The effects of temperature and frequency dispersion on sound speed in bulk poly (vinyl alcohol) poly (N-isopropylacrylamide) hydrogels caused by the phase transition.

Bulk Poly (Vinyl Alcohol) (PVA) Poly (N-isopropyl acrylamide) (PNIPAm) hydrogel, one of the thermally responsive phase transitive hydrogels, is a versatile material due to its sharp volumetric phase transition and anomalous behaviors with facile tunability by thermal stimulation. At the lower critical solution temperature (LCST) of 33 °C, the hydrogels undergo a volumetric phase transition that causes drastic, non-monotonic change in the elastic modulus, viscosity, stiffness, and speed of sound. Here, we report the temperature and frequency dependence of the speed of sound in bulk PVA-PNIPAm hydrogel as measured by means of a planar resonant cavity. The linear response theory is applied for calculation of frequency dependent speed of sound. Comparisons find standard time of flight techniques underestimate the speed of sound by up to 6%, with variation in the frequency dependent speed of sound reaching as high as 200 m/s in the ultrasonic range of 0.2-0.8 MHz. The first characterization of frequency dependent speed of sound in PVA-PNIPAm hydrogel is addressed and delineated into its phase transition behaviors as connected to temperature. The findings can lead to better characterization of mechanical properties using ultrasonic spectroscopy, and higher resolution in ultrasonic imaging applications with dispersive media.

Nonreciprocal Linear Transmission of Sound in a Viscous Environment with Broken P Symmetry.

Reciprocity is a fundamental property of the wave equation in a linear medium that originates from time-reversal symmetry, or T symmetry. For electromagnetic waves, reciprocity can be violated by an external magnetic field. It is much harder to realize nonreciprocity for acoustic waves. Here we report the first experimental observation of linear nonreciprocal transmission of ultrasound through a water-submerged phononic crystal consisting of asymmetric rods. Viscosity of water is the factor that breaks the T symmetry. Asymmetry, or broken P symmetry along the direction of sound propagation, is the second necessary factor for nonreciprocity. Experimental results are in agreement with numerical simulations based on the Navier-Stokes equation. Our study demonstrates that a medium with broken PT symmetry is acoustically nonreciprocal. The proposed passive nonreciprocal device is cheap, robust, and does not require an energy source.

Surface plasmon enhancement of broadband photoluminescence emission from graphene oxide.

The photoluminescence (PL) emission studies of both graphene oxide (GO) and partially reduced graphene oxide (rGO) have been investigated. It has been observed that GO has broadband emission from the green to near infrared range and upon reduction rGO shows blue PL emission. The broadband PL emission is due to the recombination of the electron-hole pair in the sp(2) domain embedded within the sp(3) matrix. The broadband PL emission also suggests the existence of various sizes of the sp(2) domain within the same matrix. Furthermore, PL emission from GO in the presence of an Au metal thin film has been investigated. It has been observed that the entire broadband emission from GO in the green to near infrared wavelength region is enhanced significantly at room temperature. The Au-GO interface exhibits surface plasmon resonance in the visible wavelength region and is responsible for over 10 fold enhancement in the photoluminescence at ∼2.36 eV. The electrical property measurements on the GO and rGO thin films suggested that the rGO exhibits significantly higher electrical conductivity compared to that of the GO thin film. Furthermore, the GO thin film exhibits semiconducting behaviour. These properties make the material quite suitable for fabrication of new generation photonic devices.

Effects of residual gas exposure on the field emission properties of ZnO nanorods.

We compare the effects of O2, CO2, N2, H2, and Ar residual gas exposure on the field emission (FE) properties of ZnO nanorods. In contrast to carbon nanotubes and Mo metal microtips, we find that O2 and CO2 exposures do not significantly degrade the FE properties of ZnO nanorods. However, N2 exposure significantly degrades the FE properties. We propose that this could be due to the dissociation of N2 into atomic nitrogen species and the reaction of such species with ZnO. H2 and Ar exposures are not observed to significantly degrade the FE properties.

Focused-ion-beam-assisted selective control of graphene layers: acquisition of clean-cut ultra thin graphitic film.

A focused-ion beam (FIB) and a nanomanipulator provide a novel way to selectively control and obtain a few layers of graphene. Because of its weak van der Waals force in the interlayer of graphite, the nanomanipulator could easily exfoliate a graphitic thin layer with no wrinkles on the surface from a highly oriented pyrolitic graphite (HOPG) by applying a shear force which exceeds the static interlayer shear force. Subsequently, a few layers of graphene were successfully obtained by applying a uniform shear force from a detached graphitic thin layer that had been transferred to a pre-determined site on an oxide wafer. The required shear force for clean cleavage of a graphitic thin layer was then estimated based upon experimental data. Raman scattering analysis was used to confirm the number of placed graphene layers and the placement of a few layers of graphene was projected to have about five atomic layers.

Exciton localization in vertically and laterally coupled GaN/AlN quantum dots.

