We believe that osmosis has been overlooked as a possible mechanism for observed low-salinity enhanced-oil-recovery (EOR) effects. Osmosis can occur in an oil/water/rock system when injecting low-salinity water, because the system is full of an excellent semipermeable membrane-the oil itself.In the present work, water transport through oil films was visualized both in 2D micromodels and in sandstone cores imaged in a microcomputed tomography (CT). After treating these model systems with hexamethyldisilazane (HMDS) to render them more oil-wet, water became discontinuous, and it was possible to establish osmotic gradients. Either expansion or contraction of the connate water was observed, depending on the direction of the imposed salinity gradient.Because osmosis could be the underlying mechanism for lowsalinity EOR, two changes in research strategy are proposed: Most importantly, the use of spontaneous-imbibition tests as evidence for wettability alteration in low-salinity water should be critically reinvestigated. This is because observed production could have stemmed from "osmotic expansion" of the connate water rather than wettability change. Second, much research focus should be shifted from sandstone reservoirs to fractured oil-wet carbonates. Osmosis potentially yields larger responses for the latter reservoir type, whereas from a mechanistic perspective the reason behind low-salinity EOR functioning in both sandstones and carbonates deserves further attention.
Purpose:To evaluate manganese (Mn 2ϩ )-enhanced MRI (MEMRI) and diffusion tensor imaging (DTI) as tools for detection of axonal injury and regeneration after intravitreal peripheral nerve graft (PNG) implantation in the rat optic nerve (ON). Materials and Methods:In adult Fischer rats, retinal ganglion cell (RGC) survival was evaluated in Flurogold (FG) back-filled retinal whole mounts after ON crush (ONC), intravitreal PNG, and intravitreal MnCl 2 injection (150 nmol) at 0 and 20 days post lesion (dpl). MEMRI and echoplanar DTI (DTI-EPI) was obtained of noninjured ON one day after intravitreal MnCl 2 injection, and at 1 and 21 dpl after ONC, intravitreal PNG, and intravitreal MnCl 2 injections given at 0 and 20 dpl. GAP-43 immunohistochemistry was performed after the last MRI.Results: ONC reduced RGC density in retina by 94% at 21 dpl compared to noninjured ON without MnCl 2 injections. Both intravitreal PNG and intravitreal MnCl 2 injections improved RGC survival in retina, which was reduced by 90% (ONCϩMnCl 2 ), 82% (ONCϩPNG), and 74% (ONCϩPNGϩMnCl 2 ) compared to noninjured ON. DTIderived parameters (fractional anisotropy [FA], mean diffusivity, axial diffusivity , and radial diffusivity Ќ ) were unaffected by the presence of Mn 2ϩ in the ON. At 1 dpl, CNR MEMRI and were reduced at the injury site, while at 21 dpl they were increased at the injury site compared to values measured at 1 dpl. GAP-43 immunoreactive axons were present in the ON distal to the ONC injury site. Conclusion:MEMRI and DTI enabled detection of functional and structural degradation after rat ON injury, and there was correlation between the MRI-derived and immunohistochemical measures of axon regeneration. UNLIKE AXONS IN THE PERIPHERAL NERVOUS SYS-TEM, those in the central nervous system (CNS) of adult mammals do not regenerate after injury (1,2). Failure to regenerate is attributed to a combination of axon growth arrest by myelin-associated and scar-derived inhibitory molecules (3,4), and to the absence of growth-promoting neurotrophic factors in the adult CNS (5). Several therapeutic interventions have been tested in animal models to try to promote axon regeneration in the adult mammalian CNS, including neutralizing inhibitory molecules by bacterial enzyme chondroitinase ABC (6) and administration of growthpromoting factors released, for example, from olfactory ensheathing cells and stem cells (7,8). One method that has been shown to have an effect in an optic nerve (ON) animal model is the intravitreal implantation of a peripheral nerve graft (PNG) after ON transection. Schwann cells in the PNG produce trophic factors that promote both retinal ganglion cell (RGC) survival and axon growth through the putative inhibitory environment of the injured ON, as documented in several studies (9 -11). Most studies detect regenerating axons in the CNS using traditional axon tracing techniques (e.g.,
