Impaired Permeability Research Articles

Comparative study of different enhanced oil recovery scenarios by silica nanoparticles: An approach to time-dependent wettability alteration in carbonates

Recently, nanoparticles (NPs) have been proven to be effective chemical agents for enhanced oil recovery (EOR) purposes. Many studies implemented various Nano-EOR scenarios, including slug nanofluid injection, continuous nanofluid-flooding, and pre-soaking by nanofluids. However, since the EOR performance of NPs is limited by factors such as the cost of nanofluids preparation and the potential rock permeability impairment, a lack of an efficient Nano-EOR scenario is felt. This study intends to evaluate the efficiency of the mentioned Nano-EOR scenarios to propose a more desirable Nano-EOR plan. The results showed that silica NPs could decrease interfacial tension of water/oil system from 25.1 mN/m to 9.3 mN/m. Also, wettability alteration induced by silica NPs is a time-dependent process, in which it took around 7 days for NPs to exhibit their optimal potential for wettability alteration of the carbonate rock. Equilibrium contact angle values of 66 and 23 degrees were obtained using 0.1 and 0.3 wt% of silica nanofluids. Accordingly, a 7-day shut-in period was carried out after nanofluid flooding (meaning pre-soaking by nanofluids), before flushing by low salinity water. Core flooding tests showed ultimate oil recovery values of 78 and 71% of original oil in place (OOIP) through the pre-soaking scenario by 0.1 and 0.3 wt% of silica nanofluids, which were higher than slug nanofluid injection and continuous nanofluid flooding scenarios with 49 and 38% of OOIP, respectively. Permeability reduction was intensified with nanofluids concentration and a 24% permeability impairment was achieved by injecting 0.3 wt% of silica nanofluid. Primary reasons associated with differences in oil recovery values were dynamic performance of silica NPs on wettability alteration, oil snap-off, and pore plugging due to the adsorption and straining of NPs. Findings of this study revealed the importance of an optimal Nano-EOR scenario selection in oil-wet carbonates.

“Reach the cells”: microcirculatory support

Background. Vessels of the microcirculatory tract provide regulatory, drainage, thermocontrol and signal functions. Disorders of these vessels are the part of the pathogenesis of coronary heart disease, endarteritis obliterans, Raynaud’s disease, etc. Common causes of microcirculation disorders include disorders of central and regional blood circulation, impaired blood volume and viscosity, impaired permeability of microvessel walls.
 Objective. To describe the features of microcirculatory support.
 Materials and methods. Analysis of literature sources on this topic.
 Results and discussion. In order to improve microcirculation, various drugs are used: antiplatelets, anticoagulants, antioxidants, and nitric oxide donors. The purpose of these drugs are to improve the rheological properties of blood, to improve the delivery of nutrients to the vascular wall, to regulate the vascular tone, and to improve endothelial function. Reosorbilact (“Yuria-Pharm”) opens precapillary sphincters, increases the area of blood contact with the target cell, improves tissue oxygenation and rheological properties of blood. Reosorbilact includes such components as sorbitol, basic cations (Na, Ca, K, Mg) and sodium lactate. Sorbitol is used for urgent energy needs, metabolized and stored as glycogen, has a disaggregating effect, improves microcirculation and tissue perfusion. The hyperosmolar action of Reosorbilact is to stimulate the flow of fluid from the intercellular space into the vascular bed. Correction of metabolic acidosis with Reosorbilact is slower than due to sodium bicarbonate buffer, so this solution does not cause severe fluctuations in pH. The detoxifying effect of Reosorbilact involves washing of metabolites and toxins out from damaged cells, tissues and organs, followed by their rapid excretion due to increased diuresis. The improvement of liver microcirculation and replenishment of glycogen depot, which normalizes the functional state of hepatocytes and enhances physiological detoxification, is an additional beneficial effect. Hemodilution is also important, because it allows to reduce the content of toxic metabolites in blood plasma. In addition, Reosorbilact gently stimulates peristalsis, has choleretic and cholekinetic effects, reduces bilirubin and creatinine, improves energy metabolism, stabilizes systemic hemodynamics, reduces the symptoms of pain due to anti-edematous effect, and accelerates wound healing. Reosorbilact can be considered a drug № 1 for low-volume infusion therapy. The positive hemodynamic effect of the drug is manifested within 2-3 hours. Reosorbilact promotes the transition of the hypokinetic type of blood circulation into eukinetic due to the redistribution of extracellular fluid into the vascular bed. The drug should be prescribed at a dose of 7 ml/kg of body weight for 5-7 days or until the symptoms of intoxication are reduced.
 Conclusions. 1. Vessels of the microcirculatory tract provide regulatory, drainage, thermoregulatory and signal functions. 2. Common causes of microcirculation disorders include disorders of central and regional blood circulation, disorders of blood volume and viscosity, impaired permeability of microvessel walls. 3. Reosorbilact improves tissue oxygenation and rheological properties of blood, promotes washing of metabolites and toxins out from damaged cells, normalizes the functional state of hepatocytes, stimulates peristalsis, stabilizes systemic hemodynamics.

