Biomedical subjects

Nan Yao

Publications and source records attributed to Nan Yao.

13 recordsLinked to original sources

PubMed2006

Characterization and analysis of new catalysts for a direct ethanol fuel cell.

A direct ethanol fuel cell offers an attractive, fairly high density, energy source, if an electrochemical system can be developed that efficiently carries out the 12-electron oxidation of ethanol to carbon dioxide and water. To that end, new catalyst systems must be developed along with fuel cell operating conditions that encourage the complete oxidation of ethanol, as opposed to the presently available platinum on carbon systems that tend to produce acetaldehyde (two-electron oxidation) or acetic acid (four-electron oxidation) products. It is found that a composite nanoparticulate catalyst containing platinum and tin oxide or platinum indium tin oxide allows the partial conversion of ethanol to its 12-electron oxidation products. Catalysts of this type can be formed using a modified polyol process. Elevation of the operating temperature of a proton exchange membrane fuel cell using the indicated catalysts to 130 degrees C facilitates the production of carbon dioxide and provides an improved current-voltage response.

Journal Article↗

PubMed2006

Induction of apoptotic cell death leads to the development of bacterial rot caused by Pseudomonas cichorii.

Pseudomonas cichorii is the major causal agent of bacterial rot of lettuce. Collapse and browning symptoms were observed in lettuce leaf tissue from 15 to 24 h after inoculation (HAI) with P. cichorii; superoxide anion generation was detected at 1 to 6 HAI; and cell death was induced at 6 HAI, reaching a maximum at approximately 9 and 12 HAI. Heterochromatin condensation and DNA laddering also were observed within 3 HAI. Pharmacological studies showed that induction of cell death and DNA laddering was closely associated with de novo protein synthesis, protein kinase, intracellular reactive oxygen species, DNase, serine protease, and caspase III-like protease. Moreover, chemicals, which inhibited the induction of cell death and DNA laddering, also suppressed the development of disease symptoms. These results suggest that apoptotic cell death might be closely associated with the development of bacterial rot caused by P. cichorii.

Anions↗

PubMed2006

[CAG repeats of DNA polymerase gamma in Chinese males and relationship of idiopathic male infertility to CAG repeats].

OBJECTIVE: To analyze the polymerase gamma(Polg) gene polymorphisms in Chinese idiopathic infertile males and evaluate the correlation of the polymorphisms with male infertility. METHODS: We conducted a study of Polg CAG repeats in the sperm or blood DNA of 55 asthenospermia patients, 57 oligospermia patients, 34 azoospermia patients, and 104 controls with PCR and GeneScan. Phenotypic data were available in all the subjects, including semen parameters, and clinical profiles. RESULTS: The frequency of 10/not 10 CAG genotype in asthenospermia patients was higher than in the other groups, but with no significance. CONCLUSION: Our findings have shown for the first time that there exits an ethnic difference between Chinese and European males in the number of CAG repeats of Polg gene, and that 10/not 10 CAG genotype may affect sperm motility.

Adult↗

PubMed2005

Arabidopsis ACCELERATED CELL DEATH2 modulates programmed cell death.

The Arabidopsis thaliana chloroplast protein ACCELERATED CELL DEATH2 (ACD2) modulates the amount of programmed cell death (PCD) triggered by Pseudomonas syringae and protoporphyrin IX (PPIX) treatment. In vitro, ACD2 can reduce red chlorophyll catabolite, a chlorophyll derivative. We find that ACD2 shields root protoplasts that lack chlorophyll from light- and PPIX-induced PCD. Thus, chlorophyll catabolism is not obligatory for ACD2 anti-PCD function. Upon P. syringae infection, ACD2 levels and localization change in cells undergoing PCD and in their close neighbors. Thus, ACD2 shifts from being largely in chloroplasts to partitioning to chloroplasts, mitochondria, and, to a small extent, cytosol. ACD2 protects cells from PCD that requires the early mitochondrial oxidative burst. Later, the chloroplasts of dying cells generate NO, which only slightly affects cell viability. Finally, the mitochondria in dying cells have dramatically altered movements and cellular distribution. Overproduction of both ACD2 (localized to mitochondria and chloroplasts) and ascorbate peroxidase (localized to chloroplasts) greatly reduces P. syringae-induced PCD, suggesting a pro-PCD role for mitochondrial and chloroplast events. During infection, ACD2 may bind to and/or reduce PCD-inducing porphyrin-related molecules in mitochondria and possibly chloroplasts that generate reactive oxygen species, cause altered organelle behavior, and activate a cascade of PCD-inducing events.

Apoptosis↗

PubMed2005

Nanostructure of Er3+ doped silicates.

