Corneal Blood Staining Following Autologous Blood Injection for Hypotony Maculopathy

1997 ◽  
Vol 28 (10) ◽  
pp. 866-868
Author(s):  
Ramesh S Ayyala ◽  
Robert C Urban ◽  
Mina S Krishnamurthy ◽  
David J Mendelblatt
2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Nicola Massy-Westropp ◽  
Stuart Simmonds ◽  
Suzanne Caragianis ◽  
Andrew Potter

Purpose. This study explored the effect of autologous blood injection (with ultrasound guidance) to the elbows of patients who had radiologically assessed degeneration of the origin of extensor carpi radialis brevis and failed cortisone injection/s to the lateral epicondylitis.Methods. This prospective longitudinal series involved preinjection assessment of pain, grip strength, and function, using the patient-rated tennis elbow evaluation. Patients were injected with blood from the contralateral limb and then wore a customised wrist support for five days, after which they commenced a stretching, strengthening, and massage programme with an occupational therapist. These patients were assessed after six months and then finally between 18 months and five years after injection, using the patient-rated tennis elbow evaluation.Results. Thirty-eight of 40 patients completed the study, showing significant improvement in pain; the worst pain decreased by two to five points out of a 10-point visual analogue for pain. Self-perceived function improved by 11–25 points out of 100. Women showed significant increase in grip, but men did not.Conclusions. Autologous blood injection improved pain and function in a worker’s compensation cohort of patients with chronic lateral epicondylitis, who had not had relief with cortisone injection.


2001 ◽  
Vol 132 (1) ◽  
pp. 36-40 ◽  
Author(s):  
Alan Burnstein ◽  
Darrell WuDunn ◽  
Yoko Ishii ◽  
Christian Jonescu-Cuypers ◽  
Louis B Cantor

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Arthur F Steinschneider ◽  
Che-Feng Chang ◽  
Michael H Askenase ◽  
Youxi Ai ◽  
Lauren H Sansing

Introduction: After intracerebral hemorrhage (ICH), erythrocytes contribute to secondary injury by releasing toxic hemoproteins. Our lab has previously shown that blood derived macrophages play an important role in ICH clearance but mechanisms of phagocytosis by human macrophages are unknown. This study aims to quantify eryptotic (phosphatidylserine (PtdSer)-expressing) red blood cells (RBCs) in an in vivo model of ICH, and to investigate the mechanisms that play a role in autologous eryptotic phagocytosis by human monocyte derived macrophages (huMDMs). Methods: ICH was induced in mice by autologous blood injection. The mice were sacrificed at 1 day after ICH. The brains were separated into hemispheres and digested into a single cell suspension for analysis by flow cytometry. Cells were stained with antibodies to cell surface markers and annexin V to quantify externalized PtdSer expression. Human monocytes were cultured with M-CSF for 7 days to generate huMDMs. Autologous RBCs were heat shocked (HS) to induce eryptosis. The huMDMs were cocultured with HS RBCs, HS RBCs treated with annexin V, or control RBCs. After 1 hour of coculture, the huMDMs were washed, stained and erythrophagocytosis quantified by microscopy. Results: The proportion of cells that externalized PtdSer increased by almost 20 fold at day 1 after ICH. Control brains mixed with fresh RBCs and subjected to tissue prep did not show PtdSer expression, ensuring that the PtdSer expression detected was induced in vivo (Fig A). HS RBCs increased PtdSer expression and were efficiently phagocytosed by huMDMs. Treatment of HS RBCs with annexin V to antagonize PtdSer-receptor interactions decreased RBC phagocytosis to levels comparable to control RBCs (Figs B and C). Conclusions: In vivo after ICH, erythrocytes externalize PtdSer, a cue to be engulfed by macrophages. Human macrophages phagocytose RBCs in a PtdSer-dependent mechanism. These findings highlight potential targets to enhance ICH clearance.


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