Objective To observe the clinical efficacy of atorvastatin combined with neuroendocrine antagonist in the treatment of chronic heart failure.Methods 70 patients of Wenzhou Medical College Theorem Clinical College of Cardiology Department from March 2014 to March 2015 were randomly divided into observation group and control group of 35 cases in each group.The control group were given the neuroendocrine antagonist, observation group were given atorvastatin combined with neuroendocrine antagonist treatment. The changes of related indicators were recorded. Results The aminoterminal pro-brain natriuretic peptide (NT-ProBNP) and ejection fraction in observation group were [(1264.7 ±174.6)pg/mL, (0.58 ±0.07)], which were higher than those in control group [(2106.5 ±164.8)pg/mL,(0.49 ±0.08)](P<0.05).The total effective rate in observation group was 91.43%, which was higher than 71.43%in control group(P<0.05).Conclusion Atorvastatin joint neuroendocrine antagonist in treatment of chronic heart failure has clinical exact effect with no significant side effects.

Objective To study and analyze the clinical efficacy of metoprolol combined with trimetazidine in the treatment of coronary heart disease and heart failure. Methods 80 patients with coronary heart disease and heart failure treated in our hospital from January 2015 to December 2016 were selected and randomly divided into the control group and the experimental group, with 40 cases in each group. The control group received routine treatment, including diuretics and angiotensin converting enzyme inhibitors, and the experimental group was treated with trimetazidine combined with metoprolol. The therapeutic effects of the two groups were compared and analyzed. Results After the corresponding treatment, 5 patients in the experimental group were invalid. In the control group, 14 patients were ineffective. The effective rate of treatment in the experimental group (87.5％) was significantly higher than that in the control group (65.0％), the differences were statistically significant (P<0.05). After treatment, the LVEF in the experimental group was (50.4 ± 7.7)％, and the LVEF in the control group was (45.1 ± 7.0)％. In addition, the LVEDD and LVESD indexes and LVEF in the experimental group were better than those in the control group, the differences were statistically significant (P<0.05). Conclusion The clinical effect of trimetazidine combined with metoprolol in the treatment of coronary heart disease and heart failure is better. It can improve the efficiency of treatment to some extent, and has the significance of further promotion and application.

Objective:To investigate the therapeutic effect of cardiac rehabilitation exercise on ventricular remodeling in patients with acute myocardial infarction undergoing percutaneous coronary intervention.Methods:A total of 100 patients with acute myocardial infarction undergoing percutaneous coronary intervention who received treatment in Wenzhou Central Hospital from June 2018 to June 2019 were included in this study. They were randomly divided into a rehabilitation group and a conventional treatment group ( n = 50/group). Patients in the conventional treatment group underwent conventional postoperative rehabilitation education while those in the rehabilitation group received targeted cardiac rehabilitation exercise. After surgery, all patients were followed up for 12 months. Real time three-dimensional echocardiography was used to evaluate ventricular remodeling (left ventricular ejection fraction, left ventricular end-diastolic volume , left ventricular end-systolic volume, left ventricular remodeling index) and ventricular synchrony (Tmsv-16dif, Tmsv-16sd, Tmsv16-dif%, Tmsv16-sd%) before and 3, 6 and 12 months after surgery. In addition, serum levels of ventricular remodeling indexes (fibroblast growth factor 23, PICP and PIIINP) were measured. The incidence of cardiovascular end-point events within 12 months was calculated. Results:At 3, 6 and 12 months after surgery, left ventricular ejection fraction was (51.81 ± 5.43)%, (55.88 ± 5.46)%, (55.63 ± 5.57)% in the rehabilitation group, which was significantly higher than (47.16 ± 5.38)%, (52.31 ± 5.44)%, (51.84 ± 5.59)% respectively in the conventional treatment group ( t = 4.302, 3.275, 3.396, all P < 0.05). At 3, 6 and 12 months after surgery, left ventricular end-diastolic volume was (124.65 ± 15.56) mL, (98.54 ± 14.54) mL, (99.82 ± 13.18) mL, respectively in the rehabilitation group, which was lower than (132.64 ± 16.58) mL, (112.55 ± 15.61) mL and (114.84 ± 17.35) mL, respectively in the conventional treatment group ( t = 2.485, 4.644, 4.874, all P < 0.05). At 6 and 12 months after surgery, left ventricular end-systolic volume was (52.26 ± 5.48) mL and (52.15 ± 5.32) mL respectively in the rehabilitation group, which was significantly lower than (57.92 ± 5.46) mL and (58.51 ± 5.72) mL in the conventional treatment group ( t = 5.174, 5.757, both P < 0.05). At 6 and 12 months after surgery, left ventricular remodeling index was (1.75 ± 0.42) g/mL and (1.74 ± 0.35) g/mL respectively in the rehabilitation group, which was significantly higher than (1.52 ± 0.37) g/mL and (1.50 ± 0.32) g/mL, respectively in the conventional treatment group ( t = 2.906, 3.579, both P < 0.05). At 3, 6 and 12 months after surgery, Tmsv-16dif ( t = 2.753, 4.283, 4.088, all P < 0.05), Tmsv-16sd ( t = 5.134, 4.326, 4.670, all P < 0.05), Tmsv-16dif% ( t = 7.714, 8.587, 7.800, all P < 0.05) and Tmsv16-sd% ( t = 9.004, 14.061, 10.305, all P < 0.05) respectively in the rehabilitation group, were significantly lower than those in the conventional treatment group. At 3, 6 and 12 months after surgery, fibroblast growth factor 23 ( t = 6.303, 5.053, 4.619, all P < 0.05). PICP ( t = 3.772, 2.798, 3.788, all P < 0.05) and PIIINP ( t = 3.110, 5.912, 4.294, all P < 0.05) in the rehabilitation group were significantly lower than those in the conventional treatment group. Within 12 months, the total incidence of cardiovascular end-point events in the rehabilitation group [12.00% (6/50)] was significantly lower than that in the conventional treatment [32.00% (16/50)] ( χ2 = 5.828, P < 0.05). Conclusion:Cardiac rehabilitation exercise can improve ventricular remodeling and synchrony in patients with acute myocardial infarction undergoing percutaneous coronary intervention and reduce the incidence of cardiovascular end-point events.

