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Molecular recognition (e.g., antigen-antibody, DNA-DNA, and streptavidin-biotin) is a generic, yet highly versatile and powerful strategy employed in enzyme-catalyzed signal amplification process. However, this approach is not applicable to metals, anions, and small reactive species (e.g., O2- and F-), as these molecules are too small to bind effectively to the macromolecules. In this paper, we demonstrate an enzyme-catalyzed signal amplification approach based on the controlled binding between streptavidin and target activated affinity-switchable biotin (ASB) probes, for the detection of O2- and F-, using electrochemical and fluorescent detection techniques. The underlying rationale behind this design is that, while the ASB probe would not bind with the streptavidin-enzyme conjugate due to its low binding affinity with streptavidin, in the presence of the target analyte, the ASB probe on the immobilized surface will be activated to form biotin, which can then bind with the enzyme-tagged streptavidin to initiate signal amplification process. This versatile approach can also be applied in the imaging of endogenously secreted O2- along the plasma membrane of living cells using streptavidin conjugated with multiple fluorescent dye reporters. We believe that this ASB probe strategy will be useful for a wide range of applications, such as in basic biological research and medical diagnoses, where highly specific signal enhancement is required.

Purpose Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. Materials and methods We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with platelet-derived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. Results SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. Conclusion These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.

BACKGROUND This study aimed to identify the relationship between miR-125a polymorphism rs12976445 and the post-ablation recurrence of atrial fibrillation (AF), as well as to explore the underlying mechanism of miR-125a in AF recurrence. MATERIAL AND METHODS Microarray analysis was performed to search for miRNAs potentially involved in the regulation of AF recurrence, while real-time PCR (polymerase chain reaction) and Western blot analyses were carried out to study the expression of miR-125a (microRNA-125a), IL-6R (interleukin-6 receptor), and IL-16 (interleukin-16) in different experimental groups, so as to understand the regulatory relationships among miR-125a, IL-6R, and IL-16. Subsequently, a logistic regression analysis was utilized to investigate the survival status of recurrent AF in subjects harboring different genotypes of rs12976445. RESULTS The subjects in the GG and GC/CC groups of miR-125a polymorphism rs12976445 showed no obvious difference regarding all demographic characteristics that were collected in this study. In addition, 19 miRNAs were identified as potentially involved in the regulation of AF recurrence. Among these miRNAs, 6 were upregulated and 13 were downregulated in the group with early recurrence. According to real-time PCR results, the expression of miR-125a was dramatically upregulated in LRAF (late recurrence of atrial fibrillation) as well as in subjects harboring the GG genotype. On the contrary, the level of IL-6R mRNA was dramatically downregulated in LRAF and subjects harboring the GG genotype. Furthermore, IL-6R was confirmed as a candidate target of miR-125a by a luciferase reporter assay. CONCLUSIONS MicroRNA-125a polymorphism rs12976445 plays a role in AF recurrence via the regulation of IL-6R.

Ventricular septal defect (VSD) is an uncommon complication of penetrating heart injuries, but transcatheter closure has emerged as a new technique and is widely used worldwide. In spite of high success rate and minimal operative mortality, short-term follow-up post-operation and long-term follow-up post-operation have not been observed. In the present study, we report a case of cardiac injury after stabbing himself with a dagger. The patient was diagnosed with a post-traumatic VSD with left-to-right shunt and was transferred to theatre where the defect was successfully repaired. Seven days later, on echocardiography examination, an occluder closing the defect with no residual leak was revealed. During the extensive follow-up over 10 years, no complication of occluder break, translocation and thrombosis formation occurred.

With the continuous development of wireless communication technology and the improvement in the performance of the vehicular device, the concept of Autonomous Vehicular Cloud (AVC) has emerged. Vehicular Cloud can provide abundant resources and services, but the high mobility of highway vehicle nodes leads to the network communication time is short, therefore allocated resources lost easily. This paper will focus on solving the problem of the low efficiency of the resource aggregation and distribution of the vehicle nodes in the highway scene. Based on the particularity of the Vehicular cloud in the highway, this paper introduces the checkpoint server selection mechanism which is based on mobility prediction and proposes two checkpoint server selection schemes, one is the choice of relative task initiating node stability of the vehicle node, the other is the choice of relative task executing node stability of the vehicle node. This paper uses OPNET Network simulation tool to evaluate the two schemes mentioned above based on various scenarios of different node density. Finally, the empirical conclusion is that the selected checkpoint based on mobility prediction methods is more stable, can improve the efficiency of resource aggregation and allocation, and vehicle node is more sparse, the enhanced effect is more obvious.