A New Coupled Model for Permeability-Impairment Prediction Because of Mineral Scale Deposition in Water-Injection Wells

Summary It is common to produce some percentage of water during the oil-extraction process. Conventionally, some water-disposal wells are drilled in an oil field to inject these useless and hazardous waters. Mineral scale formation is a critical issue in water-injection wells and may result in well plugging and an injection rate decrease in these wells. The two steps of mineral scale formation are scale precipitation and scale deposition. Two main mechanisms of inorganic scale precipitation are incompatibility between injected water and reservoir formation water and changes in the thermodynamic state of injected water. The injectivity of the well decreases because of deposition of supersaturated precipitated scales through the well column and near-wellbore region. Currently, limited research has been done to evaluate inorganic scale deposition, and most of the research is limited to calculation of total scaling by commercial software. In this study, the mineral scale precipitation is evaluated by software modeling and laboratory experiments in an Iranian oil field, and the effect of the scale deposition phenomenon is assessed on permeability impairment and injection rate decrease. One of the major novelties of this work is simulation of various scale-deposition models by coupling MATLAB® software coding and a reservoir simulator. The accuracy of different deposition models is analyzed by comparing them with field data (real water-injection well) and laboratory tests (coreflooding test). Finally, our simulation results show that a single deposition model could not exactly predict the scaling phenomena in the studied carbonate reservoir that is supersaturated with CaCO3 and CaSO4. It is recommended to improve the scale-formation prediction with a mixed deposition model supported by reliable static/dynamic modeling and experimental analysis.

Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease.

Over recent years, several investigations have suggested that Parkinson’s disease (PD) can be regarded as the consequence of a bowel disorder. Indeed, gastrointestinal symptoms can occur at all stages of this neurodegenerative disease and in up to a third of cases, their onset can precede the involvement of the central nervous system. Recent data suggest that enteric glial cells (EGCs) may play a major role in PD-related gastrointestinal disturbances, as well as in the development and progression of the central disease. In addition to their trophic and structural functions, EGCs are crucial for the homeostatic control of a wide range of gastrointestinal activities. The main purpose of this review was to provide a detailed overview of the role of EGCs in intestinal PD-associated alterations, with particular regard for their participation in digestive and central inflammation as well as the dynamic interactions between glial cells and intestinal epithelial barrier. Accumulating evidence suggests that several pathological intestinal conditions, associated with an impairment of barrier permeability, may trigger dysfunctions of EGCs and their shift towards a proinflammatory phenotype. The reactive gliosis is likely responsible for PD-related neuroinflammation and the associated pathological changes in the ENS. Thus, ameliorating the efficiency of mucosal barrier, as well as avoiding IEB disruption and the related reactive gliosis, might theoretically prevent the onset of PD or, at least, counteract its progression.

