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本文引用的文献

1
Stepwise or linear decrease in penetrance of type 1 diabetes with lower-risk HLA genotypes over the past 40 years.40 年来,低风险 HLA 基因型的 1 型糖尿病外显率呈逐步或线性下降。
Diabetes. 2011 Mar;60(3):1045-9. doi: 10.2337/db10-1419. Epub 2011 Feb 9.
2
Mathematical modelling of immune regulation of type 1 diabetes.1型糖尿病免疫调节的数学建模
Biosystems. 2010 Nov-Dec;102(2-3):88-98. doi: 10.1016/j.biosystems.2010.07.018. Epub 2010 Aug 11.
3
Recent progress in the genetics of diabetes.糖尿病遗传学的最新进展。
Horm Res. 2009 Jan;71 Suppl 1:17-23. doi: 10.1159/000178031. Epub 2009 Jan 21.
4
Review series on helminths, immune modulation and the hygiene hypothesis: how might infection modulate the onset of type 1 diabetes?关于蠕虫、免疫调节与卫生假说的综述系列:感染如何调节1型糖尿病的发病?
Immunology. 2009 Jan;126(1):12-7. doi: 10.1111/j.1365-2567.2008.03009.x.
5
Meta-analysis of genome-wide association study data identifies additional type 1 diabetes risk loci.全基因组关联研究数据的荟萃分析确定了更多1型糖尿病风险基因座。
Nat Genet. 2008 Dec;40(12):1399-401. doi: 10.1038/ng.249. Epub 2008 Nov 2.
6
The "perfect storm" for type 1 diabetes: the complex interplay between intestinal microbiota, gut permeability, and mucosal immunity.1型糖尿病的“完美风暴”:肠道微生物群、肠道通透性和黏膜免疫之间的复杂相互作用。
Diabetes. 2008 Oct;57(10):2555-62. doi: 10.2337/db08-0331.
7
The accelerator hypothesis and increasing incidence of type 1 diabetes.1型糖尿病的加速假说与发病率上升
Curr Opin Endocrinol Diabetes Obes. 2008 Aug;15(4):321-5. doi: 10.1097/MED.0b013e3283073a5a.
8
The rising incidence of type 1 diabetes is accounted for by cases with lower-risk human leukocyte antigen genotypes.1型糖尿病发病率的上升是由低风险人类白细胞抗原基因型的病例导致的。
Diabetes Care. 2008 Aug;31(8):1546-9. doi: 10.2337/dc08-0239. Epub 2008 May 16.
9
Worldwide childhood type 1 diabetes incidence--what can we learn from epidemiology?全球儿童1型糖尿病发病率——我们能从流行病学中学到什么?
Pediatr Diabetes. 2007 Oct;8 Suppl 6:6-14. doi: 10.1111/j.1399-5448.2007.00280.x.
10
Foxp3 and Aire in thymus-generated Treg cells: a link in self-tolerance.胸腺生成的调节性T细胞中的Foxp3和Aire:自身耐受的一个环节。
Nat Immunol. 2007 Apr;8(4):333-4. doi: 10.1038/ni0407-333.

阈值假说:解决 1 型糖尿病中先天与后天的方程式。

The threshold hypothesis: solving the equation of nurture vs nature in type 1 diabetes.

机构信息

Department of Pathology, University of Florida, College of Medicine, 1600 SW Archer Road, Gainesville, FL 32610-0275, USA.

出版信息

Diabetologia. 2011 Sep;54(9):2232-6. doi: 10.1007/s00125-011-2244-z. Epub 2011 Jul 20.

DOI:10.1007/s00125-011-2244-z
PMID:21773685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7296551/
Abstract

For more than 40 years, the contributions of nurture (i.e. the environment) and nature (i.e. genetics) have been touted for their aetiological importance in type 1 diabetes. Disappointingly, knowledge gains in these areas, while individually successful, have to a large extent occurred in isolation from each other. One reason underlying this divide is the lack of a testable model that simultaneously considers the contributions of genetic and environmental determinants in the formation of this and potentially other disorders that are subject to these variables. To address this void, we have designed a model based on the hypothesis that the aetiological influences of genetics and environment, when evaluated as intersecting and reciprocal trend lines based on odds ratios, result in a method of concurrently evaluating both facets and defining the attributable risk of clinical onset of type 1 diabetes. The model, which we have elected to term the 'threshold hypothesis', also provides a novel means of conceptualising the complex interactions of nurture with nature in type 1 diabetes across various geographical populations.

摘要

四十多年来,环境(即教养)和遗传(即天性)对 1 型糖尿病病因学的重要性一直备受推崇。令人失望的是,这些领域的知识虽各自取得了成功,但在很大程度上彼此孤立。造成这种分裂的一个原因是缺乏一个可测试的模型,该模型可以同时考虑遗传和环境决定因素在这种疾病形成中的作用,以及可能受到这些变量影响的其他疾病。为了解决这个空白,我们设计了一个模型,其基于以下假设:基于比值比,将遗传和环境的病因影响评估为相交和相互影响的趋势线,将产生一种同时评估两个方面并定义 1 型糖尿病临床发病可归因风险的方法。我们选择将这个模型称为“阈值假设”,它还为理解不同地理人群中 1 型糖尿病中环境与天性的复杂相互作用提供了一种新的方法。