Numerical Analysis of the Airflow Field and Experiments of Fiber Motion for Solution Blowing.

Solution blowing is a rapidly developing technology for the rapid and large-scale preparation of nanofibers, driven by its advantages, such as wide adaptability to raw materials, simple and safe operation, and ease of scalable production. Most of the research related to solution blowing mainly focuses on the fiber spinning and forming principle, fiber structure and properties, and the development of new materials. Limited studies have focused on the airflow field and fiber motion in solution blowing. In this paper, nine nozzles for solution blowing with varying geometrical parameters were designed by adjusting the outer nozzle diameter, inner nozzle outstretched distance, and inner nozzle diameter. The centerline airflow velocity, turbulence intensity, and velocity distribution of the solution blowing were analyzed using the numerical simulation method. The results showed that the outer nozzle diameter had the greatest influence on the air velocity and turbulence intensity. The airflow velocity increased and the turbulence intensity decreased with the increase of the outer nozzle diameter. The inner nozzle outstretched distance only affected the airflow convergence point and had less effect on the airflow velocity and turbulence intensity. The captured trajectory of the polymer jet initially shows a straight or slightly curved development that eventually diverges from the airflow field. With an increasing distance, dispersed fibers exhibit instability, including loop formation, bonding, and separation. The experimental observation of fiber morphology in the solution-blowing web further verified the instability during the fiber movement.

Indoxyl sulphate-TNFα axis mediates uremic encephalopathy in rodent acute kidney injury.

Acute kidney injury (AKI) is often accompanied by uremic encephalopathy resulting from accumulation of uremic toxins in brain possibly due to impaired blood-brain barrier (BBB) function. Anionic uremic toxins are substrates or inhibitors of organic anionic transporters (OATs). In this study we investigated the CNS behaviors and expression/function of BBB OAT3 in AKI rats and mice, which received intraperitoneal injection of cisplatin 8 and 20 mg/kg, respectively. We showed that cisplatin treatment significantly inhibited the expressions of OAT3, synaptophysin and microtubule-associated protein 2 (MAP2), impaired locomotor and exploration activities, and increased accumulation of uremic toxins in the brain of AKI rats and mice. In vitro studies showed that uremic toxins neither alter OAT3 expression in human cerebral microvascular endothelial cells, nor synaptophysin and MAP2 expressions in human neuroblastoma (SH-SY5Y) cells. In contrast, tumour necrosis factor alpha (TNFα) and the conditioned medium (CM) from RAW264.7 cells treated with indoxyl sulfate (IS) significantly impaired OAT3 expression. TNFα and CM from IS-treated BV-2 cells also inhibited synaptophysin and MAP2 expressions in SH-SY5Y cells. The alterations caused by TNFα and CMs in vitro, and by AKI and TNFα in vivo were abolished by infliximab, a monoclonal antibody designed to intercept and neutralize TNFα, suggesting that AKI impaired the expressions of OAT3, synaptophysin and MAP2 in the brain via IS-induced TNFα release from macrophages or microglia (termed as IS-TNFα axis). Treatment of mice with TNFα (0.5 mg·kg-1·d-1, i.p. for 3 days) significantly increased p-p65 expression and reduced the expressions of Nrf2 and HO-1. Inhibiting NF-κB pathway, silencing p65, or activating Nrf2 and HO-1 obviously attenuated TNFα-induced downregulation of OAT3, synaptophysin and MAP2 expressions. Significantly increased p-p65 and decreased Nrf2 and HO-1 protein levels were also detected in brain of AKI mice and rats. We conclude that AKI inhibits the expressions of OAT3, synaptophysin and MAP2 due to IS-induced TNFα release from macrophages or microglia. TNFα impairs the expressions of OAT3, synaptophysin and MAP2 partly via activating NF-κB pathway and inhibiting Nrf2-HO-1 pathway.

Experimental Study of the Airflow Field and Fiber Motion in the Melt-Blowing Process.

