Evaluation of 3D-CEUS in the Recurrence of Liver Cancer after Radiofrequency Ablation.

Background: Radiofrequency ablation (RFA) has the similar curative effects to surgery, but RFA will lead to higher postoperative local recurrence rate. 3D-CEUS is a minimally invasive examination method, which is used to analyze the sensitivity to postoperative recurrence in this study. Methods: The clinical data of 60 patients with liver cancer admitted to our hospital (February 2018-February 2020) were retrospectively analyzed. All patients were treated with RFA and were followed up with 3D-CEUS, MRI, and enhanced CT examination after surgery. The ROC curve was used to analyze the differences of different examination methods in judging postoperative recurrence. Results: For the 60 patients, 52 patients (86.7%) had a single lesion and 8 patients (13.3%) had multiple lesions, with a total of 72 lesions. After RFA, 56 lesions (77.8%) were completely inactivated and 16 lesions (22.2%) remained. Totally inactivated lesions were detected as follows: 51 (91.1%) by 3D-CEUS, 42 (75.0%) by MRI, and 50 (89.3%) by enhanced CT. During a 2-year follow-up, a total of 26 recurrent lesions were detected, 24 (92.3%) by 3D-CEUS, 12 (46.2%) by MRI, and 25 (96.2%) by enhanced CT, indicating that the sensitivity of 3D-CEUS and enhanced CT was obviously higher than that of MRI (P < 0.001), without conspicuous difference between sensitivity of 3D-CEUS and enhanced CT (P > 0.05). Conclusion: As a new imaging examination method based on artificial intelligence, 3D-CEUS has a high sensitivity in patients with liver cancer who underwent RFA, which can effectively judge the recurrence after surgery and should be widely used in practice.

Nuciferine inhibits the progression of glioblastoma by suppressing the SOX2-AKT/STAT3-Slug signaling pathway.

BACKGROUND: Nuciferine (NF), extracted from the leaves of N. nucifera Gaertn, has been shown to exhibit anti-tumor and anti-viral pharmacological properties. It can also penetrate the blood brain barrier (BBB). However, the mechanism by which NF inhibits glioblastoma (GBM) progression is not well understood. We aimed to determine the anti-tumor effect of NF on GBM cell lines and clarify the potential molecular mechanism involved. METHODS: U87MG and U251 cell lines were used in vitro to assess the anti-tumor efficacy of NF. Cytotoxicity, viability, and proliferation were evaluated by MTT and colony formation assay. After Annexin V-FITC and PI staining, flow cytometry was performed to evaluate apoptosis and cell cycle changes in NF-treated GBM cells. Wound healing and Transwell assays were used to assess migration and invasion of GBM cells. Western blot analysis, immunofluorescence staining, immunohistochemistry, and bioinformatics were used to gain insights into the molecular mechanisms. Preclinical therapeutic efficacy was mainly estimated by ultrasound and MRI in xenograft nude mouse models. RESULTS: NF inhibited the proliferation, mobility, stemness, angiogenesis, and epithelial-to-mesenchymal transition (EMT) of GBM cells. Additionally, NF induced apoptosis and G2 cell cycle arrest. Slug expression was also decreased by NF via the AKT and STAT3 signaling pathways. Interestingly, we discovered that NF affected GBM cells partly by targeting SOX2, which may be upstream of the AKT and STAT3 pathways. Finally, NF led to significant tumor control in GBM xenograft models. CONCLUSIONS: NF inhibited the progression of GBM via the SOX2-AKT/STAT3-Slug signaling pathway. SOX2-targeting with NF may offer a novel therapeutic approach for GBM treatment.

The diffuse reduction in spleen density: an indicator of severe acute pancreatitis?

We observed that acute pancreatitis (AP) was associated with diffuse reduction in spleen density (DROSD) in some patients. Furthermore, the condition of these patients was more serious, and the potential relationship between DROSD and structural and functional injury of the spleen remained unclear. Therefore, we performed a preliminary exploration of these factors. We analysed pertinent clinical data for AP patients with normal spleen density (control group) and for those with DROSD (reduction group) at the First Affiliated Hospital of Harbin Medical University (June 2013-June 2015). We measured the immunoglobulin M (IgM) B-cells of the AP patients and examined pancreatic and splenic tissues from AP rats with optical microscopy and TEM. The reduction group had a higher acute physiology and chronic health evaluation II (APACHE II) score, a longer length of stay (LOS) and lower serum calcium than the control group. The levels of triglycerides (TG) and total cholesterol (TC) did not differ significantly between the two groups. The percentage of IgM memory B-cells was significantly lower in the DROSD group than in the control group. TEM revealed that the spleen T-lymphocytes were normal in AP rats, but pyroptotic and necrotic spleen B-cells were observed in the severe AP rats. In AP, DROSD was an independent indicator of more severe conditions. Furthermore, spleen B-lymphocytes showed obvious damage at the cellular level, and the immunological function of the spleen was down-regulated when AP was associated with DROSD.

