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Biomedical subjects

J Ruan

Publications and source records attributed to J Ruan.

At least 19 recordsLinked to original sources
PubMed2005

Decomposition of mixed malodorants in a wire-plate pulse corona reactor.

Decomposition characteristics of two groups of representative mixed malodorants (1, ethanethiol + hydrogen sulfide; 2, ethanethiol + ammonia) in air were investigated employing a wire-plate pulse corona reactor. A new type of high-voltage pulse generator with a thyratron switch and a Blumlein pulse-forming network (BPFN) was used in our experiments. The experiments were conducted at a gas-flow rate of 13 m3/h. Important parameters, including peak voltage, chemical structures of malodorants, pulse frequency, and initial concentration, which influenced the removal efficiency, were investigated. The results showed that the mixed malodorants could be treated effectively by pulse corona. The removal efficiencies of 200 mg/m3 C2H5SH and 200 mg/m3 H2S for group 1 were 95.6% and 100%, respectively, which were almost equal to those of the two pollutants separately. The energy cost was about 65.1-81.4 J/L, which was 31.5-45.2% lower than for treating pollutants alone. The removal efficiencies of 105 mg/m3 C2HsSH and 40 mg/m3 NH3 for group 2 were 93.1% and almost 100%, and the energy cost was 65.1 J/L, 55.6% lower than that which was treated separately. In the case of two groups of mixed malodorants removal, NOx, 03, SO2, CO2, and CO were all observed. Moreover, some sulfur and white crystal ammonium nitrates were discovered adhering to the corona wires in the removal of groups 1 and 2, respectively. A dynamics model was developed to describe the relation of the removal efficiency with specific energy density and initial concentration. In the case of group 1 removal,the decomposition rate constants decreased as compared to the single treating. As for group 2 removal, the decomposition rate constants increased, especially for NH3. According to the results, the optimization design for the reactor and the matching of high pulse voltage source can be reckoned.

Air Pollutants↗
PubMed2003

Lack of association of group specific component haplotypes with lung function in smokers.

BACKGROUND: Airway inflammation may affect the decrease in lung function that occurs in response to cigarette smoke, and is an important pathological feature in chronic obstructive pulmonary disease (COPD). Group specific component (GC) can act as an inflammatory mediator and may therefore have important influences on the inflammatory reaction in the airway. Several reports have described associations between GC haplotypes and COPD but these remain controversial. In addition, most of these studies were based on a small number of subjects. METHODS: We have studied the contribution of GC haplotypes to the level of lung function in a large cohort of smokers with high or low lung function (mean FEV(1) % predicted 91.8 and 62.6, respectively). The frequency of the three major GC haplotypes (1S, 1F and 2) was investigated in 537 individuals with high lung function and 533 with low lung function. RESULTS: No significant difference was found in the frequency of any GC haplotype between the high and low lung function groups. There was also no significant difference between the groups in genotype frequency of the two single nucleotide polymorphisms that underlie the haplotypes. CONCLUSION: The GC haplotype does not contribute to reduced lung function in this cohort of smokers.

Adult↗
PubMed2001

Peptide methionine sulfoxide reductase from Escherichia coli and Mycobacterium tuberculosis protects bacteria against oxidative damage from reactive nitrogen intermediates.

Inducible nitric oxide synthase (iNOS) plays an important role in host defense. Macrophages expressing iNOS release the reactive nitrogen intermediates (RNI) nitrite and S-nitrosoglutathione (GSNO), which are bactericidal in vitro at a pH characteristic of the phagosome of activated macrophages. We sought to characterize the active intrabacterial forms of these RNI and their molecular targets. Peptide methionine sulfoxide reductase (MsrA; EC ) catalyzes the reduction of methionine sulfoxide (Met-O) in proteins to methionine (Met). E. coli lacking MsrA were hypersensitive to killing not only by hydrogen peroxide, but also by nitrite and GSNO. The wild-type phenotype was restored by transformation with plasmids encoding msrA from E. coli or M. tuberculosis, but not by an enzymatically inactive mutant msrA, indicating that Met oxidation was involved in the death of these cells. It seemed paradoxical that nitrite and GSNO kill bacteria by oxidizing Met residues when these RNI cannot themselves oxidize Met. However, under anaerobic conditions, neither nitrite nor GSNO was bactericidal. Nitrite and GSNO can both give rise to NO, which may react with superoxide produced by bacteria during aerobic metabolism, forming peroxynitrite, a known oxidant of Met to Met-O. Thus, the findings are consistent with the hypotheses that nitrite and GSNO kill E. coli by intracellular conversion to peroxynitrite, that intracellular Met residues in proteins constitute a critical target for peroxynitrite, and that MsrA can be essential for the repair of peroxynitrite-mediated intracellular damage.

