Core-level photoemission and work-function investigation of Na on Cu(110).
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Journal Article↗
Biomedical subjects
X Shi
Publications and source records attributed to X Shi.
Constraints on neutrino oscillations from big bang nucleosynthesis.
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Journal Article↗
Generation of free radicals in reactions of Ni(II)-thiol complexes with molecular oxygen and model lipid hydroperoxides.
The generation of free radicals from reactions of nickel(II)-thiol complexes with molecular oxygen and model lipid hydroperoxides was investigated by electron spin resonance (ESR) utilizing 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) as a spin trap. Incubation of nickel(II) [Ni(II)] with cysteine in an aerobic environment generated hydroxyl (.OH) radical, which then reacted with cysteine to generate a carbon-centered alkyl (.R) radical. Radical generation was inhibited under a nitrogen atmosphere. Model lipid hydroperoxides, cumene hydroperoxide, and t-butyl hydroperoxide enhanced the yield of these radicals and also generated an alkoxyl (.OR) radical. Radical yield decreased by approximately half under a nitrogen atmosphere. Although histidine did not cause radical formation in the reaction between Ni(II) and cumene hydroperoxide under aerobic conditions, the addition of histidine to a mixture containing Ni(II), cysteine, and cumene hydroperoxide under the same experimental conditions increased the yield of .R radical but lowered the yield of .OR and .OH radical adducts. It thus appears that histidine caused the .OH attack to be more site-specific. Similar results were obtained utilizing t-butyl hydroperoxide. Penicillamine or N-acetylcysteine yielded similar results except that under aerobic conditions, reaction between Ni(II) and N-acetylcysteine without hydroperoxide did not generate a significant concentration of free radicals. Under the same experimental conditions, cystine did not generate any detectable free radicals, suggesting an important role of the -SH group in Ni(II)-mediated free radical generation. The results indicate that free radical generation from the reaction of Ni(II)-thiol complexes and molecular oxygen, and/or lipid hydroperoxides, may play an important role in the mechanism(s) of Ni(II) toxicity and carcinogenesis.
Acetylcysteine↗
Coverage-dependent core-level binding-energy shifts of alkali-metal atoms on metal surfaces.
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Journal Article↗
Generation of free radicals from hydrogen peroxide and lipid hydroperoxides in the presence of Cr(III).
Free radical generation from H2O2 and lipid hydroperoxides in the presence of Cr(III) was investigated by electron spin resonance (ESR) spin trapping methodology. Incubation of Cr(III) with H2O2 at physiological pH generated hydroxyl (.OH) radical, the yield of which reached saturation level in about 6 min. Deferoxamine reduced the .OH radical yield by only about 20%, diethylenetriamine pentaacetic acid (DTPA) reduced it by about 70%, while cysteine, glutathione, and NADH exhibited no significant effect. The yield of .OH radical formation also depended on the pH being 15 times higher at pH 10 than that at pH 7.2. At pH 3.0, .OH radical generation became nondetectable, and addition of H2O2 to Cr(III) solution did not affect the intensity of the Cr(III) ESR signal while at pH 10, addition of H2O2 reduced the Cr(III) intensity by about 40%, showing that reaction of Cr(III) with H2O2 occurred only at higher pH. Incubation of Cr(III) with the model lipid hydroperoxides, cumene hydroperoxide and t-butyl hydroperoxide, generated lipid hydroperoxide-derived free radicals. Addition of deferoxamine or DTPA had a minor inhibitory effect on that generation. These results show that Cr(III) is capable of producing free radicals from H2O2 and lipid hydroperoxides, which may have significant implications regarding the mechanism of chromium-induced carcinogenesis.
Benzene Derivatives↗
One-electron reduction of vanadium(V) by flavoenzymes/NADPH.
