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Silicon Valley, and the U.S. tech sector more broadly, have changed the world in part by embracing a “move fast and break things” mentality popularized by Mark Zuckerberg. While it is true that the tech sector has attempted to break with such a reactive and flippant response to security concerns, including at Microsoft itself through its Security Development Lifecycle, cyberattacks continue at an alarming rate. As a result, there are growing calls from regulators around the world to change the risk equation. An example is the 2023 U.S. National Cybersecurity Strategy, which argues that “[w]e must hold the stewards of our data accountable for the protection of personal data; drive the development of more secure connected devices; and reshape laws that govern liability for data losses and harm caused by cybersecurity errors, software vulnerabilities, and other risks created by software and digital technologies.” What exact form such liability should take is up for debate. The defect model of products liability law is one clear option, and courts across the United States have already been applying it using both strict liability and risk utility framings in a variety of cases. This Article delves into the debates by considering how other cyber powers around the world—including the European Union—are extending products liability law to cover software, and it examines the lessons these efforts hold for U.S. policymakers with case studies focusing on liability for AI- generated content and Internet-connected critical infrastructure. 

Continuous perfusion is necessary to sustain microphysiological systems and other microfluidic cell cultures. However, most of the established microfluidic perfusion systems, such as syringe pumps, peristaltic pumps, and rocker plates, have several operational challenges and may be cost-prohibitive, especially for laboratories with no microsystems engineering expertise. Here, we address the need for a cost-efficient, easy-to-implement, and reliable microfluidic perfusion system. Our solution is a modular pumpless perfusion assembly (PPA), which is constructed from commercially available, interchangeable, and aseptically packaged syringes and syringe filters. The total cost for the components of each assembled PPA is USD 1–2. The PPA retains the simplicity of gravity-based pumpless flow systems but incorporates high resistance filters that enable slow and sustained flow for extended periods of time (hours to days). The perfusion characteristics of the PPA were determined by theoretical calculations of the total hydraulic resistance of the assembly and experimental characterization of specific filter resistances. We demonstrated that the PPA enabled reliable long-term culture of engineered endothelialized 3-D microvessels for several weeks. Taken together, our novel PPA solution is simply constructed from extremely low-cost and commercially available laboratory supplies and facilitates robust cell culture and compatibility with current microfluidic setups. 

Abstract Interactions between cells and their environment influence key physiologic processes such as their propensity to migrate. However, directed migration controlled by extrinsically applied electrical signals is poorly understood. Using a novel microfluidic platform, we found that metastatic breast cancer cells sense and respond to the net direction of weak (∼100 µV cm⁻¹), asymmetric, non-contact induced Electric Fields (iEFs). iEFs inhibited EGFR (Epidermal Growth Factor Receptor) activation, prevented formation of actin-rich filopodia, and hindered the motility of EGF-treated breast cancer cells. The directional effects of iEFs were nullified by inhibition of Akt phosphorylation. Moreover, iEFs in combination with Akt inhibitor reduced EGF-promoted motility below the level of untreated controls. These results represent a step towards isolating the coupling mechanism between cell motility and iEFs, provide valuable insights into how iEFs target multiple diverging cancer cell signaling mechanisms, and demonstrate that electrical signals are a fundamental regulator of cancer cell migration.