[Establishment and transfer management of veno-arterial extracorporeal membrane oxygenation in patients with difficult downtime during cardiopulmonary bypass surgery].

OBJECTIVE: To investigate the establishment method, coordination points and safe transport management strategy of vena-arterial extracorporeal membrane oxygenation (VA-ECMO) in patients with downtime difficulties during cardiopulmonary bypass (CPB). METHODS: A observation study was conducted. The patients admitted to the department of critical care medicine of the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital) from January 2020 to October 2022 were enrolled. These patients could not be separated from CPB and received VA-ECMO-assisted CPB surgery. The clinical data of the patients were recorded, including the basic information of the patients, the data of VA-ECMO establishment and transport process, the clinical indicators before and after VA-ECMO installation, the operation data of VA-ECMO and clinical outcomes. The experience was summarized from the aspects of extracorporeal membrane oxygenation (ECMO) establishment, transport process, team cooperation, and adverse events during transport. The clinical indicators before and after ECMO operation were compared. According to whether ECMO was successfully weaned, the patients were divided into a successful weaning group and a failure weaning group, and the clinical data between the two groups were compared. RESULTS: Eighteen patients who underwent VA-ECMO-assisted CPB were enrolled, including 10 males and 8 females. The average age was (56.7±12.3) years old. Preoperative left ventricular ejection fraction (LVEF) was 0.46±0.10, and the main reasons for switching to VA-ECMO assistance included right ventricular systolic weakness in 6 cases, total cardiac systolic weakness in 5 cases, left ventricular systolic weakness in 4 cases, high pulmonary arterial pressure in 2 cases, and intractable ventricular fibrillation in 1 case. Among the 18 patients transferred from CPB to VA-ECMO, 10 cases were successfully weaned and 8 cases failed. In ICU, 8 cases survived, 5 cases died, and 5 cases gave up treatment and discharged. The average time for successful CPB to VA-ECMO establishment was (24.6±7.4) minutes, initial blood flow was (3.3±0.4) L/min, and transit time was (8.4±1.5) minutes. ECMO-assisted duration averaged (82.0±69.3) hours. Adverse events occurred in 9 patients during ECMO establishment and transfer. Post-ECMO onboarding for 4 hours, significant improvements were noted in blood lactic acid (Lac), pH value, mean arterial pressure (MAP), central venous oxygen saturation (ScvO2) as compared with pre-ECMO onboarding [Lac (mmol/L): 10.5±7.0 vs. 15.2±6.8, pH value: 7.38±0.92 vs. 7.26±0.87, MAP (mmHg, 1 mmHg ≈ 0.133 kPa): 74.9±13.7 vs. 58.4±17.0, ScvO2: 0.678±0.065 vs. 0.611±0.061, all P < 0.01], and vasoactive-inotropic score (VIS) was also decreased (39.8±29.8 vs. 68.9±64.4, P < 0.01). Compared with successful weaning group, the patients in the failed weaning group exhibited higher pre-machine Lac (mmol/L: 18.8±7.8 vs. 12.3±4.3, P < 0.05), longer CPB time [minutes: 238.0 (208.8, 351.2) vs. 200.0 (185.8, 217.0), P < 0.05], and shorter ECMO-assisted time [hours: 19.5 (11.0, 58.8) vs. 94.5 (65.8, 179.8), P < 0.01]. However, there was no statistically significant difference in pre-machine pH value, ScvO2, MAP, VIS score, and initial blood flow and establishment time of ECMO between the two groups. CONCLUSIONS: VA-ECMO is an effective circulatory aid for CPB surgery that cannot be weaned after CPB. The establishment and transfer of CPB "bridge" to ECMO aid depends on multi-disciplinary treatment (MDT) cooperation. The success rate of ECMO weaning is related to the Lac and CPB duration. If it is not possible to detach from the CPB successfully, VA-ECMO should be initiated as early as possible.

Case study of colorectal endometriosis treated with endoscopic submucosal excavation.