Investigation of permeability decline due to coupled precipitation/dissolution mechanism in carbonate rocks during low salinity co-water injection

Low salinity water injection is a promising water-based enhanced oil recovery (EOR) method for carbonate rocks. However, permeability impairment resulted from competition between mineral scale precipitation and rock dissolution is not well understood due to complex injection water/formation brine/rock interactions. In this paper, simultaneous effects of rock dissolution and mineral scale precipitation in low saline co-water injection on permeability performance were investigated. A dynamic flow of water with varying ion composition considering scale precipitation/rock dissolution coupling with geochemical reactions (using PHREEQC) was developed. The proposed model was validated with outlet ion concentration of single phase coreflood data. Then, permeability decline curves were obtained for each mixing ratio of formation brine and diluted sea water. The results show that in case of co-water injection, mineral scale precipitation is the dominant mechanism in early times of flooding and can be comparable with rock dissolution quantitatively in longer time. This result is in contrast with results of sequensive injection available in literature due to lack of sufficient mixing zone between injected water and formation brine and small pore volume of injection. In addition there are three different regions in permeability curve of co-water injection which is reflecting the competition between mineral scale precipitation and rock dissolution mechanisms. Moreover, as the share of formation brine increased more than 0.5, mineral precipitation became dominant and permeability curve decreased monotonically. The model can be used for distinguishing share of different mechanisms of permeability variation during low salinity waterflooding.

The platelets behaviour in non-alcoholic fatty liver disease. A potential role for antiplatelets drugs?

Abstract Background and purpose Previous studies showed a favorable effect of aspirin, which irreversibly acetylates cyclooxygenase-1 (COX1) so preventing Thromboxane (Tx) A2 biosynthesis, in non-alcoholic steatohepatitis (NASH) and its sequelae. However, the behavior of COX1 in NASH patients is still unknown. Methods We conducted a cross-sectional study on 44 outpatients with NASH, 50 subjects with simple steatosis (NAFL) and 50 subjects without hepatic steatosis balanced for age, gender and BMI. Serum TxB2, a stable metabolite of TxA2, and urinary 11-dehydro-TxB2, as markers of COX1 activation, plasma soluble P-selectin (sP-selectin), a maker of in vivo platelet activation, serum bacterial lipopolysaccharide (LPS) and serum zonulin, a marker of gut permeability, were measured. Results Urinary 11-dehydro-TxB2 (p<0.001) and serum TxB2 (p<0.001) levels as well as sP-selectin (p<0.001) were significantly higher in patients with NASH/NAFL compared to the controls (figure 1); the markers of COX1 activation significantly correlated with sP-selectin (p<0.001). Serum LPS was higher in patients with NASH compared with NAFL and controls (p<0.001) and serum zonulin was significantly higher in patients with NASH as compared to controls (p=0.031). A positive correlation (rS=0.37; p<0.001) was observed between serum LPS and serum zonulin. Moreover, serum LPS correlated with serum and urinary 11-dehydro-TxB2 (rS=0.30; p<0.001 and rS=0.61; p<0.001, respectively) and with sP-Selectin (rS=0.32; p<0.001) (figure). At multivariate analysis, LPS above median (OR=3.15, p=0.015) and liver diagnosis (NAFL vs. Controls: OR=6.54; p<0.001 and NASH vs Controls: OR=4.54; p=0.007) were independently associated with sP-selectin above median (table). Conclusions Patients with NAFLD display enhanced platelet activation, which is associated to COX1 up-regulation. LPS increased by impaired gut permeability may favor platelet activation. Figure 1 Funding Acknowledgement Type of funding source: None

Neuroimaging patterns of chronic cerebrovascular insufficiency with evaluation of cerebral perfusion depending on the level of cognitive disorders

Aim. To evaluate the neuroimaging patterns of chronic cerebrovascular insufficiency with cerebral perfusion assessment depending on the level of cognitive impairment.Materials and methods. The 58 patients aged 50–79 years were examined: 45 patients with a diagnosis of сhronic cerebrovascular insufficiency and 13 conditionally healthy volunteers. Patients with Chronic cerebrovascular insufficiency were ranked into three subgroups depending on the severity of cognitive impartment (CI). T1-, T2, T2*- VI, DWI, FLAIR and non-contrast MR perfusion (ASL) were included in the MR-protocol (Toshiba Vantage Titan, 1.5 T). The analysis of MRM patterns of Chronic cerebrovascular insufficiency was carried out according to STRIVE criteria. The total cerebral blood flow and regional in the frontal and parietal lobes were evaluated by the ASLperfusion.Results. A relationship was found between the degree of leukoaraiosis, the type of expansion of the perivascular spaces of Virchow-Robin and the level of CI. According to ASL, total cerebral blood flow is higher in groups without CI and in patients with severe CI. There is a diffuse decrease of cerebral perfusion in patients with mild CI. This phenomenon is explained by initial impairment of the blood-brain barrier permeability, damage to the microvasculature. Relative hyperperfusion in the cortex of the frontal and parietal lobes of patients with dementia indicates the ineffectiveness of increased cortical blood flow and the resulting shunt blood flow due to the high resistance of the altered small cerebral vessels under high pulsating properties of the main arteries.Conclusion. ASL perfusion is a complementary link to the STRIVE criteria in the diagnosis of chronic cerebrovascular insufficiency. The absence of changes in cerebral perfusion in patients with subjective manifestations of chronic cerebrovascular insufficiency makes it advisable to search for new methods for the diagnosis of preclinical stages of vascular cognitive impairment.

