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Introduction: COVID-19 patients with hypotension and hypoxemia had a significantly worse outcome. The purpose of this research was to ascertain the risk factors affecting the prognoses of these patients and to develop appropriate prognostic prediction tools.Methods: From March 1, 2020, to April 16, 2020, a retrospective cohort analysis of COVID-19 patients with hypotension and hypoxemia was performed. The univariate and multivariate analyses were performed to identify the associated risk factors influencing the prognosis of COVID-19 patients with hypotension and hypoxemia, and the selected variables were then utilized to construct and validate the prediction model for these patients.Results: Three hundred and twenty-seven COVID-19 patients with hypotension and hypoxemia who met the inclusion and exclusion criteria were included in this study. Age, temperature, troponin, and blood glucose were related to mortality in COVID-19 patients with hypotension and hypoxemia in both univariate and multivariate analyses. The MFP model (multiple fractional polynomial model), full model, and stepwise model were utilized to build the prediction model, and their AUCs were, respectively, 0.902 (0.868, 0.936), 0.902 (0.868, 0.936), and 0.902 (0.868, 0.936). Because the sample size for this research was limited, we utilized bootstrapping for internal validation. The AUCs of Bootstrap full and Bootstrap stepwise were 0.902 (0.867, 0.936) and 0.902 (0.868, 0.936), respectively.Conclusion: Age, temperature, troponin, and blood glucose levels were associated with mortality in COVID-19 patients with hypotension and hypoxemia. Additionally, the prediction model developed using the variables above showed a high predictive value for predicting the prognosis of these individuals.

Background Acute kidney injury (AKI) is the most common cause of organ failure in multiple organ dysfunction syndrome (MODS) and is associated with increased mortality. This study aimed at determining the efficacy of sequential organ failure assessment (SOFA), and acute physiology and chronic health evaluation II (APACHE-II) scoring systems in assessing the prognosis of critically ill patients with AKI undergoing continuous renal replacement therapy (CRRT). At present, APACHE-II score and SOFA score were also used to evaluate and predict the prognosis of critically ill patients with AKI. Methods The predictive value of SOFA and APACHE-II scores for 28- and 90-d mortality in patients with AKI undergoing CRRT were determined by multivariate analysis, sensitivity analysis, and curve-fitting analysis. Results A total of 836 cases were included in this study. Multivariate Cox logistic regression analysis showed that SOFA scores were associated with 28- and 90-d mortality in patients with AKI undergoing CRRT. The adjusted HR of SOFA for 28-d mortality were 1.18 (1.14, 1.21), 1.24 (1.18, 1.31), and 1.19 (1.13, 1.24) in the three models, respectively, and the adjusted HR of SOFA for 90-d mortality was 1.12 (1.09, 1.16), 1.15 (1.10, 1.19), and 1.15 (1.10, 1.19), respectively. The subgroup analysis showed that the SOFA score was associated with 28-d and 90-d mortality in patients with AKI undergoing CRRT. APACHE-II score was not associated with 28- and 90-d mortality patients with AKI undergoing CRRT. Curve fitting analysis showed that SOFA scores increased had a higher prediction accuracy for 28- and 90-d than APACHE-II. Conclusions The SOFA score showed a higher accuracy of mortality prediction in critically ill patients with AKI undergoing CRRT than the APACHE-II score.