Colorectal endometriosis (CEM) is a rare and complicated form of deep invasive endometriosis. Its treatment methods include drug therapy and surgery. However, it is often difficult to alleviate symptoms and address problems, such as infertility, using drug treatment alone. Surgical intervention provides a histologic diagnosis, allows assessment of pelvic cysts or masses with features concerning for malignancy, and reduces pain by destroying the endometriotic implants. We consider surgery in women with the following: Persistent pain despite medical therapy; Contraindications to or refusal of medical therapy; Need for a tissue diagnosis of endometriosis; Exclusion of malignancy in an adnexal mass; Obstruction of the bowel or urinary tract. But there is no consensus about the surgical methods. With the rapid development of gastroenteroscopy technology in recent years, many local gastrointestinal tumors that previously required surgical resection can now be removed by endoscopic surgery. Herein, we report one case of CEM treated by endoscopic submucosal excavation (ESE) to provide a new treatment option for the radical resection of single CEM.

m6A-mediated upregulation of LINC01003 regulates cell migration by targeting the CAV1/FAK signaling pathway in glioma.

BACKGROUND: Long non-coding RNAs (lncRNAs) play important roles in the progression of glioma. Here, we examined the potential functions of a lncRNA, LINC01003, in glioma and characterized the underlying molecular mechanisms. METHODS: The GEIPA2 and Chinese Glioma Genome Atlas (CCGA) databases were employed to analyze gene expression and the overall survival curve in patients with glioma. The functions of LINC01003 in glioma growth and migration were assessed by loss-of-function experiments in vitro and in vivo. RNA sequencing was used to determine the signaling pathways effected by LINC01003. Bioinformatics analysis and RNA immunoprecipitation (RIP) assays were used to explore the mechanism underlying the N6-methyladenine (m6A) modification-dependent upregulation of LINC01003 in glioma. RESULTS: LINC01003 expression was upregulated in glioma cell lines and tissues. Higher LINC01003 expression predicted shorter overall survival time in glioma patients. Functionally, LINC01003 knockdown inhibited the cell cycle and cell proliferation and migration in glioma cells. Mechanistically, RNA sequencing revealed that LINC01003 mediated the focal adhesion signaling pathway. Furthermore, LINC01003 upregulation is induced by m6A modification regulated by METTL3. CONCLUSION: This study characterized LINC01003 as a lncRNA that contributes to tumorigenesis in glioma and demonstrated that the LINC01003-CAV1-FAK axis serves as a potential therapeutic target for glioma.

Artificial intelligence in endoscopic ultrasonography: risk stratification of gastric gastrointestinal stromal tumors.

Background: Previous studies have identified useful endoscopic ultrasonography (EUS) features to predict the malignant potential of gastrointestinal stromal tumors (GISTs). However, the results of the studies were not consistent. Artificial intelligence (AI) has shown promising results in medicine. Objectives: We aimed to build a risk stratification EUS-AI model to predict the malignancy potential of GISTs. Design: This was a retrospective study with external validation. Methods: We developed two models using EUS images from two hospitals to predict the GIST risk category. Model 1 was the four-category risk EUS-AI model, and Model 2 was the two-category risk EUS-AI model. The diagnostic performance of the models was validated with external cohorts. Results: A total of 1320 images (880 were very low-risk, 269 were low-risk, 68 were intermediate-risk, and 103 were high-risk) were finally chosen for building the models and test sets, and a total of 656 images (211 were very low-risk, 266 were low-risk, 88 were intermediate-risk, and 91 were high-risk) were chosen for external validation. The overall accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for the four-category risk EUS-AI model in the external validation sets by tumor were 74.50%, 55.00%, 79.05%, 53.49%, and 81.63%, respectively. The accuracy, sensitivity, specificity, PPV, and NPV for the two-category risk EUS-AI model for the prediction of very low-risk GISTs in the external validation sets by tumor were 86.25%, 94.44%, 79.55%, 79.07%, and 94.59%, respectively. Conclusion: We developed a EUS-AI model for the risk stratification of GISTs with promising results, which may complement current clinical practice in the management of GISTs. Registration: The study has been registered in the Chinese Clinical Trial Registry (No. ChiCTR2100051191).

Artificial Intelligence in the Prediction of Gastrointestinal Stromal Tumors on Endoscopic Ultrasonography Images: Development, Validation and Comparison with Endosonographers.

