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Excellent thermoelectric performance has been realized in trace-elements-doped n-type Mg3Bi2-xSbx materials, but the structural origin for such improved performance hasn't been fully studied, inhibiting this effective approach to better performance. Here we present the characterizations and analyses of the atomic and electronic structures associated with La dopants in polycrystalline Mg3·2Bi1·5Sb0.5 using synchrotron X-ray diffraction and X-ray absorption spectra, as well as the material's thermoelectric performance. Interstitial oxygen was observed inside the cavities of the Mg6Bi6 hexagonal cylinders in un-doped Mg3·2Bi1·5Sb0.5, which may account for its semiconducting behavior, while the La can effectively depresses the interstitial oxygen, resulting in the more negative valence state of Bi from −2.20 to −3.35. Furthermore, the thermoelectric performance of La-doped Mg3·2Bi1·5Sb0.5 has been significantly improved due to the optimized carrier concentration and the increased Hall mobility, exhibiting a zT value of ∼0.75 at 525 K.

Nitric oxide (NO) overproduction via induction of inducible nitric oxide synthase (iNOS) is implicated in vasodilatory shock in sepsis, leading to septic encephalopathy and accelerating cerebral ischemic injury. An abbreviated urea-cycle ( l -citrulline- l -arginine-NO cycle) has been demonstrated in cerebral perivascular nitrergic nerves and endothelial cells but not in normal cerebral vascular smooth muscle cell (CVSMC). This cycle indicates that argininosuccinate synthase (ASS) catalyzes l -citrulline ( l -cit) conversion to form argininosuccinate (AS), and subsequent AS cleavage by argininosuccinate lyase (ASL) forms l -arginine ( l -arg), the substrate for NO synthesis. The possibility that ASS enzyme in this cycle was induced in the CVSMC in sepsis was examined. Blood-vessel myography technique was used for measuring porcine isolated basilar arterial tone. NO in cultured CVSMC and in condition mediums were estimated by diaminofluorescein (DAF)-induced fluorescence and Griess reaction, respectively. Immunohistochemical and immunoblotting analyses were used to examine iNOS and ASS induction. l -cit and l -arg, which did not relax endothelium-denuded normal basilar arteries precontracted by U-46619, induced significant vasorelaxation with increased NO production in these arteries and the CVSMCs following 6-hour exposure to 20 μg/ml lipopolysaccharide (LPS) or lipoteichoic acid (LTA). Pre-treatment with pyrrolidine dithiocarbamate (PDTC) and salicylate (SAL) (NFκB inhibitors), aminoguanidine (AG, an iNOS inhibitor), and nitro- l -arg (NLA, a non-specific NOS inhibitor) blocked NO synthesis in the CVSMC and attenuated l -cit- and l -arg-induced relaxation of LPS- and LTA-treated arteries. Furthermore, immunohistochemical and immunoblotting studies demonstrated that expression of basal iNOS and ASS in the smooth muscle cell of arterial segments denuded of endothelium and the cultured CVSMCs was significantly increased following 6-hour incubation with LPS or LTA. This increased iNOS- and ASS-proteins expression in both preparations was inhibited by SAL, but was further increased by AG. These results indicate that LPS and LTA induce the l -cit- l -arg-NO cycle via induction of iNOS and ASS in the CVSMCs, accounting for massively increased NO-production and cerebral vasodilation in septic shock. Simultaneous inhibition of both pathways and NFκB-activation may be necessary to efficiently decrease or normalize NO production in the CVSMCs in this disease condition, and/or prevention and treatment of cerebral vessel-related brain dysfunctions. Our results further suggest to avoid using iNOS inhibitors alone which may cause upregulation of iNOS and ASS resulted from feedback-inhibition of iNOS activity. Accordingly, combined treatments with specific iNOS-activity inhibitor and inhibitor for iNOS genomic expression may provide a strategy in optimally managing brain sepsis and related encephalopathy associated with enhanced iNOS expression and NO overproduction.

