Monolayers of transition metal dichalcogenides (TMDCs) have attracted a great interest for post‐silicon electronics and photonics due to their high carrier mobility, tunable bandgap, and atom‐thick 2D structure. With the analogy to conventional silicon electronics, establishing a method to convert TMDC to p‐ and n‐type semiconductors is essential for various device applications, such as complementary metal‐oxide‐semiconductor (CMOS) circuits and photovoltaics. Here, a successful control of the electrical polarity of monolayer WSe2 is demonstrated by chemical doping. Two different molecules, 4‐nitrobenzenediazonium tetrafluoroborate and diethylenetriamine, are utilized to convert ambipolar WSe2 field‐effect transistors (FETs) to p‐ and n‐type, respectively. Moreover, the chemically doped WSe2 show increased effective carrier mobilities of 82 and 25 cm2 V−1s−1 for holes and electrons, respectively, which are much higher than those of the pristine WSe2. The doping effects are studied by photoluminescence, Raman, X‐ray photoelectron spectroscopy, and density functional theory. Chemically tuned WSe2 FETs are integrated into CMOS inverters, exhibiting extremely low power consumption (≈0.17 nW). Furthermore, a p‐n junction within single WSe2 grain is realized via spatially controlled chemical doping. The chemical doping method for controlling the transport properties of WSe2 will contribute to the development of TMDC‐based advanced electronics.

The rabbit pulmonary artery contains postsynaptic alpha-adrenoceptors which meidate smooth muscle contraction; its noradrenergic nerves contain presynaptic alpha-adrenoceptors which mediate inhibition of the release of the transmitter evoked by nerve impulses. Dose-response curves for the pre- and postsynaptic effects of eight alpha-receptor agonists were determined on superfused strips of the artery in the presence of cocaine, corticosterone and propranolo. 1. According to the concentrations which caused 20% of the maximal contraction (EC20 post), the postsynaptic rank order of potency was: adrenaline greater than noradrenaline greater than oxymetazoline greater than naphazoline greater than phenylephrine greater than tramazoline greater than alpha-methylnoradrenaline greater than methoxamine. The pA2 values of phentolamine againstoxymethazoline, phenylephrine, alpha-methylnoradrenaline and methoxamine were 7.43, 7.48, 7.59 and 7.69, respectively. 2. For the investigation of presynaptic effects, the arteries were preincubated with 3H-noradrenaline. All agonists inhibited the overflow of tritium evoked by transmural sympathetic nerve stimulation. According to the concentrations which reduced the stimulation-induced overflow by 20% (EC20 pre), the rank order of potency was: adrenaline greater than oxymetazoline greater than tramazoline greater than alpha-methylnoradrenaline greater than noradrenaline greater than naphazoline greater than phenylephrine greater than methoxamine. 10(-5) M phentolamine shifted the presynaptic dose-response curves for moradrenaline and oxymethazoline to the right. 3. The ratio EC20 pre/EC20 post was calculated for each agonist as an index of its relative post- and presynaptic potency. According to the ratios, the agonists were arbitrarily classified into three groups. Group 1 (ratio about 30: preferentially postsynaptic agonists) comprised methoxamine and phenylephrine; group 2 (ratio near 1; similar pre- and postsynaptic potencies) comprised noradrenaline, adrenaline and naphazoline; group 3 (ratio below 0.2; preferentially presynaptic agonists) comprised oxymetazoline, alpha-methylnoradrenaline and tramazoline (as well as clonidine). 4. Preferentially presynaptic and preferentially postsynaptic agonists had opposite effects on the basoconstrictor response to nerve stimulation. Methoxamine and phenylephrine either did not change or enhanced, but never reduced, the response. In contrast, oxymetazoline, alpha-methylnoradrenaline and tramazoline at low concentrations selectively inhibited the response to stimulation at low frequency (0.25-2Hz). 5. It is concluded that alpha-adrenoceptor agonists vary widely in their relative pre- and postsynaptic potencies, possibly because of structural differences between pre- and postsynaptic alpha-receptors. Pre- and postsynaptic components contribute to their overll postsynaptic effec in actively transmitting synapses. The preferential activation of presynaptic alpha-receptors results in alpha-adrenergic inhibition of synaptic transmission.

