Puzzling thermonuclear burst behaviour from the transient low-mass X-ray binary IGR J17473-2721

We investigate the thermonuclear bursting behaviour of IGR J17473-2721, an X-ray transient that in 2008 underwent a six month long outburst, starting (unusually) with an X-ray burst. We detected a total of 57 thermonuclear bursts throughout the outburst with AGILE, Swift, RXTE, and INTEGRAL. The wide range of inferred accretion rates (between <1% and about 20% of the Eddington accretion rate m-dot_Edd) spanned during the outburst allows us to study changes in the nuclear burning processes and to identify up to seven different phases. The burst rate increased gradually with the accretion rate until it dropped (at a persistent flux corresponding to about 15% of m-dot_Edd) a few days before the outburst peak, after which bursts were not detected for a month. As the persistent emission subsequently decreased, the bursting activity resumed with a much lower rate than during the outburst rise. This hysteresis may arise from the thermal effect of the accretion on the surface nuclear burning processes, and the timescale is roughly consistent with that expected for the neutron star crust thermal response. On the other hand, an undetected superburst, occurring within a data gap near the outburst peak, could have produced a similar quenching of burst activity.Comment: 18 pages, 12 figures, 1 table, accepted for publication in MNRA

Binary systems and their nuclear explosions

Peer ReviewedPreprin

The effect of metamizole and tolfenamic acid on canine and equine adipose-derived mesenchymal stem cells (ASCs) an in vitro research

The influences of NSAIDs (Nonsteroidal Anti-inflammatory Drugs) - non-selective metamizole and selectively-acting tolfenamic acid were estimated on morphology, ultrastructure, and cytophysiological activity of canine (Ca) and equine (Eq) adipose-derived mesenchymal stem cells (ASCs). The lowest concentration of metamizole (0.01 mg/mL) stimulated the viability and cytophysiological activity of Ca ASCs and did not affect cell morphology. Stimulated cells possessed a proper, fibroblastic shape, with large, eccentrically located nuclei. Similar effects to those observed in Ca ASCs were found in Eq cells treated with both drugs. Cells cultivated with the intermediate (0.1 mg/mL) doses of NSAIDs displayed proper cell morphology, whereas cells cultivated in intermediate dose (0.1 mg/mL) became more flattened. The highest concentrations (1 mg/mL) of both drugs resulted in a cytotoxic effect in Ca and Eq ASCs. Based on these results, we conclude that stimulation of Ca and Eq ASCs with metamizole as well as Eq ASCs with tolfenamic acid can lead to positive effects only when the lowest drug concentrations are applied. This study indicates a different cellular response of canine and equine ASCs treated with metamizole and tolfenamic acid. The obtained data might be potentially useful in the study of functionalized veterinary biomaterials

Retinol-binding protein 4 (RBP-4) levels do not change after oral glucose tolerance test and after dexamethasone, but correlate with some indices of insulin resistance in humans

Abstract INTRODUCTION: Secretory products from adipocytes may contribute to deterioration in glycaemic control and increased insulin resistance (IR). Retinol-binding protein 4 (RBP-4) may increase IR in mice, with elevated levels in insulin-resistant mice and humans with obesity and type 2 diabetes. However, the mechanisms regulating RBP-4 synthesis remain not fully understood. It is not clear whether short-term glucose-induced hyperglycaemia and hyperinsulinaemia as well as glucocorticosteroid-induced increase in IR might be reflected in alterations in serum RBP-4 levels in humans. In order to investigate this, we measured serum RBP-4, glucose and insulin concentrations during 75.0 gram oral glucose tolerance test (OGTT) - Study 1, as well as before and after oral administration of dexamethasone - Study 2. MATERIAL AND METHODS: Both studies included 35 subjects (8 males), age (mean +/- SD) 39.1 +/- 15.6 years, BMI 35.8 +/- 8.7 kg/m(2). Twenty-four of those subjects (5 males), age 38.7 +/- 15.1 years, BMI 34.4 +/- 8.3 kg/m(2), had 75 gram oral glucose tolerance test (OGTT) - Study 1. Blood samples were taken before (0 minutes), and at 60 and 120 minutes of OGTT. 17 subjects (3 males, 4 subjects with type 2 diabetes), age 43.1 +/- 18.1 years, BMI 36.7 +/- 9.0 kg/m(2) underwent screening for Cushing's disease/syndrome (Study 2). Dexamethasone was administered in a dose of 0.5 mg every 6 hours for 48 hours. Fasting serum concentrations of RBP-4, glucose and insulin were assessed before (D0) and after 48 hours of dexamethasone administration (D2). IR was assessed by HOMA in all non-diabetic subjects and in subjects participating in study 1 also by Insulin Resistance Index (IRI), which takes into account glucose and insulin levels during OGTT. RESULTS: Glucose administration resulted in significant increases in insulin and glucose (p < 0.0001). There was, however, no change in RBP-4 concentrations (124.1 +/- 32 mg/ml at 0 minutes, 123 +/- 35 mg/ml at 60 minutes and 126.5 +/- 37.5 mg/ml at 120 minutes of OGTT, p = ns). All subjects in Study 2 achieved suppression of cortisol below 50 nmo/l. Dexamethasone administration resulted in an increase in fasting insulin (from 11.6 +/- 6.8 to 17.1 +/- 7.2 muU/ml; p = 0.003), and an increase in HOMA (from 2.73 +/- 1.74 to 4.02 +/- 2.27; p = 0.015), although without a significant change in RBP-4 levels (119 +/- 26.8 vs. 117.5 +/- 24.8 mg/ml, p = ns). RBP-4 correlated with fasting insulin (r = 0.40, p = 0.025), fasting glucose (r = 0.41, p = 0.02) and HOMA (r = 0.43, p = 0.015), but not with IRI (r = 0.19, p = 0.31). There was, however, only a moderate correlation between HOMA and IRI (r = 0.49 [r(2) = 0.24]; p = 0.006, Spearman rank correlation), while the best correlation was obtained between the product of glucose and insulin levels at 60 min of OGTT and IRI in a non-linear model (r = 0.94 [r(2) = 0.88]; p<0.00001). In subjects who received dexamethasone, a positive correlation between RBP-4 and HOMA (p = 0.01) was lost after two days of dexamethasone administration (p = 0.61). CONCLUSIONS: RBP-4 levels do not change during oral glucose tolerance test or after a dexamethasone-induced increase in insulin resistance. This implies that it is highly unlikely that RBP-4 is involved in short-term regulation of glucose homeostasis in humans and that it responds to short-term changes in insulin resistance. A moderate correlation between RBP-4 and some insulin resistance indices (HOMA) does not exclude the fact that RBP-4 might be one of many factors that can influence insulin sensitivity in humans