The biochemical mechanism underlying vanadate-stimulated NAD(P)H oxidation is controversial. Some reports favor an exclusive role for a superoxide (O2(-)-mediated radical chain reaction, while others cite data that suggest a contribution from O2(-)-independent enzymatic pathways. We recently reported that a vanadium(IV) species accumulates over a period of about 30 min in phosphate-buffer mixtures of vanadate, NAD(P)H, and a flavoenzyme such as glutathione reductase, lipoyl dehydrogenase, or ferredoxin-NADP+ oxidoreductase. The concentration of this vanadium(IV) species was found to depend critically on the simultaneous presence of the enzyme and NAD(P)H, but not on superoxide dismutase, or a nitrogen atmosphere. It was thus concluded that the flavoenzyme/NAD(P)H system acts as a vanadate reductase. However, a subsequent report put forth an alternative hypothesis in which the accumulation of this vanadium(IV) species is ascribed to direct reduction of vanadate by NAD(P)H itself, starting when buffer-dissolved molecular O2 and H2O2 have been depleted. We have reexamined our earlier data, and carried out new measurements to evaluate the effect of dissolved oxygen and related factors on the kinetics of vanadium(IV) generation in vanadate/NAD(P)H/flavoenzyme mixtures. The new data support our earlier suggestion that the above-mentioned flavoenzymes can indeed act as NAD(P)H-dependent vanadate reductases.
Cyclic N-Oxides↗
Vanadate-mediated hydroxyl radical generation from superoxide radical in the presence of NADH: Haber-Weiss vs Fenton mechanism.
The mechanism of hydroxyl (.OH) radical generation from O2- and H2O2 by vanadate [V(V)] and the role of NADH in this reaction have been investigated using electron spin resonance (ESR) and spin trapping techniques. The results show that the reaction of V(V) with O2- (generated via xanthine/xanthine oxidase) does not generate any ESR detectable V(IV) ion or .OH radical and the addition of H2O2 has little effect on the radical yield. In the presence of NADH, however, the xanthine/xanthine oxidase/V(V) system generates .OH as well as V(IV), the formation of both of which could be suppressed by superoxide dismutase. Catalase inhibits the .OH formation but enhances V(IV) generation. Reaction of V(V) with NADH alone in the presence of phosphate buffer also causes .OH radical generation albeit at a much reduced rate, and superoxide dismutase reduces the .OH yield. These observations indicate, in contrast to earlier reports, that O2- does not reduce V(V) to V(IV) in the absence of NADH. It is concluded that vanadate generates the .OH radical via not a Haber-Weiss but a Fenton-like reaction [V(IV) + H2O2-->V(V) + .OH+OH-], the V(IV) and H2O2 being generated by V(V)-stimulated, O(2-)-dependent NADH oxidation.
Cyclic N-Oxides↗
Effect of carnosine homocarnosine and anserine on hydroxylation of the guanine moiety in 2'-deoxyguanosine, DNA and nucleohistone with hydrogen peroxide in the presence of nickel(II).
The oxidation of 2'-deoxyguanosine (dG) to 8-hydroxy-2'-deoxyguanosine (8-OH-dG) in free dG and the dG residues of DNA and nucleohistone with H2O2 in the presence of Ni(II) and histidyl oligopeptides, carnosine, homocarnosine and anserine was studied at physiological pH. The oxidation of free dG with H2O2 was enhanced by the oligopeptides, but not by Ni(II) alone. Much greater enhancement was produced by equimolar mixtures of Ni(II) with any of the oligopeptides or with L-histidine. In contrast, the oxidation of dG residues in DNA and nucleohistone with H2O2 was not affected by the oligopeptides, but was enhanced by Ni(II). The latter enhancement remained practically unchanged when Ni(II) was accompanied by equimolar amounts of homocarnosine or anserine, whereas carnosine tended to attenuate that enhancement. The extent of formation of 8-OH-dG in free dG depended on time and concentration of H2O2 and was highest at pH 7.4. An electron spin resonance study of the reaction mixture containing H2O2, Ni(II), carnosine, homocarnosine and/or anserine provided evidence for the generation of .OH radical in the reaction media. Although it has previously been concluded that carnosine, anserine and homocarnosine might serve as anti-oxidants, the present study does not support that conclusion and shows that these compounds may even act as pro-oxidants, especially when they are complexed with Ni(II). The results suggest that carnosine, homocarnosine and anserine, by enhancing oxidation of the free dG pool, may potentiate the carcinogenic effects of Ni(II) since the resulting 8-OH-dG can be misincorporated into DNA and thus produce a mutagenic lesion.
Anserine↗
Modulation of acid-induced amino acid decarboxylase gene expression by hns in Escherichia coli.
