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Cardiogenic shock (CS) often occurs in patients suffering from rapidly progressing end-stage heart failure or acute myocardial infarction. Mechanical circulatory support may be used for patients who do not respond to medication or revascularization to stabilize hemodynamics. Extracorporeal ventricular assist device (Extra-VAD) has been reported to be successful for patients with cardiogenic shock. This study aimed to evaluate the 30-day in-vivo performance and safety of a newly developed Extra-VAD with maglev centrifugal pump technology, MoyoAssist®.The study was conducted with 6 healthy ovine models, weighing 43.2 ~ 59.6 kg. Cannulation was performed with a 34 Fr venous cannula surgically connected to the left arterial appendage and a 24 Fr arterial cannula inserted into descending aorta. The pump flow rate was maintained at 2 ~ 3 L/min to provide sufficient cardiac support without suction. Activated clotting time was maintained within the range of 150 ~ 250 s.No device-related adverse events occurred throughout the study. Plasma-free hemoglobin results were within the acceptable range of ventricular assist device therapy (40 mg/dl). MGS01 had an anticoagulation management related bleeding event and was terminated on day 29. All other sheep's biochemical test results were stable. The autopsy showed no embolism or thrombus formation and no end-organ damage.This study demonstrated that the MoyoAssist® Extra-VAD is able to provide cardiac support effectively and safely and may provide a new alternative choice for patients with CS in China.

Autoimmune demyelinating diseases can be induced by an immune response against myelin peptides; however, the exact mechanism underlying the development of such diseases remains unclear. In experimental autoimmune encephalomyelitis, we found that the clearance of exogenous myelin antigen at the peak of the primary immune response is key to the pathogenesis of the disease. The generation of effector T cells requires continuous antigen stimulation, whereas redundant antigen traps and exhausts effector T cells in the periphery, which induces resistance to the disease. Moreover, insufficient antigenic stimulation fails to induce disease efficiently owing to insufficient numbers of effector T cells. When myelin antigen is entirely cleared, the number of effector T cells reaches a peak, which facilitates infiltration of more effector T cells into the central nervous system. The peripheral antigen clearance initiates the first wave of effector T cell entry into the central nervous system and induces chronic inflammation. The inflamed central nervous system recruits the second wave of effector T cells that worsen inflammation, resulting in loss of self-tolerance. These findings provide new insights into the mechanism underlying the development of autoimmune demyelinating diseases, which may potentially impact future treatments. This article is protected by copyright. All rights reserved.

As a pre-clinical assessment, the present study aimed to investigate the safety and effectiveness of a novel valved pulmonary arterial conduit constructed entirely from biomaterials by transplanting it in the outflow tract of the right ventricle in sheep. Under extracorporeal circulation, the valved pulmonary arterial conduit was used to replace the pulmonary artery of sheep with a beating heart. The performance was assessed at 30, 90 and 180 days post-surgery. Hemodynamic and structural changes were evaluated, and safety was assessed after 180 postoperative days. The hemodynamic effect and biosafety of the implant were further evaluated by observing the changes in various pressure indicators of the heart, echocardiographic results, anatomical and pathological examination results, liver and kidney functions, routine blood tests, a blood coagulation test, and other test results following implantation of the purely biotic valved conduit. The conduit was successfully implanted in 12 sheep and no mortality occurred postoperatively. During the 180-day follow-up, there was no obvious stenosis or regurgitation of the right ventricular outflow tract and pulmonary valve after valved conduit implantation. The findings of autopsy, pathology and laboratory examinations were unremarkable. The implantation of this biosynthetic vascular graft into animals meets the safety and effectiveness requirements for clinical application. This pulmonary arterial conduit has potential clinical application for children with complex congenital heart disease who require pulmonary artery reconstruction to achieve a radical cure.

Objective To investigate the expression profile of circular RNAs (circRNAs) and proposed circRNA-microRNA (miRNA) regulatory network in atrial fibrillation (AF). Methods Atrial tissues from patients with persistent AF with rheumatic heart disease and non-AF myocardium with normal hearts were collected for circRNA differential expression analyses by high-throughput sequencing. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to predict the potential functions of the differentially expressed genes and AF-related pathways. Co-expression networks of circRNA-miRNA were constructed based on the correlation analyses between the differentially expressed RNAs. Quantitative reverse transcription polymerase chain reaction (PCR) was performed to validate the results. Results A total of 108 circRNAs were found to be differentially expressed in AF. Among them, 51 were up-regulated, and 57 were down-regulated. Dysregulated circRNAs were validated by quantitative real-time PCR. The GO and KEGG pathway enrichment analyses were executed to determine the principal functions of the significantly deregulated genes. Furthermore, we constructed correlated expression networks between circRNAs and miRNAs. circRNA19591, circRNA19596, and circRNA16175 interacted with 36, 28, and 18 miRNAs, respectively; miR-29b-1-5p and miR-29b-2-5p were related to 12 down-regulated circRNAs, respectively. Conclusion Our findings provide a novel perspective on circRNAs involved in AF due to rheumatic heart disease and establish the foundation for future research of the potential roles of circRNAs in AF.

Water body extraction can help eco-environmental policymakers to intuitively grasp surface water resources. Remote sensing technology can accurately and quickly extract surface water information, which is of great significance for monitoring surface water changes. Fengyun satellite images have the advantages of high time resolution and multispectral bands. This provides important image data suitable for high-frequency surface water monitoring. Based on Fengyun 3 medium resolution spectral imager (FY-3/MERSI) data, 7 methods were applied in this study, which include single-band threshold method, water body index method, knowledge decision tree classification method, supervised classification method, unsupervised classification method, spectral matching based on discrete particle swarm optimization (SMDPSO), and improved spectral matching based on discrete particle swarm optimization with linear feature enhancement (SMDPSO+LFE). These methods were used to extract the land surface water of Poyang Lake, check the samples from the Landsat image with similar times to the FY-3 images, and calculate the classification accuracy via the confusion matrix. The results showed that the overall classification accuracy (OA) of the SMDPSO+LFE is 97.64%, and the Kappa coefficient is 0.95. To analyze the stability of the surface water extracted by SMDPSO+LFE in different regions, this paper selected eight test sites with different surface water types, landscapes, and terrains to extract surface water. Based on an analysis of the land surface water results at the eight test sites, every OA in the eight sites was higher than 94.5%, the Kappa coefficient was greater than 0.88. In conclusion, the SMDPSO+LFE is found to be the most suitable method among the 7 methods and effectively distinguish between different surface water bodies and backgrounds with good stability.

