An ultraviolet-optical flare from the tidal disruption of a helium-rich stellar core.

The flare of radiation from the tidal disruption and accretion of a star can be used as a marker for supermassive black holes that otherwise lie dormant and undetected in the centres of distant galaxies. Previous candidate flares have had declining light curves in good agreement with expectations, but with poor constraints on the time of disruption and the type of star disrupted, because the rising emission was not observed. Recently, two 'relativistic' candidate tidal disruption events were discovered, each of whose extreme X-ray luminosity and synchrotron radio emission were interpreted as the onset of emission from a relativistic jet. Here we report a luminous ultraviolet-optical flare from the nuclear region of an inactive galaxy at a redshift of 0.1696. The observed continuum is cooler than expected for a simple accreting debris disk, but the well-sampled rise and decay of the light curve follow the predicted mass accretion rate and can be modelled to determine the time of disruption to an accuracy of two days. The black hole has a mass of about two million solar masses, modulo a factor dependent on the mass and radius of the star disrupted. On the basis of the spectroscopic signature of ionized helium from the unbound debris, we determine that the disrupted star was a helium-rich stellar core.

Investigation of SiO2-Al2O3 nanolaminates for protection of silver reflectors.

H2S and particles from the atmosphere can damage silver reflectors. These defects lead to scattering and a reduction of reflectivity. With regard to these risks, the suitability of sputtered SiO2, Al2O3, and SiO2-Al2O3 nanolaminates for the protection of Ag was analyzed. The optical properties, protection properties against H2S, solubility, film stress, and protection properties against particle-induced defect formation have been investigated. Especially in the case of particle-induced defects on protected Ag, differences between the protective coatings are considerable, and the nanolaminate layers have advantageous properties.

Investigation of the refractive index repeatability for tantalum pentoxide coatings, prepared by physical vapor film deposition techniques.

Random effects in the repeatability of refractive index and absorption edge position of tantalum pentoxide layers prepared by plasma-ion-assisted electron-beam evaporation, ion beam sputtering, and magnetron sputtering are investigated and quantified. Standard deviations in refractive index between 4*10-4 and 4*10-3 have been obtained. Here, lowest standard deviations in refractive index close to our detection threshold could be achieved by both ion beam sputtering and plasma-ion-assisted deposition. In relation to the corresponding mean values, the standard deviations in band-edge position and refractive index are of similar order.

Estimation of the composition of coelectron-beam-evaporated thin-mixture films by making use of the Wiener bounds.

Material mixtures offer prospective possibilities for synthesizing coating materials with tailored optical constants. We present experimental results for mixture coatings of alumina/aluminum fluoride and alumina/hafnia deposited by electron beam evaporation. Thereby, the volume filling factors of the components are commonly estimated on the basis of deposition rates measured by quartz crystal microbalance. The interplay between the vapor fluxes from the two evaporation sources, the crosstalk between quartz crystal microbalances, and the influence of the plasma source on the tooling factors limit the accuracy of this estimation, and this has motivated us to develop an alternative approach. The general idea of our approach is based on the commonly high accuracy in thin-film optical constant determination using spectrophotometry. Therefore, these optical constants serve as a reliable input for a rather simple but robust evaluation procedure based on the concept of Wiener bounds. The consistency of the obtained results is illustrated by opposing the data to the elementary film composition estimated from energy-dispersive x-ray spectroscopy.

Protected and enhanced aluminum mirrors for the VUV.

Aluminum layers protected with fluoride coatings have been deposited by evaporation and characterized with respect to their suitability as vacuum ultraviolet (VUV) mirrors. Optical characterization has been performed by spectrophotometry, while the surface quality of the layers has been judged by means of x ray reflection, scanning electron microscopy, and atomic force microscopy. In particular, protection with aluminum fluoride results in superior VUV reflection properties. VUV reflectance values between 80% and nearly 90% have been verified even two years after deposition and exposure to the atmosphere.

[Fractures of the lateral condyle of the humerus in children : High risk of secondary dislocation with conservative treatment]. / Frakturen des Condylus radialis humeri beim Kind : Hohes Risiko der sekundären Dislokation bei konservativer Therapie.