The abuse of ketamine and amphetamine analogs is associated with incidence of hypertension and strokes involving activation of sympathetic activities. Large cerebral arteries at the base of the brain from several species receive dense sympathetic innervation which upon activation causes parasympathetic-nitrergic vasodilation with increased regional blood flow via axo-axonal interaction mechanism, serving as a protective mechanism to meet O2 demand in an acutely stressful situation. The present study was designed to examine effects of ketamine and amphetamine analogs on axo-axonal interaction-mediated neurogenic nitrergic vasodilation in porcine basilar arteries using techniques of blood-vessel myography, patch clamp and two-electrode voltage clamp, and calcium imaging. In U46619-contracted basilar arterial rings, nicotine (100μM) and electrical depolarization of nitrergic nerves by transmural nerve stimulation (TNS, 8Hz) elicited neurogenic nitrergic vasodilations. Ketamine and amphetamine analogs concentration-dependently inhibited nicotine-induced parasympathetic-nitrergic vasodilation without affecting that induced by TNS, nitroprusside or isoproterenol. Ketamine and amphetamine analogs also concentration-dependently blocked nicotine-induced inward currents in Xenopus oocytes expressing α3β2-nicotinic acetylcholine receptors (nAChRs), and nicotine-induced inward currents as well as calcium influxes in rat superior cervical ganglion neurons. The potency in inhibiting both inward-currents and calcium influxes is ketamine>methamphetamine>hydroxyamphetamine. These results indicate that ketamine and amphetamine analogs, by blocking nAChRs located on cerebral perivascular sympathetic nerves, reduce nicotine-induced, axo-axonal interaction mechanism-mediated neurogenic dilation of the basilar arteries. Chronic abuse of these drugs, therefore, may interfere with normal sympathetic-parasympathetic interaction mechanism resulting in diminished neurogenic vasodilation and, possibly, normal blood flow in the brainstem.

Vascular dysfunction plays a critical role in the pathogenesis of sepsis. We elucidated the mechanisms underlying the amelioration of lipopolysaccharide (LPS)-induced vascular inflammation by oroxylin A (OroA) post-treatment in rats. The animals were intraperitoneally injected with LPS (10 mg/kg) to induce systemic inflammation and intravenously (iv) administered OroA (15 mg/kg) 6 h after the LPS treatment. The assessments included biochemical changes in peripheral blood, vascular reactivity which was evaluated by blood-vessel myography, morphological/histological assessment of inflammation, toll-like receptor (TLR)-4-mediated interleukin-1-receptor-associated-kinase (IRAK)-4 activation, changes in adhesion molecule expression, and endothelial junctional stability in the aorta. LPS significantly enhanced the proinflammatory cytokine release, increased vascular cell adhesion molecule (VCAM)-1 expression, disrupted endothelial tight junction, reduced vascular endothelial barrier stability, and increased macrophage infiltration and accumulation in the aorta. All observed pathological changes and vascular inflammation were significantly reversed by the OroA post-treatment. Importantly, OroA suppressed the increased adhesion molecule expression and the endothelial barrier disruption by inhibiting LPS-activated IRAK-4-targeted inhibitory nuclear factor kappa B kinase (IKK) α/β complex phosphorylation, without directly affecting the interaction between LPS and TLR-4. Moreover, the iNOS activity induced by the LPS challenge was inhibited by the OroA pretreatment of the isolated aortic rings. These results suggest that OroA regulates the vascular tone by inhibiting vascular hyporeactivity caused by NO overproduction and reverses the endothelial barrier dysfunction and inflammation by inhibiting the IRAK-4-mediated IKKα/β phosphorylation. Overall, these findings suggest OroA administration as a potentially useful therapeutic approach for clinical interventions in septic shock.

