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Y Chiang

Publications and source records attributed to Y Chiang.

At least 19 recordsLinked to original sources
PubMed2006

The 2-oxocyclobutanecarboxylic acid keto-enol system in aqueous solution: a remarkable acid-strengthening effect of the cyclobutane ring.

Flash photolysis of 2-diazocyclopentane-1,3-dione in aqueous solution produced 2-oxocyclobutylideneketene, which underwent hydration to the enol of 2-oxocyclobutanecarboxylic acid; the enol then isomerized to the keto form of this acid. Rates of the ketene and enol reactions were measured in acid, base, and buffer solutions across the acidity range [H+] = 10(-1)-10(-13) M, and analysis of these data, together with rates of enolization of the keto form of 2-oxocyclobutanecarboxylic acid determined by bromine scavenging, gave keto-enol equilibrium constants as well as acidity constants of the keto and enol forms. The keto-enol equilibrum constants proved to be 2 orders of magnitude less than those reported previously for the next higher homolog, 2-oxocyclopentanecarboxylic acid, reflecting the difficulty of inserting a carbon-carbon double bond into a small, strained carbocyclic ring. The acidity constant of the enol group of 2-oxocyclobutanecarboxylate ion, on the other hand, is greater, by 4 orders of magnitude, than that of the corresponding enol in the cyclopentyl system. This remarkable increase in acidity with diminishing ring size is consistent with the enhanced s character of the orbitals used to make the exocyclic bonds of the smaller cyclobutane ring.

Journal Article↗
PubMed2003

The mandelamide keto-enol system in aqueous solution. Generation of the enol by hydration of phenylcarbamoylcarbene.

Flash photolysis of diazophenylacetamide in aqueous solution produced phenylcarbamoylcarbene, whose hydration generated a transient species that was identified as the enol isomer of mandelamide. This assignment is based on product identification and the shape of the rate profile for decay of the enol transient, through ketonization to its carbonyl isomer, as well as by the form of acid-base catalysis of and solvent isotope effects on the decay reaction. Rates of enolization of mandelamide were also determined, by monitoring hydrogen exchange at its benzylic position, and these, in combination with the ketonization rate measurements, gave the keto-enol equilibrium constant pK(E) = 15.88, the acidity constant of the enol ionizing as an oxygen acid, pQ(E)(a)= 8.40, and the acidity constant of the amide ionizing as a carbon acid pQ(K)(a)= 24.29. (These acidity constants are concentration quotients applicable at ionic strength = 0.10 M.) These results show the enol content and carbon acid strength of mandelamide, like those of mandelic acid and methyl mandelate, to be orders of magnitude less than those of simple aldehydes and ketones; this difference can be attributed to resonance stabilization of the keto isomers of mandelic acid and its ester and amide derivatives, through electron delocalization into their carbonyl groups from the oxygen and nitrogen substituents adjacent to these groups. The enol of mandelamide, on the other hand, again like the enols of mandelic acid and methyl mandelate, is a substantially stronger acid than the enols of simple aldehydes and ketones. This difference can be attributed to the electronegative nature of the oxygen and nitrogen substituents geminal to the enol hydroxyl group in the enols of mandelic acid and its derivatives; in support of this, the acidity constants of these enols correlate well with field substituent constants of these geminal groups.

Acetamides↗
PubMed2002

Flash photolytic generation and study of p-quinone methide in aqueous solution. An estimate of rate and equilibrium constants for heterolysis of the carbon-bromine bond in p-hydroxybenzyl bromide.

