SummarySplenectomy results in an increased risk of sepsis. The autogenous transplant of the spleen is an option for preserving splenic functions after total splenectomy. In this study, the capacity of animals undergoing autogenous spleen transplantation to respond to Staphylococcus aureus infection was investigated. BALB/c mice were divided into three groups: splenectomy followed by autotransplantation in the retroperitonium (AT), splenectomized only (SP) and operated non-splenectomized sham control (CT). Thirty days after surgery the mice were infected intravenously with S. aureus. Splenectomized mice had a higher number of colony-forming units (CFU) of S. aureus in liver and lungs in comparison with either AT or with CT mice (P < 0·05). Higher CFU numbers in lung of SP mice correlated with elevated production of interleukin-10 associated with a lower production of interferon-g and tumour necrosis factor-a. However, systemically, the level of tumour necrosis factor-a was higher in the SP group than in CT or AT. Lower titres of specific anti-S. aureus immunoglobulin (Ig)M and IgG1 were observed 6 days after infection in SP mice in comparison either with the AT or CT groups. Thus, splenectomy is detrimental to the immune response of BALB/c mice against infection by S. aureus which can be re-established by autogenous implantation of the spleen.

The high incidence of overwhelming postsplenectomy infection caused by Streptococcus pneumoniae can be reduced by splenic autotransplantation. In this study the effect of splenectomy and splenic autotransplantation on the immune response to S. pneumoniae infection was investigated. Balb/c mice were divided into three groups: splenectomized (SP), splenectomized and autotransplanted (AT), and sham operated control (CT). Five days post-infection the serum antibody levels were measured and the number of S. pneumoniae CFU, neutrophil accumulation and IL-17 production in the liver and lungs were investigated. SP mice showed greater number of bacteria in both organs and lower serum levels of S. pneumoniae-specific IgM, IgG1 and IgG2a antibodies. IL-17 production and neutrophil recruitment to the liver and lungs were lower in SP mice, in comparison with both the CT and the AT groups. Levels of S. pneumoniae-specific IgM, CFU counts, neutrophil accumulation and IL-17 production did not differ significantly between the CT and AT groups. These results suggest that splenic autotransplantation restores the capacity of splenectomized mice to fight S. pneumoniae infection.

Purpose The experience with 125Iodine (I125) plaque brachytherapy in the treatment of IM at the Princess Margaret Hospital/University Health Network is the subject of the report to follow. Methods All cases of IM submitted to I125 plaque radiotherapy were included. Patients' demographic, clinical, management, and follow‐up data were reviewed. Outcome measures included rates of tumor control, eye preservation, systemic metastases, and brachytherapy‐related complications. Results Fourteen IMs were included in the study. All patients had blue/green irises. Mean largest basal dimension and thickness were 7.1 +/‐ 2.1 mm (range, 4.0 to 11.5 mm) and 2.2 +/‐ 0.8 mm (range, 1.0 to 3.5 mm), respectively. Ten patients (71%) had seeding and 2 (14%) had glaucoma at presentation. Median follow‐up was 26.6 +/‐ 19.5 months (range, 6 to 72 months). Tumor control was achieved in 100% of the cases and no eye was enucleated because of radiation‐induced complications. At last visit, all patients were alive and free of metastasis. Final visual acuity was the same as or better than before treatment in 9 patients (75%). Cataract was the most common complication (8; 75%), followed by persistent glaucoma (2; 17%) and anterior uveitis (1; 8%). No other significant complication was seen during the follow‐up period. Conclusion Plaque radiotherapy is a safe and effective conservative treatment option for IM, although cataract is a common, yet treatable, complication. This treatment scheme circumvents an intraocular procedure and may avoid the dissemination of malignant cells, and provides a margin of safety in the treatment of clinically undetectable disease.

Belfort et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 3.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Background: Uveal melanoma (UM) cell lines, when exposed to blue light in vitro, show a significant increase in proliferation. In order to determine if similar effects could be seen in vivo, we investigated the effect of blue light exposure in a xenograft animal model of UM.

Purpose: We previouly demonstrated the feasibility of a human uveal melanoma GFP model in nude mice. We were able to monitor the preferential colonization of the liver by malignant cells during a 20‐day period. In this study we extended the observation period in order to observe disease progression and metastatic growth. Methods: Five hundred thousand, GFP transfected, human primary uveal melanoma cells (92.1) were injected into the tail vein of 30 nude mice at time zero. Starting at day one, five mouse per week was imaged, using an abdominal incision to expose the liver, for up to 60 minutes before sacrifice. The liver was imaged in vivo and post mortem, while the lungs, spleen, and kidney were all examined post‐mortem for GFP expression. Histopathological examination of all organs was performed to ensure that the GFP signal was arising from malignant cells. Results: In vivo imaging of the liver revealed positive GFP signal in all mice throughout the experiment. Malignant cells seeded the liver after injection, but there was no apparent tumor growth upon completion of the experiment. The micrometastatic foci remained viable without changes in size or intensity of the signal. No tumors were seen in any other organ at the end of the experiment. Histopathology confirmed that the cells emitting GFP were malignant cells. Conclusions: The results of this uveal melanoma model show great promise for understanding the previously unobservable interactions between single human uveal melanoma cells and native liver tissue. The fact that our cells successfully colonize the liver yet remain dormant for six weeks should actually mirror the disease in humans; metastases in patients takes roughly five to ten years to develop.