Service evaluation of radiographer-led vetting and protocoling of Computed Tomography (CT) scan requests in a Singapore public healthcare institution.

INTRODUCTION: A service improvement project involving the vetting and protocoling of Computed Tomography (CT) scan requests by qualified CT radiographers was initiated in 2018. AIM: This study provides a comprehensive evaluation of how a radiographer-led initiative aims to ensure that the CT scan requests received by the Radiology department are clinically appropriate, which in turn will reduce interruptions to the interpretation and reporting of imaging examinations by radiologists, who might otherwise be required to attend to clinically inappropriate and wrongly protocolled CT scan requests. METHOD: Outpatient CT scan requests received from July to October 2021 were vetted and protocolled by a qualified CT-trained radiographer for parameters which included the appropriateness of the clinical indication, adequacy of patient preparation for the scan, as well as the suitability of the requested examination protocol pertaining to the need for contrast media, multiple contrast-enhanced imaging phases, and the appropriateness of the scan range. RESULTS: Poor patient preparation and insufficient or inaccurate clinical indications were the most common findings during the vetting process (71%). Out of the 64 CT scan requests with protocol errors, 77% were attributed to contrast media type errors. The odds of incorrect CT scan requests increased with the requesting clinician's rank, while there was no such significant correlation with the clinical specialty of the requesting clinician or the CT scan type. CONCLUSION: The meticulous vetting of imaging requests helps to ensure that limited imaging hardware resources are allocated to more clinically appropriate cases, correct protocols are applied to requested imaging scans, and that patients undergoing imaging are adequately prepared, thereby enhancing overall patient care. IMPLICATIONS FOR PRACTICE: Vetting of imaging requests by radiographers, who are capable to make appropriate clinical decisions related to their enhanced level of practice ensures patient safety and optimisation of Radiology resources.

Cloning of an infectious milk-borne mouse mammary tumor virus (MMTV) DNA from a mammary tumor that developed in an endogenous MMTV-free wild mouse.

Molecular characterization of infectious mouse mammary tumor viruses (MMTVs) has been hampered due to the problem of cloning a full-length exogenous virus into a plasmid. The present report describes our strategy for obtaining a full-length clone of an exogenous MMTV from a mouse mammary tumor that arose spontaneously in a wild Chinese mouse free of endogenous MMTV and shows that the cloned virus (JYG-MMTV) is expressed in rat RBA cells. Four-week-old C58/J x CBA/CaJ female mice, free of both endogenous and exogenous MMTVs, were injected with virus-secreting RBA cells. The progeny of these mice were bred, and their offspring were tested for the presence of MMTV. These third-generation mice were found to actively produce MMTV that was shed in their milk and transmitted to their offspring. The virus was detected not only in the mammary glands of these young mice, but also in their spleens and bone marrow. These results suggest that our plasmid-cloned exogenous JYG-MMTV is infectious. This virus can now be used effectively in manipulating the various genes of JYG-MMTV and other MMTV strains to understand their structure/function relationships.

The role of LY49 NK cell subsets in the regulation of murine cytomegalovirus infections.

The distributions and functions of NK cell subsets, as defined by the expression of Ly49 NK cell receptors, were examined in murine CMV (MCMV)-infected mice. MCMV induced a reduction in NK1.1+ cell number in the spleen and an increase in the peritoneal exudate cells. Within the splenic NK1.1+ population, proportional increases in Ly49A+ and Ly49G2+ cells but decreases in Ly49C+ and Ly49D+ cells were observed 3 days post-MCMV infection, but within the peritoneal NK1.1+ cell populations there were proportional decreases in Ly49A+ cells and increases in Ly49C+, Ly49D+, and Ly49G2+ cells. Lymphocytic choriomeningitis virus did not elicit a comparable NK cell subset distribution. Lymphokine-activated killer cells were sorted into different Ly49 NK cell subsets and adoptively transferred into C57BL/6 suckling mice. Regulation of MCMV synthesis in these suckling mice was shown to be an IFN-gamma-dependent, perforin- and Cmv-1-independent process, and each NK cell subset mediated anti-viral activity. In adult C57BL/6 mice, the control of MCMV in the spleen is mediated by a perforin-dependent mechanism, regulated in part by the Cmv-1 gene, which maps closely to the Ly49 family. In vivo depletions of either one or two of the Ly49 subsets in adult mice did not affect the ability of the residual NK cells to regulate MCMV synthesis. These data provide evidence of NK cell subset distribution and function in MCMV infection, but no individual subset was required for the Cmv-1-like regulation of MCMV synthesis.