Bacterial Proteins↗
PubMed2001

Hard correlation gap observed in quench-condensed ultrathin beryllium.

We report on the tunneling density of states (DOS) in strongly disordered ultrathin Be films quench condensed at 20 K. Above 5 K, the DOS shows the well-known logarithmic anomaly at the Fermi level. Only in a narrow temperature range near 2 K is the DOS linearly dependent on energy, as predicted by Efros and Shklovskii. However, both the zero-bias conductance and the slope of the linear DOS are found to decrease drastically with decreasing temperature. Tunneling measurements at mK temperatures have revealed conclusively that a hard correlation gap opens up in the DOS.

Journal Article↗
PubMed2001

Dynamics of some neural network models with delay.

The dynamics of the neuronic model described by the one-dimensional delay functional differential equation are studied in this paper. We give a strict and detailed analysis of dynamical characteristic of this model by the Lyapunov functional approach and Hopf bifurcation proposition. Furthermore, numerical simulations, as well as Lyapunov exponents, are presented to support our conjectures about the appearance of complex dynamics such as chaos. We also investigate the dynamics of the neural network model described by the n-dimensional delay functional differential equation with a symmetrical weight matrix, and corresponding simulation results are included as concrete examples.

Artificial Intelligence↗
PubMed2001

Association of IL-1beta and IL-1 receptor antagonist haplotypes with rate of decline in lung function in smokers.

BACKGROUND: There is increasing evidence that the cytokine network is central to the immunopathology of inflammatory airway diseases. The interleukin 1 (IL-1) receptor antagonist (IL-1RN) is a naturally occurring anti-inflammatory agent that binds to the IL-1 receptor but does not possess agonist activity. Each of the genes of the IL-1 locus on chromosome 2q14 is polymorphic. The IL1RN gene contains an 86 bp tandem repeat and allele 2 of this polymorphism has been associated with various inflammatory diseases. The IL-1beta (IL1B) gene contains a promoter polymorphism (C-511T) that has been associated with inflammatory diseases and is in linkage disequilibrium with the IL1RN polymorphism. METHODS: We investigated whether polymorphisms in the IL1B and IL1RN genes were associated with rate of decline of lung function. Genotypes were determined in 284 smokers with a rapid decline in lung function and 306 smokers with no decline in lung function. RESULTS: None of the genotypes was associated with the rate of decline of lung function. However, the distribution of IL1B/IL1RN haplotypes was different between smokers with a rapid decline in lung function and those with no decline in lung function (p=0.0005). CONCLUSION: These results suggest that IL1B/IL1RN haplotypes play a role in the rate of decline in lung function in smokers.

Algorithms↗
PubMed2001

[Study on the constituents from freeze-dried power of blackberries (Rubus ursinus)].

Three Compounds were isolated from freeze-dried powder of Blackberries (Rubus ursinus L.) which showed an activity on inhibition of chemocarcinogen. The structures of them were identified as stigmasta-5,22-dien-3-ol],beta-sitosterol and beta-sitosterol-3 beta-D-glucose. All these compounds were isolated at the first time from the plant.

Fruit↗
PubMed2000

[Pharmacokinetic study on absorption of stachyose].

OBJECTIVE: To study the intestinal absorption and absorption site of stachyose, one of the oligosaccharides extracted from Rehmannia, in mice and rats. METHODS: Plasma concentration of stachyose was measured by high performance liquid chromatography (HPLC) with postcolumn fluorescence derivatization after administration of stachyose to mice by oral or intravenous injection. The absorption of stachyose in different sections of digestive tract was evaluated using the intestine loop in situ technique. The kanamycin treated mice were used to study the metabolism of stachyose in intestine. RESULTS: Absorption of stachyose in intestine after oral administration was quick but low, the bioavailability being 3.82%. The absorption rate in stomach, duodenum, jejunum and ileum was 6.03%, 13.80%, 8.33% and 0.53% respectively, no absorption was tested in large intestine. The residual rate of stachyose in the intestine of normal mice and kanamycin treated mice was 8.6% and 93.4% respectively. CONCLUSION: The intestinal absorption rate of stachyose is low, the main absorption site is the upper portion of small intestine. The unabsorbed stachyose is metabolized by the intestinal microflora.