Heart failure (HF) is an end-stage manifestation of various heart diseases and a major cause of death in patients with heart disease. Morbidity increases with age, and mortality and hospitalization remain high. This chapter will introduce definition, mechanism, diagnosis, and management of heart failure. Through the description of the pathophysiology of heart failure, to understand the current world’s cutting-edge treatment technology. Whether it is chronic heart failure or acute heart failure, it is a challenge for doctors in this era to propose effective treatment methods based on symptomatic treatment. From the traditional single drug treatment gradually to more challenging mechanical treatment evolution. In this chapter, the current effective, feasible and high survival rate treatment methods are briefly listed.

Respiratory failure is one of the major causes of mortality and morbidity all over the world. Therapeutic options to treat respiratory failure remain limited. The objective of this study was to evaluate the gas transfer performance of a newly developed miniature portable integrated pediatric pump-lung device (PediPL) with small membrane surface for respiratory support in an acute ovine respiratory failure model. The respiratory failure was created in six adult sheep using intravenous anesthesia and reduced mechanical ventilation at 2 breaths/min. The PediPL device was surgically implanted and evaluated for respiratory support in a venovenous configuration between the right atrium and pulmonary artery. The hemodynamics and respiratory status of the animals during support with the device gas transfer performance of the PediPL were studied for 4 h. The animals exhibited respiratory failure 30 min after mechanical ventilation was reduced to 2 breaths/min, indicated by low oxygen partial pressure, low oxygen saturation, and elevated carbon dioxide in arterial blood. The failure was reversed by establishing respiratory support with the PediPL after 30 min. The rates of O2 transfer and CO2 removal of the PediPL were 86.8 and 139.1 mL/min, respectively. The results demonstrated that the PediPL (miniature integrated pump-oxygenator) has the potential to provide respiratory support as a novel treatment for both hypoxia and hypercarbia. The compact size of the PediPL could allow portability and potentially be used in many emergency settings to rescue patients suffering acute lung injury.

Nickel chromium (NiCr) powders with different titanium diboride (TiB2) additions (20, 40 and 60 wt %) were prepared with a mechanical alloying method and then sprayed using an air plasma spraying technology. The microstructure and phase composite of the powders and the cross-sections of deposited coatings were analyzed with a scanning electronic microscope and X-ray diffraction. The tribological performance of the coatings was studied using a pin-on-disk tribometer at room temperature. The weight loss of the as-sprayed coating was measured by using a high accuracy weighing balance. Cr3C2-25NiCr coating was produced and tested for comparison. The morphologies of the worn surface were then investigated. Parts of debris with some scratches were found, presenting typical signs of abrasive wear and showing slight adhesive wear on the surface. The 20 wt % additive TiB2 coating demonstrated the highest microhardness and the lowest coefficient of friction. The wear resistance of the metal-ceramic composites coatings was enhanced with the addition of TiB2.

The scarcity of donor organs has led to the development of devices that provide optimal long-term respiratory or cardiopulmonary support to bridge recipients as they wait for lung and/or heart transplantation. This study was designed to evaluate the 30-day in vivo performance of the newly developed pediatric pump-lung (PediPL) for cardiopulmonary support using a juvenile sheep model. The PediPL device was placed surgically between the right atrium and descending aorta in eight sheep (25.4-31.2 kg) and evaluated for 30 days. Anticoagulation was maintained with continuous heparin infusion (activated clotting time 150-200 s). The flow rate was measured continually, and gas transfer was measured daily. Plasma free hemoglobin, platelet activation, hematologic data, and blood biochemistry were assessed twice a week. Sheep were euthanized after 30 days. The explanted devices were examined for gross thrombosis. Six sheep survived for 30-32 days. During the study, the oxygen transfer rate of the devices was 54.9 ± 13.2 mL/min at a mean flow rate of 1.14 ± 0.46 L/min with blood oxygen saturation of 95.4% ± 1.7%. Plasma free hemoglobin was 8.2 ± 3.7 mg/dL. Platelet activation was 5.35 ± 2.65%. The animals had normal organ chemistries except for surgery-related transient alterations in kidney and liver function. Although we found some scattered thrombi on the membrane surfaces of some explanted devices during the necropsy, the device function and performance did not degrade. The PediPL device was capable of providing cardiopulmonary support with long-term reliability and good biocompatibility over the 30-day duration and offers the potential option for bridging pediatric patients with end-stage heart or lung disease to heart and/or lung transplantation.

Based on several unpredictable reasons, buildings will have varying degrees of tilt damage. As for Line-Shaped buildings structure, since its own structure has a large aspect ratio, it is more prone to appear the tilt damage than other types of buildings. However, some already existed building correction methods are not suitable for line-shaped buildings. So the present study proposes and analyzes the correction method which is more effective to deal with the tilt damage of Line-Shaped buildings structure. Regarded the ancient the Screen Wall as an example, firstly the study analyzes the reasons of damage, and then puts up with corresponding methods. It can devote an available method for such projects for reference.

Large animal models serve as a critical link in the translation of basic science to clinical practice. However, large animal models of myocardial infarction (MI), especially large size MI, have been associated with high mortality because of arrhythmia. The prophylactic effect of amiodarone and lidocaine were retrospectively reviewed in our ovine MI model.A total of 114 Dorset hybrid sheep with 25%-30% MI were included in the present study. The sheep were prophylactically treated with amiodarone plus lidocaine before ligation of the four to six coronary artery branches supplying the apex of the heart (arrhythmia prevention [AP] group, n = 45) and with epinephrine (shock prevention [SP] group, n = 49), respectively. The sheep without prophylactic treatment (no prevention [NP] group, n = 20) were used as the control group. The incidence of arrhythmia requiring treatment, mortality due to arrhythmia, hemodynamics, and arterial blood gas values during surgery were analyzed in these three groups.No significant difference was found in infarct size among the three groups. The incidence of arrhythmia requiring treatment was significantly decreased in the AP group compared with that in the NP or SP groups (4.4% for AP versus 35% for NP and 45% for SP groups; P0.05). The mortality due to lethal arrhythmia was 2.2% in the AP group, significantly lower than that in the NP group (15%) or SP group (18.4%). Other than the heart rate, no significant differences were found in the hemodynamic data between the AP and NP groups. Metabolic acidosis was not observed in any group, as indicated by the pH and lactate values.Prophylactic amiodarone plus lidocaine decreased the mortality due to lethal arrhythmia after acute MI in our sheep model without significant negative effects on the hemodynamics. However, epinephrine improved the hemodynamics but also increased the mortality due to lethal arrhythmia. Thus, prophylactic amiodarone plus lidocaine is recommended to improve the stability in a large MI animal model.

