Evaluation of Stimulation Techniques for Oil Wells

The oil well stimulation is a technical measure which is by eliminating the damage of the near well-bore or building structures of high conductivity in the formation. The stimulation concludes Fill Layer Measures, Water Shutoff Measures, Separate Injection Measures, Sidetracking Drilling Measures, Fracturing, Sand Control Measures, Acidification Measures. Valid Measures, Measures to Increase the Amount of Oil, Measures Earnings, Measures of Investment Payback are the four indexes which analyze the effect of various measures. And compare the combined effect of these measures, achieve the effective increasing in the oilfield.In this paper, By synthesizing measures for each increasing oil, to evaluate the effect of increasing oil after using a variety of measures in the economic aspects

Transmission of integrin β7 transmembrane domain topology enables gut lymphoid tissue development.

Integrin activation regulates adhesion, extracellular matrix assembly, and cell migration, thereby playing an indispensable role in development and in many pathological processes. A proline mutation in the central integrin β3 transmembrane domain (TMD) creates a flexible kink that uncouples the topology of the inner half of the TMD from the outer half. In this study, using leukocyte integrin α4β7, which enables development of gut-associated lymphoid tissue (GALT), we examined the biological effect of such a proline mutation and report that it impairs agonist-induced talin-mediated activation of integrin α4β7, thereby inhibiting rolling lymphocyte arrest, a key step in transmigration. Furthermore, the α4β7(L721P) mutation blocks lymphocyte homing to and development of the GALT. These studies show that impairing the ability of an integrin β TMD to transmit talin-induced TMD topology inhibits agonist-induced physiological integrin activation and biological function in development

Selective gas detection using Mn3O4/WO3 composites as a sensing layer

Pure WO3 sensors and Mn3O4/WO3 composite sensors with different Mn concentrations (1 atom %, 3 atom % and 5 atom %) were successfully prepared through a facile hydrothermal method. As gas sensing materials, their sensing performance at different temperatures was systematically investigated for gas detection. The devices displayed different sensing responses toward different gases at specific temperatures. The gas sensing performance of Mn3O4/WO3 composites (especially at 3 atom % Mn) were far improved compared to sensors based on pure WO3, where the improvement is related to the heterojunction formed between the two metal oxides. The sensor based on the Mn3O4/WO3 composite with 3 atom % Mn showed a high selective response to hydrogen sulfide (H2S), ammonia (NH3) and carbon monoxide (CO) at working temperatures of 90 degrees C, 150 degrees C and 210 degrees C, respectively. The demonstrated superior selectivity opens the door for potential applications in gas recognition and detection

Mechanisms underlying uridine adenosine tetraphosphate-induced vascular contraction in mouse aorta: Role of thromboxane and purinergic receptors

Uridine adenosine tetraphosphate (Up4A), a novel endothelium-derived vasoactive agent, is proposed to play a role in cardiovascular disorders and induces aortic contraction through activation of cyclooxygenases (COX). We and others demonstrated that activation of A1 or A3 adenosine receptors (AR) results in vascular contraction via thromboxane (TX) A2 production. However, the mechanisms of Up4A-induced vascular contraction in mouse aorta are not understood. We hypothesize that Up4A-induced aortic contraction is through COX-derived TXA2 production, which requires activation of A1 and/or A3AR. Concentration responses to Up4A were conducted in isolated aorta. The TXB2 production, a metabolite of TXA2, was also measured. Up4A (10(-9)-10(-5) M) produced a concentration-dependent contraction >70%, which was markedly attenuated by COX and COX1 but not by COX2 inhibition. Notably, Up4A-induced aortic contraction was blunted by both TX synthase inhibitor ozagrel and TXA2 receptor (TP) antagonist SQ29548. Surprisingly, A3AR deletion had no effect on Up4A-induced contraction. Moreover, A1AR deletion or antagonism as well as A1/A3AR deletion potentiated Up4A-induced aortic contraction, suggesting a vasodilator influence of A1AR. In contrast, non-selective purinergic P2 receptor antagonist PPADS significantly blunted Up4A-induced aortic contraction to a similar extent as selective P2X1R antagonist MRS2159, the latter of which was further reduced by addition of ozagrel. Endothelial denudation almost fully attenuated Up4A-induced contraction. Furthermore, Up4A (3 μM) increased TXB2 formation, which was inhibited by either MRS2159 or ozagrel. In conclusion, Up4A-induced aortic contraction depends on activation of TX synthase and TP, which partially requires the activation of P2X1R but not A1 or A3 AR through an endothelium-dependent mechanism