The melt-blowing process involves high velocity airflow and fiber motion, which have a significant effect on fiber attenuation. In this paper, the three-dimensional airflow field for a melt-blowing slot die was measured using the hot-wire anemometry in an experiment. The fiber motion was captured online using a high-speed camera. The characteristics of the airflow distribution and fiber motion were analyzed. The results show that the melt-blowing airflow field is asymmetrically distributed. The centerline air velocity is higher than that around it and decays quickly. The maximum airflow velocity exists near the die face, in the range of 130-160 m/s. In the region of -0.3 cm < y < 0.3 cm and 0 < z < 2 cm, the airflow has a high velocity (>100 m/s). As the distance of z reaches 5 cm and 7 cm, the maximum airflow velocity reduces to 70 m/s. The amplitude of fibers is calculated, and it increases with the increase in air dispersion area which has a significant influence on fiber attenuation. At z = 1.5 cm, 2.5 cm, 4 cm, and 5.5 cm, the average fiber amplitudes are 1.05 mm, 1.71 mm, 2.83 mm, and 3.97 mm, respectively. In the vicinity of the die, the fibers move vertically downward as straight segments. With the increase in distance from the spinneret, the fiber appears to bend significantly and forms a fiber loop. The fiber loop morphology affects the velocity of the fiber movement, causing crossover, folding, and bonding of the moving fiber. The study investigated the interaction between the fiber and airflow fields. It indicates that the airflow velocity, velocity difference, and dispersion area can affect the motion of fiber which plays an important role in fiber attenuation during the melt-blowing process.

Bile duct ligation elevates 5-HT levels in cerebral cortex of rats partly due to impairment of brain UGT1A6 expression and activity via ammonia accumulation.

Hepatic encephalopathy (HE) is often associated with endogenous serotonin (5-HT) disorders. However, the reason for elevated brain 5-HT levels due to liver failure remains unclear. This study aimed to investigate the mechanism by which liver failure increases brain 5-HT levels and the role in behavioral abnormalities in HE. Using bile duct ligation (BDL) rats as a HE model, we verified the elevated 5-HT levels in the cortex but not in the hippocampus and striatum, and found that this cortical 5-HT overload may be caused by BDL-mediated inhibition of UDP-glucuronosyltransferase 1A6 (UGT1A6) expression and activity in the cortex. The intraventricular injection of the UGT1A6 inhibitor diclofenac into rats demonstrated that the inhibition of brain UGT1A6 activity significantly increased cerebral 5-HT levels and induced HE-like behaviors. Co-immunofluorescence experiments demonstrated that UGT1A6 is primarily expressed in astrocytes. In vitro studies confirmed that NH4Cl activates the ROS-ERK pathway to downregulate UGT1A6 activity and expression in U251 cells, which can be reversed by the oxidative stress antagonist N-acetyl-l-cysteine and the ERK inhibitor U0126. Silencing Hepatocyte Nuclear Factor 4α (HNF4α) suppressed UGT1A6 expression whilst overexpressing HNF4α increased Ugt1a6 promotor activity. Meanwhile, both NH4Cl and the ERK activator TBHQ downregulated HNF4α and UGT1A6 expression. In the cortex of hyperammonemic rats, we also found activation of the ROS-ERK pathway, decreases in HNF4α and UGT1A6 expression, and increases in brain 5-HT content. These results prove that the ammonia-mediated ROS-ERK pathway activation inhibits HNF4α expression to downregulate UGT1A6 expression and activity, thereby increasing cerebral 5-HT content and inducing manic-like HE symptoms. This is the first study to reveal the mechanism of elevated cortical 5-HT concentration in a state of liver failure and elucidate its association with manic-like behaviors in HE.

Detection of CSTF2 by nano fluorescent probe and its correlation with malignant biological characteristics in liver cancer.

