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For a long time normal Spark ignition and Combustion ignition engines emit toxic into the atmosphere which causes many environmental problems, like global warming, ozone layer depletion. In order to minimize this introducing an alternative way is the feasible path. Alternative sources such as compressed air, solar, wind energy can be used to minimize the effect on environment. We have converted a Spark ignition engine into compressed air engine by incorporating additional setup. Some pneumatic components are used in this conversion of engine. The pollution can be reduced, because the major power source used here is compressed air. Compressed air is produced at a very low cost when compared with fossil fuel which is used extensively. This tricycle is fixed with an engine setup. This tricycle is commercialized in way that can be used for very short distance drives.

Introduction: Pulmonary arterial hypertension (PAH) is a vascular disease characterized by an increased mean pulmonary artery (PA) pressure. Pulmonary artery smooth muscle cells (PASMCs) from PAH patients exhibit a “cancer-like” hyperproliferative and apoptosis-resistant phenotype leading to pulmonary vascular remodeling. It is believed that these alterations are influenced by epigenetic processes. However, it is still not clear which gene are the drivers. “G9a”, a histone methyltransferase, is known to be overexpressed in different types of cancer, promoting cell survival and proliferation. Given the similarities between PAH and cancer, we hypothesized that G9a could be implicated in PAH progression and pathogenesis. Methods and Results: Using Western blot (WB) and immunofluorescence (IF), we showed that G9a is significantly upregulated in distal PAs and isolated PASMCs from PAH patients (n= 6-14, pIn vitro, pharmacological G9A inhibition using BIX01294 reduces PAH-PASMC proliferation (Ki67/ EdU assays, pIn vivo , we showed that BIX01294 significantly improved established PAH in FHR (reduced RVSP and mPAP, increased SV and CO, by right heart catheterization, and attenuated pulmonary vascular remodeling, p Conclusion: We showed that G9a upregulation contributes to the pro-proliferative phenotype of PAH-PASMCs; and its inhibition represents a novel avenue to improve PAH.

Considerable efforts have been made by aero-engine manufacturers to understand, detect, attenuate, if not eliminate, high-frequency transverse screech combustion instabilities due to their destructive nature. Combustion dynamic stability problems arise in turbofan afterburners when fluctuations in the combustion energy release rates are coupled with the afterburner duct acoustics. Anti-screech liners have been used to attenuate the consequential pressure oscillations and mitigate the harmful effects of the transverse screech combustion instabilities. A versatile experimental test facility, using a single V-gutter flame holder as a driver to generate predetermined screech frequencies of interest of 1250 and 2000 Hz was used to conduct comprehensive experimental studies. Anti-screech liners of variable effectiveness with porosities of 3.5 and 10.0% were used for this investigation. The attenuation effectiveness of these liners was investigated under simulated test conditions specifically for the 2000-Hz screech frequency. For these comprehensive experimental investigations, a novel methodology to generate the predetermined screech frequency in a model afterburner test rig had been evolved. These anti-screech liners with variable effectiveness were not found to be effective in completely suppressing screech over the entire spectrum of operating conditions, probably because the complex modes present in the screech combustion instabilities, may have not been strictly transverse and the pressure amplitude may have been too large. Mitigation efforts need to be attempted at the source of generation of the screech combustion instabilities.

Large field flow visualization of the unsteady combusting flow inside a hydrogen-fueled valveless pulsejet engine has been successfully demonstrated by using a retro-reflective screen based high-speed shadowgraph technique. A rectangular cross-sectional valveless pulsejet engine with optical access has been designed, fabricated, and successfully used for demonstrating the effective use of a retro-reflective shadowgraph technique for large and spatially wide flow fields of interest. The aspect ratio of the engine considered for the study was 13.5 and the technique helped to understand the acoustically coupled combusting flow structures from the intake to the tailpipe of the pulsejet engine. A Photron FASTCAM SA4 camera was used in this study. High-speed shadowgraph videos were captured with a frame rate of 13500 frames per second with a resolution of 1024 × 272 pixels.