Objective: Cardiosphere-derived cells (CDCs) improve cardiac function and attenuate remodeling in ischemic and non-ischemic cardiomyopathy, and are currently obtained through myocardial biopsy. However, there is not any study on whether functional CDCs may be obtained through cadaveric autopsy with similar benefits in non-ischemic cardiomyopathy. Methods: Cardiac tissues from human or mouse cadavers were harvested, plated at 4°C, and removed at varying time points to culture human CDCs (CLH-EDCs) and mouse CDCs (CM-CDCs). The differentiation and paracrine effects of CDCs were also assessed. Furthermore, intramyocardial injection of cadaveric CM-CDCs was performed in an induced dilated cardiomyopathy (DCM) model. Results: With the extension of post mortem hours, the number of CLH-EDCs and CM-CDCs harvested from autopsy specimens decreased. The expressions of von Willebrand factor (VWF) and smooth muscle actin (SMA) on CDCs were gradually reduced, however, cardiac troponin I (TNI) expression increased in the 24 h group compared to the 0 h group. CLH-EDCs were also found to have similar paracrine function in the 24 h group compared to 0 h group. 8 weeks after CM-CDCs transplantion to the injured heart, mean left ventricular ejection fraction increased in both 0 h (64.99 ± 3.4%) and 24 h (62.99 ± 2.8%) CM-CDCs-treated groups as compared to the PBS treated group (53.64 ± 5.6 cm), with a decrease in left ventricular internal diastolic diameter (0.29 ± 0.08 cm and 0.32 ± 0.04 cm in 0 h and 24 h groups, vs. 0.41 ± 0.05 cm in PBS group). Conclusion: CDCs from cadaveric autopsy are highly proliferative and differentiative, and may be used as a source for allograft transplantation, in order to decrease myocardial fibrosis, attenuate left ventricular remodeling, and improve heart function in doxorubicin-induced non-ischemic cardiomyopathy.

In order to suit better for variations of coal and rock with different properties, solve the problem of big fluctuation of a cutting motor power, and ensure the durable high-efficient, high-energetic working of a shearer, a constant power speed-adjusting system of shearer cutting motor is designed based on the theory and the method of single neuron self-adaptive PID controlling, the system effects constant power function of shearer cutting motor by adjusting continually the shearer’s haulage speed. A systematic simulation model is build by using the Matlab/Simulink, and the experiment shows: the speed-adjusting system of single neuron self-adaptive PID controlling has following advantages by comparing it with a traditional controlling method: adjustment time of haulage speed decreases by 0.6s, overshoot and adjustment time of the cutting motor power lower by 2.4% and 0.27s respectively, which improves the working efficiency of the shearer by a rapid reaction speed and a good controlling property.

Moving boundary problems arise in many important applications to biology and chemistry. Comparing to the fixed boundary problem, moving boundary problem is more reasonable. To the best of our knowledge, there’s few results on the moving boundary for nonlinear first-order hyperbolic initial-boundary value problems. In the present paper, we mainly clarify the problem and show the existence and uniqueness of the solution for such kind of problems. We take a classical transform to straighten the moving boundary and develop a monotone approximation, based on upper and lower solutions technique, for solving a class of first-order hyperbolic initial-boundary value problems of moving boundary. Such an approximation results in the existence and uniqueness of the solution for the problem. The idea behind such a method is to replace the actual solution in all the nonlinear and nonlocal terms with some previous guess for the solution, then solve the resulting linear model to obtain a new guess for the solution. Iteration of such a procedure yields the solution of the original problem upon passage to the limit. A novelty of such a technique is that an explicit solution representation for each of these iterates is obtained, and hence an efficient numerical scheme can be developed. The key step is a comparison principle between consecutive guesses.

Background In this study, we investig1ated whether microRNA let-7i regulates dendric cell maturation targeting interleukin-10 (IL-10) via the Janus kinase 1–signal transducer and activator of transcription 3 (JAK1-STAT3) signal pathway subsequently prolongs rat cardiac allograft survival. Methods Quantitative real-time reverse transcriptase polymerase chain reaction, enzyme linked immunosorbent assay, and dual-luciferase assay were performed to verify whether IL-10 was the target of let-7i, and regulatory T cells were assessed by flow cytometry and immunohistochemical study. Western blot was performed to detect JAK1, STAT3, and phosphorylated STAT3 expression. Lewis recipients of Dark Agouti hearts were transfused with phosphate-buffered saline, lipopolysaccharide (LPS)-mature dendritic cells (mDCs), or let-7i–inhibitor-mDCs. Allograft survival times were recorded, and histologic studies were performed. Results Expression of IL-10 messenger RNA level and production of IL-10 were increased in let-7i–inhibitor-mDCs compared with LPS-mDCs. Luciferase activity showed that the translational level of the IL-10 luciferase reporter was decreased by let-7i mimic but increased by let-7i-inhibitor. MicroRNA let-7i inhibitor suppressed DC maturation; however, pretreatment of IL-10 small interfering RNA attenuated the suppression. Expression of JAK1, STAT3, and phosphorylated STAT3 in mDCs were suppressed by let-7i mimic, and pre-treatment of IL-10 small interfering RNA, however, were upregulated by let-7i inhibitor. Lewis recipients transfused with let-7i–inhibitor-mDCs significantly prolonged Dark Agouti cardiac allograft survival. The allografts transfused with let-7i–inhibitor-mDCs showed slight cell infiltration and significantly preserved graft structure. Inhibition of let-7i increased CD4 + CD25 + forkhead box P3 + regulatory T cells and modulated cytokine profiles in vivo and in vitro. Conclusions MicroRNA let-7i regulated DC maturation and function targeting IL-10 through the JAK1-STAT3 pathway. Moreover, transfusion of LPS-induced mDCs transfected with let-7i inhibitor induced prolonged cardiac allograft survival and generated regulatory T cells.

Repairing the panel CAD geometric model is an important pre-processing step of the finite element analysis, and widely used in the computer-aided geometric design field. This paper focused on the surface healing method of panel CAD model, which was proposed and analyzed by NURBS technology. Through the pipeline method determines the matching-curves border fast firstly, make the curves discrete points sets and on the basis of the characteristics of the matching-curves method, the surfaces were stitched. On the basis of the algorithm, a surface stitching program module was developed. The validity of algorithm was verified by healing automobile front fender parts.