The underlying molecular mechanisms of the remodeling after myocardial infarction (MI) remain unclear. The purpose of this study was to investigate the role of a survival pathway (PI3K/Akt) and an apoptosis pathway (calcineurin/BAD) in the remodeling after MI in a large animal model.Ten Dorset hybrid sheep underwent 25% MI in the left ventricle (LV, n=10). Five sheep were used as sham control. The regional strain was calculated from sonomicrometry. Apoptosis and the activation of the PI3K/Akt and calcineurin/BAD pathways were evaluated in the non-ischemic adjacent zone and the remote zone relative to infarct by immunoblotting, immunoprecipitation, and immunofluorescence staining.Dilation and dysfunction of LV were present at 12 weeks after MI. The regional strain in the adjacent zone was significantly higher than in the remote zone at 12 weeks (36.6 ± 4.0% vs 9.5 ± 3.6%, p0.05). Apoptosis was more severe in the adjacent zone than in the remote zone. The PI3K/Akt and calcineurin/BAD pathways were activated in the adjacent zone. Dephosphorylation and translocation of BAD were evident in the adjacent zone. Regional correlation between the strain and the expression of calcineurin/BAD indicated that the activation was strain-related (R(2)=0.46, 0.48, 0.39 for calcineurin, BAD, mitochondrial BAD, respectively, p0.05).The PI3K/Akt survival and calcineurin/BAD apoptotic pathways were concomitantly activated in the non-ischemic adjacent zone after MI. The calcineurin/BAD pathway is strain related and its imbalanced activation may be one of the causes of progressive remodeling after MI.

The purpose of this study was to assess the biocompatibility of a newly developed long-term wearable artificial pump-lung (APL) in a clinically relevant ovine animal model. The wearable APL device was implanted in five sheep through left thoracotomy. The device was connected between the right atrium and pulmonary artery and evaluated for 30 days. Three sheep were used as the sham control. Platelet activation was assessed by measuring platelet surface P-selectin (CD62P) expression with flow cytometry and plasma soluble P-selectin with an enzyme-linked immunosorbent assay. Thrombotic deposition on the device components and hollow fiber membranes were analyzed with digital imaging and scanning electron microscopy. Surface P-selectin of the APL and sham groups changed significantly over the study period, but without significant differences between the two groups. Soluble P-selectin for the two groups peaked in the first 24 h after the surgery. Soluble P-selectin of the APL group remained slightly elevated over the study period compared to the presurgical baseline value and was slightly higher compared to that of the sham group. Plasma free hemoglobin remained in the normal ranges in all the animals. In spite of the surgery-related alteration in laboratory tests and elevation of platelet activation status, the APL devices in all the animals functioned normally (oxygen transfer and blood pumping) during the 30-day study period. The device flow path and membrane surface were free of gross thrombus. Electron microscopy images showed only scattered thrombi on the fibers (membrane surface and weft). In summary, the APL exhibited excellent biocompatibility. Two forms of platelet activation, surgery-related and device-induced, in the animals implanted with the wearable APL were observed. The limited device-induced platelet activation did not cause gross thrombosis and impair the long-term device performance.

BACKGROUND The infant Jarvik 2000 heart is a very small, hermetically sealed, intracorporeal, axial-flow ventricular assist device (VAD) designed for circulatory support in neonates and infants. The anatomic fit, short-term biocompatibility and hemodynamic performance of the device were evaluated in a neonate piglet model. METHODS The infant Jarvik 2000 heart with two different blade profiles (low- or high-flow blade design) was tested in 6 piglets (8.8±0.9 kg). Using a median sternotomy, the pump was placed in the left ventricle through the apex without cardiopulmonary bypass. An outflow graft was anastomosed to the ascending aorta. Hemodynamics and biocompatibility were studied for 6 hours. RESULTS All 6 pumps were implanted without complication. Optimal anatomic positioning was found with the pump body inserted 2.4 cm into the left ventricle. Hemodynamics demonstrated stability throughout the 6-hour duration. The pump flow increased from 0.27 to 0.95 liter/min at increasing speeds from 18 to 31 krpm for the low-flow blade design, whereas the pump flow increased from 0.54 liter/min to 1.12 liters/min at increasing speeds from 16 krpm to 31 krpm for the high-flow blade design. At higher speeds, >80% of flow could be supplied by the device. Blood chemistry and final pathology demonstrated no acute organ injury or thrombosis for either blade design. CONCLUSIONS The infant Jarvik 2000 heart is anatomically and biologically compatible with an short-term neonate piglet model. This in vivo study demonstrates the future feasibility of this device for clinical use.

Gas leakage accident occurs frequently due to the aging of pipeline and the third-party interference. To ensure safety during the gas pipeline emergency-repair, it's necessary to detect the gas concentration in the working place. In this paper, a WSN-based monitoring system for gas emergency repairing is proposed. The monitoring system is composed of the wireless nodes and the terminal software. The wireless nodes are used to collect gas concentration, temperature, humidity, wind speed and wind direction in real time, and transmit the data to the command terminal. The terminal software then store, upload the data, and can check those data as well as alarm. In order to provide feasible reference data for alert area and evacuation zone, this paper not only studies the diffusion model of gas leakage in the air, but also studies the impact of environmental meteorological condition on the gas diffusion. The system has been proven effective and reliable in real gas emergency-repair.

Progressive cardiac remodeling, including the myopathic process in the adjacent zone following myocardial infarction (MI), contributes greatly to the development of cardiac failure. Cardiomyoplasty using bone marrow-derived mesenchymal stem cells (MSCs) has been demonstrated to protect cardiomyocytes and/or repair damaged myocardium, leading to improved cardiac performance, but the therapeutic effects on cardiac remodeling are still under investigation. Here, we tested the hypothesis that MSCs could improve the pathological remodeling of the adjacent myocardium abutting the infarct. Allogeneic ovine MSCs were transplanted into the adjacent zone by intracardiac injection 4 hours after infarction. Results showed that remodeling and contractile strain alteration were reduced in the adjacent zone of the MSC-treated group. Cardiomyocyte hypertrophy was significantly attenuated with the normalization of the hypertrophy-related signaling proteins phosphatidylinositol 3-kinase α (PI3Kα), PI3Kγ, extracellular signal-regulated kinase (ERK), and phosphorylated ERK (p-ERK) in the adjacent zone of the MSC-treated group versus the MI-alone group. Moreover, the imbalance of the calcium-handling proteins sarcoplasmic reticulum Ca2+ adenosine triphosphatase (SERCA2a), phospholamban (PLB), and sodium/calcium exchanger type 1 (NCX-1) induced by MI was prevented by MSC transplantation, and more strikingly, the activity of SERCA2a and uptake of calcium were improved. In addition, the upregulation of the proapoptotic protein Bcl-xL/Bcl-2-associated death promoter (BAD) was normalized, as was phospho-Akt expression; there was less fibrosis, as revealed by staining for collagen; and the apoptosis of cardiomyocytes was significantly inhibited in the adjacent zone by MSC transplantation. Collectively, these data demonstrate that MSC implantation improved the remodeling in the region adjacent to the infarct after cardiac infarction in the ovine infarction model.

