Modifying single-crystal silicon and trimming silicon microring devices by femtosecond laser irradiation.

Single-crystal silicon (c-Si) is a vital component of photonic devices and has obvious advantages. Moreover, femtosecond-pulsed laser interactions with matter have been widely applied in micro/nanoscale processing. In this paper, we report the modification mechanisms of c-Si induced by a femtosecond laser (350 fs, 520 nm) at different pulse fluences, along with the mechanism of this technique to trim the phase error of c-Si-based devices. In this study, several distinct types of final micro/nanostructures, such as amorphization and ablation, were analyzed. The near-surface morphology was characterized using optical microscopy, scanning electron microscopy, and atomic force microscopy. The main physical modification processes were further analyzed using a two-temperature model. By employing Raman spectroscopy, we demonstrated that a higher laser fluence significantly contributes to the formation of more amorphous silicon components. The thickness of the amorphous layer was almost uniform (approximately 30 nm) at different induced fluences, as determined using transmission electron microscopy. From the ellipsometry measurements, we demonstrated that the refractive index increases for amorphization while the ablation decreases. In addition, we investigated the ability of the femtosecond laser to modify the effective index of c-Si microring waveguides by either amorphization or ablation. Both blue and red shifts of resonance spectra were achieved in the microring devices, resulting in double-direction trimming. Our results provide further insight into the femtosecond laser modification mechanism of c-Si and may be a practical method for dealing with the fabrication errors of c-Si-based photonic devices.

A life prediction method based on MDFF and DITCN-ABiGRU mixed network model.

A single network model exhibits limitations in the life prediction of rotating machinery for the various fault types and uncertain fault occurrence. Therefore, a network prediction model combining multi-domain feature fusion (MDFF) and distributed TCN-Attention-BiGRU (DITCN-ABiGRU) is proposed to enable a more accurate life prediction of rotating machinery. Firstly, the features of vibration signals collected from multiple sensors are extracted in the time, frequency, and time-frequency domains. Subsequently, dimensionality reduction optimization is conducted on these multi-domain features to eliminate useless information features. The temporal convolutional network (TCN) model is constructed to capture the critical information reflecting the fault characteristics of rotating machinery through the attention mechanism, and the dependencies of the whole training process are captured by the BiGRU network. Finally, precise prediction of the lifespan of rotating machinery is achieved by constructing a health indicator curve (HI). The proposed methods are verified through the life prediction of rolling bearings from the IEEE PHM Challenge 2012 dataset and ball screw pairs from a designed experiment. The experimental results show that the proposed MDFF and DITCN-ABiGRU model achieves a better score and lower error than the convolutional neural network (CNN) and GRU models.

Protection of Oxygen Glucose Deprivation-Induced Human Brain Vascular Pericyte Injury: Beneficial Effects of Bellidifolin in Cellular Pyroptosis.

Pericytes play critical roles in the maintenance of brain vascular homeostasis. However, very little is currently known about how pericytes regulate ischemic stroke-induced brain injury. Inflammation is a key event in the pathobiology of stroke, in which the nod-like receptor protein-3 (NLRP3) inflammasome is involved in, triggering sterile inflammatory responses and pyroptosis. In the current study, an immortalized cell line derived from human brain vascular pericytes (HBVPs) was constructed, and it showed that HBVPs challenged with oxygen glucose deprivation (OGD) displays pronounced cellular excretion of LDH, IL-1ß, IL-18 and increased PI positive staining. Mechanistically, upon OGD treatment, NLRP3 forms an inflammasome with its adaptor protein apoptosis-associated speck-like protein, containing a caspase recruitment domain (ASC) and caspase-1, manifested as much more co-stainings of NLRP3, ASC and Caspase-1 in HBVPs, accompanied by the increased protein levels of NLRP3, ASC, caspase-1 as well as the pyroptosis-associated protein gasdermin D (GSDMD). Intriguingly, GSDMD-N shuttled to the mitochondrial membrane triggered by OGD exposure, which promoted massive mitochondria-derived ROS generation. Importantly, the invention value of the specific targets was evaluated by treatment with bellidifolin, a kind of ketone compound derived from Swertia chirayita in traditional Tibetan medicine. It showed that bellidifolin exerts beneficial effects and attenuates the formation of NLRP3/ASC/Caspase-1 complex, thereby impeding GSDMD-N shuttling and resultant ROS generation, protecting against OGD-induced HBVPs pyroptosis. Overall, these findings unravel the potential mechanisms of pericyte injury induced by OGD and indicate that bellidifolin may exert its beneficial effects on pyroptosis, thus providing new therapeutic insights into stroke.

