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Surfactant polymer (SP) flooding has become an important enhanced oil recovery (EOR) technique for the high-water cut mature oilfield. Emulsification in the SP flooding process is regarded as a powerful mark for the successful application of SP flooding in the filed scale. People believe emulsification plays a positive role in EOR. This paper uses one-dimensional homogenous core flooding experiments and parallel core flooding experiments to examine the effect of emulsification on the oil recoveries in the SP flooding process. 0.3 pore volume (PV) of emulsions which are prepared using ultralow interface intension (IFT) SP solution and crude oil with stirring method was injected into core models to mimic the emulsification process in SP flooding, followed by 0.35 PV of SP flooding to flood emulsions and remaining oil. The other experiment was preformed 0.65 PV of SP flooding as a contrast. We found SP flooding can obviously enhance oil recovery factor by 25% after water flooding in both homogeneous and heterogeneous cores. Compared to SP flooding, emulsification can contribute an additional recovery factor of 3.8% in parallel core flooding experiments. But there is no difference on recoveries in homogenous core flooding experiments. It indicates that the role of emulsification during SP flooding will be more significant for oil recoveries in a heterogeneous reservoir rather than a homogeneous reservoir.

Polymer flooding is a tertiary oil recovery technology that is very suitable for the characteristics of China’s reservoirs. However, due to the fast flow rate of polymer solution in near-well zone, the shear effect of perforation blasthole and the compacted zone results in serious loss of polymer viscosity. In this paper, the polymer used in Dagang Oilfield is studied by simulation experiment through the shearing process of perforating holes, and the influence of different perforating parameters on polymer viscosity loss is analyzed, so as to provide theoretical basis for the optimization design of perforating technology in field test. The experimental results show that, the shear effect of perforation blasthole on polymer is not obvious, and the viscosity retention rate of polymer solution is greater than 96%. The size and shape of perforation blasthole have no effect on viscosity loss of polymer solution. The shear effect of compacted zone on polymer is obvious, and the viscosity retention rate of polymer solution is lower than 64% for the target block. The viscosity loss of polymer solution increases with flow rate at compacted zone, and the decrease of permeability can increase viscosity loss of polymer solution. The higher the polymer concentration is, the stronger the shear resistance is, while the higher the molecular weight is, the weaker the shear resistance is. It is suggested that perforation gun and perforation method with deep perforation depth and low compaction degree be chosen to reduce the flow rate at compacted zone and viscosity loss of polymer solution.

A novel series of Si-bearing, nearly Ni-free economical TRIP-aided duplex stainless steels (DSSs) 19Cr-5.5Mn-0.3Ni-0.2N-xSi (x = 0.5-2.5) have been prepared to investigate effect of silicon on microstructure, tensile mechanical property and high-temperature oxidation behavior. The results have shown that the designed economical alloys have a balanced ferrite/austenite dual-phase structure after suitable solution treatment. Volume of ferrite phase increases with an increase in silicon content. Ferrite deforms by dislocation slip during tensile plastic deformation process at room temperature. However, transformation-induced plasticity effect dominates deformation mode of metastable austenite phase. The designed DSS with 1.5 wt.% Si content exhibits good combination of tensile mechanical properties, exceeding 50% in elongation and 800 MPa in ultimate tensile strength, with a sequential γ → e-martensite → α′-martensite transformation in deformed austenite phase. High-temperature oxidation resistance of DSSs could be enhanced with an increase in silicon content at 1100 °C in air due to the formation of compact and continuous Cr- and Si-rich oxide film in the inner oxide film layer.

In the wake of COVID-19, mental health providers and treatment programs are adapting rapidly to the challenges in engaging people and delivering treatment with limited guidance. This paper will explore the challenges associated with delivering treatment within coordinated specialty care (CSC) programs for people with first episode psychosis. Suggestions for treatment will take into consideration experiences with stress, changes to the pursuit of work and school, and increased time spent with families. Drawing on the experience of several CSC programs in the United States, Israel, and China, we describe the impact and modifications to the core treatment elements in CSC including medication, family interactions, supported employment and education, individual therapy, peer support and the way they are delivered. The paper includes recommendations based on experiences from CSC programs to help staff members, participants, and family members better identify, prepare, cope and respond to the unique new challenges and suggests modifications that can be made during various stages of the coronavirus pandemic.

