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As digital security demands continue to rise, physical unclonable functions (PUFs) have emerged as a potential solution for providing unique identifiers and cryptographic keys. However, conventional memory‐based PUFs have limited encoding capacity, which can compromise their security. Herein, an Ag nanowire‐based PUF that offers a high encoding capacity is introduced. The prototype PUF leverages the intrinsic topology of the nanowire network for encoding, which enables to achieve encoding capacities that are on the order of nn−2. The encoding method for a 4‐node PUF is validated and its encoding capacity distribution at binary and ternary bit levels is assessed. The ternary bit encoding method allows for more detailed differentiation of the internal topological connection structure of the PUF, resulting in a larger encoding capacity. Additionally, an authentication system that is proposed. For a 7 × 7 array PUF, the estimated decryption time is ≈1.5*1058 years, demonstrating the PUF's resistance to attacks. The Ag nanowire‐based PUF design offers a promising approach to enhancing authentication system security and overcoming limitations of existing PUFs. Further exploration of this innovative PUF technology in the realm of hardware security can have significant implications for digital security in modern devices. [ABSTRACT FROM AUTHOR]

Abstract Background The Warburg effect is well-established to be essential for tumor progression and accounts for the poor clinical outcomes of hepatocellular carcinoma (HCC) patients. An increasing body of literature suggests that circular RNAs (circRNAs) are important regulators for HCC. However, few circRNAs involved in the Warburg effect of HCC have hitherto been investigated. Herein, we aimed to explore the contribution of circFOXK2 to glucose metabolism reprogramming in HCC. Methods In the present study, different primers were designed to identify 14 circRNAs originating from the FOXK2 gene, and their differential expression between HCC and adjacent liver tissues was screened. Ultimately, circFOXK2 (hsa_circ_0000817) was selected for further research. Next, the clinical significance of circFOXK2 was evaluated. We then assessed the pro-oncogenic activity of circFOXK2 and its impact on the Warburg effect in both HCC cell lines and animal xenografts. Finally, the molecular mechanisms of how circFOXK2 regulates the Warburg effect of HCC were explored. Results CircFOXK2 was aberrantly upregulated in HCC tissues and positively correlated with poor clinical outcomes in patients that underwent radical hepatectomy. Silencing of circFOXK2 significantly suppressed HCC progression both in vitro and in vivo. Mechanistically, circFOXK2 upregulated the expression of protein FOXK2-142aa to promote LDHA phosphorylation and led to mitochondrial fission by regulating the miR-484/Fis1 pathway, ultimately activating the Warburg effect in HCC. Conclusions CircFOXK2 is a prognostic biomarker of HCC that promotes the Warburg effect by promoting the expression of proteins and miRNA sponges that lead to tumor progression. Overall, circFOXK2 has huge prospects as a potential therapeutic target for patients with HCC.

In order to increase the encoding capacity and reduce the size of the tag, this paper proposes the frequency sharing method to design a retransmitted chipless tag, which is composed of N resonators, a coupled microstrip transmission line, and the orthogonal transmitting antenna and receiving antenna. A pair of the same size resonators is placed symmetrically on both sides of the coupled microstrip transmission line. M open-ended stubs (OES) with different combinations are embedded in each resonator to obtain different resonance frequencies. The frequency sharing multi-state resonators' chipless tags are designed where N=6, M=4, and the dimension of the tag is 46 mm × 30 mm, which can generate about 212 codes. Simulation and measurement results show good agreement and feasibility of the tag design. The chipless tag is small in size, has large encoding capacity and is easy to print. This kind of tag has no silicon chip so the cost is low. It can be widely used in logistics, supermarkets and other fields to replace the barcode. [ABSTRACT FROM AUTHOR]

Background: The Warburg effect is well-established to be essential for tumor progression and accounts for the poor clinical outcomes of hepatocellular carcinoma (HCC) patients. An increasing body of literature suggests that circular RNAs (circRNAs) are important regulators for HCC. However, few circRNAs involved in the Warburg effect of HCC have hitherto been investigated. Herein, we aimed to explore the contribution of circFOXK2 to glucose metabolism reprogramming in HCC. Methods: In the present study, different primers were designed to identify 14 circRNAs originating from the FOXK2 gene, and their differential expression between HCC and adjacent liver tissues was screened. Ultimately, circFOXK2 (hsa_circ_0000817) was selected for further research. Next, the clinical significance of circFOXK2 was evaluated. We then assessed the pro-oncogenic activity of circFOXK2 and its impact on the Warburg effect in both HCC cell lines and animal xenografts. Finally, the molecular mechanisms of how circFOXK2 regulates the Warburg effect of HCC were explored. Results: CircFOXK2 was aberrantly upregulated in HCC tissues and positively correlated with poor clinical outcomes in patients that underwent radical hepatectomy. Silencing of circFOXK2 significantly suppressed HCC progression both in vitro and in vivo. Mechanistically, circFOXK2 upregulated the expression of protein FOXK2-142aa to promote LDHA phosphorylation and led to mitochondrial fission by regulating the miR-484/Fis1 pathway, ultimately activating the Warburg effect in HCC. Conclusions: CircFOXK2 is a prognostic biomarker of HCC that promotes the Warburg effect by promoting the expression of proteins and miRNA sponges that lead to tumor progression. Overall, circFOXK2 has huge prospects as a potential therapeutic target for patients with HCC. [ABSTRACT FROM AUTHOR]