Nicotinic acetylcholine receptor activation on the perivascular sympathetic nerves via axo-axonal interaction mechanism causes norepinephrine release, which triggers the neurogenic nitrergic relaxation in basilar arteries to meet the need of a brain. Donepezil and huperzine A, which are the cholinesterase inhibitors used for Alzheimer's disease therapy, exert controversial effects on nicotinic acetylcholine receptors. Therefore, we investigated how donepezil and huperzine A via the axo-axonal interaction regulate the neurogenic vasodilation of isolated porcine basilar arteries and define their action on different subtypes of the nicotinic acetylcholine receptor by using blood vessel myography, calcium imaging, and electrophysiological techniques. Both nicotine (100 μM) and transmural nerve stimulation (TNS, 8 Hz) induce NO-mediated dilation in the arteries. Nicotine-induced vasodilations were concentration-dependently inhibited by huperzine A and donepezil, with the former being 30 fold less potent than the latter. Both cholinesterase inhibitors weakly and equally decreased TNS-elicited nitrergic vasodilations. Neither huperzine A nor donepezil affected isoproterenol (a β adrenoceptor-agonist)- or sodium nitroprusside (a NO donor)-induced vasodilation. Further, huperzine A was less potent than donepezil in inhibiting nicotine-elicited calcium influxes in rodent superior cervical ganglionic neurons and inward currents in α7- and α3β2-nicotinic acetylcholine receptor-expressing Xenopus oocytes. In conclusion, huperzine A may exert less harmful effect over donepezil on maintaining brainstem circulation and on the nicotinic acetylcholine receptor-associated cognition deficits during treatment for Alzheimer's disease.

Raman scattering and polarization-dependent synchrotron radiation X-ray absorption, in combination, have been employed to examine the residual stress of undoped GaN epitaxial layers grown on Si by molecular beam epitaxy and Si-doped n-type GaN layers grown on sapphire by metalorganic chemical vapor deposition. Values of the lattice constant of different GaN films can be deduced from the interatomic distances in the second coordination shell around Ga by polarization-dependent extended X-ray absorption fine structure analysis and the strain of the films can be obtained. This result is further confirmed by Raman scattering spectra in which the phonon modes show a significant shift between different GaN epitaxial layers with different growth conditions.

S K-edge XANES and Mn-, W- and Ni-XANES and EXAFS spectra of silicate glasses synthesised at 1400 °C and 1 bar with compositions in the CaO–MgO–Al2O3–SiO2–S plus MnO, NiO, or WO3 systems were used to investigate sulphur speciation in silicate glasses. S K-edge spectra comprised a composite peak with an edge between 2470 and 2471.4 eV, which was attributed to S2−, and a peak of variable height with an edge at 2480.2–2480.8 eV, which is consistent with the presence of S6+. The latter peak was attributed to sample oxidation during sample storage. W-rich samples produced an additional lower energy peak at 2469.8 eV that is tentatively attributed to the existence of S 3p orbitals hybridised with the W 5d states. Deconvolution of the composite peak reveals that the composite peak for Mn-bearing samples fits well to a model that combines three Lorentzians at 2473.1, 2474.9 and 2476.2 eV with an arctan edge step. The composite peak for W-bearing samples fits well to the same combination plus an additional Lorentzian at 2469.8 eV. The ratio of the proportions of the signal accounted for by peaks at 2473.1 and 2476.2 eV correlates with Mn:Ca molar ratios, but not with W:Ca ratios. Spectra from Ni-bearing samples were qualitatively similar but S levels were too low to allow robust quantification of peak components. Some part of the signal accounted for by the 2473.1 eV peak was therefore taken to record the formation of Mn–S melt species, while the 2469.8 peak is interpreted to record the formation of W–S melt species. The 2474.9 and 2476.2 eV peaks were taken to be dominated by Ca–S and Mg–S interactions. However, a 1:1 relationship between peak components and specific energy transitions is not proposed. This interpretation is consistent with known features of the lower parts of the conduction band in monosulphide minerals and indicates a similarity between sulphur species in the melts and the monosulphides. S-XANES spectra cannot be reproduced by a combination of the spectra of the component element monosulphides. Mn-, W- and Ni-XANES and EXAFS for synthetic glasses without sulphide exsolution did not show any sensitivity to the presence of sulphur, which is unsurprising as S:O ratios were sufficiently low that metals would be mostly co-ordinated by O. Mn EXAFS spectra were consistent with divalent Mn in 5 co-ordinated Mn–O melt species. W spectra were consistent with tetrahedrally co-ordinated hexavalent W, most likely in scheelite-like melt species, and Ni spectra were consistent with [4] co-ordinated divalent Ni. These results indicate lower co-ordinations for both W and Ni than those inferred by some previous workers. Cation co-ordination may reflect the proportion of non-bridging oxygens, which is lower in the Ca-rich and Al-poor samples investigated here than for previous studies.

