Lincoln University - Pennsylvania

Purpose While previous research has highlighted the role of entrepreneurs in leading individual employees' behaviour in small businesses, our understanding of how they influence opportunity development in uncertain times remains limited. This study investigates how entrepreneurs in small businesses navigate uncertainty and create new opportunities. Design/methodology/approach An interpretive qualitative method was employed to understand how entrepreneurs enable their teams to overcome multiple uncertainties in the relatively unexplored business environment of Iran. The data were driven from 35 in-depth, semi-structured interviews with entrepreneurs/small business owner-managers. Findings The results of this study indicate that entrepreneurial leadership enables small businesses to overcome uncertainties and crises and create new opportunities by facilitating collective problem-solving and opportunity development. Entrepreneurial leadership fosters effectual co-creation through communicating a compelling vision, empowering employees, stimulating collective cognition, and collective action. Practical implications Entrepreneurs and managers of small businesses can use the findings of this study to rethink their approaches to environmental uncertainty by adopting entrepreneurial leadership practices that enable collective cognition and action. By fostering a compelling vision, empowering team-level decision-making, and creating a supportive environment, entrepreneurial leadership enables small firms to co-create opportunities and remain resilient during crises. Originality/value This study extends the theory of entrepreneurial leadership by illustrating how it facilitates opportunity co-creation through collective cognition and action in uncertain environments. It offers a contextualised understanding of entrepreneurial leadership as an empowering approach to enhancing small business resilience.

ABSTRACT This study presents the development of thermoplastic polyurethane (TPU) and silica aerogel powder (SAP)‐based composite coatings for enhancing the thermal insulation performance of cotton fabrics. A solvent pre‐filling and replacement method using N, N‐dimethylformamide (DMF) was employed to preserve the aerogel's porous structure during processing. By systematically varying TPU concentration (15%–25%), TPU/SAP ratio, and coating thickness (35–55 μm), the effects on thermal conductivity, mechanical durability, water repellency, and comfort were investigated. Results showed that DMF pre‐filling effectively prevented TPU infiltration into aerogel pores, improving insulation efficiency. Optimal performance was achieved at 20% TPU, a 7:3 TPU/SAP ratio, and a 55 μm thickness, yielding a low thermal conductivity of 0.1043 W m −1 K −1 , a water contact angle of 112°, and an air permeability of 7.68 mm/s. After five washing cycles, the fabric retained good insulation properties with only a 3.3% increase in thermal conductivity and a 13.2% reduction in peel strength. These findings demonstrate the feasibility of TPU/SAP/DMF coatings for durable, breathable, and thermally insulating textile applications.

Rugby tackles can cause head acceleration events (HAEs) which may acutely and chronically affect brain health. This study aimed to investigate the varying proportions, impact forces and rugby-specific factors of tackles from different directions relative to the ball carrier which may illuminate strategies to reduce injury and health risks. Boys from four youth boys’ teams in New Zealand (one U13 club: n = 19 players, 13 matches; two U16 club: n = 41, mean of 31.5 matches; one U16 representative: n = 26, 8 matches) wore instrumented mouthguards and all matches were videoed and analyzed to verify the collisions resulting in a tackle and code them based on rugby-specific and biomechanical factors (anticipation, falling, head position, face position). Of the 2539 tackles resulting in HAEs, most were front-on (56–64%). Tackle direction had no significant effect on either mean peak linear or rotational acceleration, however significantly fewer tackles from the rear resulted in impacts that would trigger an elite rugby head injury assessment than tackles from the front and side. The older and more skilled players more often had correct head positioning in front and side-on tackles, whereas almost none of the tackles from the rear had incorrect head positioning. Additional training focus should be given to tackles from the side and rear with younger players as they have poorer anticipation in these directions often resulting in higher HAE magnitude. Face up tackling seems to be best for reducing impact forces in tackles from behind, while face down tackling appears to be safest for front-on tackles.

