MicroRNA-325 targets lipocalin 15 to suppress proliferation, migration and invasion of breast cancer cells.

Introduction: Recent studies have proved the diverse roles of miRs in different cancer-related processes. This study was undertaken to determine the therapeutic implications of miR-325-3p in breast cancer. Material and methods: Expression analysis was carried out by qRT-PCR. Transfections were performed by Lipofectamine 2000 reagent. MTT assay was used for cell viability. Transwell assays were used for cell migration and invasion. Western blot analysis was used for protein expression analysis. Results: Gene expression analysis revealed miR-325 to be significantly suppressed in breast cancer tissues and cell lines. Nonetheless, ectopic expression of miR-325 resulted in suppression of the growth and colony development potential of the SK-BR-3 and CAMA-1 cells. Transwell assays showed that miR-325 overexpression also resulted in the decline of the migration and invasion of the SK-BR-3 and CAMA-1 cells. Bioinformatic analysis showed that miR-325 targets lipocalin 15 (LNC15) in breast cancer cells. LNC15 was also overexpressed in the breast cancer tissues and cell lines. However, overexpression of miR-325 caused a significant decline in the LNC15 expression in SK-BR-3 cells. Additionally, silencing of LNC15 resulted in inhibition of the growth, migration and invasion of the SK-BR-3 cells. Rescue assay showed that overexpression of LNC15 could promote the growth, migration and invasion of the miR-325 overexpressing effects. Conclusions: Taken together, the evidence shows that miR-325 acts as a tumor suppressor in breast cancer and may be used in the treatment of breast cancer.

Studying the Influence of Finite Element Mesh Size on the Accuracy of Ventricular Tachycardia Simulation.

Background: Ventricular tachycardia (VT) is a life-threatening heart condition commonly seen in patients with myocardial infarction (MI). Although personalized computational modeling has been used to understand VT and its treatment noninvasively, this approach can be computationally intensive and time consuming. Therefore, finding a balance between mesh size and computational efficiency is important. This study aimed to find an optimal mesh resolution that minimizes the need for computational resources while maintaining numerical accuracy and to investigate the effect of mesh resolution variation on the simulation results. Methods: We constructed ventricular models from contrast-enhanced magnetic resonance imaging data from six patients with MI. We created seven different models for each patient, with average edge lengths ranging from 315 to 645 µm using commercial software, Mimics. Programmed electrical stimulation was used to assess VT inducibility from 19 sites in each heart model. Results: The simulation results in the slab model with adaptive tetrahedral mesh (same as in the patient-specific model) showed that the absolute and relative differences in conduction velocity (CV) were 6.1 cm/s and 7.8% between average mesh sizes of 142 and 600 µm, respectively. However, the simulation results in the six patient-specific models showed that average mesh sizes with 350 µm yielded over 85% accuracy for clinically relevant VT. Although average mesh sizes of 417 and 478 µm could also achieve approximately 80% accuracy for clinically relevant VT, the percentage of incorrectly predicted VTs increases. When conductivity was modified to match the CV in the model with the finest mesh size, the overall ratio of positively predicted VT increased. Conclusions: The proposed personalized heart model could achieve an optimal balance between simulation time and VT prediction accuracy when discretized with adaptive tetrahedral meshes with an average edge length about 350 µm.

Effects of alirocumab on cardiovascular events and all-cause mortality: a systematic review and meta-analysis.

Evaluation of the effects of alirocumab on cardiovascular (CV) events, CV mortality and all-cause mortality. Data search was carried out using the Cochrane Library, PubMed, Web of Science and Embase. The search time is up to November 18, 2020. All randomized clinical trials (AEs) comparing alirocumab with placebo were searched. Meta-analysis was performed by Review Manager version 5.3 (The Cochrane Collaboration, Copenhagen, Denmark), and the heterogeneity between studies was tested by Cochrane's Q test and measured with I2 statistics. A total of 13 randomized controlled trials with 24,815 participants were included. Alirocumab usage can considerably lower the incidence of CV events when compared to the control group (risk ratio(RR) 0.89, 95% confidence interval(CI) 0.83-0.95). No significant difference in CV mortality between the two groups was observed (RR 0.87, 95% CI 0.74-1.04). Treatment with alirocumab has been associated with a major decrease in all-cause mortality compared to placebo (RR 0.80, 95% CI 0.66-0.96). The incidence of serious adverse events (AEs) was similar in the two groups (RR 0.94, 95% CI 0.90-0.99). Alirocumab can reduce CV events and all-cause mortality. The AEs were mild and tolerable.