Background/Aims: The accuracy of endosonographers in diagnosing gastric subepithelial lesions (SELs) using endoscopic ultrasonography (EUS) is influenced by experience and subjectivity. Artificial intelligence (AI) has achieved remarkable development in this field. This study aimed to develop an AI-based EUS diagnostic model for the diagnosis of SELs, and evaluated its efficacy with external validation. Methods: We developed the EUS-AI model with ResNeSt50 using EUS images from two hospitals to predict the histopathology of the gastric SELs originating from muscularis propria. The diagnostic performance of the model was also validated using EUS images obtained from four other hospitals. Results: A total of 2,057 images from 367 patients (375 SELs) were chosen to build the models, and 914 images from 106 patients (108 SELs) were chosen for external validation. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of the model for differentiating gastrointestinal stromal tumors (GISTs) and non-GISTs in the external validation sets by images were 82.01%, 68.22%, 86.77%, 59.86%, and 78.12%, respectively. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy in the external validation set by tumors were 83.75%, 71.43%, 89.33%, 60.61%, and 80.56%, respectively. The EUS-AI model showed better performance (especially specificity) than some endosonographers. The model helped improve the sensitivity, specificity, and accuracy of certain endosonographers. Conclusions: We developed an EUS-AI model to classify gastric SELs originating from muscularis propria into GISTs and non-GISTs with good accuracy. The model may help improve the diagnostic performance of endosonographers. Further work is required to develop a multi-modal EUS-AI system.

PLK1 protects intestinal barrier function in sepsis: A translational research.

BACKGROUND: Sepsis and its related complications are very challenging in the intensive care unit, among which intestinal barrier injury is a general manifestation. Polo-like kinase 1 (PLK1) is widely studied in cancer, while its role in sepsis is poorly understood. In this study, the efficiency of PLK1 as a marker of intestinal barrier function as well as a predictor of mortality in sepsis was evaluated. METHODS: The level of serum PLK1 was measured in septic patients (n = 51) and controls (n = 20); subsequently, its correlation with serum diamine oxidase (DAO), d-lactate, and endotoxin levels and its ability topredict mortality were analysed. The survival rate and barrier injury degree were also assessed in septic mice. RESULTS: Serum PLK1 levels were elevated in septic patients, were negatively correlated with serum DAO, d-lactate, and endotoxin levels, and had a high predictive value for 28-day mortality in patients. The serum PLK1 level in non-survivors was lower. The expression of PLK1 in the intestine was decreased in septic mice, and overexpression or inhibition of PLK1 alleviated or aggravated intestinal barrier injury, respectively, as evaluated by Chiu's score, serum levels of DAO and d-lactate, and expression of tight junction proteins. Overexpressing PLK1 also decreased the 72-hour death rate of septic mice. Further study also revealed the negative correlation of PLK1 and IL-6 in patients, and increasing or interfering with PLK1 expression reduced or increased the serum IL-6 level in mice. CONCLUSIONS: PLK1 plays a critical role in intestinal barrier function during sepsis, providing a novel perspective for sepsis therapy in the clinic.

ALTERATION IN SHEAR WAVE ELASTOGRAPHY IS ASSOCIATED WITH ACUTE KIDNEY INJURY: A PROSPECTIVE OBSERVATIONAL PILOT STUDY.

ABSTRACT: Background: Kidney stiffness could change during kidney disease. We hypothesize that acute kidney injury (AKI) would increase renal stiffness. Therefore, evaluating kidney Young's modulus (YM; a measure of tissue stiffness) using shear wave elastography (SWE) might help to diagnose AKI. Methods: This research was divided into two studies. Study A: Male C57BL/6 mice were used to observe kidney YM changes induced by sepsis-associated AKI, which was established by cecal ligation and puncture (CLP). Study B included 54 consecutive critically ill patients with or without AKI. Changes in renal YM were observed. Results: Study A: CLP mice showed a significantly higher kidney YM compared with the sham group. The YM gradually increased from CLP 0 hours to CLP 24 hours, and presented a fair relationship with the renal tubular injury score ( R2 = 0.71) and serum creatinine ( R2 = 0.73). Study B: YM was easily accessible, and the intraclass correlation coefficient ranged from 0.62 to 0.84. Kidney YM was higher in AKI patients and gradually increased from non-AKI to AKI III patients. Furthermore, the YM in the upper, middle, and lower poles of the renal cortex presented a fair relationship with kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin ( R2 ranging from 0.4 to 0.58), and the areas under the curve of the above five indicators for the diagnosis of AKI were 0.7, 0.73, 0.70, 0.74, and 0.79, respectively. Conclusion: SWE-derived estimates of renal stiffness are higher in AKI patients and sepsis-associated AKI mice. However, it has no advantage over NGAL and KIM-1. Trial Registration: Chinese Clinical Trial Registry No: ChiCTR2200061725. Retrospectively registered July 1, 2022, https://www.chictr.org.cn/showproj.aspx?proj=169359 .

