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Int. J. Mol. Sci., Volume 13, Issue 9 (September 2012), Pages 10660-12152

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Open AccessArticle Purification and Characterization of a Ginsenoside Rb1-Hydrolyzing β-Glucosidase from Aspergillus niger KCCM 11239
Int. J. Mol. Sci. 2012, 13(9), 12140-12152; https://doi.org/10.3390/ijms130912140
Received: 13 July 2012 / Revised: 24 August 2012 / Accepted: 7 September 2012 / Published: 24 September 2012
Cited by 13 | PDF Full-text (854 KB) | HTML Full-text | XML Full-text
Abstract
Rb1-hydrolyzing β-glucosidase from Aspergillus niger KCCM 11239 was studied to develop a bioconversion process for minor ginsenosides. The specific activity of the purified enzyme was 46.5 times greater than that of the crude enzyme. The molecular weight of the native enzyme
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Rb1-hydrolyzing β-glucosidase from Aspergillus niger KCCM 11239 was studied to develop a bioconversion process for minor ginsenosides. The specific activity of the purified enzyme was 46.5 times greater than that of the crude enzyme. The molecular weight of the native enzyme was estimated to be approximately 123 kDa. The optimal pH of the purified enzyme was pH 4.0, and the enzyme proved highly stable over a pH range of 5.0–10.0. The optimal temperature was 70 °C, and the enzyme became unstable at temperatures above 60 °C. The enzyme was inhibited by Cu2+, Mg2+, Co2+, and acetic acid (10 mM). In the specificity tests, the enzyme was found to be active against ginsenoside Rb1, but showed very low levels of activity against Rb2, Rc, Rd, Re, and Rg1. The enzyme hydrolyzed the 20-C,β-(1→6)-glucoside of ginsenoside Rb1 to generate ginsenoside Rd and Rg3, and hydrolyzed 3-C,β-(1→2)-glucoside to generate F2. The properties of the enzyme indicate that it could be a useful tool in biotransformation applications in the ginseng industry, as well as in the development of novel drug compounds. Full article
(This article belongs to the Special Issue Enzyme Optimization and Immobilization)
Open AccessArticle Serum Autofluorescence, a Potential Serum Marker for the Diagnosis of Liver Fibrosis in Rats
Int. J. Mol. Sci. 2012, 13(9), 12130-12139; https://doi.org/10.3390/ijms130912130
Received: 16 June 2012 / Revised: 20 August 2012 / Accepted: 2 September 2012 / Published: 24 September 2012
Cited by 7 | PDF Full-text (502 KB) | HTML Full-text | XML Full-text
Abstract
Fluctuations in serum autofluorescence (AF) intensity have recently been widely used as markers of certain diseases such as cancer. To determine the diagnostic value of serum AF intensity for liver fibrosis in rats, we induced liver fibrosis by subcutaneous injection of carbon tetrachloride
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Fluctuations in serum autofluorescence (AF) intensity have recently been widely used as markers of certain diseases such as cancer. To determine the diagnostic value of serum AF intensity for liver fibrosis in rats, we induced liver fibrosis by subcutaneous injection of carbon tetrachloride into rats. The rat serum AF intensities were detected at the excitation wavelength of 337 nm and the emission wavelength of 512 nm. The degree of liver fibrosis was evaluated by Van Gieson’s staining. The relationship between serum AF intensity and the degree of liver fibrosis was analyzed by Spearman and Pearson Correlation. The diagnostic sensitivity and specificity of the serum AF was determined by analyzing the receiver operating characteristic (ROC) curves. Our results show that the serum AF intensity in the rat liver fibrosis model increased when compared with control rats eight weeks and twelve weeks post induction of liver fibrosis. However, there was no significant difference in serum AF intensity between fibrotic and control rats at four week post induction. Furthermore, serum AF intensity correlated positively with the severity of the degree of hepatic fibrosis. ROC analysis further suggested that serum AF intensity is a valid marker for staging fibrosis. Therefore, it may potentially be developed as a novel diagnostic tool for hepatic fibrosis. Full article
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
Open AccessArticle Gelam Honey Scavenges Peroxynitrite During the Immune Response
Int. J. Mol. Sci. 2012, 13(9), 12113-12129; https://doi.org/10.3390/ijms130912113
Received: 23 July 2012 / Revised: 6 September 2012 / Accepted: 9 September 2012 / Published: 24 September 2012
Cited by 6 | PDF Full-text (248 KB) | HTML Full-text | XML Full-text
Abstract
Monocytes and macrophages are part of the first-line defense against bacterial, fungal, and viral infections during host immune responses; they express high levels of proinflammatory cytokines and cytotoxic molecules, including nitric oxide, reactive oxygen species, and their reaction product peroxynitrite. Peroxynitrite is a
[...] Read more.
