Assessment of Keratitis Severity Using Quantitative Image Analysis in an In Vivo Murine Model of Staphylococcus aureus Bacterial Keratitis.

Purpose: Bacterial keratitis (BK) severity in murine models has traditionally been measured by subjective clinical grading or quantification of ocular bacterial burden. This investigation explores an objective and repeatable quantification of slit lamp photography (SLP) images to measure BK severity.

Methods: BALB/c strain mice underwent three parallel scratches of the right cornea with subsequent inoculation of 107Staphylococcus aureus cells.

Patient-Reported Outcomes After Corneal Transplantation.

Purpose: To characterize vision-related quality of life after penetrating keratoplasty (PKP), deep anterior lamellar keratoplasty (DALK), Descemet stripping automated endothelial keratoplasty (DSAEK), and Descemet membrane endothelial keratoplasty (DMEK) using the National Eye Institute Visual Function Questionnaire (NEI-VFQ 9).

Methods: Using the Sight Outcomes Research Collaborative ophthalmology electronic health record repository, questionnaire responses were obtained from 103 PKP patients, 24 DALK patients, 42 DSAEK patients, and 50 DMEK patients undergoing postoperative examination. No exclusions were made based on preoperative diagnosis, age, complications, or comorbidities.

C-Mpl Is Expressed on Osteoblasts and Osteoclasts and Is Important in Regulating Skeletal Homeostasis.

C-Mpl is the receptor for thrombopoietin (TPO), the main megakaryocyte (MK) growth factor, and c-Mpl is believed to be expressed on cells of the hematopoietic lineage. As MKs have been shown to enhance bone formation, it may be expected that mice in which c-Mpl was globally knocked out (c-Mpl(-/-) mice) would have decreased bone mass because they have fewer MKs. Instead, c-Mpl(-/-) mice have a higher bone mass than WT controls.

GATA-1 deficiency rescues trabecular but not cortical bone in OPG deficient mice.

GATA-1(low/low) mice have an increase in megakaryocytes (MKs) and trabecular bone. The latter is thought to result from MKs directly stimulating osteoblastic bone formation while simultaneously inhibiting osteoclastogenesis. Osteoprotegerin (OPG) is known to inhibit osteoclastogenesis and OPG(-/-) mice have reduced trabecular and cortical bone due to increased osteoclastogenesis.

Pyk2 regulates megakaryocyte-induced increases in osteoblast number and bone formation.

Preclinical and clinical evidence from megakaryocyte (MK)-related diseases suggests that MKs play a significant role in maintaining bone homeostasis. Findings from our laboratories reveal that MKs significantly increase osteoblast (OB) number through direct MK-OB contact and the activation of integrins. We, therefore, examined the role of Pyk2, a tyrosine kinase known to be regulated downstream of integrins, in the MK-mediated enhancement of OBs.

Megakaryocytes regulate expression of Pyk2 isoforms and caspase-mediated cleavage of actin in osteoblasts.

The proliferation and differentiation of osteoblast (OB) precursors are essential for elaborating the bone-forming activity of mature OBs. However, the mechanisms regulating OB proliferation and function are largely unknown. We reported that OB proliferation is enhanced by megakaryocytes (MKs) via a process that is regulated in part by integrin signaling.