Distinct organ-dependent mechanisms for the control of murine cytomegalovirus infection by natural killer cells.

Antiviral mechanisms by which natural killer (NK) cells control murine cytomegalovirus (MCMV) infection in the spleens and livers of C57BL/6 mice were measured, revealing different mechanisms of control in different organs. Three days postinfection, MCMV titers in the spleens of perforin 0/0 mice were higher than in those of perforin +/+ mice, but no elevation of liver titers was found in perforin 0/0 mice. NK cell depletion in MCMV-infected perforin 0/0 mice resulted only in an increase in liver viral titers and not in spleen titers. Depletion of gamma interferon (IFN-gamma) in C57BL/6 mice by injections with monoclonal antibodies to IFN-gamma resulted in an increase of viral titers in the liver but not in the spleen. Analyses using IFN-gamma-receptor-deficient mice, rendered chimeric with C57BL/6 bone marrow cells, indicated that in a recipient environment where IFN-gamma cannot exert its effects, the depletion of NK cells caused an increase in MCMV titers in the spleens but had little effect in the liver. IFN-gamma has the ability to induce a variety of cells to produce nitric oxide, and administrating the nitric oxide synthase inhibitor N(omega)-monomethyl-L-arginine into MCMV-infected C57BL/6 mice resulted in MCMV titer increases in the liver but not in the spleen. Taken together, these data suggest that in C57BL/6 mice, there is a dichotomy in the mechanisms utilized by NK cells in the regulation of MCMV in different organs. In the spleen NK cells exert their effects in a perforin-dependent manner, suggesting a cytotoxic mechanism, while in the liver the production of IFN-gamma by NK cells may be a predominant mechanism in the regulation of MCMV synthesis. These results may explain why the Cmv-lr locus, which maps closely to genes regulating NK cell cytotoxic function, confers an NK cell-dependent resistance to MCMV infection in the spleen but not in the liver.

NK cell response to viral infections in beta 2-microglobulin-deficient mice.

Because class I MHC Ags have been implicated as modulators of target cell sensitivity to NK cell-mediated lysis, the regulation of virus infections and the fate of NK cells and their natural targets was examined in beta 2-microglobulin-deficient mice, which have defective class I MHC expression. Infections with either the NK cell-sensitive murine cytomegalovirus (MCMV) or the NK cell-resistant lymphocytic choriomeningitis virus (LCMV) significantly augmented NK cell activity in either C57BL/6 (+/+) or beta 2-microglobulin knockout (-/-) mice. Depletion of NK cells in vivo with antiserum to asialo-GM1 markedly enhanced the synthesis of MCMV but had no effect on the synthesis of LCMV in either strain of mouse. Analysis of naturally NK cell-sensitive thymocyte targets from these virus-infected -/- mice revealed no cell surface expression of class I MHC detectable by conformation-dependent or -independent Abs, but the virus infections enhanced class I expression on thymocytes from +/+ mice. The sensitivity of +/+ thymocytes to NK cell-mediated lysis was markedly reduced after in vivo poly inosinic:cytidylic and treatment or viral infection; in contrast, the sensitivity of the -/- thymocytes was significantly less affected by poly inosinic:cytidylic acid treatment or viral infection. These data indicate that the normal expression of class I MHC Ags on NK cells or their targets is not required for the antiviral functions of NK cells against a NK-sensitive virus (MCMV) nor do they protect a NK-resistant virus (LCMV) from the antiviral activity of NK cells.

Extraosseous Ewing's sarcoma: report of a case and review of literature.

Extraosseous Ewing's sarcoma is a primitive small round cell neoplasm found in children and young adults. Extraosseous Ewing's sarcoma has been recognized as being histologically indistinguishable from Ewing's sarcoma of the bone and other round cell tumors. Our study reports the clinical course and histopathologic features of this rare variant, occurring in a 13 year-old boy, who presented with a subcutaneous tumor of the right thigh without osseous involvement. Wedge resection of the tumor was done followed by chemotherapy with Actinomycin-D, Oncovin and Endoxan.