Flash photolysis of p-hydroxybenzyl acetate in aqueous perchloric acid solution and formic acid, acetic acid, biphosphate ion, and tris(hydroxymethyl)methylammonium ion buffers produced p-quinone methide as a short-lived species that underwent hydration to p-hydroxybenzyl alcohol in hydronium ion catalyzed (k(H(+)) = 5.28 x 10(4) M(-1) s(-1)) and uncatalyzed (k(uc) = 3.33 s(-1)) processes. The inverse nature of the solvent isotope effect on the hydronium ion-catalyzed reaction, k(H(+))/k(D(+)) = 0.41, indicates that this process occurs by rapid and reversible protonation of the quinone methide on its carbonyl carbon atom, followed by rate-determining capture of the p-hydroxybenzyl carbocation so produced by water, while the magnitude of the rate constant on the uncatalyzed process indicates that this reaction occurs by simple nucleophilic addition of water to the methylene group of the quinone methide. p-Quinone methide also underwent hydronium ion-catalyzed and uncatalyzed nucleophilic addition reactions with chloride ion, bromide ion, thiocyanate ion, and thiourea. The solvent isotope effects on the hydronium ion-catalyzed processes again indicate that these reactions occurred by preequilibrium mechanisms involving a p-hydroxybenzyl carbocation intermediate, and assignment of a diffusion-controlled value to the rate constant for reaction of this cation with thiocyanate ion led to K(SH) = 110 M as the acidity constant of oxygen-protonated p-quinone methide. In a certain perchloric acid concentration range, the bromide ion reaction became biphasic, and least-squares analysis of the kinetic data using a double-exponential function provided k(Br(-)) = 3.8 x 10(8) M(-1) s(-1) as the rate constant for nucleophilic capture of the p-hydroxybenzyl carbocation by bromide ion, k(ionz) = 8.5 x 10(2) s(-1) for ionization of the carbon-bromine bond of p-hydroxybenzyl bromide, and K = 4.5 x 10(5) M(-1) as the equilibrium constant for the carbocation-bromide ion combination reaction, all in aqueous solution at 25 degrees C. Comparisons are made of the reactivity of p-quinone methide with p-quinone alpha,alpha-bis(trifluoromethyl)methide as well as p-quinone methide with o-quinone methide.

Hydrocarbons, Brominated↗
PubMed2002

Flash photolytic generation of o-quinone alpha-phenylmethide and o-quinone alpha-(p-anisyl)methide in aqueous solution and investigation of their reactions in that medium. Saturation of acid-catalyzed hydration.

o-quinone alpha-phenylmethide was generated as a short-lived transient species in aqueous solution by flash photolysis of o-hydroxy-alpha-phenylbenzyl alcohol, and its rate of decay was measured in HClO4 and NaOH solutions as well as in CH3CO2H, H2PO4-, and HCO3- buffers. These data show that hydration of this quinone methide back to its benzyl alcohol precursor occurs by acid-, base-, and uncatalyzed routes. The acid-catalyzed reaction gives the solvent isotope effect kH+/kD+ = 0.34, whose inverse nature indicates that this reaction occurs via rapid preequilibrium protonation of the quinone methide on its carbonyl oxygen atom followed by rate-determining capture of the ensuing carbocationic intermediate by water, a conclusion supported by the saturation of acid catalysis in concentrated HClO4 solution. o-quinone alpha-(p-anisyl)methide was also generated by flash photolysis of the corresponding benzyl alcohol and of the p-cyanophenol ether of this alcohol as well, and its rate of decay was measured in HClO4 and NaOH solutions and in HCO2H, CH3CO2H, HN3, CF3CH2NH3+, imidazolium ion, H2PO4-, (CH2OH)3CNH3+, (CH3)3CPO3H-, and HCO3- buffers. Acid-, base-, and uncatalyzed hydration reaction routes were again found, and solvent isotope effects as well as saturation of acid catalysis, this time in dilute HClO4, confirmed a preequilibrium mechanism for the acid-catalyzed reaction. Analysis of the buffer data gave buffer-base rate constants that did not conform to the Brønsted relation, consistent with the expected nucleophilic nature of the buffer reactions.

Acids↗
PubMed2001

Keto-enol/enolate equilibria in the isochroman-4-one system. Effect of a beta-oxygen substituent.

The enol of 1-tetralone was generated flash photolytically, and rates of its ketonization were measured in aqueous HClO4 and NaOH solutions as well as in CH3CO2H, H2PO4(-), (CH2OH)3CNH3(+), and NH4(+) buffers. The enol of isochroman-4-one was also generated, by hydrolysis of its potassium salt and trimethylsilyl ether, and rates of its ketonization were measured in aqueous HClO4 and NaOH. Rates of enolization of the two ketones were measured as well. Combination of the enolization and ketonization data for isochroman-4-one gave the keto-enol equilibrium constant pK(E) = 5.26, the acidity constant of the enol ionizing as an oxygen acid p = 10.14, and the acidity constant of the ketone ionizing as a carbon acid p = 15.40. Comparison of these results with those for 1-tetralone shows that the beta-oxygen substituent in isochroman-4-one raises all three of these constants: K(E) by 2 orders of magnitude, by not quite 1 order of magnitude, and by nearly 3 orders of magnitude. The beta-oxygen substituent also retards the rate of hydronium-ion-catalyzed ketonization by more than 3 orders of magnitude. The origins of these substituent effects are discussed.