Iatrogenic (drug induced) cognitive disorders

This article discusses the clinical and pathogenetic aspects of iatrogenic (drug induced) cognitive disorders. It is emphasized that in most cases the etiology of these disorders is multifactorial in nature. In some cases, iatrogenic disorders are caused by the intake of an inadequately large dose of the drug, while in other cases, they are caused by the side effect of drugs. Disorders such as cerebral homeostasis, impaired permeability of the bloodbrain barrier and the neurochemical properties of a certain drug are important. Side effects of drug therapy in elderly patients are much more common than in patients of a younger age, which is due to a number of causes, namely the poly-pragmasy characteristic of the elderly patients, erroneous prescription of certain drugs, drug interactions, altered pharmacokinetics and pharmacodynamics, and increased sensitivity to medications. Various groups of drugs are considered, during the intake of which, neuropsychiatric disorders may occur. In this case, special attention is paid to drugs with cholinolytic properties. Neurological disorders arising from radiation therapy were analyzed separately. It was concluded that it is necessary to assess the possible adverse effect of previously prescribed drug therapy for various indications in patients with cognitive impairment.

Stress response and tolerance to perfluorooctane sulfonate (PFOS) in lettuce (Lactuca sativa)

Comprehensive understanding of stress response and tolerance to perfluorooctane sulfonate (PFOS) in plants at physiological, biochemical and molecular levels is scarce. Here, lettuce was cultivated in hydroponic media, to investigate the cross-talk among reactive oxygen species (ROS) production, oxidative damage, antioxidative defense and metabolic regulation in different parts of plants. Under exposure to 5 and 50 μg/L PFOS for 10 days, 8.8 and 82.5 ng/g dry weight (dw) PFOS were accumulated in leaves, respectively, and 150.9 and 1445.6 ng/g dw in roots, respectively·H2O2 was the dominant ROS in roots, while H2O2 and •O2− were detected in leaves. Impaired permeability of plasma membrane (58.7–88.7%, p < 0.05) and reduction in chlorophyll a (41.4–55.6%, p < 0.01) and b (38.4–41.3%, p < 0.01) were observed in leaves. The concentration of soluble proteins was elevated by 93.2–127.4% in roots (p < 0.05). Non-enzymatic antioxidants (glutathione, phenolics and carotenoids) were regulated to scavenge ROS in leaves, beside additional enzymatic antioxidants (ascorbate peroxidase, peroxidase, catalase and glutathione peroxidase) were activated in roots. Metabolomics revealed that some metabolites in primary (amino acids and carbohydrates) and secondary ((poly)phenols, terpenoids and benzylisoquinolines) metabolism were regulated, in accordance with the ROS scavenging process in plants. Our results demonstrated stress response and tolerance to PFOS were different in lettuce leaves and roots, and multiple defensive mechanisms in roots rendered high tolerance to PFOS.

