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Due to trauma and disease, bone defects endanger the healthy life of human beings. At present, the gold standard for bone defect repair is still autologous bone transplantation and allogeneic bone transplantation. However, its insufficient source, potential disease transmission and immune rejection limit its clinical application. Therefore, the development of bone repair materials plays an important role in promoting bone repair. As the interface between material and tissue, the surface of the material plays an important role in the reaction after implantation, which determines the effectiveness of defect repair treatment. With the development of surface engineering and technology, bone repair materials have developed from biological inertia to biological activity by endowing various biological functions by controlling the composition, topological morphology and structure of the material surface etc. The inspired biofunctionalisation of material surface includes the capacities of inducing osteogenesis, promoting angiogenesis, antibacterial, immune regulation etc., as well as integration of postoperative repair and treatment. The authors review the biofunctionalisation of biomaterial surface and the inspired biological effects for bone repair, mainly including physical and chemical properties of material surface to regulate osteogenesis, and functional strategy of bone repair material surface. [ABSTRACT FROM AUTHOR]

Inflammation and oxidative stress (OS) are the major pathogenic characteristics of acute kidney injury (AKI). Studies have shown that Schisandrin (Sch) could regulate inflammatory disease. However, the function and mechanism of Sch in AKI progression are still unknown. Here, we investigated Sch's potential effects and mechanism on mice's renal damage and macrophages induced by lipopolysaccharide (LPS). Sch decreased LPS‐induced inflammatory factor production while increasing the activity of related antioxidant enzymes in macrophages and mouse kidney tissues. Hematoxylin and eosin staining revealed that Sch may have the ability to profoundly inhibit inflammatory cell invasion and tissue damage caused by LPS in renal tissue. Furthermore, Western blot and immunohistochemical studies showed that Sch exerted its effects mainly through up‐regulation of nuclear factor erythroid 2‐related factor 2/heme oxygenase‐1 and inhibition of Toll‐like receptor 4‒mitogen‐activated protein kinases/nuclear factor‐kappa B pathways. Collectively, this study illustrates that Sch suppresses LPS‐stimulated AKI by descending inflammation and OS, illuminating prospective AKI treatment options. [ABSTRACT FROM AUTHOR]

In this paper, Pd‐catalyzed [4+2] decarboxylative cycloaddition of 4‐vinylbenzodioxinones with barbiturate‐derived alkenes has been developed, leading to various spirobarbiturate−chromane derivatives in high yields with excellent diastereo‐ and enantioselectivities. The scale‐up reaction and further derivation of the product were demonstrated. A plausible reaction mechanism was also proposed. [ABSTRACT FROM AUTHOR]

Transparent and homogeneous SrPb3Br8 single crystals with the size of Ø25 mm × 50 mm are grown by the modified vertical Bridgman method. X‐ray diffraction results reveal that the middle part of the crystal is pure in chemical compositions, while the tip part contains low content of Sr(PbBr3)2(H2O)5. X‐ray photoelectron spectroscopy analysis points out the absorption to C, O‐containing substances of the pristine surfaces of SrPb3Br8 wafers. The Raman results prove the low phonon energy of the SrPb3Br8 (116 cm−1). Transmission spectra demonstrate its wide transparent range (0.37–25 µm) and high transmittance in the mid‐infrared range except for several absorption lines. Moreover, Hall measurements show that the SrPb3Br8 sample is n‐type conductive at 110–300 K, and the Hall coefficient RH, resistivity ρ and mobility µH decrease as temperature increases while the carrier concentration n has an opposite trend. The conduction mechanism and scattering mechanism of SrPb3Br8 crystal at different temperatures has been studied by analyzing ln(|RH|)−T−1, n−T and µH−T curves, and the dominant donor defect ionization energy ED is calculated to be 0.077 eV. [ABSTRACT FROM AUTHOR]

Antisocial personality disorder (ASPD) is a common behavioral pattern that causes sufferers to ignore or violate the rights of others. Though its cause is still unclear, previous studies have shown that childhood maltreatment is closely related to ASPD. The NOS1AP gene is associated with various neuropsychiatric diseases, but a linkage between it and ASPD has not yet been discovered. This study recruited ASPD and non‐ASPD male subjects who had committed violent crimes from a prison in Nanjing, China. By comparing the two groups' genotypes, allele frequencies, and histories of childhood abuse, we explored the interaction between the NOS1AP gene and childhood maltreatment on the pathogenesis of ASPD. The results showed that polymorphism rs945713 in the NOS1AP gene was associated with ASPD and furthermore that this SNP may be involved in regulating the effect of childhood abuse on ASPD. This study found that childhood trauma increases the risk of ASPD in violent adult male inmates; for prisoners with ASPD, it is critical to pay attention to their childhood trauma and take early psychological intervention. [ABSTRACT FROM AUTHOR]

