[Predicting value on short-term outcome of various established risk prediction models in extracorporeal membrane oxygenation treated cardiogenic shock patients due to ST-segment elevation myocardial infarction].

Objective: To investigate the predicting value of different risk prediction models for short-term death in patients with ST-segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock and treated with extracorporeal membrane oxygenation (ECMO). Methods: This study was a retrospective case-control study. Forty patients with STEMI complicated by cardiogenic shock who hospitalized in the First Affiliated Hospital of Zhengzhou University from April 2017 to August 2021 and treated with percutaneous coronary intervention (PCI) and ECMO, were enrolled in this study. Patients were divided into survival group and death group according to their clinical outcomes at 30 days after ECMO implantation, and clinical data of the two groups were collected and analyzed. Receiver operating characteristic (ROC) curve and decision curve analysis (DCA) were used to compare the predictive value of ACEF, AMI-ECMO, Encourage and SAVE risk scores for mortality at 30 days after ECMO implantation. According to the evaluation results of DCA, the optimal risk score was selected. Kaplan-Meier curve estimating the 30-day survival after ECMO implantation was plotted by grouping risk scores with reference to previous literatures. Results: A total of 40 patients with STEMI combined with cardiogenic shock were included, age was (57.4±16.7) years, 31 (77.5%) patients were male, there were 21 (52.5%) patients in the death group and 19 (47.5%) in the survival group. Compared with the survival group, patients in the death group had higher lactic acid values, higher proportion of anterior descending artery or left main artery lesions, and a higher proportion of acute renal failure and continuous renal replacement therapy during hospitalization (all P<0.05). Compared with survival group, ACEF, AMI-ECMO and Encourage scores were higher in death group, SAVE score was lower in death group (all P<0.05). The ROC curve analysis showed that the area under the curve (AUC) of ACEF, AMI-ECMO, Encourage and SAVE scores in predicting mortality were 0.707, 0.816, 0.757, and 0.677 respectively (P>0.05). ACEF score demonstrated the highest sensitivity (90.5%) and Encourage score exhibited the highest specificity (89.5%). DCA indicated that the AMI-ECMO and Encourage scores had the best performance in predicting the 30-day mortality after ECMO therapy. Kaplan-Meier survival curve analysis showed that the 30-day mortality after ECMO implantation increased with the increase of AMI-ECMO and Encourage scores (log-rank P≤0.001). Conclusions: The 4 scoring systems are all suitable for predicting 30-day mortality after VA-ECMO therapy in patients with ST-segment elevation myocardial infarction complicated by cardiogenic shock. Among them, AMI-ECMO and Encourage scores have better predicting performance.

[Early effect of extracorporeal membrane oxygenation and factors related to early outcome in adult patients with fulminant myocarditis].

Objective: To evaluate the efficacy within the first 24 h post extracorporeal membrane pulmonary oxygenation (ECMO) and the impact of early efficacy on the prognosis of adult patients with fulminant myocarditis (FM). Methods: This retrospective case analysis study included hospitalized patients (age≥18 years) who were diagnosed with fulminant myocarditis from November 2016 to May 2021 in the First Affiliated Hospital of Zhengzhou University. Patients were divided into survival or non-survival groups according to treatment outcomes. The age, sex, treatments, drug use, ECMO use, clinical and laboratory data (before and 24 h after the use of ECMO) were analyzed. The change rate of clinical and laboratory data after 24 h use of ECMO was calculated to find differences between two groups. Multivariate logistic regression was used to analyze the related factors with in-hospital death and complication between the two groups. Results: A total of 38 FM patients treated with ECMO were included. There were 23 cases (60.5%) in the survival group, aged (39.6±13.7) years, and 17 (73.9%) cases were female. The total ECMO time was (134.4±71.3)h. There were 15 cases (39.5%) in non-survival group, aged (40.0±15.8) years, and there were 12(80.0%) female, the ECMO time was (120.1±72.4) h in this group. The proportion of tracheal intubation and continuous renal replacement therapy in the survivor group and dosage of norepinephrine within 24 h after ECMO implantation were significantly less than in non-survival group (all P<0.05). There was no significant difference in all efficacy related biochemical indexes between two groups before ECMO use. The levels of lactic acid, procalcitonin, creatinine, alanine aminotransferase, aspartate aminotransferase, creatine kinase-MB, cardiac troponin I and N-terminal B-type natriuretic peptide prosoma were significantly less in survival group than in non-survival group at 24 h after the use of ECMO (all P<0.05). Results of multivariate logistic regression analysis showed that the higher 24 h change rate of creatinine (OR=0.587, 95%CI 0.349-0.986, P=0.044) and creatine kinase-MB (OR=0.177, 95%CI 0.037-0.841, P=0.029) were positively correlated with reduced risk of in-hospital mortality. The central hemorrhage and acute kidney injury in survival group were less than in non-survivor group (P<0.05). Conclusions: After 24 h early use of ECMO in FM patients, the improvement of various efficacy related biochemical test indexes in the survival group was better than that in the non-survival group. Faster reduction of creatine kinase-MB and creatinine values within 24 h ECMO use is positively correlated with reduced risk of in-hospital mortality in adult patients with FM.