Animals↗
PubMed1999

Differential regulation of human alpha1-adrenoceptor subtypes.

We have compared the agonist-induced down-regulation of human alpha1A-, alpha1B- and alpha1D-adrenoceptors upon stable expression in rat-1 fibroblasts. During a 24-h incubation the agonist phenylephrine downregulated alpha1A- and alpha1 -adrenoceptors in a concentration-dependent manner. While maximum downregulation was similar for both subtypes, the threshold concentration for significant reductions was markedly higher for alpha1A- than for alpha(1B-adrenoceptors (10 microM vs. 100 nM). The downregulation of both subtypes by 100 microM phenylephrine was time-dependent, and significant reductions were observed already after 2-4 h. In contrast, incubation of alpha1D-adrenoceptor-expressing cells with phenylephrine increased receptor number in a time- and concentration-dependent manner. The downregulation of alpha1B-adrenoceptors by 100 microM phenylephrine for 24 h was accompanied by a matching reduction in mRNA abundance, but no such reduction was seen for alpha-adrenoceptors. These treatment conditions also caused a functional desensitization of agonist-stimulated inositol phosphate formation for alpha1A- and alpha1B- but not for alpha1D-adrenoceptors. Treatment with the phorbol ester phorbol-12-myristate-13-acetate did not change receptor density or mRNA abundance and did not cause functional desensitization. We conclude that human alpha1-adrenoceptor subtypes are differentially regulated by agonist treatment even if they are expressed in the same cell line.

Adrenergic alpha-Agonists↗
PubMed1999

Use of a cell-based, lawn format assay to rapidly screen a 442,368 bead-based peptide library.

A cell-based, lawn format assay utilizing an in situ photocleavage method has been developed that allows the rapid examination of large bead-based compound libraries as discrete molecules. The format uses frog melanophore cells in a contiguous, adherent, confluent layer in small petri dishes covered with a 0.5-1-mm layer of agarose containing 130 micron diameter TentaGel beads at a density of 2-20 beads/mm2. Employing this technique a 9-mer, 442,368-member peptide library (designed around the 13 amino acid alpha-MSH peptide sequence) made up of 12 separate pools of 36,864 peptides/pool was assayed. Initially, a fraction (approximately 10%) of each pool was scanned (approximately 3700 beads from each pool) in 60-mm petri dishes to identify the most active pools. Upon direct photocleavage of the beads with UV light (365 nm), each petri dish was photographed over a 60-min period with a CCD camera to record changes in light intensity as an index of melanosome dispersion. Active beads were those that were surrounded by a localized decrease in light transmittance indicating melanosome dispersed cells. Upon examination with a dissecting microscope, single beads centrally located to a circular array of dispersed cells were identified and removed from the agarose and sequenced by Edman degradation to determine the peptide sequence. Re-synthesized peptides were re-examined against alpha-MSH receptor to confirm and quantify the activity. Several 9-mer peptides were identified with potencies similar to the natural 13-mer peptide. This method allows for the rapid screening of large bead-based photo-cleavable peptide libraries with the advantage that each compound is screened as a discrete molecule in a well-less format.

Animals↗
PubMed1999

noxR3, a novel gene from Mycobacterium tuberculosis, protects Salmonella typhimurium from nitrosative and oxidative stress.

Reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI) produced by activated macrophages participate in host defense against the facultative intracellular pathogens Mycobacterium tuberculosis and Salmonella typhimurium. To survive within macrophages, such pathogens may have evolved ROI and RNI resistance mechanisms. ROI resistance pathways have been intensively studied. Much less is known about the mechanisms of resistance to RNI. To identify possible RNI resistance genes in M. tuberculosis, a mycobacterial library was expressed in S. typhimurium and subjected to selection by exposure to the NO donor S-nitrosoglutathione (GSNO) in concentrations sufficient to kill the vast majority of nontransformed salmonellae. Among the rare surviving recombinants was a clone expressing noxR3, a novel and previously anonymous M. tuberculosis gene predicted to encode a small, basic protein. Expression of noxR3 protected S. typhimurium not only from GSNO and acidified nitrite but also from H2O2. noxR3 is the third gene cloned from M. tuberculosis that has been shown to protect heterologous cells from both RNI and ROI. This suggests diversity in the repertoire of mechanisms that help pathogens resist the oxidative and nitrosative defenses of the host.

Amino Acid Sequence↗
PubMed1999

Homozygous Cys542-->Arg substitution in GPIIIa in a Swiss patient with type I Glanzmann's thrombasthenia.

Glanzmann's thrombasthenia (GT) arises from a qualitative or quantitative defect in the GPIIb-IIIa complex (integrin alphaIIbbeta3), the mediator of platelet aggregation. We describe a patient in whom clinical and laboratory findings typical of type I GT were found together with a second pathology involving neurological and other complications symptomatic of tuberous sclerosis. Analysis of platelet proteins by Western blotting revealed trace amounts of normally migrating GPIIb and equally small amounts of GPIIIa of slightly slower than normal migration. Flow cytometry confirmed a much decreased binding to platelets of monoclonal antibodies to GPIIb, GPIIIa or GPIIb-IIIa, and an antibody to the alphav subunit also showed decreased binding. Nonradioactive PCR single-strand conformation polymorphism analysis followed by direct sequencing of PCR-amplified DNA fragments showed a homozygous point mutation (T to C) at nucleotide 1722 of GPIIIa cDNA and which led to a Cys542-->Arg substitution in the GPIIIa protein. The mutation gave rise to a HinP1 I restriction site in exon 11 of the GPIIIa gene and allele-specific restriction enzyme analysis of family members confirmed that a single mutated allele was inherited from each parent. This amino acid substitution presumably changes the capacity for disulphide bond formation within the cysteine-rich core region of GPIIIa and its study will provide new information on GPIIb-IIIa and alphavbeta3 structure and biosynthesis.

Amino Acid Substitution↗
PubMed1998

Linkage of four polymorphisms on the alphaIIb gene.

The subunits of the platelet integrin alphaIIb beta3 are encoded by two genes located on chromosome 17. Two pathologies are associated with structural modifications of this complex: Glanzmann's thrombasthenia and alloimmune thrombocytopenia. The former is a hereditary bleeding disorder, the latter is due to an immune response linked to the presence of specific epitopes defined by single amino acid substitutions called human platelet alloantigen (HPA) systems. Analysing the alphaIIb gene from 112 independent chromosomes, we have defined two new silent polymorphisms in complete linkage disequilibrium. They are reciprocally linked to HPA-3 and a previously reported 9 pb deletion in intron 21. Linkage of these four DNA markers spanning a 5 kb fragment of genomic DNA provides a new tool for analysing alphaIIb gene pathology and evolution.

Genetic Linkage↗
PubMed1998

Double heterozygosity of the GPIIb gene in a Swiss patient with Glanzmann's thrombasthenia.

Glanzmann's thrombasthenia (GT) results from a qualitative or quantitative defect of GPIIb-IIIa complexes (integrin alphaIIbbeta3). the fibrinogen receptor on platelets. This integrin plays a critical role in platelet aggregation. In this report we describe the molecular abnormalities of a patient with clinical and laboratory findings typical of type I Glanzmann's thrombasthenia. SDS-PAGE with Western blotting revealed an absence of GPIIb but small amounts of normally migrating GPIIIa in his platelets. A non-radioactive PCR-SSCP procedure and direct sequence analysis of PCR-amplified DNA fragments showed the patient to be a compound heterozygote for mutations in the GPIIb gene. A single point mutation (G to A) at nucleotide 1064 of the cDNA derived from the mother's allele led to a Glu324 to Lys amino acid substitution in GPIIb. It was responsible for a MscI restriction site in exon 12 of the GPIIb gene. This amino acid substitution changes the electric charge between the second and third Ca++-binding domains of GPIIb. The second mutation was inherited from his father and is in exon 18 of the GPIIb gene. It was a T --> C base transition at position 1787 of GPIIb cDNA and results in a Ile565 to Thr substitution. The two GPIIb mutations identified in this study will provide new information on GPIIb-IIIa structure and biosynthesis.

