5 research outputs found

    Albumin in neural retina (a possible marker of vascular permeability).

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    <p>The retina wsa perfused to remove blood, and albumin remaining in the retina after that perfusion was interpretd as having leaked into the neural retina. Diabetes significanlty increased that albumin accumulation in wildtpe chimeras. Deletion of IL1β or TLR2/4 or MyD88 from marrow-derived cells had no significant effect on that parameter. n=5 per group.</p

    MyD88 pathways in leukocytes regulate diabetes-induced generation of superoxide by the retina.

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    <p>Diabetes caused a doubling of superoxide production by retina in wildype mice, whereas deletion of MyD88, IL-1βr or TLR2/4 only from marrow-derived cells significantly inhibited the diabetes-induced increase in superoxide generation by the retina. n=5-8 per group.</p

    Adherence of leukocytes to the endothelia of the retinal vascular wall (leukostasis) is increased in diabetes, and occurs via MyD88-dependent signalling pathways.

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    <p>Wildtype leukocytes from diabetic mice attached to the vessel wall in significantly greater numbers than did leukocytes from nondiabetic wildtypes, whereas leukocytes lacking either MyD88, TLR2/4 or IL-1βr underwent less diabetes-induced leukostasis than wildtype diabetic controls. Photomicrograph is a representative picture of a diabetic wildtyype animal. n=5 per group; representative of two repeat experiments.</p

    Cytokine production in diabetic retinas.

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    <p>Retinas from diabetic and normal mice were stimulated with TLR ligands, and retinal generation of CXCL1 and IL-6 were examined by ELISA. (A and B) retinas were incubated for 6h with 10 µg/ml of Pam3CysK (to activate TLR2), PolyI:C (TLR3), LPS (TLR4), CpG DNA (TLR9), or with IL-1ß (IL-1r). (C and D) IL-6 and CXCL1 production by retinas following incubation with media alone or containing 10 µg/ml Pam3CysK. Data are mean ± SD of three retinas per group, and are representative of two repeat experiments.</p
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