Primitive-based models of motor learning suggest that adaptation occurs by tuning the responses of motor primitives. Based on this idea, we consider motor learning as an information encoding procedure, that is, a procedure of encoding a motor skill into primitives. The capacity of encoding is determined by the number of recruited primitives, which depends on how many primitives are “visited” by the movement, and this leads to a rather counterintuitive prediction that faster movement, where a larger number of motor primitives are involved, allows learning more complicated motor skills. Here, we provide a set of experimental results that support this hypothesis. First, we show that learning occurs only with movement, that is, only with nonzero encoding capacity. When participants were asked to counteract a rotating force applied to a robotic handle, they were unable to do so when maintaining a static posture but were able to adapt when making small circular movements. Our second experiment further investigated how adaptation is affected by movement speed. When adapting to a simple (low-information-content) force field, fast (high-capacity) movement did not have an advantage over slow (low-capacity) movement. However, for a complex (high-information-content) force field, the fast movement showed a significant advantage over slow movement. Our final experiment confirmed that the observed benefit of high-speed movement is only weakly affected by mechanical factors. Taken together, our results suggest that the encoding capacity is a genuine limiting factor of human motor adaptation. NEW & NOTEWORTHY We propose a novel concept called “encoding capacity” of motor adaptation, which describes an inherent limiting-factor of our brain’s ability to learn new motor skills, just like any other storage system. By reinterpreting the existing primitive-based models of motor learning, we hypothesize that the encoding capacity is determined by the size of the movement, and present a set of experimental evidence suggesting that such limiting effect of encoding capacity does exist in human motor adaptation. [ABSTRACT FROM AUTHOR]

Physical unclonable functions (PUFs) based on uncontrollable fabrication randomness are promising candidates for anticounterfeiting applications. Currently, the most popular optical PUFs are generally constructed from the scattering, fluorescent, or Raman phenomenon of nanomaterials. To further improve the security level of optical PUFs, advanced functions transparent to the above optical phenomenon have always been perused by researchers. Herein, we propose a new type of PUF based on the photothermal effect of gold nanoparticles, which shows negligible scattering, fluorescent, or Raman responses. The gold nanoparticles are randomly dispersed onto the surface of fused silica, which can enhance the photothermal effect and facilitate high contrast responses. By tuning the areal density of the gold nanoparticles, the optimized encoding capacity (2 319 ) and the total authentication error probability (3.6428 × 10 -24 ) are achieved from our PUF due to excellent bit uniformity (0.519) and inter Hamming distances (0.503). Moreover, the intra-Hamming distance (0.044) indicates the desired reliability. This advanced PUF with invisible features and high contrast responses provides a promising opportunity to implement authentication and identification with high security.

A retransmission chipless tag with multiple U-shaped slot resonators is proposed to cut down the cost of traditional tags with chips. Multiple side-by-side U-shaped slot structures of different lengths are printed on the microstrip line, and the two terminals of the microstrip line are connected correspondingly with two orthogonal ultra-wideband (UWB) transceiver antennas to form the retransmission chipless tag. The U-shaped slot resonator has high Q values and narrow impedance bandwidth. The bandwidth that each resonator adds to the protection bandwidth is 300 MHz. Several 6-bit coding U-shaped slot resonator chipless tags are designed and fabricated for comparison and measurement. Results show that the simulation and the measurement are in agreement. The slot width of the U-shaped slot resonator and the distance between the resonators are reduced, resulting in deepened spectrum notch depth of the resonator. Decreasing the dielectric constant of the substrate or increasing the thickness of the substrate increases the spectrum notch depth of the resonator. [ABSTRACT FROM AUTHOR]

Primitive-based models of motor learning suggest that adaptation occurs by tuning the responses of motor primitives. Based on this idea, we consider motor learning as an information encoding procedure, that is, a procedure of encoding a motor skill into primitives. The capacity of encoding is determined by the number of recruited primitives, which depends on how many primitives are "visited" by the movement, and this leads to a rather counterintuitive prediction that faster movement, where a larger number of motor primitives are involved, allows learning more complicated motor skills. Here, we provide a set of experimental results that support this hypothesis. First, we show that learning occurs only with movement, that is, only with nonzero encoding capacity. When participants were asked to counteract a rotating force applied to a robotic handle, they were unable to do so when maintaining a static posture but were able to adapt when making small circular movements. Our second experiment further investigated how adaptation is affected by movement speed. When adapting to a simple (low-information-content) force field, fast (high-capacity) movement did not have an advantage over slow (low-capacity) movement. However, for a complex (high-information-content) force field, the fast movement showed a significant advantage over slow movement. Our final experiment confirmed that the observed benefit of high-speed movement is only weakly affected by mechanical factors. Taken together, our results suggest that the encoding capacity is a genuine limiting factor of human motor adaptation. NEW & NOTEWORTHY We propose a novel concept called "encoding capacity" of motor adaptation, which describes an inherent limiting-factor of our brain's ability to learn new motor skills, just like any other storage system. By reinterpreting the existing primitive-based models of motor learning, we hypothesize that the encoding capacity is determined by the size of the movement, and present a set of experimental evidence suggesting that such limiting effect of encoding capacity does exist in human motor adaptation.