Atherosclerosis is a chronic, progressive arterial disease characterized by the deposition of lipids on the inner arterial walls, leading to plaque formation and serious cardiovascular events. Traditional mouse models of atherosclerosis require prolonged dietary induction to exhibit arterial lesions due to significant differences in lipid metabolism compared to humans. In contrast, Golden hamsters share a lipid metabolic profile more closely aligned with humans. In this study, we utilized CRISPR/Cas9 to generate ApoE knockout (ApoE−/−) hamsters using, which spontaneously developed atherosclerotic lesions in the arterial wall after 8 weeks on a standard chow diet. When fed on a high-cholesterol/high-fat diet, they exhibited even more severe aortic atherosclerosis, fatty liver, and liver fibrosis. Our findings demonstrated that the ApoE−/− hamster model is highly valuable tool for translational research, offering significant potential for studying hyperlipidemia and atherosclerosis in a context more relevant to human physiology.

Abstract Background The long-term neurological outcomes for children diagnosed with neuroblastoma associated with Opsoclonus Myoclonus Syndrome (NB-OMS) are not well characterized, primarily due to the infrequency of the condition. This multicenter study sought to evaluate the rate of neurological recovery and the long-term neurodevelopmental sequelae within this patient population. Methods A retrospective study at nine Chinese medical centers (January 2015 - January 2025) involved 39 children with NB-OMS. Researchers gathered data on demographics, clinical presentation, tumor traits, treatment, and outcomes. Non-parametric tests and multivariate logistic regression identified prognostic factors. Results In this study, a cohort of 39 patients was examined, with a median age at onset of 22 months. The retroperitoneum was identified as the most prevalent tumor location, accounting for 79.5% of cases. The majority of tumors were classified within the low-risk and intermediate risk, as determined by the International Neuroblastoma Risk Group Staging System, comprising 87.2% of the sample. Follow-up was conducted for 37 patients, all of whom exhibited symptom improvement, resulting in a 100% survival rate. Nonetheless, neurological sequelae were detected in 16 children (43.2%). A higher OMS severity score at onset demonstrated a strong trend towards significance (OR = 1.42, 95% CI: 1.00-2.01, P = 0.051). Multivariate analysis revealed that delayed initiation of treatment, defined as greater than 30 days, was a significant independent risk factor for the development of sequelae (Odds Ratio [OR] = 22.98, 95% Confidence Interval [CI]: 2.67-197.63, P = 0.004). Additionally, relapse of opsoclonus-myoclonus syndrome emerged as a significant independent risk factor (OR = 13.74, 95% CI: 1.37-137.34, P = 0.026). Furthermore, the use of combination immunotherapy, consisting of corticosteroids and intravenous immunoglobulin (IVIG), was associated with a significantly reduced median time to symptom resolution compared to non-combination therapy (5 months versus 8.5 months, P = 0.001). Conclusion OMS is a chronic immune disorder often misdiagnosed, leading to treatment delays. Prompt first-line immunotherapy can quickly alleviate OMS symptoms. Early treatment and reducing relapses are crucial for better long-term outcomes. Future multicenter studies are needed to confirm the effectiveness of new immunotherapies.

Myeloid-derived suppressor cells (MDSCs) are known for their immunosuppressive effects on both innate and adaptive immunity, particularly targeting T cells, and they undergo continuous expansion during sepsis. However, the pathophysiological significance of MDSCs in sepsis-induced immunosuppression remains to be fully elucidated. In this study, we investigated the dynamic changes in MDSCs during sepsis and their contribution to sepsis-induced immunosuppression using a clinically relevant “two-hit” sepsis model. Our findings revealed that mice surviving cecal ligation and puncture (CLP) exhibited a significant accumulation and enhanced activity of MDSCs, which correlated with sepsis-related immune paralysis, impaired bacterial clearance, and heightened susceptibility to secondary infections. Importantly, administration of the liver X receptor (LXR) agonist GW3965 at the late stage of sepsis significantly restored immune function, decreased susceptibility to secondary infections, enhanced bacterial clearance, and improved prognosis by eliminating MDSCs. These results highlight the pivotal role of MDSCs in the development of sepsis-associated immunosuppression and indicate that targeting MDSCs could be a promising therapeutic approach to mitigate immunosuppression in sepsis.

