Objective. This study was aimed at identifying the potential outcome predictors, comparing the efficacy in patients with different tremor characteristics, and summarizing the adverse effect rates (AERs) of deep brain stimulation on the ventral intermediate nucleus (VIM-DBS) for essential tremor (ET). Methods. An extensive search of articles published to date in 2019 was conducted, and two main aspects were analyzed. Improvement was calculated as a percentage of change in any objective tremor rating scale (TRS) and analyzed by subgroup analyses of patients’ tremor characteristics, laterality, and stimulation parameters. Furthermore, the AERs were analyzed as follows: the adverse effects (AEs) were classified as stimulation-related, surgical-related, or device-related effects. A simple regression analysis was used to identify the potential prognostic factors, and a two-sample mean-comparison test was used to verify the statistical significance of the subgroup analyses. Results. Forty-six articles involving 1714 patients were included in the meta-analysis. The pooled improvement in any objective TRS score was 61.3% (95% CI: 0.564-0.660) at the mean follow-up visit (20.0±17.3 months). The midline and extremity symptoms showed consistent improvement (P=0.440), and the results of the comparison of postural and kinetic tremor were the same (P=0.219). In addition, the improvement in rest tremor was similar to that in action tremor (OR=2.759, P=0.120). In the simple regression analysis, the preoperative Fahn-Tolosa-Marin Tremor Rating Scale (FTM-TRS) scores and follow-up time were negatively correlated with the percentage change in any objective TRS score (P<0.05). The most common adverse event was dysarthria (10.5%), which is a stimulation-related AE (23.6%), while the rates of the surgical-related and device-related AEs were 6.4% and 11.5%, respectively. Conclusion. VIM-DBS is an efficient and safe surgical method in ET, and the efficacy was not affected by the body distribution of tremor, age at surgery, and disease duration. Lower preoperative FTM-TRS scores likely indicate greater improvement, and the effect of VIM-DBS declines over time.

Compression sutures are primarily used to treat atonic postpartum hemorrhage. We herein describe three cases of selective arterial ligation combined with B-Lynch or modified B-Lynch suture for the treatment of intractable postpartum hemorrhage unresponsive to available conservative interventions. Three pregnant women underwent a cesarean section for a macrosomic fetus, fetal distress, and oligohydramnios, respectively. All three women developed intractable postpartum hemorrhage due to uterine atony with no chance of embolization therapy. B-Lynch or modified B-Lynch suture and additional selective arterial ligation were performed using braided absorbable suture. The first woman developed postoperative hematometra and infection without response to drainage and antibiotic therapy. Although laparoscopic exploration was performed to loosen the suture line and drain the hematometra and pyometra, the necrosis and infection could not be controlled. Subtotal hysterectomy was therefore conducted, and the necrotic uterine adnexa was removed. The other two women developed subinvolution of the uterus resulting in prolonged menstruation and amenorrhea, although the uterus was preserved and the bleeding was controlled. Modified B-Lynch suture combined with vascular ligation is an invaluable technique for women with severe intractable postpartum hemorrhage. However, it can lead to serious complications such as uterine necrosis, infection, and subinvolution.

Ischemia-reperfusion injury (IRI), also called reoxygenation injury, is the outcome of inflammatory processes and oxidative damage through the induction of oxidative stress. In the clinical setting, IRI contributes to severe hepatic injury, including liver cell death by apoptosis and ferroptosis. Ferroptosis is a novel type of cell death in hepatic IRI that involves small molecules that inhibit glutathione biosynthesis or glutathione peroxidase 4 (GPX4), which is a glutathione-dependent antioxidant enzyme, causing mitochondrial damage. Currently, ferroptosis has been systematically described in neurological settings, kidney diseases and different types of cancer, while few studies have analysed the presence of ferroptosis and the regulatory mechanism of ferroptosis in hepatic IRI. Exploring the exact role played by ferroptosis in the liver following hepatic IRI in accordance with existing evidence and mechanisms could guide potential therapeutic interventions and provide a novel research avenue. Contents1. Introduction 2. Hepatic IRI 3. Brief overview of ferroptosis 4. The ferroptotic signalling pathway 5. Ferroptosis in hepatic IRI 6. Other types of regulated cell death 7. Current therapeutic strategies in hepatic IRI 8. Conclusions and future perspectives

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