rFSAV promotes Staphylococcus aureus-infected bone defect healing via IL-13- mediated M2 macrophage polarization.

Staphylococcus aureus (S. aureus) contamination commonly occurs in orthopedic internal fixation operations, leading to a delayed healing of the defected bone tissue. However, antibiotic treatments are ineffective in dealing with S. aureus bone infections due to the rise in multiple antimicrobial resistances. Here, we reported the protective effects of a recombinant five-antigen S. aureus vaccine (rFSAV) in an S. aureus infected bone defect model. In this study, we found the number of M2 macrophages markedly increased in the defect site and played a critical role in the healing of defected bone mediated by rFSAV. Mechanistically, rFSAV mediated increased level of IL-13 in bone defect site predominant M2 macrophage polarization. In summary, our study reveals a key role of M2 macrophage polarization in the bone regeneration process in S. aureus infection induced bone defect, which provide a promising application of rFSAV for the treatment of bone infection for orthopedic applications.

S-nitrosylation of RABG3E positively regulates vesicle trafficking to promote salt tolerance.

Nitric oxide (NO) is a key signaling molecule affecting the response of plants to salt stress; however, the underlying molecular mechanism is poorly understood. In this study, we conducted a phenotype analysis and found that the small GTPase RABG3E (RAB7) promotes salt tolerance in Arabidopsis thaliana. NO promotes the S-nitrosylation of RAB7 at Cys-171, which in turn helps maintain the ion balance in salt-stressed plants. Furthermore, the S-nitrosylation of RAB7 at Cys-171 enhances the enzyme's GTPase activity, thereby promoting vesicle trafficking and increasing its interaction with phosphatidylinositol phosphates-especially phosphatidylinositol-4-phosphate (PI4P). Exogenously applied PI4P increases vesicle trafficking and promotes salt tolerance depending on the S-nitrosylation of RAB7 at Cys-171. These findings illustrate a unique mechanism in salt tolerance, by which NO regulates vesicle trafficking and ion homeostasis through the S-nitrosylation of RAB7 and its interaction with PI4P.

Calcium Signaling and the Response to Heat Shock in Crop Plants.

Climate change and the increasing frequency of high temperature (HT) events are significant threats to global crop yields. To address this, a comprehensive understanding of how plants respond to heat shock (HS) is essential. Signaling pathways involving calcium (Ca2+), a versatile second messenger in plants, encode information through temporal and spatial variations in ion concentration. Ca2+ is detected by Ca2+-sensing effectors, including channels and binding proteins, which trigger specific cellular responses. At elevated temperatures, the cytosolic concentration of Ca2+ in plant cells increases rapidly, making Ca2+ signals the earliest response to HS. In this review, we discuss the crucial role of Ca2+ signaling in raising plant thermotolerance, and we explore its multifaceted contributions to various aspects of the plant HS response (HSR).

The Role of Nitric Oxide in Plant Responses to Salt Stress.

The gas nitric oxide (NO) plays an important role in several biological processes in plants, including growth, development, and biotic/abiotic stress responses. Salinity has received increasing attention from scientists as an abiotic stressor that can seriously harm plant growth and crop yields. Under saline conditions, plants produce NO, which can alleviate salt-induced damage. Here, we summarize NO synthesis during salt stress and describe how NO is involved in alleviating salt stress effects through different strategies, including interactions with various other signaling molecules and plant hormones. Finally, future directions for research on the role of NO in plant salt tolerance are discussed. This summary will serve as a reference for researchers studying NO in plants.

An Immunodominant Epitope-Specific Monoclonal Antibody Cocktail Improves Survival in a Mouse Model of Staphylococcus aureus Bacteremia.

To date, no vaccine or monoclonal antibody (mAb) against Staphylococcus aureus has been approved for use in humans. Our laboratory has developed a 5-antigen S. aureus vaccine (rFSAV), which is now under efficacy evaluation in a phase 2 clinical trial. In the current study, using overlapping peptides and antiserum from rFSAV-immunized volunteers, we identified 7 B-cell immunodominant epitopes on 4 antigens in rFSAV, including 5 novel epitopes (Hla48-65, IsdB402-419, IsdB432-449, SEB78-95, and MntC7-24). Ten immunodominant epitope mAbs were generated against these epitopes, and all of them exhibited partial protection in a mouse sepsis model. Four robust mAbs were used together as an mAb cocktail to prevent methicillin-resistant S. aureus strain 252 infection. The results showed that the mAb cocktail was efficient in combating S. aureus infection and that its protective efficacy correlated with a reduced bacterial burden and decreased infection pathology, which demonstrates that the mAb cocktail is a promising S. aureus vaccine candidate.

