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Objective To explore the efficacy of wrapping the hepatic artery with detached ligamentum teres hepatis during pancreaticoduodenectomy (PD) on preventing postoperative intra-abdominal hemorrhage. Methods A total of 186 patients who received PD in the First Affiliated Hospital of Xinjiang Medical University from June 2020 to June 2022 were divided into wrapping group (n=86) and non-wrapping group (n=100) according to whether the detached ligamentum teres hepatis was used to wrap the hepatic artery during the operation. The clinical data on perioperative and postoperative complications were collected and retrospectively analyzed in two groups. Results PD was successfully performed and completed in both groups, and there was no significant difference in age, gender, BMI, length of hospital stay, operative time and intra-operative blood loss between two groups (P＞0.05) . The incidences of pancreatic fistula, biliary fistula and abdominal infection were similar in two groups (P＞0.05) , but the incidence of postoperative bleeding in wrapping group was significantly lower than that in non-wrapping group (1.16% vs 9.00%, P＜0.05) . Logistic regression analysis showed that the pancreatic and biliary fistulas of grade B/C were the independent risk factors for postoperative abdominal bleeding after PD (P＜0.05) , and the wrapping of the hepatic artery with the detached hepatic round ligament during operation was an independent protective factor for postoperative abdominal bleeding after PD (P＜0.05) . Conclusion Wrapping the hepatic artery with detached ligamentum teres hepatis during PD surgery may reduce the incidence of postoperative abdominal bleeding and is simple, safe and feasible to perform without additional complications．

Our previous study has reported that metastasis-associated protein 2 (MTA2) plays essential roles in tumorigenesis and aggressiveness of gastric cancer (GC). However, the underlying molecular mechanisms of MTA2-mediated GC and its upstream regulation mechanism remain elusive. In this study, we identified a novel circular RNA (circRNA) generated from the MTA2 gene (circMTA2) as a crucial regulator in GC progression. CircMTA2 was highly expressed in GC tissues and cell lines, and circMTA2 promoted the proliferation, invasion, and metastasis of GC cells both in vitro and in vivo. Mechanistically, circMTA2 interacted with ubiquitin carboxyl-terminal hydrolase L3 (UCHL3) to restrain MTA2 ubiquitination and stabilize MTA2 protein expression, thereby facilitating tumor progression. Moreover, circMTA2 was mainly encapsulated and transported by exosomes to promote GC cell progression. Taken together, these findings uncover that circMTA2 suppresses MTA2 degradation by interacting with UCHL3, thereby promoting GC progression. In conclusion, we identified a cancer-promoting axis (circMTA2/UCHL3/MTA2) in GC progression, which paves the way for us to design and synthesize targeted inhibitors as well as combination therapies. [ABSTRACT FROM AUTHOR]

Drug resistance is a primary cause of chemotherapeutic failure; however, how this resistance develops is complex. A comprehensive understanding of chemotherapeutic resistance mechanisms may aid in identifying more effective drugs and improve the survival rates of patients with cancer. Insulin-like growth factor 1 receptor (IGF1R), a member of the insulin receptor family, has been extensively assessed for biological activity, and its putative contribution to tumor cell development and progression. Furthermore, researchers have attended to drugs that target IGF1R since IGF1R functions as a membrane receptor. However, how IGF1R participates in chemotherapeutic resistance remains unclear. Therefore, the present study described the IGF1R gene and its associated signaling pathways, and offered details of IGF1R-induced tumor chemoresistance associated with promoting cell proliferation, inhibition of apoptosis, regulation of ATP-binding cassette transporter proteins and interactions with the extracellular matrix. The present study offered additional explanations for tumor chemotherapy resistance and provided a theoretical basis of IGF1R and its downstream pathways for future possible chemotherapy treatment options. [ABSTRACT FROM AUTHOR]

Intestinal stem cells differentiate into absorptive enterocytes, characterised by increased brush border enzymes such as intestinal alkaline phosphatase (IAP), making up the majority (95%) of the terminally differentiated cells in the villus. Loss of integrity of the intestinal epithelium plays a key role in inflammatory diseases and gastrointestinal infection. Here, we show that the intestinal microRNA (miR)‐27a‐3p is an important regulator of intestinal epithelial cell proliferation and enterocyte differentiation. Repression of endogenous miR‐27a‐3p leads to increased enterocyte differentiation and decreased intestinal epithelial cell proliferation in mouse and human small intestinal organoids. Mechanistically, miR‐27a‐3p regulates intestinal cell differentiation and proliferation at least in part through the regulation of retinoic acid receptor α (RXRα), a modulator of Wnt/β‐catenin signalling. Repression of miR‐27a‐3p increases the expression of RXRα and concomitantly, decreases the expression of active β‐catenin and cyclin D1. In contrast, overexpression of miR‐27a‐3p mimic decreases the expression of RXRα and increases the expression of active β‐catenin and cyclin D1. Moreover, overexpression of the miR‐27a‐3p mimic results in impaired enterocyte differentiation and increases intestinal epithelial cell proliferation. These alterations were attenuated or blocked by Wnt inhibition. Our study demonstrates an miR‐27a‐3p/RXRα/Wnt/β‐catenin pathway that is important for the maintenance of enterocyte homeostasis in the small intestine. [ABSTRACT FROM AUTHOR]

Background: Abnormal levels of glutamate constitute a key pathophysiologic mechanism in epilepsy. The use of glutamate chemical exchange saturation transfer (GluCEST) imaging to measure glutamate levels in pediatric epilepsy is rarely reported in research., Purpose: To investigate hippocampal glutamate level variations in pediatric epilepsy and the correlation between glutamate and hippocampal subregional volumes., Study Type: Cross-sectional, prospective., Subjects: A total of 38 school-aged pediatric epilepsy patients with structurally normal MRI as determined by at least two independent radiologists (60% males; 8.7 ± 2.5 years; including 20 cases of focal pediatric epilepsy [FE] and 18 cases of generalized pediatric epilepsy [GE]) and 17 healthy controls (HC) (41% males; 9.0 ± 2.5 years)., Field Strength/sequence: 3.0 T; 3D magnetization prepared rapid gradient echo (MPRAGE) and 2D turbo spin echo GluCEST sequences., Assessment: The relative concentration of glutamate was calculated through pixel-wise magnetization transfer ratio asymmetry (MTR asym ) analysis of the GluCEST data. Hippocampal subfield volumes were computed from MPRAGE data using FreeSurfer., Statistical Tests: This study used t tests, one-way analysis of variance, Kruskal-Wallis tests, and Pearson correlation analysis. P < 0.05 was considered statistically significant., Results: The MTR asym values of both the left and right hippocampi were significantly elevated in GE (left: 2.51 ± 0.23 [GE] vs. 2.31 ± 0.12 [HCs], right: 2.50 ± 0.22 [GE] vs. 2.27 ± 0.22 [HCs]). The MTR asym values of the ipsilateral hippocampus were significantly elevated in FE (2.49 ± 0.28 [ipsilateral] vs. 2.29 ± 0.16 [HCs]). The MTR asym values of the ipsilateral hippocampus were significantly increased compared to the contralateral hippocampus in FE (2.49 ± 0.28 [ipsilateral] vs. 2.35 ± 0.34 [contralateral]). No significant differences in hippocampal volume were found between different groups (left hippocampus, P = 0.87; right hippocampus, P = 0.87)., Data Conclusion: GluCEST imaging have potential for the noninvasive measurement of glutamate levels in the brains of children with epilepsy., Level of Evidence: 2 TECHNICAL EFFICACY: Stage 1., (© 2024 International Society for Magnetic Resonance in Medicine.)