PubMed Health⌕ Search

Biomedical subjects

C Yan

Publications and source records attributed to C Yan.

At least 73 records · Page 4Linked to original sources
PubMed2000

Seroepidemiological investigation of feline chlamydiosis in cats and humans in Japan.

The prevalence of chlamydia antibodies in Japan was investigated in 215 cat sera, consisting of 88 sera of stray cats and 127 sera of pet cats, and 2,184 human sera, taken from 2,003 general persons and 181 small animal clinic veterinarians, by microimmunofluorescence (MIF) testing with Chlamydia psittaci Fe/Pn1 of feline origin and Prk/6BC of avian origin as antigens. The prevalence rates of anti-Fe/Pn1 antibodies were 45.5% in stray cats, 17.3% in pet cats, 1.7% in general persons and 8.8% in small animal clinic veterinarians. The prevalence rates of anti-Prk/6BC antibodies were 51.1% in stray cats, 15.0% in pet cats, 3.1% in general persons and 5.0% in small animal clinic veterinarians. These results suggested that feline chlamydia infection is widely spread in cats especially in stray cats in Japan, and suggested that feline chlamydiosis could be transmitted to people who are in close contact with infected cats.

Animals↗
PubMed2000

Temporal/spatial expression of nuclear receptor coactivators in the mouse lung.

Our laboratory has previously demonstrated that retinoic acid nuclear receptor, thyroid transcription factor-1 (TTF-1), and nuclear receptor coactivators such as cAMP response element binding protein (CREB) binding protein (CBP)/p300 and steroid receptor coactivator-1 (SRC-1) form an enhanceosome on the 5'-enhancer region of the human surfactant protein B gene. Immunohistochemistry was used to identify cells that coexpressed CBP/p300, SRC-1, retinoid X receptor, and TTF-1 in the developing and mature lung. CBP/p300 and SRC-1 were expressed in the adult mouse lung, CBP and p300 being present in both alveolar type I and type II epithelial cells and SRC-1 and TTF-1 being restricted to type II epithelial cells. CBP/p300, SRC-1, and TTF-1 were readily detected in the nuclei of developing respiratory epithelial tubules in fetal mice from embryonic days 10 to 18. CBP/p300 and SRC-1 were also detected in developing mesenchymal cells. These coactivators were coexpressed with TTF-1 and SP-B in human pulmonary adenocarcinoma cells (H441 cells) in vitro. Interaction assays with a two-hybrid reporter analysis demonstrated direct interactions among TTF-1, SRC-1, and CBP/p300 in H441 cells. These findings support a role for retinoic acid receptor and nuclear receptor coactivators in the regulation of SP-B gene expression in the respiratory epithelium.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed2000

Comparative analysis of the putative amino acid sequences of chlamydial heat shock protein 60 and Escherichia coli GroEL.

The nucleotide sequences of the gene encoding chlamydial heat shock protein 60 (cHSP60) of 7 Chlamydia psittaci strains were determined. Comparison of sequences of the cHSP60 gene among chlamydiae showed high identities of the nucleotide sequences by 81.0% or greater and of the deduced amino acid sequences by 92.2% or greater. Comparison of the amino acid sequences between chlamydia and the other bacterial HSP60s resulted in the finding of three highly conserved regions, suggesting that these regions play a role in some function. In addition, 26- or 27-functional residues in the Escherichia coli GroEL out of the 28-residues are conserved in the amino acid sequences of the cHSP60. The data suggest that the function of the cHSP60 may be the same as that of the E. coli GroEL.

Amino Acid Sequence↗
PubMed2000

A novel congenital myopathy with apoptotic changes.

We report on a female child with congenital myopathy with delayed developmental milestones and mental retardation. The most striking pathological finding was the presence of many condensed to fragmented myonuclei. DNA fragmentation was confirmed by the TUNEL method and supported by the ultrastructural characteristics of apoptotic nuclear changes. We also demonstrated immunohistochemically the activation of caspase-3 and caspase-9. This appears to be the first reported case of congenital myopathy with apoptotic process.

Apoptosis↗
PubMed2000

[Stable carbon isotope characteristics of some woody plants in warm temperate zone].