Gabapentin for phantom limb pain after amputation in pediatric oncology: a systematic review protocol.

BACKGROUND: Phantom limb pain (PLP) is a prevalent problem for children after amputation because of the chemotherapy treatment. Gabapentin is a potential option to manage PLP after amputation in pediatric oncology. However, no systematic review specifically investigated this topic. Thus, this study aims to appraise the efficacy and safety of gabapentin for post-amputation PLP in pediatric oncology. METHODS: Electronic databases (Cochrane Library, MEDLINE, EMBASE, Web of Science, CINAHL, PsychINFO, Scopus, WANGFANG, and Chinese Biomedical Literature Database) will be systematically searched from the beginning to the present without limitations to publication status and language. Primary outcome is pain intensity. Secondary outcomes are analgesic drug consumption, sleep quality, depression, anxiety, health-related quality of life, and adverse events. The treatment effect of all dichotomous outcome data will be estimated as risk ratio and 95% confidence intervals (CIs) and that of continuous outcome data will be calculated as mean difference or standardized mean difference and 95% CIs. Methodological quality of randomized controlled trials (RCTs) will be assessed using Cochrane risk of bias tool and that of case-controlled studies (CCSs) will be appraised using Newcastle-Ottawa Tool. Statistical analysis will be conducted using RevMan 5.3 software. DISCUSSION: This study will summarize up-to-date high-quality RCTs and CCSs to assess the efficacy and safety of gabapentin for PLP after amputation in pediatric oncology. The findings of this study will help to determine whether or not gabapentin is effective and safe for children with PLP after amputation. SYSTEMATIC REVIEW REGISTRATION: INPLASY202060090.

lncRNA SNHG1 cooperated with miR-497/miR-195-5p to modify epithelial-mesenchymal transition underlying colorectal cancer exacerbation.

Our study was intended to provide evidence for whether long noncoding RNA (lncRNA) SNHG1 would accelerate the epithelial-mesenchymal transition (EMT) course intrinsic in colorectal cancer (CRC) by sponging downstream miR-497-5p and miR-195-5p. We altogether collected 338 pairs of CRC and noncancerous tissues, and meanwhile purchased five CRC cell lines (i.e., SW480, HCT116, Lovo, CaCO-2, and HT29) and human embryo intestinal mucosal tissue-sourced cell line (i.e., CCC-HIE-2). The CRC cells as mentioned above were appraised regarding their potencies in proliferation, migration, and invasion, after being transfected with pcDNA3.1-SNHG1, si-SNHG1, miR-195-5p mimic/inhibitor, and miR-497-5p mimic/inhibitor. Eventually, we depended on reverse transcription-polymerase chain reaction to assess SNHG1, miR-497-5p, and miR-195-5p expressions, and the protein levels of EMT-specific molecules were determined on the strength of western blotting. It seemed that there was a high potential for highly expressed SNHG1 and lowly expressed miR-497/miR-195 to symbolize CRC patients' unfavorable prognosis (p < .05). Concurrently, CRC cells were detected with higher SNHG1 expression and lower miR-497/miR-195 expression than CCC-HIE-2 cells (p < .05). In addition, the EMT process of CRC cells was facilitated markedly against the contexts of overexpressed SNHG1 and underexpressed miR-497-5p/miR-195-5p. Intriguingly, the strength of miR-195-5p collaborating with miR-497-5p in affecting the activity of CRC cells seemed to overweigh that of miR-497/miR-195-5p alone. Besides, both miR-195-5p and miR-497-5p were subjected to in vivo and in vitro modification of SNHG1 (p < .05). Conclusively, application of lncRNA SNHG1 for treating CRC might be promising, given its dual modulation of miR-497 and miR-195 underlying CRC pathogenesis.

LncRNA NBR2 suppresses migration and invasion of colorectal cancer cells by downregulating miRNA-21.

It has been reported that lncRNA NBR2 regulates cancer metabolism. We investigated the role of NBR2 in colorectal cancer. We found that NBR2 was downregulated in colorectal cancer tissues than in adjacent healthy tissues. Decreased expression levels of NBR2 in tumor tissues were observed with the increase of clinical stages. MiRNA-21 was upregulated in colorectal cancer tissues than in adjacent healthy tissues, and was significantly and inversely correlated with NBR2. NBR2 overexpression downregulated miRNA-21 in colorectal cancer cells, while miRNA-21 overexpression failed to significantly affect NBR2 expression. NBR2 overexpression suppressed migration and invasion of colorectal cancer cells. MiRNA-21 overexpression played an opposite role and attenuated the effects of NBR2 overexpression. NBR2 overexpression did not significantly alter cancer cell proliferation. Therefore, lncRNA NBR2 inhibited colorectal cancer cell migration and invasion possibly by downregulating miRNA-21.