Introduction: Although low serum albumin (ALB) may worsen acute kidney injury (AKI), additional study is needed to establish the connection between ALB and the prognosis of critically ill patients with AKI and treated with continuous renal replacement therapy (CRRT).Methods:A secondary analysis of a bi-center, retrospective, and observational study, such as critically ill patients with AKI and treated with CRRT from January 2009 to September 2016. The univariate analysis, multi-factor regression analysis, sensitivity analysis, and curve-fitting analysis were applied to explore the association of ALB with the 28 and 90 days mortality of critically ill patients with AKI and treated with CRRT, and the removal efficiency of serum phosphorus.Results: From January 2009 to September 2016, 1,132 cases with AKI and treated with CRRT met the inclusion criteria and enrolled in this study. We found that the higher ALB before CRRT, the lower the 28- and 90-day mortality of patients with AKI and treated with CRRT, the higher removal efficiency of serum phosphorus, the adjusted hazard ratio (HR) value for 28-day mortality in the four models were separately 0.92 (0.90, 0.95), 0.91 (0.89, 0.94), 0.92 (0.89, 0.95), and 0.92 (0.89, 0.95); the adjusted HR value for 90 day mortality in the four models were 0.91 (0.89, 0.94), 0.92 (0.89, 0.95), 0.92 (0.89, 0.95), and 0.92 (0.89, 0.96); the adjusted OR value for the removal efficiency of serum phosphorus in the four models were separately −0.04 (−0.07, −0.01), −0.05 (−0.08, −0.01), −0.04 (−0.08, −0.01), and −0.04 (−0.08, −0.01). The sensitivity analysis and curve-fitting analysis also showed that ALB before CRRT was correlated with the 28 and 90 days mortality of critically ill patients with AKI and treated with CRRT and the removal efficiency of serum phosphorus.Conclusion: The higher the serum ALB before CRRT, the lower the mortality of critically ill patients with AKI and treated with CRRT, and the higher the clearance efficiency of serum phosphorus.

Sepsis is the most common cause of acute kidney injury (AKI), which is associated with increased morbidity and mortality. The molecular mechanisms underlying sepsis pathogenesis and its regulation are incompletely understood. Here we demonstrated that human AlkB homologue, ALKBH8, plays a critical role in sepsis. We found that ALKBH8 expression was down-regulated in patients with acute sepsis. Low expression of ALKBH8 was also confirmed in LPS-induced sepsis model. Functionally, we revealed that knockdown of ALKBH8 in THP-1 cells suppressed cell proliferation and promoted cell apoptosis. In contrast, overexpression of ALKBH8 enhanced cell viability and protected against oxidative damage in THP-1 cells. In addition, we demonstrated that knockdown of ALKBH8 enhanced oxidative stress and decreased selenocysteine-protein expression. Mechanistically, we found that ALKBH8 ameliorated inflammation response via blocking NFκB/NLRP3 signaling in THP-1 cells. Inhibition of ROS production by using N -acetylcysteine (NAC) antagonized the effect of ALKBH8 knockdown on inflammation response and NFκB/NLRP3 signaling activation in THP-1 cells. Taken together, these results strongly suggest that ALKBH8 is an important oxidative stress and inflammation regulator in sepsis, which might have potential clinical application in the treatment of sepsis. Ethics: All patients provided written informed consent and the study protocols were approved by the Ethics Committee of Xiʹan Jiaotong University. The investigation conforms to the principles outlined in the Declaration of Helsinki and written informed consent was obtained from all participants. Funding: The work was supported by Key Research and Development Projects of Shaanxi Province of China (2020SF-121) Shaanxi Administration of Traditional Chinese Medicine Research Program (JCMS037). Competing interests: None

Background: Acute kidney injury (AKI) requiring continuous renal replacement therapy (CRRT) is a fatal and common clinical disorder in critically ill patients. Recent studies have shown that the relationship between BMI and the outcome of patients with AKI undergoing CRRT is conflicting. Methods: A retrospective cohort study based on data reuse. Univariate analysis, multi-factor regression analysis and subgroup analyses were used to explore the association of the BMI with the 28-days mortality risk in patients with AKI undergoing CRRT. Results: From January 2009 to September 2016, a total of 1120 cases met the inclusion criteria and were enrolled in this study. The univariate analysis showed that BMI was associated with 28-days mortality of patients with AKI undergoing CRRT, its HR value was 0.98 (0.96, 0.99). The multi-factor regression analysis showed that BMI was not associated with 28-days mortality of patients with AKI undergoing CRRT in the four models, the adjusted HR value of four models were 1.00 (0.96, 1.04), 1.01 (0.97, 1.04), 1.00 (0.96, 1.04) and 1.00 (0.96, 1.04), respectively. The subgroups analyses showed that the BMI was a risk factor of the 28-days mortality in patients with AKI undergoing CRRT when GFR ≥30 mL/min, its HR value was 1.04 (1.01, 1.09). Conclusion: Higher BMI was not a protective risk of 28-day mortality in patients with AKI undergoing CRRT. Especially, when GFR ≥30 mL/min, higher BMI increased the risk of the 28-day mortality rate in patients with AKI undergoing CRRT.