It was found that the delta 13C values of the foliar, trunk, flower, and fruit of some woody plants in broad-leaved forest in warm temperate zone were affected by many factors, and showed a great interspecific difference and temporal and spatial heterogeneity. The intraspecific variation of delta 13C values was also great, with the order of Vitex negundo var. heterophylla 6.549@1000(-22.226@1000(-)-28.775@1000), Fraxinus rhynchophylla 5.706@1000(-23.687@1000(-)-29.393@1000), Jugans mandshurica 5.229@1000 (-26.146@1000-31.375@1000), Quercus liaotungensis 3.333@1000 (-24.324@1000(-)-27.657@1000), Syringa pekinensis 2.414@1000(-25.655@1000(-)-28.070@1000), and Prunus armeniaca var. ansu 2.296@1000 (-23.436@1000(-)-26.432@1000). Different organs of the same species had different delta 13C values: trunk and root barks had the low, while xylem had the highest delta 13C value. According to the relationship analysis between delta 13C value of Prunus armeniaca var. ansu xylem and environment factors, it was found that delta 13C value was strongly affected by annual mean temperature and followed by annual precipitation, mean temperature and precipitation in growth season.

Carbon Isotopes↗
PubMed2000

[Fibronectin induces matrix metalloproteinase-2 expression in ovarian cancer cells].

OBJECTIVE: To investigate the effects of extracelluar matrix proteins on matrix metalloproteinases (MMPs) expression by cancer cells, and the underlying mechanisms. METHODS: Following stimulation of SKOV3 ovarian cancer cells by fibronectin, MMPs secretion and cellular mRNA contents were assayed by gelatin-zymography and RT-PCR, respectively. The activity of MMP-2 promoter was monitored by cellular luciferase activity after the cells were transfected with MMP-2 promoter-luciferase construct. Cellular p53 contents were determined by Western blot analysis. RESULTS: Fibronectin (5 micrograms/ml) was found to stimulate the secretion of MMP-2 but not MMP-9 by SKOV3 cells. The stimulation was enhanced with the increase in fibronectin concentration. When SKOV3 cells were treated with 10 micrograms/ml fibronectin for 1 hr, the cellular MMP-2 mRNA dramatically increased. However, with increase in stimulation time, MMP-2 mRNA content decreased. Fibronectin induced an increase in luciferase activity in cells transfected with MMP-2 promoter construct, whilst curcumin (50 mumol/L), a potent transcription factor AP-1 inhibitor, could not block the fibronectin-induced increase in MMP-2 promoter activity. Fibronectin also induced an increase in p53 content of SKOV3 cells. CONCLUSION: Fibronectin stimulates ovarian cancer cells to secret MMP-2 via its enhancing effect on MMP-2 promoter activity with resultant increase in MMP-2 transcription. The effect might involve a pathway associated with p53 but independent of AP-1.

Female↗
PubMed2000

[A cross-sectional study on injuries in the residents of Shijiazhuang city].

OBJECTIVE: To comprehend current status of injury in the residents of Shijiazhuang city and to lay a foundation for prevention from injury. METHODS: A retrospective study on injury in the 21,544 residents of two and six rural villages was conducted by multi-stage stratified sampling. RESULTS: Standardized incidence rate of injury was 4.21% in Shijiazhuang city, higher in the rural than in the urban areas and higher in men than in women. The top three causes of injuries were traffic accidents, falls and poisoning. Traffic accidents and poisoning ranked the first place in the urban areas and in the rural areas, respectively. Falls occurred mostly in those aged less than 14 years and more than 60 years. Gas poisoning and traffic accidents occurred more often in those aged 15 - 34 years and traffic accidents ranked the first in the age group of 35 - 59 years old. Standardized mortality rate of injury was 48.78 per 100,000, higher in the rural than in the urban areas. Standardized mortality rate of suicide was the highest with 23.21 per 100,000 in the countryside and that of traffic accidents ranked the next. In average, 22 years of potential life lost, 17 work years of potential life lost and nine valued years of potential life lost for each death were caused by injury. Disability rate caused by injury was 1.1 percent. Direct economic loss for each case with injury cost 679.98 RMB yuan. Incidence rate for traffic accidents ranked the highest and the most severe in all injuries. CONCLUSION: Injury has become an important public health problem harmful to the people's health.

Accidental Falls↗
PubMed1999

Sensitive, universal detection for capillary electrochromatography using condensation nucleation light scattering detection.

Condensation nucleation light scattering detection (CNLSD) was coupled with a pressurized capillary electrochromatography (pCEC) system using an electrospray interface. Supplementary pressure from a high-pressure pump was used to stabilize the electrospray and electrochromatography processes. Hydrodynamic injections were made with a 20 nl injection valve, and the inherent dead volume from the valve was successfully minimized, such that plate numbers in the range of 120,000 to 350,000/m were observed. Selectivity tuning using both pressure and voltage with the pressurized capillary electrochromatography system was demonstrated. Good reproducibility, comparable sensitivities for a wide range of compounds, including carbohydrates, and limits of detection down to the 50 ng/ml level, corresponding to 1-2 pg levels, were determined without the need for derivatization, demonstrating that condensation nucleation light scattering detection is a sensitive, universal detection method for pressurized capillary electrochromatography.

