PubMed Health⌕ Search

Biomedical subjects

Yun Xia

Publications and source records attributed to Yun Xia.

At least 19 recordsLinked to original sources
PubMed2026

Genome-wide SNP data reveal geographic structure and landscape-associated genomic differentiation in a widespread lizard in arid Eastern Central Asia.

Arid landscapes provide important systems for examining how geographic structure and environmental heterogeneity shape genomic differentiation. In topographically complex desert regions, however, it remains challenging to determine whether population structure primarily reflects landscape resistance, geographic distance, or contemporary environmental variation. Here, we use genome-wide SNP data to investigate population structure, phylogenetic relationships, historical gene flow, demographic history, and landscape correlates of genomic differentiation in the variegated racerunner (Eremias vermiculata), a widespread lacertid lizard across arid Eastern Central Asia. Analyses of 164 individuals recovered six geographically structured nuclear clusters associated with major desert basins and mountain-bounded regions. Nuclear phylogenies resolved two broad regional clades corresponding to northeastern and southwestern parts of the species' range, while PCA and ADMIXTURE analyses recovered six finer-scale genetic clusters. Mitochondrial phylogenies, based on combined NCBI-derived Cyt b and COI sequences from the same individuals, recovered four deeper maternal lineages. These patterns indicate overall phylogeographic agreement between nuclear and mitochondrial datasets, with genome-wide SNPs providing finer-scale resolution of population structure. Demographic reconstructions further uncovered regionally heterogeneous Late Pleistocene histories among clusters, including signals of expansion, stability, and decline. Landscape genomic analyses revealed that genomic differentiation is primarily associated with landscape resistance, particularly elevation and land cover, as well as geographic distance, whereas contemporary environmental variables explained comparatively little variation after controlling for spatial structure. Together, our results suggest that genomic differentiation in E. vermiculata reflects the interplay of persistent landscape configuration, historical connectivity, and region-specific demographic histories across arid Eastern Central Asia. More broadly, this study highlights the value of integrating phylogeographic and landscape genomic approaches for understanding population differentiation and evolutionary history in topographically heterogeneous desert ecosystems.

Arid Eastern Central Asia↗
PubMed2006

Stimulation of adenosine A1 and A2A receptors by AMP in the submucosal plexus of guinea pig small intestine.

Actions of adenosine 5'-monophosphate (AMP) on electrical and synaptic behavior of submucosal neurons in guinea pig small intestine were studied with "sharp" intracellular microelectrodes. Application of AMP (0.3-100 microM) evoked slowly activating depolarizing responses associated with increased excitability in 80.5% of the neurons. The responses were concentration dependent with an EC(50) of 3.5 +/- 0.5 microM. They were abolished by the adenosine A(2A) receptor antagonist ZM-241385 but not by pyridoxal-phosphate-6-azophenyl-2,4-disulfonic acid, trinitrophenyl-ATP, 8-cyclopentyl-1,3-dimethylxanthine, suramin, or MRS-12201220. The AMP-evoked responses were insensitive to AACOCF3 or ryanodine. They were reduced significantly by 1) U-73122, which is a phospholipase C inhibitor; 2) cyclopiazonic acid, which blocks the Ca(2+) pump in intraneuronal membranes; and 3) 2-aminoethoxy-diphenylborane, which is an inositol (1,4,5)-trisphosphate receptor antagonist. Inhibitors of PKC or calmodulin-dependent protein kinase also suppressed the AMP-evoked excitatory responses. Exposure to AMP suppressed fast nicotinic ionotropic postsynaptic potentials, slow metabotropic excitatory postsynaptic potentials, and slow noradrenergic inhibitory postsynaptic potentials in the submucosal plexus. Inhibition of each form of synaptic transmission reflected action at presynaptic inhibitory adenosine A(1) receptors. Slow excitatory postsynaptic potentials, which were mediated by the release of ATP and stimulation of P2Y(1) purinergic receptors in the submucosal plexus, were not suppressed by AMP. The results suggest an excitatory action of AMP at adenosine A(2A) receptors on neuronal cell bodies and presynaptic inhibitory actions mediated by adenosine A(1) receptors for most forms of neurotransmission in the submucosal plexus, with the exception of slow excitatory purinergic transmission mediated by the P2Y(1) receptor subtype.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2006

Differential expression of the CD14/TLR4 complex and inflammatory signaling molecules following i.c.v. administration of LPS.