The clinical significance of circulating tumor cell (CTC) clusters in highly metastatic tumors hasn’t yet been revealed. Here, we demonstrated the diagnostic and prognostic value of CTC clusters in neuroblastoma (NB) which is the most prevalent childhood extracranial solid tumor. We employed cascaded filter deterministic lateral displacement microfluidic chips to enrich CTCs and CTC clusters in 64 newly diagnosed NB patients. CTCs and CTC clusters were identified by CD45-, GD2+/PHOX2B+, DAPI + immunofluorescence staining, with cells displaying characteristic neoplastic morphology. Among NB patients, 85.94

ObjectiveThis study aims to analyze and summarize the clinical characteristics of small intestinal adenomyosis.MethodsA retrospective study was conducted on children with small intestinal adenomyosis at our center from 2014 to 2024. The age of onset, gender, clinical symptoms, auxiliary examination results, treatment plans, and pathological characteristics of the tumors were recorded and analyzed.ResultsSix cases of small intestinal adenomyosis were analyzed. The male-to-female ratio was 5:1. The median age was 19 months, with two-thirds of the affected children being under 2 years old. Two cases were identified in newborns during the treatment of intestinal malrotation. The remaining patients developed symptoms of intussusception. Preoperative ultrasound identified pathological lead points in two cases. Among the six cases, one case's adenomyoma was located in the jejunum, while the rest was located in the ileum, with tumors ranging from 25 to 140 cm from the ileocecal region. All six patients underwent resection of the tumor segments in the small intestine followed by anastomosis; postoperative prognosis was favorable. Of the six pathological results, glandular-like structures were found in five tumors, with three cases lined with cuboidal or columnar epithelium and one case lined with stratified or squamous epithelium.ConclusionsSmall intestinal adenomyosis is observed to be more prevalent in male, with onset ages ranging from six days to four years. It frequently coexists with recurrent intussusception, making reduction with air or water enema challenging. Abdominal ultrasound typically shows tumors at the leading edge of the intussusception, with compromised blood flow signals and multiple small cystic or honeycomb-like anechoic structures. Surgery is the primary treatment and generally results in a favorable prognosis.

BACKGROUND:The Syrian hamster (Mesocricetus auratus) has shown promise as a human diseases model, recapitulating features of different human diseases including COVID-19. However, the landscape of its genome and transcriptome has not been systematically dissected, restricting its potential applications. RESULTS:Here we provide a complete analysis of the genome and transcriptome of the Syrian hamster and found that its lineage diverged from that of the Chinese hamster (Cricetulus griseus) around 29.4 million years ago. 21,387 protein-coding genes were identified, with 90.03% of the 2.56G base pair sequence being anchored to 22 chromosomes. Further comparison of the transcriptomes from 15 tissues of the Syrian hamster revealed that the Syrian hamster shares a pattern of alternative splicing modes more similar to humans, compared to rats and mice. An integrated genomic-transcriptomic analysis revealed that the Syrian hamster also has genetic and biological advantages as a superior animal model for cardiovascular diseases. Strikingly, several genes involved in SARS-COV-2 infection, including ACE2, present a higher homology with humans compared to other rodents and show the same function as their human counterparts. CONCLUSION:The detailed molecular characterisation of the Syrian hamster in the present study opens a wealth of fundamental resources from this small rodent for future research into human disease pathology and treatment.

BackgroundHepatoblastoma is the most prevalent primary hepatic malignancy in children, comprising 80% of pediatric hepatic malignancies and 1% of all pediatric malignancies. However, traditional treatments have proven inadequate in effectively curing hepatoblastoma, leading to a poor prognosis.MethodsA literature search was conducted on multiple electronic databases (PubMed and Google Scholar). A total of 86 articles were eligible for inclusion in this review.ResultThis review aims to consolidate recent developments in hepatoblastoma research, focusing on the latest advances in cancer-associated genomics, epigenetic studies, transcriptional programs and molecular subtypes. We also discuss the current treatment approaches and forthcoming strategies to address cancer-associated biological challenges.ConclusionTo provide a comprehensive summary of the molecular mechanisms associated with hepatoblastoma occurrence, this review highlights three key aspects: genomics, epigenetics, and transcriptomics. Our review aims to facilitate the exploration of novel molecular mechanisms and the development of innovative clinical treatment strategies for hepatoblastoma.

