BACKGROUND:Repetitive trans-spinal magnetic stimulation(rTSMS)can inhibit inflammatory responses following spinal cord injury.rTSMS applies magnetic field stimulation to the spinal cord region to modulate neuronal excitability and synaptic transmission,thereby promoting plasticity and repair of the nervous system. OBJECTIVE:To observe the effects of rTSMS on the Toll-like receptor 4(TLR4)/nuclear factor(NF)-κB/NLRP3 signaling pathway after spinal cord injury and explore its mechanism in promoting motor function recovery. METHODS:Male C57BL/6J mice,SPF grade,were randomly divided into sham surgery group,spinal cord injury group,and rTSMS group.The latter two groups of mice were anesthetized and the T9 vertebral plate was removed using rongeur forceps to expose the spinal cord,and the spinal cord was clamped using a small aneurysm clip for 20 seconds to establish the spinal cord injury model.Mice in the rTSMS group underwent a 21-day rTSMS intervention starting on day 1 after spinal cord injury.The stimulation lasted 10 minutes per day,5 days per week with an interval of 2 days.Basso Mouse Scale scores were used to assess motor function recovery in mice after spinal cord injury at 1,3,7,14,and 21 days after spinal cord injury.Western blot was employed to detect the expression of AQP4,apoptotic factors Bax,Bcl-2,CL-Caspase-3,inflammatory factors tumor necrosis factor-α,interferon-γ,interleukin-6,interleukin-4,and the TLR4/NF-κB/NLRP3 signaling pathway related proteins in the injured spinal cord.Oxidative stress assay kit was used to measure the activity of superoxide dismutase,glutathione peroxidase,and malondialdehyde content at the site of spinal cord injury.Immunofluorescence staining was performed to detect the expression of neuronal nuclei(NeuN). RESULTS AND CONCLUSION:The Basso Mouse Scale score in the rTSMS group was significantly higher than that in the spinal cord injury group(P<0.05).Compared with the spinal cord injury group,the rTSMS group showed a reduction in spinal cord water content.The expression of AQP4 protein,malondialdehyde content,and expression of Bax,Bcl-2,CL-Caspase-3,tumor necrosis factor-α,interferon-γ,interleukin-6,and TLR4/NF-κB/NLRP3 signaling pathway related proteins were all decreased in the rTSMS group,while the activities of superoxide dismutase and glutathione peroxidase,as well as the expression of Bcl-2,interleukin-4,and NeuN,were all increased(P<0.05).These results suggest that rTSMS downregulates the expression of proteins related to the TLR4/NF-κB/NLRP3 signaling pathway,alleviating symptoms after spinal cord injury such as spinal cord edema,oxidative stress,apoptosis,and inflammation,exerting neuroprotective effects,and thereby promoting the recovery of hindlimb motor function after spinal cord injury.

“Inflammation-cancer” transformation of chronic atrophic gastritis （CAG） refers to the process in which the gastric mucosa， in the context of CAG， progresses through stages of precancerous lesions of gastric cancer （PLGC）， such as intestinal metaplasia and dysplasia， and eventually develops into gastric cancer （GC）. In China， the incidence and mortality rates of GC rank among the highest in the world， and the proportion of GC cases caused by gastric mucosal infection and inflammation has been increasing. Modern medical treatments for CAG and PLGC mainly rely on drug therapy， endoscopic resection， and regular surveillance. Although these disease management strategies are relatively mature， they present limitations in early lesion prevention and recurrence risk control. Therefore， it is imperative to identify therapeutic approaches for CAG and PLGC that offer preventive， reversible， and recurrence-reducing benefits. With advances in research on the mechanisms underlying inflammation-cancer transformation and the integration of traditional Chinese and Western medicine， the advantages of TCM in preventing and even reversing early-stage CAG and PLGC have gradually become apparent. This review explored the mechanisms of inflammation-cancer transformation in CAG from five aspects： inflammatory microenvironment， autophagy， glycolysis， bile acids， and ferroptosis. In conjunction with TCM theory and a deeper understanding of the distinct mechanisms involved in the inflammation-cancer transformation of CAG， this review further discussed the specific mechanisms through which TCM intervened in treating CAG and PLGC， with the aim of providing theoretical support and therapeutic insights for future clinical applications.