We demonstrate nanostructural evolution resulting in highly increased photoluminescence in silicates doped with Er3+ ions. High-resolution transmission electron microscopy (HRTEM) imaging, nano-energy dispersed X-ray (NEDX) spectroscopy, X-ray diffraction (XRD) and photoluminescence analysis confirm the local composition and structure changes of the Er3+ ions upon thermal annealing. We studied two types of amorphous nanopowder: the first is of the composition SiO2/18Al2O3/2Er2O3 (SAE), synthesized by combustion flame-chemical vapor condensation, and the second is with a composition of SiO2/8Y2O3/2Er2O3 (SYE), synthesized by sol-gel synthesis (composition in mol%). Electron diffraction and HRTEM imaging clearly show the formation of nanocrystallites with an average diameter of approximately 8 nm in SAE samples annealed at 1000 degrees C and SYE samples annealed at 1200 degrees C. The volume fraction of the nanocrystalline phase increased with each heat treatment, eventually leading to complete devitrification at 1400 degrees C. Further XRD and NEDX analysis indicates that the nanocrystalline phase has the pyrochlore structure with the formula Er(x)Al(2-x)Si2O7 or Er(x)Y(2-x)Si2O7 and a surrounding silica matrix.

Journal Article↗

PubMed2005

Sodium chloride enhanced oligomerization of L-glutamic acid in aqueous solution.

The presence of NaCl was found to significantly enhance the formation of longer peptides in N,N'-carbonyldiimidazole induced oligomerization of L-glutamic acid in homogeneous aqueous solution. The enhancement was detected in the presence of as low as 0.01-M NaCl and the highest yield of longer oligomers was achieved in the presence of 1-M NaCl. The possible prebiotic relevance is discussed.

Chromatography, High Pressure Liquid↗

PubMed2004

Nitric oxide and reactive oxygen species do not elicit hypersensitive cell death but induce apoptosis in the adjacent cells during the defense response of oat.

Nitric oxide (NO) acts as a signaling molecule in many cellular responses in plants and animals. Oat plants (Avena sativa L.) evoke the hypersensitive response (HR), which shares morphological and biochemical features with mammalian apoptosis, such as DNA laddering and heterochromatin condensation, in response to the avirulent crown rust fungus (Puccinia coronata f. sp. avenae). We examined the role of NO and reactive oxygen species (ROS) in the initiation of hypersensitive cell death, which is induced by direct contact with the pathogen, and apoptotic cell death in the adjacent cells. Cytofluorimetric analysis using the fluorescent NO probe DAF and the H2O2 probe DCF demonstrated that NO and H2O2 were generated simultaneously in primary leaves at an early stage of the defense response. The NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) markedly enhanced H2O2 accumulation detected by 3,3-diaminobenzidine staining and DCF, whereas treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP) strongly suppressed it. Superoxide dismutase (SOD) increased NO accumulation, suggesting that endogenous NO may modulate the level of H2O2 by interacting with O2- in the HR lesion. Cytological observation showed that administration of cPTIO, SNAP, or SOD had no effect on elicitation of hypersensitive cell death, but clearly reduced heterochromatin condensation in the nearby cells and DNA laddering. These findings indicate that NO and ROS are not essential mediators for the initiation of hypersensitive cell death. However, NO and O2- but not H2O2 are required for the onset of apoptotic cell death in the adjacent cells, where excess NO may exert its anti-apoptotic function by regulating cellular redox state.

Apoptosis↗

PubMed2004

The mitochondrion--an organelle commonly involved in programmed cell death in Arabidopsis thaliana.

Plant cells undergoing programmed cell death (PCD) at late stages typically show chromatin condensation and endonucleolytic cleavage prior to obvious membrane or organelle ultrastructural changes. To investigate possible early PCD-associated events, we used microscopic observations and flow cytometry to quantitate mitochondrial membrane potential (DeltaPsim) changes during PCD at the single cell and population levels using Arabidopsis protoplasts. A DeltaPsim loss was commonly induced early during plant PCD and was important for PCD execution, as evidenced by the concomitant reduction of the change in DeltaPsim and PCD by cyclosporin A, which inhibits mitochondrial permeability transition pores in animal cells. DeltaPsim loss occurred prior to nuclear morphological changes and was only associated with mitochondrial cytochrome c release (an apoptotic trigger in animals) in response to one of three PCD elicitors. Three different stimuli in wild type implicated DeltaPsim changes in PCD: ceramide, protoporphyrin IX, and the hypersensitive response elicitor AvrRpt2. Additionally, the behavior of the conditional ectopic cell death mutant accelerated cell death2 and ACD2-overproducing plants also implicated DeltaPsim alteration as key for PCD execution. Because ACD2 is largely a chloroplast component in mature plants, the observation that the cell death in acd2 mutants requires changes in mitochondrial functions implicates communication between chloroplasts and mitochondria in mediating PCD activation. We suggest that DeltaPsim loss is a common early marker in plant PCD, similar to what has been documented in animals. However, unlike in animal cells, in plant cells, mitochondrial cytochrome c release is not an obligatory step in PCD control.

Apoptosis↗

PubMed2004

The role and regulation of programmed cell death in plant-pathogen interactions.

