Current T cell-based immunotherapeutic strategies show limited success in treating solid tumors due to insufficient dendritic cell (DC) activity, particularly cross-presenting conventional type 1 dendritic cells (cDC1s). DC scarcity and dysfunction hinder T cell expansion and differentiation, greatly limiting anti-tumor responses. In this study, we propose a T cell engineering strategy to enhance interaction with XCR1+ cDC1s. Adoptively transferred T cells engineered to secrete Flt3L and XCL1 (FX) promote DC trafficking and maturation and improve DC-T cell interaction, while maintaining a pool of TCF1+SlamF6+ stem-like T cells. Importantly, FX-engineered T cells trigger robust antigen spreading and potent endogenous polyclonal T cell response, enabling the recognition and elimination of tumors with heterogeneous antigens and preventing immune escape. The therapeutic efficacy of FX-armed chimeric antigen receptor (CAR)-T cells is further validated in the Flt3KO&hFLT3LG humanized mouse model. This strategy offers a promising avenue for enhancing DC-T cell interactions, paving the way for more effective immunotherapy against solid tumors.

BackgroundThe diagnosis and treatment of pancreatic adenocarcinoma (PAAD) remain clinically challenging, and new molecular markers for prognostic assessment and targeted therapy are urgently needed. The tumor microenvironment (TME) and immune invasion play an important role in pancreatic cancer development and progression. Therefore, immunotherapeutic strategies based on the TME and immune invasion may have important clinical value.MethodsIn this study, we extracted transcriptome and clinicopathological data for 179 PAAD samples from the TCGA database and evaluated the immune composition, stromal composition, and infiltrating immune cell landscape in the tumor samples. Then, we identified relevant differentially expressed genes (DEGs) and performed functional annotation and prognostic correlation analysis to identify prognostic biomarkers for pancreatic cancer, the correlation between biomarkers and tumor immune invasion was analyzed to reveal the molecular immune mechanism of pancreatic cancer. Finally, GEO databases (GES71729), GEPIA, TISIDB, TIMER databases and RT-PCR were used for further analysis.ResultsCXCL10 and CXCL11 were highly expressed in pancreatic cancer and associated with poor prognosis of patients through cell adhesion molecules chemokine signaling, cytokine-cytokine receptor interaction, natural killer cell-mediated cytotoxicity, and Toll-like receptor signaling pathways. Finally, the correlation between CXCL10 and CXCL11 and tumor immune invasion was analyzed. The results confirmed that the expression levels of CXCL10 and CXCL11 were positively correlated with the contents of CD8+ T cells. Activated memory CD4+ T cells, M1 macrophages and resting mast cells. The levels of CXCL10 and CXCL11 were related to but negatively correlated with the contents of memory B cells, Tregs and M0 macrophages.ConclusionOur study demonstrates that CXCL10 and CXCL11 are novel biomarkers of TME and immune cell infiltration in pancreatic cancer by affecting the distribution of immune cells. CXCL10 and CXCL11 may be new targets for molecular targeted therapy and immunotherapy of pancreatic cancer.

Breast cancer (BRCA) is a complex disease influenced by the tumor microenvironment, where interactions between immune cells and cancer cells play a crucial role in tumor progression and response to therapy. Understanding the intricacies of these interactions requires detailed analysis at the single-cell level, enabling the identification of specific immune cell subpopulations and their functional roles within the tumor milieu. This study comprehensively analyzed immune cell subpopulations and macrophage subtypes in BRCA using single-cell RNA sequencing technology and various computational tools. Initially, Sc-Type software accurately identified and annotated immune cell subpopulations, followed by CNV analysis using infercnv software, revealing significant CNV variations in epithelial cells. Subsequently, macrophages were re-clustered into 5 clusters, and their biological significance and functional features were assessed. CellChat analysis elucidated potential interactions between macrophage subtypes and BRCA cells, primarily through SPP1-CD44 and LGALS9-CD44 signaling networks. Additionally, CytoTRACE and Monocle were employed to analyze cellular plasticity and differentiation trajectories of macrophage subtypes. Furthermore, efferocytosis-related gene set scoring, transcription factor analysis, and risk score development were conducted, followed by immune infiltration and tumor mutation burden analysis, revealing increased immune infiltration and higher TMB levels in the high-risk group. These findings offer crucial insights into the interaction mechanisms of immune cells and macrophage subtypes within the BRCA tumor microenvironment, aiding in the understanding of tumor progression and therapeutic interventions.

