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Introduction: Decompressive craniectomy (DC) is the most common surgical procedure to manage increased intracranial pressure (ICP). Hinge craniotomy (HC), which consists of fixing the bone operculum with a pivot, is an alternative method conceived to avoid some DC-related complications; nonetheless, it is debated whether it can provide enough volume expansion. In this study, we aimed to analyze the volume and ICP obtained with HC using an experimental cadaver-based preclinical model and compare the results to baseline and DC., Methods: Baseline conditions, HC, and DC were compared on both sides of five anatomical specimens. Volume and ICP values were measured with a custom-made system. Local polynomial regression was used to investigate volume differences., Results: The area of the bone opercula resulting from measurements was 115.55 cm 2 ; the mean supratentorial volume was 955 mL. HC led to intermediate results compared to baseline and DC. At an ICP of 50 mmHg, HC offers 130 mL extra space but 172 mL less than a DC. Based on local polynomial regression, the mean volume difference between HC and the standard craniotomy was 10%; 14% between DC and HC; both are higher than the volume of brain herniation reported in the literature in the clinical setting. The volume leading to an ICP of 50 mmHg at baseline was less than the volume needed to reach an ICP of 20 mmHg after HC (10.05% and 14.95% from baseline, respectively)., Conclusions: These data confirm the efficacy of HC in providing sufficient volume expansion. HC is a valid intermediate alternative in case of potentially evolutionary lesions and non-massive edema, especially in developing countries., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.)

Uncontrolled accumulation of methylglyoxal (MG) and reactive oxygen species (ROS) occurs in hyperglycemia-induced endothelial dysfunction associated with diabetes. Resveratrol (RSV) protects the endothelium upon high glucose (HG); however, the mechanisms underlying such protective effects are still debated. Here we identified key molecular players involved in the glycative/oxidative perturbations occurring in endothelial cells exposed to HG. In addition, we determined whether RSV essentially required SIRT1 to trigger adaptive responses in HG-challenged endothelial cells. We used primary human umbilical vein endothelial cells (HUVECs) undergoing a 24-h treatment with HG, with or without RSV and EX527 (i.e., SIRT1 inhibitor). We found that HG-induced glycative stress (GS) and oxidative stress (OS), by reducing SIRT1 activity, as well as by diminishing the efficiency of MG- and ROS-targeting protection. RSV totally abolished the HG-dependent cytotoxicity, and this was associated with SIRT1 upregulation, together with increased expression of GLO1, improved ROS-scavenging efficiency, and total suppression of HG-related GS and OS. Interestingly, RSV failed to induce effective response to HG cytotoxicity when EX527 was present, thus suggesting that the upregulation of SIRT1 is essential for RSV to activate the major antiglycative and antioxidative defense and avoid MG- and ROS-dependent molecular damages in HG environment., Competing Interests: The authors declare no conflict of interest.