Suppression of lung cancer in murine model: treated by combination of recombinant human endostsatin adenovirus with low-dose cisplatin.

BACKGROUND: The sustained growth of tumors necessitates neovascularization. As one of the potent endogenous vascular inhibitors, endostatin has been widely used in antiangiogenesis therapy for tumor. Cisplatin is normally administered in chemotherapy for lung cancer but accompanied with serious side effects. In the current study, we investigated a novel chemo-antiangiogenesis therapeutic strategy to both improve toxic effects on lung cancer cells and reduce damages to normal cells in the anti-tumor therapy. METHODS: In vitro, we transduced LLC cells with Ad-hEndo and collected supernatants. Western blotting analysis of the supernatants revealed expression of endostatin. In vivo, to fully investigate the suppression effect on murine lung cancer of the combination therapy, we injected recombinant human endostatin adenovirus intratumorally plus a low dose of cisplatin intraperitoneally routinely. The tumor volume and survival time were observed. Angiogenesis was apparently inhibited within the tumor tissues and on the alginate beads. Assessment of apoptotic cells by the TUNEL assay was conducted in the tumor tissues. RESULTS: The combination treatment significantly suppressed the tumor growth and prolonged survival time of the murine LLC tumor model. This anti-tumor activity was associated with decreased microvessel density and increased apoptotic index of tumor cells. CONCLUSION: According to the results in this study, recombinant human endostatin adenovirus in combination with a low dose of cisplatin demonstrated apparent synergistic anti-tumor activity without marked toxicity. Thus, these observations may provide a rational alternative for lung cancer treatment.

Effect of DIMBOA on growth and digestive physiology of Sesamia nonagrioides (Lepidoptera: noctuidae) larvae.

The hydroxamic acid 2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one (DIMBOA) was assessed for its effect on growth and digestive physiology of larvae of the stalk corn borer Sesamia nonagrioides Lef. Nutritional indices and activities of some digestive and detoxification enzymes were determined for larvae feeding on a DIMBOA-containing diet for the first two days of the third instar (short-term feeding assays), and from neonates to third instar (long-term feeding assays). DIMBOA reduced the relative growth rate and the efficiency of conversion of ingested food without affecting the relative consumption rate in long-term feeding assays, but it had no effect in short-term assays. Moreover, elastase-like activity was significantly increased by DIMBOA in short-term feeding assays, whereas microsomal oxidase activity was increased and esterase activity was reduced in long-term feeding assays. In vitro, DIMBOA inhibited the activities of carboxypeptidases, aminopeptidase, glutathione S-transferase and esterase, but it had no effect on trypsin, chymotrypsin and elastase. The implications of the altered levels of proteases and detoxification enzyme activities on the digestive physiology of larvae feeding on DIMBOA-containing diets are discussed.

A carboxy-terminal mutant spleen focus-forming virus (SFFV) envelope glycoprotein is transport-competent, but non-leukemogenic.