Raman, X-ray diffraction and extended X-ray absorption fine structure (EXAFS) measurements of x Ba(Ni 1/3 Ta 2/3 )O 3 + (1 − x )Ba(Mg 1/3 Ta 2/3 )O 3 samples with x = 0–0.03 were performed to reveal the nickel doping effect on the microwave properties. EXAFS result clearly shows that the nickel is located on the Mg lattice site. We also found that, as the nickel concentration increases, microwave dielectric constant decreases with the Ta O and Ni O bond distances. X-ray diffraction shows that the 1:2 ordered structure is degraded with the increasing of nickel concentration. The stretching phonon of the TaO 6 octahedra, that is A 1g (O) phonon near 800 cm −1 , are strongly correlated to the microwave properties of x Ba(Ni 1/3 Mg 2/3 )O 3 + (1 − x )Ba(Mg 1/3 Ta 2/3 )O 3 samples. The large Raman shift and the large width of the A 1g (O) imply rigid but distorted oxygen octahedral structure, therefore, the effect of nickel doping lowers the dielectric constant and the Q × f value of Ba(Mg 1/3 Ta 2/3 )O 3 ceramic.

Bimetallic silver and gold nanoparticles, a core–shell type structure, have been prepared by NaBH4 reduction method. The optical absorption spectra are recorded and compared with various ratios of Ag/Au alloy nanoparticles. The absorption spectra of bimetallic nanoparticles suggested the formation of core–shell structure. On the other hand, the high resolution transmission electron microscopy image of the nanoparticles confirmed the core–shell type configuration directly. Moreover, we studied the surrounding environment of core–shell type and alloy nanoparticles around gold atoms by using extended X-ray absorption fine structure spectroscopy.

X-ray absorption near-edge spectroscopy (XANES) spectra at the Ni K-, In L 3 -, and In K-edge of Ni 3 In and Ni 13 In 9 are presented and compared with theoretical XANES spectra and site- and momentum-decomposed partial density of states derived from first-principles calculation. The agreement between theory and experiment is better for Ni 3 In than for Ni 13 In 9 . Extended X-ray absorption fine structure spectra of Ni 3 Al, Ni 3 Ga, Ni 3 In, and Ni 13 In 9 are also analyzed to yield the bonding parameters.

Pt/C, PtRu/C and PtMo/C electro catalysts were prepared in different compositions by incipient wetness impregnation method. These catalysts were characterized by X-ray diffraction (XRD) and X-ray absorption near-edge structure (XANES) to understand the miscibility into solid solution and to calculate the d-orbital vacancy, respectively. Pt with Ru and Mo forms a single alloy which was confirmed by XRD date. XANES was measured at Pt LII and LIII edges and K edges of Ru and Mo to determine the oxidation states of these metals in different compositions. Further calculations of d-orbital vacancy of Pt revealed more information that increasing the Ru or Mo content increases d-orbital vacancy. As Mo oxidizes faster than Ru, magnitude of d-orbital vacancy is high in the case of Ru compared to Mo. In situ XENES study was also conducted in methanol fuel cell to understand the oxidation states and methanol oxidation mechanism.

We report on the preparation and characterization of the variation of B′-site transition metal in Sr 2 CrMO 6 (M=Mo, W) with double perovskites structure. The magnetic susceptibility shows that Sr 2 CrMoO 6 and Sr 2 CrWO 6 are antiferromagnets with T N =40 and 30 K at H =1 T, respectively. In addition, a large magnetoresistance ratio (MR) of ∼38% ( H =3 T) at 5 K was observed in the Sr 2 CrWO 6 compound. However, the Sr 2 CrMoO 6 compound does not show any significant MR even at high fields (MR∼4%; H =3 T and 5 K). The measured O K-edge X-ray absorption is in agreement with the calculated O p -density of states for both compounds.