BACKGROUND:Ring finger protein 11 (RNF11) is integral to cell signal transduction and transcription factor regulation and is strongly connected to the beginning and progression of malignant tumors. However, the core mechanisms of RNF11 remain unknown to date. This study highlights the significant function of RNF11 in the DNA damage response. METHODS:After the CRISPR-Cas9 gene knockout of RNF11, HCT116 cells were transfected, and cell viability assays were performed to evaluate the response of tumor cells to the chemotherapy drugs after RNF11 deletion. The interaction of RNF11 with its binding proteins and its ubiquitination mechanism, along with the recruitment of KU80 to chromatin, were subsequently evaluated. RNF11 was revealed to participate in the regulation of the cell cycle and apoptosis. An HCT116 xenograft tumor model was used to validate the in vivo sensitivity of tumors to 5-FU, revealing that RNF11 is essential for regulating the responsiveness of tumor cells to chemotherapy. RESULTS:RNF11 modulates KU80 expression and participates in cell cycle regulation. The elimination of RNF11 results in the accumulation of KU80 at the DNA damage sites, induces G1 phase cell cycle arrest, and increases sensitivity to the chemotherapy drugs. Mechanistically, RNF11 regulates KU80 expression through a direct interaction and facilitates its ubiquitination while modulating apoptosis and the cell cycle, thereby participating in the cellular damage response. Furthermore, high RNF11 expression is associated with poor prognosis in patients with cancer, while RNF11 deletion impedes tumor progression and enhances the sensitivity of the xenografts to 5-FU treatment. These findings demonstrate that RNF11 is involved in the clinical tumor treatment processes and could be a target for cancer treatment. CONCLUSION:RNF11 binds with KU80, facilitates its ubiquitination, supports DNA damage repair, preserves genomic stability, and enhances the chemotherapy response in tumor cells.

Abstract Objectives To compare the risk of acute kidney injury (AKI) between hospitalized children who received intravenous contrast media for imaging examinations and those who did not. Methods This retrospective cohort study enrolled patients aged 0–18 years with serum creatinine levels before and after imaging examinations from 2015 to 2020 at Beijing Children’s Hospital. Participants were classified into an exposure group or a control group. Log-binomial regression analysis was used to estimate the adjusted risk ratio (aRR) value for the association between exposure to contrast media and consequential AKI. After which, inverse probability treatment weighting was used to reduce systematic differences in baseline characteristics among the groups. Moreover, subgroup and sensitivity analyses were performed. Finally, multivariate logistic regression analysis was performed to identify risk factors for pediatric AKI. Results In total, 3061 pediatric patients were included in the analyses (median age, 4.5 [IQR, 1.3–8.9] years, 1760 males). According the KDIGO definition of AKI, the incidence of AKI in the exposure group, and the control group were 7.4% and 6.5%, respectively; furthermore, the aRR was 1.35 (95% CI: 1.31–1.39). In patients underwent CT, the risk of AKI in the exposure group of contrast media increased compared with the control group and the aRR was 1.39 (95% CI: 1.09–1.78). However, it is not observed in patients underwent MRI (aRR: 1.36; 95% CI: 0.96–1.95). According to our subgroup analysis of pediatric patients aged ≥ 2 years (aRR: 1.38; 95% CI: 1.05–1.82) and sensitivity analysis (aRR: 1.32, 95% CI: 1.08–1.61), the risk of AKI in the exposure group was greater than that in the control group. An increased risk to exposure to contrast media was seen in females (aRR: 1.41, 95% CI: 1.05–1.89) rather than males (aRR: 1.30, 95% CI: 0.99–1.70). According to the multivariate logistic regression analyses, the baseline eGFR (OR: 1.02; 95% CI: 1.01–1.03) and comorbidities (OR: 2.97; 95% CI: 1.89–4.65) were risk factors, while age (OR: 0.87; 95% CI: 0.84–0.91) was a protective factor against AKI. Conclusion The evidence from the present study suggested that the increased risk of AKI in hospitalized children induced by intravascular contrast should not be ignored.