To develop a novel nano DNA fluorescent probe for in situ detection of CSTF2 in liver cancer (LC) and study its correlation with the development of LC, we developed nano-TiO2-DNA fluorescent probe which can bind with CSTF2 in LC samples with high efficiency. The detection process of CSTF2 did not involve the use PCR technology, and the concentration of CSTF2 can be directly observed by fluorescence intensity. This probe exhibited excellent physicochemical properties in ethyl alcohol at -20°C and could directly and selectively permeate into Hep-3B cells. By using CSTF2 Nano-TiO2-DNA probe, we found that the CSTF2 level increased greatly in LC tissue and cells, and high CSTF2 level was closely associated with high levels of tumor markers and poor prognosis in LC patients. After transfection, CSTF2 was overexpressed or silenced in Hep-3B cells, and we find that high CSTF2 level effectively increased the activity and invasion of Hep-3B cells and reduced their apoptosis. Furthermore, high CSTF2 level significantly increased the tumor volume and weight in mice models by activating PI3K/AKT/mTOR signal pathway. Therefore, CSTF2 can serve as an early biomarker of LC and a novel potential target for its treatment.

Thioacetamide-Induced Acute Liver Injury Increases Metformin Plasma Exposure by Downregulating Renal OCT2 and MATE1 Expression and Function.

Metformin plasma exposure is increased in rats with thioacetamide (TAA)-induced liver failure. The absorption, distribution, and excretion process of metformin is mainly mediated by organic cation transporters (OCTs) and multidrug and toxin extrusion transporters (MATEs). To investigate the mechanisms of the increase in TAA-induced metformin plasma exposure, we employed intestinal perfusion and urinary excretion assays to evaluate the changes in the absorption and excretion of metformin and used Western blotting to investigate the metformin-related transport proteins' expression changes and mechanisms. The results showed that neither intestinal OCT2 expression nor metformin intestinal absorption were significantly altered by TAA-induced liver failure, while significantly decreased expression and function of renal OCT2 and MATE1 as well as impaired metformin excretion were observed in TAA rats. HK-2 cells were used as an in vitro model to explore the mechanism of liver-failure-mediated downregulation in renal OCT2 and MATE1. The results demonstrated that among numerous abnormal substances that changed in acute liver failure, elevated estrogen levels and tumor necrosis factor-α were the main factors mediating the downregulation of OCT2 and MATE1. In conclusion, this study highlights the downregulation of renal OCT2 and MATE1 in liver injury and its regulatory mechanism and reveals its roles in the increase in TAA-mediated metformin plasma exposure.

Unveiling the functional paradigm of exosome-derived long non-coding RNAs (lncRNAs) in cancer: based on a narrative review and systematic review.

BACKGROUND AND PURPOSE: The intricate mechanisms underlying intercellular communication within the tumor microenvironment remain largely elusive. Recently, attention has shifted towards exploring the intercellular signaling mediated by exosomal long non-coding RNAs (lncRNAs) within this context. This comprehensive systematic review aims to elucidate the functional paradigm of exosome-derived lncRNAs in cancer. MATERIALS AND METHODS: The review provides a comprehensive narrative of lncRNA definition, characteristics, as well as the formation, sorting, and uptake processes of exosome-derived lncRNAs. Additionally, it describes comprehensive technology for exosome research and nucleic acid drug loading. This review further systematically examines the cellular origins, functional roles, and underlying mechanisms of exosome-derived lncRNAs in recipient cells within the cancer setting. RESULTS: The functional paradigm of exosome-derived lncRNAs in cancer mainly depends on the source cells and sorting mechanism of exosomal lncRNAs, the recipient cells and uptake mechanisms of exosomal lncRNAs, and the specific molecular mechanisms of lncRNAs in recipient cells. The source cells of exosomal lncRNAs mainly involved in the current review included tumor cells, cancer stem cells, normal cells, macrophages, and cancer-associated fibroblasts. CONCLUSION: This synthesis of knowledge offers valuable insights for accurately identifying exosomal lncRNAs with potential as tumor biomarkers. Moreover, it aids in the selection of appropriate targeting strategies and preclinical models, thereby facilitating the clinical translation of exosomal lncRNAs as promising therapeutic targets against cancer. Through a comprehensive understanding of the functional role of exosome-derived lncRNAs in cancer, this review paves the way for advancements in personalized medicine and improved treatment outcomes.

