Worcester Polytechnic Institute

Physiological signals are increasingly used to study stress, engagement, and user experience. Yet collecting and interpreting these signals remains difficult for students and novice researchers, who must navigate complex device setups, scattered software tools, and technical analysis workflows. This demo presents Sensei, an intelligent browser-based platform that streamlines the entire process of running small physiological studies—from connecting sensors and defining protocols to visualizing data and generating interpretations. In this demo, attendees will run a brief recording session and explore Sensei’s AI-assisted analysis tools, illustrating how intelligent support can make physiological computing more approachable for learning and early-stage research.

Tissue-engineered blood vessels (TEBVs) represent a critical advancement in vascular medicine, offering transformative potential in drug testing, regenerative therapies, and disease modeling. Current evaluation methods, however, rely heavily on destructive techniques such as histology, which preclude further use of samples and limit real-time monitoring. Ultrasound Computed Tomography (USCT) emerges as a promising alternative, enabling non-destructive, high-resolution imaging within bioreactors. While prior work has demonstrated the feasibility of USCT for TEBV monitoring using needle and tubing phantoms, this study advances the field by imaging real TEBV samples and employing histological analysis as the ground truth for validation. This paper utilizes a prototype USCT system that achieve comprehensive 360-degree reconstructions of TEBV cross-sections. Validated through both needle-phantom studies and histology comparisons, the system demonstrates high accuracy with an average measurement error of 0.03 mm and adaptability within bioreactor environments. Our results underscore USCT’s capacity for non-destructive TEBV evaluation, paving the way for enhanced monitoring during cultivation. Future developments aim to refine image reconstruction and expand clinical applications. • Developed a non-destructive USCT system for imaging TEBVs within a bioreactor. • Validated USCT’s measurement accuracy using needle phantom experiments. • USCT measurements of TEBV geometry align closely with histological results.

Macrophage antimicrobial programs are regulated not only by transcriptional networks but also by RNA processing mechanisms affecting signal transduction and effector responses. One such mechanism, alternative polyadenylation (APA), determines mRNA fate by changing the length of the 3' UTR. However, our understanding of the impact of APA on antibacterial functions and how we can manipulate it to influence infection outcomes remains limited. In this study, we identify the APA regulator CFIm25 (NUDT21) as a promoter of macrophage defense against Salmonella enterica serovar Typhimurium (STM). STM infection is known to drive macrophages toward an M2-like immunosuppressive state conducive to bacterial survival. Concurrent with this transition, the CFIm25 level is reduced, and the 3' UTRs of CFIm25 targets encoding key immune proteins, such as TAB2 and TBL1XR1, are lengthened, suggesting a role for APA changes in the response to STM. Overexpression of CFIm25 in infected macrophages blocks these Salmonella -induced 3' UTR changes, leading to greater mRNA and protein expression. Significantly, the increase in CFIm25 suppresses infection, thereby creating a more antimicrobial intracellular environment, improving macrophage survival, and reducing M2 properties that support bacterial replication. Specifically, CFIm25 enhances production of the antibacterial peptide LL-37, increases reactive oxygen species and nitric oxide levels, suppresses arginase activity and lactate production, and stimulates release of pro-inflammatory cytokines while inhibiting anti-inflammatory cytokines. Depletion studies show TAB2 mediates CFIm25's antibacterial effects by activating both MAPK and NF-kB pathways. Our findings highlight APA regulation as a potential target for boosting immune defenses and developing treatments for chronic bacterial infections.

We describe a relationship between the Lie algebra $\mathfrak{sl}_4(\mathbb C)$ and the hypercube graphs. Consider the $\mathbb C$-algebra $P$ of polynomials in four commuting variables. We turn $P$ into an $\mathfrak{sl}_4(\mathbb C)$-module on which each element of $\mathfrak{sl}_4(\mathbb C)$ acts as a derivation. Then $P$ becomes a direct sum of irreducible $\mathfrak{sl}_4(\mathbb C)$-modules $P = \sum_{N\in \mathbb N} P_N$, where $P_N$ is the $N$th homogeneous component of $P$. For $N\in \mathbb N$ we construct some additional $\mathfrak{sl}_4(\mathbb C)$-modules ${\rm Fix}(G)$ and $T$. For these modules the underlying vector space is described as follows. Let $X$ denote the vertex set of the hypercube $H(N,2)$, and let $V$ denote the $\mathbb C$-vector space with basis $X$. For the automorphism group $G$ of $H(N,2)$, the action of $G$ on $X$ turns $V$ into a $G$-module. The vector space $V^{\otimes 3} = V \otimes V \otimes V$ becomes a $G$-module such that $g(u \otimes v \otimes w)= g(u) \otimes g(v) \otimes g(w)$ for $g\in G$ and $u,v,w \in V$. The subspace ${\rm Fix}(G)$ of $V^{\otimes 3}$ consists of the vectors in $V^{\otimes 3}$ that are fixed by every element in $G$. Pick $\varkappa \in X$. The corresponding subconstituent algebra $T$ of $H(N,2)$ is the subalgebra of ${\rm End}(V)$ generated by the adjacency map $\sf A$ of $H(N,2)$ and the dual adjacency map ${\sf A}^*$ of $H(N,2)$ with respect to $\varkappa$. In our main results, we turn ${\rm Fix}(G)$ and $T$ into $\mathfrak{sl}_4(\mathbb C)$-modules, and display $\mathfrak{sl}_4(\mathbb C)$-module isomorphisms $P_N \to {\rm Fix}(G) \to T$. We describe the $\mathfrak{sl}_4(\mathbb C)$-modules $P_N$, ${\rm Fix}(G)$, $T$ from multiple points of view.