Rictor, an essential component of mTOR complex 2, undergoes caspase-mediated cleavage during apoptosis induced by multiple stimuli.

Caspase-mediated cleavage of proteins ensures the irreversible commitment of cells to undergo apoptosis, and is thus a hallmark of apoptosis. Rapamycin-insensitive companion of mTOR (rictor) functions primarily as a core and essential component of mTOR complex 2 (mTORC2) to critically regulate cellular homeostasis. However, its role in the regulation of apoptosis is largely unknown. In the current study, we found that rictor was cleaved to generate two small fragments at ~ 50 kD and ~ 130 kD in cells undergoing apoptosis upon treatment with different stimuli such as the death ligand, TRAIL, and the small molecule, AZD9291. This cleavage was abolished when caspases were inhibited and could be reproduced when directly incubating rictor protein and caspase-3 in vitro. Furthermore, the cleavage site of caspase-3 on rictor was mapped at D1244 (VGVD). These findings together robustly demonstrate that rictor is a substrate of caspase-3 and undergoes cleavage during apoptosis. These results add new information for understanding the biology of rictor in the regulation of cell survival and growth.

Upregulation of Tubulointerstitial nephritis antigen like 1 promotes gastric cancer growth and metastasis by regulating multiple matrix metallopeptidase expression.

BACKGROUND AND AIM: Tubulointerstitial nephritis antigen-like 1 (TINAGL1), as a novel matricellular protein, has been demonstrated to participate in cancer progression, whereas the potential function of TINAGL1 in gastric cancer (GC) remains unknown. METHODS: The expression pattern of TINAGL1 in GC was examined by immunohistochemistry, ELISA, real-time polymerase chain reaction, and Western blot. Correlation between TINAGL1 and matrix metalloproteinases (MMPs) was analyzed by the GEPIA website and Kaplan-Meier plots database. The lentivirus-based TINAGL1 knockdown, CCK-8, and transwell assays were used to test the function of TINAGL1 in vitro. The role of TINAGL1 was confirmed by subcutaneous xenograft, abdominal dissemination, and lung metastasis model. Microarray experiments, ELISA, real-time polymerase chain reaction, and Western blot were used to identify molecular mechanism. RESULTS: TINAGL1 was increased in GC tumor tissues and associated with poor patient survival. Moreover, TINAGL1 significantly promoted GC cell proliferation and migration in vitro as well as facilitated GC tumor growth and metastasis in vivo. TINAGL1 expression in GC cells was accompanied with increasing MMPs including MMP2, MMP9, MMP11, MMP14, and MMP16. GEPIA database revealed that these MMPs were correlated with TINAGL1 in GC tumors and that the most highly expressed MMP was MMP2. Mechanically, TINAGL1 regulated MMP2 through the JNK signaling pathway activation. CONCLUSIONS: Our data highlight that TINAGL1 promotes GC growth and metastasis and regulates MMP2 expression, indicating that TINAGL1 may serve as a therapeutic target for GC.

[A heart sound classification method based on joint decision of extreme gradient boosting and deep neural network].

Heart sound is one of the common medical signals for diagnosing cardiovascular diseases. This paper studies the binary classification between normal or abnormal heart sounds, and proposes a heart sound classification algorithm based on the joint decision of extreme gradient boosting (XGBoost) and deep neural network, achieving a further improvement in feature extraction and model accuracy. First, the preprocessed heart sound recordings are segmented into four status, and five categories of features are extracted from the signals based on segmentation. The first four categories of features are sieved through recursive feature elimination, which is used as the input of the XGBoost classifier. The last category is the Mel-frequency cepstral coefficient (MFCC), which is used as the input of long short-term memory network (LSTM). Considering the imbalance of the data set, these two classifiers are both improved with weights. Finally, the heterogeneous integrated decision method is adopted to obtain the prediction. The algorithm was applied to the open heart sound database of the PhysioNet Computing in Cardiology(CINC) Challenge in 2016 on the PhysioNet website, to test the sensitivity, specificity, modified accuracy and F score. The results were 93%, 89.4%, 91.2% and 91.3% respectively. Compared with the results of machine learning, convolutional neural networks (CNN) and other methods used by other researchers, the accuracy and sensibility have been obviously improved, which proves that the method in this paper could effectively improve the accuracy of heart sound signal classification, and has great potential in the clinical auxiliary diagnosis application of some cardiovascular diseases.