Machine learning for the micropeptide encoded by LINC02381 regulates ferroptosis through the glucose transporter SLC2A10 in glioblastoma.

Glioblastoma (GBM) is the most common primary intracranial tumor in the central nervous system, and resistance to temozolomide is an important reason for the failure of GBM treatment. We screened out that Solute Carrier Family 2 Member 10 (SLC2A10) is significantly highly expressed in GBM with a poor prognosis, which is also enriched in the NF-E2 p45-related factor 2 (NRF2) signalling pathway. The NRF2 signalling pathway is an important defence mechanism against ferroptosis. SLC2A10 related LINC02381 is highly expressed in GBM, which is localized in the cytoplasm/exosomes, and LINC02381 encoded micropeptides are localized in the exosomes. The micropeptide encoded by LINC02381 may be a potential treatment strategy for GBM, but the underlying mechanism of its function is not precise yet. We put forward the hypothesis: "The micropeptide encoded by LINC02381 regulates ferroptosis through the glucose transporter SLC2A10 in GBM." This study innovatively used machine learning for micropeptide to provide personalized diagnosis and treatment plans for precise treatment of GBM, thereby promoting the development of translational medicine. The study aimed to help find new disease diagnoses and prognostic biomarkers and provide a new strategy for experimental scientists to design the downstream validation experiments.

Ticagrelor Protects against Sepsis-Induced Acute Kidney Injury through an Adenosine Receptor-Dependent Pathway.

OBJECTIVE: Ticagrelor is a widely used anti-platelet drug. However, the mechanisms by which ticagrelor protects against sepsis-induced acute kidney injury (AKI) have not been clearly demonstrated. We designed this study to explore the protective effect of ticagrelor on sepsis-induced AKI and to explore the underlying mechanisms. METHODS: C57BL6J mice received oral ticagrelor (20 mg/kg and 50 mg/kg) for 7 days, and then caecal ligation and puncture (CLP) were performed. An adenosine receptor antagonist, CGS15943, was administered (10 mg/kg, intraperitoneal injection) to block the adenosine pathway 2 h before CLP. After 24 h, serum creatinine levels were measured. Periodic acid-Schiff (PAS) staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining were employed to analyze pathological changes and cell apoptosis. Serum concentrations of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and mRNA expression of tissue TNF-α and IL-1ß were detected. Western blotting analysis was used to determine AKT and mammalian target of rapamycin (mTOR) protein expression in the kidney. RESULTS: PAS staining showed less swelling of renal tubules, and TUNEL staining revealed less cell apoptosis in the ticagrelor group than in the CLP group. Serum creatinine levels were significantly lower in the ticagrelor group than in the CLP group. Moreover, significantly lower serum and kidney levels of TNF-α and IL-1ß were observed in the ticagrelor group. CGS15943 blocked the effects of ticagrelor. Western blotting analysis showed increased phosphorylation of AKT and mTOR in the kidneys of the 50 mg/kg ticagrelor group. The adenosine receptor antagonist inhibited the activation of AKT and mTOR. CONCLUSION: This study demonstrates that the protective effect of ticagrelor on sepsis-induced AKI depends on adenosine receptor activation and the subsequent increase of AKT and mTOR phosphorylation.

Blocking the A2B adenosine receptor alleviates myocardial damage by inhibiting spleen-derived MDSC mobilisation after acute myocardial infarction.