The integration of Artificial Intelligence (AI) and Machine Learning (ML) presents a paradigm shift for enhancing sustainability within the textile industry. This review examines the transformative potential of these technologies in fostering a circular economy, with a focus on material design, process optimisation, and end-of-life solutions. It surveys applications across textile science, from natural fibre composites to technical and smart textiles, highlighting the role of predictive modelling and ML algorithms—including neural networks, convolutional neural networks (CNNs), and random forests. These techniques are demonstrated to enhance the design of fibre-based materials, predict key properties such as tensile strength and thermal stability, and optimise manufacturing processes like dyeing and weaving. Furthermore, the review explores the significant contribution of computer vision to automated quality control, defect detection, and the assessment of garment condition for resale, thereby supporting circular business models. A central theme is the capacity of AI to drive sustainability by enabling zero-waste pattern design, improving colour prediction accuracy to reduce chemical waste, and advancing automated textile sorting for recycling. Despite this promising progress, the principal challenges identified are not algorithmic but systemic, relating to data scarcity, integration complexities, and the need for cross-sector collaboration. The review concludes by identifying critical future research directions, emphasising the need for robust, physics-informed models, the collaborative development of larger, more diverse datasets, and AI-driven Design for Disassembly (DfD) to fully realise AI's potential in creating a more innovative, efficient, and sustainable textile industry. Keywords: Artificial Intelligence; Circular Economy; Textile Recycling; Predictive Modelling; Computer Vision; Sustainable Manufacturing

Abstract Background Systemic inflammation is a hallmark of acute myocardial infarction (AMI) with residual inflammatory risk a key player in reoccurring cardiovascular events. Use of sodium-glucose cotransporter-2 inhibitors (SGLT2i) in patients with type-2 diabetes mellitus (T2DM) and AMI improves cardiovascular outcomes, yet the mechanism of action is unknown. Purpose We posit that Empagliflozin (EMPA) provides anti-inflammatory protection via suppression of the nod-like receptor protein-3 (NLRP3) inflammasome in monocyte-derived macrophages (MDMs), and that this protection is greater in early (Arm A: prescribed EMPA during AMI admission at T0, T30, T90 and T180days) versus delayed therapy (Arm B: EMPA prescribed 90days post-discharge with sampling at T90, T120 and T180days), plus appropriate controls (T0-T90). Methods Patients presenting with T2DM-AMI, eligible but not already taking an SGLT2i were recruited and randomised to Arm A (n=28) or B (n=27). Blood CD14+ monocytes were isolated and differentiated into MDMs. An inflammasome assay measured Caspase-1 activity (direct inflammasome activation) in lipopolysaccharide (0.1ug/mL) + ATP (2mM) stimulated MDMs. Quantitative RT-PCR and Lumit immunoassays measured IL1β, IL6, and TNFα gene expression/secretion. Results IL1β expression (NLRP3 priming) decreased in MDMs isolated from patients in Arm A given EMPA at T0, at all subsequent timepoints from 2.13±0.53 (T0) to 0.64±0.37 (T30; P<0.05), 0.89±0.20 (T90; P<0.05) and 0.66±0.14 (T180; P<0.05). No change in IL1β expression was observed in Arm B both without EMPA (T0-90) or when EMPA was delayed (T90-180). Caspase-1 activity decreased with EMPA in Arm A from 8677±1550 to 4751±591.7 (T0-90; P<0.05) and 3772±450.2 RLu; (T0-180; P<0.01) whilst no significant reduction in caspase-1 activity was recorded in MDMs from Arm B. Although early therapy failed to alter TNFα levels (T0-T180), EMPA prevented the early increase in TNFα gene expression in Arm B MDMs (No EMPA) at T0-T30 (0.537±0.104 to 1.148±0.236 P<0.01). EMPA also reduced TNFα release when taken immediately prior to discharge (from 5240±1201 to 2409±363.6pg/mL; P<0.05; T0-90) compared to Arm B patients without EMPA (T0-90;) or with delayed therapy (T90-180). Lastly, early initiation of EMPA reduced IL6 secretion from 2248± 609.5 (T0) to 883.3±180.4 (T30; P<0.05) and 735.2±0.5pg/mL (T180; P<0.05). In the absence of EMPA, IL6 release increased from 571.9±96.57 (T0) to 1279±243.3 (T30; P<0.05) and 1617±396pg/mL (T90; P<0.05). Levels were restored with EMPA (from 1617±396 to 661.9±82.95pg/mL; P<0.05; T90-180). Conclusion UK NICE guidelines do not stipulate if SGLT2i’s should be prescribed during admission with AMI prior to discharge, or 90days post-discharge. This study suggests that anti-inflammatory protection of EMPA on MDMs from people with T2DM who have had an AMI is greatest following early therapy, timing of which may reduce residual inflammatory risk and improve clinical outcomes.