Regulation of the thrombin/protease-activated receptor 1 axis by chemokine (CXC motif) receptor 4

The chemokine receptor CXCR4, a G protein-coupled receptor (GPCR) capable of heteromerizing with other GPCRs, is involved in many processes, including immune responses, hematopoiesis, and organogenesis. Evidence suggests that CXCR4 activation reduces thrombin/protease-activated receptor 1 (PAR1)-induced impairment of endothelial barrier function. However, the mechanisms underlying cross-talk between CXCR4 and PAR1 are not well-understood. Using intermolecular bioluminescence resonance energy transfer and proximity ligation assays, we found that CXCR4 heteromerizes with PAR1 in the HEK293T expression system and in human primary pulmonary endothelial cells (hPPECs). A peptide analog of transmembrane domain 2 (TM2) of CXCR4 interfered with PAR1:CXCR4 heteromerization. In HTLA cells, the presence of CXCR4 reduced the efficacy of thrombin to induce β-arrestin-2 recruitment to recombinant PAR1 and enhanced thrombin-induced Ca2+ mobilization. Whereas thrombin-induced extracellular signal-regulated protein kinase 1/2 (ERK1/2) phosphorylation occurred more transiently in the presence of CXCR4, peak ERK1/2 phosphorylation was increased when compared with HTLA cells expressing PAR1 alone. CXCR4-associated effects on thrombin-induced β-arrestin-2 recruitment to and signaling of PAR1 could be reversed by TM2. In hPPECs, TM2 inhibited thrombin-induced ERK1/2 phosphorylation and activation of Ras homolog gene family member A. CXCR4 siRNA knockdown inhibited thrombin-induced ERK1/2 phosphorylation. Whereas thrombin stimulation reduced surface expression of PAR1, CXCR4, and PAR1:CXCR4 heteromers, chemokine (CXC motif) ligand 12 stimulation reduced surface expression of CXCR4 and PAR1:CXCR4 heteromers, but not of PAR1. Finally, TM2 dose-dependently inhibited thrombin-induced impairment of hPPEC monolayer permeability. Our findings suggest that CXCR4:PAR1 heteromerization enhances thrombin-induced G protein signaling of PAR1 and PAR1-mediated endothelial barrier disruption.

Myrtus communis improves cognitive impairment in renovascular hypertensive rats.

Myrtus communis has anti-inflammatory, neuroprotective and anticholinesterase activities yet there have been limited studies examining effects of Myrtus communis on cognitive functions. This study investigated the possible effects of Myrtus communis on changes in the cognitive functions of experimental renovascular hypertensive rats. Fifty-six Wistar-Albino rats were equally divided into 4 groups; sham-operated control, renovascular hypertension (RVH), ramipril (RVH + Ram) and Myrtus communis extract (RVH + MC) treatment groups. Goldblatt's 2-kidney 1-clip (2K1C) method was used to induce RVH. At the end of 9 weeks of treatment, after blood pressure recording, the animals underwent new object recognition test and Morris water maze (MWM) task. Following these tests, blood brain barrier (BBB) integrity was examined in 6 animals from each group. In the others after decapitation, osteopontin and interleukin (IL)-10 levels were measured in blood samples; while matrix metalloproteinase (MMP)-13, sodium potassium adenosine triphosphatase (Na+,K+-ATPase), cluster of differentiation (CD) 36, amyloid beta (Aβ), neprilysin levels, and acetylcholinesterase (AChE) activity were investigated in hippocampal tissues. In RVH group, high systolic blood pressure decreased serum IL-10 levels, increased serum osteopontin levels and also impaired BBB permeability. Hippocampal MMP-13, CD36, Aβ, neprilysin levels and AChE activities were elevated, while there were decreases in Na+,K+-ATPase levels. In new objet recognition test, discrimination index (DI) was determined as lower in saline-treated RVH group compared to control animals. In MWM training trail, 4th day performance in finding platform was significantly reduced in saline-treated RVH group compared to control group. RVH also decreased the time spent in target quadrant in probe test of MWM task compared to control group. In both of the treatment groups, all biochemical parameters were restored in parallel with improvement in the behavioral test performances. The results of this study suggest that Myrtus communis extract may improve the cognitive dysfunctions in hypertension through antihypertensive, anti-inflammatory and anticholinesterase activities.

Gut-lymph-lung pathway mediates sepsis-induced acute lung injury.

