Instagram branding frame for Arctic artists and designers based on service design

In the remote Lapland region of Finland, Arctic artists and designers face challenges due to the limited local market and networking opportunities. This research leverages social media, notably Instagram, to boost their visibility and market presence. Grounded in digital service design and participatory design, the study employed the Double Diamond model across three phases: Interview and landscape analysis, Generating Workshops, and Prototyping. Data sources included interviews, landscape analysis, participatory workshops, and service prototypes. The data gathered shed light on Arctic artists and designers' motivations, challenges, and branding practices. It also yielded a frame with tailored 68 recommendations, covering themes, scheduling, content, and services. These recommendations facilitate branding, visibility, engagement, and efficiency

Enterovirus 71 induces degradation of TRIM38, a potential E3 ubiquitin ligase

<p>Abstract</p> <p>Background</p> <p>The tripartite motif (TRIM) proteins are a family of more than 70 members in human. However, only a few of them have been well studied. The TRIM proteins contain the conserved RING, B-box, coiled-coil, and SPRY domains, most of which are involved in protein ubiquitination. TRIM38 is a member of the TRIM protein family, which we studied in more detail here as its functions are largely unknown.</p> <p>Results</p> <p>Our study shows that, similar to other TRIM family members, TRIM38 is localized in the cytoplasm. TRIM38 increases ubiquitination of other cellular proteins and catalyzes self-ubiquitination. TRIM38 also promotes K63- and K48-linked ubiquitination of cellular proteins. An intact RING domain is important for the functions of TRIM38. In addition, enterovirus 71 infection induces TRIM38 degradation.</p> <p>Conclusions</p> <p>Our observations demonstrate that TRIM38 has E3 ubiquitin ligase activity and can be degraded during virus infection. These findings may provide insight into innate immune signaling pathways.</p

Zero Knowledge Contingent Payments for Trained Neural Networks

Nowadays, neural networks have been widely used in many machine learning tasks. In practice, one might not have enough expertise to fine-tune a neural network model; therefore, it becomes increasingly popular to outsource the model training process to a machine learning expert. This activity brings out the needs of fair model exchange: if the seller sends the model first, the buyer might refuse to pay; if the buyer pays first, the seller might refuse to send the model or send an inferior model. In this work, we aim to address this problem so that neither the buyer nor the seller can deceive the other. We start from Zero Knowledge Contingent Payment (ZKCP), which is used for fair exchange of digital goods and payment over blockchain, and extend it to Zero Knowledge Contingent Model Payment (ZKCMP). We then instantiate our ZKCMP with two state-of-the-art NIZK proofs: zk-SNARKs and Libra. We also propose a random sampling technique to improve the efficiency of zk-SNARKs. We extensively conduct experiments to demonstrate the practicality of our proposal

Rotavirus nonstructural protein 1 antagonizes innate immune response by interacting with retinoic acid inducible gene I

<p>Abstract</p> <p>Background</p> <p>The nonstructural protein 1 (NSP1) of rotavirus has been reported to block interferon (IFN) signaling by mediating proteasome-dependent degradation of IFN-regulatory factors (IRFs) and (or) the β-transducin repeat containing protein (β-TrCP). However, in addition to these targets, NSP1 may subvert innate immune responses via other mechanisms.</p> <p>Results</p> <p>The NSP1 of rotavirus OSU strain as well as the IRF3 binding domain truncated NSP1 of rotavirus SA11 strain are unable to degrade IRFs, but can still inhibit host IFN response, indicating that NSP1 may target alternative host factor(s) other than IRFs. Overexpression of NSP1 can block IFN-β promoter activation induced by the retinoic acid inducible gene I (RIG-I), but does not inhibit IFN-β activation induced by the mitochondrial antiviral-signaling protein (MAVS), indicating that NSP1 may target RIG-I. Immunoprecipitation experiments show that NSP1 interacts with RIG-I independent of IRF3 binding domain. In addition, NSP1 induces down-regulation of RIG-I in a proteasome-independent way.</p> <p>Conclusions</p> <p>Our findings demonstrate that inhibition of RIG-I mediated type I IFN responses by NSP1 may contribute to the immune evasion of rotavirus.</p

Positive correlation between fatty liver index and hyperuricemia in hypertensive Chinese adults: a H-type hypertension registry study

BackgroundFew studies have examined the relationship between fatty liver index (FLI) and hyperuricemia (HUA). This study explores the relationship between FLI and HUA in hypertensive patients.MethodsA total of 13,716 hypertensive subjects were included in the current study. FLI, a simple index calculated from triglycerides (TG), waist circumference (WC), body mass index (BMI), and γ -glutamyltransferase (GGT), was used as a useful predictor of nonalcoholic fatty liver disease (NAFLD) distribution. HUA was defined as serum uric acid ≥ 360 μmol/L for females and ≥ 420 μmol/L for males.ResultsThe mean value of total FLI was 31.8 ± 25.1. Multiple logistic analyses revealed a significant positive correlation between FLI and HUA (OR, 1.78; 95% CI: 1.69–1.87). A subgroup analysis demonstrated that the correlation between FLI (&lt; 30 vs. ≥ 30) and HUA was significant in both sexes (P for interaction = 0.006). Further analyses stratified by sex indicated a positive correlation between FLI and HUA prevalence among male and female subjects. However, the correlation between FLI and HUA was stronger in female subjects than in males (male: OR, 1.70; 95% CI: 1.58–1.83; female: 1.85; 95% CI: 1.73–1.98).ConclusionThis study demonstrates a positive correlation between FLI and HUA in hypertensive adults, but stronger in females than males

Association of TyG index and TG/HDL-C ratio with arterial stiffness progression in a non-normotensive population

Background: Cross-sectional studies have reported that insulin resistance (IR) is associated with arterial stiffness. However, the relationship between IR and arterial stiffness progression remains unclear. This study aims to evaluate the association of triglyceride glucose (TyG) index and triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio with arterial stiffness progression in a non-normotensive population. Methods: A total of 1895 prehypertensive (systolic pressure 120–139 mmHg or diastolic pressure 80–90 mmHg) or hypertensive (systolic pressure ≥ 140 mmHg or diastolic pressure ≥ 90 mmHg or using antihypertensive medication) participants were enrolled in 2013 and 2014, and followed until December 31, 2019. Arterial stiffness progression was measured by brachial-ankle pulse wave velocity (baPWV) change (absolute difference between baseline and last follow-up), baPWV change rate (change divided by following years), and baPWV slope (regression slope between examination year and baPWV). Results: During a median follow-up of 4.71 years, we observed an increasing trend of baPWV in the population. There were linear and positive associations of the TyG index and TG/HDL-C ratio with the three baPWV parameters. The difference (95% CI) in baPWV change (cm/s) comparing participants in the highest quartile versus the lowest of TyG index and TG/HDL-C ratio were 129.5 (58.7–200.0) and 133.4 (52.0–214.9), respectively. Similarly, the evaluated baPWV change rates (cm/s/year) were 37.6 (15.3–60.0) and 43.5 (17.8–69.2), while the slopes of baPWV were 30.6 (9.3–51.8) and 33.5 (9.0–58.0). The observed association was stronger in the hypertensive population. Conclusion: Our study indicates that the TyG index and TG/HDL-C ratio are significantly associated with arterial stiffness progression in hypertensive population, not in prehypertensive population