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lor, sending retrograde signals that affect the expression of nuclear genes in Brassica.

This study aimed to identify the risk factors associated with performing a difficult laparoscopic radical resection of rectal cancer, and to establish a predictive nomogram to help individual clinical treatment decisions.

A total of 977 patients with rectal cancer who underwent laparoscopic radical resection between January 2014 and December 2016 were enrolled in this study. The difficulty of laparoscopic-assisted rectal resection (LARR) was defined according to the scoring criteria reported by Escal. A logistic regression analysis was performed to identify the variables that may affect the difficulty of LARR, and a nomogram predicting the surgical difficulty was created.

A multivariate analysis demonstrated that a BMI > 28kg/m

, the distance between the tumor and the anal margin ≤ 5cm, the maximum transverse tumor diameter > 3cm tumor, interspinous distance < 10cm, history of abdominal surgery, and preoperative radiotherapy were independent risk factors and they were, therefore, included in the predictive nomogram for identifying a difficult LARR.

This study defined a difficult LARR and identified independent risk factors for a difficult operation and created a predictive nomogram for difficult LARR. This nomogram may facilitate the stratification of patients at risk for being associated with a difficult LARR for rectal cancer.

This study defined a difficult LARR and identified independent risk factors for a difficult operation and created a predictive nomogram for difficult LARR. This nomogram may facilitate the stratification of patients at risk for being associated with a difficult LARR for rectal cancer.The endogenous metabolite itaconate and its cell‑permeable derivative dimethyl itaconate (DI) have been identified as anti‑inflammatory regulators of macrophages; however, their contribution to inflammasome‑mediated pyroptosis remains unknown. click here The present study examined the molecular mechanism of DI on NLR family pyrin domain‑containing 3 (NLRP3) inflammasome assembly and NLRP3 inflammasome‑dependent pyroptosis in microglia. Lipopolysaccharide (LPS) and ATP were used to induce microglia pyroptosis in vitro; this process was confirmed by TUNEL assay, lactate dehydrogenase (LDH) detection and gasdermin D (GSDMD) expression analysis. The regulation of microglia polarization and inflammatory cytokine expression was assessed by immunofluorescence assays and ELISA. To investigate the associated mechanism of action, the expression levels of the nuclear factor erythroid 2‑related factor 2 (Nrf‑2)/heme oxygenase‑1 (HO‑1) pathway proteins were analyzed by western blotting. Finally, the regulatory effect of DI on autophagy and its association with inflammation was determined by western blotting. The present study demonstrated that DI administration inhibited NLRP3 assembly, LDH release and GSDMD cleavage. Cotreatment of DI with LPS and ATP facilitated the transition from M1 to M2, reduced inflammatory mediator expression and impeded NF‑κB phosphorylation. In addition, DI effectively reduced reactive oxygen species production through the Nrf‑2/HO‑1 pathway. Moreover, DI induced cellular autophagy, whereas inhibition of autophagy with 3‑methyladenine markedly reversed its inhibitory effect on NLRP3‑dependent pyroptosis. Taken together, the present study suggested that DI participated in the Nrf‑2/HO‑1 pathway and served a key role in microglia inflammation and NLRP3 inflammasome‑mediated pyroptosis via induction of autophagy.Following the publication of this paper, the authors have realized that they overlooked indicating that Ting Liu and Jingjing Meng contributed equally to this work. Therefore, the affiliations for this paper should have been written as follows Ting Liu1*, Jingjing Meng2* and Yu Zhang3. Departments of 1Nuclear Medicine and 2Thyroid and Breast Surgery, The Affiliated Wuhan Central Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014; 3Department of Surgery II, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, P.R. China. *Contributed equally. Furthermore, the authors have also realized that they overlooked acknowledging a source that contributed towards the paper’s funding in the Funding section of the declarations. Accordingly, the following information should have been included in the paper regarding the funding received Funding This work was partially supported by Shanghai Municipal Commission of Health and Family Planning (grant no. 201740175). The authors confirm that there are no further errors in the study, and all the authors agree to this correction. The authors regret their oversight, and apologize for any inconvenience caused. [the original article was published in Molecular Medicine Reports 22 3316‑3326, 2020, DOI 10.3892/mmr.2020.11392].Ferroptosis is critically involved in the pathophysiology of diabetic nephropathy (DN). As a bioactive peptide, salusin‑β is abundantly expressed in the kidneys. However, it is unclear whether salusin‑β participates in the pathologies of diabetic kidney damage by regulating ferroptosis. The present study found that high glucose (HG) treatment upregulated the protein expressions of salusin‑β in a dose‑ and time‑dependent manner. Genetic knockdown of salusin‑β retarded, whereas overexpression of salusin‑β aggravated, HG‑triggered iron overload, antioxidant capability reduction, massive reactive oxygen species production and lipid peroxidation in HK‑2 cells. Mechanistically, salusin‑β inactivated nuclear factor erythroid‑derived 2‑like 2 (Nrf‑2) signaling, thus contributing to HG‑induced ferroptosis‑related changes in HK‑2 cells. Notably, the protein expression of salusin‑β was upregulated by ferroptosis activators, such as erastin, RSL3, FIN56 and buthionine sulfoximine. Pretreatment with ferrostatin‑1 (a ferroptosis inhibitor) prevented the upregulated protein expression of salusin‑β in HK‑2 cells exposed to HG. Taken together, these results suggested that a positive feedback loop between salusin‑β and ferroptosis primes renal tubular cells for injury in diabetes.