The CD14/toll-like receptor 4 (TLR4) complex plays a vital role in initiating lipopolysaccharide (LPS) signaling during inflammation. In this study, we assessed innate immune responses and inflammatory transmission in the rat brain following intracerebroventricular (i.c.v.) administration of LPS. I.c.v. LPS induced the widespread increase in CD14 mRNA but did not change levels of TLR4 transcription in the brain. An increase in TLR4 immunoreactivity, coincident with cell death, leukocyte infiltration and neural tissue damage, was found in the meninges, choroid plexus and ventricular ependyma. In addition to CD14, rapid increases in gene expression of IkappaBalpha, IL-1beta, and TNF-alpha occurred along the meninges and ventricular ependyma. The response was most intense along the borders of the brain and declined in intensity in the adjacent periventricular areas and cerebral cortex. In the brain parenchyma, increased TLR4 immunoreactivity was confined to the vasculature and neighboring tissues along with strong vascular expression of IkappaBalpha and mPGES-1. These results suggest involvement of TLR4 in both brain inflammation and neural tissue injury and support the hypothesis that local diffusion and vascular transmission of inflammatory molecules are two major routes for developing inflammation in the brain.

Animals↗
PubMed2006

Neurogenic secretion mediated by the purinergic P2Y1 receptor in guinea-pig small intestine.

We tested the hypothesis that ATP is an enteric neurotransmitter that acts at P2Y1 excitatory purinergic receptors on intestinal secretomotor neurons to evoke neurogenic mucosal secretion in the guinea pig. Ussing chamber methods for studying neurogenic intestinal secretion were used to test the hypothesis. Application of ATP evoked concentration-dependent increases in short circuit current (Isc) indicative of stimulation of electrolyte secretion. MRS2179, a selective P2Y1 purinergic receptor antagonist, suppressed the ATP-evoked responses in a concentration-dependent manner with an IC50 of 0.9+/-0.1 microM. Tetrodotoxin or a selective vasoactive intestinal peptide (VPAC1) receptor antagonist suppressed or abolished the ATP-evoked responses. A selective VPAC1 receptor antagonist also suppressed Isc responses evoked by electrical field stimulation of the secretomotor neurons. Secretory responses to ATP were not suppressed by scopolamine, piroxicam nor selective adenosine receptor antagonists. Region-specific differences in responses to ATP corresponded to regional differences in the expression of mRNA transcripts for the P2Y1 receptor. Post-receptor signal transduction for the P2Y1-evoked responses involved stimulation of phospholipase C and an IP3/Ca2+-calmodulin/protein kinase C signaling cascade. Our evidence suggests that ATP is released as a neurotransmitter to stimulate neurogenic mucosal secretion by binding to P2Y1 receptors expressed by VIP-ergic secretomotor neurons.

Adenosine Diphosphate↗
PubMed2006

Distribution and chemical coding of corticotropin-releasing factor-immunoreactive neurons in the guinea pig enteric nervous system.

Immunofluorescence was used to study immunoreactivity (IR) for corticotropin-releasing factor (CRF) in the guinea pig enteric nervous system. CRF-IR was expressed in both the myenteric and the submucosal plexuses of all regions of the large and small intestine and the myenteric plexus of the stomach. CRF-IR nerve fibers were present in the myenteric and submucosal plexuses, in the circular muscle coat, and surrounding submucosal arterioles. Most of the CRF-IR fibers persisted in the myenteric and submucosal plexuses after 7 days in organotypic culture. CRF-IR was not coexpressed with tyrosine hydroxylase-IR or calcitonin gene-related peptide-IR fibers. The proportions of CRF-IR cell bodies in the myenteric plexus increased progressively from the stomach (0.6%) to the distal colon (2.8%). Most of the CRF-IR myenteric neurons (95%) had uniaxonal morphology; the remainder had Dogiel type II multipolar morphology. CRF-IR cell bodies in the myenteric plexus of the ileum expressed IR for choline acetyltransferase (56.9%), substance P (55.0%), and nitric oxide synthase (37.9%). CRF-IR never colocalized with IR for calbindin, calretinin, neuropeptide Y, serotonin, or somatostatin in the myenteric plexus. CRF-IR cell bodies were more abundant in the submucosal plexus (29.9-38.0%) than in the myenteric plexus. All CRF-IR neurons in submucosal ganglia expressed vasoactive intestinal peptide-IR and were likely to be secretomotor/vasodilator neurons. CRF-IR neurons did not express IR for the CRF(1) receptor. CRF(1)-IR was expressed in neuronal neighbors of those with CRF-IR. Collective evidence suggests that VIPergic secretomotor neurons might provide synaptic input to neighboring cholinergic neurons.

