No abstract

The solubility of H2S in aqueous solutions of 40 mass % MDEA + 5 mass % AMP, 30 mass % MDEA + 15 mass % AMP, and 22.5 mass % MDEA + 22.5 mass % AMP at (313.15, 333.15, and 353.15) K and pressure from the vapor pressure of the solutions up to 1.5 MPa using the isochoric saturation method were measured. The experimental data are presented as the partial pressure of H2S against acid gas loading (mole H2S/total moles of amine). The results showed that the H2S solubility decreases with an increase of temperature and increases with the rising of partial pressure of H2S, and also AMP concentration can improve absorption capacity of MDEA aqueous solution as [AMP]0/[MDEA]0 (ratio of AMP per MDEA concentration in fresh solutions) increases when total amine concentration is constant. The Deshmukh–Mather model and Peng–Robinson equation of state were used for liquid and vapor phase, respectively, to correlate the solubility data.

Apoptosis is the main pathological aspect of neuronal injury after cerebral ischemia–reperfusion (I/R) injury. However the detailed molecular mediators are still under debate. The aim of this study is to explore the effect of cerebral I/R on miR‐23a/TGF‐β‐activated kinase 1 binding protein 3 (TAB3)/nuclear factor kappa B (NF‐κB)/p53 axis in rat hippocampus alone and in combination with chlorogenic acid (CGA). Common carotid artery occlusion (CCAO) was performed by nylon monofilament for 20 min to establish a model of ischemic brain injury. CGA (30 mg/kg) was administered intraperitoneally (ip), 10 min prior to ischemia and 10 min before reperfusion. Examination of hippocampus neurons by terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling staining showed that the number of apoptotic neurons was elevated at 24 h after reperfusion. At the molecular levels, I/R injury resulted in an increased protein expression of p53 with a concomitant upregulation of cleaved‐caspase3/phosphorelated‐caspase3 ratio and cytochrome c level. Further miR‐23b gene expression was significantly downregulated after 24 h of reperfusion. Also, we observed increased TAB3 and NF‐κB protein expressions after 24 h following CCAO. Treatment with CGA significantly reduced the apoptotic damage and also reversed miR‐23b gene expression, TAB3 and NF‐κB protein expressions in hippocampus neurons in I/R rats. In conclusion our data suggest that miR‐23b/TAB3/NF‐κB/p53 axis could play a regulatory role in hippocampus cell death, which provide a new target for novel therapeutic interventions during transit ischemic stroke. It also demonstrated that CGA could reverse these molecular alterations indicating an effective component against hippocampus apoptotic insult following acute I/R injury.

In this paper, the effect of variations in the cladding of photonic crystal fibers (PCF) using fully-vectorial effective index method has analytically been considered. There are two important parameters in calculating effective index, that are air-hole diameter ( ) d and airhole spacing ( ).Λ The difference of effective index and cladding index has been shown in terms of wavelengths for different values of d and .Λ Another effective factor of PCF is its single-modedness, which is investigated for different design conditions in this analysis. As it is well known that the PCF can develop high negative dispersion. Therefore, It has been shown that dispersion of the PCF can be more negative/positive by changing its characteristic parameters. Also, it is shown that slope of dispersion curve changes with PCF parameters.