Timothy S. Kern

Transducin1, Phototransduction and the Development of Early Diabetic Retinopathy.

Pathophysiology of Diabetic Retinopathy: Contribution and Limitations of Laboratory Research.

Neutrophil elastase contributes to the pathological vascular permeability characteristic of diabetic retinopathy.

Successful induction of diabetes in mice demonstrates no gender difference in development of early diabetic retinopathy.

Photoreceptor cells and RPE contribute to the development of diabetic retinopathy.

Negative regulation of FOXP3 expression by c-Rel O-GlcNAcylation.

Sildenafil-evoked photoreceptor oxidative stress in vivo is unrelated to impaired visual performance in mice.

Regulation of Adrenergic, Serotonin, and Dopamine Receptors to Inhibit Diabetic Retinopathy: Monotherapies versus Combination Therapies.

A Randomized Trial of Photobiomodulation Therapy for Center-Involved Diabetic Macular Edema with Good Visual Acuity (Protocol AE).

Neutrophil-Derived Proteases Contribute to the Pathogenesis of Early Diabetic Retinopathy.

Nanomedicine platform for targeting activated neutrophils and neutrophil-platelet complexes using an α-antitrypsin-derived peptide motif.

ICAM-1 on the luminal surface of endothelial cells is induced to a greater extent in mouse retina than in other tissues in diabetes.

Defibrinogenation Ameliorates Retinal Microgliosis and Inflammation in A CX3CR1-Independent Manner.

CCR2-positive monocytes contribute to the pathogenesis of early diabetic retinopathy in mice.

Stress resilience-enhancing drugs preserve tissue structure and function in degenerating retina via phosphodiesterase inhibition.