Basic demographic characteristics and prevalence of comorbidities in acute mesenteric ischemia: a systematic review and proportional meta-analysis.

PURPOSE: The aim of this systematic review and meta-analysis was to examine and assess the basic demographic characteristics and prevalence of comorbidities in acute mesenteric ischemia (AMI) and its various subtypes. PATIENTS AND METHODS: A literature search was conducted by using the databases PubMed, EMBASE, and Google Scholar (to June 1, 2022). Random-effects or fixed-effects models were selected to pool means and proportions and their corresponding 95% confidence intervals (CI), based on heterogeneity between studies. The results of meta-analyses for basic demographic characteristics and prevalence (proportions) of each specific comorbidities of acute mesenteric ischemia (AMI) and its various subtypes were described. RESULTS: Ninety-nine studies were included in the meta-analysis, including 17,103 patients with AMI. Furthermore, 7941 patients with subclass diagnoses of AMI were identified, including 3,239 patients with arterial occlusive mesenteric ischemia (AOMI), 2,977 patients with nonocclusive mesenteric ischemia (NOMI), and 1,725 patients with mesenteric venous thrombosis (MVT). As a surgical emergency, AMI is associated with older patients and a high likelihood of multisystem comorbidities. Comorbidities of AMI involved multiple systemic diseases, including cardiovascular disease, endocrine and metabolic diseases, kidney diseases, digestive diseases, respiratory diseases, cerebrovascular diseases, vascular diseases, and cancer. CONCLUSION: The basic demographic characteristics and the prevalence of comorbidities of different subtypes of AMI are different. The management of comorbidities should be an essential part of improving the prognosis of AMI patients and may contribute to precise prevention of AMI.

Comprehensive landscape and future perspectives of long noncoding RNAs (lncRNAs) in colorectal cancer (CRC): Based on a bibliometric analysis.

This review aimed to use bibliometric analysis to sort out, analyze and summarize the knowledge foundation and hot topics in the field of long noncoding RNAs (lncRNAs) in colorectal cancer (CRC), and point out future trends to inspire related research and innovation. We used CiteSpace to analyze publication outputs, countries, institutions, authors, journals, references, and keywords. Knowledge foundations, hotspots, and future trends were then depicted. The overall research showed the trend of biomedical-oriented multidisciplinary. Much evidence indicates that lncRNA plays the role of oncogene or tumor suppressor in the occurrence and development of CRC. Besides, many lncRNAs have multiple mechanisms. lncRNAs and metastasis of CRC, lncRNAs and drug resistance of CRC, and the clinical application of lncRNAs in CRC are current research hotspots. Through insight into the development trend of lncRNAs in CRC, this study will help researchers extract hidden valuable information for further research.

A glimpse of research cores and frontiers on the relationship between long noncoding RNAs (lncRNAs) and colorectal cancer (CRC) using the VOSviewer tool.

As lncRNAs are essential participants in colorectal carcinogenesis. This study aimed to use the VOSviewer tool to access the research cores and frontiers on the relationship between lncRNAs and CRC. Our findings showed that the mechanism of lncRNA in the occurrence and development of CRC was the core theme of the field. (1) Immunotherapy and immune microenvironment of CRC and lncRNAs, (2) CRC and lncRNAs in exosomes and (3) CRC and lncRNA-targeted therapy might represent three research frontiers. A comprehensive understanding of their existing mechanisms and the search for new regulatory paradigms are the core topics of future research. This knowledge will also help us select appropriate targeting methods and select appropriate preclinical models to promote clinical translation and ultimately achieve precise treatment of CRC.

Gut Microbiota Dysbiosis in the Development and Progression of Gastric Cancer.

