Diabetes mellitus (DM) and hyperglycaemia are associated with platelet activation. The present study was designed to investigate how high glucose levels influence platelet function. Fasting human blood was incubated with different concentrations of D-glucose (5, 15 and 30 mmol/l) and other sugars without or with in vitro stimuli. Platelet activation was monitored by whole blood flow cytometry. High glucose levels enhanced adenosine diphosphate (ADP)- and thrombin receptor-activating peptide (TRAP)-induced platelet P-selectin expression, and TRAP-induced platelet fibrinogen binding. Similar effects were seen with 30 mmol/l L-glucose, sucrose and galactose. Hyperglycaemia also increased TRAP-induced platelet-leucocyte aggregation. Protein kinase C (PKC) blockade did not counteract the enhancement of platelet P-selectin expression, but abolished the enhancement of TRAP-induced platelet fibrinogen binding by hyperglycaemia. Superoxide anion scavenging by superoxide dismutase (SOD) attenuated the hyperglycaemic enhancement of platelet P-selectin expression, but did not counteract the enhancement of TRAP-induced platelet fibrinogen binding. Hyperglycaemia did not alter platelet intracellular calcium responses to agonist stimulation. Blockade of cyclo-oxygenase (COX), phosphotidylinositol-3 (PI3) kinase, or nitric oxide synthase, or the addition of insulin did not influence the effect of hyperglycaemia. In conclusion, high glucose levels enhanced platelet reactivity to agonist stimulation through elevated osmolality. This occurred via superoxide anion production, which enhanced platelet P-selectin expression (secretion), and PKC signalling, which enhanced TRAP-induced fibrinogen binding (aggregablity).
Three synthesis routes are presented here that leads to carbon-silica composites. These were characterized by nitrogen physisorption, by thermogravimetric analysis and by dynamic toluene adsorption test similar to Ashrae standard I45.1. The carbon-silica composites possess high microporosity and mesoporosity as well as large surface areas. Furthermore, the control of the microporosity as well as pore size distribution is possible because they depend on the amount of carbon used and of the synthesis route. Following routes I and III a wide micro-mesoporous pore size (1-32 nm) was obtained where as by route II narrow micro-mesoporous pore size (1-4 nm) was observed. In addition, pore diameters center in the range of 1.13-1.17 nm was observed when carbon content was 32 or 45 wt%. The dynamic adsorption of toluene was evaluated for carbon-silica composites obtained by three preparation routes at two different carbon contents, 32 and 45 wt% The results showed that a composite with 45 wt% carbon content and obtained via preparation route I gave the highest toluene adsorption capacity (27.6 wt% relative to carbon content). The large uptake capacity of this composite was attributed to the presence of high microporosity volume and a wide (1-32 nm) bimodal pore system consisting of extensive mesopore channels (2-32 nm) as well as large surface area. These capacity values of carbon-silica composites are by weight relative to carbon content and are competitive to, results obtained for commercial coconut activated carbon (31.1 wt%) and significantly better than a commercial alumina-carbon composite (9.5 wt%) at 0% efficiency.
Diabetes mellitus is associated with platelet dysfunction, and hypoglycemic treatments may counteract this diabetic alteration. We thus studied how acute hyperglycemia influences platelet function. Fast blood (n=20) was incubated with different levels of glucose (5, 15, and 30 mM) for 5 min, and without or with in vitro stimuli. Platelet activation was monitored by whole blood flow cytometry, while platelet aggregation was also measured using impedance aggregometry. Blood glucose levels had little influence on unstimulated platelets. Hyperglycemia enhanced ADP- and TRAP-induced platelet P-selectin expression. Hyperglycemia also increased TRAP-induced platelet fibrinogen binding. High glucose levels mildly increased ADP- and TRAP-induced platelet-leukocyte aggregation. The blockade of protein kinase C (PKC) slightly attenuated ADP-induced, and markedly inhibited TRAP-induced platelet activation. PKC blockade had, however, little effect on hyperglycemia effect. Platelet P-selectin expression induced by the direct PKC activator phorbol 12-myristate 13-acetate (PMA) was not augmented by hyperglycemia. Superoxide anion scavenging by superoxide dismutase (SOD) reduced, whistle cyclo-oxygenase (COX) inhibition by naproxen did not reduced the enhancing effect of platelet activation by hyperglycemia. In conclusion, acute hyperglycemia enhances platelet activation in whole blood. Superoxide anions contribute importantly to hyperglycemia-enhanced platelet activation, while other mechanisms not identified presently also contribute to hyperglycemic effects.
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