A kilonova as the electromagnetic counterpart to a gravitational-wave source.

Gravitational waves were discovered with the detection of binary black-hole mergers and they should also be detectable from lower-mass neutron-star mergers. These are predicted to eject material rich in heavy radioactive isotopes that can power an electromagnetic signal. This signal is luminous at optical and infrared wavelengths and is called a kilonova. The gravitational-wave source GW170817 arose from a binary neutron-star merger in the nearby Universe with a relatively well confined sky position and distance estimate. Here we report observations and physical modelling of a rapidly fading electromagnetic transient in the galaxy NGC 4993, which is spatially coincident with GW170817 and with a weak, short γ-ray burst. The transient has physical parameters that broadly match the theoretical predictions of blue kilonovae from neutron-star mergers. The emitted electromagnetic radiation can be explained with an ejected mass of 0.04 ± 0.01 solar masses, with an opacity of less than 0.5 square centimetres per gram, at a velocity of 0.2 ± 0.1 times light speed. The power source is constrained to have a power-law slope of -1.2 ± 0.3, consistent with radioactive powering from r-process nuclides. (The r-process is a series of neutron capture reactions that synthesise many of the elements heavier than iron.) We identify line features in the spectra that are consistent with light r-process elements (atomic masses of 90-140). As it fades, the transient rapidly becomes red, and a higher-opacity, lanthanide-rich ejecta component may contribute to the emission. This indicates that neutron-star mergers produce gravitational waves and radioactively powered kilonovae, and are a nucleosynthetic source of the r-process elements.

Fibronectin distribution in human aortic intima and atherosclerotic lesions: concentration of soluble and collagenase-releasable fractions.

Fibronectin is associated with cell attachment and migration and interacts with fibrin, collagen and glycosaminoglycans; thus, it may be a factor in the focal proliferation of smooth muscle cells and collagen in atherosclerosis. We have measured, by rocket immunoelectrophoresis, the concentrations of soluble and collagenase-releasable fibronectin in normal human aortic intima and different types of atherosclerotic lesions. Soluble fibronectin concentration showed no significant difference between normal intima and lesions, but was 6-8-times higher than expected on the basis of plasma concentration and molecular mass. The concentration free in the interstitial fluid was about 3-times the expected level, suggesting that it originates from local synthesis as well as plasma insudation. In tissue, about half the fibronectin appeared to be reversibly associated with tissue components. Incubation with collagenase released fibronectin equal to twice the soluble fraction from normal intima and early proliferative lesions. In more advanced plaques that were accumulating lipid, the amount released was significantly higher (P less than 0.05) and more than 3-times the soluble fraction, suggesting that it might be involved in lipid accumulation. However, there was no correlation between release of fibronectin and bound low-density lipoprotein.

Fibrinolysis and plasminogen concentration in aortic intima in relation to death following myocardial infarction.

In samples of human aortic intima fibrin/fibrinogen degradation products (FDP) were assayed by isoelectric focussing/immunoelectrophoresis as a possible measure of endogenous fibrinolysis, and plasminogen concentration was assayed by rocket immunoelectrophoresis as a possible marker for fibrinolytic potential. No consistent differences were found between normal intima and different types of atherosclerotic lesion, but there was marked variation between patients, and multiple samples from the same aorta showed similar levels. There was no significant correlation with age, sex, or time after death. Low concentrations of FDP and failure to recover measureable amounts of plasminogen from intima were highly associated with death in patients who had suffered a recent myocardial infarction. In aortas from which 3 or more samples of intima and lesions were obtained (n = 16), no FDP were found in 3 (total of 12 samples); all of these were from patients who died following myocardial infarction. Low levels were present in the 4th patient with myocardial infarction. No plasminogen was found in 10 of 11 aortas from patients dying after myocardial infarction (total of 46 samples with no plasminogen), but it was present in 10 of 17 aortas from patients dying of other causes (X2 = 7.6, P less than 0.01). Where both were assayed, FDP were not found in any samples which did not contain plasminogen. Low levels of FDP and absence of plasminogen were associated with increased involvement with atherosclerosis. There was no relation between intimal and serum plasminogen levels, and prothrombin and low density lipoprotein were present in all samples from which no plasminogen was recovered. The results indicate that in some patients, particularly those dying after myocardial infarction, there is decreased fibrinolysis and fibrinolytic potential in the arterial intima, and this may result in increased intimal accumulation of fibrin.