Objectives: This study aims to explore gut microbiota dysbiosis in the histological stages of gastric cancer (GC). Methods: Feces samples and clinical characteristics were collected from patients with different stages of GC, including 15 superficial gastritis (SG), 13 atrophic gastritis (AG), 8 gastric mucosal atypical hyperplasia (GMAH), and 15 advanced GC cases. The diversity and composition of gut microbiota among the four groups were determined by sequencing the V4 region of bacterial 16S rRNA genes. Results: Reduced gut microbial alpha diversity and altered dissimilarity of the microbial community structure were found among the four groups. In addition, 18 species, 6 species, 6 species, and 16 species of bacteria were enriched in the SG, AG, GMAH, and GC groups, respectively, using the linear discriminant analysis (LDA) effect size (LEfSe) analyses. Besides, we found that two new genera, Scardovia and Halomonas, are associated with GC and the metabolic pathways of Genetic information processing and Circulatory System were more abundant in the GC group compared with noncancer groups. Conclusions: We identified differences in microbial compositional changes across stages of GC. Six genera and two metabolic pathways were more abundant in the GC group than noncancer groups, suggesting that these findings may contribute to the therapy strategies in GC in the near feature.

Green Innovation, Corporate Environmental Ethics, and Competitive Advantages of Chinese Automobile Industry During COVID-19: Corporate Environmental Management as Moderator.

Objective: The main purpose of this study is to investigate the impact of green product and process innovation on the competitive advantages of the Chinese automobile industry during coronavirus disease 2019 (COVID-19). This study also examined the mediating role of corporate environmental ethics (CEE) and the moderating role of corporate environmental management in the relationship between the green product and process innovation on the competitive advantages of the Chinese automobile industry during COVID-19. Methods: This study used a quantitative approach of research with the cross-sectional method for the collection of data. This study also used purposive sampling for the collection of data from the production managers of the automobile industry of China. The structural equation modeling-partial least squares (SEM-PLS) is used to analyze the data. Results: The results of direct effects indicated that green product innovation has a significant and positive effect on the corporate advantages (ß = 0.294, t = 2.868) and green process innovation also has a significant and positive effect on the corporate advantages (ß = 0.350, t = 3.276). Moreover, green product innovation has also a significant effect on corporate advantages (ß = 0.334, t = 4.258) and green product innovation has also a significant effect on corporate advantages (ß = 0.269, t = 3.202). Significance: The research in this domain about the antecedents of green innovation is still minimal in the previous literature. One of the antecedents of the green innovation, corporate environmental ethics is discussed in this study; thus, it provides the understanding of green innovation as the mediator which would mediate the relationship between corporate environmental ethics and competitive advantage in the auto manufacturing industry of China. Novelty: This study is among very few to examine the relationship between green innovation, corporate environmental ethics, corporate environmental management, and competitive advantages of the Chinese automobile industry during COVID-19.

A two-stage reconstruction method for complex networked system with hidden nodes.

Reconstructing the interacting topology from measurable data is fundamental to understanding, controlling, and predicting the collective dynamics of complex networked systems. Many methods have been proposed to address the basic inverse problem and have achieved satisfactory performance. However, a significant challenge arises when we attempt to decode the underlying structure in the presence of inaccessible nodes due to the partial loss of information. For the purpose of improving the accuracy of network reconstruction with hidden nodes, we developed a robust two-stage network reconstruction method for complex networks with hidden nodes from a small amount of observed time series data. Specifically, the proposed method takes full advantage of the natural sparsity of complex networks and the potential symmetry constraints in dynamic interactions. With robust reconstruction, we can not only locate the position of hidden nodes but also precisely recover the overall network structure on the basis of compensated nodal information. Extensive experiments are conducted to validate the effectiveness of the proposed method and superiority compared with ordinary methods. To some extent, this work sheds light on addressing the inverse problem, of which the system lacks complete exploration in the network science community.

The Mechanism of Long Non-coding RNA in Cancer Radioresistance/Radiosensitivity: A Systematic Review.