SODD promotes glucose uptake of colorectal cancer cells via AKT pathway.

Altered glucose metabolism has been found in a variety of malignant diseases and recognized as one of the hallmarks of cancer. However, the molecular mechanism behind it is far from well understood. In current study, we found silencer of death domains (SODD) regulates glucose uptake of colorectal cancer cells. When cultured under low level of glucose, SODD overexpressing RKO and SW1417 cells generated more colonies, compared with control cells, in clonogenic assay. SODD upregulation enhanced RKO and SW1417 cells viability. Furthermore, SODD induced more GLUT1 (Glucose transporter 1) expression and enhanced glucose uptake. AKT phosphorylation was upregulated in SODD overexpression cells. Moreover, inhibition of GLUT1 or AKT could reverse SODD induced glucose uptake enhancement. In conclusion, our findings indicate that SODD positively regulates glucose uptake and may be a potential therapeutic target of colorectal cancer.

Mir-30d suppresses cell proliferation of colon cancer cells by inhibiting cell autophagy and promoting cell apoptosis.

MiR-30 family plays an important role in the tumorigenesis of human cancers. The aim of the study is to investigate the role of miR-30d in human colon cancer cell lines and explore the molecular mechanism in the proliferation of colon cancer cells. The expression of miR-30d was determined by real-time polymerase chain reaction assay in colon cancer cell lines (HCT15, HCT116, HT-29, DLD-1, and SW480) and the results demonstrated that miR-30d level was significantly decreased in human colon cancer cell lines, compared with normal colon epithelial cell line. Transfection with miR-30d mimics inhibited cell proliferation, and transfection with miR-30d inhibitors significantly promoted cell viability of colon cancer cells. Furthermore, TargetScan analysis predicted that miR-30d interacted with messenger RNA on its 3' untranslated region of ATG5, phosphoinositide 3-kinase, and Beclin1 to negatively regulate cell autophagy in colon cancer cells. Moreover, transfection with miR-30d induced cell arrest at G2/M phase of HT-29 cells. Overexpression of miR-30d mimics inhibited cell viability probably due to the inhibition of cell autophagy and promotion of cell apoptosis. Thus, MiR-30d inhibited cell autophagy by directly targeting messenger RNA of ATG5, phosphoinositide 3-kinase, and Beclin1 and promoted cell apoptosis of human colon cancer cells. It is helpful to clarify the function of miR-30d in tumorigenesis of human cancers.

Knockdown of miR-27a sensitizes colorectal cancer stem cells to TRAIL by promoting the formation of Apaf-1-caspase-9 complex.

MicroRNAs have been proved to participate in multiple biological processes in cancers. For developing resistance to cytotoxic drug, cancer cells, especially the cancer stem cells, usually change their microRNA expression profile to survive in hostile environments. In the present study, we found that expression of microRNA-27a was increased in colorectal cancer stem cells. High level of microRNA-27a was indicated to induce the resistance to TNF-related apoptosis-inducing ligand (TRAIL). Knockdown of microRNA-27a resensitized colorectal cancer stem cells to TRAIL-induced cell death. Mechanically, the gene of Apaf-1, which is associated with the mitochondrial apoptosis, was demonstrated to be the target of microRNA-27a in colorectal cancer stem cells. Knockdown of microRNA-27a increased the expression level of Apaf-1, thus enhancing the formation of Apaf-1-caspase-9 complex and subsequently promoting the TRAIL-induced apoptosis in colorectal cancer stem cells. These findings suggested that knockdown of microRNA-27a in colorectal cancer stem cells by the specific antioligonucleotides was potential to reverse the chemoresistance to TRAIL. It may represent a novel therapeutic strategy for treating the colorectal cancer more effectively.

Protective effects of heparin on endothelial cells in sepsis.