Monocytes and macrophages are part of the first-line defense against bacterial, fungal, and viral infections during host immune responses; they express high levels of proinflammatory cytokines and cytotoxic molecules, including nitric oxide, reactive oxygen species, and their reaction product peroxynitrite. Peroxynitrite is a short-lived oxidant and a potent inducer of cell death. Honey, in addition to its well-known sweetening properties, is a natural antioxidant that has been used since ancient times in traditional medicine. We examined the ability of Gelam honey, derived from the Gelam tree (Melaleuca spp.), to scavenge peroxynitrite during immune responses mounted in the murine macrophage cell line RAW 264.7 when stimulated with lipopolysaccharide/interferon-γ (LPS/IFN-γ) and in LPS-treated rats. Gelam honey significantly improved the viability of LPS/IFN-γ-treated RAW 264.7 cells and inhibited nitric oxide production—similar to the effects observed with an inhibitor of inducible nitric oxide synthase (1400W). Furthermore, honey, but not 1400W, inhibited peroxynitrite production from the synthetic substrate 3-morpholinosydnonimine (SIN-1) and prevented the peroxynitrite-mediated conversion of dihydrorhodamine 123 to its fluorescent oxidation product rhodamine 123. Honey inhibited peroxynitrite synthesis in LPS-treated rats. Thus, honey may attenuate inflammatory responses that lead to cell damage and death, suggesting its therapeutic uses for several inflammatory disorders. Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
Open AccessArticle Photophysical Behaviors of Single Fluorophores Localized on Zinc Oxide Nanostructures
Int. J. Mol. Sci. 2012, 13(9), 12100-12112; https://doi.org/10.3390/ijms130912100
Received: 16 July 2012 / Revised: 6 September 2012 / Accepted: 12 September 2012 / Published: 24 September 2012
Cited by 4 | PDF Full-text (454 KB) | HTML Full-text | XML Full-text
Abstract
Single-molecule fluorescence spectroscopy has now been widely used to investigate complex dynamic processes which would normally be obscured in an ensemble-averaged measurement. In this report we studied photophysical behaviors of single fluorophores in proximity to zinc oxide nanostructures by single-molecule fluorescence spectroscopy and
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Single-molecule fluorescence spectroscopy has now been widely used to investigate complex dynamic processes which would normally be obscured in an ensemble-averaged measurement. In this report we studied photophysical behaviors of single fluorophores in proximity to zinc oxide nanostructures by single-molecule fluorescence spectroscopy and time-correlated single-photon counting (TCSPC). Single fluorophores on ZnO surfaces showed enhanced fluorescence brightness to various extents compared with those on glass; the single-molecule time trajectories also illustrated pronounced fluctuations of emission intensities, with time periods distributed from milliseconds to seconds. We attribute fluorescence fluctuations to the interfacial electron transfer (ET) events. The fluorescence fluctuation dynamics were found to be inhomogeneous from molecule to molecule and from time to time, showing significant static and dynamic disorders in the interfacial electron transfer reaction processes. Full article
(This article belongs to the Special Issue Advances in Single Molecule Spectroscopy)
Open AccessTechnical Note Microsatellite Markers for the Chameleon Grasshopper (Kosciuscola tristis) (Orthoptera: Acrididae), an Australian Alpine Specialist
Int. J. Mol. Sci. 2012, 13(9), 12094-12099; https://doi.org/10.3390/ijms130912094
Received: 4 September 2012 / Revised: 18 September 2012 / Accepted: 19 September 2012 / Published: 24 September 2012
