Surface oxidation effect on the electrical behaviour of Bi2Te2Se nanoplatelets.

Charge transport in topological insulators is notably influenced by moisture and air in the surrounding environment. At present, however, little is known about the detailed composition of the oxidized surface and its impact on the electrical characteristics of these materials. Here, we investigate the surface oxide formation on the topological insulator Bi2Te2Se (BTS) and how this affects its electrical behavior. While ambient exposure of BTS nanoplatelets predominantly creates surface hydroxyl groups, oxygen plasma treatment yields a compact, few-nanometer thick surface oxide layer. The plasma causes p-type doping, accompanied by a decrease of the effective platelet thickness, the interplay of which is manifested in a resistance maximum as a function of plasma treatment time. It is furthermore demonstrated that the structural integrity of the plasma-derived surface oxide is sufficient to enable its use as a gate insulator layer in combination with a top gate.

Ultrahigh magnetically responsive microplatelets with tunable fluorescence emission.

Tuning the optical properties of suspensions by controlling the orientation and spatial distribution of suspended particles with magnetic fields is an interesting approach to creating magnetically controlled displays, microrheology sensors, and materials with tunable light emission. However, the relatively high concentration of magnetic material required to manipulate these particles very often reduces the optical transmittance of the system. In this study, we describe a simple method of generating particles with magnetically tunable optical properties via sol-gel deposition and functionalization of a continuous layer of silica on ultrahigh magnetically responsive (UHMR) alumina microplatelets. UHMR microplatelets with tunable magnetic response in the range of 15-36 G are obtained by the electrostatic adsorption of 2 to 13% of superparamagnetic iron oxide nanoparticles (SPIONs) on the alumina surface. The magnetized platelets are coated with a 20-50 nm layer of SiO2 through the controlled hydrolysis and condensation reactions of tetraethylorthosilicate (TEOS) in an NH3/ethanol mixture. Finally, the silica surface is covalently modified with an organic fluorescent dye by conventional silane chemistry. Because of the anisotropic shape of the particles, control of their orientation and distribution using magnetic fields and field gradients enables easy tuning of the optical properties of the suspension. This strategy allows us to gain both spatial and temporal control over the fluorescence emission from the particle surface, making the multifunctional platelets interesting building blocks for the manipulation of light in colloid-based smart optical devices and sensors.

Sugars communicate through water: oriented glycans induce water structuring.

Cells are coated with a glycocalyx-a layer of carbohydrate-containing biomolecules, such as glycoproteins. Although the structure and orientation of the cell-surface glycans are frequently regarded as being random, we have found, using α-1-acid glycoprotein and antitrypsin as model systems for surface glycans, that this is not the case. A glycoprotein monolayer was adsorbed onto hydrophilic and hydrophobic substrates. Surface-force measurements revealed that the orientation of the glycans with respect to the aqueous solution has a profound effect on the structure of vicinal water. The glycan antennae of the surface-adsorbed glycoproteins apparently impose an ordering on the water, resulting in a strong repulsive force over some tens of nanometers with superposed film-thickness transitions ranging from ≈0.7 to 1.8 nm. When the glycan orientation is modified by chemical means, this long-range repulsion disappears. These results may provide an explanation as to why the multiantennary structure is ubiquitous in glycoproteins. Although direct, specific interactions between glycans and other biomolecules are essential for their functionality, these results indicate that glycans' long-range structuring of water may also influence their ability to interact with biomolecules in their vicinity.

Prenatal caffeine causes long lasting behavioral and neurochemical changes.

The effects of prenatal exposure to caffeine were studied on later physical development, behavior and brain neurochemistry. Daily doses (150, 300 or 450 mg/L) of caffeine were given to rat dams during the last week of pregnancy. Prenatal caffeine exposure resulted in a number of behavioral and neurochemical changes in the offspring which were long lasting and dose related. The low dose (150 mg/L) of prenatal caffeine caused hyperactivity in an open-field. The high dose of caffeine caused learning disabilities in complex visual and auditory discrimination learning paradigms while simple motor learning or a spatial orientation task were not affected. Both male and female offspring showed some behavioral effects of caffeine exposure. The medium and high doses of caffeine resulted in weight gain that was observable as early as 35 days of age and increased progressively with age. This weight gain was associated with increased food intake. The neurochemical studies carried out at 2-3 months of age revealed an increase in choline uptake in hippocampus, mainly in the animals treated with the lower doses of caffeine and higher protein concentration (microgram/mg wet tissue) in the cortex or hippocampus of offspring exposed to the higher doses of caffeine. At 15 months of age, choline uptake in the frontal cortex was significantly reduced in the animals prenatally exposed to the 300 and 450 mg/L dose.