“Inflammation-cancer” transformation of chronic atrophic gastritis （CAG） refers to the process in which the gastric mucosa， in the context of CAG， progresses through stages of precancerous lesions of gastric cancer （PLGC）， such as intestinal metaplasia and dysplasia， and eventually develops into gastric cancer （GC）. In China， the incidence and mortality rates of GC rank among the highest in the world， and the proportion of GC cases caused by gastric mucosal infection and inflammation has been increasing. Modern medical treatments for CAG and PLGC mainly rely on drug therapy， endoscopic resection， and regular surveillance. Although these disease management strategies are relatively mature， they present limitations in early lesion prevention and recurrence risk control. Therefore， it is imperative to identify therapeutic approaches for CAG and PLGC that offer preventive， reversible， and recurrence-reducing benefits. With advances in research on the mechanisms underlying inflammation-cancer transformation and the integration of traditional Chinese and Western medicine， the advantages of TCM in preventing and even reversing early-stage CAG and PLGC have gradually become apparent. This review explored the mechanisms of inflammation-cancer transformation in CAG from five aspects： inflammatory microenvironment， autophagy， glycolysis， bile acids， and ferroptosis. In conjunction with TCM theory and a deeper understanding of the distinct mechanisms involved in the inflammation-cancer transformation of CAG， this review further discussed the specific mechanisms through which TCM intervened in treating CAG and PLGC， with the aim of providing theoretical support and therapeutic insights for future clinical applications.

Objective:To investigate the efficacy and safety of venetoclax combined with the decitabine, cytarabine, and homoharringtonine (HHT) regimen and donor lymphocyte infusion (DLI) for the preventive and salvage therapy of pediatric acute myeloid leukemia (AML) /myelodysplastic syndrome (MDS) after allogeneic hematopoietic stem cell transplantation (HSCT) .Methods:A total of 29 relapsed pediatric/minimal residual disease-positive AML after HSCT were recruited at the Peking University Institute of Hematology from January 1, 2021, to June 1, 2023. They were treated with the above combination regimen and administered with DLI after 24-48 hours at the end of chemotherapy, and the treatment response and adverse reactions were regularly assessed.Results:The overall response rate (ORR) was 75.8%, CR rate was 88.9% (8/9) in the hematologic relapse group, and MRD negativity rate was 61.1% (11/18) in the MRD-positive group. The incidence of agranulocytosis, anemia, and thrombocytopenia with a classification above grade 3 were 100%, 82.7%, and 100%, respectively. The median time of the granulocyte deficiency period was 15 days. Acute graft-versus-host diseases (aGVHD) with a classification of grades Ⅲ-Ⅳ occurred in 11.1% of the patients after DLI, while moderate or severe cGVHD occurred in 7.4% of the patients. The single risk factor for ORR was MNC counts of less than 10×10 8/kg, and the relapse occurred within 100 days. At a median follow-up of 406 days, the 1-year OS was 65%, and the 1-year OS was 57% in the group with no reaction ( P=0.164) compared with 71% in the group who had an overall reaction. Conclusion:The combined regimen based on the DAC, VEN, and modified HA regimen showed a high response rate in the salvage therapy for pediatric AML after the relapse of HSCT. However, bridging to transplantation should be performed immediately after remission to result in a long survival rate.

Objective To investigate the risk factors for identifying local tumor progression(LTP)in patients with hepatocellular carcinoma(HCC)after radiofrequency ablation(RFA)and to establish a predictive model.Methods The clinical data of 122 HCC patients treated by RFA were analyzed retrospectively,and then the patients were divided into positive and negative LTP groups according to that whether LTP occurred within 12 months after RFA.The risk factors of LTP were determined using univariate and multivari-ate analysis,and the predictive model was constructed based on these factors and the internal validation was conducted.Results The results of this study showed that multiple number,diameter＞2 cm,rough margin,and adjacent to large blood vessels of the tumor could be independent predictors of LTP,which were further incorporated into constructing the predictive model.Internal validation results showed that the area under the curve(AUC)of receiver operating characteristic(ROC)curve was 0.815[95％confidence interval(CI)0.735-0.895],indicating the model with high differentiation ability.The calibration curve was drawn and the Hosmer-Lemeshow goodness-fit test showed that the model had good stability(P＞0.05).The decision curve suggested that the model had good clinical application value.Conclusion The independent risk factors of LTP of HCC after RFA are multiple number,diameter＞2 cm,rough margin,and adjacent to large blood vessels of the tumor.When the predictive model is integrated with the above factors,it can poten-tially predict the risk of local tumor and may offer useful guidance for individual treatment and follow-up.