BACKGROUND: Myeloid-derived suppressor cell (MDSC) mobilisation is an important immune event in acute myocardial infarction (AMI). The A2B adenosine receptor (A2BAR) plays key role in regulating MDSC function, but its specific involvement in MDSC mobilisation in AMI remains unclear. METHODS: In AMI patients, the circulating MDSC ratio and A2BAR mRNA expression were measured. A mouse AMI model was established by left anterior descending coronary artery (LADCA) ligation. MDSCs were analysed by FACS and immunofluorescence staining (of heart tissue). A2BAR mRNA expression was assessed by qRT-PCR. Myocardial injury was detected by HE staining. Myocardial cell apoptosis was analysed by immunohistochemistry. Cardiac systolic function was evaluated by transthoracic echocardiography. RESULTS: In AMI patients, the circulating MDSC ratio was increased and positively correlated with A2BAR mRNA expression (r = 0.86, p < 0.01). In AMI model mice, the percentage of MDSCs was increased in the circulation and infarcted heart and decreased in the spleen. MRS-1754-mediated A2BAR inhibition decreased the MDSC ratio in the circulation and infarcted heart and prevented the decrease in MDSC number in the spleens of mice with AMI. A2BAR blockade inhibited myocardial cell apoptosis, alleviated myocardial inflammatory injury, and improved myocardial systolic function in the AMI mouse model. Similar results were found in mice after splenectomy. Additionally, spleen-derived MDSC injection increased the MDSC ratio in the infarcted heart, increased myocardial cell apoptosis, aggravated myocardial injury, and decreased cardiac systolic function in mice with AMI. CONCLUSION: Blocking A2BAR alleviates myocardial damage and improves myocardial systolic function through inhibition of spleen-derived MDSC mobilisation after AMI. Key MessagesSpleen-derived MDSC mobilisation aggravates myocardial inflammatory injury within 24 h of AMI.A2BAR promotes spleen-derived MDSC mobilisation within 24 h of AMI.Blocking A2BAR improves myocardial systolic function through inhibition of spleen-derived MDSC mobilisation.

Effect of Dexmedetomidine on Intestinal Barrier in Patients Undergoing Gastrointestinal Surgery-A Single-Center Randomized Clinical Trial.

INTRODUCTION: Gastrointestinal failure results in death in critically ill patients. This study aimed to explore the effect of dexmedetomidine (DEX) on intestinal barrier function and its mechanism in critically ill patients undergoing gastrointestinal surgery. METHODS: Patients undergoing gastrointestinal surgery were randomized into the DEX group (n = 21) or midazolam (MID) group (n = 21). Sufentanil was used for analgesia in both groups. In the DEX group, DEX was loaded (1 µg/kg) before sedation and infused (0.7 µg/kg/h) during sedation. In the MID group, MID was loaded (0.05 mg/kg) before sedation and infused (0.1 mg/kg/h) during sedation. The mean arterial pressure , heart rate , borborygmus resumption time , first defecation time, length of intensive care unit stay, and length of hospital stay were observed. The diamine oxidase (DAO), D-lactate , TNF-α, IL-6, and α7nAChR levels in plasma or hemocytes were detected before the start of sedation (0 h) and after sedation (24 h). RESULTS: No significant differences in age, sex, body mass index, Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores were noted (P > 0.05). The mean arterial pressure between 0 h and 24 h showed no significant difference between the groups (P > 0.05), but the heart rate was significantly lower in the DEX group (P = 0.042). The borborygmus resumption time was significantly earlier in the DEX group (P = 0.034). The lengths of intensive care unit stay (P = 0.016) and hospital stay (P = 0.031) were significantly shorter in the DEX group. The TNF-α level in the DEX group was lower at 24 h than 0 h. The D-lactate level was significantly lower in the DEX group than the MID group at 24 h (P = 0.016). The expression of α7nAChR in the DEX group was significantly higher at 24 h than 0 h (P < 0.05). CONCLUSIONS: DEX maintained intestinal barrier integrity in patients undergoing gastrointestinal surgery through the cholinergic anti-inflammatory pathway.

Development of a nomogram for prediction of postoperative sore throat in patients under general anaesthesia: a single-centre, prospective, observational study.