The stability of styrene-divinyl benzene copolymer (SDB)-supported Pt (Pt/SDB) catalysts for destruction of volatile-organic-compound (VOC) in wastewater was examined. The test reaction was wet oxidation of water-containing aliphatic alcohol and formaldehyde at 140 degrees C and 90 psig for 40 h. The catalytic performance tests indicated that activity of the Pt/SDB catalysts could be maintained for VOC concentration of 3 wt.%, whereas the catalysts deactivated rapidly for 10 wt.% VOC containing wastewater. In order to investigate the nature of catalyst deactivation, extended X-ray absorption fine structure (EXAFS) and X-ray absorption near edge (XANES) spectroscopy were used to characterize the fresh and used catalysts. After the reaction, there is no oxidation of Pt clusters observed in EXAFS and XANES spectroscopy suggesting that the oxidation reaction takes places via the adsorbed oxygen. The spectroscopy results further indicated that deactivation of the catalysts were mainly caused by the increase of Pd particle size. After the reaction, the Pt-Pt coordination number has no significant change for the 3 wt.% wastewater whereas increase from 5.6 to 6.2 for 10 wt.% wastewater. Combined with the fact that the catalysts fractured during the reactions, we suggested that Pt agglomeration was mainly caused by thermal migration of the metal clusters.

Large cerebral arteries at the base of the brain from several species are innervated by dense sympathetic adrenergic nerves, and parasympathetic cholinergic and nitrergic nerves. Norepinephrine (NE) and acetylcholine (ACh) released from the respective nerves are not the primary postsynaptic transmitters for vasoconstriction and dilation. Evidence has been presented to indicate that nitric oxide (NO) is the predominant transmitter for cerebral vasodilation. NE and ACh act as presynaptic transmitters in modulating NO release and therefore cerebral vascular tone. This transmitter mechanism in the large cerebral arteries appears to be different from that in the smaller vessels.

Nanocrystalline CeO2 samples were prepared via precipitation from aqueous cerium(IV) sulfate solution under a controlled pH. After being subjected to calcination at various temperatures to yield different particle sizes, the local structure around Ce atom was investigated by using EXAFS spectroscopy at Ce K-edge. The first shell CeO distance was found to be slightly shorter with small CeO2 particles, indicating a contraction of the lattice. There exists a significant growth in coordination number of the second cell CeCe when the particle size became larger. In terms of Debye–Waller factor (σ2), the first three coordination shells showed a consistent trend, i.e. the degree of disorder increases with reduced particle size. Moreover, σ2 of the second shell was found to be smaller than that of the first shell for all samples.

The presence of close apposition between the adrenergic and the non-adrenergic or nitrergic nerve terminals in large cerebral arteries in several species is well documented. The axo-axonal distance between these different types of nerve terminals is substantially closer than the synaptic distance between the adventitial nerve terminals and the outermost layer of smooth muscle in the media. This feature suggests that a functional axo-axonal interaction between nerve terminals is more likely to occur than that between the nerve and muscle. Thus, transmitters released from one nerve terminal may modulate release of transmitters from the neighboring nerve terminals, resulting in a neurogenic response. We have reported that nicotine-induced nitric oxide (NO)-mediated neurogenic vasodilation is dependent on intact sympathetic innervation in porcine and cat cerebral arteries. Evidence also has been presented to indicate that nicotine acts on alpha7-nicotinic receptors located on sympathetic nerve terminals, resulting in release of norepinephrine which then diffuses to act on beta2-adrenoceptos located on the neighboring nitrergic nerve terminals to release NO and therefore vasodilation. The predominant facilitatory effect of beta2-adrenoceptors in releasing NO is compromised by presynaptic alpha2-adrenoceptors located on the same nerves. Activation of cerebral sympathetic nerves may cause NO-mediated dilation in large cerebral arteries at the base of the brain.

We previously reported that oroxylin A, a polyphenolic compound, was a potent inhibitor of lipopolysaccharide (LPS)-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). In the present study, three oroxylin A structurally related polyphenols isolated from the Chinese herb Huang Qui, namely baicalin, baicalein, and wogonin, were examined for their effects on LPS-induced nitric oxide (NO) production and iNOS and COX-2 gene expressions in RAW 264.7 macrophages. The results indicated that these three polyphenolic compounds inhibited LPS-induced NO production in a concentration-dependent manner without a notable cytotoxic effect on these cells. The decrease in NO production was in parallel with the inhibition by these polyphenolic compounds of LPS-induced iNOS gene expression. However, these three compounds did not directly affect iNOS enzyme activity. In addition, wogonin, but not baicalin or baicalein, inhibited LPS-induced prostaglandin E2 (PGE2) production and COX-2 gene expression without affecting COX-2 enzyme activity. Furthermore, N-nitro-L-arginine (NLA) and N-nitro-L-arginine methyl ester (L-NAME) pretreatment enhanced LPS-induced iNOS (but not COX-2) protein expression, which was inhibited by these three polyphenolic compounds. Wogonin, but not baicalin or baicalein, similarly inhibited PGE2 production and COX-2 protein expression in NLA/LPS or L-NAME/LPS-co-treated RAW 264.7 cells. These results indicated that co-treatment with NOS inhibitors and polyphenolic compounds such as wogonin effectively blocks acute production of NO and, at the same time, inhibits expression of iNOS and COX-2 genes.

