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Background: The incidence of duodenal adenocarcinoma is increasing, with limited studies on this disease published. This multicenter retrospective study aimed to analyze the clinicopathologic features of duodenal adenocarcinoma and identify prognostic factors for postoperative survival., Methods: Demographic characteristics, clinicopathologic features, treatment outcomes, and survival of patients with duodenal adenocarcinoma undergoing surgical treatment at 16 Chinese medical centers from 2012 to 2023 were retrospectively analyzed., Results: Among the 2,189 patients with duodenal adenocarcinoma included, 50.07% had extra-ampullary duodenal adenocarcinoma and 49.93% had peri-ampullary duodenal adenocarcinoma. The 1-, 3-, and 5-year overall survival rates for patients who underwent radical surgery were 91.78%, 69.30%, and 55.86%, respectively. The median overall survival was 73 months (range, 64-84), and the median progression-free survival was 64 months (range, 52-76). No differences in survival were observed between the laparotomy and minimally invasive surgery groups (log-rank P = .562); furthermore, no significant between-group differences in operation time, lymph node dissection, postoperative complications, or in-hospital mortality were observed (P > .05). The minimally invasive surgery group experienced less intraoperative blood loss (250 mL vs 100 mL, P < .001), fewer intraoperative blood transfusions (24.97% vs 18.84%, P = .002), and shorter hospital stays (28 days vs 23 days, P < .001). Multivariate Cox regression analysis revealed that advanced age, advanced stage, longer operation time, intraoperative blood transfusion, and postoperative hemorrhage were independent risk factors for poor prognosis., Conclusion: Radical surgery was associated with favorable overall survival among patients with duodenal adenocarcinoma, and no difference in survival was observed between patients with extra-ampullary duodenal adenocarcinoma and peri-ampullary duodenal adenocarcinoma. Minimally invasive surgery is a reliable alternative for duodenal adenocarcinoma treatment., Competing Interests: Conflicts of Interest/Disclosure The authors have no relevant financial disclosures., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Pancreatic cancer is a malignancy with high mortality. Once diagnosed, effective treatment strategies are limited and the five-year survival is extremely poor. Recent studies have shown that zinc finger proteins play important roles in tumorigenesis, including pancreatic cancer. However, it remains unknown on the clinical significance, function and underlying mechanisms of zinc finger protein 488 (ZNF488) during the development of pancreatic cancer., Methods: The clinical relevance of ZNF488 and stearoyl-CoA desaturase 1 (SCD1) was examined by analyzing the data from The Cancer Genome Atlas (TCGA) and immunohistochemical staining of the tissue microarray. Gain-of-function and loss-of-function experiments were performed by transfecting the cells with overexpressing lentivirus and siRNAs or shRNA lentivirus, respectively. The function of ZNF488 in pancreatic cancer was assessed by CCK8, colony formation, EdU staining, PI/Annexin V staining and xenografted tumorigenesis. Chip-qPCR assay was conducted to examine the interaction between ZNF488 and the promoter sequence of SCD1. Transcription activity was measured by dual luciferase reporter assay. mRNA and protein expression was detected by qRT-PCR and immunoblotting experiment, respectively. Fatty acid was quantified by gas chromatography mass spectrometry., Results: ZNF488 was overexpressed in pancreatic cancer samples compared with normal tissues. High expression of ZNF488 predicted the poor prognosis of the patients. In vitro, ZNF488 upregulation contributed to the EuU cooperation, proliferation and colony formation of MIAPaCa-2 and PANC-1 cells. Based on PI/Annexin V and trypan blue staining results, we showed that ZNF488 suppressed the ferroptosis and apoptosis of pancreatic cancer cells. Mechanistically, ZNF488 directly interacted with the promoter sequence of SCD1 gene and promoted its transcription activity, which resulted in enhanced palmitoleic and oleic acid production, as well as the peroxidation of fatty acid. In vivo, ZNF488 overexpression promoted the xenograted tumorigenesis of PANC-1, which was reversed by SCD1 knockdown. Importantly, combination of erastin and SCD1 inhibitors A939572 completely blunted the growth of ZNF488 overexpressed MIAPaCa-2 and PANC-1 cells. Usage of A939572 or erastin recovered the sensitivity of pancreatic cancer cells to the treatment of gemcitabine. Lastly, we found a positive correlation between ZNF488 and SCD1 in pancreatic cancer patients based on TCGA and immunohistochemical staining results., Conclusion: Overexpression of ZNF488 suppresses the ferroptosis and apoptosis to support the growth and tumorigenesis of pancreatic cancer through augmentation of SCD1-mediated unsaturated fatty acid metabolism. Combination of SCD1 inhibitors, ferroptosis inducers or gemcitabine could be applied for the treatment of pancreatic cancer with overexpression of ZNF488., (© 2023. The Author(s).)