Pulmonary arterial hypertension (PAH) is a progressive disorder characterized by a sustained elevation of pulmonary artery (PA) pressure, right ventricular failure, and premature death. Enhanced proliferation and resistance to apoptosis (as seen in cancer cells) of PA smooth muscle cells (PASMCs) is a major pathological hallmark contributing to pulmonary vascular remodeling in PAH, for which current therapies have only limited effects. Emerging evidence points toward a critical role for Enhancer of Zeste Homolog 2 (EZH2) in cancer cell proliferation and survival. However, its role in PAH remains largely unknown. The aim of this study was to determine whether EZH2 represents a new factor critically involved in the abnormal phenotype of PAH-PASMCs. We found that EZH2 is overexpressed in human lung tissues and isolated PASMCs from PAH patients compared to controls as well as in two animal models mimicking the disease. Through loss- and gain-of-function approaches, we showed that EZH2 promotes PAH-PASMC proliferation and survival. By combining quantitative transcriptomic and proteomic approaches in PAH-PASMCs subjected or not to EZH2 knockdown, we found that inhibition of EZH2 downregulates many factors involved in cell-cycle progression, including E2F targets, and contributes to maintain energy production. Notably, we found that EZH2 promotes expression of several nuclear-encoded components of the mitochondrial translation machinery and tricarboxylic acid cycle genes. Overall, this study provides evidence that, by overexpressing EZH2, PAH-PASMCs remove the physiological breaks that normally restrain their proliferation and susceptibility to apoptosis and suggests that EZH2 or downstream factors may serve as therapeutic targets to combat pulmonary vascular remodeling.

Adiponectin (ADN) is a crucial mediator of insulin sensitivity and vascular health. The discoveries of the adiponectin receptors AdipoR1 and AdipoR2 (R1 and R2) prompted efforts to identify ADN-mimetics. R1 and R2 are especially difficult drug targets due to the complex higher-order structures of ADN as well as challenges in creating receptor knock-out cell lines. We approached R1 and R2 as possible targets beginning with a rigorous validation of the ligand and receptors. ADN preparations from multiple internal and external sources were characterized in physicochemical, cell binding and in vitro assays (pAMPK/pACC and ceramidase). It is important to note that ADN from only one source passed this evaluation. This ADN triggered in vitro activities associated with this protein, including stimulation of phosphorylation of ACC (EC50 = 9.3 ug/ml), calcium influx (EC50 = 2.2 ug/ml), glucose uptake, fatty acid oxidation and ceramidase activity. With a biologically active ADN preparation identified, we strove to understand the interactions of ADN with R1 and R2. However, both R1 and R2 are ubiquitously expressed, complicating the in vitro confirmation of receptor-dependent functional activity. We selected HAP1 cells, an ADN-responsive haploid CML derived line well-suited for gene deletion via CRISPR-Cas9 technology, to generate R1, R2 and R1/R2 deficient cells. Surprisingly, the stimulatory activity of adiponectin in pACC and ceramidase assays in HAP1 cells deficient in R1, R2 or both R1 and R2 were indistinguishable from those in wild type HAP1 cells. In addition, transient overexpression of R1 in HAP1 cells or pretreatment with antibodies to block R1 did not alter their pACC responses to ADN. These data indicate R1 and R2 are not responsible for all the in vitro biological activity attributed to ADN and suggest that there must be other yet unidentified receptors for ADN. Disclosure J.W. Gunnet: Employee; Self; Janssen Research & Development. W. Li: None. Y. Wang: None. J.A. Chavez: None. M. Husovsky: None. R. Meng: None. W. Lang: None. J.R. Jeyaseelan: Employee; Self; Janssen Pharmaceuticals, Inc.. G.W. Caldwell: None. S. Edavettal: Employee; Self; Janssen Research & Development.