Carbohydrates↗
PubMed1999

Opposing effects of reactive oxygen species and cholesterol on endothelial nitric oxide synthase and endothelial cell caveolae.

Synthesis of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS) is critical for normal vascular homeostasis. eNOS function is rapidly regulated by agonists and blood flow and chronically by factors that regulate mRNA stability and gene transcription. Recently, localization of eNOS to specialized plasma membrane invaginations termed caveolae has been proposed to be required for maximal eNOS activity. Because caveolae are highly enriched in cholesterol, and hypercholesterolemia is associated with increased NO production, we first studied the effects of cholesterol loading on eNOS localization and NO production in cultured bovine aortic endothelial cells (BAECs). Caveolae-enriched fractions were prepared by OptiPrep gradient density centrifugation. Treatment of BAECs with 30 microgram/mL cholesterol for 24 hours stimulated significant increases in total eNOS protein expression (1.50-fold), eNOS associated with caveolae-enriched membranes (2.23-fold), and calcium ionophore-stimulated NO production (1.56-fold). Because reactive oxygen species (ROS) contribute to endothelial dysfunction in hypercholesterolemia, we next studied the effects of ROS on eNOS localization and caveolae number. Treatment of BAECs for 24 hours with 1 micromol/L LY83583, a superoxide-generating napthoquinolinedione, decreased caveolae number measured by electron microscopy and prevented the cholesterol-mediated increases in eNOS expression. In vitro exposure of caveolae-enriched membranes to ROS (xanthine plus xanthine oxidase) dissociated caveolin more readily than eNOS from the membranes. These results show that cholesterol treatment increases eNOS expression, whereas ROS treatment decreases eNOS expression and the association of eNOS with caveolin in caveolae-enriched membranes. Our data suggest that oxidative stress modulates endothelial function by regulating caveolae formation, eNOS expression, and eNOS-caveolin interactions.

Animals↗
PubMed1999

The modulation of excitatory synaptic transmission by adenosine in area CA1 of the rat hippocampus is temperature dependent.

We tested the possibility that extracellular adenosine concentration varies with tissue temperature by measuring the tonic adenosinergic inhibition of excitatory synaptic transmission at different temperatures in the in vitro rat hippocampus. Application of the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) enhanced population excitatory postsynaptic potentials (EPSPs) by antagonizing tonic adenosinergic inhibition; this effect was greatest at 25 degrees C, and was progressively reduced at 35 and 37.5 degrees C. These results demonstrate that tonic adenosinergic inhibition is inversely related to temperature. In a second experiment, an exogenous A1 agonist, N6-cyclohexyladenosine (CHA), was applied to slices to inhibit evoked EPSPs. CHA inhibition of EPSPs was greater at 35 than at 25 degrees C, demonstrating that the reduced adenosinergic inhibition at higher temperatures is not a result of reduced A1 receptor function.

Adenosine↗
PubMed1999

Fluid shear stress stimulates big mitogen-activated protein kinase 1 (BMK1) activity in endothelial cells. Dependence on tyrosine kinases and intracellular calcium.

Mitogen-activated protein (MAP) kinases including ERK1/2 and JNK play an important role in shear stress-mediated gene expression in endothelial cells (EC). A new MAP kinase termed big MAP kinase 1 (BMK1/ERK5) has been shown to phosphorylate and activate the transcription factor MEF2C, which is highly expressed in EC. To determine the effects of shear stress on BMK1, bovine aortic EC were exposed to steady laminar flow (shear stress = 12 dynes/cm2). Flow activated BMK1 within 10 min with peak activation at 60 min (7.1 +/- 0.6-fold) in a force-dependent manner. Flow was the most powerful activator of BMK1, significantly greater than H2O2 or sorbitol. An important role for non-Src tyrosine kinases in flow-mediated BMK1 activation was demonstrated by inhibition with herbimycin A, but not with the Src inhibitor PP1 or overexpression of kinase-inactive c-Src. BMK1 activation was calcium-dependent as shown by inhibition with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxymethyl ester or thapsigargin. As shown by specific inhibitors or activators, flow-mediated BMK1 activation was not regulated by the following: intracellular redox state; intracellular NO; protein kinase A, C, or G; calcium/calmodulin-dependent kinase; phosphatidylinositol 3-kinase; or arachidonic acid metabolism. In summary, flow potently stimulates BMK1 in EC by a mechanism dependent on a tyrosine kinase(s) and calcium mobilization, but not on c-Src, redox state, or NO production.