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted by the Editor-in-Chief because several results reported in the manuscript were plagiarized from the following article published in 2014 by Zhang et al.: Zhang Z, Zhang L, Zhou C, Wu H. Ketamine inhibits LPS-induced HGMB1 release in vitro and in vivo. Int Immunopharmacol 2014;23:14–26. The editor was contacted by the editor of International Immunopharmacology, who had been alerted regarding the presence of duplicate figures in the two articles. Examination of the articles confirmed that data in Figures 1, 2, and 11 in the paper by Wang et al. appeared to have been plagiarized from the paper by Zhang et al. The corresponding author of the paper by Wang et al. was not able to provide a satisfactory explanation or the original related data to refute the allegation., (Crown Copyright © 2015. Published by Elsevier Inc. All rights reserved.)

Objectives: To characterize alterations in continuous EEG monitoring that occurs during and after intravenous infusion of human albumin or furosemide in patients with intracerebral hemorrhage., Methods: Patients were rapidly administered 20% human albumin 50 ml or furosemide 40 mg intravenously with continuous EEG monitoring for 3h before and after drug infusion in the neurological intensive care unit. Visual and spectral analyses of EEG recordings before and after mannitol administration were carried out., Results: The study consisted of 20 patients. Of 14 patients with human albumin treatment, a decrease in the slowing activity was visually noted in 9 cases after the drug infusion. The spectral analysis demonstrated that albumin-induced EEG changes increased in alpha power and decreased in delta power in the lesion hemispheres, especially in the central and middle temporal areas. The effects occurred after 30 min and were maximal 1h after the end of the infusion, then remained significant for 2h post-infusion. Of 6 patients with furosemide treatment, the EEG recordings before, during, and after the furosemide infusion were not statistically significantly different by visual and quantitative analyses., Conclusions: The results support the opinion that the available EEG monitoring techniques offer an inexpensive, non-invasive, and consistently reproducible technique for reflecting the therapeutic effects of therapeutics in lowering ICP and antiedema in stroke patients.

Objectives: To evaluate the usefulness of continuous EEG monitoring of stroke patients during and after intravenously infused mannitol., Methods: Patients were rapidly administered 50 g of intravenous mannitol solution with continuous EEG monitoring for 3h pre- and post-drug infusion in the neurological intensive care unit. Visual and spectral analyses of EEG recording pre- and post-mannitol infusion were carried out., Results: The study consisted of 47 patients. Of 38 patients with intracranial hemorrhage, 33 had abnormal EEG findings pre-mannitol administration. After mannitol therapy, visual analysis of the drug-induced EEG changes showed that the EEG findings were unchanged in 13 patients, demonstratively improved in 22 patients, and worse in 3 patients. The spectral analysis demonstrated that mannitol-induced EEG changes increased in alpha power and decreased in delta power in the lesion hemispheres, especially in the central and middle temporal areas. Maximal effects occurred 30 min post-mannitol infusion, and remained significant for 2h post-infusion. Of the 9 patients with cerebral infarction, only one with diffuse background slowing of one-side dominance pre-mannitol improved after the infusion of mannitol., Conclusions: The results of our investigation indicated that continuous EEG monitoring of mannitol treatment can reflect the brain edema, raised ICP in stroke patients, and provide assessment the drugs effects of antiedema and intracranial pressure lowering in vivo.