ObjectiveTo study central venous oxygen saturation (ScyO2) in controlled hemorrhagic shock rabbits resuscitation process as a transfusion trigger and traditional transfusion trigger of comparison.MethodsSelection New Zealand pure line of rabbit 32 only,simple randonly divided into 4 groups,groups A and B for the observation group,groups C and D as control group,groups of eight only.A,B,C,D four groups respectively by ScvO2 ≤70％,ScvO2 ≤75％,hemoglobin (Hb)≥8g/dl,blood loss for the whole blood volume≥30％ as transfusion trigger.From right femoral artery bloodletting 10 minute inside,made the MAP to about (40 ± 5 )mmHg,and maintained the blood pressure 60 minutes,established controlled hemorrhagic shock rabbits of animal model.And then started to resuscitate,with colloid and crystalloid infusion according to the proportion 1∶2,infusion rate of about 10 ～ 15ml/( kg · h),according to the blood pressure and heart rate,and proper adjustment according to the different requirements of each group conducted a blood transfusion.Monitoring based value,shock,shock treatment 30 minutes,60 minutes,120 minutes,180 minutes all time points,and various indexes of blood loss,blood transfusions,crystalloid and colloid fluid volume and so on.ResultsIn shock treatment observation group A late blood pressure,pH,BE,HCO3-,O2ER etc compared with the other three groups had obvious statistical differences ( P ＜ 0.05 ),group B with C and D two groups at the same time points each monitoring were no significant differences ( P ＞0.05 ).The volume of transfusion group C was most,compared with the other three groups were significant difference ( P ＜ 0.05 ),group D of blood transfusions than A,B two groups (P ＜ 0.05 ),groups A and B infused colloid fluid,crystal fluid volume than groups C and D ( P ＜ 0.05 ),each group blood lossed without significant difference.ConclusionScvO2 for controlled hemorrhagic shock rabbit resuscitation monitoring can guide controlled hemorrhagic shock rabbit of blood transfusions,according to ScvO2 ≤75％ transfusion with traditional according to Hb or blood loss transfusion trigger comparison,can achieve the same resuscitation effect,and can more accurately and individualized guide transfusion,reduce unnecessary blood transfusions,save resources.