Animals↗
PubMed1999

NMR studies of the structure and dynamics of peptide E, an endogenous opioid peptide that binds with high affinity to multiple opioid receptor subtypes.

Structural and dynamic properties of opioid peptide E have been examined in an sodium dodecyl sulfate (SDS) micelle. Structural and dynamic studies both indicate that this peptide exhibits greater segmental mobility than typical structured proteins. An nmr structural analysis of adrenal peptide E in SDS micelles indicated the presence of two well-defined beta-turns, one at the N-terminus encompassing residues 3 to 6, and the second in the region between residues 15 and 18. Certain side chain dihedral angles were also remarkably well defined, such as the chi 1 angle of F4, which exhibited a trans configuration. These calculated structures were based on a set of 9.5 restraints per residue. The backbone dynamics of peptide E in SDS micelles were examined through an analysis of 15N-relaxation parameters. An extended model-free analysis was used to interpret the relaxation data. The overall rotational correlation time is 19.7 ns. the average order parameter S2 is 0.66 +/- 0.15. The N-terminal loop region residues including G3 to R6 have an average order parameter of 0.70 +/- 0.23. The average order parameter lies somewhere between that observed for a random coil (e.g., S2 = 0.3) and that of a well-defined tertiary fold (e.g., S2 = 0.86). This suggests that peptide E in SDS micelles adopts a restricted range of conformations rather than a random coil. Based on the helical structure recently obtained for the highly homologous kappa-agonist dynorphin-A(1-17) and the beta-turn in the same region of peptide E, it is reasonable to assume that these two elements of secondary structure reflect different receptor subtype binding geometries. The intermediate order parameters observed for peptide E in an SDS micelle suggest a degree of dynamic mobility that may enable facile interconversion between helical and beta-turn geometries in the N-terminal agonist domain.

Amino Acid Sequence↗
PubMed1999

Inhibition of hSP-B promoter in respiratory epithelial cells by a dominant negative retinoic acid receptor.

Retinoic acid (RA) receptors (RARs) belong to the nuclear hormone receptor superfamily and play important roles in lung differentiation, growth, and gene regulation. Surfactant protein (SP) B is a small hydrophobic protein synthesized and secreted by respiratory epithelial cells in the lung. Expression of the SP-B gene is modulated at the transcriptional and posttranscriptional levels. In the present work, immunohistochemical staining revealed that RAR-alpha is present on day 14.5 of gestation in the fetal mouse lung. To assess whether RAR is required for SP-B gene transcription, a dominant negative mutant human (h) RAR-alpha403 was generated. The hRAR-alpha403 mutant was transcribed and translated into the truncated protein product by reticulocyte lysate in vitro. The mutant retained DNA binding activity in the presence of retinoid X receptor-gamma to an RA response element in the hSP-B promoter. When transiently transfected into pulmonary adenocarcinoma epithelial cells (H441 cells), the mutant hRAR-alpha403 was readily detected in the cell nucleus. Cotransfection of the mutant hRAR-alpha403 repressed activity of the hSP-B promoter and inhibited RA-induced surfactant proprotein B production in H441 cells, supporting the concept that RAR is required for hSP-B gene transcription in vitro.

Animals↗
PubMed1999

Regulation of mouse SP-B gene promoter by AP-1 family members.

The regulatory role of activator protein-1 (AP-1) family members in mouse surfactant protein (SP) B (mSP-B) promoter function was assessed in the mouse lung epithelial cell line MLE-15. Expression of recombinant Jun B and c-Jun inhibited mSP-B promoter activity by 50-75%. Although c-Fos expression did not alter mSP-B transcription, Jun D enhanced mSP-B promoter activity and reversed inhibition of mSP-B by c-Jun or Jun B. A proximal AP-1 binding site (-18 to -10 bp) was identified that overlaps a thyroid transcription factor-1 binding site. Mutation of this proximal AP-1 site blocked both Jun B inhibition and Jun D enhancement and partially blocked c-Jun inhibition of promoter activity. Promoter deletion mutants were used to identify additional sequences mediating the inhibitory effects of c-Jun in the distal region from -397 to -253 bp. The AP-1 element in this distal site (-370 to -364 bp) is part of a composite binding site wherein AP-1, cAMP response element binding protein, thyroid transcription factor-1, and nuclear factor I interact. Point mutation of the distal AP-1 binding site partially blocked c-Jun-mediated inhibition of the SP-B promoter. Both stimulatory (Jun D) and inhibitory (c-Jun/Jun B) effects of AP-1 family members on mSP-B promoter activity are mediated by distinct cis-acting elements in the mSP-B 5'-flanking region.