BACKGROUND: Fractures of the lateral condyle of the humerus in children are articular fractures with difficult diagnostics due to the incompletely ossified elbow joint. The aim of this study was to evaluate the method of treatment at initial presentation and to analyze the frequency of subsequent displacement during follow-up. MATERIAL AND METHOD: Retrospective analysis of the frequency of primary fracture dislocation and subsequent displacement of fractures of the lateral condyle of the humerus in children under 16 years of age between 2004 and 2021. Conventional radiographs in two planes at the time of the accident and in the follow-up after 5-7 days were evaluated. RESULTS: A total of 285 fractures of the lateral condyle of the humerus were evaluated. The average age was 5.3 years. Of the fractures 109 (38.3%) were directly surgically treated in cases of primary displacement and 176 fractures (61.7%) were not primarily displaced and were initially treated conservatively. During follow-up, subsequent displacement was evident in 46 fractures (26.1%). A total of 130 fractures (45.6%) were treated conservatively and 155 fractures (54.4%) were treated surgically using open joint visualization and screw osteosynthesis or K­wire osteosynthesis. CONCLUSION: Fractures of the lateral condyle of the humerus occur more frequently in a certain age group and require targeted radiological diagnostics. Nondisplaced fractures can be treated conservatively but essential radiological follow-up shows a high number of subsequent displacements, so that open surgical stabilization is often necessary.

Revealing the quantum nature of the voltage-induced conductance changes in oxygen engineered yttrium oxide-based RRAM devices.

In this work, the quasi-analog to discrete transition occurring in the current-voltage characteristic of oxygen engineered yttrium oxide-based resistive random-access memory (RRAM) devices is investigated in detail. In particular, the focus of our research is not on the absolute conductance values of this characteristic but on the magnitude of its conductance changes occurring during the reset process of the device. It is found that the detected changes correspond to conductance values predominantly of the order of the quantum unit of conductance G0 = 2e2/h, where e is the electron charge and h the Planck constant. This feature is observed even at conductance levels far above G0, i.e. where electron transport is seemingly diffusive. It is also observed that such behavior is reproducible across devices comprising yttrium oxide layers with different oxygen concentrations and measured under different voltage sweep rates. While the oxygen deficiency affects the total number of quantized conductance states, the magnitude of the changes in conductance, close to 1 G0, is invariant to the oxygen content of the functional layer.

Familial hyperinsulinism maps to chromosome 11p14-15.1, 30 cM centromeric to the insulin gene.

Familial hyperinsulinism (HI) is the most common cause of persistent neonatal hyperinsulinaemic hypoglycemia. Linkage analysis in 15 families (12 Ashkenazi Jewish, 2 consanguineous Arab, 1 non-Jewish Caucasian) mapped HI to chromosome 11p14-15.1 (lod score = 9.5, theta = 0 at D11S921). Recombinants localized the disease locus to the 6.6 cM interval between D11S926 and D11S928. In Jewish families, association (p = 0.003) with specific D11S921/D11S419 haplotypes suggested a founder effect. This locus, which is important for normal glucose-regulated insulin secretion, represents a candidate gene for studies of other diseases of beta-cell dysfunction including non-insulin-dependent diabetes mellitus (NIDDM).

Combined application of EPANET and empirical model for possible formation of trihalomethanes in water distribution network of Chattogram city to identify potential carcinogenic health risk zone.