Animals↗
PubMed2006

Ecophysiology of a group of uncultured Gammaproteobacterial glycogen-accumulating organisms in full-scale enhanced biological phosphorus removal wastewater treatment plants.

The presence of glycogen-accumulating organisms (GAOs) in enhanced biological phosphorus removal (EBPR) plants can seriously deteriorate the biological P-removal by out-competing the polyphosphate-accumulating organisms (PAOs). In this study, uncultured putative GAOs (the GB group, belonging to the Gammaproteobacteria) were investigated in detail in 12 full-scale EBPR plants. Fluorescence in situ hybridization (FISH) revealed that the biovolume of the GB bacteria constituted 2-6% of total bacterial biovolume. At least six different subgroups of the GB bacteria were found, and the number of dominant subgroups present in each plant varied between one and five. Ecophysiological investigations using microautoradiography in combination with FISH showed that, under aerobic or anaerobic conditions, all subgroups of the GB bacteria could take up acetate, pyruvate, propionate and some amino acids, while some subgroups in addition could take up formate and thymidine. Glucose, ethanol, butyrate and several other organic substrates were not taken up. Glycolysis was essential for the anaerobic uptake of organic substrates. Polyhydroxyalkanoates (PHA) but not polyphosphate (polyP) granules were detected in all GB bacterial cells. Polyhydroxyalkanoate formation after anaerobic uptake of acetate was confirmed by measuring the increase in fluorescence intensity of PHA granules inside GB bacterial cells after Nile blue staining. One GB subgroup was possibly able to denitrify, and several others were able to reduce nitrate to nitrite. PAOs were also enumerated by FISH in the same treatment plants. Rhodocyclus-related PAOs and Actinobacteria-related PAOs constituted up to 7% and 29% of total bacterial biovolume respectively. Rhodocyclus-related PAOs always coexisted with the GB bacteria and showed many physiological similarities. Factors of importance for the competition between the three groups of important bacteria in EBPR plants are discussed.

Acetates↗
PubMed2006

Platelet-activating factor in the enteric nervous system of the guinea pig small intestine.

Platelet-activating factor (PAF) is a proinflammatory mediator that may influence neuronal activity in the enteric nervous system (ENS). Electrophysiology, immunofluorescence, Western blot analysis, and RT-PCR were used to study the action of PAF and the expression of PAF receptor (PAFR) in the ENS. PAFR immunoreactivity (IR) was expressed by 6.9% of the neurons in the myenteric plexus and 14.5% of the neurons in the submucosal plexus in all segments of the guinea pig intestinal tract as determined by double staining with anti-human neuronal protein antibody. PAFR IR was found in 6.1% of the neurons with IR for calbindin, 35.8% of the neurons with IR for neuropeptide Y (NPY), 30.6% of the neurons with IR for choline acetyltransferase (ChAT), and 1.96% of the neurons with IR for vasoactive intestinal peptide (VIP) in the submucosal plexus. PAFR IR was also found in 1.5% of the neurons with IR for calbindin, 51.1% of the neurons with IR for NPY, and 32.9% of the neurons with IR for ChAT in the myenteric plexus. In the submucosal plexus, exposure to PAF (200-600 nM) evoked depolarizing responses (8.2 +/- 3.8 mV) in 12.4% of the neurons with S-type electrophysiological behavior and uniaxonal morphology and in 12.5% of the neurons with AH-type electrophysiological behavior and Dogiel II morphology, whereas in the myenteric preparations, depolarizing responses were elicited by a similar concentration of PAF in 9.5% of the neurons with S-type electrophysiological behavior and uniaxonal morphology and in 12.0% of the neurons with AH-type electrophysiological behavior and Dogiel II morphology. The results suggest that subgroups of secreto- and musculomotor neurons in the submucosal and myenteric plexuses express PAFR. Coexpression of PAFR IR with ChAT IR in the myenteric plexus and ChAT IR and VIP IR in the submucosal plexus suggests that PAF, after release in the inflamed bowel, might act to elevate the excitability of submucosal secretomotor and myenteric musculomotor neurons. Enhanced excitability of motor neurons might lead to a state of neurogenic secretory diarrhea.

