Optical study of electron and acoustic phonon confinement in ultrathin-body germanium-on-insulator nanolayers.

Nanoelectronics require semiconductor nanomaterials with high electron mobility like Ge nanolayers. Phonon and electron states in nanolayers undergo size-dependent changes induced by confinement and surface effects. Confined electrons and acoustic phonons determine layer optical, electric and thermal properties. Despite scientific and practical significance, their experimental studies in individual nanolayers are still lacking. Thanks to recent progress in the fabrication of high-quality nanolayers, here, we report the thickness dependencies of Raman spectra of acoustic phonons and optical spectra of electrons confined in germanium-on-insulator (GeOI) nanolayers with thicknesses TGeOI = 1-20 nm. We show that for TGeOI > 5 nm, both GeOI acoustic phonon Raman spectra and the E1 electron energy gap display dependencies on TGeOI which are reasonably described by the corresponding phonon and electron confinement theories. Accordingly, TGeOI can be probed using acoustic phonon Raman spectra at TGeOI > 5 nm. However, both confinement theories fail to describe GeOI thickness dependencies at TGeOI < 5 nm. We attribute this discrepancy to an increased influence of the Ge-GeO2 interface disorder with TGeOI reduction. The acoustic phonon data suggest a decrease of Ge normal-to-the-layer longitudinal sound velocity. Generation of interface-disorder-induced dispersionless phonons might contribute to this. The change in GeOI phonon properties at TGeOI < 5 nm might influence E1(TGeOI) dependence via a change in the GeOI electron-phonon interaction. We demonstrate that the Al2O3 coating improves the agreement between experimental and confinement theories, probably, via reduction of disorder at the Ge-GeOx-Al2O3-interface. Our results are important for control of nanolayer-confined electrons and phonons with benefits for modern and future nanoelectronic devices.

Effects of the Chinese herbal medicines Bupleuri radix, Ginseng radix, and Zingiberis rhizoma on lymphatic vessel activity in rats.

The aim of the present study was to determine the effects of the Chinese herbal medicines Bupleuri radix, Ginseng radix and Zingiberis rhizoma on spontaneous lymphatic vessel activity. The effect of each herbal medicine on in vivo lymphatic flow was examined by injection of dye into the femoral regions of rats after feeding with the herbal medicines. In an in vitro study, spontaneous changes in diameter of the rat thoracic duct were monitored, and each segment was exposed to each herbal medicine. In the in vivo study, 100% of the right iliac lymphatic node were positively stained in the herbal medicine group, whereas only 40% of the node were positively stained in the control group. In the in vitro study, Bupleuri radix and Ginseng radix increased the amplitude of spontaneous activity of lymphatic vessels in a concentration-dependent manner with or without L-NAME, an NO synthase inhibitor. The results indicated that the herbal medicines Bupleuri radix and Ginseng radix activated spontaneous lymphatic vasomotion and lymph flow, and the mechanisms of this effect seem to be independent of endothelial cells.

Inhibitory effects of the anesthetics propofol and sevoflurane on spontaneous lymphatic vessel activity in rats.

BACKGROUND: The effects of propofol and sevoflurane on lymphatic vessel activity are unknown. This study aimed to clarify the effects of these anesthetics on lymphatic vessel activity in rats by the use of a technique for mechanical removal of the endothelium. METHODS: The authors first examined the effects of propofol (8 mg/kg) and sevoflurane (2.0%) on in vivo lymphatic flow by injection of dye into the femoral regions of rats. In the in vitro study, the ends of the vessel segments of rat thoracic duct were connected to a syringe and stopcock, respectively. Spontaneous changes in diameter of each segment were monitored, and the extraluminal side of each segment was exposed to propofol (1 x 10(-6) approximately 3 x 10(-5) M) or sevoflurane (0.5 approximately 2.0%). Endothelial function was eliminated by perfusion of air into the lumen. RESULTS: In the dye uptake study, 80% of iliac lymphatic nodes were positively stained in a control group, whereas only 10% and 20% were positively stained in propofol and sevoflurane groups, respectively. In the in vitro study, both of the anesthetics significantly decreased the amplitude of spontaneous activity of lymphatic vessels with or without endothelial function. Sevoflurane inhibited the frequency of lymphatic vessel activity but propofol had no effect on it. When the endothelial function was eliminated, both anesthetics decreased the frequency of spontaneous activity of lymphatic vessels. CONCLUSIONS: Propofol and sevoflurane seem to have some different effects on endothelial function, which regulates the pacemaking of spontaneous contraction of lymphatic vessels.

