To determine whether herpes simplex virus type 1 (HSV-1) infection causes oxidative stress and lipid peroxidation in cultured neural cells, mouse P19 embryonal carcinoma cells were differentiated...

To better understand the pathogenesis of herpes simplex virus type 1 (HSV-1) infections of the nervous system, concentrations of F4-neuroprostanes (F4-NP) and F2-isoprostanes (F2-IP) in the murine...

To assess whether intravitreal rituximab 1 mg/0.1 cc penetrates the retina of Dutch-belted rabbits. Two right eyes of two rabbits were injected with intravitreal rituximab 1 mg/0.1 mL, and one right eye of one rabbit was injected with intravitreal tissue plasminogen activator (tPA) 12.5 microg/0.1 mL, as a protein control. The three left eyes received no intravitreal injections. The rabbits were killed; the eyes were enucleated and immediately frozen at -80 degrees C. Rituximab was detected using rabbit antihuman IgG (whole molecule) peroxidase conjugated antibody. tPA was detected using an antihuman IgG with a sheep antihuman tPA antibody conjugated with peroxidase. There was staining in all retinal layers of the two eyes injected with intravitreal rituximab, and no staining of the retina in the eye injected with intravitreal tPA. The three control eyes showed no staining in any retinal layer. Intravitreal rituximab at a dose of 1 mg/0.1 cc penetrates the retina of Dutch-belted rabbits while the control intravitreal tPA at a dose of 12.5 microg/0.1 cc does not.

Cancer stem cells have increased resistance against a variety of anti-tumor treatment modalities. Vasculogenic mimicry (VM) patterns are present in numerous malignant tumor types, represent the formation of perfusion pathways by tumor cells, and their presence in tumors is associated with adverse outcome. Earlier we have shown that VM-forming tumor cells in three-dimensional (3D) uveal melanoma cultures have increased resistance against cytotoxic agents and oncolytic herpes simplex virus-mediated destruction. The purpose of the current study was to explore the possibility that this increased resistance of VM-forming tumor cells is due to a cancer stem cell phenotype. The expression of cancer stem cell marker cluster of differentiation 271 (CD271) was determined in traditional two-dimensional (2D) and 3D cultures of C918 uveal melanoma cells by fluorescent immunocytochemistry. We found that the VM-forming tumor cell subpopulation in 3D cultures expressed CD271. In contrast, cells grown in 2D cultures and tumor cell subpopulations not participating in VM formation in 3D cultures were negative for CD271. These findings suggest that VM-forming uveal melanoma cells acquire a cancer stem cell-like phenotype that may play a role in the increased therapy resistance of these cells.