Cited by 3 | PDF Full-text (143 KB) | HTML Full-text | XML Full-text
Abstract
A set of polymorphic loci was characterised using an enrichment library for the Australian alpine specialist, the chameleon grasshopper (Kosciuscola tristis), an atypical grasshopper known for its remarkable temperature-controlled colour change. The number of alleles per locus ranged from three to
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A set of polymorphic loci was characterised using an enrichment library for the Australian alpine specialist, the chameleon grasshopper (Kosciuscola tristis), an atypical grasshopper known for its remarkable temperature-controlled colour change. The number of alleles per locus ranged from three to 20 and observed heterozygosity from 0.16 to 0.76. These are the first microsatellite markers for a non-endangered Australian alpine animal and will inform questions of gene flow across the sky islands of this unique and threatened region. Full article
Open AccessArticle Development of New Microsatellite Markers for Salvia officinalis L. and Its Potential Use in Conservation-Genetic Studies of Narrow Endemic Salvia brachyodon Vandas
Int. J. Mol. Sci. 2012, 13(9), 12082-12093; https://doi.org/10.3390/ijms130912082
Received: 9 August 2012 / Revised: 30 August 2012 / Accepted: 5 September 2012 / Published: 24 September 2012
Cited by 18 | PDF Full-text (780 KB) | HTML Full-text | XML Full-text
Abstract
Nine new microsatellite markers (SSR) were isolated from Salvia officinalis L. A total of 125 alleles, with 8 to 21 alleles per locus, were detected in a natural population from the east Adriatic coast. The observed heterozygosity, expected heterozygosity, and polymorphic information content
[...] Read more.
Nine new microsatellite markers (SSR) were isolated from Salvia officinalis L. A total of 125 alleles, with 8 to 21 alleles per locus, were detected in a natural population from the east Adriatic coast. The observed heterozygosity, expected heterozygosity, and polymorphic information content ranged from 0.46 to 0.83, 0.73 to 0.93 and 0.70 to 0.92, respectively. New microsatellite markers, as well as previously published markers, were tested for cross-amplification in Salvia brachyodon Vandas, a narrow endemic species known to be present in only two localities on the Balkan Peninsula. Out of 30 microsatellite markers tested on the natural S. brachyodon population, 15 were successfully amplified. To obtain evidence of recent bottleneck events in the populations of both species, observed genetic diversity (HE) was compared to the expected genetic diversity at mutation-drift equilibrium (HEQ) and calculated from the observed number of alleles using a two-phased mutation model (TPM). Recent bottleneck events were detected only in the S. brachyodon population. This result suggests the need to reconsider the current threat category of this endemic species. Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
Open AccessArticle Several Lipid-Related Gene Polymorphisms Interact with Overweight/Obesity to Modulate Blood Pressure Levels
Int. J. Mol. Sci. 2012, 13(9), 12062-12081; https://doi.org/10.3390/ijms130912062
Received: 17 August 2012 / Revised: 12 September 2012 / Accepted: 13 September 2012 / Published: 24 September 2012
Cited by 12 | PDF Full-text (3473 KB) | HTML Full-text | XML Full-text
Abstract
Little is known about the interactions of single nucleotide polymorphisms (SNPs) and overweight/obesity on blood pressure levels. The present study was undertaken to detect 10 lipid-related gene SNPs and their interactions with overweight/obesity on blood pressure levels. Genotyping of ATP-binding cassette transporter A1
[...] Read more.
