EXCESS MOLAR VOLUMES AND DEVIATIONS IN VISCOSITY OF THE BINARY MIXTURES OF 1-PENTANOL + AROMATIC HYDROCARBONS AT T = 298.15 K

The densities, ρ and viscosities, η of pure 1-Pentanol, toluene, ethylbenzene, propylbenzene, and those of their binary mixtures covering the whole composition range have been measured at 298.15 K under atmospheric pressure. Excess molar volumes, E Vm , partial molar volumes, Vi , deviations in viscosity, ∆η and excess free energies of activation, E G# ∆, have also been calculated from the ρ and η data. To obtain correlation coefficients and standard deviations E Vm , ∆η and E G# ∆were fitted to Redlich–Kister type function in terms of mole fraction. In the whole range of composition, E Vm were found to be positive for 1-pentanol + ethylbenzene and + propylbenzene, but 1-pentanol + toluene system showed negative E Vm in the alcohol-rich region for. The ∆η and E G# ∆ values were the negative for all the binary mixtures

EXCESS MOLAR VOLUMES AND DEVIATIONS IN VISCOSITY OF THE BINARY MIXTURES OF 1-PENTANOL + AROMATIC HYDROCARBONS AT T = 298.15 K

The densities, ρ and viscosities, η of pure 1-Pentanol, toluene, ethylbenzene, propylbenzene, and those of their binary mixtures covering the whole composition range have been measured at 298.15 K under atmospheric pressure. Excess molar volumes, E Vm , partial molar volumes, Vi , deviations in viscosity, ∆η and excess free energies of activation, E G# ∆, have also been calculated from the ρ and η data. To obtain correlation coefficients and standard deviations E Vm , ∆η and E G# ∆were fitted to Redlich–Kister type function in terms of mole fraction. In the whole range of composition, E Vm were found to be positive for 1-pentanol + ethylbenzene and + propylbenzene, but 1-pentanol + toluene system showed negative E Vm in the alcohol-rich region for. The ∆η and E G# ∆ values were the negative for all the binary mixtures

A study of the properties of an oil-based drilling fluid with using emulsifier EM-4

The issue of maintaining the potential productivity of the well is one of the most urgent tasks of the oil and gas industry nowadays. Due to the development of deposits with complex deposits and low-permeability productive layers, the issues of increasing the flow rate of wells due to the qualitative opening of reservoirs were of fundamental importance. The drilling fluid with an oil base (OBM) does not adversely affect the properties of oil and gas collectors, also it has good lubricating properties, reducing the wear of drill bits and bits. This paper is devoted to comparing the properties of drilling muds prepared using the industrial emulsifier Cleave FM and the new synthesized emulsifier EM-4. Emulsifier EM-4 is a solution of N- (2-hydroxyethyl) amides of fatty acids in a mixture of mono- and diglycerides of fatty acids

Надежность стержневых конструкций мостов (ферм)

Rationale: The chemokine CXCL12 (CXC motif ligand 12) and its receptor CXCR 4 (CXC motif receptor 4) direct the recruitment of smooth muscle progenitor cells (SPCs) in neointima formation after vascular injury. Lysophosphatidic acid (LPA) induces CXCL12 and neointimal accumulation of smooth muscle cells (SMCs) in uninjured arteries. Thus, we hypothesize that LPA may regulate CXCL12-mediated vascular remodelling. Objectives: We evaluated the role of LPA receptors in initiating CXCL12-dependent vascular repair by SPCs. Methods and Results: Wire-induced carotid injury was performed in apolipoprotein E(-/-) mice on western-type diet. LPA receptor expression was studied by immunostaining and quantitative RT-PCR. LPA receptors LPA(1) and LPA(3) were detected in the media of uninjured arteries and in the injury-induced neointima. LPA(3) mRNA was upregulated and LPA(1) mRNA downregulated at one week after injury. The LPA(1/3) antagonist Ki16425 inhibited neointima formation by 71% and reduced both relative neointimal SMCs and the macrophage content. Additionally, neointimal hypoxia-inducible factor-1 alpha and CXCL12 expression, the injury-induced peripheral stem cell antigen-1 (Sca-1)(+)/Lin(-) SPC mobilization, and the neointimal recruitment of Sca-1(+)SMCs were inhibited by Ki16425. In wild type mice, LPA20:4 increased CXCL12 and hypoxia-inducible factor-1 alpha expression in carotid arteries as early as 1 day following short-term endoluminal incubation. LPA20: 4-induced SPC mobilization and neointima formation were blocked by Ki16425, LPA(1)- and LPA(3)-specific small interfering (si) RNA, and the CXCR4 antagonist POL5551. Ki16425 reduced LPA20: 4-mediated neointimal recruitment of SPC as demonstrated by 2-photon microscopy in bone marrow chimeric mice after repopulation with SM22-LacZ transgenic, hematopoietic cells. Moreover, POL5551 decreased the neointimal accumulation of CXCR4(+) SMCs. Conclusions: LPA(1) and LPA(3) promote neointima formation through activation of CXCL12-mediated mobilization and recruitment of SPCs. (Circ Res. 2010; 107: 96-105.