This review attempts to unveil the possible mechanisms underlying how gut lymph affects lung and further gives rise to acute respiratory distress syndrome, as well as potential interventional targets under the condition of ischemia-reperfusion injury. We searched electronic databases including PubMed, MEDLINE, Cochrane Central Register of Controlled Trials, Google Scholar, Web of Science, and Embase to identify relevant literatures published up to December 2019. We enrolled the literatures including the Mesh Terms of “gut lymph or intestinal lymph and acute lung injury or acute respiratory distress syndrome.” Gut is considered to be the origin of systemic inflammation and the engine of multiple organ distress syndrome in the field of critical care medicine, whereas gut lymph plays a pivotal role in initiation of ischemia-reperfusion injury-induced acute respiratory distress syndrome. In fact, in the having been established pathologic model of sepsis leading to multiple organ dysfunction named by Gut Lymph theory, a variety of literatures showed the position and role of changes in gut lymph components in the initiation of systemic inflammatory response, which allows us to screen out potential intervention targets to pave the way for future clinic and basic research.

Secondary Sclerosing Cholangitis in Critically Ill Patients Alters the Gut–Liver Axis: A Case Control Study

Secondary sclerosing cholangitis in critically ill patients (SC-CIP) occurs after long-term intensive care treatment. This study aimed to assess the gut–liver axis in SC-CIP. Stool microbiome composition, gut permeability, bacterial translocation and serum bile acid profiles of 18 SC-CIP patients compared to 11 patients after critical illness without liver disease (CIP controls), 21 patients with cirrhosis and 21 healthy controls were studied. 16S rDNA was isolated from stool and sequenced using the Illumina technique. Diamine oxidase, zonulin, soluble CD14 (sCD14) and lipopolysaccharide binding protein were measured in serum and calprotectin in stool. Serum bile acids were analyzed by high-performance liquid chromatography-mass spectrometry (HPLC-MS). Reduced microbiome alpha diversity and altered beta diversity were seen in SC-CIP, CIP controls and cirrhosis compared to healthy controls. SC-CIP patients showed a shift towards pathogenic taxa and an oralization. SC-CIP, CIP controls and cirrhotic patients presented with impaired gut permeability, and biomarkers of bacterial translocation were increased in SC-CIP and cirrhosis. Total serum bile acids were elevated in SC-CIP and cirrhosis and the bile acid profile was altered in SC-CIP, CIP controls and cirrhosis. In conclusions, observed alterations of the gut–liver axis in SC-CIP cannot solely be attributed to liver disease, but may also be secondary to long-term intensive care treatment.

Methylglyoxal-Induced Dysfunction in Brain Endothelial Cells via the Suppression of Akt/HIF-1α Pathway and Activation of Mitophagy Associated with Increased Reactive Oxygen Species.

Methylglyoxal (MG) is a dicarbonyl compound, the level of which is increased in the blood of diabetes patients. MG is reported to be involved in the development of cerebrovascular complications in diabetes, but the exact mechanisms need to be elucidated. Here, we investigated the possible roles of oxidative stress and mitophagy in MG-induced functional damage in brain endothelial cells (ECs). Treatment of MG significantly altered metabolic stress as observed by the oxygen-consumption rate and barrier-integrity as found in impaired trans-endothelial electrical resistance in brain ECs. The accumulation of MG adducts and the disturbance of the glyoxalase system, which are major detoxification enzymes of MG, occurred concurrently. Reactive oxygen species (ROS)-triggered oxidative damage was observed with increased mitochondrial ROS production and the suppressed Akt/hypoxia-inducible factor 1 alpha (HIF-1α) pathway. Along with the disturbance of mitochondrial bioenergetic function, parkin-1-mediated mitophagy was increased by MG. Treatment of N-acetyl cysteine significantly reversed mitochondrial damage and mitophagy. Notably, MG induced dysregulation of tight junction proteins including occludin, claudin-5, and zonula occluden-1 in brain ECs. Here, we propose that diabetic metabolite MG-associated oxidative stress may contribute to mitochondrial damage and autophagy in brain ECs, resulting in the dysregulation of tight junction proteins and the impairment of permeability.

