Perioperative complication incidence and risk factors for retroperitoneal neuroblastoma in children: analysis of 571 patients.

BACKGROUND: Surgery plays an important role in the treatment of neuroblastoma. Perioperative complications may impact the course of neuroblastoma treatment. To date, comprehensive analyses of complications and risk factors have been lacking. METHODS: Patients with retroperitoneal neuroblastoma undergoing tumor resection were retrospectively analyzed between 2014 and 2021. The data collected included clinical characteristics, operative details, operative complications and postoperative outcomes. Risk factors for perioperative complications of retroperitoneal neuroblastoma were analyzed. RESULTS: A total of 571 patients were enrolled in this study. Perioperative complications were observed in 255 (44.7%) patients. Lymphatic leakage (28.4%), diarrhea (13.5%), and injury (vascular, nerve and organ; 7.5%) were the most frequent complications. There were three operation-related deaths (0.53%): massive hemorrhage (n = 1), biliary tract perforation (n = 1) and intestinal necrosis (n = 1). The presence of image-defined risk factors (IDRFs) [odds ratio (OR) = 2.09, P < 0.01], high stage of the International Neuroblastoma Risk Group staging system (INRGSS) (OR = 0.454, P = 0.04), retroperitoneal lymph node metastasis (OR = 2.433, P = 0.026), superior mesenteric artery encasement (OR = 3.346, P = 0.003), and inferior mesenteric artery encasement (OR = 2.218, P = 0.019) were identified as independent risk factors for perioperative complications. CONCLUSIONS: Despite the high incidence of perioperative complications, the associated mortality rate was quite low. Perioperative complications of retroperitoneal neuroblastoma were associated with IDRFs, INRGSS, retroperitoneal lymph node metastasis and vascular encasement. Patients with high-risk factors should receive more serious attention during surgery but should not discourage the determination to pursue total resection of neuroblastoma. Video Abstract (MP4 94289 KB).

Screening of xylene degrading bacteria and optimization of their degradation characteristics in heavily polluted areas.

Aiming at the problems of high xylene concentration and difficult removal in heavily polluted areas, high-efficient degrading bacteria of volatile organic compounds (VOCs) xylene in heavily polluted areas were selected and screened from sewage sludge, and their degradation characteristics were studied. The response surface methodology (RSM) optimized the optimal degradation conditions. The results showed that the screened degrading strain was identified as Klebsiella by the 16SrDNA technology and named H-16. During the start-up phase of the reactor, the removal rate of xylene by strain H-16 fluctuated, and it was stable above 71.3% for 150 min. At 40°C, the degradation rate is the highest, reaching 63.25%. With an increasing inoculum amount of strain H-16, the degradation rate of xylene gradually increased, and the degradation rate could reach 86.1% when the inoculation amount was 25%. A neutral environment was more conducive to the degradation and removal of xylene. Through the analysis of the model and RSM, the optimal conditions for the degradation of xylene by H-16 were obtained: 38.89°C, pH 6.94 and 18.07%. GC-MS results showed that the possible degradation pathway of xylene began with demethylation, formation of pentene diacid by benzene ring cleavage, and finally oxidation to generate CO2 and H2O.

Potential exploration of Fe3O4/biochar from sludge as the media of bioretention system and its comparison with conventional media.

The selection and configuration of soil media are a core issue of the bioretention system. A porous carbon material of Fe3O4/biochar (BSF) was prepared by adding pickling wastewater to modified sludge biochar, which could serve as a good adsorption performance and cheap media for bioretention system. Through the analytic hierarchy process (AHP), different media were evaluated according to their characteristics. By comparing the characteristics of BSF to bio-ceramic (BC), zeolite (ZE), and activated carbon (AC), it was found that BSF has a larger specific surface area and pore volume. The hydrological characteristics of the medium were also tested. The results show that BSF has better water-absorbing quality and hydraulic conductivity than the other three media, but the water-retention property of the medium seems to be inferior. BSF has stable adsorption performance for ammonia nitrogen (NH4+-N) and total phosphorus (TP) in rainwater. Its high adsorption capacity is maintained at 5-35°C, but it is very susceptible to pH factors. The adsorption process by BSF and other media conforms to pseudo-second-order kinetics and the Langmuir model in rainwater. In general, the performance of BSF is shown to be superior to BC, ZE, and AC, making it a potential medium for bioretention system.