Animals↗
PubMed2006

[Time distribution of ventricular arrhythmias in patients with Brugada syndrome].

OBJECTIVE: To study the characterization of time distribution of ventricular arrhythmias in patients with Brugada syndrome (BrS) using Holter monitoring and ICD follow-up. METHODS: Patients with BrS [all male, mean age (41.07 +/- 11.49) years], were divided into ventricular fibrillation (VF) group (n = 7) and no ventricular fibrillation (N-VF) group (n = 7). Premature ventricular capture (PVC) and VF episodes were detected by Holter monitoring and ICD recording. RESULTS: The 24 hours total number of PVCs ranged from 0 to 74 (mean 9.61 +/- 17.23) in most of the patients and were similar between VF group and N-VF group. The percentage of PVC episodes in VF group was significantly higher than that in N-VF group from nocturnal time to early morning (22:00 to 7:00, 98.67% vs. 44.14%, P < 0.01). There were total 75 VF episodes during (23.18 +/- 17.96) months' follow-up in 5 patients with BrS, 93.3% of which occurred from nocturnal time to early morning (22:00 to 7:00). CONCLUSIONS: The episodes of PVC were enriched from nocturnal time to early morning in BrS patients, this time distribution could be a new noninvasive risk stratification factor for BrS. The episodes of VF in BrS patients were also enriched from nocturnal time to early morning and this time characteristic of episodes of VF could be used to guide drug therapy.

Adult↗
PubMed2006

[Screening and their anti-tumor activity of antisense oligodeoxynucleotides targeting KDR mRNA in breast cancer MCF-7 cells].

OBJECTIVE: To screen the antisense oligodeoxynucleotides (asONs) which could hybridize with KDR (kinase insert domain-containing receptor) mRNA in an effective and specific way and to explore their anti-tumor effects on breast cancer MCF-7 cell line in vitro. METHODS: The asONs were firstly selected using oligodeoxynucleotides library hybridization or computer prediction, then their hybridization ability with KDR mRNA was further tested with oligonucleotide microarray. The asONs with strong hybridization intensity were selected. Their inhibitory effects on MCF-7 cells proliferation and KDR expression were assayed by MTT, RT-PCR and Western blotting assay, respectively. RESULTS: In 13 asONs selected with oligodeoxynucleotides library hybridization, 8 (8/13, 61.5%) showed strong hybridization signals, while such was only 1 in 17 asONs designed by computer prediction. 9 asONs with strong hybridization intensity were selected and synthesized with phosphorothioated modification. All these asONs inhibited the MCF-7 cells proliferation in a dose-dependent manner, in which asON4 and asON7 screened by oligodeoxynucleotides library in combination with oligonucleotide microarray were the most effective, with inhibitory rates of 51.6% and 62.2% at 0.8 micromol/L, respectively. The KDR expression at mRNA and protein levels was reduced by both the two asONs, in a dose-dependent manner. CONCLUSION: asONs screened by oligodeoxynucleotides library hybridization are well consistent with that chosen with oligonucleotide microarray. The combination of oligodeoxynucleotides library with oligonucleotide microarray is an effective approach of asONs screening. The asONs targeting KDR mRNA showed prominent anti-tumor activity on breast cancer MCF-7 cells.

Breast Neoplasms↗
PubMed2005

A kinetically controlled trans bifunctionalized organoimido derivative of the Lindqvist-type hexamolybdate: synthesis, spectroscopic characterization, and crystal structure of (n-Bu4N)2{trans-[Mo6O17(NAr)2]} (Ar = 2,6-dimethylphenyl).