Acute-On-Chronic Liver Failure ; blood ; pathology ; Case-Control Studies ; Cytochrome Reductases ; metabolism ; Humans ; Prospective Studies ; alpha-Fetoproteins ; metabolism

Objective To investigate the effects of peroxisome proliferator-activated receptor α( PPARα) on macrophage-mediated inflammatory responses with the interference of lipopolysaccharide and the possible mechanism.Methods The bone marrow stem cells were isolated from the femora of mice.The granulocyte-macrophage colony stimulating factor ( GM-CSF) was used to stimulate the in vitro differentiation from bone marrow stem cells into primary macrophages.An in vitro model with cultured cells expressing in-flammatory cytokines was established by treating the primary macrophages with lipopolysaccharide ( LPS) .A specific chemical agonist, Wy-14643, was used to activate PPARα. Autophagy inhibitors including 3-methyladenine (3-MA) and small interfering RNA against Atg7 ( Atg7 siRNA) were used to inhibit the autophagy.Western blot assay was performed to detect the expression of autophagy-related proteins ( Atg5, Atg7, Beclin-1 and LC3).The transcriptional levels of TNF-α, IL-1β, IL-6, Atg5, Atg7 and Beclin-1 were analyzed by qRT-PCR.Results Compared with the macrophages treated with LPS alone, those pretreated with various concentrations of Wy-14643 (10 μmol/L, 25 μmol/L and 50 μmol/L) showed inhibited ex-pression of proinflammatory cytokines ( TNF-α,IL-1βand IL-6) and enhanced expression of autophagy-relat-ed proteins (Atg5, Atg7 and Beclin-1) at mRNA level in a dose-dependent manner.The expression of auto-phagy-related proteins (Atg5, Atg7, Beclin-1 and LC3) by macrophages was promoted with the pretreatment of Wy-14643 as indicated by Western blot assay.The transcriptional levels of TNF-α, IL-1βand IL-6 were increased in Wy-14643 pretreated-macrophages after stimulation with 3-MA or Atg7 siRNA .Conclusion PPARαsuppressed the macrophage-mediated inflammatory responses by promoting autophagy, suggesting that the PPARα-autophagy pathway might be one of the signaling pathways regulating LPS induced-inflamma-tory responses.

Objective To analyze the role of cysteinyl aspartate specific proteinase-1 (caspase-1) in a mouse model of D-galactosamine (D-GalN) and lipopolysaccharide (LPS) induced acute liver failure (ALF) and to study the possible mechanism. Methods C57BL/ 6 mice were randomly divided into four groups including control group, Z-WEHD-FMK (caspase-1 inhibitor) treatment group, ALF model group and Z-WEHD-FMK-treated ALF group. The mouse model of ALF was established by intraperitoneally injec-ting the mice with D-GalN (450 mg/ kg) and LPS (10 μg/ kg). The damages in liver tissues were evaluated based on the histopathological examination and the levels of alanine transaminase (ALT) and aspartate trans-aminase (AST) in serum samples. Western blot assay was performed to analyze the expression of caspase-1 and the phosphorylation of glycogen synthase kinase 3β (GSK-3β). The qRT-PCR was used to measure the expression of inflammatory cytokines at transcriptional level. Results The expression of caspase-1 at both mRNA and protein levels were gradually increased during the development of ALF. Compared with the mice with ALF, those in the Z-WEHD-FMK-treated ALF group showed less severe liver damages on histopatholog-ical examination and decreased levels of ALT and AST in serum samples [ALT: (479. 2±39. 5) U/ L vs (998. 5±60. 4 ) U/ L, P<0. 05; AST: ( 478. 5±28. 6) U/ L vs ( 1 180. 7±91. 4) U/ L, P<0. 05]. The expression of TNF-α, IL-1β, IL-18 and IL-33 at transcriptional level were significantly suppressed in mice with ALF upon the Z-WEHD-FMK intervention. Results of the Western blot assay indicated that Z-WEHD-FMK suppressed the activities of GSK-3β by enhancing its phosphorylation. Conclusion This study demon-strated that caspase-1 could promote the activation of GSK-3β resulting in the development of inflammation responses and liver damages during the development of ALF in mice.