PINK1 deficiency in gastric cancer compromises mitophagy, promotes the Warburg effect, and facilitates M2 polarization of macrophages.

Cancer cells are typically characterized by abnormal quality control of mitochondria, production of reactive oxygen species (ROS), dysregulation of the cell redox state, and the Warburg effect. Mutation or depletion of PTEN-induced kinase 1 (PINK1) or Parkin leads to mitophagy defects and accumulation of malfunctioning mitochondria, and is often detected in a variety of tumors. However, PINK1's role in the progression of gastric cancer (GC) remains unclear, with its main effect being on mitochondrial turnover, metabolic reprogramming, and tumor microenvironment (TME) alteration. To address these issues, we first assessed the expression levels of PINK1, mitophagy-associated molecules, ROS, HIF-1α, glycolysis-associated genes, and macrophage signatures in GC tissues and matched tumor-adjacent normal samples. In addition, GC cell lines (AGS and MKN-45) and xenograft mouse models were used to determine the mechanism by which PINK1 regulates mitophagy, metabolic reprogramming, tumor-associated macrophage (TAM) polarization, and GC progression. We found that PINK1 loss correlated with advanced stage GC and poorer overall survival. GC tissues with lower PINK1 levels showed compromised mitophagy signaling and enhanced glycolytic enzyme expression. In vitro experiments demonstrated that PINK1 deficiency promoted GC cell proliferation and migration through the inhibition of mitophagy, production of mitochondrial ROS, stabilization of HIF-1α, and facilitation of the Warburg effect under both normoxic and hypoxic conditions. Moreover, PINK1 deficiency in GC cells promoted TAM polarization toward the M2-like phenotype. Reintroduction of PINK1 or inhibition of HIF-1α effectively repressed PINK1 deficiency-mediated effects on GC cell growth, metabolic shift, and TAM polarization. Thus, mitophagy defects caused by PINK1 loss conferred a metabolic switch through accumulation of mtROS and stabilization of HIF-1α, thereby facilitating the M2 polarization of TAM to remodel an immunosuppressive microenvironment in GC. Our results clarify the mechanism between PINK1 and GC progression and may provide a novel strategy for the treatment of GC.

Retraction notice to "PINK1 deficiency in gastric cancer compromises mitophagy, promotes the Warburg effect, and facilitates M2 polarization of macrophages" [Cancer Lett. 529 (2022) 19-36].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief and authors. Following the publication of the above article, the Editor was notified by a concerned reader that the authors supplied duplicated images. Specifically, that in Fig. 5 A, both FACS panels are identical and in Fig 5E, two different proteins (HK2 and PDK1) have the same western blot. After checking the data in relation with Fig. 5A and E, the authors have confirmed that the two pictures indeed have the problems of duplication. The authors reported that this problem came from the authors' unintentional behavior, which may be due to a copy and paste error in the manner of image processing. The authors sincerely apologize for the inconvenience caused to our Editors and readers. Due to this duplication error, the authors and Editor have made the decision to retract this paper.

Bioremediation of a saline-alkali soil polluted with Zn using ryegrass associated with Fusariumincarnatum.

Biotechnological strategies have become effective in the remediation of polluted soils as they are cost-effective and do not present a risk of secondary pollution. However, using a single bioremediation technique (microorganism or plant) is not suitable for achieving a high remediation rate of polluted saline-alkali soils with heavy metals. Therefore, the present study aims to assess the effects and mechanisms of combined ryegrass and Fusarium incarnatum on the zinc (Zn)-polluted saline-alkali soil over 45 days. According to the obtained results, the combined Fusarium incarnatum-ryegrass showed the highest remediation rate of 49.35% after 45 days, resulting in a significantly lower soil Zn concentration than that observed in the control group. In addition, the inoculation of Fusarium incarnatum showed a positive effect on the soil EPS secretion. The soil protein contents ranged from 0.035 to 0.055 mg/kg, while the soil polysaccharide contents increased from 0.25 to 0.61 mg/g. The soil microbial flora and ryegrass showed resistance to saline and alkaline stresses through the secretion of extracellular polysaccharides. The three-dimensional fluorescence spectrum (3D-EEM) confirmed that EPS in the soil was mainly a fulvic acid-like substance. The fluorescein diacetate (FDA) hydrolase activity in the saline-alkali soil was first increased due to the effect of Fusarium incarnatum and then decreased to a minimum value of 96 µg/(g·h). In addition, the Fusarium incarnatum inoculation improved the diversity and richness of soil fungi. Although the Fusarium incarnatum inoculation had a slight effect on the germination of ryegrass, it increased the biomass and enrichment coefficient. The results revealed a translocation factor (TF) value of 0.316 at 45 days after ryegrass sowing, showing significant enrichment of the soil Zn heavy metal zinc in the ryegrass roots.