BackgroundSulfotransferase family 2B member 1 (SULT2B1) is involved in regulating cell proliferation, migration and metabolism. However, there is still dispute regarding whether SULT2B1 acts as an oncogene or a suppressor, and the intrinsic mechanisms in modulating tumor progression need to be further elucidated.MethodsThis work aims to reveal the relationship among SULT2B1, AKT, PKM2 signaling and glycolytic pathways, and provided a theoretical basis for SULT2B1 as a potential therapeutic target for CRC.Bioinformatics methods, immunohistochemistry (IHC) and immunoblotting assays were performed to analyze the correlation between SULT2B1 and colorectal cancer (CRC). The effect of SULT2B1 on cell proliferation and migration were investigated by several phenotypic experiments in vitro and animal studies. The SULT2B1 interacting proteins were determined by immunofluorescence, immunoprecipitation and GST-pull down assays. Immunoblotting and mCherry-GFP-LC3 assays were performed to analysis autophagy. Chromatin immunoprecipitation (CHIP) assay was utilized to detect the effect of SULT2B1 in regulating transcription. Small molecule agonist/antagonist was used to modify protein activity and therefore analyze the mutual relationships.ResultsSULT2B1 is a predictive biomarker that is abnormally overexpressed in CRC tissues. Overexpression of SULT2B1 promoted cell proliferation and migration, while its knockout suppressed these processes. Furthermore, SULT2B1 could directly interact with the oncogene AKT and thereby enhance the activity of AKT-mTORC1 signaling. Furthermore, PKM2 was found to bind with SULT2B1, and regulated by SULT2B1 at both transcription and degradation levels. Moreover, blocking glycolysis attenuated the promoting effect of OE-SULT2B1.ConclusionSULT2B1 acts as an oncogene in CRC via modulating the AKT/PKM2 axis, therefore making it a promising diagnostic and therapeutic target for CRC.

Objective This study aimed to investigate the association between white matter hyperintensity (WMH) burden and pial collaterals in acute strokes caused by intracranial large artery occlusion treated with mechanical thrombectomy in the anterior circulation, focusing on stroke subtypes. Methods Consecutive patients undergoing mechanical thrombectomy between December 2019 and June 2022 were retrospectively screened. The Fazekas scale assessed WMH burden. Pial collaterals were categorized as either poor (0–2) or good (3–4) based on the Higashida score. A multivariable analysis was used to determine the relationship between WMH burden and pial collaterals. Subgroup analyses delved into associations stratified by stroke subtypes, namely cardioembolism (CE), tandem lesions (TLs), and intracranial atherosclerosis (ICAS). Results Of the 573 patients included, 274 (47.8%) demonstrated poor pial collaterals. Multivariable regression indicated a strong association between extensive WMH burden (Fazekas score of 3–6) and poor collaterals [adjusted OR 3.04, 95% CI 1.70–5.46, P < 0.001]. Additional independent predictors of poor collaterals encompassed ICAS-related occlusion (aOR 0.26, 95% CI 0.09–0.76, P = 0.014), female sex (aOR 0.63, 95% CI 0.41–0.96, P = 0.031), and baseline Alberta Stroke Program Early Computed Tomography scores (aOR 0.80, 95% CI 0.74–0.88, P < 0.001). Notably, an interaction between extensive WMH burden and stroke subtypes was observed in predicting poor collaterals ( P = 0.001), being pronounced for CE (adjusted OR 2.30, 95% CI 1.21–4.37) and TLs (adjusted OR 5.09, 95% CI 2.32–11.16), but was absent in ICAS (adjusted OR 1.24, 95% CI 0.65–2.36). Conclusions Among patients treated with mechanical thrombectomy for anterior circulation large artery occlusion, extensive WMH burden correlates with poor pial collaterals in embolic occlusion cases (CE and TLs), but not in ICAS-related occlusion.

BACKGROUND:The Oxford Classification was proposed as an independent prognostic indicator in IgA nephropathy (IgAN). However, most studies on the subject focus on adults instead of children. OBJECTIVES:Using a meta-analysis to appraise the predictive roles of the Oxford classification for the prognosis of pediatric patients with IgAN. METHODS:All cohort studies regarding the analysis of the association between poor kidney-related prognosis (GFR categories G2-G5) according to the Kidney Disease Improving Global Outcomes (KDIGO) Guideline in pediatric patients with IgAN and five pathologic lesions in the Oxford Classification were included. Hazard ratios (HRs) regarding the association between the Oxford classification and prognosis of pediatric patients with IgAN were synthesized using random effect models. The risk of bias in studies was assessed based on the Newcastle-Ottawa scale. RESULTS:Fourteen articles were included with 5679 IgAN patients and 710 endpoint outcome events occurred. M1 was associated with a higher risk of poor kidney-related prognosis compared with M0, pooled HR (1.79; 95%CI, 1.46-2.19; p < 0.001, random effect model). S1 and T1 or T2 increased the risk of poor kidney-related prognosis (pooled HR, 2.13; 95%CI, 1.68-2.70; p < 0.001; pooled HR, 2.64; 95%CI, 1.81-3.86; p < 0.001, respectively, estimated by random effect model). Compared with C0, C1, or C2 was also associated with an increased risk of poor kidney-related prognosis in the subgroup analysis of Asian and other populations. Evidence to indicate that E1 increased the risk of poor kidney-related prognosis was marginal.