Biodegradative arginine decarboxylase and lysine decarboxylase, encoded by adi and cadA, respectively, are induced to maximal levels when Escherichia coli is grown anaerobically in rich medium at acidic pH. Mutants formed by transposon mutagenesis, namely, GNB725, GNB729, GNB88, GNB824, and GNB837, exhibited considerably elevated expression at pH 8.0 compared with the corresponding parental strain. Southern hybridization and chromosome mapping showed that the above mutants contained a transposon within the hns gene. Several plasmids from an E. coli library able to complement these mutants by restoring normal pH induction were independently isolated and were found to contain the hns gene. These results suggest a role for the DNA-binding protein H-NS in affecting the activation of these acid-induced genes.
Bacterial Outer Membrane Proteins↗
Hemodynamic responses to graded lower body positive pressure.
Fourteen healthy young men were exposed to progressive increases in lower body positive pressure (LBPP) from 0 to 40 Torr in the supine position. Central venous pressure (CVP) increased 1.09 mmHg (P < 0.05) at 5 Torr LBPP. Between 20 and 40 Torr LBPP CVP increased 0.85 mmHg, resulting in a total increase of 2.06 mmHg (P < 0.05). During 0-20 Torr LBPP mean arterial pressure (MAP) increased from 86 to 89 mmHg with a slope of 0.15 mmHg/Torr LBPP. Stroke volume and cardiac output were significantly increased at 20 Torr LBPP. Beyond 20 Torr LBPP, MAP increased to 95 mmHg at 40 Torr (P < 0.05) with a slope of 0.32 mmHg/Torr LBPP. Forearm blood flow increased above rest at 40 Torr LBPP (P < 0.05). However, neither peripheral nor forearm vascular resistance decreased significantly from rest. Despite the significant increases in MAP, heart rate was unchanged above 20 Torr LBPP. These data suggest that LBPP produces increases in CVP at 0-20 Torr by translocation of blood volume from the legs to the thorax. At LBPP > 20 Torr, further increases in CVP and MAP were produced by other mechanisms possibly related to an activation of intramuscular pressure-sensitive receptors.
Adult↗
Carotid baroreflex responsiveness to lower body positive pressure-induced increases in central venous pressure.
Lower body positive pressure (LBPP) was applied at 4 and 30 Torr to increase central venous pressure (CVP). CVP increased with LBPP (r = 0.55, P < 0.01), and the increases were significant at 4 and 30 Torr (7.4 and 7.8 mmHg) from the control (6.0 mmHg). During LBPP cardiac output increased, which was significantly related to the increase in CVP (r = 0.63, P < 0.01). The carotid baroreflex was elicited by trains of neck pressure and suction from 40 to -65 Torr. The carotid-cardiac and carotid-vasomotor baroreflex responses were assessed by determining the maximal gains of heart rate (HR) interval and intraradial mean arterial pressure (MAP) to changes in carotid sinus pressure using a logistic model. The carotid-cardiac and carotid-vasomotor baroreflex gains were negatively related to LBPP, and at 30 Torr, both gains (5.6 ms/mmHg and -0.14 mmHg/mmHg) were significantly smaller than the control (12.4 ms/mmHg and -0.24 mmHg/mmHg). The decreases in carotid-cardiac and carotid-vasomotor baroreflex sensitivity during LBPP were primarily associated with the increases in CVP (r = -0.52, P < 0.01, and r = -0.74, P < 0.01, respectively). These data suggest that the increases in CVP and/or central blood volume diminish the sensitivity of the carotid baroreflex control of HR and MAP by enhancing the tonic inhibitory influence from the cardiopulmonary baroreceptors.
Adult↗
Aortic baroreflex control of heart rate during hypertensive stimuli: effect of fitness.
We examined the aortic baroreflex control of heart rate (HR) in seven healthy young men of average fitness (AF) and seven of high fitness (HF). The fitness level was determined by maximal oxygen uptake (AF = 42.9 +/- 1.1, HF = 62.3 +/- 1.8 ml.kg-1.min-1). Aortic baroreflex control of HR was determined during a steady-state increase of mean arterial pressure (MAP; AF, +15.0 +/- 2.1 and HF, +18.3 +/- 0.8 mmHg) with phenylephrine (PE) infusion combined with positive neck pressure (NP; AF, 18 +/- 2.0 and HF, 20 +/- 0.8 mmHg) to counteract the increased carotid sinus pressure and with low levels of lower body negative pressure to counteract the increased central venous pressure. There was no group difference in the increased MAP or NP, nor was there stage difference in MAP within either group during PE infusion. However, the isolated cardiac-aortic baroreflex gains (i.e., delta HR/delta MAP) were significantly less in the HF (0.16 +/- 0.02 and 0.14 +/- 0.03 beats.min-1.mmHg-1) than in the AF (0.52 +/- 0.08 and 0.59 +/- 0.07 beats.min-1.mmHg-1) subjects at PE + NP and PE + NP + lower body negative pressure. We concluded that during steady-state increases in MAP, the sensitivity of aortic baroreflex control of HR was significantly less in the HF than in the AF subjects.