Diagnosis and Treatment of Retroperitoneal Infection.

Background: Retroperitoneal infection is a persistent and widespread infectious disease that is difficult to treat. It is usually caused by secondary complications such as inflammation, damage, or perforation of adjacent organs in the retroperitoneal space. Pathogenic bacteria invade the retroperitoneal space through retroperitoneal and interstitial organs, peripheral tissue, and the blood. As a result, infections mostly arise from severe acute pancreatitis, acute colonic diverticulitis, inflammatory bowel disease, kidney abscess, and biliary tract injury. Initially manifested by the presence of lumbago, this disease spreads easily, is persistent, and is often misdiagnosed. Methods: Review and synthesis of pertinent literature and guidelines pertaining to abdominal infection and retroperitoneal infection. Results: Recent data indicate that mortality rates associated with retroperitoneal infection have been increasing annually. Early diagnosis and treatment have been shown to improve the prognosis. In the early stage, infection is insidious and lacks typical symptoms, and is primarily diagnosed with computed tomography (CT). Strategies that control the source of infection, rational use of antibiotic agents, and nutritional interventions are the primary approaches to treat the infections. Emergence of minimally invasive drainage technologies, including the ultrasound/CT-guided puncture and drainage, percutaneous nephroscope puncture and drainage, and drainage using a catheter through an abdominal puncture device (trocar) have shortened the treatment cycle and disease burden. However, current diagnosis and treatment for retroperitoneal infection are not sufficiently effective because some patients do not show typical clinical manifestations. Moreover, sensitivity and specificity of available auxiliary examination methods are not supported by sufficient evidence-based medical research. Additionally, there are no uniform standards on the timing of surgical intervention and treatment options. Therefore, we summarized the progresses on current diagnosis and treatment approaches for retroperitoneal infection.

Long noncoding RNA DLGAP1-AS2 facilitates Wnt1 transcription through physically interacting with Six3 and drives the malignancy of gastric cancer.

The long noncoding RNA (lncRNA) DLGAP1-AS2 has recently been characterized as an oncogenic lncRNA in several cancers. However, its biological roles and clinical significance in gastric cancer (GC) remains barely understood. In this study, we performed a systematic analysis of DLGAP1-AS2 expression with data from the TCGA and GEO database as well as our clinic GC samples. In agreement with previous studies, our findings demonstrated that DLGAP1-AS2 was significantly up-regulated in GC and its high expression was associated with poor prognosis, suggesting that DLGAP1-AS2 might be a putative oncogenic lncRNA of GC. Loss of DLGAP1-AS2 restricted cell proliferation, migration, and invasion in GC cell lines. Mechanically, Wnt1 was identified as the downstream target of DLGAP1-AS2 by using bioinformatics analysis coupled with qPCR and Western blot assays. Furthermore, DLGAP1-AS2 was found to directly interact with the transcriptional repressor Six3, and this interaction hampered Six3 binding to the promoter regions of the Wnt1 gene, thereby leading to transcriptional activation of Wnt1. Consequently, GC cells lacking DLGAP1-AS2 showed a decreased Wnt1 expression and weakened Wnt/ß-catenin signaling. Further, Six3 silencing could reverse the above effects, highlighting a pivotal role of Six3 in the DLGAP1-AS2-mediated activation of Wnt/ß-catenin signaling. Either genetic (Wnt1 knockdown) or pharmacological (LF3) inhibition of Wnt/ß-catenin signaling could effectively abolish the activation of Wnt/ß-catenin signaling by Six3 depletion, thereby preventing GC cell malignant transformation. Taken together, our results suggest that DLGAP1-AS2 functions as an oncogenic factor by directly interacting with Six3 to relieve its suppression on Wnt1 expression, thereby driving the malignancy of GC. DLGAP1-AS2/Six3/Wnt1/ß-catenin signaling axis might serve as a promising diagnostic and therapeutic target for GC.