Pancreatic cancer (PC) has poor prognosis. PRKAA1 (AMPK-alpha 1) is the catalytic subunit of 5'-adenylateactivated protein kinase (AMPK), which plays a critical role in multiple stages of tumorigenesis and development. However, the biological mechanisms of PRKAA1 in the tumor microenvironment have not been well studied. In this study, we performed a combined analysis of data from TCGA and GTEx databases to determine whether PRKAA1 is differentially expressed in a variety of tumors. Kaplan-Meier curve and Cox regression analyses indicated that the differential expression of PRKAA1 affected overall survival in a variety of tumors and was an independent prognostic factor for Brain Lower Grade Glioma (LGG), Brain Lower Grade Glioma (LAML), Liver hepatocellular carcinoma (LIHC), Pancreatic adenocarcinoma (PAAD), and Pancreatic adenocarcinoma (KICH). PRKAA1 was closely associated with various immune profiles, suggestingthat PRKAA1 can be used for direct immunotherapy. We investigated the role of PRKAA1 in PC cells. We found that the downregulation of PRKAA1 expression reduced the proliferation, migration, and invasion of PC cells. In addition, we found that PRKAA1 regulated PC progression, possibly through the PI3K/AKT signaling pathway. Treatment of cells with the AKT inhibitors MK2206 and GSK2110183 revealed that the PRKAA1 overexpression group was less sensitive to AKT inhibitors than the negative control group. Taken together, PRKAA1 can be used as a potential prognostic marker and new target for tumor immunotherapy.

Background: Chaperonin-containing tailless complex polypeptide 1 subunit 6A (CCT6A) is mainly located in the cytoplasm and considered to be involved in various biological processes in tumors. However, its function and the intrinsic mechanism need to be further elucidated. Methods: Multi-omics analysis was used to evaluate the correlation between CCT6A expression and prognosis of patients, as well as its immune value. CCT6A was knockout by CRISPR-Cas9, and overexpressed by transfecting plasmids in colorectal cancer (CRC) cells. Cell proliferation was analyzed by MTS, EDU staining and colony growth assay, and cell migration was monitored by wound healing assay and Transwell assay. The phosphor-kinase array kit and immunoblotting assay was utilized to explore the potential molecular mechanisms. Results: CCT6A was highly expressed in multiple tumor tissues and significantly correlated with the prognosis of patients. It was also associated with the immune infiltration, immune correlation and prognosis in CRC. CCT6A was highly expressed in CRC biopsies as well as fresh CRC tissues. Meanwhile, knockout of CCT6A reduced cell proliferation, cell cycle and cell migration. On the contrary, overexpression of CCT6A exhibited the opposite phenotypes. Moreover, we identified that HSPD1 and non-phosphorylated P53 were highly increased in CCT6A overexpressed cells, which are involved in regulating tumorigenesis. Conclusions: Therefore, CCT6A positively regulated cell proliferation/migration in CRC cells, and suggesting CCT6A has a high immunological value and is associated with CRC progression, which makes it a potential therapeutic target for CRC.

Trabeculectomy (TRAB) traditionally has been the gold-standard surgical treatment for primary open-angle glaucoma (POAG), while gonioscopy-assisted transluminal trabeculotomy (GATT) is an emerging minimally invasive surgery used for the treatment of various open-angle glaucoma (OAG) types. In this study, we aimed to compare the efficacy and safety between GATT and TRAB for the treatment of POAG. This cohort study included eyes with POAG that underwent a single GATT (30 eyes) or TRAB (34 eyes). Follow-up was conducted at 1 day, 1 week, and 1, 3, 6, and 12 months postoperatively. Intraocular pressure (IOP), the numbers of glaucoma medication, visual field mean deviation, peripapillary retinal nerve fiber layer thickness, surgical time, and complications were analyzed. Success criteria were defined as IOP ≤ 21 mmHg and ≥ 20

