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Abstract IntroductionThe endothelial glycocalyx regulates vascular permeability, inflammation, and coagulation, and acts as a mechanosensor. The loss of glycocalyx can cause endothelial injury and contribute to several microvascular complications and, therefore, may promote diabetic retinopathy. Studies have shown a partial loss of retinal glycocalyx in diabetes, but with few molecular details of the changes in glycosaminoglycan (GAG) composition. Therefore, the purpose of our study was to investigate the effect of hyperglycemia on GAGs of the retinal endothelial glycocalyx. MethodsGAGs were isolated from rat retinal microvascular endothelial cells (RRMECs), media, and retinas, followed by liquid chromatography-mass spectrometry assays. Quantitative real-time polymerase chain reaction was used to study mRNA transcripts of the enzymes involved in GAG biosynthesis. Results and ConclusionsHyperglycemia significantly increased the shedding of heparan sulfate (HS), chondroitin sulfate (CS), and hyaluronic acid (HA). There were no changes to the levels of HS in RRMEC monolayers grown in high-glucose media, but the levels of CS and HA decreased dramatically. Similarly, while HA decreased in the retinas of diabetic rats, the total GAG and CS levels increased. Hyperglycemia in RRMECs caused a significant increase in the mRNA levels of the enzymes involved in GAG biosynthesis (including EXTL-1,2,3, EXT-1,2, ChSY-1,3, and HAS-2,3), with these increases potentially being compensatory responses to overall glycocalyx loss. Both RRMECs and retinas of diabetic rats exhibited glucose-induced alterations in the disaccharide compositions and sulfation of HS and CS, with the changes in sulfation including N,6-O-sulfation on HS and 4-O-sulfation on CS. 

ABSTRACT Gravitational wave (GW) observatories are discovering binary neutron star mergers (BNSMs), and in at least one event we were able to track it down in multiple wavelengths of light, which allowed us to identify the host galaxy. Using a catalogue of local galaxies with inferred star formation histories and adopting a BNSM delay time distribution (DTD) model, we investigate the dependence of BNSM rate on an array of galaxy properties. Compared to the intrinsic property distribution of galaxies, that of BNSM host galaxies is skewed towards galaxies with redder colour, lower specific star formation rate, higher luminosity, and higher stellar mass, reflecting the tendency of higher BNSM rates in more massive galaxies. We introduce a formalism to efficiently make forecast on using host galaxy properties to constrain DTD models. We find comparable constraints from the dependence of BNSM occurrence distribution on galaxy colour, specific star formation rate, and stellar mass, all better than those from dependence on r-band luminosity. The tightest constraints come from using individual star formation histories of host galaxies, which reduces the uncertainties on DTD parameters by a factor of three or more. Substantially different DTD models can be differentiated with about 10 BNSM detections. To constrain DTD parameters at 10 per cent precision level requires about one hundred detections, achievable with GW observations on a decade time-scale.