Objective To analyse the role of anticoagulation therapy in cardiopulmonary resuscitation (CPR) following an in-hospital cardiac arrest. Methods This single-centre retrospective cohort study enrolled patients treated with in-hospital CPR that met the inclusion and exclusion criteria. The patients were divided into a without anticoagulation group and an anticoagulation group. The main outcome measures were the restoration of spontaneous respiration, restoration of sinus rhythm (ROSR), restoration of spontaneous circulation (ROSC) and the hospital mortality. Results The study analysed 344 patients: 272 in the without anticoagulation group and 72 in the anticoagulation group. Multiple logistic regression analyses demonstrated that anticoagulation therapy improved ROSR (adjusted odds ratio [OR] 2.21, 95% confidence interval [CI] 1.23, 3.96) and ROSC (adjusted OR 1.91, 95% CI 1.08, 3.40), but it did not improve the restoration of spontaneous respiration (adjusted OR 1.64, 95% CI 0.72, 3.76) and hospital survival (adjusted OR 0.90, 95% CI 0.40, 1.99). Conclusion Anticoagulation therapy improved ROSR and ROSC, but did not decrease the mortality rate of hospitalized patients undergoing CPR following in-hospital cardiac arrest.

Background: Acute renal injury (AKI) is the most common cause of organ failure in multiple organ dysfunction syndrome and is associated with higher mortality, especially for patients requiring continuous renal replacement therapy (CRRT). At present, no effective approaches are in place to predict the prognosis of patients with AKI undergoing CRRT. Methods: A retrospective cohort study was carried to determine whether sequential organ failure assessment (SOFA) score may be a more valuable prognostic indicator than acute physiology and chronic health evaluation II (APACHE-II) score in patients with AKI undergoing CRRT. The multivariate analysis, sensitivity analysis, receiver operating characteristics (ROC) curve and decision curve analysis (DCA) were performed to determine the predictive value of SOFA and APACHE-II scores on 28- and 90-day mortality. Results: From January 2009 to September 2016, a total of 1128 cases were included. Multivariate logistic regression analysis showed that both APACHE-II and SOFA scores were associated with 28- and 90-day mortality of patients with AKI undergoing CRRT. The adjusted odds ratios (ORs) for SOFA and APACHE-II scores associated with 28-day mortality were 1.38 (1.27, 1.51) and 1.04 (1.01, 1.07), respectively, and the adjusted ORs for SOFA and APACHE-II scores associated with 90-day mortality were 1.40 (1.28, 1.52) and 1.04 (1.01, 1.07), respectively. decision curve analysis and receiver operating characteristics analyses showed that SOFA had a higher prediction accuracy than APACHE-II for 28- and 90-day mortality. The AUCs of SOFA and APACHE-II for 28-day mortality were 0.70 (0.67, 0.73) and 0.62 (0.58, 0.65), and for 90-day mortality, the AUCs were 0.71 (0.68, 0.78) and 0.62 (0.58, 0.65), respectively. Conclusion: SOFA score revealed higher accuracy than APACHE-II score in predicting the prognosis of critically ill patients with AKI undergoing CRRT.

Objective To investigate the association between serum phosphate levels and the risk of 28-day mortality in critically-ill patients with septic acute kidney injury (AKI) undergoing continuous renal replacement therapy (CRRT). Methods This retrospective cohort study analysed data from critically-ill patients with septic AKI who underwent CRRT between January 2009 and September 2016. Demographic, clinical and routine biochemical data were retrieved from a database and analysed to identify risk factors for 28-day mortality. Results A total of 796 patients were included in the analyses. Multivariate regression analyses showed that phosphate (0 h), phosphate (24 h) and delta phosphate were associated with the 28-day mortality in patients with septic AKI undergoing CRRT. The adjusted odds ratios (95% confidence interval) were 1.12 (1.03, 1.22), 1.22 (1.14, 1.30) and 1.12 (1.04, 1.20) for phosphate (0 h), phosphate (24 h) and delta phosphate, respectively. Curve fitting and threshold analyses showed that when phosphate (0 h) was between 5.6 mg/dl and 8.7 mg/dl, phosphate (24 h) was >3.8 mg/dl and delta phosphate was >–1, the 28-day mortality risk increased significantly. Conclusion In patients with septic AKI undergoing CRRT, serum phosphate level was associated with the prognosis of patients in terms of 28-day mortality.

