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Purpose: To evaluate the effectiveness and safety of diazepam in maintaining stable intraoperative blood pressure (BP) in hypertensive patients undergoing vitrectomy under nerve block anesthesia.Methods: A total of 180 hypertensive patients undergoing vitrectomy with nerve block anesthesia were randomized into two groups. The intervention group was given oral diazepam 60 min before operation, while the control group was given oral placebo 60 min before operation. The primary outcome is the effective rate of intraoperative BP control, defined as systolic blood pressure (SBP) during the operation maintained < 160 mmHg at all timepoints. The logistic regression model will be performed to analyze the compare risk factors for ineffective BP control.Results: The effective rate of intraoperative SBP control in the diazepam group was significant higher than that in the placebo group from 15 min to 70 min of the surgery (P < 0.05). The proportion of patients with SBP ≥ 180 mmHg at any timepoint from operation to 1 h postoperation was higher in the placebo group (12.22%) than in the diazepam group (2.22%) (P = 0.0096). We observed that the change in SBP from baseline consistently remained higher in the placebo group than in the diazepam group. In the logistic regression analysis, age, years of diagnosed hypertension and SBP 1h before surgery were significant risk factors for ineffective BP control.Conclusion: This study provides robust evidence supporting the effectiveness of oral diazepam as a pre-surgery intervention in maintaining stable blood pressure during vitrectomy in hypertensive patients.Trial Registration: Chinese Clinical Trial Registry (ChiCTR), ChiCTR2100041772. [ABSTRACT FROM AUTHOR]

Purpose: Human trabecular meshwork cell (HTMC) dysfunction results in imbalanced aqueous humor inflow and outflow, leading to an increase in intraocular pressure (IOP). Uncontrolled high IOP can promote the occurrence of glaucoma, an irreversible optic neuropathy. Here, we explored whether the long non-coding RNA plasmacytoma variant translocation 1 (lncRNA PVT1)/microRNA-29a-3p (miR-29a-3p) axis could ameliorate HTMC dysfunction under oxidative stress by modulating the expression of the proangiogenic factor vascular endothelial growth factor (VEGFA) and the profibrotic factor metalloproteinase-2 (MMP-2)., Methods: HTMCs were cultured under H 2 O 2 -induced oxidative stress for 48 h. The expression of lncRNA PVT1, miR-29a-3p, VEGFA, MMP-2, intracellular adhesion molecule-1 (ICAM-1), and alpha-smooth muscle actin (α-SMA) was detected by reverse transcription quantitative real-time polymerase chain reaction, western blotting, and immunofluorescence. Interference experiments were conducted via the transfection of HTMCs with small interfering RNA (siRNA) targeting lncRNA PVT1 or miR-29a-3p mimics. A luciferase reporter assay was undertaken to identify the presence of a miR-29a-3p binding site in lncRNA PVT1. Flow cytometry and Transwell and Cell Counting Kit-8 assays were employed to evaluate HTMC functions under oxidative stress with different treatments., Results: In HTMCs, the expression of lncRNA PVT1 was induced by H 2 O 2 treatment, whereas that of miR-29a-3p was inhibited. The levels of angiogenic factors (VEGFA, ICAM-1) and fibrosis-associated mediators (MMP-2, α-SMA) were upregulated in HTMCs under oxidative stress. The siRNA-mediated suppression of lncRNA PVT1 or the upregulation of miR-29a-3p significantly suppressed the expression of VEGFA, MMP-2, ICAM-1, and α-SMA. A luciferase reporter assay confirmed that lncRNA PVT1 directly targeted miR-29a-3p and acted as a miR-29a-3p sponge. The knockdown of lncRNA PVT1 restored the level of miR-29a-3p in H 2 O 2 -treated HTMCs, thereby inhibiting VEGFA and MMP-2, its target mRNAs. HTMC dysfunction, including increased apoptosis and decreased cell mobility and viability, could be effectively ameliorated by lncRNA PVT1 downregulation or miR-29a-3p overexpression under oxidative stress., Conclusion: LncRNA PVT1 has potential as a therapeutic target for inhibiting VEGFA and MMP-2, thus protecting HTMCs, suppressing the progression of fibrosis, and, consequently, improving the outcome of glaucoma filtration surgery., Competing Interests: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Qiaoyun Gong reports financial support was provided by 10.13039/501100001809National Natural Science Foundation of China., (© 2023 The Authors. Published by Elsevier Ltd.)

Diabetic foot ulcers (DFUs) remain a devastating threat to human health. While hydrogels are promising systems for DFU-based wound management, their effectiveness is often hindered by the immune response and hostile wound microenvironment associated with the uncontrollable accumulation of reactive oxygen species and hypoxia. Here, we develop a therapeutic wound dressing using a biomimetic hydrogel system with the decoration of catalase-mimic nanozyme, namely, MnCoO@PDA/CPH. The hydrogel can be designed to match the mechanical and electrical cues of skins simultaneously with H 2 O 2 -activated oxygenation ability. As a proof of concept, DFU-based rat models are created to validate the therapeutic efficacy of the MnCoO@PDA/CPH hydrogel in vivo. The results indicate that the developed hydrogel can promote DFU healing and improve the quality of the healed wound as featured by alleviated proinflammatory, increased re-epithelialization, highly ordered collagen deposition, and functional blood vessel growth.