Occurrence of neonicotinoid insecticides and their metabolites in tooth samples collected from south China: Associations with periodontitis.

Neonicotinoid insecticides (NEOs) are widely used in agricultural production processes in China and worldwide. NEOs have been an increasing concern because of their potential toxicity to nontarget organisms. However, studies that focused on human exposure to NEOs in China are limited. In this study, levels of six parent NEOs (p-NEOs), namely imidacloprid (IMI), acetamiprid (ACE), clothianidin (CLO), dinotefuran (DIN), thiamethoxam (THIX), and thiacloprid (THI), and three metabolites (m-NEOs), such as 5-hydroxy-imidacloprid (5-OH-IMI), 1-methyl-3-(tetrahydro-3-furyl methyl) urea (UF), and N-desmethyl-acetamiprid (N-dm-ACE) were measured in 127 tooth samples collected from South China. P-NEOs and m-NEOs are frequently detected (76%-93%) in tooth samples, with median levels of 0.03-1.20 ng/g. UF is the most abundant NEOs in tooth samples (36%). Females have higher NEO levels than males, and gender-related differences in NEO levels are found. Associations among most p-NEOs are also found (p < 0.05), indicating the source of human exposure to p-NEOs is related. However, no significant relationships (p > 0.05) between levels of m-NEOs and their corresponding p-NEOs are found, suggesting that exogenous m-NEOs contribute to exposure. We have also examined the associations between human NEOs exposure and periodontitis, and associations between NEO exposure and periodontitis are observed (OR = 2.63-7.33; 95% CI = 1.01-21.1, p-trend < 0.05). Our results suggest that NEO levels are associated with increased odds of prevalent periodontitis. This study is the first to report about p-NEOs and m-NEOs in tooth samples collected from South China.

Biomechanical effect of anterior talofibular ligament injury in Weber B lateral malleolus fractures after lateral plate fixation: A finite element analysis.

OBJECTIVE: To determine the biomechanical effect of anterior talofibular ligament injury in Weber B lateral malleolus fractures after lateral plate fixation. METHOD: A three-dimensional model was established based on CT images from a healthy volunteer. The simulation of lateral malleolus fracture, and the modeling and assembly of plate were completed by referring to characteristics of Weber B lateral malleolus fractures, as well as the technical characteristics of open reduction and internal fixation of lateral plate. Operating conditions were set up for groups A-D. The proximal end of the model was restrained in all four groups, 200N of upward force and 100N of backward force were applied at anterior of talus head in order to simulate the dorsiflexion of ankle joint. Biomechanical differences of the lateral plate were observed under various conditions of different ligament ruptures. RESULTS: The maximum stress value of group A was the smallest, approximately 78.47N, while that of group C was the largest, approximately 238.83N. The maximum stress value of group B was about 91.69N; and that of group D was about 184.08N. Importantly, location of the maximum stress in group D (CUT ATaF) was displaced from the posterior edge to the anterior edge of the plate, which was different from those of the other three groups. CONCLUSIONS: The anterior talofibular ligament injury may be a major contributing factor to the stress of lateral plate fixation following Weber B lateral malleolus fracture. It should be considered as an essential risk factor for evaluation of the stability in these fractures.

CD8 T cell-derived perforin aggravates secondary spinal cord injury through destroying the blood-spinal cord barrier.

Perforin plays an important role in autoimmune and infectious diseases, but its function in immune inflammatory responses after spinal cord injury (SCI) has received insufficient attention. The goal of this study is to determine the influence of perforin after spinal cord injury (SCI) on secondary inflammation. Compared recovery from SCI in perforin knockout (Prf1-/-) and wild-type(WT)mice, WT mice had significantly lower the Basso mouse score (BMS), CatWalk XT, and motor-evoked potentials (MEPs) than Prf1-/- mice. Spinal cord lesions were also more obvious through glial fibrillary acidic protein (GFAP), Nissl, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining. Furthermore, the blood-spinal cord barrier (BSCB) disruption was more severe and inflammatory cytokine levels were higher. Flow cytometry indicated that perforin mainly originated from CD8 T cells. With flow cytometry and enzyme-linked immunosorbent assay (ELISA), human cerebrospinal fluid (CSF) yielded similar results. Together, this study firstly demonstrated that CD8 T cell-derived perforin is detrimental to SCI recovery in the mouse model. Mechanistically, this effect occurs because perforin increases BSCB permeability, causing inflammatory cells and related cytokines to infiltrate and disrupt the nervous system.

LINC00673 silencing inhibits cell migration and invasion by suppressing PI3K/AKT signaling in glioma.

LINC00673 is an oncogene that plays a key role in various cancer types. However, the role of LINC00673 in glioma remains unclear. In this study, we examined its expression in glioma cells by quantitative real-time PCR and found higher expression of LINC00673 in glioma cells compared with that in normal human astrocytes. Furthermore, LINC00673 silencing inhibited the migration and invasion of U87MG and U118MG cells, phosphoinositide 3-kinase (PI3K) expression, and AKT phosphorylation. Moreover, activation of the PI3K/AKT signaling pathway by insulin-like Growth factor-1 abolished the inhibitory effect of LINC00673 silencing on the migration and invasion of U87MG and U118MG cells. In conclusion, LINC00673 silencing inhibits glioma cell migration and invasion by suppressing the PI3K/AKT signaling pathway, and it is a potential therapeutic target for the treatment of metastatic glioma.

Finite element analysis of the influence of anterior talofibular ligament injury on Hook test results.

AIM: To determine whether the anterior talofibular ligament injury will influence the Hook test result. METHOD: A three-dimensional model of the ankle was established based on CT scan of a healthy volunteer and ligament attachment through references; Four groups (A-D) of operating conditions were set up. In group A, the anterior and posterior ligaments of the inferior tibiofibular joint were cut off and the anterior talofibular ligament was kept intact; in group B, all the anterior and posterior tibiofibular ligaments and the anterior talofibular ligament were cut off; in group C, the medial and lateral ligaments of the ankle joint and the inferior tibiofibular ligament were kept intact; in group D, only the talofibular ligament was cut off and other ligaments were kept intact. The proximal end of the model was restrained in all four groups, an outward pulling force of 100N perpendicular to the fibula was applied, and displacement and rotation of the distal end of the fibula in the four groups was observed. RESULTS: When the inferior tibiofibular joint injury was associated with an anterior talofibular ligament injury, the Hook test indicated about 3.19mm of displacement of the distal end of the fibula, and obvious external rotation occurred due to increased activity of the anterior border of the fibula. In the other groups, a single inferior tibiofibular joint injury or a single anterior talofibular ligament injury did not increase displacement or rotation of the distal end of the fibula.