Background To provide long-term ambulatory cardiopulmonary and respiratory support for adult patients, a novel wearable artificial pump-lung device has been developed. The design features and in vitro and acute in vivo performance of this device are reported. Methods This device features a uniquely designed hollow-fiber membrane bundle integrated with a magnetically levitated impeller that together form one ultracompact pump-lung device, which can be placed like current paracorporeal ventricular assist devices to allow ambulatory support. The device is 117 mm in length and 89 mm in diameter and has a priming volume of 115 ml. In vitro hydrodynamic, gas transfer and biocompatibility experiments were carried out in mock flow-loops using ovine blood. Acute in vivo characterization was conducted in an ovine model by surgically implanting the device between right atrium and pulmonary artery. Results The in vitro results show that the device with a membrane surface area of 0.8 m 2 was capable of pumping blood from 1 to 4 liters/min against a wide range of pressures and transferring oxygen at a rate of up to 180 ml/min at a blood flow of 3.5 liters/min. Standard hemolysis tests demonstrated low hemolysis at the targeted operating condition. The acute in vivo results also confirmed that the device can provide sufficient oxygen transfer with excellent biocompatibility. Conclusions Based on in vitro and acute in vivo study findings, this highly integrated wearable pump-lung device can provide efficient respiratory support with good biocompatibility and it is ready for long-term evaluation.

Background. The purpose of this study was to evaluate the long-term in-vivo hemodynamics, gas transfer, and biocompatibility of an integrated artificial pump-lung (APL) developed for ambulatory respiratory support. Methods. The study was conducted in an ovine model by surgically placing the APL between the right atrium and pulmonary artery. Nine sheep were implanted. Heparin was infused as an anticoagulant. The device flow, gas transfer, and plasma free hemoglobin were measured daily. Hematologic data, platelet activation, and blood biochemistry were assessed twice a week. After 30 days, the sheep were euthanized for postmortem examination. The explanted devices were examined for gross thrombosis. Results. Five sheep survived for 29 to 31 days and were electively terminated. Four sheep died or were terminated early owing to mechanical failure of intravenous lines or device. The APL devices in the 5 long-term animals were capable of delivering an oxygen transfer rate of 148 18 mL/min at a flow rate of 2.99 0.46 L/min with blood oxygen saturation of 96.7% 1.3%. The device flow and oxygen transfer were stable over 30 days. The animals had normal end-organ functions except for surgery-related transient alteration in kidney function, liver function, and cell and tissue injury. There was no hemolysis. The device flow path and membrane surface were free of gross thrombus. Conclusions. The APL exhibited the capability of providing respiratory support with excellent biocompatibility, long-term reliability, and the potential for bridging to lung transplant.

Background The mechanism underlying left ventricular remodeling and reverse remodeling in the setting of mechanical support following acute myocardial infarction (MI) is unclear. We tested the hypothesis that left ventricular assist device (LVAD) unloading can decrease apoptotic signals after MI. Methods An MI model was created in 16 sheep by coronary artery ligation. Eight were unloaded with a LVAD during the first 2 weeks after MI and observed for 10 more weeks. Myocardial tissue was collected from the nonischemic adjacent zone and the remote zone. Proteins in the apoptotic matrix metalloproteinases (MMPs)-2/c-Jun N-terminal kinase (JNK) and prosurvival β1D-integrin/focal adhesion kinase (FAK) pathway were quantified. Results Increased TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) positive nuclei were observed in the MI group and to a lesser extent in the LVAD group (6.18 ± 0.26 versus 0.82 ± 0.18; p 0.05). Pro-MMP-2, MMP-2, JNK, and phosphorylated (p)-JNK were all elevated in the adjacent zone of the MI-only group but not in the adjacent zone of the LVAD-supported group. There were higher levels of prosurvival p-FAK in the LVAD-supported group than in the MI group. Conclusions MMP-2/JNK apoptotic and β1D-integrin/FAK survival pathways are activated in the nonischemic adjacent zone after MI in adult sheep. LVAD unloading of approximately 50% cardiac output for 2 weeks attenuates remodeling in part by its negative effect on stretch-induced apoptosis and inhibition of MMP-2 activity.

Recent studies have suggested that loss of RUNX3 expression is involved with gastric tumor metastasis. However, the precise mechanism of RUNX3-mediated suppression of tumor metastasis remains elusive. We aimed to clarify the effect of RUNX3 on tumor metastasis in gastric cancer cell lines and tumors. Immunohistochemistry revealed that RUNX3 was significantly decreased in metastatic gastric cancer. Gelatin zymography and Western blot showed that instead of regulating matrix metalloproteinase 9 (MMP9) expression, RUNX3 expression inhibited MMP9 enzyme activity, and this was consistent with the upregulation of tissue inhibitor of metalloproteinases 1 (TIMP1) by RUNX3. TIMP1 siRNA treatment impaired RUNX3-mediated suppression of gastric cancer cell invasion. Reporter assays demonstrated regulation of TIMP-1 by RUNX3. Two RUNX3 binding sites were identified in the TIMP-1 promoter and direct interaction of RUNX3 with the TIMP-1 promoter was confirmed in vitro and in vivo. These findings provide evidence for RUNX3-mediated suppression of gastric cancer invasion and metastasis and define a novel molecular mechanism that for the metastasis-inhibiting activity of RUNX3. These data may be applied in the development of RUNX3 for gastric cancer metastasis diagnostics and therapeutics.