The magnetostriction of Fe-Ga alloys is significantly affected by the Ga content, which displays two positive peaks with increasing Ga concentration. This work presents a systematic structural investigation of rapidly-cooled Fe-Ga alloys by the synchrotron-based high-energy x-ray diffraction. Ga-rich clusters are evidenced for the alloys beyond the first magnetostriction peak, which is identified by the anomalous peak broadening for the (200) fundamental reflection and a shrink of lattice parameter. The generation of Ga-rich clusters in A2 matrix results in the sudden decrease of magnetostriction after the first magnetostriction peak. These findings are important for designing high-performance Fe-Ga magnetostrictive alloys by structural tuning.

In order to ensure the rationality of screed structure design and reliability of structure strength, the structural finite element model of paver screed was established with the aid of APDL language. The static and dynamic characteristics of the screed are analysed based on the finite element method. Results show that maximum principal stress of screed in the bar is 113Mpa, maximum deformation is 1.82mm, the screed meets the normal demand both in intensity and rigidity. Natural frequencies and according vibration model of screed were obtained from finite element modal analysis, the first-order natural frequency in a vibrator adjustable frequency range, so working frequency should avoid the first-order natural frequency, and the change rule of strain and stress amplitudes of screed with the vibration frequency was obtained from harmonic response analysis. The structural static and dynamic analysis of screed provides the basis for the structure design and the adjustment of construction parameters.

Background and purpose: A prostamide analogue, bimatoprost, has been shown to be effective in reducing intraocular pressure, but its precise mechanism of action remains unclear. Hence, to elucidate the molecular mechanisms of this effect of bimatoprost, we focused on pharmacologically characterizing prostaglandin FP receptor (FP) and FP receptor variant (altFP) complexes. Experimental approach: FP receptor mRNA variants were identified by reverse transcription-polymerase chain reaction. The FP-altFP4 heterodimers were established in HEK293/EBNA cells co-expressing FP and altFP4 receptor variants. A fluorometric imaging plate reader was used to study Ca2+ mobilization. Upregulation of cysteine-rich angiogenic protein 61 (Cyr61) mRNA was measured by Northern blot analysis, and phosphorylation of myosin light chain (MLC) by western analysis. Key results: Six splicing variants of FP receptor mRNA were identified in human ocular tissues. Immunoprecipitation confirmed that the FP receptor is dimerized with altFP4 receptors in HEK293/EBNA cells co-expressing FP and altFP4 receptors. In the studies of the kinetic profile for Ca2+ mobilization, prostaglandin F2α (PGF2α) elicited a rapid increase in intracellular Ca2+ followed by a steady state phase. In contrast, bimatoprost elicited an immediate increase in intracellular Ca2+ followed by a second phase. The prostamide antagonist, AGN211335, selectively and dose-dependently inhibited the bimatoprost-initiated second phase of Ca2+ mobilization, Cyr61 mRNA upregulation and MLC phosphorylation, but did not block the action of PGF2α. Conclusion and implications: Bimatoprost lacks effects on the FP receptor but may interact with the FP-altFP receptor heterodimer to induce alterations in second messenger signalling. Hence, FP-altFP complexes may represent the underlying basis of bimatoprost pharmacology.

Background and Purpose: The prostamides (prostaglandin-ethanolamides) and prostaglandin (PG) glyceryl esters are biosynthesized by COX-2 from the respective endocannabinoids anandamide and 2-arachidonyl glycerol. Agonist studies suggest that their pharmacologies are unique and unrelated to prostanoid receptors. This concept was further investigated using antagonists. Experimental Approach: The isolated feline iris was used as a key preparation, where prostanoid FP receptors and prostamide activity co-exist. Activity at human recombinant FP and other prostanoid receptors was determined using stable transfectants. Key Results: In the feline iris, AGN 204396 produced a rightward shift of the dose-response curves for prostamide F2α and the prostamide F2α analog bimatoprost but did not block the effects of PGF2α and synthetic FP receptor agonists. Studies on human recombinant prostanoid receptors confirmed that AGN 204396 did not behave as a prostanoid FP receptor antagonist. AGN 204396 exhibited no antagonism at DP and EP1-4, but was a highly effective TP receptor antagonist. Contrary to expectation, the FP receptor antagonist AL-8810 efficaciously contracted the cat iris. AGN 204396 did not affect AL-8810 induced contractions, demonstrating that AL-8810 and AGN 204396 are pharmacologically distinct. Unlike AL-8810, the ethylamide derivate of AL-8810 was not an agonist. Al-8810 did not block prostamide F2α activity. Finally, AGN 204396 did not block PGE2-glyceryl ester activity. Conclusions and Implications: The ability of AGN 204396 to selectively block prostamide responses suggests the existence of prostamide sensitive receptors as entities distinct from receptors recognizing PGF2α and PGE2-glyceryl ester. British Journal of Pharmacology (2007) 150, 342–352. doi:10.1038/sj.bjp.0706989