Risk factors of infected pancreatic necrosis secondary to severe acute pancreatitis.

BACKGROUND: Severe acute pancreatitis (SAP) remains a clinical challenge with considerable morbidity and mortality. An early identification of infected pancreatic necrosis (IPN), a life-threatening evolution secondary to SAP, is obliged for a more preferable prognosis. Thus, the present study was conducted to identify the risk factors of IPN secondary to SAP. METHODS: The clinical data of patients with SAP were retrospectively analyzed. Univariate and multivariate logistic regression analyses were sequentially performed to assess the associations between the variables and the development of IPN secondary to SAP. A receiver operating characteristic (ROC) curve was created for each of the qualified independent risk factors. RESULTS: Of the 115 eligible patients, 39 (33.9%) progressed to IPN, and the overall in-hospital mortality was 11.3% (13/115). The early enteral nutrition (EEN) (P=0.0092, OR=0.264), maximum intra-abdominal pressure (IAP) (P=0.0398, OR=1.131) and maximum D-dimer level (P=0.0001, OR=1.006) in the first three consecutive days were independent risk factors associated with IPN secondary to SAP. The area under ROC curve (AUC) was 0.774 for the maximum D-dimer level in the first three consecutive days and the sensitivity was 90% and the specificity was 58% at a cut-off value of 933.5 µg/L; the AUC was 0.831 for the maximum IAP in the first three consecutive days and the sensitivity was 95% and specificity was 58% at a cut-off value of 13.5 mmHg. CONCLUSIONS: The present study suggested that the maximum D-dimer level and/or maximum IAP in the first three consecutive days after admission were risk factors of IPN secondary to SAP; an EEN might be helpful to prevent the progression of IPN secondary to SAP.

The apoptosis of peripheral blood lymphocytes promoted by hyperbaric oxygen treatment contributes to attenuate the severity of early stage acute pancreatitis in rats.

The aim of this study was to investigate the immunoregulatory effects of hyperbaric oxygen (HBO) via promoting the apoptosis of peripheral blood lymphocytes (PBLs) to attenuate the severity of early stage acute pancreatitis (AP) in rats. Additionally, the persistence of the HBO treatment effects was evaluated. One hundred and twenty male Wistar rats were randomized into four groups: sham, AP, AP + normobaric oxygen (NBO), and AP + HBO. Each group consisted of 30 rats. Four hours after the induction of AP, the 30 rats in the AP + NBO group were given normobaric oxygen treatment with 100 % oxygen at 1 atm for 90 min. The 30 rats in the AP + HBO group received 100 % oxygen at 2.5 atm for 90 min, with a compression/decompression time of 15 min. The 30 rats in the AP group remained untreated. At 6, 12, and 24 h after the induction of AP, surviving rats from each group were sacrificed, and the blood and tissue samples were collected for the following measurements: the partial pressure of oxygen (PaO2) and oxygen saturation (SaO2) of the arterial blood, the levels of serum amylase, lipase, interleukin-2 (IL-2), interferon-γ (IFN-γ), interleukin-10 (IL-10), hepatocyte growth factor (HGF), and reactive oxygen species (ROS), and the mitochondrial membrane potential (∆Ψm) of the PBLs. The expression levels of procaspase-3, caspase-3, procaspase-9, and caspase-9 were also evaluated in the PBLs. Additionally, the apoptosis of PBLs was assessed, and the pancreatic tissues were subjected to a histopathological analysis by pathological grading and scoring. The histopathology of the lung, liver, kidney, duodenum, and heart was also analyzed at 12 h after the induction of AP. Significant differences were found at 6 and 12 h after AP induction. The HBO treatment significantly elevated the PaO2 and SaO2 levels, and the ROS levels in the PBLs. Additionally, HBO downregulated the levels of amylase and lipase. The HBO treatment also reduced the ∆Ψm levels, upregulated the expression of caspase-3 and caspase-9, and increased the apoptosis rate of the PBLs. Moreover, the HBO treatment decreased the serum concentrations of IL-2, IFN-γ and HGF, and reduced the pathological scores of the pancreatic tissue. The histopathological changes of the lung, liver, kidney, duodenum, and heart were also improved. A significant elevation of IL-10 occurred only at the 12-h time point. However, no obvious differences were found at the 24-h time point. This study demonstrated that the HBO treatment can promote the apoptosis of PBLs via a mitochondrial-dependent pathway and inhibit the inflammatory response. These immunoregulatory effects may play an important therapeutic role in attenuating the severity of early stage AP. The repeated administration of HBO or the use of HBO in combination with other approaches may further improve outcomes.