Human mitochondrial Mrs2 protein (hsaMrs2p) is a magnesium transporter in mitochondria inner membrane. It was identified as an upregulated gene in a multidrug-resistant (MDR) gastric cancer cell line compared to its parental cells by subtractive hybridization. To further explore the role of hsaMrs2p in MDR of gastric cancer cells, the cDNA encoding hsaMrs2p was generated and mouse antisera against hsaMrs2p was raised with recombinant hsaMrs2p as the immunogen. HsaMrs2p expression could positively regulate adriamycin resistance of SGC7901/ADR cells both in vitro and in vivo. Further study showed that hsaMrs2p increased adriamycin-releasing index. Its upregulation inhibited adriamycin-induced apoptosis, probably by suppressing Bax induced cytochrome C release from mitochondria. Additionally, hsaMrs2p promoted cell growth and cells with decreased hsaMrs2p exhibited significant inhibition of cell growth with G(1) cell cycle arrest. By enhanced hsaMrs2p expression, p27 was downregulated whereas cyclinD1 was upregulated. Our results provide new insights into the function of hsaMrs2p that may be a promising target for MDR reversal therapy.

Surgical repair and endovascular stent-graft placement are both therapies for thoracic aortic dissection. A combination of these two approaches may be effective in patients with type A dissection. In this study, we evaluated the prognosis of this combined technique. From December 2003 to December 2006, 15 patients with type A dissection were admitted to our institute; clinical data were retrospectively reviewed. Follow-up was performed at discharge and approximately 12 months after operation. Endovascular stent-graft placement by interventional radiology and surgical repair for reconstruction of aortic arch was performed in all patients. Total arch replacement for distal arch aneurysm was carried out under deep hypothermia with circulatory arrest; antegrade-selected cerebral perfusion was used for brain protection. Four patients concomitantly received a coronary artery bypass graft. Hospital mortality rate was 6.7%; the patient died of cerebral infarction. Neurological complications developed in two patients. Multi-detector-row computed tomography scans performed before discharge revealed complete thrombosis of the false lumen in six patients and partial thrombosis in eight patients. At the follow-up examination, complete thrombosis was found in another three patients, aortic rupture, endoleaks, or migration of the stent-graft was not observed and injuries of peripheral organs or anastomotic endoleaks did not occur. For patients with aortic type A dissection, combining intervention and surgical procedures is feasible, and complete or at least partial thrombosis of the false lumen in the descending aorta can be achieved. This combined approach simplified the surgical procedures and shortened the circulatory arrest time, minimizing the necessity for further aortic operation.

Background: Engineered tissue heart valves may become a promising therapeutics for heart valve disease. Compared with synthetic materials, acellular porcine scaffolds are considered as suitable matrices for tissue-engineered heart valves for the mechanical and structural properties of native tissue. Whether acellular porcine scaffolds can cause infection in recipients with porcine endogenous retrovirus (PERV) is critical for evaluating the safety of transplantation of tissue-engineered heart valves based on acellular porcine scaffolds. This study was completed to evaluate the risk of PERV transmission for application of acellular porcine aortic valves (PAVs). Methods: Native aortic valves obtained from Chinese pigs of different species were acellularized by our modified detergent-enzymatic acellularization procedure. Polymerase chain reaction and reverse transcriptase polymerase chain reaction for pol sequences were used to detect PERV infection. In vitro, ovine endothelial cells (ECs) were inoculated and cocultured with supernatants of porcine aortic endothelial cells (PAECs) and acellualr PAVs, respectively. On 7th day, DNA and RNA of ovine ECs were isolated and tested for PERV. In vivo, acellular PAVs were implanted in the descending thoracic aorta in 40 sheep. Blood samples from the sheep and implanted acellular PAVs were collected 24 months after operation and tested for PERV. Results: All cells were removed from the PAVs. Acellularized PAVs were repopulated by autologous cells of the host 24 months after implantation. PERV was detected in all native PAVs, porcine blood samples, acellularized PAVs and ovine ECs inoculated with supernatants of PAECs; no PERV was detected in ovine ECs cocultured with acellularized PAVs, ovine blood samples, and implanted acellular PAVs. Conclusions: Acellularized PAVs processed by modified detergent-enzymatic acellularization procedure can be used for cardiovascular tissue-engineered grafts as matrix scaffolds without risk of PERV transmission.

The effect of adenosine postconditioning on myocardial protection in cardiac surgery remains uncertain. The present study evaluated the safety, feasibility, and beneficial effect of adenosine postconditioning as an adjunct to predominantly used cold-blood cardioplegic myocardial protection method in the setting of heart valve replacement operations.Sixty patients with rheumatic heart valve disease undergoing heart valve replacement operations were randomized to an adenosine (1.5 mg/kg) or saline (as control) bolus injection through an arterial catheter immediately after the aorta cross-clamp was removed. The surgical indications were similar in both groups, and heart valve replacement was successful in all patients.The extubation time and postoperative hospital time were similar in both groups. Compared with the control group, however, the inotrope scores in the intensive care unit (ICU) were much lower (p0.01), and the ICU time was significantly shorter (p0.05) in adenosine group. More important, cardiac troponin I release was less in the adenosine group, especially at 12 and 24 hours after reperfusion (p0.01), and total cardiac troponin I release estimated with the area under curve was also significantly reduced during the first 24 hours after reperfusion (p0.01).A 1.5-mg/kg bolus administration of adenosine through an arterial catheter immediately after the aorta cross-clamp is removed is feasible and well tolerated in patients undergoing heart valve replacement. An adenosine postconditioning adjunct to high potassium cold blood myocardial protection is related to less troponin I release, less inotropic drug use, and shorter ICU stay.

Gas pipeline leakage accidents often happen and cause loss of property and life. Thus the emergency-repair is very important. To ensure safety during the gas pipeline emergency-repair, it's necessary to detect the gas concentration in the working place. Existing detection method needs special worker detect the field gas concentration with the hand-held detection equipment. The detection work is not only boring but also a waste of manpower, and at the same time it is inconvenient to monitor a large field. So a new kind of detection method which can provide real-time and large area detection is necessary. In order to solve this situation, this paper introduces a new monitoring system using wireless sensor network technology in the gas detection, which can tremendously help the repair work.