It is commonly known that animal pathogens often target and suppress programmed cell death (pcd) pathway components to manipulate their hosts. In contrast, plant pathogens often trigger pcd. In cases in which plant pcd accompanies disease resistance, an event called the hypersensitive response, the plant surveillance system has learned to detect pathogen-secreted molecules in order to mount a defence response. In plants without genetic disease resistance, these secreted molecules serve as virulence factors that act through largely unknown mechanisms. Recent studies suggest that plant bacterial pathogens also secrete antiapoptotic proteins to promote their virulence. In contrast, a number of fungal pathogens secrete pcd-promoting molecules that are critical virulence factors. Here, we review recent progress in determining the role and regulation of plant pcd responses that accompany both resistance and susceptible interactions. We also review progress in discerning the mechanisms by which plant pcd occurs during these different interactions.

Apoptosis↗

PubMed2004

Scanning probe microscopy in catalysis.

This review discusses the recent progress in the application of scanning probe microscopy (SPM) in catalysis. SPM proves to be an invaluable technique for imaging catalytic surfaces and interfaces. Most SPM research is related to the structural and morphological transformation associated with catalyst preparation and use. Real-time SPM observation of surface dynamics including adsorption, diffusion and reaction, provides invaluable insights to the mechanism of catalysis. SPM is also used to shape and manipulate surfaces and surface processes. Fabrication of nanostructured catalysts, direct manipulation of adsorbed atoms and molecules and tip-mediated reactions are some examples of new SPM approach in catalyst research.

Adsorption↗

PubMed2003

Ceramides modulate programmed cell death in plants.

The balance between the bioactive sphingolipid ceramide and its phosphorylated derivative has been proposed to modulate the amount of programmed cell death (PCD) in eukaryotes. We characterized the first ceramide kinase (CERK) mutant in any organism. The Arabidopsis CERK mutant, called accelerated cell death 5, accumulates CERK substrates and shows enhanced disease symptoms during pathogen attack and apoptotic-like cell death dependent on defense signaling late in development. ACD5 protein shows high specificity for ceramides in vitro. Strikingly, C2 ceramide induces, whereas its phosphorylated derivative partially blocks, plant PCD, supporting a role for ceramide phosphorylation in modulating cell death in plants.

Apoptosis↗

PubMed2002

Mitochondrial oxidative burst involved in apoptotic response in oats.

Apoptotic cell response in oats is induced by victorin, a host-selective toxin secreted by Cochliobolus victoriae and thought to exert toxicity by inhibiting mitochondrial glycine decarboxylase (GDC) in Pc-2/Vb oats. We examined the role of mitochondria, especially the organelle-derived production of reactive oxygen species (ROS), in the induction of apoptotic cell death. Cytofluorimetric analysis showed that victorin caused mitochondrial deltaPsim breakdown and mitochondrial oxidative burst. Ultrastructural analysis using a cytochemical assay based on the reaction of H2O2 with CeCl3 detected H2O2 eruption at permeability transition pore-like sites on the mitochondrial membrane in oat cells treated with victorin. ROS generation preceded the apoptotic cell responses seen in chromatin condensation and DNA laddering. Both aminoacetonitrile (a specific GDC inhibitor) and antimycin A (a mitochondrial complex III inhibitor) also induced mitochondrial H2O2 eruption, and led to the apoptotic response in oat cells. ROS scavengers such as N-acetyl-l-cysteine and catalase suppressed the mitochondrial oxidative burst and delayed chromatin condensation and DNA laddering in the victorin- or antimycin A-treated leaves. These findings indicate possible involvement of mitochondria, especially mitochondrial-derived ROS generation, as an important regulator in controlling apoptotic cell death in oats.

Acetylcysteine↗

PubMed2002

Apoptotic cell death is a common response to pathogen attack in oats.

We have examined the characteristics of cell death induced by pathogen infection in oats with respect to following hallmark apoptotic features: DNA laddering, chromatin condensation, and electron microscopic-terminal deoxynucleotidyl transferase-mediated UTP end labeling positive response. A wide range of plant pathogens representing different levels of parasitism in susceptible and resistant interactions were used for the inocula, which include (i) an obligate parasite, Puccinia coronata f. sp. avenae (the crown rust fungus); (ii) a facultative biotroph parasite, Magnaporthe grisea (the blast fungus); (iii) pathogenic bacteria, Pseudomonas syringae pv. atropurpurea and P. syringae pv. coronafaciens (the halo or stripe blights of oats); and (iv) Ryegrass mottle virus. Surprisingly, any of the pathogens used induced most of the apoptotic features in oat cells at and around the infection sites, indicating that apoptotic cell death is a common phenomenon in oats during pathogen attack. The localization and the timing of apoptotic cell death during a course of infection were, however, quite different depending on the interactions (compatible or incompatible) and the pathogens (fungi, bacteria, or viruses). Possible roles of apoptotic cell death in the susceptible and resistant interactions are discussed.

Apoptosis↗