BackgroundSplenic littoral cell angioma (LCA) is an exceptionally uncommon malignant potential vascular tumor with infrequent occurrences in pediatric patients. Due to its reliance on histopathological analysis for diagnosis, LCA may be mistakenly identified as other splenic tumors. Patients with LCA may experience anemia or thrombocytopenia, but peripheral blood pancytopenia is infrequent.Case reportA 14-year-old boy presented with peripheral blood pancytopenia, necessitating hospitalization after splenomegaly was identified during a physical examination. Following the exclusion of hematological disorders, a splenectomy was conducted; histopathological examination confirmed the diagnoses of LCA. No metastases or recurrences were observed during the 8-month follow-up. To the best of our knowledge, this case represents the first instance of LCA associated with pancytopenia in a pediatric patient.ConclusionLCA can lead to iron-deficiency anemia or thrombocytopenia, with rare occurrences of pancytopenia, potentially resulting in misdiagnosis as a hematological disorder. Surgical intervention remains an effective treatment for LCA.

To examine the potential correlation between chemotherapy and the risk of individual of second primary endometrial cancer (SEC) in patients with rectal cancer (RC) and assess survival outcomes. The study employed the Surveillance, Epidemiology, and End Results database (SEER) as the primary data source, it encompasses a substantial cohort of patients diagnosed with RC between 1975 and 2018. This study involved a total of 30,847 individuals diagnosed with RC, of whom 168 individuals (5.45‰) experienced SEC. Among them, 107 patients (3.47‰) received chemotherapy treatment, while 61 patients (1.98‰) did not receive chemotherapy. The analysis of the overall occurrence of SEC revealed a significant association between SEC and chemotherapy treatment. Univariate and multivariate analyses confirmed a significant association between chemotherapy treatment and an increased risk of developing SEC in RC patients. Upon implementation of a dynamic analysis on the variables of relative risk and standardized incidence ratios, the results revealed that the likelihood of SEC escalated in tandem with advancing age. The examination of patients who developed SEC after receiving and not receiving chemotherapy revealed no substantial disparities in the 10-year overall survival (OS) and (cancer-specific survival) CSS rates. The results were the same after propensity score matching. Nevertheless, a notable discrepancy emerged when comparing the OS and CSS rates at 10 years between patients afflicted with SEC subsequent to chemotherapy and those afflicted with primary endometrial cancer, and the result was the same situation in the no-chemotherapy group. The use of chemotherapy in RC patients has been associated with an increased probability of developing specific SEC. Therefore, it is imperative to prioritize efforts aimed at reducing chemotherapy-related SEC occurrences and improving the prognosis of affected individuals.

BACKGROUND:The effectiveness and safety of intravenous thrombolysis before mechanical thrombectomy (MT) in large cerebral infarctions remains uncertain. This study compares bridging MT, which includes intravenous thrombolysis, to direct MT without it. METHODS:Data from 298 patients with anterior circulation large cerebral infarctions, assessed via non-enhanced CT (ASPECTS 0-5), who underwent MT in two-center cohort studies, were analyzed. Primary outcomes focused on independent ambulation (modified Rankin Scale scores 0-3) at 90 days post-stroke. Safety outcomes included parenchymal hemorrhage (PH) rates and mortality. We conducted a sensitivity analysis considering the timing from symptom onset to imaging within 4.5 hours. Additionally, a meta-analysis of 17 studies involving 3527 patients assessed the interventions' effectiveness and safety, with further scrutiny of high-quality studies (Newcastle-Ottawa Scale ratings 7-9) to increase robustness of results. RESULTS:No significant differences were found in 90-day independent ambulation between the bridging MT and the direct MT group (adjusted odds ratio [aOR] 1.15, 95% CI 0.68-1.94). Rates of PH and mortality were also similar across groups. These outcomes were consistent in the subgroup imaged within 4.5 hours of symptom onset. The meta-analysis supported these outcomes, showing no improvement in ambulation (aOR 1.16, 95% CI 0.82-1.64) or reduction in PH with bridging MT. Further analysis of high-quality studies supported these results. CONCLUSIONS:The cohort study and meta-analysis provide Class II evidence indicating no significant differences in functional outcomes or hemorrhagic risks between bridging and direct MT for large cerebral infarctions. This suggests that direct MT might be a viable alternative to bridging MT.