Despite the significant contribution of the Fontan procedure to the therapy of complex congenital heart diseases, many patients progress to failure of their Fontan circulation. The use of ventricular assist devices to provide circulatory support to these patients remains challenging. In the current study, a continuous axial-flow pump was used to support a univentricular Fontan circulation. A modified Fontan circulation (atrio-pulmonary connection) was constructed in six Yorkshire piglets (8-14 kg). A Dacron conduit (12 mm) with two branches was constructed to serve as a complete atrio-pulmonary connection without the use of cardiopulmonary bypass. The Impella pump was inserted into the conduit through an additional Polytetrafluoroethylene (PTFE) graft in five animals. Hemodynamic data were collected for 6 hours under the supported Fontan circulation. The control animal died after initiating the Fontan circulation independent of resuscitation. Four pump supported animals remained hemodynamically stable for 6 hours with pump speeds between 18,000 rpm and 22,000 rpm (P1-P3). Oxygen saturation was maintained between 95% and 100%. Normal organ perfusion was illustrated by blood gas analysis and biochemical assays. A continuous axial-flow pump can be used for temporal circulatory support to the failing Fontan circulation as "bridge" to heart transplantation or recovery.

Aims Shear stress-induced apoptosis is one of the leading problems in seeding cells of tissue-engineered blood vessels (TEBVs). We aim to determine the human bone mesenchymal stem cell (hBMSC) apoptosis under shear stress and its possible mechanism. Main methods hBMSCs were subjected to 3-, 10-, and 30-dyn/cm2 shear stress in vitro. Cell multiplication and apoptosis were analyzed by flow cytometry. Apoptosis-related genes were screened by a microarray and evidenced by real-time polymerase chain reaction (RT-PCR). hBMSCs were treated with the human recombinant cell inhibitor of apoptosis protein 1 (cIAP1) and its inhibitor, direct IAP-binding protein with low pl (DIABLO), and then cell apoptosis was analyzed. Key findings Exposure to shear stress (3 dyn/cm2 for > 6 h) activated apoptosis progress of hBMSCs. However, the same degree of shear stress (3 dyn/cm2 for 6 h) did not induce apoptosis. Microarray screening and RT-PCR revealed that Bcl-2-related ovarian killer (BOK) and apoptotic protease-activating factor 1 (APAF1), key molecules of the mitochondrial apoptosis pathway, were markedly upregulated under 3-dyn/cm2 shear stress. Then, we observed that cIAP1, a Caspase 9 inhibitor, was elevated under 3 dyn/cm2 at short-time exposure (2 or 6 h), and it was reduced at long-time exposure (24 h). When treated with human recombinant cIAP1, Caspase 3 activity and LDH release of hBMSCs were decreased, and vice versa when treated with DIABLO. Significance cIAP1 attenuates hBMSC apoptosis when cells were exposed to shear stress through the regulation of the BOK–APAF1–Caspase 9–Caspase 3 pathway. It may present a pharmacological target to enhance hBMSC biological function in the application of TEBVs.

Wireless multimedia sensor networks constitute a powerful technology particularly suitable for environmental monitoring. With regard of fire detection and prevention in buildings, fire images acquired by WMSNs provide visual information of fire, which contributes to a more accurate recognition. This paper presents a design scheme of early fire detection system in buildings based on WMSNs. We adopt the traditional fire detection sensors together with the CMOS image sensors, and process those data at the acquisition side, using DSP chips, instead of at the monitoring side, in which way less data need to be transferred through the wireless network. Thus, it makes a more reasonable and energy saving fire detection system. The traditional fire detection method used is to implement basic detection of suspicious fire area and a fire image detection method, based on the static image features and the dynamic image features of fire, is applied in the system to enhance detection precision.

Background Device availability of mechanical circulatory or respiratory support to the right heart has been limited. The purpose of this study was to investigate the effect of right heart unloading and respiratory support with a wearable integrated artificial pump-lung (APL). Methods The APL device was placed surgically between the right atrium and pulmonary artery in 7 sheep. Anti-coagulation was performed with heparin infusion. The device's ability to unload the right ventricle (RV) was investigated by echocardiograms and right heart catheterization at different bypass flow rates. Hemodynamics and echocardiographic data were evaluated. APL flow and gas transfer rates were also measured at different device speeds. Results Hemodynamics remained stable during APL support. There was no significant change in systemic blood pressure and cardiac index. Central venous pressure, RV pressure, RV end-diastolic dimension and RV ejection fraction were significantly decreased when APL device flow rate approached 2 liters/min. Linear regression showed significant correlative trends between the hemodynamic and cardiac indices and device speed. The oxygen transfer rate increased with device speed. The oxygen saturation from the APL outlet was fully saturated (>95%) during support. The impact of APL support on blood elements (plasma free hemoglobin and platelet activation) was minimal. Conclusions APL device support significantly unloaded the RV with increasing device speed. The device also provided stable hemodynamics and respiratory support in terms of blood flow and oxygen transfer. The right heart unloading performance of this wearable device needs to be evaluated further in an animal model of right heart failure with long-term support.

Heart transplantation still remains the best choice of treatment for many kinds of end-stage heart diseases, but the side-effects of immunosuppressive agents and cardiac allograft vasculopathy (CAV) remain the main two obstacles in improving the long outcome of cardiac allografts. Mesenchymal stem cells (MSCs) are nonhematopoietic pluripotent cells that retain the ability to undergo differentiation into cells of different lineages. What's more, MSCs have been demonstrated to exert many profound inhibitory effects on many lymphocytic subpopulations such as T cells, regulatory T cells, and dendritic cells in vitro. In vivo studies also suggested that MSCs could be used to attenuate immune-mediated disorders such as transplant rejection and autoimmune diseases including rheumatoid arthritis, multiple sclerosis and GVHD. Hepatocyte growth factor (HGF) is a pleiotropic factor that plays an important role in protecting infarcted myocardial by its antiapoptotic, antifibrotic and angiogenic effects. And also it was suggested that the administration of HGF could effectively suppress acute and chronic cardiac allograft rejection. We based our hypothesis on that HGF-modified MSCs would engraft stably in recipient and interact with important immune cells such as T cells, B cells and dendritic cells, then stable immune tolerance be induced possibly by both immunomodulation of MSCs and cardioprotective and immunomodulative effects of HGF. Further work is necessary to highlight the specific underlying mechanisms.