Journal Article↗
PubMed2001

Keto-enol/enolate equilibria in the N-acetylamino-p-methylacetophenone system. Effect of a beta-nitrogen substituent.

The cis-enol of N-acetylamino-p-methylacetophenone was generated flash photolytically and its rates of ketonization in aqueous HClO(4) and NaOH solutions as well as in HCO(2)H, CH(3)CO(2)H, H(2)PO(4)(-), (CH(2)OH)(3)CNH(3)(+), and NH(4)(+) buffers were measured. Rates of enolization of N-acetylamino-p-methylacetophenone to the cis-enol were also measured by hydrogen exchange of its methylene protons, and combination of the enolization and ketonization data gave the keto-enol equilibrium constant pK(E) = 5.33, the acidity constant of the enol ionizing as an oxygen acid pQ(a)(E)= 9.12, and the acidity constant of the ketone ionizing as a carbon acid pQ(a)(K)= 14.45. Comparison of these results with corresponding values for p-methylacetophenone itself shows that the N-acetylamino substituent raises all three of these equilibrium constants: K(E) by 3 orders of magnitude, Q(a)(E) by 1 order of magnitude, and Q(a)(K)by 4 orders of magnitude. This substituent also retards the rate of H+ catalyzed enol ketonization by 4 orders of magnitude. The origins of these substituent effects are discussed.

Acetophenones↗
PubMed2001

Flash photolytic generation of ortho-quinone methide in aqueous solution and study of its chemistry in that medium.

Flash photolysis of o-hydroxybenzyl alcohol, o-hydroxybenzyl p-cyanophenyl ether, and (o-hydroxybenzyl)trimethylammonium iodide in aqueous perchloric acid and sodium hydroxide solutions, and in acetic acid and biphosphate ion buffers, produced o-quinone methide as a short-lived transient species that underwent hydration back to benzyl alcohol in hydrogen-ion catalyzed (k(H+) = 8.4 x 10(5) M(-1) s(-1)) and hydroxide-ion catalyzed (k(HO)- = 3.0 x 10(4) M(-1) s(-1)) reactions as well as an uncatalyzed (k(UC) = 2.6 x 10(2) s(-1)) process. The hydrogen-ion catalyzed reaction gave the solvent isotope effect k(H+)/k(D)+ = 0.42, whose inverse nature indicates that this process occurs by rapid and reversible equilibrium protonation of the carbonyl oxygen atom of the quinone methide, followed by rate-determining capture of the carbocation so produced by water. The magnitude of the rate constant of the uncatalyzed reaction, on the other hand, indicates that this process occurs by simple nucleophilic addition of water to the methylene group of the quinone methide. Decay of the quinone methide is also accelerated by acetic acid buffers through both acid- and base-catalyzed pathways, and quantitative analysis of the reaction products formed in these solutions shows that this acceleration is caused by nucleophilic reactions of acetate ion rather than by acetate ion assisted hydration. Bromide and thiocyanate ions also accelerate decay of the quinone methide through both hydrogen-ion catalyzed and uncatalyzed pathways, and the inverse nature of solvent isotope effects on the hydrogen-ion catalyzed reactions shows that these reactions also occur by rapid equilibrium protonation of the quinone methide carbonyl oxygen followed by rate-determining nucleophilic capture of the ensuing carbocation. Assignment of an encounter-controlled value to the rate constant for the rate-determining step of the thiocyanate reaction leads to pK(a) = -1.7 for the acidity constant of the carbonyl-protonated quinone methide.

Acetic Acid↗
PubMed2001

Fetal intra-nigral ventral mesencephalon and kidney tissue bridge transplantation restores the nigrostriatal dopamine pathway in hemi-parkinsonian rats.

