Some harvesting system transforming energy wastes of compressed air to electricity

Energy harvesting devices are self-powered systems which are associated with input ambient energy and convert such energy to electrical one. In this study, we focus on input ambient energy deriving from compressed air. Using arbitrary pneumatic machine, the compressed air after work - with its typical parameters as overpressure 6 bar or higher and variable volume flow - is exhausted to atmosphere. This generates energy losses. We have constructed some device which transforms the loss of compressed air energy to electricity. It illustrates the principle of action very well and does not perturb operation of pneumatic machines being source of energy losses

Platelet Na+/H+ exchanger activity in patients with coronary heart disease confirmed by selective arteriography and the disturbances of carbohydrate metabolism

WSTĘP. Wzmożoną aktywność antyporterów Na+/H+ (NHE, sodium/proton exchanger) opisywano u chorych z nadciśnieniem tętniczym, niewyrównaną cukrzycą typu 1 i typu 2 oraz nefropatią cukrzycową. Podjęto również próby kliniczne zastosowania inhibitorów NHE1 u chorych z ostrymi zespołami wieńcowymi. Celem pracy autorów była ocena aktywności płytkowych antyporterów Na+/H+ oraz wybranych czynników ryzyka miażdżycy u pacjentów poddanych badaniu koronarograficznemu, w zależności od współistniejących zaburzeń gospodarki węglowodanowej i zaawansowania choroby niedokrwiennej serca. MATERIAŁ I METODY. Pomiaru aktywności antyportera Na+/H+ w osoczu bogatopłytkowym dokonano metodą optyczną u 55 chorych w wieku 57,3 ± 6,6 roku, z dodatnim wynikiem testu wysiłkowego [7 osób z upośledzoną tolerancją glukozy (IGT, impaired glucose tolerance) i 14 chorych na cukrzycę typu 2] oraz u 32 zdrowych osób w wieku 48,4 ± 9,0 lat. WYNIKI. U pacjentów, u których występowały zmiany w naczyniach wieńcowych, aktywność antyportera Na+/H+ była istotnie wyższa niż u osób w grupie kontrolnej (4,36 ± 0,90 × 10-3 × s-1 vs. 3,18 ± 0,55 × 10-3 × s-1, p = 0,000001). Nie zaobserwowano natomiast znamiennych różnic w aktywności antyportera Na+/H+ w zależności od liczby zwężonych tętnic wieńcowych. Nie stwierdzono także różnic w aktywności płytkowego antyportera Na+/H+ u chorych z nadciśnieniem tętniczym (4,48 ± 0,92 × 10-3 × s-1 vs. 4,34 ± 0,88 × 10-3 × s-1) oraz z IGT i cukrzycą typu 2, chociaż w każdej z tych podgrup aktywność antyporterów była istotnie wyższa niż w grupie kontrolnej. Wykazano natomiast istotną zależność między aktywnością antyportera a wskaźnikiem masy ciała (BMI, body mass index) pacjentów (r = 0,30, p = 0,047). WNIOSKI. Badania autorów sugerują wzmożoną aktywność płytkowych antyporterów Na+/H+ u osób z chorobą niedokrwienną serca, jednak zagadnienie to wymaga dalszych badań.INTRODUCTION. Enhanced activity of Na+/H+ exchangers (NHE, sodium/proton exchanger) has been previously described in patients with arterial hypertension, poorly controlled type 1 and type 2 diabetes and nephropathy. There were also clinical trials with NHE1 inhibitors in patients with acute coronary syndromes. The aim of our study was the estimation of platelet Na+/H+ exchanger activity and selected risk factors in patients referred for coronary angiography, dependent on the disturbances of carbohydrate metabolism and atherosclerotic lesions. MATERIAL AND METHODS. Platelet Na+/H+ exchanger activity was measured in platelet rich plasma, using an optical swelling assay, in 55 consecutive patients (7 with impaired glucose tolerance [IGT] and 14 with type 2 diabetes) with positive exercise test (mean age 57.3 ± 6.6 years) and in 32 healthy subjects (mean age 48.4 ± 9.0 years). RESULTS. Na+/H+ exchanger activity was markedly increased in patients with coronary heart disease in comparison to the controls (4.36 ± 0.90 × 10-3 × s-1 vs 3.18 ± 0.55 × 10-3 × s-1, p = 0.000001). However, there was no significant differences between subjects with 1-, 2- and 3-vessel disease, nor with and without arterial hypertension (4.48 ± 0.92 × 10-3 × s-1 vs 4.34 ± 0.88 × 10-3 × s-1), as well as between patients with normal glucose tolerance, IGT and type 2 diabetes, however the mean values in each group were significantly higher than in the controls. Na+/H+ exchanger activity correlated with BMI (r = 0.30, p = 0.047). CONCLUSIONS. Our study suggests enhanced activity of platelet Na+/H+ exchanger in patients with coronary heart disease, but the problem needs further investigations

Involvement of Na+/H+ exchanger in desmopressin-induced platelet procoagulant response.