Role of the Peli1-RIPK1 Signaling Axis in Methamphetamine-Induced Neuroinflammation.

Severe neurological inflammation is one of the main symptoms of methamphetamine (meth)-induced brain injury. Studies have demonstrated that meth exposure facilitates neuroinflammation via Pellino E3 ubiquitin protein ligase 1 (Peli1)-mediated signaling. However, the involved mechanisms remain incompletely understood. Herein, we used Peli1-/- mice and Peli1-knockdown microglial BV2 cells to decipher the roles of Peli1 and downstream signaling in meth-induced neuroinflammation. After meth administration for seven consecutive days, Peli1-/- mice exhibited better learning and memory behavior and dramatically lower interleukin (IL)-1ß, tumor necrosis factor (TNF)-α, and IL-6 levels than wild-type mice. Moreover, in vitro experiments revealed that Peli1 knockdown significantly attenuated the meth-induced upregulation of cytokines. Besides, meth markedly activated and increased the levels of receptor-interacting protein kinase 1 (RIPK1), and Peli1 knockout or knockdown prevented these effects, indicating that RIPK1 participated in meth-induced Peli1-mediated inflammation. Specifically, treating the cells with necrostatin-1(Nec-1), an antagonist of RIPK1, remarkably inhibited the meth-induced increase in IL-1ß, TNF-α, and IL-6 expression, confirming the involvement of RIPK1 in Peli1-mediated neuroinflammation. Finally, meth induced a dramatic transfer of the mixed lineage kinase domain-like protein, a downstream effector of RIRK1, to the cell membrane, disrupting membrane integrity and causing cytokine excretion. Therefore, targeting the Peli1-RIPK1 signaling axis is a potentially valid therapeutic approach against meth-induced neuroinflammation.

A Sensor for Broken Wire Detection of Steel Wire Ropes Based on the Magnetic Concentrating Principle.

Electromagnetic testing is the most widely used technique for the inspection of steel wire ropes. As one of the electromagnetic detecting approaches, the magnetic flux leakage (MFL) method has the best effect for the detection of broken wires. However, existing sensors based on MFL method still have some problems. (1) The size of the permanent magnet exciter is usually designed according to experience or rough calculation, and there is not enough depth analysis for its excitation performance; (2) Since the detectable angular range for a single Hall component is limited, Hall sensor arrays are often employed in the design of MFL sensors, which will increase the complexity of the subsequent signal processing due to the extensive use of Hall components; (3) Although the new magneto-resistance sensor has higher sensitivity, it is difficult to be applied in practice because of the requirement of the micron-level lift-off. To solve these problems, a sensor for the detection of broken wires of steel wire ropes based on the principle of magnetic concentration is developed. A circumferential multi-circuit permanent magnet exciter (CMPME) is employed to magnetize the wire rope to saturation. The traditional Hall sensor array is replaced by a magnetic concentrator to collect MFL. The structural parameters of the CMPME are optimized and the performance of the magnetic concentrator is analyzed by the finite element method. Finally, the effectiveness of the designed sensor is verified by wire breaking experiment. 1-5 external broken wires, handcrafted on the wire rope with a diameter of 24 mm, can be clearly identified, which shows great potential for the inspection of steel wire ropes.

Taurine enhances the protective effect of Dexmedetomidine on sepsis-induced acute lung injury via balancing the immunological system.

Sepsis, an overwhelming systemic inflammatory disease, is the leading cause of acute lung injury (ALI). Despite plenty of researches have been done, effective drugs treating septic ALI are still eagerly needed in the clinic. Dexmedetomidine (Dex), a potent alpha-2 adrenoreceptor agonist, has been reported to possess antioxidant, anti-apoptosis and anti-inflammatory abilities. Taurine, a kind of intracellular free amino acid, has been used to treat various diseases. This study aimed to explore the combination effect of Dex and Taurine on septic ALI and the underlying mechanism in vivo. The establishment of septic ALI was set up in SD rats by cecal ligation and puncture (CLP) operation. Results indicated that Dex or Taurine could reduce septic ALI-induced cell apoptosis via decreasing caspase-3 activity. However, the combination of Dex or Taurine produced greater effect. Besides that, Dex combined with Taurine could better promote cell proliferation with remarkably elevated Ki67 expression. The combination of Dex and Taurine significantly suppressed the activation of NF-κB pathway via inhibiting P65 phosphorylation and P65 nuclear translocation, leading to the down-regulation of interleukin (IL)-6 and IL-1ß. Moreover, co-administration of Dex and Taurine alleviated the imbalance of Th1/Th2 induced by septic ALI to a great extent. All in all, our study suggested the synergistic therapeutic effect of Dex and Taurine on septic ALI.