The aim of glaucoma therapy is to preserve vision by reducing intraocular pressure (IOP). Following recent National Eye Institute sponsored studies, it is becoming increasingly apparent that every mmHg of extra IOP lowering counts. Bimatoprost is the newest and most effective addition to the physician's armamentarium of ocular hypotensive drugs. Direct clinical comparisons have demonstrated that it is more efficacious than the prostaglandin (PG) FP receptor agonist prodrugs, latanoprost and travoprost, as well as a β-adrenoceptor antagonist, timolol, alone or in fixed combination with the carbonic anhydrase inhibitor, dorzolamide. Moreover, patients that are refractory to latanoprost therapy may be successfully treated with bimatoprost. Such evidence provides support, at the clinical level, for the contention that bimatoprost is pharmacologically distinct from PG FP receptor agonist prodrugs. Bimatoprost is a structural analog of PGF2α-ethanolamide (prostamide F2α), which is formed from the endocannabinoid anandamide by a biosynthetic pathway involving cyclooxygenase-2 (COX-2). Their pharmacology is remarkably similar, such that bimatoprost may be regarded as a prostamide mimetic. The target receptor for bimatoprost and the prostamides appears unique and unrelated to PG- and endocannabinoid-sensitive receptors. Extensive ocular distribution/metabolism studies in non-human primates demonstrate that bimatoprost is not a prodrug, it remains essentially intact. Its profound ocular hypotensive effects may, therefore, be attributed to its prostamide-mimetic properties.

Regulator of G protein signaling (RGS) proteins act as GTPase-activating proteins (GAPs) for Galpha subunits and negatively regulate G protein-coupled receptor signaling. Using RGS5 gene-specific RT-PCR, we have identified a novel alternative splicing variant of RGS5 mRNA in human ocular tissues. The alternative splicing of RGS5 mRNA occurred at position +44 (GenBank NM_003617), spliced out 174 bp (+44 to +218 bp) of the coding region, and encoded an RGS5s protein with a 108 amino acid N-terminal deletion. This study is the first to document alternative splicing of an RGS5 gene. We therefore studied RGS5 and RGS5s mRNA distribution in human tissues. In the eye, RGS5s was found to be highly expressed in the ciliary body and trabecular meshwork. It was also expressed in the kidney, brain, spleen, skeletal muscle and small intestine, but was not detectable in the liver, lung, heart. RGS5s was not found in monkey and rat ocular tissues, indicating species specificity for the eye. Comparing the recombinant RGS5 and RGS5s expression in HEK293/EBNA cells, RGS5s was present almost exclusively in the cytosolic fraction, whereas RGS5 was present in both membrane and cytosolic fractions. The data suggest that the N-terminal of RGS5 may be important for protein translocation to the cell membrane. Both RGS5 and RGS5s antagonized the rapid phosphorylation of p44/42 MAP kinase induced by Galphai coupled cannibinoid receptor-1 activation. RGS5, but not RGS5s, inhibited the Ca2+ signaling initiated by activation of Galphaq coupled angiotensin II receptors (AT1) and prostaglandin FP receptors. Cotransfection of RGS5s with RGS5 resulted in the blockade of RGS5 actions with respect to inhibition of the signal transduction initiated by activation of both AT1 and FP receptor, suggesting that RGS5s may contain functional domains that compete with RGS5 in the regulation of the Galphaq coupled AT1 and FP receptors. The unique expression pattern, cellular localization and functions of RGS5s suggest that RGS5s may play a critical role in the regulation of intracellular signaling pathways.

