Confinement loss prediction in diverse anti-resonant fibers through neural networks.

In this work, genetic algorithm (GA) is employed to optimize convolutional neural networks (CNNs) for predicting the confinement loss (CL) in anti-resonant fibers (ARFs), achieving a prediction accuracy of CL magnitude reached 90.6%, which, to the best of our knowledge, represents the highest accuracy to date and marks the first instance of using a single model to predict CL across diverse ARF structures. Different from the previous definition of ARF structures with parameter groups, we use anchor points to describe these structures, thus eliminating the differences in expression among them. This improvement allows the model to gain insight into the specific structural characteristics, thereby enhancing its generalization capabilities. Furthermore, we demonstrate a particle swarm optimization algorithm (PSO), driven by our model, for the design of ARFs, validating the model's robust predictive accuracy and versatility. Compared with the calculation of CL by finite element method (FEM), this model significantly reduces the cost time, and provides a speed-up method in fiber design driven by numerical calculation.

circAP1M2 activates ATG9A-associated autophagy by inhibiting miR-1249-3p to promote cisplatin resistance in oral squamous cell carcinoma.

Cisplatin (CDDP) is the first-line chemotherapeutic agent for oral squamous cell carcinoma (OSCC). Susceptibility to drug resistance during treatment is a significant challenge in enhancing the therapeutic efficacy of OSCC. Autophagy is an essential element to guarantee the cancer cells' survival under chemo-stress conditions. We established a cisplatin-resistant OSCC cell line (CAL27/CDDP) and showed that circAP1M2 is a remarkably upregulated circular RNA in OSCC. Knockdown of circAP1M2 contributes to reversing cisplatin chemoresistance in vivo, while enhanced autophagic activity in cisplatin-resistant OSCC cells contributes to chemoresistance. Mechanistically, we showed that circAP1M2 induces autophagy-associated cisplatin resistance via the miR-1249-3p-ATG9A axis in OSCC cells. This study provides insights into the specific influence of a newly identified circular RNA circAP1M2 in OSCC regarding drug abuse and the treatment of a broad range of cancers that can benefit from cisplatin.

Antiresonant fiber structures based on swarm intelligence design.

In this work, we obtained a new, to the best of our knowledge, structure of anti-resonant fiber (ARF) by an adaptive particle swarm optimization (PSO) algorithm. Different from the prior method of stacking elemental parts and optimizing parameters through experience or algorithm, we decompose some classic structures into points and optimize the positions of these points through swarm intelligence. The fiber structure is reconstructed by interpolation, and some new structures with low confinement loss (CL) and high higher order mode extinction ratio (HOMER) are obtained. These novel ARFs exhibit similar structural characteristics, and are named as "the bulb-shaped ARFs". Among these structures, the minimum achieved CL is 2.21 × 10-5dB/m at 1300 nm and the maximum achieved HOMER exceeds 14,000. This work provides a method with high degree of freedom in the design of non-uniform cross-section waveguides and helps to discover new fiber structures.

[Mechanism of the dentino-enamel junction on the resist-crack propagation of human teeth by the finite element method].

OBJECTIVE: This study aims to identify the crack tip stress intensity factor of the propagation process, crack propagation path, and the changes in the shape of the crack tip by the finite element method. METHODS: The finite element model of dentino-enamel junction was established with ANSYS software, and the length of the initial crack in the single edge was set to 0.1 mm. The lower end of the sample was fixed. The tensile load of 1 MPa with frequency of 5 Hz was applied to the upper end. The stress intensity factor, deflection angle, and changes in the shape of the crack tip in the crack propagation were calculated by ANSYS. RESULTS: The stress intensity factor suddenly and continuously decreased in dentino-enamel junction as the crack extended. A large skewed angle appeared, and the stress on crack tip was reduced. CONCLUSION: The dentino-enamel junction on human teeth may resist crack propagation through stress reduction.

Glucocorticoids activate the local renin-angiotensin system in bone: possible mechanism for glucocorticoid-induced osteoporosis.

Bone metabolism disorder has been identified to play a vital role in the pathogenesis of glucocorticoid-induced osteoporosis (GIOP). The local renin-angiotensin system (RAS) in bone is newly defined to be closely related to the bone metabolism. However, it is unknown whether the local RAS is involved in GIOP. Adult male New Zealand white rabbits were treated with saline, dexamethasone (DXM) alone, or DXM combined with perindopril. The expression of main RAS components in trabecular bone was examined at mRNA and/or protein levels. Bone metabolism was analyzed using dual-energy X-ray absorptiometry, histomorphometry, biomechanics, biochemical techniques, and quantitative RT-PCR. The expressions of local bone angiotensin II, angiotensin types 1 and 2 receptors, and angiotensin-converting enzyme at mRNA and/or protein levels increased when DXM-induced osteoporosis was present. Whereas, perindopril significantly blocked the activation of the local RAS and partially reversed GIOP. Mineralizing surface, mineral apposition rate, and bone formation rate were decreased by DXM, along with serum osteocalcin being downregulated. These changes were then reversed by the use of perindopril. Osteoclast number, osteoclast surface, and eroded surface increased after the administration of DXM, and urinary deoxypyridinoline was upregulated. These were also inhibited when perindopril was given. Quantitative RT-PCR using RNA isolated from the lumbar vertebrae revealed an increase in the SOST expression and a decrease in the Runx2 expression, whereas the receptor activator of nuclear factor-κB ligand/osteoprotegerin ratio and the expression of tartrate resistant acid phosphatase were increased, which were all inhibited by perindopril. The results of this study provide evidence for the role of local RAS is involved in GIOP, and GIOP may be ameliorated by blocking the activation of local RAS in the bone.