Background and purpose: Radioresistance remains a significant challenge in tumor therapy. This systematic review aims to demonstrate the role of long non-coding RNA (lncRNA) in cancer radioresistance/radiosensitivity. Material and methods: The electronic databases Pubmed, Embase, and Google Scholar were searched from January 2000 to December 2021 to identify studies addressing the mechanisms of lncRNAs in tumor radioresistance/sensitivity, each of which required both in vivo and in vitro experiments. Results: Among the 87 studies identified, lncRNAs were implicated in tumor radioresistance/sensitivity mainly in three paradigms. 1) lncRNAs act on microRNA (miRNA) by means of a sponge, and their downstream signals include some specific molecular biological processes (DNA repair and chromosome stabilization, mRNA or protein stabilization, cell cycle and proliferation, apoptosis-related pathways, autophagy-related pathways, epithelial-mesenchymal transition (EMT), cellular energy metabolism) and some signaling mediators (transcription factors, kinases, some important signal transduction pathways) that regulate various biological processes. 2) lncRNAs directly interact with proteins, affecting the cell cycle and autophagy to contribute to tumor radioresistance. 3) lncRNAs act like transcription factors to initiate downstream signaling pathways and participate in tumor radioresistance. Conclusion: lncRNAs are important regulators involved in tumor radioresistance\sensitivity. Different lncRNAs may participate in the radioresistance with the same regulatory paradigm, and the same lncRNAs may also participate in the radioresistance in different ways. Future research should focus more on comprehensively characterizing the mechanisms of lncRNAs in tumor radioresistance to help us identify corresponding novel biomarkers and develop new lncRNA-based methods to improve radioresistance.

Reconstruction of Tree Network via Evolutionary Game Data Analysis.

As one of the most effective technologies for network reconstruction, compressive sensing can recover signals from a small amount of observed data through sparse search or greedy algorithms in the assumption that the unknown signal is sufficiently sparse on a specific basis. However, there often occurs loss of precision even failure in the process of reconstruction without enough prior information. Therefore, the purpose of this article is to solve the problem of low reconstruction accuracy by mining implicit structural information in the network. Specifically, we propose a novel and efficient algorithm (MCM_TRA) for reconstructing the structure of the K -forked tree network. Based on evolutionary game dynamics, the modified clustering method (MCM) classifies all nodes into two sets, then a two-stage reconstruction algorithm (TRA) is illustrated to recover the node signals in different sets. The experimental results demonstrate that the MCM_TRA enhances the reconstruction accuracy prominently than previous algorithms. Moreover, extensive sensitivity analysis shows that the reconstruction effect can be promoted for a broad range of parameters, which further indicates the superiority of the proposed method.

Inhibition of SUMO2/3 antagonizes isoflurane-induced cancer-promoting effect in hepatocellular carcinoma Hep3B cells.

Surgery for patients with complicated liver cancer often results in a long exposure to anesthesia with an increase in side effects. Continued long-term exposure to isoflurane may promote liver cancer progression. Small ubiquitin-like modifier (SUMO) 2 and 3, also known as SUMO2/3, conjugates to substrate proteins when cells undergo acute stress. However, whether or not SUMO2/3 is involved in isoflurane-mediated liver cancer progression is unknown. In the present study, hepatocellular carcinoma (HCC) cells were exposed to 2% isoflurane for 12 h, followed by 36 h of drug withdrawal, and the formation of SUMO2/3 conjugates and cancer behavioral characteristics were studied. The results demonstrated that the formation of SUMO2/3 conjugates was significantly increased following HCC cells being exposed to isoflurane for 0.5 h, and continued to increase for 48 h, even after the drug had been withdrawn. Furthermore, isoflurane-exposed HCC cells exhibited increased proliferation and invasion activity during the subsequent observation period. SUMO specific protease 3 (SENP3), which inhibits the binding of SUMO2/3 to its target proteins, was overexpressed and it was discovered that isoflurane-induced SUMOylation was significantly inhibited, and accordingly, the proliferation and invasion abilities of HCC cells were decreased to a certain extent. These findings indicated that SUMO2/3 is involved in the progression of HCC cells, at least in the Hep3B cell line, induced by the anesthetic isoflurane, and that inhibition of SUMO2/3 may antagonize the response. These results provided a novel target for decreasing the adverse reactions occurring in patients with HCC during anesthesia, particularly those who are exposed to isoflurane for long periods of time.