We have previously demonstrated that intranigral transplantation of fetal ventral mesencephalic (VM) tissue and nigrostriatal administration of glial cell line-derived neurotrophic factor (GDNF) restores striatal dopamine input in hemiparkinsonian rats. Since it has been found that GDNF is highly expressed in fetal kidney, we examined the possibility that fetal kidney tissue may provide trophic support, similar to GDNF, to an intranigral dopamine (DA) transplant and restore the nigrostriatal pathway. Adult Sprague-Dawley rats were anesthetized and unilaterally injected with 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. Completeness of the lesion was evaluated by measuring amphetamine-induced rotation. One month after 6-OHDA lesioning, fetal VM cells were grafted into the lesioned nigral area followed by transplantation of fetal kidney tissue or vehicle along a pathway from nigra to striatum. Animals receiving these transplants showed a significant decrease both in amphetamine-induced rotation and in postural asymmetry 1 to 3 months after grafting. Immunocytochemical studies demonstrated tyrosine hydroxylase (TH) positive fiber tracts in the lesioned striatum. Control animals that received vehicle injection after the intranigral graft or no transplantation showed no alterations in amphetamine-induced turning and no TH-positive fibers in the lesioned striatum. These results indicate that combinations of fetal nigral and kidney transplants may restore the nigrostriatal DA pathway in Parkinsonian rats. As fetal kidney contains a variety of trophic proteins, it may provide a synergistic admixture to optimally promote DA fiber outgrowth.

Amphetamine↗
PubMed2000

Generation of the enol of methyl mandelate by flash photolysis of methyl phenyldiazoacetate in aqueous solution and study of rates of ketonization of this enol in that medium.

Flash photolysis of methyl phenyldiazoacetate in aqueous solution produced phenylcarbomethoxycarbene, whose hydration generated a short-lived transient species that was identified as the enol isomer of methyl mandelate. This assignment is supported by the shape of the rate profile for decay of the enol transient, through ketonization to its carbonyl isomer, as well as by solvent isotope effects and the form of acid-base catalysis of the ketonization reaction. Comparison of the present results with previously published information on the enol of mandelic acid shows some interesting and readily understandable similarities and differences.

Azo Compounds↗
PubMed1999

Engraftment of MDR1 and NeoR gene-transduced hematopoietic cells after breast cancer chemotherapy.

To determine whether the multidrug resistance gene MDR1 could act as a selectable marker in human subjects, we studied engraftment of peripheral blood progenitor cells (PBPCs) transduced with either MDR1 or the bacterial NeoR gene in six breast cancer patients. This study differed from previous MDR1 gene therapy studies in that patients received only PBPCs incubated in retroviral supernatants (no nonmanipulated PBPCs were infused), transduction of PBPCs was supported with autologous bone marrow stroma without additional cytokines, and a control gene (NeoR) was used for comparison with MDR1. Transduced PBPCs were infused after high-dose alkylating agent therapy and before chemotherapy with MDR-substrate drugs. We found that hematopoietic reconstitution can occur using only PBPCs incubated ex vivo, that the MDR1 gene product may play a role in engraftment, and that chemotherapy may selectively expand MDR1 gene-transduced hematopoietic cells relative to NeoR transduced cells in some patients.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Specific down-regulation of annexin II expression in human cells interferes with cell proliferation.

The protein-tyrosine kinase substrate annexin II is a growth regulated gene whose expression is increased in several human cancers. While the precise function of this protein is not understood, annexin II is proposed to be involved in multiple physiological activities, including DNA synthesis and cell proliferation. Targeted disruption of the annexin II gene affects calcium signaling, tyrosine phosphorylation and apoptosis, indicating the important physiological role of this protein. We used a transient co-transfection assay to regulate annexin II expression in human HeLa, 293 and 293T cells, and measured the effects of annexin II down regulation on DNA synthesis and proliferation. Transfection of cells with an antisense annexin II vector results in inhibition of cell division and proliferation, with concomitant reduction in annexin II message and protein levels. Cellular DNA synthesis is significantly reduced in antisense transfected cells. Replication extracts made from antisense transfected cells have significantly reduced efficiency to support SV40 in vitro DNA replication, while the extracts made from sense transfected cells are fully capable of replication. Our results indicate an important role of annexin II in cellular DNA synthesis and cell proliferation.

Annexin A2↗
PubMed1999

Differential modulation by copper and zinc of P2X2 and P2X4 receptor function.

