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Giant cell tumor of bone (GCTB) is a rare bone tumor often necessitating surgical intervention, radiation therapy, or treatment with bisphosphonates or denosumab. 99mTc-MDP bone scintigraphy for GCTB has limited specificity, and the relatively high uptake of 18F-FDG in GCTB makes it challenging to differentiate it from other benign bone tumors. More specific detection and treatment modalities for GCTB are needed to enhance patient monitoring and outcomes. Prostate Specific Membrane Antigen (PSMA) is present in the neovasculature of various tumors, yet unexplored in GCTB. PSMA-targeted imaging and radiotherapeutic agents Locametz and Pluvicto are a powerful theranostic pair for detecting and treating PSMA-positive metastatic tumors, including those in bone, and thus have considerable potential to be repurposed for GCTB. This study aimed to determine if the vasculature of GCTB was PSMA-positive and whether targeting it with PSMA-specific agents was feasible. Using bone core samples from 28 GCTB patients and 9 negative controls, we present the first robust detection of PSMA on the tumor vasculature of GCTB. To demonstrate the potential repurposed use of PSMA-targeted agents in detecting and treating GCTB, we used a PSMA-specific fluorescent probe (FAM-C6-1298) as a model for these radiopharmaceutical agents. Incubation of fresh GCTB tissue samples with FAM-C6-1298 showed increased fluorescence intensity compared to controls, indicating successful targeting of PSMA in GCTB tissue. In conclusion, our data established that PSMA is not only present in the tumor vasculature of GCTB patient tissue but can be effectively targeted with repurposed PSMA-specific radiopharmaceuticals for diagnosis and therapy. [ABSTRACT FROM AUTHOR]

Diversity enriches the educational experience by improving intellectual engagement, self-motivation, citizenship, cultural engagement, and academic skills like critical thinking, problem-solving, and writing for students of all races. Faculty role models from similar backgrounds are essential for students from traditionally underrepresented groups as it sends a powerful message of support, belonging, and the confidence to pursue higher education. However, in the biomedical sciences, the percentage of historically underrepresented tenure-track faculty is far lower than that of their white colleagues. For this to change, a strong strategic plan and commitment from the university are imperative. This scoping review will assess the size and scope of available peer-reviewed research literature on diversity programs that aim to increase the recruitment and retention of biomedical sciences research faculty and are implemented and evaluated at American Universities. The information provided in this scoping review will help universities identify novel, successful diversity-based approaches for recruiting and retaining biomedical science faculty that might suit their own unique academic and geographic needs and be incorporated into their diversity initiatives and policies. The review follows the Population-Concept-Context methodology for Joanna Briggs Institution Scoping Reviews. Relevant peer-reviewed studies published in English between June 1, 2012, to June 1, 2022, will be identified from the following electronic databases; MEDLINE (PubMed), Scopus (Elsevier), EMBASE (Elsevier), CINAHL (EBSCO), and ERIC (EBSCO). The search strings using the key variables "biomedical research faculty," "recruitment/retention," "diversity/ minority/ underrepresented, and "mentoring" will be conducted using Boolean logic. Two independent reviewers will conduct all title and abstract screening, followed by a full article screening and data extraction. Due to the possible heterogeneity of the studies, we hope to use either a narrative analysis and/or descriptive figures/tables to depict the results. [ABSTRACT FROM AUTHOR]

CD13/Aminopeptidase N is a transmembrane metalloproteinase that is expressed in many tissues where it regulates various cellular functions. In inflammation, CD13 is expressed on myeloid cells, is up-regulated on endothelial cells at sites of inflammation and mediates monocyte/endothelial adhesion by homotypic interactions. In animal models the lack of CD13 alters the profiles of infiltrating inflammatory cells at sites of ischaemic injury. Here, we found that CD13 expression is enriched specifically on the pro-inflammatory subset of monocytes, suggesting that CD13 may regulate trafficking and function of specific subsets of immune cells. To further dissect the mechanisms regulating CD13-dependent trafficking we used the murine model of thioglycollate-induced sterile peritonitis. Peritoneal monocytes, macrophages and dendritic cells were significantly decreased in inflammatory exudates from global CD13KO animals when compared with wild-type controls. Furthermore, adoptive transfer of wild-type and CD13KO primary myeloid cells, or wild-type myeloid cells pre-treated with CD13-blocking antibodies into thioglycollate-challenged wild-type recipients demonstrated fewer CD13KO or treated cells in the lavage, suggesting that CD13 expression confers a competitive advantage in trafficking. Similarly, both wild-type and CD13KO cells were reduced in infiltrates in CD13KO recipients, confirming that both monocytic and endothelial CD13 contribute to trafficking. Finally, murine monocyte cell lines expressing mouse/human chimeric CD13 molecules demonstrated that the C-terminal domain of the protein mediates CD13 adhesion. Therefore, this work verifies that the altered inflammatory trafficking in CD13KO mice is the result of aberrant myeloid cell subset trafficking and further defines the molecular mechanisms underlying this regulation. [ABSTRACT FROM AUTHOR]