Tailoring low-dimensional structures of bismuth on monolayer epitaxial graphene.

To improve graphene-based multifunctional devices at nanoscale, a stepwise and controllable fabrication procedure must be elucidated. Here, a series of structural transition of bismuth (Bi) adatoms, adsorbed on monolayer epitaxial graphene (MEG), is explored at room temperature. Bi adatoms undergo a structural transition from one-dimensional (1D) linear structures to two-dimensional (2D) triangular islands and such 2D growth mode is affected by the corrugated substrate. Upon Bi deposition, a little charge transfer occurs and a characteristic peak can be observed in the tunneling spectrum, reflecting the distinctive electronic structure of the Bi adatoms. When annealed to ~500 K, 2D triangular Bi islands aggregate into Bi nanoclusters (NCs) of uniform size. A well-controlled fabrication method is thus demonstrated. The approaches adopted herein provide perspectives for fabricating and characterizing periodic networks on MEG and related systems, which are useful in realizing graphene-based electronic, energy, sensor and spintronic devices.

Analysis of trends in water quality: constructed wetlands in metropolitan Taipei.

Meandering through the most densely populated metropolitan areas of Taipei, Taiwan, the Danshui River and its tributaries have undergone the construction of 14 wetlands since 2004, as a means to improve water quality. This study was conducted to examine the functional capabilities associated with treating non-point source pollution through these riparian wetlands. Trend analysis was used to differentiate dissolved oxygen, biochemical oxygen demand, suspended solids, ammonia, and Escherichia coli, among 13 sampling sites using both functions of a Mann-Kendall test and a seasonal Mann-Kendall test. The results show that water quality in Taipei metropolitan rivers has been improving since increasing the number of constructed wetlands and connecting households to the public sewage system. The concentration of pollutants such as those influencing biochemical oxygen demand have gradually declined in drought seasons because riparian wetlands contribute a base flow to dilute riverine pollutants. This paper indicates that the creation of treatment systems influences dissolved oxygen conditions at the municipal scale, suggesting that constructed wetlands could stabilize water quality during extreme hydrological events and improve water quality particularly in times of drought.

Diminished short-term heart rate variability predicts inducible ventricular tachycardia.

PURPOSE: The purpose of this study is to determine whether short-term heart rate variability (HRV) can be used successfully to predict inducible ventricular tachycardia (VT). METHODS: A high-speed (300 mm/s) electrocardiographic recording was obtained in 32 patients in the supine position prior to programmed ventricular stimulation. Beat-to-beat RR intervals (in milliseconds) were derived from an 11-beat strip (10 RR intervals). Logistic regression was used to study the relationship between several variables and a dichotomous dependent variable (inducible, clinical, or electrocardiographic evidence of VT). RESULTS: Of 32 patients, 12 had inducible VT (inducible VT group) and 20 had no clinical or electrocardiographic evidence of VT (control group). Mean short-term HRV values were significantly lower in those with inducible VT than in the control group in all patients (25+/-15 ms, n=12 vs 67+/-22 ms, n=20; p<0.0001) and in patients with coronary artery disease or congestive heart failure or both (22+/-13 ms, n=11 vs 63+/-23 ms, n=11; p<0.0001). For the group as a whole, short-term HRV was < or =50 ms in 11 of 12 patients (92%) with inducible VT, but was < or =50 ms in only 3 of 20 control subjects (15%; p<0.001). As a result of a stepwise selection procedure conducted within the logistic regression, only the short-term HRV was found to be predictive of inducible VT (p<0.0001). CONCLUSION: Short-term HRV is significantly lower in subjects with inducible VT than in those without clinical or electrocardiographic evidence of VT. The probability of developing sudden death increases substantially when short-term HRV decreases below 50 ms.

Brain and plasma tetrahydroisoquinolines in rats: effects of chronic ethanol intake and diet.

Brain concentrations of salsolinol (SAL), a simple tetrahydroisoquinoline (sTIQ) condensation product of dopamine (DA) and acetaldehyde, are reported to increase in chow-fed rats drinking ethanol/H2O ad libitum. However, our analyses showed that rat chow contains traces of SAL and, as previously reported, appreciable 3,4-dihydroxyphenylalanine (DOPA), a sTIQ precursor. To examine the effect of consumption of ethanol in a DOPA- and SAL-free diet on endogenous sTIQs, we analyzed two brain regions and blood plasma of rats undergoing prolonged intake (3 weeks and 23 weeks) of liquid diet containing 6.6% ethanol or isocaloric carbohydrate. SAL and three other DA-related sTIQs were quantitated using capillary gas chromatography/mass spectrometry in the selected ion mode with deuterated standards. In accord with studies on ethanol/chow-fed rats, sTIQ concentrations in hypothalamus were elevated after 3 weeks of ethanol, although after 23 weeks, hypothalamic sTIQs were either unchanged or reduced (O-methylated SAL). Furthermore, sTIQ concentrations in corpus striatum and, with one exception, plasma were not altered by ethanol ingestion for either duration. (However, 23 weeks of ethanol intake significantly reduced the striatal concentrations of DA and its acid metabolite, presumably reflecting neurotoxicity.) Reasoning that DOPA in diet might underlie the reported ethanol-dependent increases in striatal sTIQs, we found that L-DOPA supplementation (500 micrograms/rat/day) of EtOH/liquid diet-fed rats for 13 weeks tended to increase striatal SAL. Overall, the data indicate that elevations in endogenous sTIQ concentrations due to prolonged ethanol intake depend on the brain region, duration of intake, and even associated dietary constituents. In that regard, the higher striatal SAL concentrations in rats drinking ethanol ad libitum could have been facilitated by DOPA and perhaps SAL consumed in lab chow.