A kinetically controlled trans bifunctionalized organoimido derivative of hexamolybdate, (n-Bu(4)N)(2){trans-[Mo(6)O(17)(NAr)(2)]} (Ar = 2,6-dimethylphenyl) 1, in which the two 2,6-dimethylphenylimido groups are bonded to hexamolybdate at the trans positions, has been successfully synthesized in ca. 60% yield under mild reaction conditions. Its trans structure has been confirmed by a single-crystal X-ray diffraction study. In the crystals, cluster anions of 1 self-assemble into a 3D netlike structure via two different kinds of C-H...O hydrogen bondings, in which 1D supramolecular rectangular channels containing tetrabutylammonium cations form along the a axis. Compound 1 has also been characterized by (1)H NMR, IR, and UV-vis spectroscopic studies. UV-vis-near-IR reflectance spectroscopy measurements reveal the compound's nature of semiconductivity with an optical energy gap of 2.55 eV.

Journal Article↗
PubMed2005

Effective siRNA targets screening for human telomerase reverse transcriptase.

AIM: To study the inhibitory effects of siRNAs targeting different hTERT sequences and to screen the effective siRNA sequence. METHODS: Five double-stranded siRNAs targeting coding and non-coding regions of hTERT gene were designed and synthesized by T7 transcription system in vitro. siRNA4 sequence was screened by full length gene targeting technique and the rest of the siRNA sequences were selected randomly. After being purified by ethanol precipitation, the siRNAs were transfected to the human hepatocellular carcinoma cell (HepG2) by Lipofectamine 2000. At 48-72 h after siRNAs transfection, MTT assay, RT-PCR and Western-blot were applied to evaluate the effects of siRNAs on cell growth, mRNA and protein expression level of hTERT gene, respectively. RESULTS: Compared to the control cells, the cells treated with the five double-stranded siRNAs exhibited different degrees of inhibition of cell proliferation in a dose-dependent manner. siRNA2 and siRNA4, exhibited obvious effects of inhibiting hTERT mRNA and protein expression in HepG2 cells. CONCLUSION: siRNAs targeting different hTERT sequences have significantly various inhibitory effects on hTERT gene expression. The siRNA sequence screened by full length gene targeting technique has comparable inhibitory effect with the rest siRNA sequences screened by random selection, suggesting that siRNAs and antisense oligonucleic acids may have the same effective target sites. Compared with chemical synthesis method, synthesizing double-stranded siRNA by T7 transcription system in vitro is a rapid, simple, and inexpensive method suitable for screening high-effect siRNA targeting site for specific gene.

Carcinoma, Hepatocellular↗
PubMed2005

Expression of type 1 corticotropin-releasing factor receptor in the guinea pig enteric nervous system.

Reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, electrophysiological recording, and intraneuronal injection of the neuronal tracer biocytin were integrated in a study of the functional expression of corticotropin-releasing factor (CRF) receptors in the guinea pig enteric nervous system. RT-PCR revealed expression of CRF1 receptor mRNA, but not CRF2, in both myenteric and submucosal plexuses. Immunoreactivity for the CRF1 receptor was distributed widely in the myenteric plexus of the stomach and small and large intestine and in the submucosal plexus of the small and large intestine. CRF1 receptor immunoreactivity was coexpressed with calbindin, choline acetyltransferase, and substance P in the myenteric plexus. In the submucosal plexus, CRF1 receptor immunoreactivity was found in neurons that expressed calbindin, substance P, choline acetyltransferase, or neuropeptide Y. Application of CRF evoked slowly activating depolarizing responses associated with elevated excitability in both myenteric and submucosal neurons. Histological analysis of biocytin-filled neurons revealed that both uniaxonal neurons with S-type electrophysiological behavior and neurons with AH-type electrophysiological behavior and Dogiel II morphology responded to CRF. The CRF-evoked depolarizing responses were suppressed by the CRF1/CRF2 receptor antagonist astressin and the selective CRF1 receptor antagonist NBI27914 and were unaffected by the selective CRF2 receptor antagonist antisauvagine-30. The findings support the hypothesis that the CRF1 receptor mediates the excitatory actions of CRF on neurons in the enteric nervous system. Actions on enteric neurons might underlie the neural mechanisms by which stress-related release of CRF in the periphery alters intestinal propulsive motor function, mucosal secretion, and barrier functions.