Application of Transition-Metal Catalysis, Biocatalysis, and Flow Chemistry as State-of-the-Art Technologies in the Synthesis of LCZ696.

LCZ696 is a novel treatment for patients suffering from heart failure that combines the two active pharmaceutical ingredients sacubitril and valsartan in a single chemical compound. While valsartan is an established drug substance, a new manufacturing process suitable for large-scale commercial production had to be developed for sacubitril. The use of chemocatalysis, biocatalysis, and flow chemistry as state-of-the-art technologies allowed to efficiently build up the structure of sacubitril and achieve the defined performance targets.

Cyclic nucleotide-gated ion channel 6 mediates thermotolerance in Arabidopsis seedlings by regulating nitric oxide production via cytosolic calcium ions.

BACKGROUND: We previously reported the involvement of nitric oxide (NO) and cyclic nucleotide-gated ion channel 6 (CNGC6) in the responses of plants to heat shock (HS) exposure. To elucidate their relationship with heat tolerance in Arabidopsis thaliana, we examined the effects of HS on several groups of seedlings: wild type, cngc6, and cngc6 complementation and overexpression lines. RESULTS: After HS exposure, the level of NO was lower in cngc6 seedlings than in wild-type seedlings but significantly elevated in the transgenic lines depending on CNGC6 expression level. The treatment of seeds with calcium ions (Ca2+) enhanced the NO level in Arabidopsis seedlings under HS conditions, whereas treatment with EGTA (a Ca2+ chelator) reduced it, implicating that CNGC6 stimulates the accumulation of NO depending on an increase in cytosolic Ca2+ ([Ca2+]cyt). This idea was proved by phenotypic observations and thermotolerance testing of transgenic plants overexpressing NIA2 and NOA1, respectively, in a cngc6 background. Western blotting indicated that CNGC6 stimulated the accumulation of HS proteins via NO. CONCLUSION: These data indicate that CNGC6 acts upstream of NO in the HS pathway, which improves our insufficient knowledge of the initiation of plant responses to high temerature.

Antiproliferative Activity of Carnosic Acid is Mediated via Inhibition of Cell Migration and Invasion, and Suppression of Phosphatidylinositol 3-Kinases (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway.

BACKGROUND Lung cancer is one of the leading causes of cancer-related mortalities worldwide and majority of these deaths result from non-small cell lung cancer (NSCLC). The primary objective of this research was to determine the anticancer potential of carnosic acid, a plant derived abietane diterpene, against human lung cancer cells, as well as to determine its effects on cell migration and invasion, apoptosis, and the PI3K/AKT/m-TOR signaling pathway. MATERIAL AND METHODS Cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay; fluorescence microscopy using acridine orange/ethidium bromide stain and Comet assay were used to study cellular apoptosis. In vitro wound healing assay was used to study effects on cell migration; Transwell assay was used to study cell invasion after drug treatment. Western blot assay was used to study effects of carnosic acid on the PI3K/AKT/m-TOR signaling pathway. RESULTS It was shown that carnosic acid could inhibit the growth of A-549 human non-small cell lung carcinoma cells dose-dependently showing an IC50 value of 12.5 µM. This growth inhibition of A-549 cells was mediated via apoptotic cell death as observed by fluorescence microscopy showing nuclear fragmentation and chromatin condensation. Carnosic acid, dose-dependently, also inhibited cell migration and invasion. Finally, western blot assay revealed that carnosic acid also led to inhibition of the PI3K/AKT/m-TOR signaling pathway. CONCLUSIONS In conclusion, our results showed that Carnosic acid has the potential to inhibit cancer cell growth in A-549 lung cancer cells by activating apoptotic death, inhibiting cell migration and invasion and suppressing PI3K/AKT/m-TOR signaling pathway.

Arabidopsis CaM1 and CaM4 Promote Nitric Oxide Production and Salt Resistance by Inhibiting S-Nitrosoglutathione Reductase via Direct Binding.