ABSTRACT:The adenosine concentration and forkhead box protein (Foxp3) expression in T regulatory cells (T regs ) are increased during sepsis. However, the mechanism by which adenosine induces Foxp3 expression is incompletely understood. A cecal ligation and puncture (CLP) model was constructed using C57BL/J mice. The plasma adenosine concentration and Foxp3 expression in splenic T regs were increased consistently for 15 days after sepsis onset. Analysis of the mean fluorescence intensity of Foxp3 and adenosine concentration in the same mice revealed a linear correlation. In the CLP model, adenosine 2a receptor (A2aR) blockade inhibited Foxp3 expression in T regs . In vitro activation of A2aR promoted Foxp3 expression in T regs and facilitated secretion of extracellular vesicles. Transcriptome sequencing revealed that A2aR blockade led to changes in cyclic adenosine monophosphate response element-binding protein (CREB) transcription in T regs in our sepsis model. Use of adenosine or A2aR agonists promoted CREB expression, CREB phosphorylation at S133, T reg expression of Foxp3, and enhanced inhibition of proliferation of cluster of differentiation (CD)4+ lymphocytes. A2aR blockade or inhibition of CREB expression inhibited Foxp3 expression in T regs . In the CLP model, use of CREB inhibitors could inhibit Foxp3 expression and reduce the bacterial load. In summary, adenosine in sepsis promotes CREB phosphorylation via A2aR which, in turn, upregulates Foxp3 expression in T regs .

Background:Acute lung injury (ALI) caused by hypobaric hypoxia (HH) is frequently observed in high-altitude areas, and it is one of the leading causes of death in high-altitude-related diseases due to its rapid onset and progression. However, the pathogenesis of HH-related ALI (HHALI) remains unclear, and effective treatment approaches are currently lacking.Methods:A new mouse model of HHALI developed by our laboratory was used as the study subject (Chinese patent No. ZL 2021 1 1517241 X). Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the messenger RNA (mRNA) expression levels of PDZ-binding kinase (PBK), sirtuin 1 (SIRT1), and PTEN-induced kinase 1 (PINK1) in mouse lung tissue. Hematoxylin and eosin staining was used to observe the main types of damage and damaged cells in lung tissue, and the lung injury score was used for quantification. The wet-dry (W/D) ratio was used to measure lung water content. Enzyme-linked immunosorbent assay was used to detect changes in inflammatory factors and oxidative stress markers in the lungs. Western blotting verified the expression of various mitochondrial autophagy-related proteins. The 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimi-dazoylcarbocyanine iodide (JC-1) method was used determined the health status of mitochondria based on changes in mitochondrial membrane potential. Transmission electron microscopy was used to directly observe the morphology of mitochondria. Multicolor immunofluorescence was used to observe the levels of mitochondrial autophagy markers. Other signaling pathways and molecular mechanisms that may play a role in epithelial cells were analyzed via through RNA sequencing.Results:Low pressure and hypoxia caused pathological changes in mouse lung tissue, mainly ALI, leading to increased levels of inflammatory factors and intensified oxidative stress response in the lungs. Overexpression of PBK was found to alleviate HHALI, and activation of the p53 protein was shown to abrogate this therapeutic effect, while activation of SIRT1 protein reactivated this therapeutic effect. The therapeutic effect of PBK on HHALI is achieved via the activation of mitochondrial autophagy. Finally, RNA sequencing demonstrated that besides mitochondrial autophagy, PBK also exerts other functions in HHALI.Conclusions:Overexpression of PBK inhibits the expression of p53 and activates SIRT1-PINK1 axis mediated mitochondrial autophagy to alleviate HHALI.

Oncolytic viruses (OVs) possess the unique ability to selectively replicate within tumor cells, leading to their destruction, while also reversing the immunosuppression within the tumor microenvironment and triggering an antitumor immune response. As a result, OVs have emerged as one of the most promising approaches in cancer therapy. However, the effective delivery of intravenously administered OVs faces significant challenges imposed by various immune cells within the peripheral blood, hindering their access to tumor sites. Notably, neutrophils, the predominant white blood cell population comprising approximately 50%-70% of circulating white cells in humans, show phagocytic properties. Our investigation revealed that the majority of oncolytic vaccinia viruses (VV) are engulfed and degraded by neutrophils in the bloodstream. The depletion of neutrophils using the anti-LY6G Ab (1-A8) resulted in an increased accumulation of circulating oncolytic VV in the peripheral blood and enhanced deposition at the tumor site, consequently amplifying the antitumor effect. Neutrophils heavily rely on PI3K signaling to sustain their phagocytic process. Additionally, our study determined that the inhibition of the PI3Kinase delta isoform by idelalisib (CAL-101) suppressed the uptake of oncolytic VV by neutrophils. This inhibition led to a greater presence of oncolytic VV in both the peripheral blood and at the tumor site, resulting in improved efficacy against the tumor. In conclusion, our study showed that inhibiting neutrophil functions can significantly enhance the antitumor efficacy of intravenous oncolytic VV.