OBJECTIVE: This study aims to observe the protective effects of heparin on endothelial cells in sepsis and explore the involved signal pathway regulated by heparin. Methods Human vascular endothelial cells were treated by TNFα in vitro to simulate the inflammatory environment when sepsis occurred. They were intervened by heparin and the expression levels of soluble thrombomodulin (sTM) and serum activated protein C (APC) were detected by ELISA, the regulatory mechanism of heparin improving vascular endothelial cells injury induced by TNFα was detected by Western Blotting method, the methylation of histone in the gene promoter region of endothelial nitric oxide synthase (eNOS) and monocyte chemotactic protein-1 (MCP-1) were detected using chromatin immunoprecipitation method. Results Heparin could inhibit the secretion of sTM and APC protein and the expression of MCP-1 gene which involved in NF-κB signal pathway. Conclusions Heparin could protect vascular endothelial cells from injury induced by TNFα and sepsis, the mechanisms were related with the effects of heparin on the histone methylation of promoter region and the regulation of heparin on the MAPK and NF-κB signal pathways. These results provide a theoretical basis for the application of heparin in the prevention and treatment of vascular disease related with sepsis.

miR-205 regulates A549 cells proliferation by targeting PTEN.

miR-205 is an epithelial-specific miRNA and has been shown to orchestrate some cellular processes such as epithelial mesenchymal transition (EMT) and differentiation fate of stem cells in mammary gland. miR-205 play a part of a tumor suppressor in human cancers. However, the role of miR-205 in lung cancer is unclear. In this study, we detected the expression level of miR-205 in 46 cases clinical lung cancer specimens and adjacent normal tissues by stem-loop RT-PCR. We found that the expression of miR-205 was significantly increased in lung cancer specimens compared to adjacent normal tissues (P < 0.01). Furthermore, we observed the expressions of PTEN protein and mRNA in lung cancer tissues and adjacent normal tissues by methods of western blot and Real time PCR respectively. We found that the expressions of PTEN protein and mRNA was significantly decreased in lung cancer specimens compared to adjacent normal tissues. And then, we found there is a negative relationship between the expression of miR-205 and PTEN mRNA in lung cancer by analyzed. To validate whether PTEN was direct targets of miR-205, a dual-luciferase reporter assay was employed, the result showed that PTEN is a target gene of MiR-205. In subsequent experiments, we examined the expressions of PTEN protein and mRNA after transfection of miR-205 mimics or inhibitor into A549 cells, and A549 cell proliferation was measured by CCK-8 tests. We found that the expression of PTEN protein and mRNA in A549 cells were significantly down-regulated or up-regulated after miR-205 mimics and miR-205 inhibitors transfected into, and miR-205 could inhibits A549 cells proliferation. These results indicate that miR-205 might inhibitor the proliferation of A549 cells by regulating the expression of PTEN.

[Antagonistic effect and mechanism of Rosuvastatin on myocardial apoptosis in rats with acute myocardial infarction].

OBJECTIVE: To investigate the protective effect of Rosuvastatin on myocardial cells in rats with acute myocardial infarction and its possible mechanism. METHODS: Rats were randomly assigned to four groups: Control group, Sham group, AMI and Rosuvastatin group. The levels of lactate dehydrogenase (LDH) and creatine jubase (CK), the vitality of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were detected by assay kits and the levels of C-reactive protein (CRP), tumor necrosis factor (TNF) alpha and interleukin (IL)-6 expression were detected by enzyme linked immunosorbent assay (ELISA). TTC/Evans blue staining was used to determine the relative myocardial infarction area, HE staining was used to detect pathologic changes and myocardial apoptosis was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL). What's more, Western blot was used to detect the protein expression of B-cell lymphoma-2 (Bcl-2), Bax, cleaved-Caspase-3, Rock1, Rock2, I-κB and NF-κBp65. RESULTS: The model of acute myocardial infarction rats was established. Compared with Sham group, the myocardial pathological changes were more severe, and the apoptosis number, the production of inflammatory factors and oxidative damage were significantly increased in AMI group. Compared with AMI group, the relative area of infarction myocardium (43% ± 4% vs 31% ± 8%, P=0.004 3) was dramatically reduced, the levels of LDH (2 545.45 ± 613.67 U/L vs 1 573.43 ± 373.72 U/L, P=0.02) and CK (7.49 ± 1.75 U/ml vs 4.42 ± 1.28 U/ml, P=0.04) in serum were significantly lower (P<0.01), the myocardial pathological damage degree was relieved, the apoptosis number (41% ± 8% vs 23% ± 6%, P=0.014 7) was significantly decreased, the expression of Bax (1.17 ± 0.10 vs 0.57 ± 0.08, P=0.003) and cleaved-Caspase-3 (1.31 ± 0.07 vs 0.70 ± 0.01, P=0.004) were dramatically reduced, and the expression of Bcl-2 (0.19 ± 0.01 vs 0.32 ± 0.01, P=0.003) was enhanced in Rosuvastatin group. Furthermore, the production of inflammatory factors and oxidative damage were effectively alleviated (P<0.05), the protein expression of Rock1, Rock2 and NF-κBp65 were declined in Rosuvastatin group (P<0.01). CONCLUSION: Rosuvastatin can effectively alleviate the cardiomyocyte apoptosis induced by acute ischemia, and its main mechanism may be the inhibition on RhoA/ROCK activation and the oxidative stress and inflammation reaction mediated by it.