Oxidative decarboxylation of salsolinol-1-carboxylic acid to 1,2-dehydrosalsolinol: evidence for exclusive catalysis by particulate factors in rat kidney.

The decarboxylation of salsolinol-1-carboxylic acid (1-methyl-6,7-dihydroxy-1,2,3,4- tetrahydroisoquinoline-1-carboxylic acid), a novel endogenous catecholic adduct of dopamine and pyruvic acid, was examined in nuclei-free homogenates of rat liver, whole brain, and kidney, as well as in buffer only. Liquid chromatographic analysis of incubations for varying times (30 min to 5 h) showed that the tetrahydroisoquinoline substrate decarboxylated oxidatively, forming one product, 1-methyl-6,7-dihydroxy-3,4-dihydroisoquinolines (1,2-dehydrosalsolinol). No salsolinol was apparent, even with added NADPH. In buffer, decarboxylation occurred by an apparent oxygen radical-mediated process: it was stimulated by cupric ion or elevated pH, and was suppressed by EDTA, superoxide dismutase, metal ion removal with Chelex-100, or low pH (less than 6). In liver or brain, the conversion was qualitatively and quantitatively similar to that in buffer; thus there was no evidence for enzyme involvement. In kidney, however, dehydrosalsolinol formation was significantly greater than that in liver, brain, or buffer, and preboiling reduced it nearly to buffer values. The heat-labile kidney activity, displaying a pH maximum ca. 9, was localized in the particulate fractions. It was blocked completely by N-ethylmaleimide. Added superoxide dismutase was only slightly inhibitory; catalase and dimethyl sulfoxide, a hydroxyl radical trap, were uneffective. Lack of inhibition by indomethacin ruled against peroxidative involvement of kidney prostaglandin synthetase. Physiological amounts of a cofactor for amino acid decarboxylases, pyridoxal-5'-phosphate, also had no effect. The oxidative decarboxylation of 1-carboxylated salsolinol by kidney fractions appears mainly due to a sulfhydryl-containing particulate factor unique to or relatively concentrated in that organ. Its identity, substrate specificity, and possible significance, particularly in alcoholism, where elevated salsolinol-1-carboxylic acid levels have been reported, remain to be ascertained.

Inhibition of catechol-O-methyltransferase by 6,7-dihydroxy-3,4-dihydroisoquinolines related to dopamine: demonstration using liquid chromatography and a novel substrate for O-methylation.

We report that 6,7-dihydroxy-3,4-dihydroisoquinolines related to dopamine are potent inhibitors of catechol-O-methyltransferase (COMT), but are not apparent substrates for the enzyme in vitro or in vivo. Three dihydroxy (catecholic) dihydroisoquinolines, including the 1-benzyl (DesDHP) and the 1-methyl (DSAL) analogs, were found to inhibit COMT activity in rat liver supernatant more effectively than the well-known inhibitor, tropolone. Inhibition of O-methylation was uncompetitive with substrate, and O-methylated products of the catecholic dihydroisoquinolines were undetectable. For these in vitro studies, a facile liquid chromatographic assay was developed utilizing as a site-specific substrate, 1-methyl-6,7-dihydroxy-tetrahydroisoquinoline-1-carboxylate (salsolinol-1-carboxylate). This catechol produces only one phenolic product isomer when incubated with liver supernatant and S-adenosylmethionine. Following central injection of DSAL in rats, inhibition of brain COMT in vivo was indicated by the reduced brain levels of homovanillic acid, but not of 3,4-dihydroxyphenylacetic acid. Furthermore, O-methylated DSAL metabolites could not be detected in brain by liquid or gas chromatography. We suggest that 6,7-dihydroxy-dihydroisoquinolines are "nonmethylatable" COMT inhibitors because they exist as quinoidal tautomers resembling pyridones or tropolones rather than as catechols. Quinoid formation is supported by the fluorescence and ultraviolet spectra for DSAL and its O-methyl derivatives. The experiments reveal a new class of COMT inhibitors that may be of pharmacological and mechanistic value. Additionally, 3,4-dihydroisoquinolines could arise endogenously via oxidation of the 1,2,3,4-tetrahydroisoquinolines which are ingested or produced from cellular catecholamine condensations. However, it is unlikely that dihydroisoquinoline (e.g., DSAL) concentrations necessary to inhibit COMT significantly would be attained via endogenous pathways.