Allergic reaction to the silicone is rare in children and as a result very little experience has been reported on symptom and treatment. We presented a case involving a child who experienced prolonged ascites following a surgery of placing an abdominal drainage tube, characterized by the ongoing drainage of clear, light-yellow fluid at a rate of 250 mL/day through the drainage tube for 36 days. Examination of the ascitic fluid revealed an abnormal elevation in eosinophil proportion, which exhibited positive response to anti-allergic treatment. Subsequent to the removal of the drainage tube, the ascites gradually resolved. In conclusion, we presented here the first and youngest case of allergic ascites associated with drainage tube after surgery of ovarian mucinous cystadenoma, it is imperative not to overlook the possibility of drainage tube allergy in the diagnostic process.

Abstract Backgroud: The Syrian hamster (Mesocricetus auratus) has shown promise as a human diseases model, recapitulating features of different human diseases including the emerging COVID-19. However, the landscape of its genome and transcriptome has not been systematically dissected, restricting its potential applications. Results: Here we provide a complete analysis of the genome and transcriptome of the Syrian hamster and found that its lineage diverged from that of the Chinese hamster (Cricetulus griseus) around 29.4 million years ago. 21,387 protein-coding genes were identified, with 90.03% of the 2.56G base pair sequence being anchored to 22 chromosomes. The further comparison of the transcriptomes from 15 tissues of the Syrian hamster disclosed that Syrian hamster shares a pattern of alternative splicing modes more similar to humans, compared to rats and mice. A integrated genomic-transcriptomic analysis revealed that Syrian hamster also has genetic and biological advantages as a superior animal model for cardiovascular diseases. Strikingly, several genes involved in SARS-COV-2 infection including ACE2present a higher homology with humans than other rodents and show the same function as the human counterparts. Conclusion: The detailed molecular characterisation of the Syrian hamster in the present study opens a wealth of fundamental resources from this small rodent for future research into human disease pathology and treatment.

Abstract Objective: To establish a novel mouse model of acute myocardial injury induced by hypobaric hypoxia and improve the relevant evaluation system. Methods: Using the plateau simulator made by our institute (which has e Chinese invention patent, patent number: ZL 2021 1 1517241. X), Babl/c mice were continuously exposed to the extreme altitude, low pressure and hypoxia environment for 0h-216h. PET/CT was used to evaluate the metabolic function of myocardial cells in mice by injecting 18F-FDG in vivo. the changes of cardiac function and morphology was observed in mice by cardiac ultrasound. FITC-BSA was injected into the tail vein to verify the leakage function of blood vessels in the heart tissue of mice. HE staining, Masson staining, CD163 and CD34 immunohistochemical staining get used to verify the degree of myocardial injury, fibrosis, inflammatory cell infiltration and angiogenesis in mice. Results: The myocardial metabolic function of Babl/c mice in hypobaric hypoxia environment was enhanced at the early stage of exposure, and then gradually weakened. With the extension of time, the heart rate gradually accelerated, the myocardial morphology changed significantly, the myocardial pathological changes and damage gradually increased, the role of vascular leakage gradually increased, the infiltration of inflammatory cells increased, and the myocardial fibrosis increased significantly.