1. Using gene chip technology, we first identified that PGF(2alpha) (FP agonist) and Butaprost (EP(2) agonist) induced about a five-fold upregulation of Nur77 mRNA expression in hFP-HEK 293/EBNA and hEP(2)-HEK293/EBNA cells. Northern Blot analysis revealed that PGF(2alpha)- and Butaprost-induced upregulation of Nur77 expression are dose- and time-dependent. 2. Both PGF(2alpha) and Butaprost upregulated Nur77 gene expression through the protein kinase C (PKC) pathway. These data are the first showing a link between EP(2) receptor stimulation and protein kinase C activation. Calcineurin was found to be involved downstream of the PKC pathway in PGF(2alpha)-induced Nur77 expression, but not in Butaprost-induced Nur77 expression. 3. We also used Nur77 as a marker gene to compare the effects of PGF(2alpha), Butaprost, and Bimatoprost (a prostamide) on Nur77 expression in human primary trabecular meshwork and ciliary smooth muscle (SM) cells, which are target cells for antiglaucoma drugs. The results showed that PGF(2alpha) and Butaprost, but not Bimatoprost, induced upregulation of Nur77 expression in human TM cells. PGF(2alpha), but not Bimatoprost, dramatically induced upregulation of Nur77 mRNA expression in human ciliary SM cells, whereas Butaprost slightly upregulated Nur77 mRNA expression in SM cells. 4. Nur77 promoter deletion analysis indicated that PGF(2alpha), but not Bimatoprost, activated Nur77 promoter-luciferase reporter in hFP-HEK 293/EBNA cells. Butaprost was less efficacious in inducing Nur77 promoter-luciferase reporter activity in hEP(2)-HEK293/EBNA cells relative to PGF(2alpha) in the comparable assay. The data for Nur77 promoter functional analysis were matched to the Northern blot analysis. 5. It appears that PGF(2alpha) and Butaprost activate Nur77 transcription mechanisms through the activation of FP and EP(2) receptor-coupled signaling pathways, whereas Bimatoprost stimulates neither FP nor EP(2) receptors.

Connective tissue growth factor (CTGF) and Cyr61 (cysteine-rich angiogenic protein 61) are members of the CCN gene family that encode multifunctional, extracellular matrix-associated signaling proteins. Because the mechanism of action of certain anti-glaucoma drugs involves extracellular matrix remodeling of ocular ciliary muscle, with a resultant increase in drainage of aqueous humor from the eye, we compared the effects of three pharmacologically distinct ocular hypotensive agents on Cyr61 and CTGF gene expression. Thus, prostaglandin F2alpha (PGF2alpha) (FP receptor agonist), Butaprost (EP2 receptor agonist), and Bimatoprost (a prostamide) were compared. Using Affymetrix gene chip technology, we first identified that PGF2alpha dramatically up-regulated Cyr61 and CTGF mRNA expression in HEK 293/EBNA cells (hFP-HEK 293/EBNA). Northern blot further confirmed the Cyr61 and CTGF up-regulation is in a dose- and time-dependent manner. PGF2alpha-induced up-regulation of Cyr61 appeared to exclusively involve the Rho pathway, and up-regulation of CTGF was via multiple intracellular pathways. Because prostamide receptors are, to date, defined only at the pharmacological level, Bimatoprost effects on Cyr61 and CTGF were studied in the isolated feline iris sphincter preparation, a tissue highly responsive to prostamides. Both PGF2alpha and Bimatoprost up-regulated Cyr61 mRNA expression in the cat iris tissue. Only PGF2alpha up-regulated CTGF mRNA expression in the cat iris. Therefore, PGF2alpha and Bimatoprost appear to interact with different receptors populations in the cat iris, according to their markedly different effects on CTGF. Activation of prostaglandin EP2 receptors (Gs-coupled) also up-regulated Cyr61 but not CTGF mRNA expression in the isolated cat iris. Similar data were observed in human primary ciliary smooth muscle cells. Thus, despite quite different signal transduction pathways, FP receptor stimulation up-regulates CTGF and Cyr61. The prostamide analog Bimatoprost and an EP2-selective agonist affects only Cyr61.