Blotting, Western↗
PubMed1998

Family screening for a Glanzmann's thrombasthenia mutation using PCR-SSCP.

Genetic counselling is often requested in Glanzmann's thrombasthenia, but measurements of GPIIb-IIIa density on platelets are often too inconclusive to allow a precise assessment of whether prospective parents are obligate heterozygotes for this disease by this measure alone. The recent application of PCR technology to Glanzmann's thrombasthenia has resulted in the identification of a large number of mutations, i.e. insertions/ deletions, splicing defects, in the genes for both GPIIb and GPIIIa. Among the reported abnormalities is an intronic G-->A substitution at the splice donor site of intron 15 in the GPIIb gene of a European gypsy tribe. This gives rise to an abnormal splicing, of an 8-bp deletion located at the 3' end of exon 15, a reading-frame shift and a premature stop codon in the mRNA for GPIIb. In applying PCR-SSCP to the elucidation of the genetic defects of a series of Glanzmann's patients, we have found the above-cited abnormality in three more gypsy families in France. The presence of the mutation was initially established by sequencing the amplified fragment, and its presence in family members was confirmed by both PCR-SSCP and HphI restriction analysis. Evaluation of the intronic G-->A mutation enabled genetic counselling to prospective parents within these families.

Journal Article↗
PubMed1998

Reclassification of Thermomonospora and Microtetraspora.

Almost complete 16S rRNA sequences from seven Thermomonospora strains, Thermomonospora curvata, Thermomonospora formosensis, Thermomonospora fusca, Thermomonospora mesophila, Thermomonospora chromogena, Thermomonospora alba and Thermomonospora mesouviformis (a synonym of Thermomonospora alba) were determined and subjected to phylogenetic analysis together with the sequences from all the representative members of the suborder Streptosporangineae. On the basis of phylogenetic, chemotaxonomic and phenotypic evidence, the transfer is proposed of Thermomonospora formosensis to the genus Actinomadura as Actinomadura formosensis comb. nov., Thermomonospora mesophila to the genus Microbispora as Microbispora mesophila comb. nov., and Thermomonospora fusca and Thermomonospora alba to a new genus, Thermobifida gen. nov., which belongs to the family Nocardiopsaceae, as Thermobifida fusca comb. nov. and Thermobifida alba comb. nov. Thermobifida alba is designated the type species of the genus. The transfer is also proposed of all species of the Microtetraspora pusilla group, which were transferred from Actinomadura, to a new genus, Nonomuria gen. nov., as Nonomuria africana comb. nov., Nonomuria angiospora comb. nov., Nonomuria fastidiosa comb. nov., Nonomuria ferruginea comb. nov., Nonomuria flexuosa comb. nov., Nonomuria helvata comb. nov., Nonomuria polychroma comb. nov., Nonomuria pusilla comb. nov., Nonomuria recticatena comb. nov., Nonomuria roseola comb. nov., Nonomuria roseoviolacea comb. nov., Nonomuria rubra comb. nov., Nonomuria salmonea comb. nov., Nonomuria spiralis comb. nov. and Nonomuria turkmeniaca comb. nov. Nonomuria pusilla is designated the type species of the genus.

Actinomycetales↗
PubMed1997

A novel antioxidant gene from Mycobacterium tuberculosis.

Among the major antimicrobial products of macrophages are reactive intermediates of the oxidation of nitrogen (RNI) and the reduction of oxygen (ROI). Selection of recombinants in acidified nitrite led to the cloning of a novel gene, noxR1, from a pathogenic clinical isolate of Mycobacterium tuberculosis. Expression of noxR1 conferred upon Escherichia coli and Mycobacterium smegmatis enhanced ability to resist RNI and ROI, whether the bacteria were exposed to exogenous compounds in medium or to endogenous products in macrophages. These studies provide the first identification of an RNI resistance mechanism in mycobacteria, point to a new mechanism for resistance to ROI, and raise the possibility that inhibition of the noxR1 pathway might enhance the ability of macrophages to control tuberculosis.

Amino Acid Sequence↗