OBJECTIVES: Postoperative sore throat (POST) is very common in patients under general anaesthesia. However, there is no effective clinical predictive model for reducing its occurrence. The objective of this study was to estimate the risk factors for POST in patients after general anaesthesia by designing a nomogram. DESIGN: A prospective study. SETTING: This study was conducted in a large tertiary hospital. PARTICIPANTS: Patients aged 18-85 years old who received general anaesthesia with either an endotracheal tube or supraglottic airway and of American Society of Anesthesiologists classification level Ⅰ-III. RESULTS: A total of 442 patients were enrolled in this study, with a POST incidence of 44.1%. The results showed that younger age (≤55 years), surgical site (head and neck surgery), duration of anaesthesia (≥4 hours) and history of chronic pharyngitis were independent risk factors for POST in general anaesthesia patients. Receiver operating characteristic (ROC) curves and calibration curves were used to evaluate the nomogram. The area under the ROC curve was 0.784 and the C-index was 0.779. CONCLUSION: A nomogram combining age, surgical site, duration of anaesthesia and history of chronic pharyngitis is potentially useful in predicting POST under general anaesthesia. TRIAL REGISTRATION NUMBER: ChiCTR-ROC-17013258; Post-results.

Triggering receptor expressed on myeloid cells-2 promotes survival of cardiomyocytes after myocardial ischemic injury through PI3K/AKT pathway.

Background: Previous studies have already revealed that triggering receptor expressed on myeloid cells-2 (TREM2) plays a significant protective role during the pathogenesis of ischemia injury in both brain and liver. This study aims to investigate the effect of TREM2 in myocardial ischemic injury. Methods: The mice myocardial infarction (MI) model was established via left anterior descending coronary artery ligation. TREM2 expression was examined with RT-PCR and Western blot. Whereafter, mice were randomly divided into control, sham, MI, Ad.TREM2 transfection group and Ad.Null transfection group. Recombinant adenovirus containing the gene coding full-length mouse TREM2 and EGFP (Ad.TREM2) or control vector containing EGFP gene only (Ad.Null) were immediately intramyocardial injected after left anterior descending ligated. After 7 days of MI, HE, Masson and TUNEL staining were performed to find the myocardial injury, infarcted size and cell apoptosis. Besides, echocardiography was performed to determine cardiac function. In addition, Western blot was performed to check the activity of PI3K/AKT signaling pathway in myocardial tissue. Furthermore, the plasma concentrations of TREM2 in 19 coronary artery disease (CAD) patients and 8 healthy controls were measured. Results: Compared with the sham group, TREM2 expression was significantly up-regulated in cardiac tissue in mice with MI. Cardiac tissue in mice transfected with Ad.TREM2 was demonstrated with alleviated injury, reduced infarct size, and decreased number of apoptotic cells. Echocardiography revealed that heart function was significantly improved in Ad.TREM2 transfection mice. Also, TREM2 transfection significantly activated the phosphorylation of AKT. At last, the plasma concentration of TREM2 was significantly elevated in patients with CAD and correlated with the severity of CAD. Conclusions: TREM2 may curb myocardial ischemia injury via activating PI3K/AKT signal pathway. Besides, plasma TREM2 may be treated as a potential biomarker in the diagnosis of CAD to reflect the severity of coronary stenosis.

Comparison of filter life span and solute removal during continuous renal replacement therapy: convection versus diffusion - A randomized controlled trial.

INTRODUCTION: This study aimed to investigate whether continuous veno-venous hemodiafiltration (CVVHDF) has a different filter life span and molecular solutes clearance when compared to continuous veno-venous hemofiltration (CVVH). METHODS: Sixty patients were enrolled in this study and randomly assigned to the CVVHDF (n = 30) or CVVH (n = 30) groups. Demographics, laboratory tests, urea, creatinine, IL-6, ß2-microglobulin, and myoglobulin clearance were recorded. RESULTS: Patients in the CVVH group had a shorter median time of filter life span compared with those in the CVVHDF group (20 vs. 37.5 h, p = 0.002). Urea and creatinine clearance were not significantly different between groups over time (p > 0.05). IL-6, ß2-microglobulin, and myoglobulin clearance were higher in the CVVH group. The transmembrane pressure (TMP) was significantly higher in the CVVH group. CONCLUSION: The use of CVVHDF may lead to a longer filter life span and lower clearance of medium and large molecules without affecting the small molecular solute clearance. TRIAL REGISTRATION: Chinese Clinical Trial Register (ChiCTR), ChiCTR2000029873. Registered 16 February 2020, http://www.chictr.org.cn/showproj.aspx?proj=49528.