The study identifies potential carcinogenic health risk-zone of Chattogram city for the occurrence of trihalomethanes (THMs) at its water distribution network. The EPANET-THMs simulation model along with an empirical model have been adopted in the study to predict THMs content of supply water of the distribution network of the city's Karnaphuli service area. The empirical model has estimated THMs level of supply water based on influential water quality parameters, and few of these have been used as pre-set values for subsequent EPANET simulation. The simulation (R2= 0.7) shows that THMs' concentrations throughout the network vary from 33 to 486 µg/L. Around 60% of total junctions showed THMs concentrations above 150 µg/L, while that is above 50 µg/L for most (99%) of the junctions. Residual Free chlorine, one of the precursors for the THMs formation in distribution line, has also been simulated by EPANET considering varying applied chlorine dose at the water purification unit and wall (Kw) and bulk (Kb) decay constants. The simulated free residual chlorine peaks are found to be closer to the actual values with chlorine dose of 2 mg/L, and decay constants, Kw = 1 d-1 and Kb = 1 d-1. A mean lifetime total risk of cancer due to the presence of THMs has been found to be very high. Spatial distribution of carcinogenic risk shows that the central zone of the service area is the most vulnerable zone, followed by the western and northern zone. The first ever zone wise risk identification could be used as baseline data for operational and regulatory purposes and may raise awareness among the city's inhabitants. Furthermore, the application of EPANET in combination with an empirical model could be an effective tool for predicting THMs' concentration in water distribution networks in developing countries like Bangladesh to minimize the expenses of measuring THMs.

Pancreatic and duodenal homeobox gene 1 induces expression of insulin genes in liver and ameliorates streptozotocin-induced hyperglycemia.

Insulin gene expression is restricted to islet beta cells of the mammalian pancreas through specific control mechanisms mediated in part by specific transcription factors. The protein encoded by the pancreatic and duodenal homeobox gene 1 (PDX-1) is central in regulating pancreatic development and islet cell function. PDX-1 regulates insulin gene expression and is involved in islet cell-specific expression of various genes. Involvement of PDX-1 in islet-cell differentiation and function has been demonstrated mainly by 'loss-of-function' studies. We used a 'gain-of-function' approach to test whether PDX-1 could endow a non-islet tissue with pancreatic beta-cell characteristics in vivo. Recombinant-adenovirus-mediated gene transfer of PDX-1 to the livers of BALB/C and C57BL/6 mice activated expression of the endogenous, otherwise silent, genes for mouse insulin 1 and 2 and prohormone convertase 1/3 (PC 1/3). Expression of PDX-1 resulted in a substantial increase in hepatic immunoreactive insulin content and an increase of 300% in plasma immunoreactive insulin levels, compared with that in mice treated with control adenovirus. Hepatic immunoreactive insulin induced by PDX-1 was processed to mature mouse insulin 1 and 2 and was biologically active; it ameliorated hyperglycemia in diabetic mice treated with streptozotocin. These data indicate the capacity of PDX-1 to reprogram extrapancreatic tissue towards a beta-cell phenotype, may provide a valuable approach for generating 'self' surrogate beta cells, suitable for replacing impaired islet-cell function in diabetics.

[Elastic, stable intramedullary nailing of pertrochanteric femoral fractures in children (<6-8 years)]. / Elastisch-stabile intramedulläre Nagelung pertrochantärer Femurfrakturen im Kleinkindesalter (<6 bis 8 Jahre).

OBJECTIVE: Minimally invasive, sufficiently stable for movement and partial weight bearing, osteosythesis of pertrochanteric femoral fractures in children < 6-8 years using elastic, stable intramedullary nailing (ESIN). INDICATIONS: Proximal, pertrochanteric femoral fractures Delbet type IV in children < 6 years. CONTRAINDICATIONS: Comminuted fractures, femoral neck fractures. SURGICAL TECHNIQUE: By inserting three elastic titanium nails (TEN), prebent in the proximal third, retrograde into the femur, a stable 3­point support stabilizes the proximal fragment. For further improvement of stability, EndCaps can be used. POSTOPERATIVE MANAGEMENT: Partial weight bearing (sole-contact) for 4-5 weeks. X­ray controls immediately after surgery and after 4-5 weeks. No sports for 3 months. RESULTS: In our patient population we have good experience with this technique for very rare pertrochanteric fractures in children younger than 6-8 years. With minimally invasive access, exercise-stable administration can be achieved without a pelvic leg cast.

Neuronal nitric oxide synthase protects the pancreatic beta cell from glucolipotoxicity-induced endoplasmic reticulum stress and apoptosis.