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A search was performed for presynaptic, release-modulating receptor systems on the post-ganglionic sympathetic nerves of rabbit pulmonary artery. Strips of the artery were preincubated with (-)-3H-noradrenaline and then superfused and stimulated transmurally. 1. Tetrodotoxin, guanethidine, and omission of calcium all suppressed the stimulation-evoked overflow of tritium, thus confirming selective release from noradrenergic neurones. 49% of the stimulation-evoked overflow of total consisted of 3H-noradrenaline, 22% of 3H-3,4-dihydroxyphenyglycol (DOPEG), and 9% of 3H-normetanephrine. Cocaine virtually abolished the evoked overflow of 3H-DOPEG; further addition of corticosterone also abolished that of 3H-normetanephrine. In the presence of cocaine plus corticosterone, unmetabolized 3H-noradrenaline accounted for 86% of the stimulation-evoked overflow of total tritium. The overflow evoked per pulse was 2.2 X 10(-5) of the tritium content of the tissue (1 Hz); it increased 2-fold when the frequency was raised to 8 Hz. 2. Presynaptic alpha-adrenoceptors have previously been demonstrated in this tissue (Starke et al., 1975b). High concentrations of isoprenaline reduced the stimulation-evoked overflow of tritium, presumably by alpha-adrenergic inhibiton. No presynaptic effect of up to 10(-5) M normetanephrine and metanephrine was found. 3. Dopamine slightly diminished the stimulation-evoked overflow of tritium, but only at 100 times the inhibitory threshold concentration of noradrenaline (which is 10(-8) M; Starke et al., 1975b), probably through activation of presynaptic alpha-adrenoceptors. Apomorphine failed to reduce the evoked overflow whether the superfusion medium contained cocaine and corticosterone or not. 4. Isoprenaline (10(-9) -10(-6) M) did not change the evoked overflow whether the medium contained cocaine and corticosterone or not, and whether the frequency was 1 or 2 Hz. Propranolol also had no effect. 5. Angiotensin II increased the stimulation-evoked overflow both in the absence and in the presence of cocaine and corticosterone. Equieffective concentrations of angiotensin I were 10 times higher. Saralasin had no effect, whereas 1-Sar,8-Ile-angiotensin produced a small increase. Both of the latter peptides behaved as presynaptic antagonists of angiotensin II. A presynaptically supramaximal concentration of the alpha-adrenergic agonist oxymetazoline prevented the facilitatory action of yohimbine, but not that of angiotensin II. Separation of 3H-compounds showed that angiotensin II caused a proportionate increase in stimulation-evoked overflow of 3H-noradrenaline, 3H-DOPEG, and 3H-normetanephrine; this finding rules out any inhibition of noradrenaline uptake mechanisms. 6. 10(-4) -10(-3) M acetylcholine caused hexamethonium-sensitive acceleration of basal tritium outflow. Much lower concentrations (10(-7) M and higher) reduced the overflow evoked by electrical stimulation. The evoked overflow of 3H-noradrenaline, 3H-DOPEG, and 3H-normetanephrine was proportionately decreased...

The development of bulk synthetic processes to prepare functional nanomaterials is crucial to achieve progress in fundamental and applied science. Transition-metal chalcogenide (TMC) nanowires, which are one-dimensional (1D) structures having three-atom diameters and van der Waals surfaces, have been reported to possess a 1D metallic nature with great potential in electronics and energy devices. However, their mass production remains challenging. Here, a wafer-scale synthesis of highly crystalline transition-metal telluride nanowires is demonstrated by chemical vapor deposition. The present technique enables formation of either aligned, atomically thin two-dimensional (2D) sheets or random networks of three-dimensional (3D) bundles, both composed of individual nanowires. These nanowires exhibit an anisotropic 1D optical response and superior conducting properties. The findings not only shed light on the controlled and large-scale synthesis of conductive thin films but also provide a platform for the study on physics and device applications of nanowire-based 2D and 3D crystals.

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The aim of this study was to investigate the psychiatric problems and characteristics among children of child abuse (CA). Specifically, the authors investigated whether attention-deficit/hyperactivity disorder (ADHD) symptoms were exhibited before or after CA. A total of 39 abused child inpatients who were treated at Aichi Children's Health and Medical Center, Aichi, Japan, (mean age, 10.7 ± 2.6; mean IQ scores, 84.1 ± 19.3) were included in the study. The most frequent diagnosis was dissociative disorder in 59% of abused subjects. ADHD was diagnosed in 18% of abused subjects, and 71% of ADHD children had comorbid dissociative disorder. A total of 67% of all CA subjects fulfilled the ADHD criteria A according to DSM-IV-TR, however, only 27% of those fulfilled the criteria before CA. The subjects of dissociative disorder fulfilled ADHD criteria A more frequently than those of non-dissociative disorder (P = 0.013), and this result led to an increase in the frequency of the apparent ADHD. The rate of ADHD-suspected parents in the subjects who fulfilled ADHD criteria A after CA was significantly lower than those who fulfilled it before CA (P = 0.005). While it is difficult to distinguish ADHD from dissociative disorder, abused children may have increased apparent ADHD due to dissociative disorder. Further studies should be conducted in order to explore the distinct biological differences between ADHD before CA and the subjects who fulfilled ADHD criteria A after CA.

An acyl-CoA hydrolase, referred to as hBACH, was purified from human brain cytosol. The enzyme had a molecular mass of 100 kDa and 43-kDa subunits, and was highly active with long-chain acyl-CoAs, e.g. a maximal velocity of 295 micromol/min/mg and K(m) of 6.4 microM for palmitoyl-CoA. Acyl-CoAs with carbon chain lengths of C(8-18) were also good substrates. In human brain cytosol, 85% of palmitoyl-CoA hydrolase activity was titrated by an anti-BACH antibody, which accounted for over 75% of the enzyme activity found in the brain tissue. The cDNA isolated for hBACH, when expressed in Escherichia coli, directed the expression of palmitoyl-CoA hydrolase activity and a 44-kDa protein immunoreactive to the anti-BACH antibody, which in turn neutralized the hydrolase activity. The hBACH cDNA encoded a 338-amino acid sequence which was 95% identical to that of a rat homolog. The hBACH gene spanned about 130 kb and comprised 9 exons, and was mapped to 1p36.2 on the cytogenetic ideogram. These findings indicate that the long-chain acyl-CoA hydrolase present in the brain is well conserved between man and the rat, suggesting a conserved role for this enzyme in the mammalian brain, and enabling genetic studies on the functional analysis of acyl-CoA hydrolase.