A Comprehensive Way to Access Hospital Death Prediction Model for Acute Mesenteric Ischemia: A Combination of Traditional Statistics and Machine Learning.

PURPOSE: This study aimed to use traditional statistics and machine learning to develop and validate prediction models for predicting hospital death in patients with AMI and compare these models' performance. PATIENTS AND METHODS: Data were retrieved from the Medical Information Mart for Intensive Care (MIMIC III) electronic clinical database. A total of 338 eligible AMI patients were divided into a training cohort (n = 238) and a validation cohort (n = 100), and all patients were divided into survival groups and nonsurvival groups according to patients' hospital outcomes. The performance of the traditional statistics prediction model and the optimal machine learning prediction model was evaluated and compared with respect to discrimination, calibration, and clinical utility in the validation cohort. RESULTS: Univariate and multivariate logistic regression analyses identified the following independent risk factors associated with hospital death for AMI in the training cohort, including diastolic blood pressure, blood lactate, blood creatinine, age, blood pH, and red blood cell distribution width. Both the nomogram (AUC = 77.0%, 67.9-86.1%) and optimal machine learning model (AUC = 82.9%, 74.9-91.0%) achieved good discrimination and calibration in the validation cohort. Decision curves analysis showed that the optimal machine learning model has a greater net benefit than that of nomogram in this study. CONCLUSION: The nomogram achieved a concise and relatively accurate prediction of hospital death in patients with AMI, the machine learning model also has good discrimination and seems to have better clinical utility. Traditional statistics may help infer the relationship between risk factors and hospital death, while machine learning may contribute to a more accurate prediction. Traditional statistics and machine learning are complementary in developing the prediction model for hospital death of AMI. Therefore, a combination of nomogram-machine learning (Nomo-ML) predictive model may improve care and help clinicians make AMI management-related decisions.

Clinical Features and Factors Affecting Postoperative Mortality for Obstructive Acute Mesenteric Ischemia in China: A Hospital- Based Survey.

PURPOSE: The study aimed to report the clinical manifestation and identify the risk factors for postoperative mortality in patients who were diagnosed with obstructive acute mesenteric ischemia (AMI) based on a survey of a hospital in western China. PATIENTS AND METHODS: We reviewed clinical data of 108 patients with obstructive AMI at West China Hospital, Sichuan University, from 2011 to 2017. Clinical characteristic was described and compared. Factors affecting postoperative survival were analyzed. RESULTS: A total of 108 obstructive AMI cases were included in this study, with an overall average age of 57.1 years, including 58 arterial occlusive mesenteric ischemia (AOMI) and 50 mesenteric venous thrombosis (MVT). AOMI patients were older and had a significantly higher frequency of these comorbidities, including heart disease, hypertension, and diabetes. In comparison, MVT had a significantly higher proportion of male patients and a higher frequency of liver disease. A total of 77 patients underwent laparotomy, and the 30-day postoperative mortality rate was 29.9%. Multivariate logistic regression analysis showed that the time interval from admission to surgery (adjust OR 1.19; 95% CI [1.07-1.34], P = 0.005), platelet count (adjust OR = 0.98; 95% CI [0.97-0.99], P = 0.008) and AOMI (adjust OR = 5.55; 95% CI [1.36-22.55], P = 0.017) were independent predictors of 30-day mortality after exploratory laparotomy for obstructive AMI. Further analysis of the 45 AOMI showed that the time interval from admission to surgery (adjustOR 1.22; 95% CI [1.01-1.47], P = 0.036) and platelet count (adjustOR = 0.98; 95% CI [0.97-0.99], P = 0.020) were independent risk factors for 30-day postoperative mortality of AOMI. CONCLUSION: Early identification of AOMI, improving the efficiency of enhanced CT examination, strengthening doctor-patient communication, active laparotomy, and optimize platelet management may also help reduce the overall short-term mortality of obstructive AMI. Building the multidisciplinary team model of diagnostic imaging, vascular intervention, and surgical treatment to manage obstructive AMI may be urgently needed in western China.