Compartmentalization of water in human atherosclerotic lesions. Changes in distribution and exclusion volumes for plasma macromolecules.

High concentrations of LDL and other plasma macromolecules are present in normal aortic intima and early proliferative atherosclerotic lesions that have not yet accumulated lipid. Their compartmentalization within the tissue water was estimated from the concentrations of low density lipoprotein (LDL), alpha 2-macroglobulin (alpha 2-M), and albumin in interstitial fluid and adjacent intimal tissue. Interstitial fluid was collected on filter paper inserted into natural strip planes in the intima; macromolecules in interstitial fluid and tissue were assayed by rocket immunoelectrophoresis directly from the papers or tissue. From their concentrations in interstitial fluid and total tissue water, the fractional and absolute volumes in which they were distributed (distribution volume) or from which they were excluded (exclusion volume) were calculated for each macromolecule. Compared with normal intima, the distribution volume increased by 60% and the exclusion volume by 95% in early gelatinous lesions; exclusion volume fraction was linearly related to molecular mass. In more advanced lesions, there was disproportionate exclusion of LDL and alpha 2-M. Their distribution volumes decreased and their concentrations in interstitial fluid increased; the concentration showed a significant inverse relation with distribution volume (regression coefficient, b = -0.53, p less than 0.01). Redistribution of tissue water may concentrate LDL in interstitial fluid, and contribute to its extracellular deposition.

Low-density lipoprotein concentration in interstitial fluid from human atherosclerotic lesions. Relation to theories of endothelial damage and lipoprotein binding.

Increased endothelial permeability to low-density lipoprotein (LDL) is believed to be an initiating factor for atherosclerotic lesions. Concentrations of LDL, alpha 2-macroglobulin and albumin were measured by immunoassay in interstitial fluid collected from normal intima and atherosclerotic lesions of human aortas. The concentration of LDL in interstitial fluid from normal intima was twice the concentration in the patient's serum. In early proliferative (gelatinous) lesions the amount of interstitial fluid was consistently increased but its LDL concentration varied between 80 and 200% of adjacent normal intima. Highest concentrations of LDL were found in interstitial fluid from more advanced proliferative lesions, but the amount was reduced, suggesting a shift in tissue water. LDL was consistently low in interstitial fluid from fatty streaks comprised of lipid-filled cells, and in four of 12 lesions it was absent although alpha 2-macroglobulin and albumin concentrations were normal. Electrophoretic mobility of LDL, reflecting surface charge, was unchanged or increased in interstitial fluid from normal intima and fatty streaks, but decreased in gelatinous lesions. The ratio of LDL to alpha 2-macroglobulin and albumin in interstitial fluid was higher than in adjacent intact tissue. The results do not support the idea that increased endothelial permeability to LDL initiates atherogenesis.

Variability of the electrophoretic mobility of low density lipoprotein. Comparison of interstitial fluid from human aortic intima and serum.

Interstitial fluid was collected from human aortic intima and the low density lipoprotein (LDL) was compared with serum LDL by two-dimensional immunoelectrophoresis. In half the samples derived from normal intima the migration rate was within +/- 10% of migration of LDL in serum, but in the remaining samples it was higher, indicating an increase in net negative charge on the molecule. By contrast, in most samples of interstitial fluid from gelatinous thickenings the migration rate of LDL was lower than in serum, indicating reduction in net negative charge. To test for the effect of different electrolyte concentrations in interstitial fluid and serum, migration of alpha 2-macroglobulin (alpha 2-M) was measured simultaneously in both. This showed no significant difference between interstitial fluid and serum, and varied by less than 2% between different serum samples. However, the mobility of LDL relative to alpha 2-M showed a remarkable variation, ranging from 80.9 to 127.1% of alpha 2-M mobility in interstitial fluid and from 58.6 to 115.9% in 23 serum samples. In serum, LDL relative mobility showed no correlation with general acid-base status, as indicated by serum bicarbonate levels, with fatty meals or diabetic keto-acidosis, or with extent of glycosylation of haemoglobin. This suggested that the variation in surface charge is intrinsic to the molecule and not a transient reflection of the plasma environment. Experimental alterations in the surface charge of LDL change its interaction with smooth muscle cells and macrophages in vitro, and its mitogenic properties. This raises the possibility that physiological variation in the surface charge of LDL in different subjects could alter its atherogenic potential.