Chimeric antigen receptor T cell immunotherapy has achieved promising therapeutic effects in the treatment of hematological malignancies. However, there are still many obstacles, including on-target off-tumor antigen expression, that prevent successful application to solid tumors. We designed a tumor microenvironment (TME) regulated system chimeric antigen receptor T (MRS.CAR-T) which can only be auto-activated in the solid TME. B7-H3 was selected as the target antigen for esophageal carcinoma. An element comprising a human serum albumin (HSA) binding peptide and a matrix metalloproteases (MMPs) cleavage site was inserted between the 5' terminal signal peptide and single chain fragment variable (scFv) of the CAR skeleton. Upon administration, HSA bound the binding peptide in MRS.B7-H3.CAR-T effectively and promoted proliferation and differentiation into memory cells. MRS.B7-H3.CAR-T was not cytotoxic in normal tissues expressing B7-H3 as the antigen recognition site in the scFv was cloaked by HSA. The anti-tumor function of MRS.B7-H3.CAR-T was recovered once the cleavage site was cleaved by MMPs in the TME. The anti-tumor efficacy associated with MRS.B7-H3.CAR-T cells was improved compared to classic B7-H3.CAR-T cells in vitro and less IFN-γ was released, suggesting a treatment that may induce less extent of cytokine release syndrome-mediated toxicity. In vivo, MRS.B7-H3.CAR-T cells had strong anti-tumor activity and were safe. MRS.CAR-T represents a novel strategy to improve the efficacy and safety of CAR-T therapy in solid tumors.

Background : Acute pancreatitis（AP） is a severe disorder that leads to high morbidity and mortality. Appropriate reference genes are important for gene analysis in AP. This study sought to study the expression stability of several reference genes in the golden Syrian hamster, a model of AP. Methods : AP was induced in golden Syrian hamster by intraperitoneal injection of ethanol（1.35 g/kg） and palmitoleic acid（2 mg/kg）. The expression of candidate genes, including Actb, Gapdh, Eef2, Ywhaz, Rps18, Hprt1, Tubb, Rpl13a, Nono, and B2m, in hamster pancreas at different time points（1, 3, 6, 9, and 24 h） posttreatment was analyzed using quantitative polymerase chain reaction. The expression stability of these genes was calculated using Best Keeper, Comprehensive Delta CT, Norm Finder, and ge Norm algorithms and Ref Finder software. Results : Our results show that the expression of these reference genes fluctuated during AP, of which Ywhaz and Gapdh were the most stable genes, whereas Tubb, Eef2, and Actb were the least stable genes. Furthermore, these genes were used to normalize the expression of TNF-α messenger ribonucleic acid in inflamed pancreas. Conclusions : In conclusion, Ywhaz and Gapdh were suitable reference genes for gene expression analysis in AP induced in Syrian hamster.

Clinically, thymoma patients are often complicated with myasthenia gravis (MG). Dexamethasone, a glucocorticoid with anti-inflammatory effects, could be used as an immunosuppressant for thymoma-associated MG, but the mechanism of action remains to be explored. In this study, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, weighted gene co-expression network analysis (WGCNA) of potential targets was performed by screening the intersection targets of dexamethasone and thymoma-associated MG from the database. Furthermore, the key targets and core active components were identified by topological analysis of the protein-protein interaction (PPI) network. Molecular docking technology was applied to screen the complexes with stable binding of dexamethasone and core targets. Patients with thymoma were divided into two groups according to whether they received dexamethasone before operation, and immunohistochemistry and western blot were used to verify the selected target of dexamethasone in treating thymoma-associated MG. The results showed that the action pathway of dexamethasone on the disease was closely enriched to phosphatidylinositol 3-kinase (PI3K)-protein kinase B (PKB/AKT), mammalian target of rapamycin (mTOR) signaling pathways. The expressions of AKT1 and its downstream molecule mTOR in the thymoma microenvironment of thymoma-associated MG patients who did not receive dexamethasone before operation were higher than those in the group receiving dexamethasone before operation. This study demonstrates that dexamethasone can promote apoptosis through the AKT-mTOR pathway for the treatment of thymoma-associated MG, as validated by network pharmacology predictions and clinical specimen experiments, and can be verified by large-scale clinical trials in the future. This study also provides theoretical support and new research perspectives for this disease.

