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Supplemental Material for Retrospective Evaluation of Splenic Artery Embolization Outcomes in the Management of Blunt Splenic Trauma: A Single Centre Experience at a Large Level 1 Trauma Centre by C O’Rourke, H McKee, DO Wijeyaratnam, J Bajwa, L Tremblay, and E David in Canadian Association of Radiologists Journal

Sclerostin (Sost) is a negative regulator of bone formation and blocking its function via antibodies has shown great therapeutic promise by increasing both bone mass in humans and animal models. Sclerostin deletion in Sost KO mice (Sost-/- ) causes high bone mass (HBM) similar to sclerosteosis patients. Sost-/- mice have been shown to display an up to 300% increase in bone volume/total volume (BV/TV), relative to age-matched controls. It has been postulated that the main source of skeletal sclerostin is the osteocyte. To understand the cell-type specific contributions to the HBM phenotype described in Sost-/- mice, as well as to address the endocrine and paracrine mode of action of sclerostin, we examined the skeletal phenotypes of conditional Sost loss-of-function (SostiCOIN/iCOIN ) mice with specific deletions in (1) the limb mesenchyme (Prx1-Cre; targets osteoprogenitors and their progeny); (2) midstage osteoblasts and their progenitors (Col1-Cre); (3) mature osteocytes (Dmp1-Cre); and (4) hypertrophic chondrocytes and their progenitors (ColX-Cre). All conditional alleles resulted in significant increases in bone mass in trabecular bone in both the femur and lumbar vertebrae, but only Prx1-Cre deletion fully recapitulated the amplitude of the HBM phenotype in the appendicular skeleton and the B-cell defect described in the global KO. Despite WT expression of Sost in the axial skeleton of Prx1-Cre deleted mice, these mice also had a significant increase in bone mass in the vertebrae, but the sclerostin released in circulation by the axial skeleton did not affect bone parameters in the appendicular skeleton. Also, both Col1 and Dmp1 deletion resulted in a similar 80% significant increase in trabecular bone mass, but only Col1 and Prx1 deletion resulted in a significant increase in cortical thickness. We conclude that several cell types within the Prx1-osteoprogenitor-derived lineages contribute significant amounts of sclerostin protein to the paracrine pool of Sost in bone. © 2018 The Authors. Journal of Bone and Mineral Research Published by Wiley Periodicals, Inc.

A 50-year-old carpenter died in Western Pennsylvania of rabies on January 4, 1979. He had been hospitalized in an intensive care unit for 28 days. The diagnosis was made postmortem from light and electron microscopic examination of central nervous system tissue. Immunofluorescence studies confirmed the diagnosis later. No animal exposure was confirmed in this case. The clinical and neuropathologic findings of the patient are correlated. The importance of recognizing rabies and the protection of personnel who perform autopsies on these patients is emphasized. In addition, rabies should be considered in the differential diagnosis of radiculomyelitis (Guillain-Barre syndrome) and, in general, in any case of meningoencephalitis.

Iron and copper increased the decomposition of nitrite significantly during the first two hours of reaction when 150 parts per million (ppm) of nitrite and nitrogen was added to an acidic soil. Manganese was found to have a slight effect. There was no additional effect of the added metals after two hours reaction time. The higher concentration of metals was not effective in catalyzing the decomposition of the added nitrite in nitrogen. All the added nitrite nitrogen was not recovered and the deficit could be due to the formation of nitrogen gas.