Polyphenols are major components of many traditional herbal remedies, which exhibit several beneficial effects including anti-inflammation. The exact mechanism of the anti-inflammatory action of polyphenols, however, has not been determined. In the present study, we examined the effects of eight different polyphenols isolated from Chinese herbs, including two flavonoids (myricitrin and oroxylin A), four ellagitannins (penta-O-galloyl-beta-glucopyranose, woodfordin C, oenothein B, and cuphiin D1), and two anthraquinones (emodin and physcion), on lipopolysaccharide (LPS)-induced nitric oxide (NO) production, and inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) gene expression in RAW264.7 macrophages. The results indicated that only oroxylin A and emodin concentration-dependently inhibited LPS-induced NO production. The remaining compounds slightly inhibited LPS-induced NO production only at the highest concentration examined. Furthermore, oroxylin A inhibited the expression of LPS-induced iNOS and COX-2 proteins and mRNAs without an appreciable cytotoxic effect on RAW264.7 cells. Emodin also inhibited LPS-induced iNOS protein as potently as oroxylin A, but it inhibited LPS-induced iNOS mRNA expression only slightly and did not affect COX-2 mRNA and proteins. This was consistent with the findings that oroxylin A but not emodin or physcion inhibited prostaglandin E(2) synthesis induced by LPS. The inhibitory effects of oroxylin A on LPS-induced iNOS and COX-2 gene expression were also demonstrated in Bcl-2-overexpressing RAW264.7 macrophages, suggesting that oroxylin A inhibition of iNOS and COX-2 expression was not due to its antioxidant effect. Furthermore, oroxylin A but not emodin blocked nuclear factor-kappaB (NF-kappaB) binding and transcriptional activation associated with decreased p65 proteins in the nucleus induced by LPS. These results indicated that oroxylin A, an active component in Huang Qin, inhibited LPS-induced iNOS and COX-2 gene expression by blocking NF-kappaB activation, whereas emodin inhibition of LPS-induced iNOS expression may be mediated by a different transcription factor.

The Pakuashan anticline is uniquely suited for study of the forward and lateral growth of fault-related folds. The Pakuashan ridge development arises from the late Quaternary uplift of the most external thrust zone of the western foothills of Taiwan. From Kaoshiung to Taichung, recent and active westward thrusting occurs at the front of the foothills. The Pakuashan anticline, trending N 150°E in the northern part to N 000° in the southern part, has been active throughout the Quaternary period. This activity is marked by geological structures, tectonic geomorphology and seismicity. A multisource and multiscale approach to study of the continental collision setting has been undertaken to combine tectonics, sedimentology and geomorphology. Studies of fracture patterns allow identification of two main features of stress orientations: a WNW/ESE compression direction, and E–W and N–S extension directions. Quantitative geomorphic parameters have been used to define the morphotectonic evolution and to infer tectonic style along the mountain front. Geomorphic evidence provides significant information on the processes that govern lateral propagation of an active anticline. Quaternary terraces are uplifted, tilted and folded over the Pakuashan ridge. Drainage systems in areas of active compression give information on the thrust zone structures and their development. Steep drainage and high local relief indicate that the Pakuashan anticline forms a well-defined zone of high uplift, especially in the southern part. The two main controls on drainage in that area are rock strength in the hanging wall and propagation of the deformation towards the south.