Purpose:To assess magnitude and duration of changes in myocardial longitudinal relaxation rate (R 1 ) in humans following infusion of the manganese (Mn) releasing contrast agent MnDPDP (Mn-dipyridoxyl-diphosphate). Materials and Methods:Fifteen healthy volunteers were divided into three groups. After initial myocardial and liver R 1 measurements using an inversion recovery (IR) turbo fast low-angle shot (FLASH) sequence at 1.5 Tesla, the groups were given different doses of intravenous MnDPDP: 5, 10 and 15 mol/kg body weight, respectively, over 30 minutes. R 1 measurements were then repeated at 1, 2, 4, 8, and 24 hours after the infusion ended. Results:The left ventricular wall R 1 prevalue was 0.98 second -1 (Ϯ0.04). R 1 increased on average (all 15 subjects) 0.41 second -1 (Ϯ0.09). The increase was present one hour after the end of the infusion, remained relatively constant the next two hours, and then declined gradually. After 24 hours, there was still a moderate R 1 elevation present, with an average R 1 -value of 1.16 (Ϯ0.05). There were only small differences in myocardial R 1 responses between the three doses investigated, which was contrasted by a marked dose-response in liver tissue. Conclusion:MnDPDP gave a significant and prolonged rise in myocardial R 1 even at a dose of 5 mol/kg. The R 1 -values in the myocardium did not increase linearly with higher doses. THE USE OF manganese-containing contrast agents in magnetic resonance imaging (MRI) for the study of the myocardium has been debated for several years. The background for this interest in manganese is that myocardial cells actively accumulate manganese ions (Mn 2ϩ ) through voltage-dependent slow calcium channels in the cell membrane (1-4). This has raised the question of whether intracellular manganese can be used as a contrast agent for MRI-based myocardial viability diagnosis.Thus far, several research groups have studied myocardial effects of manganese in MRI. Early studies showed that manganese contrast could be used to demarcate infarcted regions in animal hearts, first in excised hearts (5,6), and later on in images obtained with live animals (7-9). The accumulated manganese led to markedly increased longitudinal relaxation rates (R 1 ) in normal myocardium (3,8 -11). Theoretically, the relationship between the concentration of contrast agent in a tissue and the corresponding R 1 should be close to linear. Southon et al (11) demonstrated a steady increase in myocardial R 1 in pigs with intravenous doses of manganese dipyridoxyl diphosphate (MnDPDP) up to 20 mol/kg. Both Bremerich et al (8) and Wendland et al (9) found that R 1 -values increased with increasing doses of MnDPDP in rat myocardium. Both studies used doses of 25, 50, and 100 mol/kg, given over 1.5 and 3 minutes, respectively. Both showed an initial higher rise in R 1 in infarcted myocardium 5-10 minutes after the infusions than in normal myocardium. However, these initial high R 1 -values in infarcted myocardium decreased with time, while normal myocardium had a steady increa...
Purpose: To develop an in vivo MR method for evaluation of myocardial calcium channel activity through quantification of apparent unidirectional manganese influx constants following manganese dipyridoxyl-diphosphate (MnDPDP) infusions. Materials and Methods:A total of 10 healthy volunteers were divided in two groups, and received 5 mol of MnD-PDP per kg of body weight intravenously in a 1.5 Tesla scanner over five or 30 minutes, respectively. A fast inversion recovery gradient echo sequence was used to estimate pre-and postcontrast R 1 values and to measure signal changes following infusions. By assuming equal longitudinal relaxivity (r 1 ) of the contrast in all tissue compartments, signal changes in blood and myocardial tissue yielded temporal input and tissue contrast concentrations respectively. Through a two-tissue compartment model, apparent unidirectional influx constants (K i ) for myocardial manganese accumulation were estimated.Results: Consistent values for K i in left ventricular wall were found, with a mean value of 5.96 mL/100 g/minute (SD ϭ 0.49; N ϭ 10). No statistical significant differences in K i were found between the two infusion groups. Conclusion:Since unidirectional manganese accumulation depends upon intact myocyte membranes with functioning calcium channels, the use of unidirectional manganese influx rates may be a valuable research tool for in vivo studies of myocyte functioning in myocardial disease.
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