Work


Below are summaries of published and in-progress projects and earlier work in biology and materials science.

Code of Practice on Disinformation

Press coverage: The Verge, The Guardian, TechCrunch, Forbes, BBC

In September of 2023, TrustLab released a first-of-its kind study that measures the prevalence and sources of misinformation across major social platforms.  The measurement study was commissioned as part of the European Commission’s Code of Practice, the world's first self-regulatory instrument to fight disinformation.  Key metrics examined are discoverability, relative post engagement, absolute post engagement, and properties about disinformation actors, including ratio of disinformation actors, their account activities, and engagement with other users. The 71-page study provides a benchmark for policy evaluation and for the monitoring of disinformation over time. The test included prevalence and sources of disinformation across six major social media platforms (Facebook, Instagram, LinkedIn, TikTok, Twitter, and YouTube) in three countries: Poland, Slovakia, and Spain. 

Full Report link: trustlab.com/codeofpractice-disinformation

Novel Composite Hinge Fabrication Method

Presented to peers and colleagues in the Program for Research in Science and Engineering (PRISE), communicating technical materials science research to a broad public audience. Associated manuscript in preparation for Advanced Functional Materials in progress. Under the mentorship of Dr. Anne Meeussen and Asst. Prof. Kaitlyn Becker.

Metamaterials are physical structures with counterintuitive properties that emerge from their internal architecture. With thoughtful design, they can be used to manipulate optical, acoustic, and thermal fields. We focus on a paradigmatic mechanical metamaterial based on a mechanism of counter-rotating hinged squares. It has received significant attention due to its effective negative Poisson’s ratio and ability to propagate solitary pulses. Realization of this metamaterial at large scales requires the ability to fabricate robust hinges capable of large rotations at low energy cost. Current strategies rely on living hinges, whose compliance is determined by the hinge geometry. By fabricating composite hinges from silicone and textiles, we’ve expanded the hinge design space to reach lower bending energy with greater durability than living hinges. We assess the impact of multi-material use on energy cost of deformation, structure durability, and transmission loss. By comparing composite and living hinges in single hinge (n=1), small array (n=4), and large array (n = 190) scenarios, we illustrate both the scalability of composite hinge properties and the feasibility of their fabrication. This work provides a guide for fabricating composite hinges and for exploring the potential of composite fabrication to strengthen and optimize metamaterials for practical use.

Chang, A. (2022). “Composite hinges control designer properties of architected materials.” 

Characterization of a Cellular Response to Highly Mutated Eukaryotic Cells

Mutations fuel evolution and accumulate naturally as organisms age. Although most mutations are deleterious, eukaryotic cells can survive surprisingly high mutation burdens. We investigated the origins of this behavior, creating independent Saccharomyces cerevisiae lineages with thousands of different genetic variants. As new mutations accumulated, their fitness cost progressively decreased. Concomitantly, cells mounted a coherent and adaptive gene expression program that is distinct from previously characterized stress responses. A similar program arises in hypermutated human cancers. Inhibiting components of this eukaryotic mutation burden response (EMBR) selectively killed burdened cells but not their ancestors. The transcriptional regulator Ume6, an essential component of the Rpd3L histone deacetylase complex, and its interactions with the Hsp70 protein Ssb1, are crucial for EMBR activation. Our data establish that EMBR buffers the fitness consequences of new genetic variants, and also represents a vulnerability of cancer and infectious disease that could be targeted therapeutically.

Zabinsky, R., Mares, J., She, R., Zeman, M., Chang, A., Talbot, J., Campbell, E. A., Monzavi, T.,  Silvers, T. R., Jarosz, D. F. "A Stress Response that Allows Highly Mutated Eukaryotic Cells to Survive and Proliferate." [paper under review] 

RNA Helicases' Role in Buffering Mutation Cost

Invited to present at the Research Symposium in Barton Science Centre, Tonbridge School, England during British Science Week. Represented Los Altos High School Advanced Scientific Investigations class to an international audience of peers and scientists. Under the mentorship of postdoctoral fellow Rebecca Zabinsky and Dr. Jonathan Mares. 

The Eukaryotic Mutation Burden Response is a conserved transcriptional stress response used by cells to buffer the impact of mutations on growth rate. However, its mechanisms and regulation are not fully understood. RNA helicases are proteins that prevent and resolve misfolded RNAs. DEAD-box RNA helicases have exhibited buffering activity in Escherichia coli, and may be involved similarly in the budding yeast Saccharomyces cerevisiae by allowing mutated mRNA to escape stable misfolded states, thereby restoring translation initiation efficiency and participation of the mutated mRNA in normal cellular functions. I use the auxin-inducible degron system to investigate this potential behavior of DEAD-box RNA helicases Ded1 and Dbp2. My data establish that the AID system is functional and has negligible side effects on the growth rate, setting a precedent for the following experiments in mutated cell lines. Comparing the growth rate of the auxin-induced and uninduced strains will reveal the extent to which Ded1 and Dbp2 play a role in buffering mutation cost, potentially opening new doors to targeted RNA helicase cancer research and therapy that predicts and prevents the survival of mutating cells.

Chang, A. (2020) “Determining the role of RNA Chaperones Ded1 and Dbp2 in buffering mutation cost in S. cerevisiae.”