Differential pressor response to intravenous ephedrine during recovery from deliberate hypotension.

STUDY OBJECTIVE: To determine whether nitroglycerin or trimethaphan alters pressor response to intravenous (i.v.) ephedrine. DESIGN: Prospective, randomized study. SETTING: Operating room of a university hospital. PATIENTS: 60 ASA physical status I female patients scheduled for mastectomy. INTERVENTIONS: Patients were assigned to one of six groups (n = 10 in each). Group 1: nitroglycerin + normal saline (NS) i.v., Group 2: nitroglycerin + ephedrine 0.1 mg/kg i.v., Group 3: nitroglycerin + ephedrine 0.15 mg/kg i.v., Group 4: trimethaphan + NS i.v., Group 5: trimethaphan + ephedrine 0.1 mg/kg i.v., and Group 6: trimethaphan + ephedrine 0.15 mg/kg i.v. MEASUREMENTS: Hemodynamic responses to ephedrine following withdrawal of vasodilators were observed for 15 minutes. MAIN RESULTS: Ephedrine increased heart rate and mean blood pressure. After ephedrine 0.1 mg/kg i.v., the maximum pressor response in the trimethaphan group was approximately twofold that of the nitroglycerin group (p = 0.038). CONCLUSIONS: Ephedrine restored BP more easily in those patients who had received trimethaphan compared with those who had received nitroglycerin for deliberate hypotension.

Role of endothelium-derived hyperpolarizing factor in phenylephrine-induced oscillatory vasomotion in rat small mesenteric artery.

BACKGROUND: In small mesenteric arteries, endothelium-derived hyperpolarizing factor (EDHF) in addition to endothelium-derived relaxing factors (EDRFs) including NO plays an important role in acetylcholine-induced vasodilation. It has been reported that EDRFs play an important role in alpha(1)-adrenoceptor agonist-induced oscillatory vasomotion and in limiting vasoconstrictor response to the agonists; however, contribution of EDHF to the alpha(1)-agonist-induced oscillation is unknown. METHODS: Rat small mesenteric arteries were isolated and cannulated at each end with a glass micropipette. The vessels were immersed in a bath (37 degrees C) containing physiologic saline solution. Changes in vessel diameter were measured using an optical density video detection system. RESULTS: Denudation of the endothelium and inhibition of NO synthesis caused a leftward shift in the concentration-response relation for phenylephrine in the mesenteric arteries, whereas inhibition of cyclooxygenase by indomethacin had no effect. Blockade of Ca2+-activated K+ (K(Ca)) channels by charybdotoxin and apamin caused a further leftward shift in the concentration-response relation in the vessels pretreated with Nomega-nitro-l-arginine methylester and indomethacin. Phenylephrine at concentrations higher than 10(-6) m caused endothelium-dependent oscillatory vasomotion, which was reduced but not abolished after combined inhibition of the cyclooxygenase and NO synthase pathways. However, the K(Ca) channel blockers completely abolished the remaining component of oscillation. CONCLUSIONS: Endothelially-derived NO is an important modulator of sustained agonist-induced vasoconstriction. NO, as well as endothelially-derived cyclooxygenase products and EDHF, also contribute significantly to phenylephrine-induced oscillatory vasomotion.

Bronchospasm induced by propofol in a patient with sick house syndrome.

IMPLICATIONS: Propofol is often used in patients with asthma, but it can induce bronchospasm. We report a patient with sick house syndrome (nonspecific complaints of mucosal irritation, headache, nausea, and chest symptoms) who suffered bronchospasm. This case suggests that propofol is not always a safe anesthetic for patients with asthma, especially drug-induced asthma.