Objective: To describe the relationship of change in retinal vessel diameters to the subsequent 6-year incidence and progression of diabetic retinopathy (DR) and incidence of proliferative diabetic retinopathy (PDR) and macular edema (ME) in persons with diabetes mellitus.
Design: A total of 1098 persons with diabetes who had DR graded from fundus photographs and had computer-assisted measurements of the central retinal arteriolar equivalent (CRAE) and central retinal venular equivalent(CRVE) participated in examinations in 1980-1982, 1984-1986, and 1990-1992.
Results: During the first 4-year period, the mean change in CRAE and CRVE was −0.37 and 2.54 μm, respectively.The 6-year incidence and progression of DR and the incidence of PDR and ME from 1984-1986 to 1990-1992 were 56%, 39%, 15%, and 11%, respectively. In multivariate analyses, while controlling for duration, diabetes type, and other factors, an increase of 10 μm in CRVE from 1980-1982 to 1984-1986 was associated with increases in the 6-year incidence of DR (odds ratio [OR],1.26; 95% CI, 1.10-1.43), progression of DR (OR, 1.21;95% CI, 1.12-1.30), incidence of PDR (OR, 1.19; 95%CI, 1.07-1.32), and incidence of ME (OR, 1.16; 95% CI,1.03-1.31). No interactions of these associations by diabetes type were found (data not shown). Change in CRAE was unrelated to the incidence or progression of DR (data not shown).
Conclusions: Independent of DR severity level, glycemic control, and other factors, widening of the retinal venular but not arteriolar diameter was associated with subsequent incidence and progression of DR. The CRVE may provide additional information regarding the risk of incidence and progression of DR beyond traditional risk factors.
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http://dx.doi.org/10.1001/archophthalmol.2011.2560 | DOI Listing |
Neurol Neuroimmunol Neuroinflamm
March 2025
Department of Neurology with Institute of Translational Neurology, University Hospital 4 Münster, Germany.
Background And Objectives: Levels of activated complement proteins in the CSF are increased in people with multiple sclerosis (MS) and are associated with clinical disease severity. In this study, we determined whether complement activation profiles track with quantitative MRI metrics and liquid biomarkers indicative of disease activity and progression.
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JCO Clin Cancer Inform
January 2025
Emory University School of Medicine, Atlanta, GA.
Purpose: Immune checkpoint inhibitors (ICIs) have demonstrated promise in the treatment of various cancers. Single-drug ICI therapy (immuno-oncology [IO] monotherapy) that targets PD-L1 is the standard of care in patients with advanced non-small cell lung cancer (NSCLC) with PD-L1 expression ≥50%. We sought to find out if a machine learning (ML) algorithm can perform better as a predictive biomarker than PD-L1 alone.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Center for Mitochondrial and Epigenomic Medicine, The Children's Hospital of Philadelphia, Philadelphia, PA 19104.
Mitochondrial DNA (mtDNA) is highly polymorphic, and host mtDNA variation has been associated with altered cancer severity. To determine the basis of this mtDNA-cancer association, we analyzed conplastic mice with the C57BL/6J (B6) nucleus but two naturally occurring mtDNA lineages, and , where mitochondria generate more oxidative phosphorylation (OXPHOS)-derived reactive oxygen species (mROS). In a cardiac transplant model, Foxp3+ T regulatory (Treg) cells supported long-term allograft survival, whereas Treg cells failed to suppress host T effector (Teff) cells, leading to acute rejection.
View Article and Find Full Text PDFJ Proteome Res
January 2025
Department of Thoracic Surgery, Ningbo No.2 Hospital, Ningbo, 315010 Zhejiang, China.
Arch Pharm Res
January 2025
Laboratory of Biochemistry and Immunology, College of Veterinary Medicine, Chungbuk National University, Cheongju, 28644, Republic of Korea.
Despite significant progress in the field of human breast cancer research and treatment, there is a consistent increase in the incidence rate of 0.5 percent annually, posing challenges in the development of effective novel therapeutic strategies. The failure rate of drugs in clinical trials stands at approximately 95%, primarily attributed to the limitations and lack of reliability of existing preclinical models, such as mice, which do not mimic human tumor biology.
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