Dopamine has been shown to induce pial arterial relaxation and constriction in several species. Its mode of action on pial veins, however, remains unclarified. The vasomotor effect of dopamine on porcine pial veins was, therefore, examined using an in vitro tissue bath technique. The results indicated that dopamine constricted exclusively isolated ring segments of pial veins in the presence or absence of active muscle tone. The constriction induced by dopamine was not affected by Nω-nitro- l -arginine ( l -NNA, 2×10−5 M) or indomethacin (10−5 M). Only in few preparations was the constriction induced by maximum concentration of dopamine potentiated by l -NNA, suggesting that dopamine at high concentrations may release NO or a NO-related substance. In the presence of l -NNA (2×10−5 M), dopamine-induced constriction was inhibited by phentolamine and yohimbine (but not prazosin) in a concentration-dependent manner with maximum inhibition at 10−6 M. SKF38393 and 6-bromo-APB (selective dopamine D1 receptor agonists) and LY171555 (a selective dopamine D2 receptor agonist) also induced pial venous constriction exclusively in the presence of l -NNA. The constriction was not affected by phentolamine (10−6 M). The order of potency for these agonists in the presence of phentolamine, propranolol, guanethidine and l -NNA was: 6-bromo-APB>SKF38393>dopamine>LY171555. The dopamine-induced constriction in the presence of phentolamine was further inhibited by both SCH23390 (a selective dopamine D1 receptor antagonist) and sulpiride (a selective dopamine D2 receptor antagonist), but was not affected by dopamine D3 or D4 receptor antagonists. These results indicate that dopamine at low and high concentrations induces exclusively constriction of isolated porcine pial veins. The constriction is mediated by postsynaptic α2-adrenoceptors, and dopamine D1 and D2 receptors.

The major structures of the Western Foothills of Taiwan mainly consist of NNE-SSW-trending folds and imbricated west-vergent thrust systems. The additional occurrence of N140°E-striking oblique structures was revealed through a multisource approach involving a Digital Elevation Model (DEM), a study of drainage network anomalies, aerial photographs, Side-Looking Airborne Radar (SLAR) images and SPOT-P and Landsat images. These structures are described from north to south based on new field analyses (including stratigraphy and tectonics studies). They are also compared to seismic data and geodetic reconstruction, in order to evaluate their present-day activity. These N140°E major morphostructures are interpreted as left-lateral transfer fault zones, either inherited from the Eurasian passive margin and/or newly formed in the cover in response to the presence of basement highs within the foreland basin (Peikang and Kuanyin highs). The Sanyi and the Chishan transfer fault zones display a high seismic activity; the distribution of earthquakes and the related focal mechanisms confirm the left-lateral movement along N140°E directions. The Chiayi, Chishan, and Fengshan fault zones act presently as transfer fault zones, as indicated by GPS data. The associated N70°E- to N100°E-trending faults result from the reactivation of normal faults of the Eurasian passive margin as right-lateral strike-slip faults in the Foothills during the Plio-Quaternary collision in Taiwan. We conclude that multisource and multiscale geomorphic studies combined with tectonic analysis in the field yield a significant contribution to the understanding of the structural and kinematic development of the Western Foothills at the front of the Taiwan collision belt.

indexof 5-HT1Areceptorfunctionin humans.To examineif 5-HTIA receptor function is involved in the pathophysiologyof bipolar depression, we measured the cortisol, hypothermic and behavioral responses to ipsapironein 8 patients with bipolar depressionand 26 normalcontrols. After obtaininga blood samplefor baseline cortisol levels and measuringbodytemperature,a singledose of 0.3 mg/kgof ipsapironewas given orally to all the subjects and further bloodsand temperaturereadingswere obtainedevery 30minutesfor 3 hours.The results showedthat the administrationof ipsapironeled to a significant increase in cortisol release and a significant decrease in body temperature both in bipolar depressed patients and normal controls. There was no significant difference in the cortisol or hypothermic responses to ipsapirone between groups. However, there was a significant positive correlation between the Hamilton depression rating (HAMD)scores and the hypothermicresponsein the depressed patients, while the HAMD scores were not significantly correlated with the cortisol response. Comparing our findings with those of previous studies, we suggest that the alterations in 5-HTIA receptor sensitivity in depressed patients may be related to the severity of depression,and that they may only be reflected in those patients who have more severe depression.