This article discusses a case of sporotrichosis, a chronic fungal infection, in a 56-year-old male patient. The patient presented with erythema and nodules on the right side of his face, and dermoscopy revealed the presence of the "blackish-red dot sign." The diagnosis was confirmed through mycological examination, and treatment with oral itraconazole led to complete healing. The article suggests that further research is needed to explore the potential of the "blackish-red dot sign" as a diagnostic clue and to evaluate its effectiveness in treatment evaluation. The study was supported by funding from West China Hospital, Sichuan University, and the National Key Research and Development Program of China. [Extracted from the article]

Novel dual physically cross‐linked (DPC) hydrogels with great tensile strength, ultrahigh elongation, and promising repairability are designed by introducing cellulose nanocrystal (CNC) or hydrophobized CNC (CNC‐C8) into polymers physically cross‐linked by hydrophobic forces. C18 alkyl chain is grafted to N‐[3‐(dimethylamino)propyl]methacrylamide (DMAPMA) for hydrophobic monomer (DMAPMA‐C18), and C8 to CNC surface for hydrophobic CNC (CNC‐C8). CNC‐C8 (or CNC) DPC hydrogels are synthesized, with monomers N,N‐dimethylacrylamide (DMAc) and DMAPMA‐C18 polymerized to form the first network physically cross‐linked by hydrophobic interactions, on which the secondary cross‐linking points are formed by hydrophobic interactions between CNC‐C8 and DMAPMA‐C18, electrostatic interactions between CNC‐C8 (or CNC) and DMAPMA, as well as hydrogen bonding between CNC‐C8 (or CNC) and DMAc. Compared with optimum CNC DPC hydrogels of the highest tensile strength (238 ± 8 kPa), the optimum CNC‐C8 DPC hydrogel with 0.0675 w/v% DMAPMA‐C18 and 0.4 w/v% CNC‐C8 possesses stronger tensile strength of 331 ± 32 kPa and excellent elongation of 4268% ± 1446% as well, demonstrating the enhanced mechanical property of the hydrogel by introduced hydrophobic interactions. In addition, such DPC hydrogel can be facilely repaired with tetrahydrofuran (THF) on the cut surfaces while retaining good tensile stress and elongation behaviors. [ABSTRACT FROM AUTHOR]

This study discusses the association between blood pressure (BP) variability at different time periods within first 24 hours after admission and the functional outcome in acute ischemic stroke (AIS). We observed BP variability within first 24 hours after admission and evaluated the association between BP variability at different time periods (4 am-8 am, 10 am-2 pm, 4 pm-8 pm, 10 pm-2 am) and the functional outcome in AIS. National Institute of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS) were applied to evaluate short- (7 days) and long-term functional outcome. The 24 hours after admission and early morning (4 am-8 am) systolic blood pressure (SBP) variability were associated with poor outcome at day 7 (adjusted OR = 1.567, 95% CI = 1.076-2.282; adjusted OR = 1.507, 95% CI = 1.028-2.209, respectively). Compared with the impact of the 24-hour BP variability on long-term functional outcome, the early morning SBP was proved to be a strongly independent predictor for functional outcome at 3 months (adjusted OR = 1.505, 95% CI = 1.053-2.152), 6 months (adjusted OR = 1.560, 95% CI = 1.048-2.226), and 12 months (adjusted OR = 1.689, 95% CI = 1.104-2.584). The BP variability in other time period groups was shown to have no influence on functional outcome. In addition, attempts to explain early morning BP variability with baseline characteristic factors at admission found that baseline SBP is the most influential (2.71%) factor. About 95.87% of the SBP variability in early morning was unexplained. In our study, early morning SBP variability is the strongest independent predictor for functional outcome in (AIS) patients, and baseline SBP after admission should be monitored as a control indicator of early morning SBP variability in the treatment of AIS patients. [ABSTRACT FROM AUTHOR]

The most prevalent pathological features of many neurodegenerative diseases are the aggregation of misfolded proteins and the loss of certain neuronal populations. Autophagy, as major intracellular machinery for degrading aggregated proteins and damaged organelles, has been reported to be involved in the occurrence of pathological changes in many neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis. In this review, we summarize most recent research progress in this topic and provide a new perspective regarding autophagy regulation on the pathogenesis of neurodegenerative diseases. Finally, we discuss the signaling molecules in autophagy-related pathways as therapeutic targets for the treatment of these diseases. [ABSTRACT FROM AUTHOR]

Corneal neovascularization ( CNV) is a common pathological change in ocular surface diseases. It is not only the factor that affects vision but also the main cause for corneal graft failure. Based on the mechanism of CNV, many achievements have been developed to suppress the formation of CNV. There are certain novel drugs such as aflibercept, gold nanoparticles, and netrins which provide us with new clues to treat CNV. However, we still need to develop more effective therapeutic drugs. It is of great significance to develop new effective drugs to suppress the occurrence of CNV. In this paper, recent drug therapies for CNV are reviewed. The electronic database (PubMed) is searched for relative basic research and randomized clinical trials that are published recently. [ABSTRACT FROM AUTHOR]