Shaping the Future of Cardiovascular Disease by 3D Printing Applications in Stent Technology and its Clinical Outcomes.

Cardiovascular disease (CVD) is a leading cause of death worldwide. In recent years, 3D printing technology has ushered in a new era of innovation in cardiovascular medicine. 3D printing in CVD management encompasses various aspects, from patient-specific models and preoperative planning to customized medical devices and novel therapeutic approaches. In-stent technology, 3D printing has revolutionized the design and fabrication of intravascular stents, offering tailored solutions for complex anatomies and individualized patient needs. The advantages of 3D-printed stents, such as improved biocompatibility, enhanced mechanical properties, and reduced risk of in-stent restenosis. Moreover, the clinical trials and case studies that shed light on the potential of 3D printing technology to improve patient outcomes and revolutionize the field has been comprehensively discussed. Furthermore, regulatory considerations, and challenges in implementing 3D-printed stents in clinical practice are also addressed, underscoring the need for standardization and quality assurance to ensure patient safety and device reliability. This review highlights a comprehensive resource for clinicians, researchers, and policymakers seeking to harness the full potential of 3D printing technology in the fight against CVD.

Stem cell expression of the AML1/ETO fusion protein induces a myeloproliferative disorder in mice.

The t(8;21)(q22;q22) translocation, present in 10-15% of acute myeloid leukemia (AML) cases, generates the AML1/ETO fusion protein. To study the role of AML1/ETO in the pathogenesis of AML, we used the Ly6A locus that encodes the well characterized hematopoietic stem cell marker, Sca1, to target expression of AML1/ETO to the hematopoietic stem cell compartment in mice. Whereas germ-line expression of AML1/ETO from the AML1 promoter results in embryonic lethality, heterozygous Sca1(+/AML1-ETO ires EGFP) (abbreviated Sca(+/AE)) mutant mice are born in Mendelian ratios with no apparent abnormalities in growth or fertility. Hematopoietic cells from Sca(+/AE) mice have markedly extended survival in vitro and increasing myeloid clonogenic progenitor output over time. Sca(+/AE) mice develop a spontaneous myeloproliferative disorder with a latency of 6 months and a penetrance of 82% at 14 months. These results reinforce the notion that the phenotype of murine transgenic models of human leukemia is critically dependent on the cellular compartment targeted by the transgene. This model should provide a useful platform to analyze the effect of AML1/ETO on hematopoiesis and its potential cooperation with other mutations in the pathogenesis of leukemia.