Near-field and time-resolved photoluminescence measurements show evidence of exciton localization in vertically and laterally coupled GaN quantum dots (QDs). The binding energies in multiple period QDs (MQDs) are observed to be stronger by more than six times compared to single period QDs (SQDs). Excitons in MQDs have a short (450 ps) lifetime and persist at room temperature, while SQDs exhibit extraordinarily long (>5 ns) lifetime at 10 K due to reduced spatial overlap of electron and hole wave functions in strained QDs.

Ultrashort-pulse-controlled all-optical modulation by interband and intersubband transitions in doped quantum wells.

The optimum condition for achieving highly efficient ultrafast all-optical pulse modulation by modification of the absorption of a pulsed interband light field by ultrasubband control-light pulses in a doped quantum well is investigated. The modulation efficiency in the femtosecond domain can be maximized by an intersubband control light with a pulse width (200 fs) that is comparable with the phase-relaxation time of the system and an intensity that is close to the intersubband saturation intensity.

Nutritional and hormonal control of glucose and fructose utilization by lung.

Whereas glucose is a major substrate for pulmonary lipid synthesis, fructose has also been suggested as a potential substrate. In vivo pulmonary fatty acid synthesis is depressed in hormonally deprived conditions, such as diabetes, and this can be modified by fructose feeding, but not by glucose feeding. In this study the glucose and fructose utilizations were compared in normal, diabetic and fasting states using isolated perfused rat lungs. When (U-14C)- or (5-3H)-glucose was used as substrate, glucose utilization by lung was reduced by 50% in both the fasting and diabetic animals compared to the normal controls. Using (U-14C)-glucose as substrate, the incorporation of (14C)-label in various metabolites of glucose was significantly depressed. For example, this reduction was 50% in lactate, pyruvate and CO2, 15% in ethanol-insoluble fraction, 65% in neutral lipids, 75% in phospholipids, 80% in fatty acid moiety, 40% in deacylated fraction and 10% in the polysaccharide fractions. Refeeding the fasted animals or insulin treatment to the diabetic animals restored these depressed (14C)-recoveries to the normal levels. Fructose utilization was less than 10% of glucose utilization, but remained unaffected by fasting and diabetic states. In addition, pulmonary hexokinase enzyme activity was lowered significantly in fasting and diabetic animals, whereas fructokinase enzyme activity was not altered. Despite the low rate of fructose utilization, these results suggest that fructose may serve as an alternative substrate for pulmonary phospholipid synthesis when glucose utilization is significantly depressed.

Thyroid hormone regulation of beta-adrenergic receptors and catecholamine sensitive adenylate cyclase in foetal heart.

The effect of thyroid hormone on the beta-adrenergic receptor in foetal cardiac membranes was analysed by measuring the binding of (-)[3H]DHA. The specific activities (per mg protein) of beta-adrenergic receptors decreased with advancing gestational age, whereas the total activities (per heart) increased under the similar conditions. The change in the binding affinities was not statistically significant. 1; 3,5,3'-L-triiodothyronine (T3) stimulated the (-)[3H]DHA binding capacities of the cardiac membranes of foetuses of all age groups. The enhancement in the receptor activity was completely inhibited actinomycin D or cycloheximide. The contents of epinephrine, norepinephrine and cAMP increased with advancing gestational age; but T3 had no significant effect on the catecholamines or cAMP. Similarly, the activities of the basal, NaF stimulated and Gpp(NH)p stimulated adenylate cyclase remained unaltered by T3, but the activities increased progressively with foetal maturity. The absolute values of catecholamine stimulated adenylate cyclase activities in the hearts of T3 treated foetuses were, however, higher compared to those in the untreated foetuses. The enhancement of the activities were totally blocked by the action of actinomycin D, cycloheximide or propranolol. Our results indicate that thyroid hormone enhances the number of beta-adrenergic receptor binding sites by synthesizing new receptor proteins resulting in increased catecholamine sensitivity.

Potentiation of surfactant release in fetal lung by thyroid hormone action.

Thyroid hormone has been shown to accelerate fetal lung development, but the mechanisms by which this hormone acts are yet unknown. Since this hormone may act indirectly by potentiating the action of endogenous catecholamines, we studied this mechanism by measuring beta-adrenergic receptors in fetal lung. Fetal rabbits at 27 days of gestation were treated with triiodothyronine (T3), 100 micrograms/100 g, in the presence and absence of propranolol, 200 micrograms/100 g, or actinomycin D, 20 micrograms/100 g. Fetuses were killed by decapitation either after 4 or 24 h of T3 treatment. The beta-adrenergic antagonist l-[3H]dihydroalprenolol was used to directly estimate the number and affinity of beta-adrenergic receptor in lung membranes. T3 increased the number of beta-adrenergic receptors in fetal lung, but the affinity of binding did not change. The enhancement of binding capacity after 4 h of T3 treatment was not inhibited by actinomycin D. However, 24-h T3-mediated stimulation was partially blocked by actinomycin D. In addition, T3 stimulated the catecholamine content, adenylate cyclase activity, and adenosine 3',5'-cyclic monophosphate content of lung. T3 increased the lecithin-to-sphingomyelin ratio, phosphatidylglycerol, and disaturated phosphatidylcholine content of the pulmonary lavage fluid. These parameters were completely inhibited by propranolol after 4 h and partially inhibited by actinomycin D after 24 h. Thus thyroid hormone enhances lung maturation by increasing the number of beta-adrenergic receptors in fetal lung.