Salt is a major threat to plant growth and crop productivity. Calmodulin (CaM), the most important multifunctional Ca2+ sensor protein in plants, mediates reactions against environmental stresses through target proteins; however, direct proof of the participation of CaM in salt tolerance and its corresponding signaling pathway in vivo is lacking. In this study, we found that AtCaM1 and AtCaM4 produced salt-responsive CaM isoforms according to real-time reverse transcription-polymerase chain reaction analyses; this result was verified based on a phenotypic analysis of salt-treated loss-of-function mutant and transgenic plants. We also found that the level of nitric oxide (NO), an important salt-responsive signaling molecule, varied in response to salt treatment depending on AtCaM1 and AtCaM4 expression. GSNOR is considered as an important and widely utilized regulatory component of NO homeostasis in plant resistance protein signaling networks. In vivo and in vitro protein-protein interaction assays revealed direct binding between AtCaM4 and S-nitrosoglutathione reductase (GSNOR), leading to reduced GSNOR activity and an increased NO level. Overexpression of GSNOR intensified the salt sensitivity of cam4 mutant plants accompanied by a reduced internal NO level, whereas a gsnor deficiency increased the salt tolerance of cam4 plants accompanied by an increased internal NO level. Physiological experiments showed that CaM4-GSNOR, acting through NO, reestablished the ion balance to increase plant resistance to salt stress. Together, these data suggest that AtCaM1 and AtCaM4 serve as signals in plant salt resistance by promoting NO accumulation through the binding and inhibition of GSNOR. This could be a conserved defensive signaling pathway in plants and animals.

A High Precision Real-time Premature Ventricular Contraction Assessment Method based on the Complex Feature Set.

This paper presents a high precision and low computational complexity premature ventricular contraction (PVC) assessment method for the ECG human-machine interface device. The original signals are preprocessed by integrated filters. Then, R points and surrounding feature points are determined by corresponding detection algorithms. On this basis, a complex feature set and feature matrices are obtained according to the position feature points. Finally, an exponential Minkowski distance method is proposed for PVC recognition. Both public dataset and clinical experiments were utilized to verify the effectiveness and superiority of the proposed method. The results show that our R peak detection algorithm can substantially reduce the error rate, and obtained 98.97% accuracy for QRS complexes. Meanwhile, the accuracy of PVC recognition was 98.69% for the MIT-BIH database and 98.49% for clinical tests. Moreover, benefiting from the lightweight of our model, it can be easily applied to portable healthcare devices for human-computer interaction.

An Improved Convolutional Neural Network Based Approach for Automated Heartbeat Classification.

With age, our blood vessels are prone to aging, which induces cardiovascular disease. As an important basis for diagnosing heart disease and evaluating heart function, the electrocardiogram (ECG) records cardiac physiological electrical activity. Abnormalities in cardiac physiological activity are directly reflected in the ECG. Thus, ECG research is conducive to heart disease diagnosis. Considering the complexity of arrhythmia detection, we present an improved convolutional neural network (CNN) model for accurate classification. Compared with the traditional machine learning methods, CNN requires no additional feature extraction steps due to the automatic feature processing layers. In this paper, an improved CNN is proposed to automatically classify the heartbeat of arrhythmia. Firstly, all the heartbeats are divided from the original signals. After segmentation, the ECG heartbeats can be inputted into the first convolutional layers. In the proposed structure, kernels with different sizes are used in each convolution layer, which takes full advantage of the features in different scales. Then a max-pooling layer followed. The outputs of the last pooling layer are merged and as the input to fully-connected layers. Our experiment is in accordance with the AAMI inter-patient standard, which included normal beats (N), supraventricular ectopic beats (S), ventricular ectopic beats (V), fusion beats (F), and unknown beats (Q). For verification, the MIT arrhythmia database is introduced to confirm the accuracy of the proposed method, then, comparative experiments are conducted. The experiment demonstrates that our proposed method has high performance for arrhythmia detection, the accuracy is 99.06%. When properly trained, the proposed improved CNN model can be employed as a tool to automatically detect different kinds of arrhythmia from ECG.

MicroRNA-30c suppresses the pro-fibrogenic effects of cardiac fibroblasts induced by TGF-ß1 and prevents atrial fibrosis by targeting TGFßRII.

Atrial fibrosis serves as an important contributor to atrial fibrillation (AF). Recent data have suggested that microRNA-30c (miR-30c) is involved in fibrotic remodelling and cancer development, but the specific role of miR-30c in atrial fibrosis remains unclear. The purpose of this study was to investigate the role of miR-30c in atrial fibrosis and its underlying mechanisms through in vivo and in vitro experiments. Our results indicate that miR-30c is significantly down-regulated in the rat abdominal aortic constriction (AAC) model and in the cellular model of fibrosis induced by transforming growth factor-ß1 (TGF-ß1). Overexpression of miR-30c in cardiac fibroblasts (CFs) markedly inhibits CF proliferation, differentiation, migration and collagen production, whereas decrease in miR-30c leads to the opposite results. Moreover, we identified TGFßRII as a target of miR-30c. Finally, transferring adeno-associated virus 9 (AAV9)-miR-30c into the inferior vena cava of rats attenuated fibrosis in the left atrium following AAC. These data indicate that miR-30c attenuates atrial fibrosis via inhibition of CF proliferation, differentiation, migration and collagen production by targeting TGFßRII, suggesting that miR-30c might be a novel potential therapeutic target for preventing atrial fibrosis.

