Acoustic-convective interference in transfer functions of methane/hydrogen and pure hydrogen flames

We investigate the occurrence and source of modulations in the gain and phase of flame transfer functions (FTF) measured in perfectly premixed, bluff body stabilised CH4=H2 and pure H2 flames. The modulations are shown to be caused by flow disturbances originating from the upstream geometry, in particular the grub screws used to centre the bluff body, indicative of a more generalised phenomenon of convective wave propagation. Velocity measurements are performed at various locations around the injector dump plane, inside the injector pipe, and in the wake of the bluff body to provide detailed insight into the flow. Peaks corresponding to natural shedding frequencies of the grub screws appear in the unforced velocity spectra and it is found that the magnitude of these convective modes depends on their location. Flame imaging and PIV measurements show that these disturbances do not show up in the mean velocity and flame shape which appear approximately axisymmetric. However, the urms and vrms fields capture a strong asymmetry due to convective disturbances. To further quantify the role of these convective disturbances, hydrodynamic transfer functions are constructed from the forced cold flow, and similar modulations observed in the FTFs are found. A strong correlation is obtained between the two transfer functions, subsequently, the modulations are shown to be centered on the vortex shedding frequency corresponding to the first convective mode. The reason behind the excitation of the first mode is due to a condition that states that for acoustic-convective interaction to be possible, the shedding (convective) frequency needs to be lower than the cut-off frequency of the flame response. This condition is shown to be more relevant for hydrogen flames compared to methane flames due to their shorter flame lengths and thus increased cut-off frequency

Long-term consumption of an obesogenic high fat diet prior to ischemia-reperfusion mediates cardioprotection via Epac1-dependent signaling

Background: Obesity is still considered a risk factor for cardiovascular disease, although more recent knowledge also suggests obesity to be associated with reduced morbidity and mortality - the “obesity paradox”. This study explores if long-term feeding of an obesogenic high fat diet renders the myocardium less susceptible to ischemic-reperfusion induced injury via Epac-dependent signaling. Methods: Wild type (wt), Epac1 (Epac1−/− ) and Epac2 (Epac2−/− ) deficient mice were fed a high fat (HFD) or normal chow diet (ND) for 33 ± 1 weeks. Six experimental groups were included: (1) control wt ND (wt ND), (2) control wt HFD (wt HFD), (3) Epac1−/− mice on ND (Epac1−/− ND), (4) Epac1−/− mice on HFD (Epac1−/− HFD), (5) Epac2−/− mice on ND (Epac2−/− ND), and (6) Epac2−/− mice on HFD (Epac2−/− HFD). Isolated ex vivo mice hearts were perfused in a constant pressure Langendorff mode, and exposed to 30min of global ischemia (GI) and 60min of reperfusion. Endpoints were infarct size and functional recovery. Results: All groups fed a HFD presented with significantly enhanced body weight, visceral fat content and reduced glucose clearance compared to corresponding ND groups. Although the HFD cohorts presented with an overall comparable systemic capability to clear glucose, the Epac1−/− HFD group presented with glucose levels slightly above the human diabetes criteria at the end of the intraperitoneal glucose tolerance test (ipGTT). Moreover, the HFD significantly reduced infarct size in both wild type (wt HFD 41.3 ± 5.5% vs. wt ND 58.0 ± 9.8%, p < 0.05) and Epac2−/− cohorts (Epac2−/− HFD 34.4 ± 7.2% vs. Epac2−/− ND 56.5 ± 3.8%, p < 0.05). Interestingly, however, the HFD did not reduce infarct size in Epac1−/− deficient mice hearts (Epac1−/− HFD 65.1 ± 5.1% vs. Epac1−/− ND 56.1 ± 3.5%, ns.). Conclusion: Epac1-dependent signaling is involved in mediating the cardioprotection afforded by long-term feeding of an obesogenic high fat diet in mice hearts

Steroidogenic Factor-1 and The Gonadotrope-Specific Element Enhance Basal and Pituitary Adenylate Cyclase-Activating Polypeptide-Stimulated Transcription of the Human Glycoprotein Hormone {alpha}-Subunit Gene in Gonadotropes

In the anterior pituitary, expression of the common glycoprotein hormone {alpha}-subunit ({alpha}GSU) is mediated in part by multiple response elements residing in the distal promoter (-435 bp). One such site is the gonadotrope-specific element (GSE), which is bound by the orphan nuclear receptor steroidogenic factor-1 (SF-1) and confers pituitary adenylate cyclase-activating polypeptide (PACAP)-stimulated {alpha}GSU expression. Here we investigated the functional importance of the GSE and SF-1 phosphorylation in both basal and stimulated {alpha}GSU transcription. Mutation of the GSE reduced basal and PACAP-stimulated {alpha}GSU promoter activity in the {alpha}T3-1 gonadotrope cell line. Overexpression of wild-type SF-1, but not an S203A mutant form of SF-1, enhanced basal and PACAP-stimulated {alpha}GSU promoter activity. The effect of PACAP on {alpha}GSU promoter activity was inhibited after overexpression of MAPK phosphatase. Helix assembly of the SF-1 ligand-binding domain was stimulated by PACAP in vitro via a MAPK-dependent pathway, as determined using a mammalian two-hybrid assay. PACAP quickly activated MAPK (within 5 min) and also resulted in elevated levels of phospho-cAMP response element-binding protein and phospho-SF-1, as judged by a specific antiphospho-S203 antibody; this effect was blocked by the MAPK kinase inhibitor, UO126. Collectively, these data demonstrate that SF-1 binds to the GSE and activates both basal and PACAP-stimulated {alpha}GSU transcription, which is further increased by phosphorylation at Ser203 via MAPK. These data suggest strongly that the induction of {alpha}GSU gene expression by peptide hormone signaling is coupled directly to the posttranslational status of SF-1