AIMS/HYPOTHESIS: Cytokines stimulate nitric oxide production in pancreatic beta cells, leading to endoplasmic reticulum (ER) stress and apoptosis. Treatment of beta cells with glucose and NEFA induces nitric oxide synthase (NOS) as well as ER stress. However, the role of NO in glucolipotoxicity-induced ER stress in beta cells is not clear. METHODS: We studied the effect of high glucose and palmitate levels on NOS isoform production in rat and Psammomys obesus islets and in insulinoma-1E beta cells. The effects of neuronal NOS (nNOS) inhibition by small interfering RNA or by N (omega)-nitro-L-arginine methyl ester (L-NAME) on beta cell function, ER stress and apoptosis under conditions of glucolipotoxicity were investigated. RESULTS: Overnight incubation of rat and P. obesus islets at 22.2 mmol/l glucose with 0.5 mmol/l palmitate induced the production of nNOS but not inducible NOS (iNOS), in contrast with the robust stimulation of iNOS by cytokines. NOS inhibition by L-NAME did not prevent the decrease in glucose-stimulated insulin secretion and proinsulin biosynthesis or the depletion of islet insulin content observed under conditions of glucolipotoxicity. Moreover, treatment of beta cells with palmitate and L-NAME together resulted in marked activation of the IRE1alpha and PERK pathways of the unfolded protein response. This was associated with increased JNK phosphorylation and apoptosis in islets and beta cells. Moreover, partial nNos knockdown increased JNK phosphorylation and CHOP production, leading to apoptosis. CONCLUSIONS/INTERPRETATION: In beta cells subjected to glucolipotoxic conditions, chronic inhibition of NOS exacerbates ER stress and activates JNK. Therefore, induction of nNOS is an adaptive response to glucolipotoxicity that protects beta cells from stress and apoptosis.

Glucose regulation of ß-cell stress in type 2 diabetes.

In type 2 diabetes, the ß-cell is exposed to chronic hyperglycaemia, which increases its metabolic activity, with excess generation of reactive oxygen species (ROS) as a consequence. ROS accumulation induces both oxidative and endoplasmic reticulum (ER) stress, which may lead to ß-cell dysfunction and apoptosis. Recent data suggest that oxidative and ER stress are interconnected, although the mechanisms involved in nutrient regulation of the different stress pathways are dissimilar. Several components of the oxidative and ER stress machineries have important roles in the physiological response to glucose and are thus necessary for normal ß-cell function. Glucose stimulates signalling pathways that provide crucial messages for ß-cell adaptation to metabolic stress; however, the same pathways may eventually lead to apoptosis. Dynamic, temporally fluctuating activation of stress signalling is probably required for the maintenance of ß-cell survival, whereas its persistent activation results in ß-cell dysfunction and apoptosis. Thus, stress signalling is a 'double-edged sword' that may promote adaptation or apoptosis according to the balance between the divergent outputs of the various pathways. Developing new strategies for ß-cell protection based on inhibition of oxidative and/or ER stress requires comprehensive understanding of the switch from ß-cell adaptation to ß-cell apoptosis under conditions of metabolic stress, such as occurs under hyperglycaemic conditions.

Insulin counteracts glucotoxic effects by suppressing thioredoxin-interacting protein production in INS-1E beta cells and in Psammomys obesus pancreatic islets.

AIMS/HYPOTHESIS: In type 2 diabetes, glucose toxicity leads to beta cell apoptosis with decreased beta cell mass as a consequence. Thioredoxin-interacting protein (TXNIP) is a critical mediator of glucose-induced beta cell apoptosis. Since hyperglycaemia leads to elevated serum insulin, we hypothesised that insulin is involved in the regulation of TXNIP protein levels in beta cells. METHODS: We studied the production of TXNIP in INS-1E beta cells and in islets of Psammomys obesus, an animal model of type 2 diabetes, in response to glucose and different modulators of insulin secretion. RESULTS: TXNIP production was markedly augmented in islets from diabetic P. obesus and in beta cells exposed to high glucose concentration. In contrast, adding insulin to the culture medium or stimulating insulin secretion with different secretagogues suppressed TXNIP. Inhibition of glucose and fatty acid-stimulated insulin secretion with diazoxide increased TXNIP production in beta cells. Nitric oxide (NO), a repressor of TXNIP, enhanced insulin signal transduction, whereas inhibition of NO synthase abolished its activation, suggesting that TXNIP inhibition by NO is mediated by stimulation of insulin signalling. Treatment of beta cells chronically exposed to high glucose with insulin reduced beta cell apoptosis. Txnip knockdown mimicking the effect of insulin prevented glucose-induced beta cell apoptosis. CONCLUSIONS/INTERPRETATION: Insulin is a potent repressor of TXNIP, operating a negative feedback loop that restrains the stimulation of TXNIP by chronic hyperglycaemia. Repression of TXNIP by insulin is probably an important compensatory mechanism protecting beta cells from oxidative damage and apoptosis in type 2 diabetes.