[This corrects the article DOI: 10.1016/j.apsb.2021.03.002.].

Objective To investigate the clinical features, liver histological features, and diagnostic and treatment methods for patients with myeloproliferative neoplasms (MPN) with portal hypertension as the main manifestation. Methods A retrospective analysis was performed for related data of the patients who attended the hospital due to portal hypertension and were finally diagnosed with MPN in Liver Research Center, Beijing Friendship Hospital, from January 2019 to February 2022, including clinical manifestation, liver pathological features, treatment, and follow-up results. Results Nine patients were included in this study, and all the patients had splenomegaly and esophageal and gastric varices, while portal vein thrombosis was observed in eight patients. All patients had normal or slightly abnormal liver function and routine blood test results. Six patients underwent liver biopsy, without the formation of fibrous septum and pseudolobule, and hepatic extramedullary hematopoiesis was observed in two patients. All nine patients underwent bone marrow biopsy and genetic testing, among whom six had essential thrombocythemia and three had primary myelofibrosis, and genetic testing revealed JAK - 2V617F gene mutation in seven patients and CALR gene mutation in two patients. Conclusion MPN is one of the rare causes of portal hypertension and has the clinical manifestations of esophageal and gastric varices, splenomegaly, and even megalosplenia, without the manifestations of hypersplenism such as leukopenia and thrombocytopenia. Detection of the JAK - 2V617F and CALR genes can improve the diagnostic rate of MPN.

[This corrects the article DOI: 10.1016/j.apsb.2021.03.002.].

Objective:To investigate the risk factors of invasive fungal disease after haploid hematopoietic stem cell transplantation in children with acute leukemia.Methods:Four hundred and two children (median age 10 years) with acute leukemia, undergoing haplo-HSCT at this institutute from January 2016 to December 2020,were analyzed retrospectively according to the diagnosis criteria of IFD. The basic information and preoperative indicators of the children were collected, including gender, age, primary disease, remission status of primary disease, and previous IFD history. Postoperative indicators were collected, including long-term granulocyte deficiency time, high-dose glucocorticoids, using CD25 monoclonal antibody, acute and chronic graft-versus-host disease. Count data are expressed as example (%), and comparisons between groups are made using the continuously multifactorial corrected Chi-square test or Fisher exact probability method. Logistic regression model was used to analyze the risk factors of IFD after haplo-HSCT in children.Results:Among 402 cases, 250 were male and 152 were female. The median age at transplantation was 10 years, and the age range was 9 months to 17 years 7 months. Before transplantation, 390 cases achieved complete remission of the primary disease, 9 cases had partial remission, and 3 cases had no remission. The implantation time of neutrophils ranged from +10 to 24 days, with a median time of 12 days. IFD occurred in 17 cases (4.2%), of which 3 cases (0.7%) were proven IFD and 14 cases (3.5%) were probable IFD. IFD occurred from 13 to 275 days after transplantation, with a median time of 30 days. The lungs were the most common site of infection (88.2%,15/17). The multivariate Logistic regression analysis showed that age >10 years old ( P=0.046, odds ratio =3.05, 95% confidence interval: 1.02~9.13), the use of high-dose corticosteroids ( P=0.005, odds ratio =7.72, 95% confidence interval: 1.85~32.20) were risk factors for IFD after haplo-HSCT in children. Conclusions:IFD is an important complication after haplo-HSCT in children with acute leukemia. Age >10 years and the use of high-dose corticosteroid are risk factors for IFD after haplo-HSCT in children with acute leukemia.

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