BACKGROUND Type 2 diabetes mellitus is a global public health problem. Prediabetes may be reversed by weight loss, diet, and lifestyle changes. However, without intervention, between 30-50% of individuals with prediabetes develop type 2 diabetes. This retrospective population study was conducted to develop a predictive model of prediabetes and incident type 2 diabetes mellitus using data from 2004 to 2015 from the DRYAD Japanese hospital database. MATERIAL AND METHODS A retrospective longitudinal population study was conducted using the DRYAD database from Murakami Memorial Hospital, Gifu, Japan, to construct a predictive model for prediabetes and incident type 2 diabetes mellitus in the population. Univariate analysis and multivariate analysis were performed to identify the variables that were associated with prediabetes. These variables were used to construct (75% samples) and verify (25% samples) the predictive model. RESULTS From 2004 to 2015, a total of 11,113 cases were identified. Multivariate logistic regression analysis included the six variables of age, waist circumference, smoking history, the presence of fatty liver, fasting blood glucose (FBG), and glycated hemoglobin (HbA1c) level. Data were used to construct (75% samples) and verify (25% samples) in a predictive model. The area under the receiver operating characteristic (ROC) curve (AUC) of the predictive model was 0.87 (0.85-0.89) in the training cohort and 0.87 (0.86-0.90) in the validation cohort. CONCLUSIONS A prognostic model based on six variables was predictive for incident type 2 diabetes mellitus and prediabetes in a healthy population in Japan.

Myocardial infarction (MI) is one of the most serious cardiovascular diseases associated with myocardial ischemia/reperfusion (I/R) injury. Glaucocalyxin A (GLA) is a biologically active ent-kauranoid diterpenoid that has been found to ameliorate myocardial I/R injury in mice. However, the mechanism has not been fully investigated. In the present study, we aimed to investigate the effect of GLA on rat cardiomyocytes H9c2 cells exposed to hypoxia/reoxygenation (H/R). The results showed that GLA treatment improved cell viability of H/R-stimulated H9c2 cells. Administration with GLA suppressed the H/R-stimulated reactive oxygen species (ROS) production in H9c2 cells. GLA also elevated the activities of antioxidant enzymes, including superoxide dismutase and glutathione peroxidase in H/R-stimulated H9c2 cells. Moreover, GLA prevented H/R-stimulated cell apoptosis in H9c2 cells, as evidenced by increased bcl-2 expression, decreased bax expression, as well as reduced caspase-3 activity. Furthermore, GLA enhanced the activation of protein kinase B (Akt)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in H9c2 cells exposed to H/R. Additionally, treatment with LY294002 reserved the protective effects of GLA on H/R-stimulated oxidative injury in H9c2 cells. In conclusion, these findings suggested that GLA protected H9c2 cells from H/R-stimulated oxidative damage, which was mediated by the Akt/Nrf2/HO-1 signaling pathway. Thus, GLA might be a promising therapeutic agent for the prevention and treatment of myocardial I/R.