Balancing needs and means: the dilemma of the beta-cell in the modern world.

The insulin resistance of type 2 diabetes mellitus (T2DM), although important for its pathophysiology, is not sufficient to establish the disease unless major deficiency of beta-cell function coexists. This is demonstrated by the fact that near-physiological administration of insulin (CSII) achieved excellent blood glucose control with doses similar to those used in insulin-deficient type 1 diabetics. The normal beta-cell adapts well to the demands of insulin resistance. Also in hyperglycaemic states some degree of adaptation does exist and helps limit the severity of disease. We demonstrate here that the mammalian target of rapamycin (mTOR) system might play an important role in this adaptation, because blocking mTORC1 (complex 1) by rapamycin in the nutritional diabetes model Psammomys obesus caused severe impairment of beta-cell function, increased beta-cell apoptosis and progression of diabetes. On the other hand, under exposure to high glucose and FFA (gluco-lipotoxicity), blocking mTORC1 in vitro reduced endoplasmic reticulum (ER) stress and beta-cell death. Thus, according to the conditions of stress, mTOR may have beneficial or deleterious effects on the beta-cell. beta-Cell function in man can be reduced without T2DM/impaired glucose tolerance (IGT). Prospective studies have shown subjects with reduced insulin response to present, several decades later, an increased incidence of IGT/T2DM. From these and other studies we conclude that T2DM develops on the grounds of beta-cells whose adaptation capacity to increased nutrient intake and/or insulin resistance is in the lower end of the normal variation. Inborn and acquired factors that limit beta-cell function are diabetogenic only in a nutritional/metabolic environment that requires high functional capabilities from the beta-cell.

Antireflection of transparent polymers by advanced plasma etching procedures.

Self-organized nanostructures that provide antireflection properties grow on PMMA caused by plasma ion etching. A new procedure uses a thin initial layer prior to the etching step. Different types of antireflective structures can now be produced in a shorter time and with fewer limitations on the type of polymer that can be used. The durability of the structured surfaces can be improved by the deposition of additional thin films.

Calcium dependence of ionophore A23187-induced lymphocyte cytotoxicity.

Concentrations of the divalent cation ionophore, A23187, optimal for the transformation of human and pig lymphocytes, were cytotoxic to lymphocytes from rats and mice. The biochemical effects associated with A23187-induced cytolysis in rat thymocytes included inhibition of [3H]uridine uptake and incorporation into macromolecules and stimulation of [14C]-alpha-aminoisobutyric acid uptake. The biochemical effects, as well as the reduction in the number of viable cells, were dose dependent and were blocked by the omission of ionic calcium from the incubation medium. At a given ionophore concentration, the magnitude of lysis of thymocytes was proportional to the concentration of Ca2+ in the extracellular medium. Sr2+ was less effective than was Ca2+ in supporting A23187-induced thymocyte lysis. A comparison of the lytic response of lymphocytes of various origins showed that extracellular Ca2+ plays a role in ionophore-induced cytolysis in thymocytes and lymph node lymphocytes but not in mouse lymphosarcoma P1798 cells.

Binding, internalization, and degradation of insulin in vascular endothelial cells.

