Virtual Reality Simulation-Based Training in Image-Guided Breast Intervention in Low- and Middle-Income Countries.

Online education has revolutionized global radiology education for low- and middle-income countries (LMICs). However, procedures requiring hands-on training, such as breast biopsies, are primarily taught through in-person sessions and patient interaction. Virtual reality (VR) offers an immersive way to simulate these sessions remotely. This Viewpoint presents an experience with an ultrasound-guided breast biopsy VR platform that may allow radiology residents in LMICs to practice breast interventions and provide all trainees with shared procedural experiences.

Ultrafast MR imaging findings of 2 different subtypes in a male patient with bilateral breast cancer.

Bilateral breast cancer in males is an exceedingly rare diagnosis. In this case report, we will discuss the ultrafast sequence findings of a bilateral male breast cancer with different subtypes on his staging dynamic contrast enhanced (DCE) MRI with ultrafast technique. A 94-year-old male presented with bilateral palpable complaints in his breasts. Diagnostic mammography and ultrasound images demonstrated bilateral irregular masses with nipple retraction. Biopsies were performed and the histopathologic examination revealed invasive breast carcinoma of no special type in 1 breast and invasive micropapillary carcinoma in the other breast. Staging MRI with ultrafast sequence showed significant enhancement differences between 2 different subtypes, correlating with the different levels of tumor aggressiveness. Different ultrafast metrics, such as time-to-enhancement and maximum slope, may help to differentiate between several subtypes of breast cancer and serve as prognostic indicators. This case report discusses the application of ultrafast sequence in predicting breast cancer subtypes in a male patient with bilateral disease.

Angiotensin II-induced Hypertension is Reduced by Deficiency of P-selectin Glycoprotein Ligand-1.

Identification of inflammatory mediators that regulate the vascular response to vasopressor molecules may aid in the development of novel therapeutic agents to treat or prevent hypertensive vascular diseases. Leukocytes have recently been shown to be capable of modifying blood pressure responses to vasopressor molecules. The purpose of this study was to test the hypothesis that deficiency of the leukocyte ligand, Psgl-1, would reduce the pressor response to angiotensin II (Ang II). Mice deficient in Psgl-1 (Psgl-1-/-) along with wild-type (WT) controls were treated for 2 weeks with a continuous infusion of Ang II. No differences in blood pressure between the groups were noted at baseline, however after 5 days of Ang II infusion, systolic blood pressures were higher in WT compared to Psgl-1-/- mice. The pressor response to acute administration of high dose Ang II was also attenuated in Psgl-1-/- compared to WT mice. Chimeric mice with hematopoietic deficiency of Psgl-1 similarly showed a reduced pressor response to Ang II. This effect was associated with reduced plasma interleukin-17 (IL-17) levels in Psgl-1-/- mice and the reduced pressor response was restored by administration of recombinant IL-17. In conclusion, hematopoietic deficiency of Psgl-1 attenuates Ang II-induced hypertension, an effect that may be mediated by reduced IL-17.

Hematopoietic Deficiency of miR-223 Attenuates Thrombosis in Response to Photochemical Injury in Mice.

Some studies have shown that levels of MicroRNA (miR)-223 derived from platelets in the plasma are reduced following inhibition of platelet function, while others have shown a correlation between low plasma miR-223 and high on-treatment platelet reactivity. The present study seeks to investigate the role of miR-223 in arterial thrombosis. A model of photochemical-induced carotid thrombosis was applied to miR-223 deficient mice and littermate (WT) controls. Mice deficient in miR-223 exhibited significantly prolonged times to occlusive thrombosis compared to WT mice indicating a protective effect of miR-223 deficiency. Bone marrow transplantation experiments confirmed that the hematopoietic pool of miR-223 was responsible for differences in thrombosis times. Transfusion of either WT platelets or extracellular vesicles derived from WT platelets were both sufficient to shorten thrombosis times in miR-223 deficient recipients. The effect of platelet transfusions on IGF-1R was explored. These experiments revealed that vascular IGF-1R was down-regulated by platelet miR-223. Furthermore, inhibition of IGF-1R abolished the protection conferred by miR-223 deficiency on thrombosis. In conclusion, platelet miR-223 is a regulator of arterial thrombosis following endothelial injury through effects on vascular wall IGF-1R. This study indicates that platelet miR-223 is a potential therapeutic target for prevention of arterial thrombosis.

Psgl-1 Deficiency is Protective against Stroke in a Murine Model of Lupus.

Systemic lupus erythematosus (SLE) is associated with an elevated risk of vascular complications, including premature stroke. Therapies targeting leukocyte recruitment may be beneficial in reducing vascular complications associated with SLE. Lupus was induced in female wild-type (WT) and P-selectin glycoprotein ligand-1 deficient (Psgl-1(-/-)) mice with pristane. Stroke was induced following photochemical injury to the middle cerebral artery (MCA). Stroke size was increased in pristane-treated WT mice compared to non-pristane-treated WT controls. However, stroke size was not increased in pristane-treated Psgl-1(-/-) mice compared to controls, despite evidence of increased nephritis in Psgl-1(-/-) mice. Pristane-treated WT mice showed elevated anti-dsDNA, anti-snRNP, CXCL1, and MCP-1 levels compared to untreated mice; however levels of anti-snRNP, MCP-1, and CXCL1 were reduced in pristane-treated Psgl-1(-/-) mice compared to pristane-treated WT mice. Infiltration of neutrophils and macrophages at the cerebral infarction site were reduced in pristane-treated Psgl-1(-/-) mice compared to pristane-treated WT mice. In conclusion, the increase in stroke size associated with lupus is prevented by Psgl-1 deficiency while nephritis is exacerbated. Therapies targeting Psgl-1 may be useful in the management of SLE patients at high risk of acute vascular complications although elucidation of downstream pathways will be necessary to identify targets that do not promote nephritis.