High-Order Fiber Mode Beam Parameter Optimization for Transport and Rotation of Single Cells

Optical tweezers are becoming increasingly important in biomedical applications for the trapping, propelling, binding, and controlled rotation of biological particles. These capabilities enable applications such as cell surgery, microinjections, organelle extraction and modification, and preimplantation genetic diagnosis. In particular, optical fiber-based tweezers are compact, highly flexible, and can be readily integrated into lab-on-a-chip devices. Taking advantage of the beam structure inherent in high-order modes of propagation in optical fiber, LP11, LP21, and LP31 fiber modes can generate structured radial light fields with two or more concentrations in the cross-section of a beam, forming multiple traps for bioparticles with a single optical fiber. In this paper, we report the dynamic modeling and optimization of single cell manipulation with two to six optical traps formed by a single fiber, generated by either spatial light modulation (SLM) or slanted incidence in laser-fiber coupling. In particular, we focus on beam size optimization for arbitrary target cell sizes to enable trapped transport and controlled rotation of a single cell, using a point matching method (PMM) of the T-matrix to compute trapping forces and rotation torque. Finally, we validated these optimized beam sizes experimentally for the LP21 mode. This work provides a new understanding of optimal optical manipulation using high-order fiber modes at the single-cell level

Camalexin Induces Apoptosis via the ROS-ER Stress-Mitochondrial Apoptosis Pathway in AML Cells

Camalexin is a phytoalexin that accumulates in various cruciferous plants upon exposure to environmental stress and plant pathogens. It was shown that camalexin has potent antitumor properties, but its underlying mechanisms are still elusive. In the present study, we evaluated the effects of camalexin on human leukemic cells and normal polymorph nuclear cells. CCK-8 assay was used to determine cell viability after camalexin treatment. Apoptosis, intracellular reactive oxygen species (ROS) levels, and loss of mitochondrial membrane potential (MMP) were measured by flow cytometry. The activity of SOD, catalase, and ratio of GSH/GSSG were assayed. ER stress and apoptotic signaling pathway was examined by Western blot. Xenograft mice were used to verify the effect of camalexin in vivo. Our results indicated that camalexin inhibited viability of leukemic but not normal polymorph nuclear cells. Furthermore, camalexin induces apoptosis via the mitochondrial pathway in a caspase-dependent manner. We also observed ER stress is located upstream of apoptosis induced by camalexin. Besides, ROS levels, SOD activity, CAT activity, and GSSG levels were significantly enhanced while the GSH level was decreased after treatment of camalexin. In addition, the generation of ROS is critical for the ER stress and apoptosis induced by camalexin. Finally, administration of camalexin suppresses xenograft tumor graft growth without obvious toxicity. Taken together, this study indicates that camalexin exerts antitumor effects against leukemia cells via the ROS-ER stress-mitochondrial apoptosis pathway