. Finally, we highlighted their limitations and future directions. In light of advances in precision medicine and multi-omics technologies, future research in genomic medicine promises to lead to innovative ideas that are relevant to disease prevention and novel drugs for cognitive aging.

|keywords=* Alzheimer’s diseases
* SNP–SNP interactions
* age-related cognitive decline
* biomarker
* cognitive aging
* gene–gene interactions
* neurodegeneration
* single-nucleotide polymorphisms
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5702307
}}