Adolescent↗
Forearm vascular responses to baroreceptor unloading at the onset of dynamic exercise.
To determine the extent to which reflexes accompanying muscular exercise (associated with central command) interact with cardiopulmonary (CP) baroreceptor-mediated reflexes controlling forearm vascular resistance (FVR), we examined the forearm vasoconstrictor response at the onset of dynamic exercise, with and without CP baroreflex unloading, in 10 physically active men. CP baroreceptors were unloaded by application of lower body negative pressure (LBNP) at rest and during five 4-min bouts of supine exercise at 25 and 32 degrees C. Exercise intensities were 10 (essentially no load) and 100 W, and LBNP was applied at -10, -20, -30, and -40 mmHg during rest and at -20 and -40 mmHg during exercise. Resting FVR was 33.0 +/- 3.2 and 14.0 +/- 2.7 resistance units, and cardiac stroke volume (SV) was 117 +/- 7 and 126 +/- 9 ml/beat at 25 and 32 degrees C, respectively. We found a linear relationship between the increase in FVR and decrease in SV during LBNP; the slope of the relationship was significantly lower at 32 degrees C (FVR = 51.7-0.29SV) than at 25 degrees C (FVR = 123-0.79SV). At the onset of 100-W exercise without LBNP, FVR increased significantly to 50.2 +/- 9.0 and 21.2 +/- 3.2 units at 25 and 32 degrees C, respectively, whereas SV was unchanged. Application of -40-mmHg LBNP reduced SV significantly to 68 +/- 5 and 71 +/- 6 ml/beat and increased FVR significantly to 89.0 +/- 11.3 and 36.3 +/- 7.6 units at 25 and 32 degrees C, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Mechanisms of hydroxyl free radical-induced cellular injury and calcium overloading in alveolar macrophages.
Excessive production of reactive oxygen radicals by alveolar macrophages is proposed to play an important role in oxidative lung injury. A major product oxygen radical formation is the highly reactive hydroxyl radical (.OH) generated via a biologic Fenton reaction. In addition to its known ability to induce lipid peroxidation, recent studies have suggested that the .OH may exert its cytotoxic effect through the alteration of [Ca2+]i homeostasis. To test this potential mechanism as well as to investigate the relationship between .OH and Ca2+ overloading in cytotoxic injury, isolated rat alveolar macrophages were exposed to externally generated radical system, H2O2 (0.01 to 1 mM) and Fe2+ (1 mM) and their [Ca2+]i levels and cell injury were monitored using quantitative fluorescence microscopy with the aid of the specific Ca2+ indicator, Fura-2, and membrane integrity indicator, propidium iodide. Electron spin resonance measurements using the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) confirmed the production of the .OH radical by this system. Upon the addition of the radicals, the macrophages displayed a rapid initial rise in [Ca2+]i which was followed by a slower but more pronounced [Ca2+]i elevation that reached a level 3 to 5 times higher than the basal level. This process preceded cell death as evident by nuclear propidium iodide fluorescence. Depletion of extracellular Ca2+ inhibited both the [Ca2+]i response and cell injury. Preincubation of the cells with the Ca2+ channel blocker verapamil or .OH radical scavenger mannitol similarly inhibited the [Ca2+]i rise and loss of viability. Firefly luciferase assay of cellular ATP content demonstrated that the alterations in [Ca2+]i following .OH treatment preceded the depletion of ATP.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[Morphological study on acupuncture in interfering experimental cerebral infarction in rats. II. Change of ischemic area in cerebral interior].
