Baicalin administration could rescue high glucose-induced craniofacial skeleton malformation by regulating neural crest development.

Hyperglycemia in pregnancy can increase the risk of congenital disorders, but little is known about craniofacial skeleton malformation and its corresponding medication. Our study first used meta-analysis to review the previous findings. Second, baicalin, an antioxidant, was chosen to counteract high glucose-induced craniofacial skeleton malformation. Its effectiveness was then tested by exposing chicken embryos to a combination of high glucose (HG, 50 mM) and 6 µM baicalin. Third, whole-mount immunofluorescence staining and in situ hybridization revealed that baicalin administration could reverse HG-inhibited neural crest cells (NCC) delamination and migration through upregulating the expression of Pax7 and Foxd3, and mitigate the disordered epithelial-mesenchymal transition (EMT) process by regulating corresponding adhesion molecules and transcription factors (i.e., E-cadherin, N-cadherin, Cadherin 6B, Slug and Msx1). Finally, through bioinformatic analysis and cellular thermal shift assay, we identified the AKR1B1 gene as a potential target. In summary, these findings suggest that baicalin could be used as a therapeutic agent for high glucose-induced craniofacial skeleton malformation.

Cord blood-derived biologics lead to robust axonal regeneration in benzalkonium chloride-injured mouse corneas by modulating the Il-17 pathway and neuropeptide Y.

BACKGROUND: Umbilical cord blood-derived therapeutics, such as serum (UCS) and platelet-rich plasma (UCPRP), are popular treatment options in clinical trials and can potentially be utilized to address a clinically unmet need caused by preservatives, specifically benzalkonium chloride (BAK), present in ophthalmic formulations. As current clinical interventions for secondary injuries caused by BAK are suboptimal, this study will explore the feasibility of utilizing UCS and UCPRP for cornea treatment and investigate the underlying mechanisms associated with this approach. METHODS: Mice's corneas were administered BAK to induce damage. UCS and UCPRP were then utilized to attempt to treat the injuries. Ocular tests were performed on the animals to evaluate recovery, while immunostaining, RNA-seq, and subsequent bioinformatics analysis were conducted to investigate the treatment mechanism. RESULTS: BAK administration led to widespread inflammatory responses in the cornea. Subsequent treatment with UCS and UCPRP led to the downregulation of immune-related 'interactions between cytokine receptors' and 'IL-17 signaling' pathways. Although axonal enhancers such as Ngf, Rac2, Robo2, Srgap1, and Rock2 were found to be present in the injured group, robust axonal regeneration was observed only in the UCS and UCPRP treatment groups. Further analysis revealed that, as compared to normal corneas, inflammation was not restored to pre-injury levels post-treatment. Importantly, Neuropeptide Y (Npy) was also involved in regulating immune responses, indicating neuroimmune axis interactions. CONCLUSIONS: Cord blood-derived therapeutics are feasible options for overcoming the sustained injuries induced by BAK in the cornea. They also have potential applications in areas where axonal regeneration is required.

Construction of a virtual reality platform for computer-aided navigation Lingnan bone setting technique.

To establish a standard Traditional Chinese medicine (TCM) bone setting technique, standardize the operation and inherit the TCM bone setting technique. This project was based on the interactive tracking of bone setting techniques with a dedicated position tracker, the motion tracking of bone setting techniques based on RGBD (Red Green Blue Depth) cameras, the digital analysis of bone setting techniques, and the design of the virtual reality platform for bone setting techniques. These key technical researches were combined to construct an interactive bone setting technique. The virtual simulation system can reproduce the implementation process of the expert's bone setting technique. The user can observe the implementation of the manipulative technique from multiple angles; through human-computer interaction, the whole process of implementation of the bone setting technique can be simulated, and the movement and reduction of the affected bone can be observed at the same time. It can be used as a teaching and training system for assisting bone setting techniques. Students can use the system to carry out repeated self-training, and can instantly compare with the standard techniques of the expert database, breaking the traditional teaching mode of 'expected and unspeakable' and avoid directly using patients. Therefore, this research makes it possible to reduce teaching costs, reduce risks, improve teaching quality, and make up for the lack of teaching conditions. It is very positive for the inheritance of the traditional Chinese 'intangible culture' of bone setting techniques, and to promote the digitalization and standardization of bone setting techniques.