PINK1-mediated mitophagy protects against hepatic ischemia/reperfusion injury by restraining NLRP3 inflammasome activation.

Activation of nucleotide-binding domain leucine-rich repeat containing family pyrin domain containing 3 (NLRP3) inflammasome in Kupffer cells (KCs) contributes significantly to hepatic ischemia/reperfusion (I/R) injury, while the mechanism of how NLRP3 inflammasome is regulated remains less well defined. Recent evidence has showed that mitophagy acts as a central player for maintaining mitochondrial homeostatis through elimination of damaged mitochondria, leading to the prevention of hyperinflammation triggered by NLRP3 activation. In this study, we aimed at investigating the potential role of PTEN-induced kinase 1 (PINK1)-mediated mitophagy in hepatic I/R injury. C57BL/6 mice subjected to partial warm hepatic I/R or primary KCs exposed to anoxia/reoxygenation (A/R) was used as in vivo or in vitro model, respectively. Mitophagy was measured by protein levels of PINK1, Parkin, LC3B-II, TOMM20 and p62. NLRP3, caspase-1 and IL-1ß at mRNA and/or protein levels were used as indicators of inflammasome activation. Our results demonstrated remarkable hepatic inflammation and NLRP3 inflammasome activation during hepatic I/R, along with increased PINK1-mediated mitophagy. Notably, overexpression of PINK1 in vivo attenuated hepatic I/R injury, ROS production, NLRP3 activation and hepatic inflammation. In parallel, A/R challenge in vitro also triggered NLRP3 activation in KCs accompanied by increase in mitophagy. Enhanced mitophagy mediated by PINK1 overexpression further inhibited NLRP3 activation and reversed the KC-mediated inflammatory injury to hepatocytes. Kinase-dead mutation of PINK1 completely abolished the above protective effects by PINK1. Blocking of mitophagy/autophagy by silencing of PINK1/Parkin, ATG5, NDP52 or OPTN showed the totally opposite effects, respectively. Treatment with different autophagic inhibitors also consistently reversed the PINK1-mediated effects, suggesting that an intact PINK1-mediated mitophagy signaling was crucial for ablation of NLRP3 signaling in the presence of A/R. Together, these results support a critical role of PINK1-mediated mitophagy in mitochondrial quality control for KC activation and function in hepatic I/R.

Long noncoding RNA ARHGAP27P1 inhibits gastric cancer cell proliferation and cell cycle progression through epigenetically regulating p15 and p16.

Long noncoding RNAs (lncRNAs) have emerged as important regulators in the development and progression of gastric cancer (GC). ARHGAP27P1 is a pseudogene-derived lncRNA, and it has been found to be associated with GC in our preliminary study, but this association has not been studied further. Herein, we confirmed that ARHGAP27P1 was significantly downregulated in GC tissues, plasma and cells. Low expression of ARHGAP27P1 was closely associated with advanced TNM stage, increased invasion depth and lymphatic metastasis. Low ARHGAP27P1 expression also predicted a poor prognosis in GC patients. Functionally, overexpression of ARHGAP27P1 inhibited proliferation, invasion, and migration in GC cells, while silencing of ARHGAP27P1 showed the opposite effects. Mechanistic investigations showed that ARHGAP27P1 had a key role in G0/G1 arrest. We further demonstrated that ARHGAP27P1 was associated with Jumonji-domain containing 3 (JMJD3) and that this association was required for the demethylation of H3K27me3, thereby epigenetically activating expression of p15, p16 and p57. Moreover, knockdown of JMJD3, p15, or p16 consistently reversed the inhibitory effects of ARHGAP27P1 in cell proliferation and cell cycle progression. Taken together, these results suggest that lncRNA ARHGAP27P1, as a novel cell cycle regulator, may serve as a potential target for GC prevention and treatment in human GC.