Successful extracorporeal membrane oxygenation resuscitation of patient with cardiogenic shock induced by phaeochromocytoma crisis mimicking hyperthyroidism: A case report.

A 29-year-old woman presented to the emergency department with the acute onset of palpitations, shortness of breath, and haemoptysis. She reported having an abortion (56 days of pregnancy) 1 week before admission because of hyperthyroidism diagnosis during pregnancy. The first diagnoses considered were cardiomyopathy associated with hyperthyroidism, acute left ventricular failure, and hyperthyroidism crisis. The young woman's cardiocirculatory system collapsed within several hours. Hence, venoarterial extracorporeal membrane oxygenation (VA ECMO) was performed for this patient. Over the next 3 days after ECMO was established, repeat transthoracic echocardiography showed gradual improvements in biventricular function, and later the patient recovered almost completely. The patient's blood pressure increased to 230/130 mm Hg when the ECMO catheter was removed, and then the diagnosis of phaeochromocytoma was suspected. Computed tomography showed a left suprarenal tumour. The tumour size was 5.8 cm × 5.7 cm with central necrosis. The vanillylmandelic acid concentration was 63.15 mg/24 h. Post-operation, pathology confirmed phaeochromocytoma. To our knowledge, this is the first case report of a patient with cardiogenic shock induced by phaeochromocytoma crisis mimicking hyperthyroidism which was successfully resuscitated by VA ECMO.

Ticagrelor alleviates sepsis-induced myocardial injury via an adenosine-dependent pathway in a mouse sepsis model.

PURPOSE: The purpose of this study was to determine whether ticagrelor, a classic anti-platelet drug, has a therapeutic effect on sepsis-induced myocardial injury. METHODS: The C57BL6J mice received oral ticagrelor (10, 25 and 50 mg/kg) for seven days after which cecum ligation and puncture (CLP) were performed. An adenosine-receptor antagonist (CGS15943) was administered two hours before CLP. After 24 h, cardiac function was measured using cardiac echocardiography, then the heart and blood were collected. Hematoxylin and eosin (HE) staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL staining) were used to observe pathological changes and cardiomyocyte apoptosis. Plasma concentration of TNF-α, IL-6 and adenosine and myocardial tissue levels of TNF-α and IL-6 were determined. Survival analysis was performed. Western blot was used to determine the expression of a signalling protein in the myocardial tissue. RESULTS: The HE and TUNEL staining showed less inflammatory cell infiltration and less cardiomyocyte apoptosis in the ticagrelor group. Cardiac echocardiography showed preserved heart function in the ticagrelor group. Plasma TNF-α, IL-6 and relative expression of TNF-α and IL-6 in myocardial tissue were significantly lower in the ticagrelor group. Plasma adenosine levels were significantly higher in the ticagrelor group. Adenosine-receptor antagonists significantly blocked the protective effect of ticagrelor. Ticagrelor reduced the mortality of sepsis mice, and this reduction was blocked by the adenosine-receptor antagonist. Western blot showed that ticagrelor activated the phosphorylation of AKT and mTOR. Adenosine-receptor antagonists inhibited the activation of AKT and mTOR. CONCLUSION: The protective effect of ticagrelor was dependent on adenosine-receptor activation, with downstream upregulation of phosphorylation of AKT and mTOR.

Asymptomatic Mediastinal Extra-adrenal Paraganglioma as a Cause of Sudden Death: A Case Report.

A 23-year-old female patient was referred for treatment of a posterior mediastinal tumour. There was no history of hypertension or headache and no other complaints. The patient's blood pressure increased to 210/125 mmHg after surgically manipulating the tumour, subsequently reversing to severe hypotension (25/15 mmHg) immediately after the tumour was removed. The life-threatening and irreversible blood pressure drop was difficult to treat with fluid and vasopressors, and the patient ultimately died of cardio-respiratory failure. Asymptomatic paraganglioma can be non-functional but can also be fatal. For any lump in the thoracic cavity, paraganglioma should be ruled out.

[One case of acute kidney injury caused by praziquantel].

This paper reported one case of acute kidney injury caused by praziquantel.