Little is known about the interactions of single nucleotide polymorphisms (SNPs) and overweight/obesity on blood pressure levels. The present study was undertaken to detect 10 lipid-related gene SNPs and their interactions with overweight/obesity on blood pressure levels. Genotyping of ATP-binding cassette transporter A1 (ABCA-1) V825I, acyl-CoA:cholesterol acyltransferase-1 (ACAT-1) rs1044925, low density lipoprotein receptor (LDL-R) AvaII hepatic lipase gene (LIPC) −250G > A, endothelial lipase gene (LIPG) 584C > T, methylenetetrahydrofolate reductase (MTHFR) 677C > T, the E3 ubiquitin ligase myosin regulatory light chain-interacting protein (MYLIP) rs3757354, proprotein convertase subtilisin-like kexin type 9 (PCSK9) E670G, peroxisome proliferator-activated receptor delta (PPARD) +294T > C, and Scavenger receptor class B type 1 (SCARB1) rs5888 was performed in 978 normal weight and 751 overweight/obese subjects. The interactions were detected by factorial regression analysis. The genotypes of ACAT-1 AC, LIPC GA and AA, and SCARB1 TT; LDL-R A-A- and LIPC GA; and SCARB1 TT were interacted with overweight/obesity to increase systolic, diastolic blood pressure (SBP, DBP) and pulse pressure (PP) levels; respectively. The genotypes of ACAT-1 CC; ACAT-1 AA and CC were interacted with overweight/obesity to decrease SBP, PP levels (p < 0.01–0.001); respectively. The differences in blood pressure levels between normal weight and overweight/obese subjects might partly result from different interactions of several SNPs and overweight/obesity. Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
Open AccessArticle Genetic Diversity Characterization of Porcine Reproductive and Respiratory Syndrome Virus Isolates in Romania, Based on Phylogenetic Analysis
Int. J. Mol. Sci. 2012, 13(9), 12046-12061; https://doi.org/10.3390/ijms130912046
Received: 2 August 2012 / Revised: 27 August 2012 / Accepted: 5 September 2012 / Published: 21 September 2012
Cited by 5 | PDF Full-text (1396 KB) | HTML Full-text | XML Full-text
Abstract
Porcine reproductive and respiratory syndrome (PRRS) is a disease produced by the (PRRS) virus, characterized by endemic evolution in the majority of countries, which remains in actuality being a permanent threat to health and economic free farms, as well as for those infected.
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Porcine reproductive and respiratory syndrome (PRRS) is a disease produced by the (PRRS) virus, characterized by endemic evolution in the majority of countries, which remains in actuality being a permanent threat to health and economic free farms, as well as for those infected. The aim of this study was to evaluate the genetic diversity of Romanian PRRSV isolates from the four most important pig farms in Romania by comparing the nucleotide sequences obtained for ORF5 and ORF7 with a wide range of sequences from GenBank belonging to the main types of PRRSV; the type 1. Eighteen different sequences were obtained for ORF5 gene and 10 for ORF7 gene. One Romanian isolate (Rom3) was found in three of the four different investigated farms. The phylogenetic analysis revealed that the Romanian PRRSV nucleotide sequences clustered in three groups within the subtype 1 of the virus. The analysis of amino acid sequences evidenced for GP5 and N-nucleocapsid proteins confirmed that the Romanian virus belonged to type 1. Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
Open AccessArticle A Computational Study of Calcium(II) and Copper(II) Ion Binding to the Hyaluronate Molecule
Int. J. Mol. Sci. 2012, 13(9), 12036-12045; https://doi.org/10.3390/ijms130912036
Received: 8 June 2012 / Revised: 28 August 2012 / Accepted: 6 September 2012 / Published: 20 September 2012
Cited by 4 | PDF Full-text (228 KB) | HTML Full-text | XML Full-text
Abstract
The hyaluronate molecule is a negatively charged polysaccharide that performs a plethora of physiological functions in many cell tissues depending on its conformation. In the present paper, molecular modeling at three levels of theory and two basis sets was used to gain a
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The hyaluronate molecule is a negatively charged polysaccharide that performs a plethora of physiological functions in many cell tissues depending on its conformation. In the present paper, molecular modeling at three levels of theory and two basis sets was used to gain a deeper insight in the complex molecular structure of calcium(II) and copper(II) hyaluronate. Simulation results were compared with the experimental data (EXAFS or X-ray). It was found that B3LYP does not properly reproduce the experimental data while the HF and M06 methods do. Simulation data confirm that the N-acetyl group of the N-acetylglucosamine residue does not participate in the coordination bonding to the calcium(II) or copper(II) ion, as evident from the experimental data. Full article
(This article belongs to the Section Physical Chemistry, Theoretical and Computational Chemistry)
Open AccessReview Inhibition of GTRAP3-18 May Increase Neuroprotective Glutathione (GSH) Synthesis
Int. J. Mol. Sci. 2012, 13(9), 12017-12035; https://doi.org/10.3390/ijms130912017
Received: 9 July 2012 / Revised: 6 August 2012 / Accepted: 10 September 2012 / Published: 20 September 2012
Cited by 17 | PDF Full-text (1049 KB) | HTML Full-text | XML Full-text
Abstract
Glutathione (GSH) is a tripeptide consisting of glutamate, cysteine, and glycine; it has a variety of functions in the central nervous system. Brain GSH depletion is considered a preclinical sign in age-related neurodegenerative diseases, and it promotes the subsequent processes toward neurotoxicity. A
[...] Read more.