In vivo, the chemokine CCL19 and its receptor CCR7 control T cell retention in lymph nodes, while the lipid chemoattractant spingosine-1-phosphate (S1P) drives T cell egress from lymphoid organs. CCL19 is known to activate actin polymerization at the leading edge of migrating cells, generating a mode of motility driven by lamellipodial protrusions. In contrast, we showed recently that S1P induces a transient lamellipodial response, followed by pressure-driven bleb-based motility. Here, we elucidate the mechanisms controlling S1P responses in naïve T cells. We show that S1P signals through S1PR1, with coupling through Gai. In contrast to CCR7, which signals through Gai to induce sustained Rac1 activation, S1PR1 engagement yields only weak and transient Rac1 activation; the dominant response is sustained activation of RhoA. This pathway, together with a pathway involving phospholipase C and myosin light chain kinase, results in phosphorylation of myosin regulatory light chain (MLC) and enhanced myosin contractility. Inhibition of mTORC2 blocks MLC phosphorylation, consistent with evidence that tension sensing by mTORC2 can couple Rac1 and RhoA signaling during leukocyte migration. Surprisingly, although RhoA pathway inhibitors blocked S1P-induced MLC phosphorylation and blebbing, they failed to block S1P-dependent chemotaxis. This led to the identification of a second arm of the S1P response: WNK1-dependent phosphorylation of SPAK1 and OSXR1, proteins that regulate ion channels and water influx. Partial WNK1 inhibition, together with inhibition of myosin contractility, was sufficient to block S1P-induced blebbing and chemotaxis, indicating that S1P-driven T cell migration involves coordinate activation of myosin contractility and water influx.

The heart adapts to cardiac demand via chemical modifications of contractile myofilament proteins. Many of these modifications, such as phosphorylation, occur in proteins' intrinsically disordered regions (IDRs). These IDRs, though challenging to study, are recognized as dynamic, tunable regulators of protein function. Since cardiac dysfunction often involves altered posttranslational modifications (PTMs) in myofilament proteins, understanding how IDR changes affect protein and myofilament behavior is crucial. We hypothesized that PTMs, primarily phosphorylation, regulate ABLIM1 (a myofilament protein) by altering its IDR conformational ensemble, thereby modulating its binding to other myofilament proteins. We tested this using multiscale modeling (including molecular dynamics simulations) to predict ABLIM1's conformational ensembles pre- and postphosphorylation at sites altered in a canine model of heart failure with reduced GSK3β activity. A state-based contraction model then rationalized the physiological consequences. Our data show that local physicochemical alterations from phosphorylation in ABLIM1's IDRs significantly affect its conformational ensemble. This ensemble change subsequently influences the ability of its LIM domains to interact with titin. Furthermore, using the contraction model, we show that a reduced ability to recruit myosin heads for cross-bridge formation, resulting from the modified LIM domain/titin interactions, provides a mechanism that elucidates previous findings of diminished length-dependent activation. These findings offer critical molecular insights, reframing IDRs not merely as structural noise but as key, tunable elements that control protein interactions and ultimately impact mechanical behavior in the sarcomere. This work bridges molecular disorder and biomechanical function, providing a new perspective to understand dynamic control and dysfunction in cardiomyocyte contraction.

Robert Sapolsky argues that free will requires complete independence from uncontrollable influences. We claim this criterion is overly demanding and misaligned with ordinary understandings of free will. To assess folk intuitions, we presented 197 American participants with five scenarios in which a person's behavior was shaped by uncontrollable factors. In four cases—preferences, genetic traits, brain function, and advertising—most participants judged the person to possess free will. A fifth scenario involving a compliance drug served as a control; here, most participants denied free will. These findings suggest that laypeople consider free will compatible with certain external influences. Thus, Sapolsky's conception diverges from common usage. While his strict definition may rule out free will, our results support the viability of a more moderate and widely endorsed conception. Any attempt to refute free will must first demonstrate that the definition used captures its common meaning.