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In order to overcome the difficulties that current attack graph model cannot reflect real-time network attack events,a method is proposed including a forward risk probability update algorithm and a forward-backward combined risk probability update algorithm,which meets the needs of real-time analyzing network security.It first performs specific quantitative analysis on the uncertainty of each node in the graph,and uses Bayesian networks to calculate their static probabilities.After that,it updates the dynamic probability of each node along the forward and backward paths according to the real-time network security events,instantly reflecting the changes of external conditions and assessing real-time risk levels across the network.Experimental results show that the method can calibrate and adjust the risk probability of each node according to the actual situation,which helps the network operator correctly understand the dangerous levels of the network and make better decision for defense and prevention of the next attack.

A lightweight and high-strength water-soluble core mold for composites was prepared by hot-air drying method using aqueous solution of polyvinylpyrrolidone as the adhesive and hollow glass beads, gypsum and graphite as the matrix materials. The effects of adhesive content and matrix material on the mechanical properties and dissolution rates of the water-soluble core mold were investigated. The effect of modification methods on the mechanical properties of water-soluble core molds was investigated, and the microscopic morphology of the modified water-soluble core mold was observed by scanning electron microscopy (SEM), and its modification mechanism was initially explored. The results shows that the density of water-soluble core mold is 0.46~0.58 g/cm³, and the high-temperature treatment and the compounding of glass beads with different scales of particle size are the effective means of modification. The flexural strength of the water-soluble core can reach 7.46 MPa, the compression strength reaches 7.45 MPa, and the dissolution rate is 1.11 g/min before the modification, while the flexural strength of the modified core mold can reach 13.21 MPa, the compression strength reaches 13.45 MPa, and the dissolution rate is 6.34 g/min. The comprehensive performance of the water-soluble core mold can meet the requirements of the composite molding process, and it provides a solution for the integrated molding of the hollow profiled composites. [ABSTRACT FROM AUTHOR]

Objective Methods Results Conclusions This study aimed to investigate whether flow fluid shear stress (FFSS)‐mediated signal transduction affects the function of Piezo1 ion channel in chondrocyte and to further explore the role of mechanical overloading in development of temporomandibular joint osteoarthritis (TMJ OA).Immunohistochemical staining was used to determine the expression of Piezo1 in TMJ OA tissue collected from rat unilateral anterior crossbite (UAC) models. Chondrocytes harvested from normal adult SD rats were treated with FFSS (0, 4, 8, 12 dyn/cm2) in vitro. Immunofluorescent staining, real‐time polymerase chain reaction, western blotting, flow cytometry and phalloidin assay were performed to detect the changes of cellular morphology as well as the expression of Piezo1 and certain pro‐inflammatory and degradative factors in chondrocyte.Immunohistochemical analysis revealed that significantly increased Piezo1 expression was associated with UAC stimulation (p < .05). As applied FFSS escalated (4, 8 and 12 dyn/cm2), the expression levels of Piezo1, ADAMTS‐5, MMP‐13 and Col‐X gradually increased, compared with the non‐FFSS group (p < .05). Administering Piezo1 ion channel inhibitor to chondrocytes beforehand, it was observed that expression of ADAMTS‐5, MMP‐13 and Col‐X was substantially decreased following FFSS treatment (p < .05) and the effect of cytoskeletal thinning was counteracted. The activated Piezo1 ion channel enhanced intracellular Ca2+ excess in chondrocytes during abnormal mechanical stimulation and the increased intracellular Ca2+ thinned the cytoskeleton of F‐actin.Mechanical overloading activates Piezo1 ion channel to promote pro‐inflammation and degradation and to increase Ca2+ concentration in chondrocyte, which may eventually result in TMJ OA. [ABSTRACT FROM AUTHOR]

Chondromyxoid fibroma (CMF) is an extremely rare cartilaginous tumor, accounting for less than 1 % of benign bone tumor. Most CMFs are found in the metaphysis of long bones. This study aimed to present a patient with temporomandibular joint (TMJ)-CMF involving pterygopalatine space and the skull base, and to discuss its epidemiology, clinical characteristics and management thereof. A 56-year-old Chinese Han woman visited our hospital with a chief complaint of facial asymmetry and progressive limitation of mouth opening due to this mass expanding upwardly to the auriculotemporal region. A computed tomography presented the wormlike osteolysis of the right condylar head presenting with swelling, cloudy flocculent ground-glass opacity, relatively clear boundary, thin bone in the middle of the cranial fossa, low continuity, and involving the temporomandibular joint. Incisional biopsy confirmed a diagnosis of TMJ-CMF. Using digital technique to determine the boundary of the lesion and reconstruct the normal glenoid fossa, the temporalis myofascial flap was transplanted between titanium mesh and condyle so as to reconstruct the disk after complete resection of the tumor. The patient's facial profile is symmetrical, with a mouth opening of 45 mm; there was no local recurrence, no complications such as cerebrospinal fluid fistula and cerebral hernia during 1-year follow-up period. To date, a review of the literature yielded only one case occurred in the TMJ was previously evaluated by radiology. To our knowledge, this is the second case of primary CMF in the TMJ. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) as a ubiquitous toxic heavy metal is reported to affect the nervous system. Selenium (Se) has been shown to have antagonistic effects against heavy metal toxicity. In addition, it shows potential antioxidant and anti‐inflammatory properties. Thus, the purpose of this study was to determine the possible mechanism of brain injury after high Cd exposure and the mitigation of Nano‐selenium (Nano‐Se) against Cd‐induced brain injury. In this study, the Cd‐treated group showed a decrease in the number of neurons in brain tissue, swelling of the endoplasmic reticulum and mitochondria, and the formation of autophagosomes. Nano‐Se intervention restored Cd‐caused alterations in neuronal morphology, endoplasmic reticulum, and mitochondrial structure, thereby reducing neuronal damage. Furthermore, we found that some differentially expressed genes were involved in cell junction and molecular functions. Subsequently, we selected eleven (11) related differentially expressed genes for verification. The qRT‐PCR results revealed the same trend of results as determined by RNA‐Seq. Our findings also showed that Nano‐Se supplementation alleviated Cx43 phosphorylation induced by Cd exposure. Based on immunofluorescence colocalization it was demonstrated that higher expression of GFAP and lower expressions of Cx43 were restored by Nano‐Se supplementation. In conclusion, the data presented in this study establish a direct association between the phosphorylation of Cx43 and the occurrence of autophagy and neuroinflammation. However, it is noteworthy that the introduction of Nano‐Se supplementation has been observed to mitigate these alterations. These results elucidate the relieving effect of Nano‐Se on Cd exposure‐induced brain injury. [ABSTRACT FROM AUTHOR]