The purpose of this study was to assess the biocompatibility of a newly developed long-term wearable artificial pump-lung (APL) in a clinically relevant ovine animal mode. The wearable APL device was implanted in five sheep through a left thoracotomy. The device was connected between the right atrium (RA) and pulmonary artery (PA) and evaluated for 30 days. Three sheep were used as the sham control. Platelet activation was assessed by measuring platelet surface P-selectin (CD62P) expression with flow cytometry and plasma soluble P-selectin with an enzyme-linked immunosorbent assay (ELISA). Thrombotic deposition on the device components and hollow fiber membranes (HFM) were analyzed with digital imaging and scanning electron microscopy (SEM). Surface P-selectin of the APL and sham groups changed significantly over the study period, but without significant differences between the two groups. Soluble P-selectin for the two groups peaked in the first 24 hours after the surgery. Soluble P-selectin of the APL group remained slightly elevated over the study period compared to the pre-surgical baseline value and was slightly higher compared to that of the sham group. Plasma free hemoglobin (PFH) remained in the normal ranges in all the animals. In spite of the surgery related alteration in laboratory tests and elevation of platelet activation status, the APL devices in all the animals functioned normally (oxygen transfer and blood pumping) during the 30 day study period. The device flow path and membrane surface were free of gross thrombus. Electron microscopy images showed only scattered thrombi on the fibers (membrane surface and weft). In summary, the APL exhibited excellent biocompatibility. Two forms of platelet activation, surgery related and device induced, in the animals implanted with the wearable APL were observed. The limited device-induced platelet activation did not cause gross thrombosis and impair the long-term device performance.

There is a scarcity of source material available in animal models appropriate to test pediatric-size blood pump design for assisting the left ventricle. A juvenile ovine animal model was developed to evaluate two pediatric ventricular assist devices (VADs). The child-size Jarvik 2000 and CircuLite VADs were tested with this model. The 33 in vivo experiments were retrospectively studied to evaluate the reliability of the animal model. Dorset hybrid juvenile sheep (20~36 kg) were used to evaluate the small pediatric VADs. Under general anesthesia, a left lateral thoracotomy was performed through the fifth intercostal space. The devices were implanted between the left ventricle apex and the descending aorta without cardiopulmonary bypass. Heparin was infused continuously for anticoagulation therapy. Support duration averaged 26.7 ± 19.6 days. Completion of 75.7% (25/33) experiments was done as intended. The animals were docile and did not require sitters beyond the immediate operative period. Complication includes leg injury, graft infection, gastrointestinal bleeding, intravenous line disconnection, weight loss, renal failure, red urine, (one for each) and pulmonary failure in two. Activated clotting time was adjusted via continuous intravenous heparin to 150-200 seconds. Reliable hemodynamics and biocompatibility data were collected for evaluate pediatric intracorporeal VADs in the animal model. The juvenile sheep model is reliable, reproducible, and translatable for testing pediatric VADs. These experiments provided vital information for improvement of the devices and for clinical application in the future.

To evaluate the effects of prearrest heparin administration on lung quality in a model of donation after cardiac death (DCD), and to assess the potential application of ex vivo lung perfusion (EVLP) in the identification of better grafts from the DCD donor pool.Cardiac death was induced by electric shock in 10 pigs. One group received a prearrest heparin dose of 300 units/kg (H group, n = 5) and the other did not (NH group, n = 5). Animals remained at room temperature for 1 hour without ventilation, defining the warm ischemic time. After harvest, the lungs underwent 6 hours of cold ischemia before being evaluated with EVLP for 4 hours.Static compliance 28 ± 3 versus 29 ± 2 (Cstat-cm H2O), pulmonary vascular resistance (PVR) 593 ± 127 versus 495 ± 70 (PVR-dyn·s/cm), and oxygenation 327 ± 32 versus 330 ± 28 (ΔPO2-mm Hg) remained stable from the beginning until the end of EVLP in the H group. In the NH group, Cstat started to decline after the first hour (25 ± 2 vs 21 ± 2), ΔPO2 after hour 2 (265 ± 44 vs 207 ± 44), and PVR started to increase after hour 3 (765 ± 132 vs 916 ± 168). Significant differences between the groups were observed at the end of EVLP (P0.001). Parameters of lung quality after EVLP also showed significant differences between the groups: wet weight-to-dry weight ratio (P0.001), protein in the bronchial lavage (P0.01), Na + K-ATPase activity (P0.001), and E-selectin (P0.001) in the perfusate.Prearrest heparin administration improved organ function by preserving endothelial homeostasis. EVLP proved to be a useful platform for assessing DCD lungs, providing reliable means of discriminating injured grafts.

Diabetes exacerbates ischemic heart disease morbidity and mortality via incompletely understood mechanisms. Although adiponectin (APN) reduces myocardial ischemia/reperfusion (MI/R) injury in nondiabetic animals, whether APN's cardioprotective actions are altered in diabetes, a pathologic condition with endogenously reduced APN, has never been investigated. High-fat diet (HD)–induced diabetic mice and normal diet (ND) controls were subjected to MI via coronary artery ligation, and given vehicle or APN globular domain (gAPN, 2 μg/g) 10 min before reperfusion. Compared to ND mice (where gAPN exerted pronounced cardioprotection), HD mice manifested greater MI/R injury, and a tripled gAPN dose was requisite to achieve cardioprotective extent seen in ND mice (i.e., infarct size, apoptosis, and cardiac function). APN reduces MI/R injury via AMP-activated protein kinase (AMPK)–dependent metabolic regulation and AMPK-independent antioxidative/antinitrative pathways. Compared to ND, HD mice manifested significantly blunted gAPN-induced AMPK activation, basally and after MI/R (p

Aims Mesenchymal stem cells (MSCs) can ameliorate myocardial infarction (MI) injury. However, older-donor MSCs seem less efficacious than those from younger donors, and the contributing underlying mechanisms remain unknown. Here, we determine how age-related expression of pigment epithelium-derived factor (PEDF) affects MSC therapeutic efficacy for MI. Methods and results Reverse transcriptase–polymerized chain reaction and enzyme-linked immunosorbent assay analyses revealed dramatically increased PEDF expression in MSCs from old mice compared to young mice. Morphological and functional experiments demonstrated significantly impaired old MSC therapeutic efficacy compared with young MSCs in treatment of mice subjected to MI. Immunofluorescent staining demonstrated that administration of old MSCs compared with young MSCs resulted in an infarct region containing fewer endothelial cells, vascular smooth muscle cells, and macrophages, but more fibroblasts. Pigment epithelium-derived factor overexpression in young MSCs impaired the beneficial effects against MI injury, and induced cellular profile changes in the infarct region similar to administration of old MSCs. Knocking down PEDF expression in old MSCs improved MSC therapeutic efficacy, and induced a cellular profile similar to young MSCs administration. Studies in vitro showed that PEDF secreted by MSCs regulated the proliferation and migration of cardiac fibroblasts. Conclusions This is the first evidence that paracrine factor PEDF plays critical role in the regulatory effects of MSCs against MI injury. Furthermore, the impaired therapeutic ability of aged MSCs is predominantly caused by increased PEDF secretion. These findings indicate PEDF as a promising novel genetic modification target for improving aged MSC therapeutic efficacy.