To investigate the improving effect of Litchi Seed Aqueous Extracts on learning and memory obstacles model and its mechanism.The learning and memory obstacles model was incluced by subcutoneous injection of D-galactose (500 mg/kg) for 8 weeks. The model group and treatment groups were given huperzine A (0.4 mg/kg) and Litchi Seed Aqueous Extracts (15,60 g/kg) respectively for 4 weeks by ig at the 5th week. After huperzine A and Litchi Seed Aqueous Extracts treatment for 4 weeks, water maze test was used to determine the ability of mice's spatial learning and memory. The contents of advanced glycation end products (AGEs) in serum, the content of nitric oxide (NO) and acetylcholine (Ach), the activity of nitric oxide synthase (NOS) and acetylcholinesterase (AchE) in the brain tissue were detected.Litchi Seed Aqueous Extracts significantly ameliorated the learning and memory ability in mice, decreased the level of AGEs in serum, and reduced the content of NO and activity of NOS in brain tissues. No significantly influence was observed for the Ach and Ach-E in brain tissues.Litchi Seed Aqueous Extracts possesses improving the learning and memory effects on the model mice induced by D-galactose, which may be related to inhibiting too much AGEs and NO formation and reducing damage in the brain cells.

To study the effects of berberine on hypertensive renal injury model in rats fed by enriched high fat-salt-fructose diet .hypertensive renal injury model was esteblished by feeding enriched high fat-salt-fructose diet for 8 weeks. On the basis of animal blood pressure, hypertensive rats were randomly divided into model group (10 rats, distilled water), captopril group (10 rats,25 mg/kg), berberine high dose group (10 rats, 300 mg/kg) and low dose group (10 rats, 100 mg/kg). These rats were fed by enriched high fat-salt-fructose diet and treated by intragastric administration with drugs for 4 weeks. And normal control group (10 rats) was set Blood pressure was determined at 0, 4, 8, 10, 12 weekend,and after 4 weeks of drugs treatment, getting urine to determine urine protein, taking blood serum to determine blood urea nitrogen, serum creatinine,GHb,MDA and activity of SOD. The content of H2O2 and GSH-Px and activity of CAT in kidney tissues were determined also.Compared with normal control group, blood pressure, urine protein, blood urea nitrogen, serum creatinine and MDA and GHb in serum of model rats obviously increased (P0.01), the activity of SOD decreased (P0.01), higher content of H2O2 and lower content of GSH-Px and activity of CAT (P0.01) in the kidney tissues. Treated with berberine for 4 weeks, elevated blood pressure and heightened levels of urine protein, blood urea nitrogen and serum creatinine in model rats were depressed significantly (P0.01), and elevated the activity of SOD, lowed the levels of MDA and GHb in blood serum (P0.01). At the same time, berberine increased the activities of GSH-Px and CAT (P0.01) and slightly lowed the content of H2O2 in the kidney tissues.Berberine has protecting effects on the hypertensive renal impairment model rats fed by enriched high fat-salt-fructose diet, which are concerned with elevated antioxidant capability in body and kidney tissues.

To observe the effect of Semen Litchi containing serum on proliferation and apoptosis of HepG2 cells.The Semen litchi or CTX containing serum and control serum were prepared by serologic pharmacology method. MTT assay was used to observe the proliferation inhibition rate of HepG2 cells after incubated with different kinds of drug's containing serum. Nuclear morphological features of HepG2 cells were detected by fluorescencemicroscopy after staining with Hochest33258. The apoptosis rate of HepG2 cells in each group was detected by flow cytometry.The cell viability and the apoptosis rate of HepG2 cells in Semen Litchi containing serum groups were higher than that of control group, and the results of fluorescencemicroscopy observation showed the nuclear morphological change of apoptosis.Semen Litchi can inhibit the proliferation of HepG2 cells, the acting mechanism may be concerned with cell apoptosis.