The products concentrations in traditional acetone-butanol (AB) fermentation are too low that large amount of energy has to be consumed in the distillation and product recovery process. Aiming at direct utilization of the fermentation products, in this study, optimization of property-improved biodiesel manufacturing process coupled with AB extractive fermentation was conducted, under the condition of using the biodiesel originated from waste cooking oil as the extractant and high concentrated corn flour medium. The effect of biodiesel/broth volume ratio, waste supernatant recycle ratio, and electronic carrier addition on the major process performance index was carefully investigated. Under the optimized condition, the biodiesel quality was improved with the cetane value increased from 51.4 to 54.4; "actual butanol yield" reached to a level of 18%, and waste supernatant recycle ratio exceeded 50%. In this way, elimination of energy-consuming product recovery process and realization of "energy-saving & waste minimization" industrial production target advocated by the state government, could be potentially expected.
Bioelectric Energy Sources ; Butanols ; chemistry ; Fermentation ; Gasoline ; Zea mays ; metabolism

Objective To analyze the role of a key intracellular signaling molecule GSK3β in hepatocyte apoptosis induced by endoplasmic reticulum stress (ERS).Methods Using mouse hepatoma cell lines(Hepa 1) as cell apoptosis model triggered by tunicamycin,an endoplasmic reticulum stress inducer.One hour before Hepa 1 apoptosis induced by tunicamycin,SB216763 specifically inhibited the activity of GSK3β.Living cells/apoptotic cells were detected using acetoxymethyl (AM)/propidium iodide (PI) staining; Furthermore,the measurement of lactate dehydrogenase(LDH) of cell culture supernatant to evaluate the apoptosis.We detect p-GSK3β,GSK3β,the ERS-related protein(GRP78,CHOP and caspase-12) and caspase-3,cleaved caspase-3 protein expression using Western blot.Results Endoplasmic reticulum stress induced by tunicamycin promotes GSK3β activity; Inhibition of GSK3β activity alleviates endoplasmic reticulum stress:the expression of GRP78,CHOP and caspase-12 expression are inhibited.At the same time,GSK3β activity inhibition significantly reduced the endoplasmic reticulum stress-induced apoptosis:compared to cell apoptosis model group,the intervention group of SB216763 showed that the level of LDH decreased significantly,and PI staining of apoptotic cells was also significant reduction.Western blot results showed that the inhibition of GSK 3 β activity reduced reactive cleaved caspase-3 protein.Conclusion GSK3β is an important signaling molecule in the apoptosis pathway induced by endoplasmic reticulum stress ;Endoplasmic reticulum stress promotes hepatocyte apoptosis by mediating GSK3β.

Objective: To investigate the role of the glycogen synthase kinase 3β (GSK3β) and the peroxisome proliferator-activated receptor alpha (PPARα) signaling pathway in acute liver failure and related mechanisms in a mouse model of acute liver failure induced by D-galactosamine/lipopolysaccharide (D-GalN/LPS). Methods: C57BL/6 mice were given intraperitoneal injection of D-GalN/LPS to establish a mouse model of acute liver failure. SB216763 was used to inhibit the activity of GSK3β and PPARα siRNA was used to inhibit the expression of PPARα. Western blotting was used to measure the expression of PPARα protein. The changes in liver pathology were observed to evaluate liver injury, and the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured to assess liver function. Quantitative real-time PCR was used to measure the mRNA expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-12p40 (IL-12p40), and PPARα. A one-way analysis of variance was used for comparison of means between multiple groups; the least significant difference test was used for data with homogeneity of variance, and the Games-Howell method was used for data with heterogeneity of variance. Results: In the mice with liver failure induced by D-GalN/LPS, GSK3β inhibition promoted the mRNA and protein expression of PPARα (F = 13.18 and 301.36, P = 0.00 and 0.00). In the mice with acute liver failure induced by D-GalN/LPS, GSK3β inhibition alleviated liver bleeding, inflammation, and necrosis and reduced the serum levels of ALT (F = 25.16, P = 0.000) and AST (F = 12.96, P = 0.001), as well as the mRNA expression of TNF-α (F = 32.17, P = 0.00), IL-1β (F = 11.57, P = 0.005), and IL-12p40 (F = 14.17, P = 0.015) in liver tissue. The inhibition of PPARα expression reversed the liver-protecting effect of GSK3β inhibition, which manifested as aggravation in liver bleeding, inflammation, and necrosis, increases in the serum levels of ALT (F = 25.16, P = 0.001) and AST (F = 12.96, P = 0.000), and an increase in the mRNA expression of TNF-α (F = 32.17, P = 0.00), IL-1β (F = 11.57, P = 0.024), and IL-12p40 (F = 14.17, P = 0.001) in liver tissue. Conclusion In mice with acute liver failure induced by D-GalN/LPS, the GSK3β-PPARα-inflammatory factor signaling pathway may play an important role. GSK3β inhibition has a protective effect in mice with acute liver failure possibly by activating the inhibitory inflammatory factor of PPARα.