The effects of mild maternal stress during pregnancy on the behavior of rat pups.

Mild maternal stress in the form of chronic daily subcutaneous injections of saline or the vehicle for diazepam to pregnant rats was shown to result in some long term, subtle but reliable, changes in the behavior of the offspring. The same vehicle given for the same period of time in the dam's drinking water, without injection had no effect on the development of later behavior of rat pups. Chronic prenatal injections of saline or vehicle for diazepam, used in many experiments as controls for the evaluation of drug effects were shown to have some long lasting behavioral effects in the offspring of the treated dams. The series of experiments reported here compared the offspring of saline or vehicle injected dams to those of uninjected dams on a variety of developmental measurements, an open field behaviour and on learning performance in a complex brightness discrimination maze.

Prenatal monosodium glutamate causes long-lasting cholinergic and adrenergic changes in various brain regions.

Prenatal monosodium glutamate (MSG) given through the mother's diet was found previously to cause behavioral changes in the offspring, including learning disabilities. In the present study, neurochemical parameters were measured in the brains of prenatally exposed rats at various ages throughout development up to adulthood. At 15 days of age, choline uptake and choline acetyltransferase (ChAT) activity in the frontal cortex were significantly reduced (by 80 and 25%, respectively) in MSG-exposed animals, whereas the same cholinergic parameters in hippocampus were not changed. During later development, choline uptake gradually increased, until in adulthood it became significantly higher in MSG-exposed animals than in the controls. This enhancement was found in both males and females. Our previous study showed that only the male offspring were learning disabled. Choline uptake and ChAT activity were enhanced in the hippocampus of adult male animals. Norepinephrine (NE) uptake was reduced (by 25%) in the frontal cortex of males only. There was no change in NE uptake in the hypothalamus.

Prenatal and early postnatal exposure to zimelidine: behavioral, neurochemical and histological findings in rats.

Zimelidine (5 mg/kg/day s.c.) was administered to pregnant rats from day 10 to day 20 of gestation. The development and later open field and learning capacities of their offspring were compared to those of saline injected and untreated dams. The development and behavior of prenatally zimelidine exposed offspring resembled those of the untreated rather than the saline injected group. Pups that were nursed by zimelidine treated mothers, however, showed behavioral deficits compared to those that were nursed by saline injected dams. Prenatal or early postnatal exposure to the 5HT uptake inhibitor zimelidine did not affect 5HT uptake and release measured at 3 months of age. Histological examination of major organs of prenatally zimelidine exposed animals showed no pathological changes.

The effect of antibodies to gangliosides on Ca2+ channel-linked release of gamma-aminobutyric acid in rat brain slices.

Antibodies to GM1 ganglioside enhance the release of gamma-aminobutyric acid (GABA) from rat brain slices induced by depolarization with either 40 mM K+ or 200 microM veratrine. Three new observations are now reported. (a) GABA release induced by the Ca2+ ionophore A23187 was not affected by these antibodies. Because this Ca2+ ionophore causes transmitter release by bypassing depolarization-induced opening of Ca2+ channels, this result suggests that gangliosides participate either in the functioning of such Ca2+ channels or in the Na+ channels involved in depolarization. (b) The enhancement (by antibodies to GM1 ganglioside) of GABA release induced by high K+ levels occurred in the presence of tetrodotoxin (0.01 microM). (c) GABA release induced by veratrine in the absence of Ca2+ was not affected by the antibodies. These latter two observations indicate that Na+ channels are not involved in the action of the antibodies. We conclude that this evidence points to the participation of gangliosides in Ca2+ channel functions involved in GABA release in rat brain slices.

Differential vulnerability of male and female rats to the timing of various perinatal insults.

The results of five experiments showed that exposure to diazepam, hypoxia and monosodium glutamate during the prenatal or early postnatal period of rapid brain development may result in different behavioral consequences depending on the timing of the exposure rather than the nature of the agent. Moreover, male and female offspring may be affected differently by the same agent at different periods of development. Prenatal insults of various kinds impair the later performance of males but not the females in a complex learning task, while postnatal insults seem to affect detrimentally this same behavior in both males and females. The effects of perinatal insults on maze learning and open field activity do not lend themselves to explanation by "feminization" or "masculinization" of behavior caused by interference with prenatal gonadal hormones.

Some long-lasting neurochemical effects of prenatal or early postnatal exposure to diazepam.