Spatial dynamics of TRAIL death receptors in cancer cells.

TNF-related apoptosis inducing ligand (TRAIL) selectively induces apoptosis in cancer cells without harming most normal cells. Currently, multiple clinical trials are underway to evaluate the antitumor activity of recombinant human TRAIL (rhTRAIL) and agonistic antibodies that target death receptors (DRs) 4 or 5. It is encouraging that these products have shown a tolerated safety profile in early phase studies. However, their therapeutic potential is likely limited by the emergence of tumor drug resistance phenomena. Increasing evidence indicates that TRAIL DRs are deficient on the plasma membrane of some cancer cells despite their total protein expression. Notably, the lack of surface DR4/DR5 is sufficient to render cancers resistant to TRAIL-induced apoptosis, regardless of the status of other apoptosis signaling components. The current review highlights recent findings on the dynamic expression of TRAIL death receptors, including the regulatory roles of endocytosis, autophagy, and Ras GTPase-mediated signaling events. This information could aid in the identification of novel predictive biomarkers of tumor response as well as the development of combinational drugs to overcome or bypass tumor drug resistance to TRAIL receptor-targeted therapies.

Hydrogen peroxide acts upstream of nitric oxide in the heat shock pathway in Arabidopsis seedlings.

We previously reported that nitric oxide (NO) functions as a signal in thermotolerance. To illustrate its relationship with hydrogen peroxide (H2O2) in the tolerance of Arabidopsis (Arabidopsis thaliana) to heat shock (HS), we investigated the effects of heat on Arabidopsis seedlings of the following types: the wild type; three NADPH oxidase-defective mutants that exhibit reduced endogenous H2O2 levels (atrbohB, atrbohD, and atrbohB/D); and a mutant that is resistant to inhibition by fosmidomycin (noa1, for nitric oxide-associated protein1). After HS, the NO levels in atrbohB, atrbohD, and atrbohB/D seedlings were lower than that in wild-type seedlings. Treatment of the seedlings with sodium nitroprusside or S-nitroso-N-acetylpenicillamine partially rescued their heat sensitivity, suggesting that NO is involved in H2O2 signaling as a downstream factor. This point was verified by phenotypic analyses and thermotolerance testing of transgenic seedlings that overexpressed Nitrate reductase2 and NOA1, respectively, in an atrbohB/D background. Electrophoretic mobility shift assays, western blotting, and real-time reverse transcription-polymerase chain reaction demonstrated that NO stimulated the DNA-binding activity of HS factors and the accumulation of HS proteins through H2O2. These data indicate that H2O2 acts upstream of NO in thermotolerance, which requires increased HS factor DNA-binding activity and HS protein accumulation.

Dendritic cell-glioma fusion activates T lymphocytes by elevating cytotoxic efficiency as an antitumor vaccine.

BACKGROUND: Hybrid cells produced by fusions of tumor and dendritic cells (DC) have demonstrated remarkable efficacy for priming the anti-tumor immune response. In the current study, we examined the antitumor activity of cytotoxic T lymphocytes (CTLs) primed in response to a tumor vaccine comprising a glioma-DC fusion as part of a therapeutic against glioma. MATERIAL AND METHODS: Primary cultured glioma cells were fused with peripheral blood DC under conditions of polyethylene glycol (PEG) incubation. Glioma cell suspensions were designated as three groups to include (1) CTL-effective cell group activated by fused cells; (2) CTL-effective cell group stimulated by co-cultured glioma cells and DC cells; and (3) lymphocyte-only group as a control, which was not stimulated by the DC. Cytotoxicity of CTLs on glioma cells was accessed by MTT assay in vitro. RESULTS: Glioma cells with peripheral blood DC were cultured and fused. The killing effect of CTLs pre-activated by fused cells was significantly higher than that of the co-culture CTL group with unsensitized lymphocytes (p < 0.01). The killing activity, as measured by an enhanced efficiency ratio, was increased significantly in the co-cultures of fused cells with CTL groups (p < 0.01). CONCLUSIONS: The glioma-dendritic cell fusion vaccine possessed a more effective anticancer activity by stimulating the effector activity of CTLs.