Hydrate Plugging and Flow Remediation during CO2 Injection in Sediments

Successful geological sequestration of carbon depends strongly on reservoir seal integrity and storage capacity, including CO2 injection efficiency. Formation of solid hydrates in the near-wellbore area during CO2 injection can cause permeability impairment and, eventually, injectivity loss. In this study, flow remediation in hydrate-plugged sandstone was assessed as function of hydrate morphology and saturation. CO2 and CH4 hydrates formed consistently at elevated pressures and low temperatures, reflecting gas-invaded zones containing residual brine near the injection well. Flow remediation by methanol injection benefited from miscibility with water; the methanol solution contacted and dissociated CO2 hydrates via liquid water channels. Injection of N2 gas did not result in flow remediation of non-porous CO2 and CH4 hydrates, likely due to insufficient gas permeability. In contrast, N2 as a thermodynamic inhibitor dissociated porous CH4 hydrates at lower hydrate saturations (&lt;0.48 frac.). Core-scale thermal stimulation proved to be the most efficient remediation method for near-zero permeability conditions. However, once thermal stimulation ended and pure CO2 injection recommenced at hydrate-forming conditions, secondary hydrate formation occurred aggressively due to the memory effect. Field-specific remediation methods must be included in the well design to avoid key operational challenges during carbon injection and storage.

Tail-Oxidized Cholesterol Enhances Membrane Permeability for Small Solutes.

Cholesterol renders mammalian cell membranes more compact by reducing the amount of voids in the membrane structure. Because of this, cholesterol is known to regulate the ability of cell membranes to prevent the permeation of water and water-soluble molecules through the membranes. Meanwhile, it is also known that even seemingly tiny modifications in the chemical structure of cholesterol can lead to notable changes in membrane properties. The question is, how significantly do these small changes in cholesterol structure affect the permeability barrier function of cell membranes? In this work, we applied fluorescence methods as well as atomistic molecular dynamics simulations to characterize changes in lipid membrane permeability induced by cholesterol oxidation. The studied 7β-hydroxycholesterol (7β-OH-chol) and 27-hydroxycholesterol (27-OH-chol) represent two distinct groups of oxysterols, namely, ring- and tail-oxidized cholesterols, respectively. Our previous research showed that the oxidation of the cholesterol tail has only a marginal effect on the structure of a lipid bilayer; however, oxidation was found to disturb membrane dynamics by introducing a mechanism that allows sterol molecules to move rapidly back and forth across the membrane—bobbing. Herein, we show that bobbing of 27-OH-chol accelerates fluorescence quenching of NBD-lipid probes in the inner leaflet of liposomes by dithionite added to the liposomal suspension. Systematic experiments using fluorescence quenching spectroscopy and microscopy led to the conclusion that the presence of 27-OH-chol increases membrane permeability to the dithionite anion. Atomistic molecular dynamics simulations demonstrated that 27-OH-chol also facilitates water transport across the membrane. The results support the view that oxysterol bobbing gives rise to successive perturbations to the hydrophobic core of the membrane, and these perturbations promote the permeation of water and small water-soluble molecules through a lipid bilayer. The observed impairment of permeability can have important consequences for eukaryotic organisms. The effects described for 27-OH-chol were not observed for 7β-OH-chol which represents ring-oxidized sterols.

Neutrophil Extracellular Traps Impair Intestinal Barrier Function during Experimental Colitis.

Aberrant neutrophil extracellular trap (NET) formation and the loss of barrier integrity in inflamed intestinal tissues have long been associated with inflammatory bowel disease (IBD). However, whether NETs alter intestinal epithelium permeability during colitis remains elusive. Here, we demonstrated that NETs promote the breakdown in intestinal barrier function for the pathogenesis of intestinal inflammation in mouse models of colitis. NETs were abundant in the colon of mice with colitis experimentally induced by dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Analysis of the intestinal barrier integrity revealed that NETs impaired gut permeability, enabling the initiation of luminal bacterial translocation and inflammation. Furthermore, NETs induced the apoptosis of epithelial cells and disrupted the integrity of tight junctions and adherens junctions. Intravenous administration of DNase I, an enzyme that dissolves the web-like DNA filaments of NETs, during colitis restored the mucosal barrier integrity which reduced the dissemination of luminal bacteria and attenuated intestinal inflammation in both DSS and TNBS models. We conclude that NETs serve a detrimental factor in the gut epithelial barrier function leading to the pathogenesis of mucosal inflammation during acute colitis.