Action Potentials↗
PubMed2005

Angiotensin receptors and actions in guinea pig enteric nervous system.

Actions of ANG II on electrical and synaptic behavior of enteric neurons in the guinea pig small intestine were studied. Exposure to ANG II depolarized the membrane potential and elevated neuronal excitability. The number of responding neurons was small, with responses to ANG II in 32% of submucosal neurons and 25% of myenteric neurons. Hyperpolarizing responses were evoked by ANG II in 45% of the neurons. The hyperpolarizing responses were suppressed by alpha2-noradrenergic receptor antagonists, which suggested that the hyperpolarizing responses reflected stimulation of norepinephrine release from sympathetic neurons. Exposure to ANG II enhanced the amplitude and prolonged the duration of noradrenergic inhibitory postsynaptic potentials and suppressed the amplitude of both fast and slow excitatory postsynaptic potentials. The selective ANG II(1) receptor (AT1R) antagonists, ZD-7115 and losartan, but not a selective AT2R antagonist (PD-123319), suppressed the actions of ANG II. Western blot analysis and RT-PCR confirmed expression of AT1R protein and the mRNA transcript for the AT1R in the enteric nervous system. No expression of AT2R protein or mRNA was found. Immunoreactivity for AT1R was expressed by the majority of neurons in the gastric antrum and small and large intestine. AT1R immunoreactivity was coexpressed with calbindin, choline acetyltransferase, calretinin, neuropeptide Y, and nitric oxide synthase in subpopulations of neurons. The results suggest that formation of ANG II might have paracrine-like actions in the enteric nervous system, which include alterations in neuronal excitability and facilitated release of norepinephrine from sympathetic postganglionic axons. The enhanced presence of norepinephrine is expected to suppress fast and slow excitatory neurotransmission in the enteric microcircuits and to suppress neurogenic mucosal secretion.

Angiotensin II↗
PubMed2005

[Preparation and characterization of indomethacin/poly(N-isopropylacrylamide)-beta-cyclodextrin complex with temperature-sensitivity].

AIM: To synthesize poly(N-isopropylacrylamide)/cyclodextrin conjugate (PNIPA-beta-CD) as thermosensitive drug carrier, incorporate indomethacin into the conjugate and evaluate the drug release from the carrier in vitro. METHODS: PNIPA-beta-CD was synthesized by introducing carboxyl terminated PNIPA into the primary hydroxy group of beta-CD. The obtained conjugate was characterized by FTIR, 1H NMR and DSC. The indomethacin/PNIPA-beta-CD complex was prepared by lyophilization. In vitro drug release from the complex was carried out at 25 degrees C and 37 degrees C respectively. RESULTS: Thermosensitive PNIPA-beta-CD was synthesized successfully. The LCST is 35 degrees C, as measured by turbidity method. The drug release from indomethacin/PNIPA-beta-CD complex was slower at 37 degrees C than that at 25 degrees C. CONCLUSION: Thermosensitive PNIPA-beta-CD with molecular inclusion capacity is a potential carrier for drug sustained release.

Acrylic Resins↗
PubMed2005

[Study on the molecular epidemiology of Stenotrophomonas maltophilia infection in patients on mechanical ventilation].

OBJECTIVE: To investigate a potential outbreak of Stenotrophomonas maltophilia (pma) infection occurred in patients on mechanical ventilation in a respiratory ICU (RICU) and to track the infective origins by antibiotype and pulsed-field gel electrophoresis (PFGE) typing methods. METHODS: (1) Thirteen pma strains were isolated from 9 patients on mechanical ventilation (9 strains), hand swabs of medical staffs in RICU (2 strains) and fiberscope used for intubations and aspiration (2 strains) from December, 2002 to February, 2003. (2) Sixteen strains gathered from different wards during the period of 1997 - 2000 were collected and used as control. (3) Antibiotic susceptibility data of all strains were collected. (4) Homology of the strains was analyzed by the methods of antibiotype and PFGE genotype. RESULTS: Of the 9 pma isolated from patients on mechanical ventilation, eight had identical PFGE genotype. The isolates from two RICU staffs and two fiberscope displayed the same genotype with the eight patients above. Seven of the 9 isolates shared an identical antibiotype. The consistent rate of antibiotype with PFGE genotype was 85% (11/13). There were 11 PFGE genotypes and 9 antibiotypes in 16 strains of the control group, which indicated that they came from different clones. CONCLUSIONS: Eight pma strains of patients in RICU came from the same clone. This result proved that clone transmission occurred in patients on mechanical ventilation. Contaminated fiberscope and hands of staffs may be the infective origin and the route of transmission.