Role of CXCL12 and endothelial HIF-1alpha in atherosclerotic lesion stabilization

Atherosclerosis is a chronic inflammatory process where pro-inflammatory cytokines and chemokines mediate the continuous recruitment of inflammatory cells and thereby increase lesion inflammation. The chronic inflammation in atherosclerosis damages the structural components of lesions, such as SMCs and collagen, by increasing degradation and apoptosis, which promotes lesion vulnerability to hemodynamic stress. Hence, treatment strategies to stabilize advanced rupture prone lesions should aim at decreasing the lesion inflammation and increasing the structural components, which would increase the biomechanical strength of the lesions. Treatment with ex vivo expanded SPCs induces stable lesions in mice model of atherosclerosis. Moreover, elevation in plasma CXCL12 level for short duration mobilizes SPCs from BM. Furthermore, LPA-mediated HIF-1alpha expression in injured carotid artery up-regulates CXCL12, which leads to recruitment of BM-derived SPCs to the lesion site via CXCR4. Recruited SPCs differentiate to SMCs and contributes to the neointimal growth. Therefore, the effect of CXCL12 treatment on stabilization of vulnerable lesions was studied. Application of CXCL12 transiently increased SPCs in the circulation by eliminating the physiological CXCL12 gradient between the BM and circulation. Repeated treatment with CXCL12 reduced the lesional macrophage content without affecting the lesion size. Moreover, FC thickness, and the lesional SMC and collagen-I content were also increased by CXCL12. The induction of a stable lesion phenotype by CXCL12 was due to increased recruitment of SPCs from the circulation, which differentiated specifically to lesional SMCs. Recruitment of SPCs was in part due to increased expression of CXCL12 in lesions after CXCL12 treatment presumably mediated by HIF-1alpha. Furthermore, CXCL12 treatment had no effect on inflammatory cell mobilization or recruitment. Of note, the stable lesion phenotype with increased SMCs, collagen and decreased macrophages was sustained even in the absence of further CXCL12 treatment, which subjected application of CXCL12 as a potential therapeutic approach for treating unstable lesions. To study the role of endothelial HIF-1a in atherosclerosis, Apoe-/- mice with an EC specific deletion of Hif1a were studied. Endothelial deletion of HIF-1alpha reduced the lesion size and lesional macrophage content in aortas in diet-atherosclerosis and in disturbed flow induced atherosclerosis in the carotid artery. Interestingly no effect on lesional SMCs and collagen-I was observed, which suggests that endothelial HIF-1alpha is involved primarily in monocyte recruitment to the lesion site. Moreover, HIF-1alpha was up-regulated in ECs by the pro-atherogenic factors moxLDL, unsaturated LPA, and AT-2. Furthermore, stimulation of ECs with moxLDL and LPA20:4 increased transcription and translation of CXCL1 in an HIF- 1alpha- and LPA receptor-dependent manner. Silencing of HIF-1alpha reduced monocyte adhesion to moxLDL- and LPA20:4-stimulated ECs. Thus, these findings suggest that endothelial HIF-1alpha participates in the early recruitment of monocytes by augmenting monocyte adhesion to the endothelium via increased synthesis of CXCL1 and thus drives the inflammatory response in atherosclerosis

Role of CXCL12 and endothelial HIF-1alpha in atherosclerotic lesion stabilization

Atherosclerosis is a chronic inflammatory process where pro-inflammatory cytokines and chemokines mediate the continuous recruitment of inflammatory cells and thereby increase lesion inflammation. The chronic inflammation in atherosclerosis damages the structural components of lesions, such as SMCs and collagen, by increasing degradation and apoptosis, which promotes lesion vulnerability to hemodynamic stress. Hence, treatment strategies to stabilize advanced rupture prone lesions should aim at decreasing the lesion inflammation and increasing the structural components, which would increase the biomechanical strength of the lesions. Treatment with ex vivo expanded SPCs induces stable lesions in mice model of atherosclerosis. Moreover, elevation in plasma CXCL12 level for short duration mobilizes SPCs from BM. Furthermore, LPA-mediated HIF-1alpha expression in injured carotid artery up-regulates CXCL12, which leads to recruitment of BM-derived SPCs to the lesion site via CXCR4. Recruited SPCs differentiate to SMCs and contributes to the neointimal growth. Therefore, the effect of CXCL12 treatment on stabilization of vulnerable lesions was studied. Application of CXCL12 transiently increased SPCs in the circulation by eliminating the physiological CXCL12 gradient between the BM and circulation. Repeated treatment with CXCL12 reduced the lesional macrophage content without affecting the lesion size. Moreover, FC thickness, and the lesional SMC and collagen-I content were also increased by CXCL12. The induction of a stable lesion phenotype by CXCL12 was due to increased recruitment of SPCs from the circulation, which differentiated specifically to lesional SMCs. Recruitment of SPCs was in part due to increased expression of CXCL12 in lesions after CXCL12 treatment presumably mediated by HIF-1alpha. Furthermore, CXCL12 treatment had no effect on inflammatory cell mobilization or recruitment. Of note, the stable lesion phenotype with increased SMCs, collagen and decreased macrophages was sustained even in the absence of further CXCL12 treatment, which subjected application of CXCL12 as a potential therapeutic approach for treating unstable lesions. To study the role of endothelial HIF-1a in atherosclerosis, Apoe-/- mice with an EC specific deletion of Hif1a were studied. Endothelial deletion of HIF-1alpha reduced the lesion size and lesional macrophage content in aortas in diet-atherosclerosis and in disturbed flow induced atherosclerosis in the carotid artery. Interestingly no effect on lesional SMCs and collagen-I was observed, which suggests that endothelial HIF-1alpha is involved primarily in monocyte recruitment to the lesion site. Moreover, HIF-1alpha was up-regulated in ECs by the pro-atherogenic factors moxLDL, unsaturated LPA, and AT-2. Furthermore, stimulation of ECs with moxLDL and LPA20:4 increased transcription and translation of CXCL1 in an HIF- 1alpha- and LPA receptor-dependent manner. Silencing of HIF-1alpha reduced monocyte adhesion to moxLDL- and LPA20:4-stimulated ECs. Thus, these findings suggest that endothelial HIF-1alpha participates in the early recruitment of monocytes by augmenting monocyte adhesion to the endothelium via increased synthesis of CXCL1 and thus drives the inflammatory response in atherosclerosis