Glutathione (GSH) is a tripeptide consisting of glutamate, cysteine, and glycine; it has a variety of functions in the central nervous system. Brain GSH depletion is considered a preclinical sign in age-related neurodegenerative diseases, and it promotes the subsequent processes toward neurotoxicity. A neuroprotective mechanism accomplished by increasing GSH synthesis could be a promising approach in the treatment of neurodegenerative diseases. In neurons, cysteine is the rate-limiting substrate for GSH synthesis. Excitatory amino acid carrier 1 (EAAC1) is a neuronal cysteine/glutamate transporter in the brain. EAAC1 translocation to the plasma membrane promotes cysteine uptake, leading to GSH synthesis, while being negatively regulated by glutamate transport associated protein 3-18 (GTRAP3-18). Our recent studies have suggested GTRAP3-18 as an inhibitory factor for neuronal GSH synthesis. Inhibiting GTRAP3-18 function is an endogenous mechanism to increase neuron-specific GSH synthesis in the brain. This review gives an overview of EAAC1-mediated GSH synthesis, and its regulatory mechanisms by GTRAP3-18 in the brain, and a potential approach against neurodegeneration. Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
Open AccessArticle Anti-Epidermal Growth Factor Receptor (EGFR) Antibodies Overcome Resistance of Ovarian Cancer Cells to Targeted Therapy and Natural Cytotoxicity
Int. J. Mol. Sci. 2012, 13(9), 12000-12016; https://doi.org/10.3390/ijms130912000
Received: 16 July 2012 / Revised: 5 September 2012 / Accepted: 11 September 2012 / Published: 20 September 2012
Cited by 9 | PDF Full-text (493 KB) | HTML Full-text | XML Full-text
Abstract
The poor outcome of advanced ovarian cancer under conventional therapy stimulated the exploration of new strategies to improve therapeutic efficacy. In our preclinical in vitro study we investigated a combination of targeted therapy and immunotherapy. Combination treatment with the anti-EGFR-antibody Cetuximab, related tyrosine
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The poor outcome of advanced ovarian cancer under conventional therapy stimulated the exploration of new strategies to improve therapeutic efficacy. In our preclinical in vitro study we investigated a combination of targeted therapy and immunotherapy. Combination treatment with the anti-EGFR-antibody Cetuximab, related tyrosine kinase inhibitors (TKI) and cytolytic NK cells was tested against different ovarian cancer cell lines and primary tumour cells cultured from patient ascites. We found that selected ovarian cancer cells were susceptible to cetuximab and anti-EGFR-TKI-treatment, while the majority of cell lines were resistant to single or combination treatment with both substances. In addition, most ovarian cancer cells displayed low susceptibility to natural cytotoxicity of unstimulated NK cells. Notably, NK cytotoxicity against resistant ovarian cancer cells could be effectively enhanced by addition of Cetuximab mediating antibody-dependent cellular cytotoxicity (ADCC). Neither natural cytotoxicity nor ADCC of NK cells were negatively affected by the presence of TKIs. ADCC could be further increased when NK cells were pre-stimulated with monocytes and the immunostimulatory mycobacterial protein PstS-1. Our data suggest that targeted antibody therapy could be beneficial even against resistant tumour cells by augmenting supplementary cytolytic NK functions. Future studies should evaluate the combination of targeted therapy and immunotherapeutic approaches in patients with advanced ovarian cancer being resistant to standard treatment. Full article
(This article belongs to the Special Issue Advances in Molecular Oncology (special issue))
Open AccessReview Common Fragile Sites: Genomic Hotspots of DNA Damage and Carcinogenesis
Int. J. Mol. Sci. 2012, 13(9), 11974-11999; https://doi.org/10.3390/ijms130911974
Received: 17 July 2012 / Revised: 9 August 2012 / Accepted: 5 September 2012 / Published: 20 September 2012
Cited by 26 | PDF Full-text (425 KB) | HTML Full-text | XML Full-text
Abstract
Genomic instability, a hallmark of cancer, occurs preferentially at specific genomic regions known as common fragile sites (CFSs). CFSs are evolutionarily conserved and late replicating regions with AT-rich sequences, and CFS instability is correlated with cancer. In the last decade, much progress has
[...] Read more.