Bacterial Typing Techniques↗
PubMed2004

Estrogen induces nitric oxide production via activation of constitutive nitric oxide synthases in human neuroblastoma cells.

Although it is becoming increasingly evident that nitric oxide (NO) mediates some of estrogen's actions in the brain, the effects of estrogen on NO production through NO synthases (NOS) in neuronal cells have not yet been identified. Here we assessed changes in NO production induced by 17beta-estradiol (E2) in cells of neuronal origin using human SK-N-SH neuroblastoma cells, which we show express all three isoforms of NOS. Involvement of NOS isoforms in E2-induced NO production was examined using isoform-specific NOS inhibitors. E2 (10(-10)-10(-6) m) induced rapid increases in NO release and changes in endothelial NOS (eNOS) expression, which were blocked by ICI 182,780, an antagonist of estrogen receptors. Increased levels of NO release and NOS activity induced by E2 were blocked by N5-(1-Imino-3-butenyl)-L-ornithine, a neuronal NOS inhibitor, and N(5)-(1-Iminoethyl)-L-ornithine, an eNOS inhibitor, but not by 1400W, an inducible NOS inhibitor. These results demonstrate that E2-stimulated NO production occurs via estrogen receptor-mediated activation of the constitutive NOSs, neuronal NOS and eNOS. The E2-induced NO increase was abolished when extracellular Ca2+ was removed from the medium or after the addition of nifedipine, an L-type channel blocker, and was partially inhibited using 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester, an intracellular Ca2+ chelator. However, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester itself also caused an increase in NO release that was blocked by 1400W, suggesting that inducible NOS mediates this response. Together these data reveal that constitutive NOS activities are responsible for E2-induced NO production in neuroblastoma cells and that differential activation of NOS isoforms in these cells occurs in response to different treatments.

Calcium↗
PubMed2004

Action of bradykinin in the submucosal plexus of guinea pig small intestine.

Intracellular recording methods with "sharp" microelectrodes were used to study actions of bradykinin (BK) on electrical behavior of morphologically identified neurons and the identification and localization of BK receptors in the submucosal plexus of guinea pig small intestine. Exposure to BK depolarized the membrane potential and elevated excitability in submucosal neurons with AH-type electrophysiological behavior and Dogiel II multipolar morphology and in neurons with S-type electrophysiological behavior and uniaxonal morphology. BK-evoked depolarizing responses were associated with increased neuronal input resistance in AH-type neurons and decreased input resistance in S-type neurons. The selective B(2) BK receptor antagonists HOE-140 (icatabant acetate) and WIN64338 [(S)-4[2-bis(cyclohexylamino)methyleneamino]-3-(2-napthalenyl)-1-oxopropylamino]benzyl tributyl phosphonium chloride hydrochloride], but not the selective B(1) receptor antagonists des-arg(10)-HOE-140 and des-arg(9)-leu(8)-BK, suppressed the BK-evoked responses. The selective B(2) receptor agonist Kallidin, but not the selective B(1) receptor agonist des-arg(9)-BK mimicked the excitatory action of BK. Western blot analysis and reverse transcription-polymerase chain reaction confirmed the expression of B(2) receptor protein and mRNA. Binding studies with a fluorescently labeled BK(2) antagonist found expression of B(2) receptors on a majority of the ganglion cells. B(2) receptors occupied 82% of the neurons that expressed immunoreactivity for neuropeptide Y, 75% of the neurons that expressed vasoactive intestinal peptide, 84% of the neurons that expressed substance P, 71% of the neurons that expressed choline acetyltransferase, and all neurons that expressed calbindin immunoreactivity. The results suggest that the B(2) receptor mediates the excitatory action of BK on submucosal plexus neurons. Pathophysiological significance of the excitatory actions on secretomotor neurons might be stimulated mucosal secretion and the secretory diarrhea associated with intestinal inflammatory states.

Animals↗