The Friend spleen focus-forming virus (F-SFFV) codes for a transport-defective leukemogenic envelope glycoprotein designated as gp52. We have previously shown that the external domain of gp52 carries the determinants responsible for its transport defect. Consistent with this idea, truncated gp52 molecules that lack a hydrophobic membrane anchor were transport-defective, and were not secreted from cells. In this report, we describe the construction of a mutant SFFV envelope gene that codes for altered gp52 molecules in which the carboxyl-terminal hydrophobic residues are replaced with exogenous hydrophilic residues encoded by the vector-derived sequences. The mutant env gene was expressed using the retroviral expression vector, pLXSN, and the mutant envelope protein was found to be transport-competent, and efficiently secreted from the cells. However, M-MuLV pseudotypes of the retroviral vectors expressing the mutant genome were found to be non-leukemogenic in mice.

The hydrophobic membrane-spanning sequences of the gp52 glycoprotein are required for the pathogenicity of Friend spleen focus-forming virus.

Friend spleen focus-forming virus (SFFV) codes for a transport-defective envelope glycoprotein designated gp52, which is responsible for the leukemogenic properties of the virus. gp52 is a monotopic integral membrane protein anchored in the membrane by a stretch of hydrophobic amino acid residues located near the carboxy terminus of the molecule. We have constructed a mutant SFFV envelope gene in which the sequences that code for the hydrophobic membrane-spanning domain have been deleted, and we expressed this gene by using recombinant vaccinia virus vectors or retroviral vectors. The mutant SFFV envelope gene was found to encode a truncated glycoprotein (gp52t) which was also transport defective; a majority of gp52t remained cell associated, while a small proportion of the molecules underwent oligosaccharide processing. The processed form of gp52t was secreted from the cells. Retroviral vectors carrying the mutant SFFV envelope gene were found to be nonpathogenic in adult mice. These results indicate that the hydrophobic membrane-spanning region of gp52 is required for pathogenicity of SFFV and suggest that these sequences may play a role in signal transduction. The results also indicate that the transport defect of SFFV gp52 is due to structural features of the ectodomain of the molecule.

Inhibition of virus-induced cell fusion by apolipoprotein A-I and its amphipathic peptide analogs.

Apolipoprotein A-I (apoA-I), the major protein component of serum high-density lipoproteins (HDL), was found to inhibit herpes simplex virus (HSV)-induced cell fusion at physiological (approximately 1 microM) concentrations, whereas HDL did not exert any inhibitory effect. Lipid-associating, synthetic amphipathic peptides corresponding to residues 1-33 (apoA-I[1-33]) or residues 66-120 (apoA-I[66-120]) of apoA-I, also inhibited HSV-induced cell fusion, whereas a peptide corresponding to residues 8-33 of apoA-I (apoA-I[8-33]), which fails to associate with lipids, did not exert any inhibitory effect. These results suggest that lipid binding may be a prerequisite for peptide-mediated fusion inhibition. Consistent with this idea, a series of lipid-binding 22-amino-acid-residue-long synthetic amphipathic peptides that correspond to the amphipathic helical domains of apoA-I (A-I consensus series), or 18-residue-long model amphipathic peptides (18A series), were found to exert variable levels of fusion-inhibitory activity. The extent of fusion-inhibitory activity did not correlate with hydrophobic moment, hydrophobicity of the nonpolar face, helix-forming ability, or lipid affinity of the different peptides. Peptides in which the nonpolar face was not interrupted by a charged residue displayed greater fusion-inhibitory activity. Also, the presence of positively charged residues at the polar-nonpolar interface was found to correlate with higher fusion-inhibitory activity.

Indirect spectrophotometric determination of cyanide by means of the colour reaction of silver with cadion 2B in presence of triton X-100.

Silver gives a colour reaction with cadion 2B in the presence of the non-ionic surfactant Triton X-100, and the suppression of the colour by competitive complexation of the silver can be used for the spectrophotometric determination of cyanide. Cyanide in waste water can be separated by distillation from other ions that also interfere, and then determined.