Desmopressin (DDAVP) action on platelets is associated with the development of procoagulant response but the underlying mechanism of this phenomenon is not known. We investigated whether this effect of DDAVP might be due to activation of plasma membrane Na+/H+ exchanger. The DDAVP-induced platelet procoagulant response, measured as phospholipid-dependent thrombin generation, was dose dependent and significantly weaker than that produced by collagen or monensin (mimics Na+/H+ antiport). Both the DDAVP- and collagen-produced procoagulant responses were less pronounced in the presence of EIPA, an Na+/H+ exchanger inhibitor. Flow cytometry studies revealed that in vitro treatment of platelets with DDAVP or collagen was associated with the appearance of both degranulated (and fragmented) and swollen cells. The DDAVP-evoked rise in size and granularity heterogeneity was similar to that produced by collagen or monensin and was not observed in the presence of EIPA. Using flow cytometry and annexin V-FITC as a probe for phosphatidylserine (PS) we demonstrated increased and uniform binding of this marker to all subsets of DDAVP-treated platelet population. The DDAVP-evoked PS expression was dose dependent, strongly reduced by EIPA and weaker than that caused by monensin or collagen. As judged by optical swelling assay, DDAVP in a dose dependent manner produced a rise in platelet volume. The swelling was inhibited by EIPA and its kinetics was similar to that observed in the presence of monensin. Electronic cell-sizing measurements showed an increase in mean platelet volume and a decrease in platelet count and platelet crit upon treatment with DDAVP. DDAVP elicited a slow (much slower than collagen) alkalinization of platelet cytosol. Altogether the data indicate an involvement of Na+/H+ exchanger in the generation of procoagulant activity in DDAVP-treated platelets

The role of Na+/H+ exchanger in serotonin secretion from porcine blood platelets

This study was undertaken to evaluate whether a link exists between the activation of protein kinase C (PKC), operation of Na+/H+ exchanger (NHE), cell swelling and serotonin (5-HT) secretion in porcine platelets. Activation of platelets by thrombin or phorbol 12-myristate 13-acetate (PMA), a PKC activator, initiated a rapid rise in the activity of Na+/H+ exchanger and secretion of 5-HT. Both thrombin- and PMA-evoked activation of Na+/H+ exchanger was less pronounced in the presence of ethyl-isopropyl-amiloride (EIPA), an NHE inhibitor, and by GF 109203X, a PKC inhibitor. Monensin (simulating the action of NHE) caused a dose-dependent release of 5-HT that was not abolished by GF 109203X or EGTA. Lack of Na+ in the suspending medium reduced thrombin-, PMA-, and monensin-evoked 5-HT secretion. GF 109203X nearly completely inhibited 5-HT release induced by PMA-, partly that induced by thrombin, and had no effect on 5-HT release induced by monensin. EIPA partly inhibited 5-HT release induced by thrombin and nearly totally that evoked by PMA. Electronic cell sizing measurements showed an increase in mean platelet volume upon treatment of cells with monensin, PMA or thrombin. The PMA- and thrombin-evoked rise in mean platelet volume was strongly reduced in the presence of EIPA. As judged by optical swelling assay monensin and PMA produced a rapid rise in platelet volume. The swelling elicited by PMA was inhibited by EIPA and its kinetics was similar to that observed in the presence of monensin. Hypoosmotically evoked platelet swelling did not affect platelet aggregation but significantly potentiated thrombin-evoked release of 5-HT and ATP. Taken together, these results show that in porcine platelets PKC may promote 5-HT secretion through the activation of NHE. It is hypothesized that enhanced Na+/H+ antiport may result in a rise in cell membrane tension (due to cell swelling) which in turn facilitates fusion of secretory granules with the plasma membrane leading to 5-HT secretion

Peroxynitrite can affect platelet responses by inhibiting energy production

Peroxynitrite (ONOO-) strongly inhibits agonist-induced platelet responses. However, the mechanisms involved are not completely defined. Using porcine platelets, we tested the hypothesis that ONOO- reduces platelet aggregation and dense granule secretion by inhibiting energy production. It was found that ONOO- (25-300 µM) inhibited collagen-induced dense granule secretion (IC50 = 55 ± 7 µM) more strongly than aggregation (IC50 = 124 ± 16 µM). The antiaggregatory and antisecretory effects of ONOO- were only slightly (5-10%) reduced by 1H-[1,2,4]-oxadiazolo-[4,3-α]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylate cyclase. In resting platelets ONOO- (50-300 µM) enhanced glycolysis rate and reduced oxygen consumption, in a dose dependent manner. The ONOO- effects on glycolysis rate and oxygen consumption were not abolished by ODQ. The extent of glycolysis stimulation exerted by ONOO- was similar to that produced by respiratory chain inhibitors (cyanide and antimycin A) or an uncoupler (2,4-dinitrophenol). Stimulation of platelets by collagen was associated with a rise in mitochondrial oxygen consumption, accelerated lactate production, and unchanged intracellular ATP content. In contrast to resting cells, in collagen-stimulated platelets, ONOO- (200 µM) distinctly decreased the cellular ATP content. The glycolytic activity and oxygen consumption of resting platelets were not affected by 8-bromoguanosine 3',5'-cyclic monophosphate. Blocking of the mitochondrial ATP production by antimycin A slightly reduced collagen-induced aggregation and strongly inhibited dense granule secretion. Treatment of platelets with ONOO- (50-300 µM) resulted in decreased activities of NADH : ubiquinone oxidoreductase, succinate dehydrogenase and cytochrome oxidase. It is concluded that the inhibitory effect of ONOO- on platelet secretion and to a lesser extent on aggregation may be mediated, at least in part, by the reduction of mitochondrial energy production