ObjectiveRecent therapeutic advances have greatly enhanced the survival rates of patients with neuroblastoma (NB). However, the outcomes of neuroblastoma patients in China, particularly those with high-risk (HR) NB, remain limited.MethodWe retrospectively analyzed the clinical data and outcomes of NB patients who were treated at a tertiary pediatric cancer facility in China between January 2013 and October 2021.ResultsA total of 117 NB patients were recruited. Patients with very low-risk (VLR), low-risk (LR), intermediate-risk (IR), and HR-NB patients made up 4%, 27%, 15%, and 54% of total patient population, respectively. Patients diagnosed between 2013 and 2018 were treated according to the protocol of Sun Yat-Sen University Cancer Center and those diagnosed between 2019 and 2021 were treated according to the COG ANBL0531 or ANBL0532 protocol with or without autologous stem cell transplantation (ASCT). The 5-year EFS and OS of all risk groups of patients were 67.29% and 77.90%, respectively. EFS and OS were significantly decreased in patients with higher risk classifications (EFS: VLR/LR vs IR vs HR: 97.22% vs 67.28% vs 51.83%; ***P = .001; OS: VLR/LR vs IR vs HR: 97.06% vs 94.12% vs 64.38%; *P = .046). In HR-NB patients treated according to the COG protocol between 2019 and 2021, the 3-year OS of patients who received tandem ASCT was significantly greater than those who did not receive ASCT (93.33% % vs 47.41%; *P = .046; log-rank test). EFS was not significantly different between patients with and without ASCT (72.16% vs 60.32%).ConclusionOur findings show that patients with lower risk classification have a positive prognosis for survival. The prognosis of patients with HR-NB remains in need of improvement. ASCT may enhance OS in HR-NB patients; however, protocol adjustment may be necessary to increase EFS in these patients.

Inflammatory bowel disease (IBD), encompassing Crohn's disease and ulcerative colitis, is a chronic autoimmune disorder characterized by inflammation. However, currently available disease-modifying anti-IBD drugs exhibit limited efficacy in IBD therapy. Furthermore, existing therapeutic approaches provide only partial relief from IBD symptoms and are associated with certain side effects. In recent years, a novel category of nanoscale membrane vesicles, known as plant-derived exosome-like nanoparticles (PDENs), has been identified in edible plants. These PDENs are abundant in bioactive lipids, proteins, microRNAs, and other pharmacologically active compounds. Notably, PDENs possess immunomodulatory, antitumor, regenerative, and anti-inflammatory properties, making them particularly promising for the treatment of intestinal diseases. Moreover, PDENs can be engineered as targeted delivery systems for the efficient transport of chemical or nucleic acid drugs to the site of intestinal inflammation. In the present study, we provided an overview of PDENs, including their biogenesis, extraction, purification, and construction strategies, and elucidated their physiological functions and therapeutic effects on IBD. Additionally, we summarized the applications and potential of PDENs in IBD treatment while highlighting the future directions and challenges in the field of emerging nanotherapeutics for IBD therapy.

CD19-targeted chimeric antigen receptor-modified T (CD19 CAR-T) cell therapy has been demonstrated as one of the most promising therapeutic strategies for treating B cell malignancies. However, it has shown limited treatment efficacy for diffuse large B cell lymphoma (DLBCL). This is, in part, due to the tumor heterogeneity and the hostile tumor microenvironment. Human interleukin-12 (IL-12), as a potent antitumor cytokine, has delivered encouraging outcomes in preclinical studies of DLBCL. However, potentially lethal toxicity associated with systemic administration precludes its clinical application. Here, an armed CD19 CAR expressing hypoxia-regulated IL-12 was developed (CAR19/hIL12ODD). In this vector, IL-12 secretion was restricted to hypoxic microenvironments within the tumor site by fusion of IL-12 with the oxygen degradation domain (ODD) of HIF1α. In vitro, CAR19/hIL12ODD-T cells could only secrete bioactive IL-12 under hypoxic conditions, accompanied by enhanced proliferation, robust IFN-γ secretion, increased abundance of CD4+, and central memory T cell phenotype. In vivo, adoptive transfer of CAR19/hIL12ODD-T cells significantly enhanced regression of large, established DLBCL xenografts in a novel immunodeficient Syrian hamster model. Notably, this targeted and controlled IL-12 treatment was without toxicity in this model. Taken together, our results suggest that armed CD19 CARs with hypoxia-controlled IL-12 (CAR19/hIL12ODD) might be a promising and safer approach for treating DLBCL.

Here, we present a case with genetically confirmed SCN. The main symptom of the child was recurring fever. The combination of antibiotics combined with G-CSF injection was proved to be insufficient, and the patient developed ''solid'' liver abscess. After undergoing surgical anatomical hepatic lobectomy, the child's infection symptoms showed improvement. The postoperative culture of the purulent material from the liver infection lesion revealed an infection with Staphylococcus aureus. Our case raises the possibility of pathogen sources and routes of infection, clinical characteristics, and effective treatment for SCN patients with concomitant liver abscess.