Permeability Impairment and Salt Precipitation Patterns During CO2 Injection Into Single Natural Brine‐Filled Fractures

AbstractFormation dry‐out in fracture‐dominated geological reservoirs may alter the fracture space, impair rock absolute permeability, and cause a significant decrease in well injectivity. In this study, we numerically model the dry‐out processes occurring during supercritical CO2 (scCO2) injection into single brine‐filled fractures and evaluate the potential for salt precipitation under increasing effective normal stresses in the evaporative regime. We use an open‐source, parallel finite‐element framework to numerically model two‐phase flow through 2‐D fracture planes with aperture fields taken from naturally fractured granite cores at the Grimsel Test Site in Switzerland. Our results reveal a displacement front and a subsequent dry‐out front in all simulated scenarios, where higher effective stresses caused more flow channeling, higher rates of water evaporation, and larger volumes of salt precipitates. However, despite the larger salt volumes, the permeability impairment was lower at higher effective normal stresses. We conclude that the spatial distribution of the salt, precipitated in fractures with heterogeneous aperture fields, strongly affects the absolute permeability impairment caused by formation dry‐out. The numerical simulations assist in understanding the behavior of the injectivity in fractures and fracture networks during subsurface applications that involve scCO2 injection into brine.

Pore-scale insights into sludge formation damage during acid stimulation and its underlying mechanisms

Acid-oil emulsion and sludge formation are known as two major formation damage mechanisms and the reason for failure of some acid treatments. The published studies in this area focus primarily on core- to well/reservoir-scale and it is fairly unclear how acid-oil interaction at the pore-scale leads to the formation damage observed at the macro- or core-scale. In this paper, dynamic, micro-scale experiments were designed and executed to investigate the acid-induced formation damage using microfluidic approach. In addition, a series of so-called static (microscope) tests were performed in which acid-crude oil compatibility tests were conducted on a glass slide followed by microscopic observation to better analyze the micromodel results.The results show that sludge precipitation occurred right at the interface of the crude oil and acid; either with the residual oil film on the pore wall, at the acid-oil displacement menisci or acid-oil interfaces in the emulsion. Although, it is theoretically assumed that the reaction between acid and crude oil is fast, the results highlight that the damage is intensified by increasing the exposure time up to 8 hours. Besides, the acid type and concentration showed to have considerable impact on the acid-sludge and emulsion formation. The dynamic results indicate that increasing live acid concentration from 15 wt% to 28 wt% caused about 27.5% more permeability impairment due to sever pore-bridging, while spent acid did not result in any acid-sludge deposit. Furthermore, the role of ferric ion, as a transfer catalyst facilitating the two-phase contact, was visually confirmed through static tests. The dynamic tests also indicated 13% more permeability reduction when 3000 ppm ferric ion was present during 28 wt% HCl injection compared with the free-iron case.Emulsion analysis at the pore-scale showed that acid emulsion critically plugs the pore throats and intensify acid-sludge depositions. Size of acid-oil emulsion droplets was found to be distance-dependent such that as the acid permeated deeper into the porous medium the emulsions became finer and denser causing increased damage.Mitigating formation damage requires underpinning the mechanisms, the microfluidic approach can assist in identifying whether sludge precipitation or emulsion formation are the chief mechanisms and can serve as a fast, intermediate step before conducting the time intensive acidizing experiments at core-scale.

Machine learning-based models for predicting permeability impairment due to scale deposition

Water injection is one of the robust techniques to maintain the reservoir pressure and produce trapped oil from oil reservoirs and improve an oil recovery factor. However, incompatibility between injected water and reservoir water causes an unflavored issue named “scale deposition.” Owing to the deposited scales, effective permeability of a reservoir reduced, and pore throats might be plugged. To determine formation damage owing to scale deposition during a water injection process, two well-known machine learning methods, least squares support vector machine (LSSVM) and artificial neural network (ANN), are employed in the present paper. To improve the performance of the LSSVM method, a metaheuristic optimization algorithm, genetic algorithm (GA), is used. The constructed LSSVM model is examined using real formation damage data samples experimentally measured, which was reported in the literature. According to the obtained outputs of the above models, LSSVM has a high performance based on the correlation coefficient, and infinitesimal uncertainty based on a relative error between the model predictions and the corresponding actual data samples was less than 15%. Outcomes from this study indicate the useful application of the LSSVM approach in the prediction of permeability reduction due to scale deposition, and it can lead to a better and more reliable understanding of formation damage effects through water flooding without expensive laboratory measurements.