To study the pathological changes of blood glucose, serum lipid, insulin resistance, liver function, liver cell denaturalization of total glucosides of paeony on nonalcoholic fatty liver rats caused by insulin resistance and discuss the acting mechanism.Adult SD rats were maintained on high-fat-sugar-salt diet for 56 days. In the 57th day, their fasting blood glucose (FBG) and 2-hours blood glucose after oral glucose tolerance test (OGTT-2 hBG) were mensurated, according to which and the weight the rats were divided randomly into nonalcoholic fatty liver model group, metformin group (0.2 g x kg(-1)) and total glucosides of paeony group (high dosage 0.15 g x kg(-1), low dosage 0.05 g x kg(-1)). All the rats were still administered the same diet and given different drugs by intragastric administration for 28 days. In the 29th day, all of them were killed and the blood was sampled to measure the levels of blood glucose [FBG, OGTT-2 hBG, fasting insulin (Fins)] and serum lipid [free fatty acids (FFA), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C)], then the HOMA insulin resistance index (HOMA-IRI, fasting glucosexinsulin) and insulin sensitivity index (ISI) were counted. The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), cholinesterase (ChE), superoxide dismutase (SOD) and the contents of malondialdehyde (MDA) were measured also. Livers were weighed and collected to be observed the pathological changes.Compared with normal group, in nonalcoholic fatty liver model group the levels of Fins and IRI were increased obviously (P0.01), ISI were decreased (P0.01), FFA, TG, TC, LDL-C were increased (P0.01), HDL-C were decreased (P0.05); the content of MDA were increased (P0.05), the activities of SOD were decreased (P0.01); AST, ALT and ChE were increased (P0.05, or P0.01), the pathological changes of liver fat were severe (P0.01). In glucosides of paeony group and metformin group, hyperinsulinaemia and insulin resistence were resisted (P0.05, or P0.01); the levels of FFA, TG, TC, LDL-C were decreased and HDL-C were increased (P0.05, or P0.01); the activities of AST, ALT, ChE were decreased (P0.05, or P0.01) and SOD were increased (P0.01). The contents of MDA were decreased (P0.05). The levels of FBG and 2 hBG in metformin group were decreased but in total glucosides of paeony group were not decreased obviously.Total glucosides of paeony may protect liver function and modulate serum lipid for the fatty liver rats caused by insulin resistance, and its action mechanism may be concerned with enhancing insulin sensitivity and antioxidative ability, decreasing serum lipid.

To observe the improvement effects of puerarin on glycated brain damages in rat model induced by D-galactose.The model rats of protein glycation were induced by intraperitoneal administration of D-galactose (150 mg x kg(-1) x d(-1)) for 8 weeks, and all rats were treated with puerarin (high dose 300 mg x kg(-1), middle dose 150 mg x kg(-1), low dose 75 mg x kg(-1)) for 6 weeks. The activity of aldose reductase in red blood cells, the amount of glycated products (fructosamine in serum, glycohaemoglobin, advanced glycation end-products) and AGEs in brain tissue, calcium ion in brain cells were measured. Moreover, mitochondria in brain hippocampus cells were observed under electronic microscope.High dose and middle dose of puerarin can decrease the activity of aldose reductase in red blood cells (P0.01), and inhibit the formation of glycation products significantly in model rats induced by D-galactose (P0.01). Also, puerarin can decrease the content of AGEs in brain and the level of calcium ions in brain cells (P0.05, P0.01), and decrease lesions degree in mitochondria in brain hippocampus cells.Puerarin can produce the protective effects on glycated brain damages through inhibiting the glycation reaction in rats induced by D-galactose.

To measure the effect of addition of heparin to adriamycin (ADM) on cell proliferation and apoptosis in CNE2 cells and investigate the possible molecular mechanisms of heparin and ADM interactions.Cell viability and cell cycle were determined by MTT assay and flow cytometry. Apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and agarose gel electrophoresis. The expression of Bax, Bcl-2, p53, and p21 was examined by Western blot.ADM (5 mg/L) alone inhibited the growth of CNE2 cells, which was magnified when heparin was added. ADM elicited typical apoptotic morphologic changes. Compared with ADM or heparin alone, ADM plus heparin obviously enhanced the number of TUNEL positive cells from 12.6 % 1.1 % to 65.7 % 1.3 %, and the DNA ladder was more clearly observed. After exposure to different concentrations of heparin (with or without ADM) for 24 h, CNE2 cells were accumulated in G0/G1 phase. There was a decrease in the number of cells in S phase by the combined heparin and ADM treatment compared to heparin or ADM alone. The ratio of Bax/Bcl-2 was elevated, and p53 and p21 mRNA were over-expression.Heparin and ADM appear to interact in a synergistic manner, which may be related to the over-expression of p53 and p21 mRNA and the elevated ratio of Bax/Bcl-2 mRNA.