Animals↗
PubMed1999

Blockade of GABAA receptors facilitates induction of NMDA receptor-independent long-term potentiation.

An N-methyl-D-aspartate (NMDA)-independent form of long-term potentiation (LTP), which depends on postsynaptic, voltage-dependent calcium channels (VDCCs), has been demonstrated in area CA1 of hippocampus. GABA acting at GABAA receptors limits postsynaptic depolarization during LTP induction. Blockade of GABAA receptors should therefore enhance activation of postsynaptic VDCCs and facilitate the induction of this NMDA receptor-independent, VDCC-dependent LTP. In agreement with this hypothesis, pharmacological blockade of GABAA receptors in the in vitro rat hippocampal slice increased the magnitude of LTP resulting from a normally effective, high-frequency (200 Hz) tetanic stimulation protocol. In addition, GABAA receptor blockade allowed a lower frequency (25 Hz) and normally ineffective tetanic stimulation protocol to induce this form of LTP. Intracellular recordings from CA1 pyramidal cells revealed that blocking GABAA receptors during tetanic stimulation allowed greater postsynaptic depolarization, increased the number of postsynaptic action potentials fired during the tetanization, and also increased the duration of synaptically evoked action potentials. To mimic the increased action potential firing observed when GABAA receptors were blocked, we paired 25-Hz antidromic stimulation with 25-Hz orthodromic stimulation. Paired antidromic + orthodromic 25-Hz stimulation induced NMDA receptor-independent LTP, whereas neither antidromic nor orthodromic stimulation alone induced LTP. Increased action potential firing can therefore at least partially account for the facilitation of NMDA receptor-independent LTP caused by blockade of GABAA receptors. This conclusion is consistent with prior studies demonstrating that action potentials are particularly effective stimuli for the gating of VDCCs in CA1 pyramidal cell dendrites.

2-Amino-5-phosphonovalerate↗
PubMed1999

Evidence for involvement of group II/III metabotropic glutamate receptors in NMDA receptor-independent long-term potentiation in area CA1 of rat hippocampus.

Previous studies implicated metabotropic glutamate receptors (mGluRs) in N-methyl-D-aspartate (NMDA) receptor-independent long-term potentiation (LTP) in area CA1 of the rat hippocampus. To learn more about the specific roles played by mGluRs in NMDA receptor-independent LTP, we used whole cell recordings to load individual CA1 pyramidal neurons with a G-protein inhibitor [guanosine-5'-O-(2-thiodiphosphate), GDPbetaS]. Although loading postsynaptic CA1 pyramidal neurons with GDPbetaS significantly reduced G-protein dependent postsynaptic potentials, GDPbetaS failed to prevent NMDA receptor- independent LTP, suggesting that postsynaptic G-protein-dependent mGluRs are not required. We also performed a series of extracellular field potential experiments in which we applied group-selective mGluR antagonists. We had previously determined that paired-pulse facilitation (PPF) was decreased during the first 30-45 min of NMDA receptor-independent LTP. To determine if mGluRs might be involved in these PPF changes, we used a twin-pulse stimulation protocol to measure PPF in field potential experiments. NMDA receptor-independent LTP was prevented by a group II mGluR antagonist [(2S)-alpha-ethylglutamic acid] and a group III mGluR antagonist [(RS)-alpha-cyclopropyl-4-phosphonophenylglycine], but was not prevented by other group II and III mGluR antagonists [(RS)-alpha-methylserine-O-phosphate monophenyl ester or (RS)-alpha-methylserine-O-phosphate]. NMDA receptor-independent LTP was not prevented by either of the group I mGluR antagonists we examined, (RS)-1-aminoindan-1,5-dicarboxylic acid and 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester. The PPF changes which accompany NMDA receptor-independent LTP were not prevented by any of the group-selective mGluR antagonists we examined, even when the LTP itself was blocked. Finally, we found that tetanic stimulation in the presence of group III mGluR antagonists lead to nonspecific potentiation in control (nontetanized) input pathways. Taken together, our results argue against the involvement of postsynaptic group I mGluRs in NMDA receptor-independent LTP. Group II and/or group III mGluRs are required, but the specific details of the roles played by these mGluRs in NMDA receptor-independent LTP are uncertain. Based on the pattern of results we obtained, we suggest that group II mGluRs are required for induction of NMDA receptor-independent LTP, and that group III mGluRs are involved in determining the input specificity of NMDA receptor-independent LTP by suppressing potentiation of nearby, nontetanized synapses.

Animals↗