Recent clinical observations have indicated that nonlethal mechanical trauma significantly increases myocardial infarction risk even in the presence of completely normal coronary arteries. We investigated the molecular mechanisms responsible for exacerbation of ischemic myocardial injury after nonlethal mechanical trauma with a special focus on the role of tumor necrosis factor α and its potential downstream effector adiponectin, a novel adipokine with anti-inflammatory and cardioprotective properties.Laboratory study.University research unit.Male adult adiponectin knockout mice and wild-type mice.The animals were subjected to nonlethal mechanical trauma using the Noble-Collip drum (40 rpm ± 5 mins) followed by myocardial ischemia/reperfusion injury 7 days posttrauma. We also investigated the effects of neutralizing tumor necrosis factor α with etanercept and exogenous adiponectin supplementation on ischemic myocardial injury after trauma.Trauma significantly sensitized myocardium to ischemia/reperfusion injury as evidenced by increased apoptosis, enlarged infarct size, and decreased cardiac function. Plasma adiponectin concentrations were reduced after traumatic injury (the nadir occurring 3 days posttrauma), an effect abrogated by etanercept-mediated tumor necrosis factor α blockade. The downregulation of adiponectin was accompanied by increased myocardial superoxide and nitric oxide generation and peroxynitrite formation. Both etanercept and exogenous adiponectin supplementation (on day 3 posttrauma or 10 mins before reperfusion on day 7 posttrauma) markedly inhibited oxidative/nitrative stress and ischemia/reperfusion injury in posttraumatic ischemic/reperfused hearts of wild-type mice, whereas only adiponectin supplementation (but not tumor necrosis factor α inhibition) substantially attenuated posttraumatic ischemia/reperfusion injury in adiponectin knockout mice.Tumor necrosis factor α-induced downregulation of adiponectin and the resultant enhanced oxidative/nitrative stress are involved in exacerbated posttraumatic ischemic myocardial injury. Therapeutic approaches blocking tumor necrosis factor α production or restoring adiponectin might have prophylactic value against secondary myocardial ischemic injury after a primary nonlethal mechanical trauma.

Aims Evidence has indicated U50,488H, a selective κ-opioid receptor (κ-OR) agonist, administered before ischemia attenuates apoptosis and infarction during ischemia and reperfusion (I/R). However, it remains unclear whether U50,488H postconditioning reduces apoptosis during I/R. This study was designed, therefore, to test the hypothesis that U50,488H administered at the onset of reperfusion inhibits cardiomyocyte apoptosis and to investigate the underlying mechanisms. Main methods Male Sprague–Dawley rats were subjected to myocardial ischemia and reperfusion(MI/R) and were randomized to receive either vehicle, U50,488H, U50,488H plus Nor-BNI, a selective κ-OR antagonist, U50,488H plus wortmannin, a specific inhibitor of phosphoinositide 3′-kinase (PI3K), or U50,488H plus L-NAME, a nitric oxide synthase inhibitor (NOS inhibitor), immediately prior to reperfusion. In vitro study was performed on cultured neonatal cardiomyocytes subjected to simulated ischemia/reperfusion. Key findings Treatment with U50,488H resulted in increases in Akt and endothelial nitric oxide synthase (eNOS) phosphorylation with secondary NO production both in vivo and in vitro and these effect were completely blocked by wortmannin and specific Akt inhibitor(AI). L-NAME treatment had no effect on Akt and eNOS phosphorylation; but, significantly reduced NO production. Moreover, treatment with U50,488H markedly reduced myocardial apoptotic death. Treatment with wortmannin and specific Akt inhibitor abolished the anti-apoptotic effect of U50,488H. L-NAME also significantly attenuated the anti-apoptotic effect of U50,488H. Significance These results demonstrate that U50,488H administered immediately prior to reperfusion increases Akt phosphorylation through a PI3-kinase-dependent mechanism and reduces postischemic myocardial apoptosis. Phosphorylation of eNOS with secondary NO production contribute significantly to the anti-apoptotic effect of U50,488H postconditioning.

This research was carried out to investigate the effect of basic fibrous growth factor (bFGF) controlled release hydrogel nanoparticles on the proliferation and differentiation of mesenchymal stem cells. The dex-GMA-bFGF-NPs were prepared by an improved emulsion polymerization method; their morphology, size and encapsulated ratio were assessed by routine procedure. Dynamic dialysis method was used to determine the release characteristics of dex-GMA-bFGF-NPs in vitro. The secondary culture MSCs were divided into four groups according the different ingredients being added into the DMEM culture medium: free bFGF group (A), blank dex-GMA nanoparticles group (B), dex-GMA-bFGF nanoparticles group (C), nothing group (D). The proliferation of cultured MSCs was measured by using cell counting method, MTT method and flow cytometry. ALP kit was used to evaluate the ALP activity of the MSCs to show the differentiation of the cells by adding the dex-GMA-bFGF-NPs to the DMEM culture medium (C group) or bFGF only (A group). B group and D group were taken as the controls. The results were analyzed by statistical analysis software (SPSS11.0). All results showed that the shape of dex-GMA-bFGF-NPs was spherical. The encapsulated ratio was 88% and more than 85% of the encapsulated bFGF could be released during 14 days. The in vitro cellular study showed the control release of bFGF from nanoparticles could promote the proliferation of MSCs. After 12 days, the cell number in groups A, B and C was (21.97 +/- 0.25) x 10(4) cells/ml, (12.43 +/- 0.13) x 10(4) cells/ml, (27.45 +/- 0.78) x 10(4) cells/ml and (12.03 +/- 0.43) x 10(4) cells/ml, with the difference being statistically significant among them (P0.05). The flow cytometry revealed that the G2/M+S percentage in group C was the highest at 4-8 days after plate culture(P0.05). During the first 3 days, the proliferation and differentiation of BMSCs between group A and group B were of no significance (P0.05), but were much faster than those of group C and D. After 7 days, dex-GMA-bFGF-NPs could enhance BMSCs proliferation and differentiation continually, but bFGF had no enhancement any more, the difference between group A and group B became more significant (P0.05). So we made the conclusions the bFGF loading dex-GMA hydrogel nanoparticles can release bFGF more than 21 days and can promote the proliferation and differentiation of the BMSCs through a long period of controlled release of bFGF. Dex-GMA-bFGF-NPs may be an ideal controlled release carrier for bioactive growth factors.