[Indwelling position and bacterial colonization of peripheral venous indwelling needles in patients with cardiovascular diseases].

OBJECTIVE: To study the characteristics of infections associated with peripheral venous indwelling needles and to explore the best indwelling position in patients with cardiovascular diseases from the perspective of bacteriology. METHODS: A total of 240 hospitalized patients from the Department of Cardiovascular Diseases, Xiangya Hospital, Central South University between November 2009 to July 2010 were randomly selected, and were divided into 3 groups according to the indwelling position and the indwelling time: a back of hand group (n=80), a forearm group (n=80) and a foot group (n=80). The above 3 groups were also divided into 4 subgroups according to the indwelling time (T1: 48 h ≤ t < 72 h; T2: 72 h ≤ t ≤ 96 h; T3: 96 h < t ≤ 120 h; and T4: 120 h < t ≤ 168 h) (20 patients in each subgroup). The bacteria of samples from puncture position of the skin were respectively cultured and identified after skin disinfection, needle pulling out and sample puncture from the indwelling needle catheters, respectively. RESULTS: 1) After the skin disinfection, there was no bacterium in the skin samples of puncture position. 2) When the needles were pulled out, there was bacterial growth in the skin samples of puncture position in 41 patients in the 3 groups, and the bacterium was not detected in samples of the 3 groups at T1 and T2 period. There was no significant difference in the positive rate of bacterial culture in the 3 groups at T3 and T4 period (P<0.05). 3) When the needles were pulled out. There was bacterial growth in the samples of indwelling needle catheters in 10 patients in the 3 groups; no bacterium was detected in the back of hand group and the forearm group at T1, T2, T3 and T4 period. In the foot group, there was no bacterium growth in the samples of indwelling needle catheters at T1 and T2 period, but there was bacterial growth in 4 patients at T3 period and in 6 patients at T4 period. There was significant difference in the positive rate of bacterial culture in the samples of indwelling needle catheters in the 3 groups (P<0.05). CONCLUSION: The best indwelling position for peripheral venous indwelling needles is the forearm in patients with cardiovascular diseases.

[Knowledge, attitude and behavior on blood lipid among people participated in health examination in Changsha and the influential factors].

OBJECTIVE: To evaluate the knowledge, attitude and behavior on blood lipid among people in Changsha and to provide evidences for prevention and control of blood lipid abnormality. METHODS: A total of 400 cases were randomly selected on the questionnaire of the knowledge, attitude and behavior on blood lipid in ordinary adults who participate in health examination in Xiangya Hospital. Blood lipid related physical examination was conducted at the same time. The health examination participants were divided into several groups according to their sex, age, degree of education, marriage and family income. The influential factors for knowledge, attitude and behavior were analyzed. RESULTS: The knowledge score of blood lipid for health examination participants was 18.33±8.67 (total score 37), the attitude score was 6.63±2.45 (total score 9) and the behavior score was 8.32±2.65 (total score 16). The scores of female was higher than that of male in the terms of knowledge and behavior (both P< 0.05); the scores in the 40-49 age group were lower than those in the other age groups (all P< 0.05); the scores in the junior high school group were lower than those in the other education groups (all P< 0.05); the scores in the family group with less than 2 000 yuan income were lower than those in other family groups with different income (all P< 0.05). The multiple stepwise regression analysis showed that: 1) the knowledge on blood lipid score was influenced by ages and education background (both P< 0.05); 2) while the attitude of blood lipid was influenced by four factors such as education background, systemic blood pressure, blood sugar and triglyceride(all P< 0.05); 3) the behavior on blood lipid was influenced by five factors such education background, triglyceride, systemic blood pressure, blood sugar and ages (all P< 0.05). CONCLUSION: The knowledge, attitude and behavior on blood lipid among health examination participants were mostly influenced by education background, gender and ages. Thus, clinical medical staff should prevent the blood lipid abnormality through the health education and improve the knowledge in normal people. The group of 40-49 age male should be thought as the primary intervention subjects. The knowledge, attitude and behavior on blood lipid among the general population is also related to individual's blood pressure, blood sugar and triglyceride. So the clinical medical staff should also improve the knowledge of blood lipid, blood pressure and blood sugar in general population for improving their attitude and unhealthy habits. In addition, the active control of blood sugar and blood pressure can enhance the overall health status of the general population.