Apolipoprotein E (apoE) and apoJ are lipid carriers produced in the brain primarily by glial cells. A variety of glial-activating stimuli induce a parallel upregulation of both apolipoproteins expression in vivo and in vitro. To further characterize the cell type and mechanisms by which apoE and apoJ expression are upregulated in activated glia, mixed glial cultures from neonatal rat cortex were treated with the endotoxin lipopolysaccharide (LPS). LPS induced dose-dependent increases in apoJ and decreases in apoE expression and secretion with maximum effects at 1-10 ng/mL and 0.1-1 microg/mL, respectively. Experiments with enriched astroglial and microglial cultures demonstrated that apoE and apoJ expression are predominantly microglial and astroglial, respectively. Given the pivotal role that nuclear factor-kappa B (NF-kappa B) plays in glial activation, we assessed its possible role in mediating apoE and apoJ expression by activated glia. LPS robustly increased NF-kappa B activation in mixed glial cultures. Two NF-kappa B inhibitors, aspirin (10 mM) and MG-132 (0.1 microM), blocked basal apoE and apoJ secretion as well as LPS-induced apoJ secretion. These data demonstrate that glial apoE and apoJ expression are independently regulated by LPS in microglia and astroglia, respectively, and that activated microglia are the predominant source of apoE in mixed glial cultures. The transcription factor NF-kappa B appears to be a critical mediator of LPS-stimulated apoJ expression from astroglia.

We investigate the propagation of the spatial soliton in cylindrical strongly nonlocal media by a novel method of image beam of light. The effect of the boundary on the soliton acting as the dynamic force for the soliton steering is equivalent to the force between the soliton beam and the image beam. The trajectory of the soliton is analytically studied which is in good agreement with the experimental results., Comment: 3 Pages, 3 figures

The fractional Fourier transform (FRFT) naturally exists in the strongly nonlocal nonlinear (SNN) media and the propagation of optical beams in SNN media can be simply regarded as a self-induced FRFT. Through FRFT technic the evolution of fields in SNN media can be conveniently dealt with and an arbitrary square-integrable input field presents generally as a revivable higher order spatial soliton which reconstructs its profile periodically after every 4 times of Fourier transforms. The self-induced FRFT would illuminate the prospect of the SNN media in new applications such as continuously tunable nonlinearity-induced FRFT devices., Published in Phys. Rev. A

Regulator of G protein signaling (RGS) proteins act as GTPase-activating proteins (GAPs) for Galpha subunits and negatively regulate G protein-coupled receptor signaling. Using RGS5 gene-specific RT-PCR, we have identified a novel alternative splicing variant of RGS5 mRNA in human ocular tissues. The alternative splicing of RGS5 mRNA occurred at position +44 (GenBank NM_003617), spliced out 174 bp (+44 to +218 bp) of the coding region, and encoded an RGS5s protein with a 108 amino acid N-terminal deletion. This study is the first to document alternative splicing of an RGS5 gene. We therefore studied RGS5 and RGS5s mRNA distribution in human tissues. In the eye, RGS5s was found to be highly expressed in the ciliary body and trabecular meshwork. It was also expressed in the kidney, brain, spleen, skeletal muscle and small intestine, but was not detectable in the liver, lung, heart. RGS5s was not found in monkey and rat ocular tissues, indicating species specificity for the eye. Comparing the recombinant RGS5 and RGS5s expression in HEK293/EBNA cells, RGS5s was present almost exclusively in the cytosolic fraction, whereas RGS5 was present in both membrane and cytosolic fractions. The data suggest that the N-terminal of RGS5 may be important for protein translocation to the cell membrane. Both RGS5 and RGS5s antagonized the rapid phosphorylation of p44/42 MAP kinase induced by Galphai coupled cannibinoid receptor-1 activation. RGS5, but not RGS5s, inhibited the Ca2+ signaling initiated by activation of Galphaq coupled angiotensin II receptors (AT1) and prostaglandin FP receptors. Cotransfection of RGS5s with RGS5 resulted in the blockade of RGS5 actions with respect to inhibition of the signal transduction initiated by activation of both AT1 and FP receptor, suggesting that RGS5s may contain functional domains that compete with RGS5 in the regulation of the Galphaq coupled AT1 and FP receptors. The unique expression pattern, cellular localization and functions of RGS5s suggest that RGS5s may play a critical role in the regulation of intracellular signaling pathways.