The treatment principle of liver cancer is mainly based on clinical stage. The early and middle stage patients were mainly treated by surgery and local treatment. The middle and late stage patients were mainly treated by comprehensive treatment. It is known that the survival and prognosis of patients with advanced hepatocellular carcinoma can be improved by targeted therapy and immunotherapy. In the era of molecular targeted therapy and immunotherapy, identifying predictive biomarkers are important for the successful implementation of personalized medicine. For the diversification treatment of hepatocellular carcinoma, how to effectively predict the treatment response and prognosis of hepatocellular carcinoma is an urgent clinical problem. Radiomics reveals in a quantitative manner the macroscopic tissue heterogeneity that is indirectly related to microscopic tissue heterogeneity, which cannot be recognized by the naked eye. The classification and stage of the tumors can be evaluated effectively, as well as the prognosis of the patients. This article reviews the correlation between radiomics and pathological characteristics, genotype and immune characteristics, treatment response and prognosis of hepatocellular carcinoma.

肠道微生物群具有多种生理功能,在宿主健康和肠道内环境稳定中起着关键作用.肿瘤的放疗会导致肠道菌群紊乱、免疫失调,引起急慢性炎症.同时,肠道菌群及其代谢物会影响放疗的效果和不良反应发生.现已发现应用益生菌、抗生素、粪便移植、菌群代谢物等改变宿主肠道菌群的方法具有预防和治疗放射性肠炎、增加放射敏感性及增强放疗效果的作用.文章就肠道菌群对肿瘤放疗的影响进行综述.

目的 采用内镜下活检胃癌组织块肾筋膜下移植法建立NOD/SCID小鼠胃癌异位移植瘤模型,观察其MRI表现,为研究胃癌个体化治疗临床前实验提供适宜的动物模型.材料与方法 将2020年12月—2021年2月在兰州大学第二医院经病理及影像确诊的9例晚期胃癌患者内镜下活检的约1 cm3新鲜肿瘤组织种植到NOD/SCID小鼠右侧肾筋膜下.种植后每周行1次MRI检查至发现肾筋膜下成瘤,继续观察4周,采用T2WI序列测量并计算肿瘤体积,然后处死小鼠,取出瘤组织,将游标卡尺测量的肿瘤体积与最后一次MRI测量结果进行对比,并对移植瘤进行病理学检查.结果 异位移植瘤T1WI呈等低混杂信号,T2WI呈等高信号,增强后明显不均匀强化,肿瘤向前挤压肾脏变形.MRI与游标卡尺测量肿瘤体积分别为(512.12±25.52)mm3、(506.95±29.24)mm3,差异无统计学意义(t=0.808,P=0.436).病理结果显示移植前后肿瘤组织学保持一致性.结论 本研究建立的胃癌异位移植瘤模型保持了原发肿瘤的组织学特性,可活体"再现"人类疾病;MRI能够敏感地发现肾筋膜下是否成瘤,且准确量化肿瘤大小,本模型可作为观察人类胃癌个体化治疗临床前实验的动物模型.

Objective: To evaluate the feasibility of free-hand bedside catheterization using axial computed tomography (CT) in patients with brain hemorrhage after ischemic revascularization. Methods: Patients who received revascularization therapy and underwent bedside catheterization were consecutively screened from December 2020 to July 2022. Revascularization included intravenous thrombolysis with or without mechanical thrombectomy, balloon angioplasty, and stenting. The catheter trajectory was designed according to the axial CT along the long axis of the hematoma body and projected onto the scalp at the calculated distance and angle. Urokinase was used locally to drain the hematoma. Results: In 12 patients (mean age 66 ± 8 years), an 86% reduction in hematoma volume was found after catheter drainage, from 48.6 ± 20.4 ml to 6.7 ± 5.7 ml (P＜0.001). In accordance with the reduction of the hematoma volume, the Glasgow Coma Scale improved from 7 (6.5–8) to 10 (7–10.5) (P = 0.031). Four patients (33.3%) achieved good outcomes (modified Rankin Scale 0–3) at the 180-day follow-up. All-cause mortality was 25%. One patient experienced active hemorrhage. No bacterial brain infections were observed. Conclusions: Free-hand bedside catheterization according to axial CT localization is feasible for treating extensive revascularization-related hematoma after ischemic stroke.

Background: Since the first successful open pancreaticoduodenectomy (OPD) that performed in 1935, several major landmarks have been achieved in the field such as the performance of the first laparoscopic pancreaticoduodenectomy (LPD) 28 years ago and the first robotic pancreaticoduodenectomy (RPD) 19 years ago. Numerous studies have justified the efficacy and safety of RPD and its popularity has been increasing significantly in recent years. As an updated technique, robotic system is superior to laparoscope with both theoretical and technical advantages.