Changes in the uptake of various neurotransmitters were measured in the frontal cortex and hippocampus of male and female rats that were exposed to diazepam through the placenta or through the mother's milk during the prenatal or early postnatal period of rapid brain development. Earlier studies from our laboratory showed that early diazepam exposure has long-lasting behavioral consequences. The present results show that prenatally diazepam-exposed rat pups show significant reduction in choline uptake in the frontal cortex at 10 days of age. At 60 days of age, both pre- and postnatally exposed males, but not females, show significant differences from controls in terms of choline uptake, whereas postnatally exposed females whose behavior was shown previously to be profoundly affected by the diazepam exposure showed significant increase in gamma-aminobutyric acid (GABA) uptake in the hippocampus and reduction of 5-hydroxytryptamine (5HT) uptake in the cortex at 60 days of age.

The effect of exposure to diazepam through the placenta or through the mother's milk. Histological findings in slices of rat brain.

Exposure to diazepam during the prenatal or early postnatal developmental period has been reported to result in later behavioural deficits. In the present study morphological changes in the brains of rats that were exposed to diazepam (DZP) prenatally or through the mother's milk postnatally were investigated. The results showed that prolonged prenatal exposure (16 days) to diazepam (10 mg/kg) resulted in characteristic and extensive pathological changes, i.e. gliosis and perivascular cuffing in the brains of the rats. These changes could be observed under the light microscope a long time after exposure to the drug had been terminated. Limiting the prenatal exposure to a single trimester of 7 days reduced somewhat the number of lesions but did not prevent their occurrence. Rats exposed to diazepam postnatally through the mothers' milk showed very few lesions.

Prenatal monosodium glutamate (MSG) treatment given through the mother's diet causes behavioral deficits in rat offspring.

The present study reports various developmental and behavioral changes in the offspring of rat dams that received monosodium glutamate (MSG) in the drinking water all through the second and third trimesters of pregnancy. Three main effects were observed in the MSG exposed offspring: (1) juvenile obesity; (2) reduced general activity levels; (3) a specific type of learning disability in discrimination learning involving choice between simultaneously present positive and negative stimuli.

The effects of exposure to diazepam during various stages of gestation or during lactation on the development and behavior of rat pups.

In the present study we have investigated the effects of diazepam (DZP) (10 mg/kg) treatment of rat dams during different periods of gestation or during lactation on the development and behavior of their offspring. The results show that DZP exposure during different phases of early development has differing effects on later behavior. Exposure during mid-gestation resulted in early and transient hyperactivity, but no learning or memory deficits at 2 months of age were observed. However, both late prenatal and early postnatal exposure to DZP resulted in significant behavioral changes. Late prenatal treatment caused no hyperactivity but resulted in poor performance on the learning and retention of a choice discrimination task, while early postnatal exposure resulted in consistent and lasting hyperactivity and in substantial discrimination learning and retention deficits at 2 months of age.

Millions of medical care dollars for indigents.

The medically indigent, a group traditionally underserved with health care, can obtain some needed free services from Hill-Burton facilities. These facilities (hospitals, nursing homes, clinics, and agencies) received Hill-Burton funds for their building programs and have, as a result, an obligation to provide a certain amount of uncompensated medical care to a defined medically indigent population. Health systems agencies (HSAS) or other interested agencies and groups can play an integral role in highlighting the Hill-Burton Program and helping the medically indigent obtain free care, This paper describes the Hill-Burton Program and explains how one HSA identified the Hill-Burton facilities in its area, determined the extent of their obligations, obtained allocation plans, and publicized and promoted the available health care services. From the interest shown by the community it was apparent that the HSA had provided a much needed and appreciated service that could be duplicated across the country by HSAS or other community groups.

Delayed post hypoxic transient amnesia is not associated with electrical brain seizures.

Rats rendered hypoxic by brief exposure to N2 after learning an avoidance response go into convulsions and subsequently become amnestic. Overt convulsions can be avoided whilst yet producing delayed post-hypoxic transient amnesia (DPHTA) by using 2% O2 in N2 in place of pure N2. The experiments reported here show that with this gas mixture, the ECoG shows hardly any of the electrical activity associated with seizures which occurs with N2. It is concluded that electrical seizures are not associated with the mechanism responsible for DPHTA.

Enhancement of depolarization-induced release of gamma-aminobutyric acid from brain slices by antibodies to ganglioside.

The effect of antibodies to GM1 ganglioside on release of neurotransmitters from rat brain slices was studied. Depolarization-induced (40 mM-KCl or veratrine) release of gamma-aminobutyric acid was markedly enhanced. Depolarization-induced release of norepinephrine was only slightly enhanced, whereas that of serotonin was unaffected. No effect on spontaneous release was observed for any of these three neurotransmitters. These results show that antibodies that can bind to synaptic membrane antigens may alter neurotransmitter release and that antibodies directed against GM1 ganglioside exhibit a measure of specificity in producing such an effect.