[Effects of telmisartan on inflammation and fibrosis after acute myocardial infarction in rats].

OBJECTIVE: To explore the protection mechanisms of telmisartan on inflammation and fibrosis after myocardial infarction in rats. METHODS: The model of acute myocardial infarction (AMI) was established by ligating left anterior descending coronary artery. The surviving rats were divided into AMI (AMI) and telmisartan treatment (telmisartan) groups. And another sham operation group (sham) was designated (n = 8). At the end of study, total heart weight (THW), left ventricular weight (LVW) and weight index were measured; myocardial infarction and inflammatory reactions detected by hematoxylin and eosin and Masson staining; the serum levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNFα), monocyte chemotactic protein-1 (MCP-1), interleukin-6 (IL-6) and interleukin-1 beta (IL-1ß) by enzyme-linked immunosorbent assay (ELISA); the levels of transforming growth factor 1 (TGFß1), collagen I, collagen III and MMP9 mRNA in myocardial tissue by reverse transcription-polymerase chain reaction (RT-PCR); the expressions of TGFß1, collagen I, collagen III, matrix metallopeptidase 9 (MMP9) and nuclear factor-kappa B (NF-κB) by Western blot. RESULTS: Compared with sham group, significant pathological changes of myocardium occurred in AMI group. The serum levels of CRP [(472 ± 132) vs (104 ± 28) ng/ml], TNFα [(229 ± 41) vs (18 ± 5) pg/ml], MCP-1[(558 ± 116) vs (158 ± 20) pg/ml], IL-6 [(404 ± 63) vs (21 ± 4) pg/ml] and IL-1ß [(625 ± 145) vs (189 ± 34) pg/ml] increased (P < 0.05). RT-PCR analysis showed that the expression levels of TGFß1, collagen I, collagen III and MMP9 increased significantly. The results of Western blot were consistent and NF-κB was activated significantly (P < 0.05). Compared with AMI group, the above-mentioned indicators decreased obviously in telmisartan group (P < 0.05). CONCLUSION: Telmisartan may regulate inflammation and myocardial fibrosis after acute myocardial infarction by signaling pathways of NF-κB and TGFß in rats.

Red blood cell count as an indicator of microvascular complications in Chinese patients with type 2 diabetes mellitus.

BACKGROUND: Rheological disorders of red blood cells (RBC) and decreased RBC deformability have been involved in the development of diabetic microangiopathy. However, few studies have evaluated the association of RBC count with microvascular complications in patients with type 2 diabetes mellitus (T2DM). The purpose of this study was to investigate the association of RBC count with microvascular complications in patients with T2DM. METHODS: This study involved 369 patients with T2DM: 243 with one or more microvascular complications and 126 without microvascular complications. Anticoagulated blood was collected and analyzed in an automated blood cell counter. The presence of risk factors for microvascular complications was determined. RESULTS: The proportion of patients with microvascular complications increased as the RBC count decreased (P < 0.001). After adjustment for known risk factors for microvascular complications by logistic regression analysis, lower quartiles of RBC count were associated with a higher risk of microvascular complications compared with the reference group composed of the highest quartile (first quartile, odds ratio 4.98, 95% confidence interval 1.54-6.19, P = 0.008; second quartile, odds ratio 3.21, 95% confidence interval 1.17-5.28, P = 0.024). CONCLUSION: A decreased RBC count is associated with microvascular complications in Chinese patients with T2DM. The RBC count is a potential marker to improve further the ability to identify diabetic patients at high risk of microvascular complications.

Emodin, a naturally occurring anthraquinone, ameliorates experimental autoimmune myocarditis in rats.