Using computer technology to digitally record bone-setting manipulations.Construct a virtual simulation system for interactive bone-setting manipulation.Promote the digitization and standardization of bone-setting techniques.

Dry eye syndrome: comprehensive etiologies and recent clinical trials.

Dry eye syndrome (DES) is multifactorial and likely to be a cause of concern more so than ever given the rapid pace of modernization, which is directly associated with many of the extrinsic causative factors. Additionally, recent studies have also postulated novel etiologies that may provide the basis for alternative treatment methods clinically. Such insights are especially important given that current approaches to tackle DES remains suboptimal. This review will primarily cover a comprehensive list of causes that lead to DES, summarize all the upcoming and ongoing clinical trials that focuses on treating this disease as well as discuss future potential treatments that can improve inclusivity.

Low-dose minocycline mediated neuroprotection on retinal ischemia-reperfusion injury of mice.

Purpose: The aim of this study was to investigate the effect of minocycline (MC) on the survival of retinal ganglion cells (RGCs) in an ischemic-reperfusion (I/R) injury model of retinal degeneration. Methods: Retinal I/R injury was induced in the left eye of mice for 60 min by maintaining intraocular pressure at 90 mmHg. Low- or high-dose MC (20 or 100 mg/kg, respectively) was administered by intravenous injection at 5 min after the retinal ischemic insult and then administered once daily until the mice were euthanized. RGCs and microglial cells were counted using immunofluorescence staining. Functional changes in the RGCs were evaluated using electroretinography. The visual function was assessed using an optokinetic test. Results: The data demonstrated that the effect of MC was dose dependent. Low-dose MC showed protective effects, with reduced RGC loss and microglial activation, while the high-dose MC showed damage effects, with more RGC loss and microglial activation when compared with the vehicle group. The electroretinography and optokinetic test results were consistent with the morphologic observations. Conclusions: These data suggested that appropriate concentrations of MC can protect the retina against retinal ischemic-reperfusion injury, while excessive MC has detrimental effects.

Seed-targeting anti-miR-21 inhibiting malignant progression of retinoblastoma and analysis of their phosphorylation signaling pathways.

MiR-21 acts as a ubiquitous oncogene in major classes of human cancers and is a potential target for therapeutic intervention. However, the relative expression of miR-21 in retinoblastoma is poorly understood. Here we detected miR-21 expression in HXO-RB44 cell line human normal retinal tissues and retinoblastoma (Rb) tissue specimens, and studied its function using an 8-mer tiny seed-targeting anti-miR-21 (t-anti-miR-21). RT-PCR revealed that miR-21 was highly overexpressed in HXO-RB44 cells and Rb tissue specimens compared with normal human retinal tissues. The localization and transfection efficiency of t-anti-miR-21 and the cell cycle distribution were detected by confocal microscopy and flow cytometry. In addition, we found that t-anti-miR-21 led to a significant inhibition of retinoblastoma cell proliferation, migration and colony formation in vitro, with a similar effect to anti-miR-21. Anti-miR-21 down-regulated the miR-21 level, whereas both 8-mer t-anti-miR-21 and 15-mer m-anti-miR-21 had no impact on miR-21 expression levels. Finally, the phosphorylation signaling pathway, down-regulated by t-anti-miR-21, was integrated by KEGG assay, which elucidated the potential mechanisms of inhibition of miR-21 in retinoblastoma. Taken together, knockdown of miR-21 in the HXO-RB44 cell is capable of inhibiting cancer progression in retinoblastoma. Seed-targeting t-anti-miR-21 was a novel strategy for mir-21-based therapeutics and drug discovery.