The interaction of insulin with the vascular endothelium was studied using bovine aortic endothelial cells in monolayer cultures. Confluent cell cultures exhibited specific binding of 125I-insulin to high- and low-affinity cell surface receptor sites. Binding was reversible, saturable, and accompanied by internalization and degradation of the bound hormone in a temperature- and time-dependent manner. Pre-exposure of the cultures to insulin resulted in a time-dependent reduction in the availability of cell surface receptors (downregulation). It is concluded that the occurrence of reversible insulin binding and of insulin degradation in endothelial cells supports the concept that the vascular endothelium compartment may regulate the level of insulin in the circulation.

Interaction between genetic and dietary factors determines beta-cell function in Psammomys obesus, an animal model of type 2 diabetes.

The gerbil Psammomys obesus develops nutrition-dependent diabetes. We studied the interaction between diet and diabetic predisposition for beta-cell function. A 4-day high-energy (HE) diet induced a 3-, 4-, and 1.5-fold increase in serum glucose, insulin, and triglycerides, respectively, in diabetes-prone (DP) but not diabetes-resistant (DR) P. obesus. Hyperglycemia and concurrent 90% depletion of islet immunoreactive insulin stores were partially corrected by an 18-h fast. In vitro early insulin response to glucose was blunted in both DR and DP perifused islets. The HE diet augmented early and late insulin response in DR islets, whereas in DP islets, secretion progressively declined. Dose-response studies showed a species-related increase in islet glucose sensitivity, further augmented in DP P. obesus by a HE diet, concomitant with a decreased threshold for glucose and a 55% reduction in maximal response. These changes were associated with a fourfold increase in glucose phosphorylation capacity in DP islets. There were no differences in islet glucokinase (GK) and hexokinase (HK) Km; however, GK Vmax was 3.7- to 4.6-fold higher in DP islets, and HK Vmax was augmented 3.7-fold by the HE diet in DP islets. We conclude that the insulin-resistant P. obesus has an inherent deficiency in insulin release. In the genetically predisposed P. obesus (DP), augmented islet glucose phosphorylation ability and diet-induced reduction of the glucose threshold for secretion may lead to inadequate insulin secretion and depletion of insulin stores in the presence of caloric abundance. Thus, genetic predisposition and beta-cell maladaptation to nutritional load seem to determine together the progression to overt diabetes in this species. It is hypothesized that similar events may occur in obese type 2 diabetic patients.

Hyperglycemia-induced beta-cell apoptosis in pancreatic islets of Psammomys obesus during development of diabetes.

The gerbil Psammomys obesus develops nutrition-dependent diabetes associated with moderate obesity. The disease is characterized by initial hyperinsulinemia, progressing to hypoinsulinemia associated with depleted pancreatic insulin stores. The contribution of changes in beta-cell turnover to insulin deficiency was investigated in vivo during transition to overt diabetes. Normo glycemic diabetes-prone P. obesus animals who were given a high-calorie diet developed hyperglycemia within 4 days, which was found to be associated with a progressive decline in pancreatic insulin content. This was accompanied by a transient increase in beta-cell proliferative activity and by a prolonged increase in the rate of beta-cell death, culminating in disruption of islet architecture. The hypothesis that "glucotoxicity" was responsible for these in vivo changes was investigated in vitro in primary islet cultures. Exposure of islets from diabetes-prone P. obesus to high glucose levels resulted in a dose-dependent increase in beta-cell DNA fragmentation. In contrast, high glucose levels did not induce DNA fragmentation in rat islets, whereas islets from a diabetes-resistant P. obesus line exhibited a reduced and delayed response. Aminoguanidine did not prevent glucose-induced beta-cell DNA fragmentation in vitro, suggesting that formation of nitric oxide and/or advanced glycation end products plays no major role. Elevated glucose concentrations stimulated beta-cell proliferation in both rat and P. obesus islets. However, unlike the marked long-lasting effect in rat islets, only a transient and reduced proliferative response was observed in P. obesus islets; furthermore, beta-cell proliferation was inhibited after prolonged exposure to elevated glucose levels. These results suggest that hyperglycemia-induced beta-cell death coupled with reduced proliferative capacity may contribute to the insulin deficiency and deterioration of glucose homeostasis in P. obesus. Similar adverse effects of hyperglycemia could play a role in the evolution of type 2 diabetes in genetically susceptible individuals.