Myocarditis is an inflammatory disease of the heart and a major cause of dilated cardiomyopathy that can lead to heart failure and sudden death in young adults. Giant cell myocarditis is a severe heart disease of unknown causes and is defined histopathologically as diffuse myocardial necrosis with multinucleated giant cells in the absence of sarcoid-like granulomata. Giant cell myocarditis is often studied using a model of experimental autoimmune myocarditis (EAM) in rats. Emodin is an important component of traditional Chinese herb rhubarb, and has well-documented anti-inflammatory effect. The current study determined the potential efficacy of emodin using a rat model of EAM. Male Lewis rats (6 weeks of age) were immunized on days 0 and 7 with a porcine cardiac myosin at both footpads to induce EAM. Simultaneously with the immunization, rats received emodin (50 mg/kg/day) or distilled water by intragastric administration for 3 weeks (8 animals/group). Likewise, eight animals were immunized with adjuvant alone and treated with distilled water. The immunization significantly enlarged the hearts due to inflammatory lesions. Emodin treatment significantly improved left ventricular (LV) function and reduced the severity of myocarditis, as reflected by echocardiographic and histopathological examination. Emodin treatment decreased the serum levels of proinflammatory cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-1ß. Nuclear factor-κBp65 (NF-κBp65), a rapid-response transcription factor that regulates proinflammatory cytokines, in the myocardial tissue was also suppressed in the treated rats. In conclusion, emodin could ameliorate EAM, at least in part, by decreasing the production of proinflammatory cytokines TNF-α and IL-1ß.

[Study of the effects of mechanical ventilation on the heart function of patients with echocardiography].

OBJECTIVE: To study the effects of different positive end expiratory pressure (PEEP) levels on the heart function of patients undergoing mechanical ventilation (MV) with echocardiography. METHODS: Thirty six critical patients with respiratory failure undergoing MV were divided into two groups according to the cardiac index (CI). The left heart function was measured with echocardiography at different PEEP levels (0, 4, 7, 10, 14 cm H(2)O, 1 cm H(2)O=0.098 kPa). RESULTS: In the normal cardiac function group (CI≥2.0 L×min(-1) ×m(-2) , n=17), an increase in PEEP had no significant effects on left ventricular systolic function [left ventricular end systolic volume (LVESV), left ventricular end diastolic volume (LVEDV), cardiac output (CO), ejection fraction (EF)]. The increase in PEEP had no significant effect on left ventricular diastolic function [mitral early diastolic filling velocity (E), late diastolic filling velocity (A), the ratio of E/A, early diastolic velocity (Ve), late diastolic velocity (Va), the ratio of Ve/Va, left ventricular end diastolic pressure (LVEDP)]. In the poor cardiac function group (CIP<2.0 L×min(-1) ×m(-2), n=19), when PEEP was increased to 10 cm H(2)O and 14 cm H(2)O, compared with PEEP 0, left ventricular systolic function indexes including LVESV (ml: 21.2±1.2 vs. 18.2±1.4 as 10 cm H(2)O) was significantly higher, i.e. LVEDV (ml: 42.6±2.4, 40.1±1.9 vs. 44.5±3.5), CO (L: 2.3±0.6, 2.1±0.7 vs. 2.6±0.7), EF (0.40±0.02, 0.39±0.02 vs. 0.42±0.02) were decreased (all P<0.05); left ventricular diastolic function indexes including A (cm/s: 88.5±15.2, 93.2±18.7 vs. 76.0±9.0), Va (cm/s: 14.3±4.5, 15.8±5.3 vs. 12.0±1.2), LVEDP [mm Hg (1 mm Hg=0.133 kPa): 15.3±2.0, 16.9±2.8 vs. 10.7±2.5] were significantly higher; E (cm/s: 73.6±15.4, 63.2±16.4 vs. 83.1±20.1), the ratio of E/A (0.83±0.10, 0.68±0.20 vs. 1.10±0.20), Ve (cm/s: 11.7±1.8, 10.4±2.0 vs. 13.8±2.8), the ratio of Ve/Va (0.8±0.1 , 0.6±0.2 vs. 1.2±0.2) were decreased (all P<0.05). CONCLUSION: Under the same condition of MV, change in PEEP levels (0-14 cm H(2)O) do not produce any obvious effect in the normal cardiac function group, on the other hand when PEEP≥10 cm H(2)O left heart function is significantly lowered in the poor cardiac function group. Optimal PEEP may improve the cardiac function.