Genomic instability, a hallmark of cancer, occurs preferentially at specific genomic regions known as common fragile sites (CFSs). CFSs are evolutionarily conserved and late replicating regions with AT-rich sequences, and CFS instability is correlated with cancer. In the last decade, much progress has been made toward understanding the mechanisms of chromosomal instability at CFSs. However, despite tremendous efforts, identifying a cancer-associated CFS gene (CACG) remains a challenge and little is known about the function of CACGs at most CFS loci. Recent studies of FATS (for Fragile-site Associated Tumor Suppressor), a new CACG at FRA10F, reveal an active role of this CACG in regulating DNA damage checkpoints and suppressing tumorigenesis. The identification of FATS may inspire more discoveries of other uncharacterized CACGs. Further elucidation of the biological functions and clinical significance of CACGs may be exploited for cancer biomarkers and therapeutic benefits. Full article
(This article belongs to the Special Issue DNA Damage and Repair in Degenerative Diseases)
Open AccessReview The Emerging Roles of ATP-Dependent Chromatin Remodeling Enzymes in Nucleotide Excision Repair
Int. J. Mol. Sci. 2012, 13(9), 11954-11973; https://doi.org/10.3390/ijms130911954
Received: 2 August 2012 / Revised: 30 August 2012 / Accepted: 31 August 2012 / Published: 20 September 2012
Cited by 22 | PDF Full-text (484 KB) | HTML Full-text | XML Full-text
Abstract
DNA repair in eukaryotic cells takes place in the context of chromatin, where DNA, including damaged DNA, is tightly packed into nucleosomes and higher order chromatin structures. Chromatin intrinsically restricts accessibility of DNA repair proteins to the damaged DNA and impacts upon the
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DNA repair in eukaryotic cells takes place in the context of chromatin, where DNA, including damaged DNA, is tightly packed into nucleosomes and higher order chromatin structures. Chromatin intrinsically restricts accessibility of DNA repair proteins to the damaged DNA and impacts upon the overall rate of DNA repair. Chromatin is highly responsive to DNA damage and undergoes specific remodeling to facilitate DNA repair. How damaged DNA is accessed, repaired and restored to the original chromatin state, and how chromatin remodeling coordinates these processes in vivo, remains largely unknown. ATP-dependent chromatin remodelers (ACRs) are the master regulators of chromatin structure and dynamics. Conserved from yeast to humans, ACRs utilize the energy of ATP to reorganize packing of chromatin and control DNA accessibility by sliding, ejecting or restructuring nucleosomes. Several studies have demonstrated that ATP-dependent remodeling activity of ACRs plays important roles in coordination of spatio-temporal steps of different DNA repair pathways in chromatin. This review focuses on the role of ACRs in regulation of various aspects of nucleotide excision repair (NER) in the context of chromatin. We discuss current understanding of ATP-dependent chromatin remodeling by various subfamilies of remodelers and regulation of the NER pathway in vivo. Full article
(This article belongs to the Special Issue Excising DNA Damage from Chromosomes: Entry Visas and Exit Strategies)
Open AccessArticle Room Temperature Radiolytic Synthesized Cu@CuAlO2-Al2O3 Nanoparticles
Int. J. Mol. Sci. 2012, 13(9), 11941-11953; https://doi.org/10.3390/ijms130911941
Received: 7 July 2012 / Revised: 2 September 2012 / Accepted: 9 September 2012 / Published: 20 September 2012
Cited by 8 | PDF Full-text (1889 KB) | HTML Full-text | XML Full-text
Abstract
Colloidal Cu@CuAlO2-Al2O3 bimetallic nanoparticles were prepared by a gamma irradiation method in an aqueous system in the presence of polyvinyl pyrrolidone (PVP) and isopropanol respectively as a colloidal stabilizer and scavenger of hydrogen and hydroxyl radicals. The gamma