Occluding unilateral middle cerebral artery (MCAO) of rat, the ischemic volume within cerebrum shown by nitroblue tetrazolium (N-BT) histochemistry method and effect of acupuncture were observed dynamically. 18 hs after MCAO, the ischemic area began to extend from cerebral cortex into subcortical area. 36 hs after MCAO, there was a large ischemic area in cortical and subcortical area, whose volume occupied 20.7 percent of the whole. Whereas the ischemic area in the cortex disappeared in the acupuncture group, the ischemic volume reduced to 6.3 percent of the whole. The experiment pointed out that the acupuncture is an effective therapeutic procedure for cerebral infarction.
Acupuncture Therapy↗
Laboratory interproximal access efficacy comparison of a rippled bristles toothbrush and a flat manual toothbrush.
The Colgate Plus Rippled Bristles toothbrush and the Oral-B 40 toothbrush were compared using a laboratory device designed to stimulate clinical toothbrushing motions and pressures and measure interproximal access efficacy. The toothbrushing time was sixty seconds for each vertical or horizontal toothbrushing sequence and for each of the three brushing weights tested (250, 500 or 750 grams). Interproximal access efficacy was determined by measuring the maximum width of the brushing stroke on pressure-sensitive paper placed around simulated anterior or posterior teeth. Twenty-four toothbrushes of each design were evaluated for each toothbrushing motion, tooth shape and toothbrushing weight. With vertical toothbrushing motions, the Colgate Rippled toothbrush had significantly higher (p < 0.001) interproximal access efficacy means compared to the Oral-B 40 toothbrush, on anterior tooth shapes at the 250 and 500 grams of brushing weights and on posterior tooth shapes at all of the brushing weights tested. Using the horizontal toothbrushing motion on anterior teeth, the interproximal access efficacy for the Colgate Rippled toothbrush was significantly higher (p < 0.05) than the Oral-B 40 toothbrush at 250 and 500 grams of brushing weights. With horizontal toothbrushing across posterior-shaped teeth, interproximal access efficacy values for the Colgate Rippled toothbrush were significantly higher (p < 0.05-0.001) than the Oral-B 40 toothbrush at all of the brushing weights tested. When the various parameters tested were combined for all brushing weights, both brushing motions or both tooth shapes, interproximal access efficacy means for the Colgate Rippled toothbrush were higher (p < 0.05-0.001) than the combined means for the Oral-B toothbrush. When all factors tested were combined, total interproximal access efficacy for the Colgate Rippled toothbrush was significantly superior (p<0.001) to the Oral-B 40 toothbrush.
Analysis of Variance↗
[Morphological study on acupuncture in interfering experimental cerebral infarction in rat. I. Compensation of cerebral PIA mater artery in cerebral surface].
Occluding unilateral middle cerebral artery (MCAo) of rat, the compensatory blood vessels (CBV) within ischemic area in cerebral surface shown by cerebral perfusion and effect of acupuncture were observed dynamically. Perfusing immediately after MCAo, there was no any blood vessel in the ischemic area. In acupuncture group, the CBV had extended a lot from anastomotic network of cerebral pia mater (ACA-MCA, PCA-MCA) located in marginal zone of ischemic area 3 hs after MCAo. 6.24 and 48 hs after MCAo, the CBV increased much more than control group (non-acupuncture) P < 0.01. The experiment pointed out that there existed a serious vasospasm in the MCA system in initial stage of MCAo, which led up to decompensation in the ischemic area. The acupuncture can remit the vasospasm, and reverse the deteriorated process in early.
Acupuncture Therapy↗
[An evaluation of DNA fingerprinting with oligonucleotide probe for forensic purposes].
The synthetic oligonucleotide probe (CAC)5/(GTG)5 for DNA, fingerprinting was studied in this paper. The incomplete pattern of DNA fingerprints was obtained from bloodstains up to three years old, which were kept at room temperature. The identical results were achieved from various human organ tissues of the same individual. DNA fingerprints from vaginal swabs was the same as that obtained from the male donor's blood. The discernible DNA fingerprints were obtained with as little as 250ng of genomic DNA. Besides, using restriction enzyme Hae III instead of Hinf I to digest human DNA, the highly polymorphic hybridization pattern was also obtained. A practical case was tested by Hinf I and Hae III digestion, respectively. The results demonstrated that the (CAC)5/(GTG)5 was a suitable probe for DNA fingerprinting in forensic practice.
Base Sequence↗