Preoperative Risk Factors for Short-Term Postoperative Mortality of Acute Mesenteric Ischemia after Laparotomy: A Systematic Review and Meta-Analysis.

OBJECTIVE: Our objective was to comprehensively present the evidence of preoperative risk factors for short-term postoperative mortality of acute mesenteric ischemia after laparotomy. METHODS: PubMed, Embase, and Google Scholar were searched from January 2000 to January 2020. Studies evaluating the postoperative risk factors for short-term postoperative mortality of acute mesenteric ischemia after laparotomy were included. The outcome extracted were patients' demographics, medical history, and preoperative laboratory tests. RESULTS: Twenty studies (5011 patients) met the inclusion criteria. Studies were of high quality, with a median Newcastle-Ottawa Scale Score of 7. Summary short-term postoperative mortality was 44.38% (range, 18.80%-67.80%). Across included studies, 49 potential risk factors were examined, at least two studies. Meta-analysis of predictors based on more than three studies identified the following preoperative risk factors for higher short-term postoperative mortality risk: old age (odds ratio [OR], 1.90, 95% confidence interval [CI], 1.57-2.30), arterial occlusive mesenteric ischemia versus mesenteric venous thrombosis (OR, 2.45, 95% CI 1.12-5.33), heart failure (OR 1.33, 95% CI 1.03-1.72), renal disorders (OR 1.61, 95% CI 1.24-2.07), and peripheral vascular disease (OR 1.38, 95% CI 1.00-1.91). Nonsurvivors were older (standardized mean difference [SMD], 0.32, 95% CI 0.24-0.40), had higher creatinine levels (SMD 0.50, 95% CI 0.25-0.75), and had lower platelet counts (SMD -0.32, 95% CI -0.50 to -0.14). CONCLUSION: The short-term postoperative mortality of acute mesenteric ischemia who underwent laparotomy is still high. A better understanding of these risk factors may help in the early identification of high-risk patients, optimization of surgical procedure, and improvement of perioperative management.

Dexamethasone inhibits stemness maintenance and enhances chemosensitivity of hepatocellular carcinoma stem cells by inducing deSUMOylation of HIF­1α and Oct4.

It has been controversial whether patients with hepatocellular carcinoma (HCC) should receive glucocorticoid therapy during chemotherapy. Recent studies have demonstrated that glucocorticoids increase the therapeutic sensitivity of tumors to some chemotherapeutic drugs, but the specific mechanism remains unclear. In the present study, dexamethasone (Dex) was used to treat HCC stem cells. The results demonstrated that Dex reduced stemness maintenance and self­renewal of HCC stem cells, promoted epithelial­to­mesenchymal transition, inhibited migration and angiogenesis and, more importantly, increased cell sensitivity to the herpes simplex virus thymidine kinase/ganciclovir drug system in vitro and in vivo. Further mechanistic analyses demonstrated that Dex inhibited small ubiquitin­like modifier (SUMO) modification of several proteins in HCC stem cells, including hypoxia­inducible factor (HIF)­1α, an important hypoxia tolerance protein, and octamer­binding transcription factor 4 (Oct4), a crucial stemness maintenance protein. Inducing deSUMOylation of HIF­1α and Oct4 reduced their accumulation in the nucleus, thereby inhibiting tumor angiogenesis and stemness maintenance. These findings provide a new perspective to the study of the mechanism underlying the anti­hepatocarcinogenesis effects of Dex. Due to the few side effects of glucocorticoids at low doses and their anti­inflammatory effects, the appropriate combination of glucocorticoids and chemotherapeutic drugs is expected to improve the survival of HCC patients and their prognosis.