Alessandra Macciotta ,1,2 Carlotta Sacerdote,3 Claudia Giachino,1 Chiara Di Girolamo,1 Matteo Franco,1 Yvonne T van der Schouw,4 Raul Zamora-Ros,5 Elisabete Weiderpass,6 Cloé Domenighetti,7 Alexis Elbaz ,7 Thérèse Truong,7 Claudia Agnoli,8 Benedetta Bendinelli,9 Salvatore Panico,10 Paolo Vineis ,11 Sofia Christakoudi,11,12 Matthias B Schulze,13,14,15 Verena Katzke,16 Rashmita Bajracharya,16 Christina C Dahm,17 Susanne Oksbjerg Dalton,18,19 Sandra M Colorado-Yohar,20,21,22 Conchi Moreno-Iribas,23 Pilar Amiano Etxezarreta,21,24,25 María José Sanchez,21,26,27 Nita G Forouhi,28 Nicholas Wareham,28 Fulvio Ricceri 1.
Additional supplemental material is published online only. To view, please visit the journal online (https://doi.org/ 10.1136/jech-2024-222734). For numbered affiliations see end of article.
Correspondence to
Professor Carlotta Sacerdote; 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 NW and FR contributed equally. Received 10 July 2024 Accepted 19 November 2024© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ Group
To cite: Macciotta A, Sacerdote C, Giachino C, et al. J Epidemiol Community Health Epub ahead of print:[please include Day MonthYear]. doi:10.1136/jech- 2024-222734
ABSTRACT
Introduction Observational studies have shown that more educated people are at lower risk of developing type 2 diabetes (T2D). However, robust study designs are needed to investigate the likelihood that such a relationship is causal. This study used genetic instruments for education to estimate the effect of education on T2D using the Mendelian randomisation (MR) approach.
Methods Analyses have been conducted in the European Prospective Investigation into Cancer and Nutrition (EPIC)- InterAct study (more than 20000 individuals), a case-cohort study of T2D nested in the EPIC cohort. Education was measured as Years of Education and Relative Index of Inequality. Prentice-weighted Cox models were performed to estimate the association between education and T2D. One-sample MR analyses investigated whether genetic predisposition towards longer education was associated with risk of T2D and investigated potential mediators of the
Results MR estimates indicated a risk reduction of about 15% for each year of longer education on the risk of developing T2D, confirming the protective role estimated by observational models (HR 0.96, 95% CI 0.95 to 0.96). MR analyses on putative mediators showed a significant role of education on body mass index, alcohol consumption, adherence to the Mediterranean diet and smoking habits.
Conclusion The results supported the hypothesis that higher education is a protective factor for the risk of developing T2D. Based on its position in the causal chain, education may be antecedent of other known risk factors for T2D including unhealthy behaviours. These findings reinforce evidence obtained through observational study designs and bridge the gap between correlation and causation.
Stephanie J. Hanna1 · Rachel H. Bonami2,3,4,5 · Brian Corrie6,7 · Monica Westley8 · Amanda L. Posgai9 · Eline T. Luning Prak10 · Felix Breden6,7 · Aaron W. Michels11 · Todd M. Brusko9,12,13 · Type 1 Diabetes AIRR Consortium
Received: 26 May 2024 / Accepted: 19 August 2024 / Published online: 29 October 2024
© The Author(s) 2024
Extended author information available on the last page of the article
Abstract
Human molecular genetics has brought incredible insights into the variants that confer risk for the development of tissuespecific autoimmune diseases, including type 1 diabetes. The hallmark cell-mediated immune destruction that is characteristic of type 1 diabetes is closely linked with risk conferred by the HLA class II gene locus, in combination with a broad array of additional candidate genes influencing islet-resident beta cells within the pancreas, as well as function, phenotype and trafficking of immune cells to tissues. In addition to the well-studied germline SNP variants, there are critical contributions conferred by T cell receptor (TCR) and B cell receptor (BCR) genes that undergo somatic recombination to yield the Adaptive Immune Receptor Repertoire (AIRR) responsible for autoimmunity in type 1 diabetes. We therefore created the T1D TCR/ BCR Repository (The Type 1 Diabetes T Cell Receptor and B Cell Receptor Repository) to study these highly variable and dynamic gene rearrangements. In addition to processed TCR and BCR sequences, the T1D TCR/BCR Repository includes detailed metadata (e.g. participant demographics, disease-associated parameters and tissue type). We introduce the Type 1 Diabetes AIRR Consortium goals and outline methods to use and deposit data to this comprehensive repository. Our ultimate goal is to facilitate research community access to rich, carefully annotated immune AIRR datasets to enable new scientific inquiry and insight into the natural history and pathogenesis of type 1 diabetes.
Keywords AIRR · AIRR Data Commons · Autoantibodies · B cell receptors · FAIR data · Next-generation sequencing · Single-cell RNA-seq · T cell receptors · Type 1 diabetes
Abbreviations
AAb Autoantibody/autoantibodies
ADC AIRR Data Commons
AIM Activation-induced marker
AIRR Adaptive Immune Receptor Repertoire
AIRR-seq AIRR sequencing
BCR B cell receptor
CDR3 Complementarity determining region 3
FAIR Findable, Accessible, Interoperable, Reusable
GEO Gene Expression Omnibus
HPAP Human Pancreas Analysis Program
IEDB Immune Epitope Database
MiAIRR Minimal information about AIRR
ML Machine learning
pLN Pancreatic lymph node(s)
SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2
scRNA-seq Single-cell RNA-seq
SRA Sequence Read Archive
T1D TCR/BCR Repository The Type 1 Diabetes T Cell Receptor and B Cell Receptor Repository
TCR T cell receptor
TCRβ T cell receptor β chain
Tfh T follicular helper
Treg Regulatory T cell(s)
VDJ Variable, diversity and joining gene segments
Stephanie J. Hanna and Rachel H. Bonami contributed equally to this work. Aaron W. Michels and Todd M. Brusko contributed equally as joint senior authors.
Members of the Type 1 Diabetes AIRR Consortium are listed in the Acknowledgements.
原创: 十六点五 中山二院糖尿病足中心
当各大商场又响起刘德华的“恭喜你发财、恭喜你发财”的歌声,当广州逐步走向“空城”的时候,我们知道,春节又要来到了。兄弟科室不停地在“封科”,病房几乎已经完全空掉时候,我们糖尿病足的病房满满的,换药的专科护士过得那个充实啊,就好像春节与我们无关。
经过反复权衡掂量,以及与患者、患者家属沟通,决定对于患者生长比较好的右足采取“点状植皮”,以加速患者伤口愈合,减少伤口的渗出。在进行植皮之前,首先再次对伤口进行清创,尽可能清除可能影响植皮效果的组织,之后装负压(2019年1月24日),准备下周四(2019年1月31日)在手术台上拆负压,直接植皮,之后再装负压,以促进植皮的贴敷,增加植皮的成功率。
2019年1月22日,对患者的足进行了第一次清创,效果如下:
由于各种原因,患者到中心的合作医院治疗了整整两个星期。在不断的微信沟通下,合作医院的医生进行了不懈的努力,患者继续向保足的方向又前进了几步。
伤口世界平台生态圈,以“关爱人间所有伤口患者”为愿景,连接、整合和拓展线上和线下的管理慢性伤口的资源,倡导远程、就近和居家管理慢性伤口,解决伤口专家的碎片化时间的价值创造、诊疗经验的裂变复制、和患者的就近、居家和低成本管理慢性伤口的问题。
2019广东省医疗行业协会伤口管理分会年会
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