Fructose utilization by lung.

We have examined the role of fructose as a substrate for the mammalian lung. Isolated and ventilated rat lungs were perfused for 2 h in the presence of either [U-14C]- or [5-3H]fructose. Fructose utilization, 3H2O production, and lactate and pyruvate production were measured. Insulin had no effect on the production of radiolabeled lactate. The 14C label from [U-14C]fructose was incorporated into the neutral lipids, phospholipids, fatty acid moiety, and deacylated fraction of lung. The apparent Km and maximum velocity of enzyme reaction for fructose utilization were 0.5 mM and 75 nmol X h-1 X g dry wt-1, respectively. Recovery of fructose 1-phosphate and fructose 1,6-diphosphate after perfusion with fructose, as well as detection of fructokinase, aldolase, and triokinase activities in the lung homogenates, suggested that fructose had been metabolized via phosphorylation through fructose 1-phosphate. Activities of fructose-metabolizing enzymes were not altered by the induction of diabetes, hypophysectomy, or starvation. These results suggest that mammalian lungs may utilize fructose to synthesize fatty acids, which in turn are used for phospholipid biosynthesis. The utilization of fructose by lung does not seem to be affected by nutritional or hormonal conditions.

Effects of superoxide anions on the (Na + K)ATPase system in rat lung.

Oxygen-derived free radicals have been shown to alter endothelial cell functions in lung. Enzymatically generated superoxide anions inactivated (Na + K)ATPase activity and caused lipid peroxidation in lung. Superoxide dismutase or allopurinol, but not ATP, protected this oxy radical-mediated depression of ATPase activity.

Pulmonary and hepatic fatty acid synthesis. III. Control of hexose monophosphate shunt pathway by 3,5,3'-L-triiodothyronine.

The hexose monophosphate shunt (HMPS) pathway activities were measured in lung and liver by estimating the relative conversion of [1-14C]-glucose and [6-14C]-glucose into 14CO2 as well as by assaying the glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities. The HMPS activities were depressed in the livers of diabetic and hypophysectomized rats and enhanced by 3,5,3'-L-triiodothyronine (T3) or insulin. The hepatic HMPS activities were stimulated to supranormal levels when normal rats were injected with T3. T3-mediated stimulation of hepatic enzyme activities was dependent on the dose and duration of the hormonal treatment. Half-lives of T3-induced synthesis and degradation of glucose 6-phosphate dehydrogenase were 20 and 96 h, respectively, and of 6-phosphogluconate dehydrogenase were 19 and 90 h, respectively. Although HMPS activity was found in lung, the activities of the HMPS pathway dehydrogenase did not vary with the alteration of hormonal conditions, nor the activities were stimulated by the action of T3 or insulin.

Effect of ischemia on fatty acid metabolism in fetal lung.

The effects of ischemia on in vivo fatty acid metabolism in fetal lung were studied using rabbit fetuses of 25 to 28 gestational age. Ischemia was produced by inflating the aortic balloon thereby reducing the uterine blood flow. Ischemic insult resulted significant increase in lactate/pyruvate and NADH/NAD ratios and decrease in ATP/ADP ratio in fetal lung. Levels of CoA, acetyl CoA, carnitine and acetyl carnitine decreased while those of long chain acyl CoA and long chain acyl carnitine enhanced. Tissue content of these metabolites returned to normal after 2 hr stabilization following 20 min of ischemic insult. Ischemia also caused small increase in lipogenesis and neutral lipid content of fetal lungs. Our results thus suggest that beta-oxidation in fetal lung is inhibited and becomes rate-limiting for fatty acid oxidation during ischemia. Sudden occurrence of hypoxia or ischemia in the fetus is a typical challenge for the obstetricians. The patients occasionally suffer from neurological injury following cerebral hypoxemia. The hypoxic insult may also affect the respiratory activity significantly. For example, acute alveolar hypoxia causes pulmonary vasoconstriction by damaging pulmonary vascular smooth muscle (1) and results in reduction of fatty acid oxidation by limiting the ATP supply required for metabolic processes (2). Hypoxia has also been shown to decrease the rate of palmitate incorporation into phospholipids (3), inhibit rate of fatty acid synthesis (3) and depress rate of incorporation of fatty acid and phosphatidic acid into lipids (4). Despite the fact that fatty acids represent a major substrate for energy metabolism in lung, no work has been done on the fatty acid metabolism in fetal lung. The present study was designed to determine the fate of fatty acid oxidation in fetal lung during ischemic challenge. The levels of acyl CoA and acylcarnitine intermediates were also measured in order to determine the rate-controlling steps of fatty acid metabolism in the fetal lung.