2,411 research outputs found
Overview of NASA supported Stirling thermodynamic loss research
NASA is funding research to characterize Stirling machine thermodynamic losses. NASA's primary goal is to improve Stirling design codes to support engine development for space and terrestrial power. However, much of the fundamental data is applicable to Stirling cooling and heat pump applications. The research results are reviewed. Much was learned about oscillating flow hydrodynamics, including laminar/turbulent transition, and tabulated data was documented for further analysis. Now, with a better understanding of the oscillating flow field, it is time to begin measuring the effects of oscillating flow and oscillating pressure level on heat transfer in heat exchanger flow passages and in cylinders
Comparison of GLIMPS and HFAST Stirling engine code predictions with experimental data
Predictions from GLIMPS and HFAST design codes are compared with experimental data for the RE-1000 and SPRE free piston Stirling engines. Engine performance and available power loss predictions are compared. Differences exist between GLIMPS and HFAST loss predictions. Both codes require engine specific calibration to bring predictions and experimental data into agreement
Reconstructive Intracranial Vascular Surgery
It is scarcely less than two decades since the initial cautious explorations of reconstructive surgery for the prevention of cerebral infarction caused by extracranial vascular disease began. The next years recorded an accumulative experience in the field of vascular surgery. Early clinical investigations led to the discovery that extracranial vascular disease is a major cause of cerebral infarction or stroke. Estimates indicate, however, that only 30-40% of the patients with cerebrovascular insufficiency have significant extracranial occlusive disease. For this larger group of patients, previous surgical methods offer no hope. It is the purpose of this report to review the current status of our clinical explorations in the area of reconstructive intracranial vascular surgery
On the theory of complex rays
The article surveys the application of complex-ray theory to the scalar Helmholtz equation in two dimensions.
The first objective is to motivate a framework within which complex rays may be used to make predictions about wavefields in a wide variety of geometrical configurations. A crucial ingredient in this framework is the role played by Sp{} in determining the regions of existence of complex rays. The identification of the Stokes surfaces emerges as a key step in the approximation procedure, and this leads to the consideration of the many characterizations of Stokes surfaces, including the adaptation and application of recent developments in exponential asymptotics to the complex Wentzel--Kramers--Brilbuin expansion of these wavefields
MARKET FAILURE IN MULTIPHASE ELECTRIC POWER DEVELOPMENT FOR AGRICULTURAL IRRIGATION
The adoption of multiphase electric power for electric irrigation has been limited in an area characterized by extremely rapid expansion of irrigated acreage despite production cost advantages. Theoretical and empirical evidence of failure in the existing market for multiphase power development are presented. Alternative development mechanisms are presented and discussed.Resource /Energy Economics and Policy,
Aging and aerobic fitness affect the contribution of noradrenergic sympathetic nerves to the rapid cutaneous vasodilator response to local heating
Sedentary aging results in a diminished rapid cutaneous vasodilator response to local heating. We investigated whether this diminished response was due to altered contributions of noradrenergic sympathetic nerves; assessing 1) the age-related decline and, 2) the effect of aerobic fitness. We measured skin blood flow (SkBF)(laser-Doppler flowmetry) in young (24±1 yr) and older (64±1 yr) endurance-trained and sedentary men (n=7 per group) at baseline and during 35 min of local skin heating to 42 °C at three forearm sites: 1) untreated; 2) bretylium tosylate (BT), preventing neurotransmitter release from noradrenergic sympathetic nerves; and 3) yohimbine and propranolol (YP), antagonising α- and β-adrenergic receptors. SkBF was converted to cutaneous vascular conductance (CVC) (SkBF/mean arterial pressure) and normalized to maximal CVC (%CVCmax) achieved by skin heating to 44 °C. Pharmacological agents were administered using microdialysis. In the young trained, the rapid vasodilator response was reduced at the BT and YP sites (P0.05) but treatment with BT did (P>0.05). Neither BT nor YP treatments affected the rapid vasodilator response in the older sedentary group (P>0.05). These data suggest that the age-related reduction in the rapid vasodilator response is due to an impairment of sympathetic-dependent mechanisms, which can be partly attenuated with habitual aerobic exercise. Rapid vasodilation involves noradrenergic neurotransmitters in young trained men, and non-adrenergic sympathetic cotransmitters (e.g.,
neuropeptide Y) in young sedentary and older trained men, possibly as a compensatory mechanism. Finally, in older sedentary men, the rapid vasodilation appears not to involve the sympathetic system
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PRMT5 regulates epigenetic changes in suppressive TH1-like iTregs in response to IL-12 treatment
Background: Induced regulatory T cells (iTregs) are a heterogeneous population of immunosuppressive T cells with therapeutic potential. Treg cells show a range of plasticity and can acquire T effector-like capacities, as is the case for T helper 1 (Th1)-like iTregs. Thus, it is important to distinguish between functional plasticity and lineage instability. Aplastic anemia (AA) is an autoimmune disorder characterized by immune-mediated destruction of hematopoietic stem and progenitor cells in the bone marrow (BM). Th1-like 1 iTregs can be potent suppressors of aberrant Th1-mediated immune responses such as those that drive AA disease progression. Here we investigated the function of the epigenetic enzyme, protein arginine methyltransferase 5 (PRMT5), its regulation of the iTreg-destabilizing deacetylase, sirtuin 1 (Sirt1) in suppressive Th1-like iTregs, and the potential for administering Th1-like iTregs as a cell-based therapy for AA.