Differential Modulation by Copper and Zinc of P2X2 and P2X4 Receptor Function. The modulation by Cu2+ and Zn2+ of P2X2 and P2X4 receptors expressed in Xenopus oocytes was studied with the two-electrode, voltage-clamp technique. In oocytes expressing P2X2 receptors, both Cu2+ and Zn2+, in the concentration range 1-130 microM, reversibly potentiated current activated by submaximal concentrations of ATP. The Cu2+ and Zn2+ concentrations that produced 50% of maximal potentiation (EC50) of current activated by 50 microM ATP were 16.3 +/- 0.9 (SE) microM and 19.6 +/- 1.5 microM, respectively. Cu2+ and Zn2+ potentiation of ATP-activated current was independent of membrane potential between -80 and +20 mV and did not involve a shift in the reversal potential of the current. Like Zn2+, Cu2+ increased the apparent affinity of the receptor for ATP, as evidenced by a parallel shift of the ATP concentration-response curve to the left. However, Cu2+ did not enhance ATP-activated current in the presence of a maximally effective concentration of Zn2+, suggesting a common site or mechanism of action of Cu2+ and Zn2+ on P2X2 receptors. For the P2X4 receptor, Zn2+, from 0.5 to 20 microM enhanced current activated by 5 microM ATP with an EC50 value of 2.4 +/- 0.2 microM. Zn2+ shifted the ATP concentration-response curve to the left in a parallel manner, and potentiation by Zn2+ was voltage independent. By contrast, Cu2+ in a similar concentration range did not affect ATP-activated current in oocytes expressing P2X4 receptors, and Cu2+ did not alter the potentiation of ATP-activated current produced by Zn2+. The results suggest that Cu2+ and Zn2+ differentially modulate the function of P2X2 and P2X4 receptors, perhaps because of differences in a shared site of action on both subunits or the absence of a site for Cu2+ action on the P2X4 receptor.

Adenosine Triphosphate↗
PubMed1999

Paclitaxel chemotherapy after autologous stem-cell transplantation and engraftment of hematopoietic cells transduced with a retrovirus containing the multidrug resistance complementary DNA (MDR1) in metastatic breast cancer patients.

The MDR1 multidrug resistance gene confers resistance to natural-product anticancer drugs including paclitaxel. We conducted a clinical gene therapy study to determine whether retroviral-mediated transfer of MDR1 in human hematopoietic cells would result in stable engraftment, and possibly expansion, of cells containing this gene after treatment with myelosuppressive doses of paclitaxel. Patients with metastatic breast cancer who achieved a complete or partial remission after standard chemotherapy were eligible for the study. Hematopoietic stem cells (HSCs) were collected by both peripheral blood apheresis and bone marrow harvest after mobilization with a single dose of cyclophosphamide (4 g/m2) and daily filgrastim therapy (10 microg/kg/day). After enrichment for CD34+ cells, one-third of each collection was incubated ex vivo for 72 h with a replication-incompetent retrovirus containing the MDR1 gene (G1MD) in the presence of stem-cell factor, interleukin 3, and interleukin 6. The remaining CD34+ cells were stored without further manipulation. All of the CD34+ cells were reinfused for hematopoietic rescue after conditioning chemotherapy with ifosfamide, carboplatin, and etoposide regimen. After hematopoietic recovery, patients received six cycles of paclitaxel (175 mg/m2 every 3 weeks). Bone marrow and serial peripheral blood samples were obtained and tested for the presence of the MDR1 transgene using a PCR assay. Six patients were enrolled in the study and four patients received infusion of genetically altered cells. The ex vivo transduction efficiency, estimated by the PCR assay, ranged from 0.1 to 0.5%. Three of the four patients demonstrated engraftment of cells containing the MDR1 transgene. The estimated percentage of granulocytes containing the MDR1 transgene ranged from a maximum of 9% of circulating nucleated cells down to the limit of detection of 0.01%. One patient remained positive for the MDR1 transgene throughout all six cycles of paclitaxel therapy, whereas the other 2 patients showed a decrease in the number of cells containing the transgene to undetectable levels. Despite the low level of engraftment of MDR1-marked cells, a correlation was observed between the relative number of granulocytes containing the MDR1 transgene and the granulocyte nadir after paclitaxel therapy. No adverse reactions to the genetic manipulation procedures were detected. Therefore, engraftment of human HSCs transduced with the MDR1 gene can be achieved. However, the overall transduction efficiency and stable engraftment of gene-modified HSCs must be improved before MDR1 gene therapy and in vivo selection with anticancer drugs can be reliably used to protect cancer patients from drug-related myelosuppression.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Intercellular communication mediates the bystander effect during herpes simplex thymidine kinase/ganciclovir-based gene therapy of human gastrointestinal tumor cells.

