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        Clinicopathological Analysis and Treatment of Adult Patients with Inflammatory Myofibroblastic Tumor: A 15-Year Single- Center Study

        Xin Liu,Chengcheng Gong,Jieyun Zhang,Wanjing Feng,Yanjing Guo,Youzhou Sang,Chunmeng Wang,Yong Chen,Jian Wang,Lin Yu,Xiaowei Zhang,Zhiguo Luo 대한암학회 2023 Cancer Research and Treatment Vol.55 No.3

        Purpose Inflammatory myofibroblastic tumor (IMT) is a rare mesenchymal malignancy that occurs primarily in children and adolescents. The clinical and pathological features of IMT in adult patients are not well understood.Materials and Methods We retrospectively searched for records of adult patients with IMT at Fudan University Shanghai Cancer Center from 2006 to 2021. Clinicopathological data, treatments, and outcomes were collected and analyzed.Results Thirty adult patients with IMT, mostly women (60.0%), were included. The median age of the patients was 38 (21-77). The most common primary site was abdominopelvic region (53.3%), followed by lungs (20.0%). Seven patients had an abdominal epithelioid inflammatory myofibroblast sarcoma (EIMS). The positivity rate of anaplastic lymphoma kinase (ALK) was 81.5% (22/27). Sixteen patients with advanced ALK-positive disease received crizotinib, with an objective response rate (ORR) of 81.3% and a disease control rate of 87.5%. The median progression-free survival was 20.8 months. EIMS was associated with more aggressive behavior; however, the prognosis was similar to that of non-EIMS patients after treatment with an ALK inhibitor. At a median follow-up time of 30 months (95% confidence interval [CI], 13.6 to 46.4), the 5-year overall survival was 77% (95% CI, 66 to 88) in all patients.Conclusion Adult IMTs appeared more aggressive, with a higher incidence of recurrence and metastases, and patients with EIMS had more aggressive cases. Treatment with ALK inhibitors resulted in a high ORR and a durable response, which suggested that ALK inhibitors could be used as a first-line treatment option in adult patients with ALK-positive advanced IMT.

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        A Novel Approach in Spinal Cord Stimulation for Enhancing Gastric Motility: A Preliminary Study on Canines

        ( Lei Tu ),( Payam Gharibani ),( Yi Yang ),( Bo Zhang ),( Feng Ji ),( Jieyun Yin ),( Jiande D Z Chen ) 대한소화기 기능성질환·운동학회 2020 Journal of Neurogastroenterology and Motility (JNM Vol.26 No.1

        Background/Aims Gastroparesis is commonly seen in patients with diabetes and functional dyspepsia with no satisfactory therapies. Dysautonomia is one of the main reasons for the imbalanced motility. We hypothesized that spinal cord stimulation (SCS) is a viable therapy for gastroparesis via the autonomic modulation to improve gastric motility. The aim is to find an optimal method of SCS for treating gastroparesis. Methods Eight healthy-female dogs were implanted with a gastric cannula, a duodenal cannula, 2 multi-electrode spinal leads, and an implantable pulse generator. Gastric motility index (MI) was used to determine the best stimulation location/parameters of SCS. Optimized SCS was used to improve glucagon-induced gastroparesis. Results With fixed parameters, SCS at Thoracic 10 (T10) was found most effective for increasing gastric MI (37.8%, P = 0.013). SCS was optimized with different parameters (pulse width: 0.05-0.6 msec, frequency: 5-500 Hz, motor threshold: 30-90%) on T10. Our findings revealed that 0.5 msec, 20 Hz with 90% motor threshold at T10 were the best parameters in increasing MI. Glucagon significantly delayed gastric emptying, and this inhibitory effect was partially blocked by SCS. Gastric emptying at 120 minutes was 25.6% in the control session and 15.7% in glucagon session (P = 0.007 vs control), while it was 22.9% with SCS session (P = 0.041 vs glucagon). SCS with the optimal parameters was found to maximally enhance vagal activity and inhibit sympathetic activity assessed by the spectral analysis of heart rate variability. Conclusions SCS with optimized stimulation location and parameters improves gastric motility in healthy-dogs and accelerates gastric emptying impaired by glucagon via enhancing vagal activity.

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