Methods: We generated Th1-like iTregs by culturing iTregs with IL-12, then assessed their suppressive capacity, expression of iTreg suppression markers, and enzymatic activity of PRMT5 using histone symmetric arginine di-methylation (H3R2me2s) as a read out. We used ChIP sequencing on Th1 cells, iTregs, and Th1-like iTregs to identify H3R2me2s-bound genes unique to Th1-like iTregs, then validated targets using CHiP-qPCR. We knocked down PRMT5 to validate its contribution to Th1-like iTreg lineage commitment. Finally we tested the therapeutic potential of Th1-like iTregs using a Th1-mediated mouse model of AA.
Results: Exposing iTregs to the Th1 cytokine, interleukin-12 (IL-12), during early events of differentiation conveyed increased suppressive function. We observed increased PRMT5 enzymatic activity, as measured by H3R2me2s, in Th1-like iTregs, which was downregulated in iTregs. Using ChIP-sequencing we discovered that H3R2me2s is abundantly bound to the Sirt1 promoter region in Th1-like iTregs to negatively regulate its expression. Furthermore, administering Th1-like iTregs to AA mice provided a survival benefit.
Conclusions: Knocking down PRMT5 in Th1-like iTregs concomitantly reduced their suppressive capacity, supporting the notion that PRMT5 is important for the superior suppressive capacity and stability of Th1-like iTregs. Conclusively, therapeutic administration of Th1-like iTregs in a mouse model of AA significantly extended their survival and they may have therapeutic potential
S-Glutathionylation of Protein Disulfide Isomerase Regulates Estrogen Receptor α Stability and Function
S-Glutathionylation of cysteine residues within target proteins is a posttranslational modification that alters structure and function. We have shown that S-glutathionylation of protein disulfide isomerase (PDI) disrupts protein folding and leads to the activation of the unfolded protein response (UPR). PDI is a molecular chaperone for estrogen receptor alpha (ERα). Our present data show in breast cancer cells that S-glutathionylation of PDI interferes with its chaperone activity and abolishes its capacity to form a complex with ERα. Such drug treatment also reverses estradiol-induced upregulation of c-Myc, cyclinD1, and P21Cip, gene products involved in cell proliferation. Expression of an S-glutathionylation refractory PDI mutant diminishes the toxic effects of PABA/NO. Thus, redox regulation of PDI causes its S-glutathionylation, thereby mediating cell death through activation of the UPR and abrogation of ERα stability and signaling
MGST1, a GSH transferase/peroxidase essential for development and hematopoietic stem cell differentiation.
We show for the first time that, in contrast to other glutathione transferases and peroxidases, deletion of microsomal glutathione transferase 1 (MGST1) in mice is embryonic lethal. To elucidate why, we used zebrafish development as a model system and found that knockdown of MGST1 produced impaired hematopoiesis. We show that MGST1 is expressed early during zebrafish development and plays an important role in hematopoiesis. High expression of MGST1 was detected in regions of active hematopoiesis and co-expressed with markers for hematopoietic stem cells. Further, morpholino-mediated knock-down of MGST1 led to a significant reduction of differentiated hematopoietic cells both from the myeloid and the lymphoid lineages. In fact, hemoglobin was virtually absent in the knock-down fish as revealed by diaminofluorene staining. The impact of MGST1 on hematopoiesis was also shown in hematopoietic stem/progenitor cells (HSPC) isolated from mice, where it was expressed at high levels. Upon promoting HSPC differentiation, lentiviral shRNA MGST1 knockdown significantly reduced differentiated, dedicated cells of the hematopoietic system. Further, MGST1 knockdown resulted in a significant lowering of mitochondrial metabolism and an induction of glycolytic enzymes, energetic states closely coupled to HSPC dynamics. Thus, the non-selenium, glutathione dependent redox regulatory enzyme MGST1 is crucial for embryonic development and for hematopoiesis in vertebrates
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