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Colloidal Cu@CuAlO2-Al2O3 bimetallic nanoparticles were prepared by a gamma irradiation method in an aqueous system in the presence of polyvinyl pyrrolidone (PVP) and isopropanol respectively as a colloidal stabilizer and scavenger of hydrogen and hydroxyl radicals. The gamma irradiation was carried out in a 60Co gamma source chamber with different doses up to 120 kGy. The formation of Cu@CuAlO2-Al2O3 nanoparticles was observed initially by the change in color of the colloidal samples from colorless to brown. Fourier transform infrared spectroscopy (FTIR) confirmed the presence of bonds between polymer chains and the metal surface at all radiation doses. Results of transmission electron microscopy (TEM), energy dispersive X-ray spectrometry (EDX), and X-ray diffraction (XRD) showed that Cu@CuAlO2-Al2O3 nanoparticles are in a core-shell structure. By controlling the absorbed dose and precursor concentration, nanoclusters with different particle sizes were obtained. The average particle diameter increased with increased precursor concentration and decreased with increased dose. This is due to the competition between nucleation, growth, and aggregation processes in the formation of nanoclusters during irradiation. Full article
(This article belongs to the Section Materials Science)
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Open AccessArticle A Soluble Receptor for Advanced Glycation End-Products Inhibits Hypoxia/Reoxygenation-Induced Apoptosis in Rat Cardiomyocytes via the Mitochondrial Pathway
Int. J. Mol. Sci. 2012, 13(9), 11923-11940; https://doi.org/10.3390/ijms130911923
Received: 28 June 2012 / Revised: 5 September 2012 / Accepted: 11 September 2012 / Published: 20 September 2012
Cited by 12 | PDF Full-text (2783 KB) | HTML Full-text | XML Full-text
Abstract
Severe myocardial dysfunction and tissue damage resulting from ischemia/reperfusion (I/R) is a common clinical scenario in patients with certain types of heart diseases and therapies such as thrombolysis, percutaneous coronary intervention, coronary artery bypass grafting, and cardiac transplantation. The underlining mechanism of endogenous
[...] Read more.
Severe myocardial dysfunction and tissue damage resulting from ischemia/reperfusion (I/R) is a common clinical scenario in patients with certain types of heart diseases and therapies such as thrombolysis, percutaneous coronary intervention, coronary artery bypass grafting, and cardiac transplantation. The underlining mechanism of endogenous cardiac protection after I/R injury has been a focus of current research. Growing evidences suggests that soluble receptor for advanced glycation end-products (sRAGE) has a cardioprotective effect; however, its role in I/R injury remains unclear. We hypothesized that exogenous administration of sRAGE during hypoxia/reoxygenation (H/R) induces cardioprotection by inhibiting cardiomyocyte apoptosis via multiple signals, involving mitochondrial membrane potential (MMP), the mitochondrial permeability transition pore (mPTP), mitochondrial cytochrome c, caspase-3, Bcl-2 and Bax. Neonatal rat cardiomyocytes underwent hypoxia for 3-h followed by 2-h reoxygenation or were treated with sRAGE for 10 min before H/R. Compared with H/R alone, sRAGE pretreatment reduced H/R-induced cardiomyocyte apoptosis from 27.9% ± 5.9% to 9.4% ± 0.7% (p < 0.05). In addition, sRAGE treatment significantly inhibited H/R-induced mitochondrial depolarization and mPTP opening, reduced mitochondrial cytochrome c leakage, caspase-3 and caspase-9 activity, and decreased the ratio of Bax to Bcl-2. Therefore, we conclude that the exogenous administration of sRAGE during H/R is involved in cardioprotection by inhibiting apoptosis via the mitochondrial pathway, which, if further confirmed in vivo, may have important clinical implications during H/R. Full article
(This article belongs to the collection Programmed Cell Death and Apoptosis)
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