Intuitive Analysis of the Microtribological Behavior of Copper-Coated Graphite-Graphite/Cu Composites with High Graphite Contents.

To improve the combination of graphite and copper, the friction and wear of a graphite/copper composite with a high content of graphite (50 wt %), copper-coated graphite were used to modify it. To observe the distribution law of each phase in the material and the change of composite surface structure after the friction and wear experiment, scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were used to characterize the micro-structure, friction film, debris, and friction cross section of the composites. The results show that the large particle size of copper-coated graphite is anisotropic in the material, which helps to form a friction film with a high graphite content on the contact surface. TEM images of the friction film and debris directly reflect the structure changes of graphite and copper during friction; under normal load and shear force, interlamellar detachment and interlamellar fracture of graphite occur, and its edge is folded and crimped, resulting in the loss of an ordered state in some regions, which results in the instability of crystal lattice and the transition from an ordered to disordered state of graphite, resulting in the (002) halo ring in FFT results. Severe plastic deformation and oxidation reactions occur in copper, and copper oxides are formed, forming a high-strength and smooth oxide film in the metal-rich area and improving the wear resistance of the material. TEM images of the friction section directly show that an inverted triangular deformation zone is formed on the surface of the sample after friction and wear experiments. The edge of the deformation zone is stepped, consisting of a drag zone and an accumulation zone, and the surface of the contact zone is covered by a carbon film.

Development pattern of ocular biometric parameters and refractive error in young Chinese adults: a longitudinal study of first-year university students.

BACKGROUND: The increase in the prevalence of myopia has become a matter of serious public health concern, and few studies to date have examined the ocular biometric parameters of myopia in young Chinese adults. This study aimed to investigate the longitudinal ocular biometric and refractive development of first-year university students and the influence of near work. METHODS: This study included 526 first-year university students from Tianjin Medical University (mean age, 18.34 years; 313 females and 213 males). From 2016 to 2018, participants underwent ocular biometry measurements and subjective refraction annually. Near-work activities such as the use of electronic devices, online games, reading, and writing as well as demographic data were recorded by questionnaires. RESULTS: The prevalence of myopia in this population from 2016 to 2018 was 92.40%, 92.59%, and 92.97%, respectively. Importantly, the prevalence of high myopia increased significantly from 20.91% to 28.33% (P < .001). The spherical equivalent refraction was significantly more myopic by approximately - 0.38 D (from - 4.18 ± 2.44 to - 4.56 ± 2.57 D; P < .001) during the period. The axial length, central corneal thickness, and lens thickness became significantly different (all P < .05), and the axial length significantly increased by 0.12 mm during 2 years (P < .001). Using binary logistic regression analysis, the data indicated that spending more time on online games (odds ratio, 2.09; 95% confidence interval, 1.33-3.29) could speed up the progression of myopia (P < .05). CONCLUSIONS: This study showed that the prevalence of high myopia continued to increase in undergraduate students over 2 years. Baseline myopia correlated with myopic shift, the time spent on online games, and parental myopia were significantly associated with an increase in myopia in these young adult populations.

MED1 Downregulation Contributes to TGFß-Induced Metastasis by Inhibiting SMAD2 Ubiquitination Degradation in Cutaneous Melanoma.

Metastasis is the main reason for the high mortality of patients and indeed a difficult task in the treatment of cutaneous melanoma. Therefore, it is of great clinical value to explore the molecular mechanism of cutaneous metastatic melanoma and develop novel therapies. MED1, acting as a factor required for activator-dependent transcription, is reported to be involved in carcinogenesis and progression. In this study, we found that MED1 was highly expressed in patients with cutaneous melanoma. MED1 downregulation could induce cellular epithelial-to-mesenchymal transition and promote migration, invasion, and metastasis of cutaneous melanoma in vivo and in vitro. Further analysis showed that in Med1 knockdown cells, the TGFß/SMAD2 signaling pathway mediated an increase in epithelial-to-mesenchymal transition phenotype and migration. The opposite results were observed after treatment with TGFß inhibitors. To further explore the mechanism, we found that MED1 interacted with SMAD2, and MED1 downregulation could protect SMAD2 from degradation by inhibiting SMAD2 ubiquitination. Together, these results suggest that MED1 inhibited TGFß signaling pathway to reduce cell epithelial-to-mesenchymal transition phenotype and migration through SMAD2 ubiquitination in the metastasis of cutaneous melanoma. Our findings elucidated the role of MED1 in the metastasis of cutaneous melanoma and provided a target for the therapeutic strategies of cutaneous melanoma.

Deficiency of vitamin D receptor in keratinocytes augments dermal fibrosis and inflammation in a mouse model of HOCl-induced scleroderma.

Scleroderma, characterized by extensive fibrosis and vascular alterations, involves excessive fibroblast activation, uncontrolled inflammation, and abnormal collagen deposition. Previous studies showed that administrations of either 1,25(OH)2D3 or vitamin D analog effectively decreased or reversed skin fibrosis by regulating the extracellular matrix homeostasis. The actions of 1,25(OH)2D3 are mediated by the vitamin D receptor (VDR), a transcription regulator crucial for skin homeostasis. Although evidence suggests that keratinocyte-fibroblast interaction influences the development of scleroderma, the role of keratinocytes in scleroderma remains unknown. Here, we demonstrated that the ablation of VDR in keratinocytes greatly exacerbated dermal fibrosis in HOCl-induced scleroderma in mice. The deficiency of VDR in the epidermis marked increased dermal thickness, inflammatory cell infiltration, and severe collagen deposition in comparison to the control group in HOCl-treated skin. Moreover, significant elevations in expression levels of mRNA for collagen overproduction (Col1A1, Col1A2, Col3A1, α-SMA, MMP9, TGF-ß1) and proinflammatory cytokines (IL-1ß, IL-6, CXCL1, CXCL2) were observed in VDR conditional KO versus control mice following HOCl treatment. Collectively, these results suggest that VDR in keratinocytes plays a pivotal role in scleroderma progression, and the interplay between keratinocytes and fibroblasts deserves more attention regarding the exploration of the pathogenesis and treatment for scleroderma.