A bystander effect is described when nontransduced or genetically unmodified cells are killed during death of genetically modified tumor cells transduced with a suicide gene. The "bystander effect" greatly enhances the efficacy of the herpes simplex virus-thymidine kinase/ganciclovir (HSV-TK/GCV) gene therapy approach for cancer. The mechanism of the bystander effect is controversial. In this study, we examined the role of intercellular gap junction communication (GJIC) for the bystander effect in human gastrointestinal tumor cells. Our results show that the extent of the bystander effect varied amongst the tumor cell lines; pancreatic cancer cells BXPC-3 exhibited excellent bystander effects in vitro and in vivo studies whereas other gastrointestinal tumor cell lines such as pancreatic cancer cells MIAPACA-2, and colon cancer cells HT-29 showed poor bystander effects. Bystander effects were only found in the presence of cell-to-cell contact. The extent of the bystander effect was independent of the level of HSV-TK activity in the transduced tumor cells and was correlated with GJIC as demonstrated by an in vitro dye-transfer assay. Expression of the mRNA levels of gap junction protein connexin 43 was 8- to 26-fold or greater and connexin 26 gene expression was 2- to 229-fold greater in BXPC-3 cells compared to HT-29, MIAPACA-2, and PANC3 cells. Our results suggest that intercellular communication is essential for the bystander effect. The correlation between GJIC and the extent of the bystander effect suggest a role for GJIC in mediating the bystander effect. Analysis of tumors for GJIC or expression of gap junction proteins may identify the subset of patients suitable for gene therapy with the HSV-TK/GCV approach.

Animals↗
PubMed1998

Retrovirus-mediated transfer of the herpes simplex type I thymidine kinase gene in alloreactive T lymphocytes.

We have demonstrated in previous studies that retrovirus-mediated transfer of the herpes simplex thymidine kinase (HS-tk) and neomycin phosphotransferase (neo) genes in CD3/IL-2 stimulated primary T lymphocytes followed by G418 selection resulted in T cells retaining both interleukin-2 (IL-2) and alloresponsiveness and specifically inhibited by ganciclovir (GCV). A clinical trial examining the therapeutic potential of such gene-modified donor T cells after allogeneic bone marrow transplantation is presently underway. In the present study, we have investigated the feasibility and consequences of replacing polyclonal stimulation of T cells by an allogeneic stimulation prior to retrovirus-mediated gene transfer. Exposure of allostimulated primary donor T lymphocytes to retrovirus-containing supernatant resulted in T cells resistant to G418 while maintaining a strong, GCV-sensitive, allogeneic response when subsequently restimulated with the initial allogeneic cells. Control nontransduced cells identically stimulated exhibited a weaker, GCV-insensitive, allogeneic proliferative response. The transduced T cells were also capable of GCV-sensitive alloreactivity when exposed to third-party cells with, however, a lower proliferative response than that seen with the allogeneic cells used for stimulation at the time of transduction. Importantly, this difference in the proliferative responses was not observed with control nontransduced cells identically stimulated. A similar response pattern was observed with respect to pre-cytotoxic T lymphocyte (CTL) frequencies. Overall, retrovirus-mediated gene transfer after an allogeneic stimulation can lead to efficient transduction and the pattern of alloreactivity of the HS-tk-expressing cells is consistent with the preferential transduction of alloantigen-specific dividing T cells. Such an approach could be used to generate cells both strongly alloreactive and GCV-sensitive for in vivo therapeutic use.

Antimetabolites↗
PubMed1998

HREM and STEM of intergranular films at zinc oxide varistor grain boundaries.

Grain boundaries in model ZnO-Bi2O3 and ZnO-Bi2O3-CoO varistors and a commercial multicomponent varistor have been characterized by high-resolution electron microscopy (HREM) and scanning transmission electron microscopy (STEM), in order to determine the relationship between Bi grain boundary segregation and formation of thin intergranular films. By controlling Bi2O3 content, applied pressure and temperature, the grain boundary Bi excess has been systematically varied from nearly zero to GammaBi = 1 x 1015 cm-2 ( approximately 1 monolayer), as measured by HB 603 STEM using an area-scan method. HREM shows that intergranular amorphous films are clearly distinguishable in samples with GammaBi > 8 x 1014 cm-2. These films range in thickness, depending on the Bi excess, from 0.6 to 1.5 nm. Similar films of approximately 1 nm thickness are widely observed in the commercial varistor. The composition of the films is a ZnO-Bi2O3 solid solution, which is in all cases more enriched in ZnO than the bulk eutectic liquid. The Bi-doped grain boundaries in ZnO varistors therefore contain an intergranular amorphous film which has not only an equilibrium thickness, but also a distinct equilibrium composition.

Journal Article↗