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Biomedical subjects

X Liu

Publications and source records attributed to X Liu.

At least 127 records · Page 7Linked to original sources
PubMed2004

The regulation of glucose-excited neurons in the hypothalamic arcuate nucleus by glucose and feeding-relevant peptides.

Glucosensing neurons in the hypothalamic arcuate nucleus (ARC) were studied using electrophysiological and immunocytochemical techniques in neonatal male Sprague-Dawley rats. We identified glucose-excited and -inhibited neurons, which increase and decrease, respectively, their action potential frequency (APF) as extracellular glucose levels increase throughout the physiological range. Glucose-inhibited neurons were found predominantly in the medial ARC, whereas glucose-excited neurons were found in the lateral ARC. ARC glucose-excited neurons in brain slices dose-dependently increased their APF and decreased their ATP-sensitive K+ channel (KATP channel) currents as extracellular glucose levels increased from 0.1 to 10 mmol/l. However, glucose sensitivity was greatest as extracellular glucose decreased to <2.5 mmol/l. The glucokinase inhibitor alloxan increases KATP single-channel currents in glucose-excited neurons in a manner similar to low glucose. Leptin did not alter the activity of ARC glucose-excited neurons. Although insulin did not affect ARC glucose-excited neurons in the presence of 2.5 mmol/l (steady-state) glucose, they were stimulated by insulin in the presence of 0.1 mmol/l glucose. Neuropeptide Y (NPY) inhibited and alpha-melanocyte-stimulating hormone stimulated ARC glucose-excited neurons. ARC glucose-excited neurons did not show pro-opiomelanocortin immunoreactivity. These data suggest that ARC glucose-excited neurons may serve an integrative role in the regulation of energy balance.

Alloxan↗
PubMed2003

Very large magnetoresistance in lateral ferromagnetic (Ga,Mn)as wires with nanoconstrictions.

We have fabricated (Ga,Mn)As nanostructures in which domain walls can be pinned by sub-10 nm constrictions. Controlled by shape anisotropy, we can switch the regions on either side of the constriction to either parallel or antiparallel magnetization. All samples exhibit a positive magnetoresistance, consistent with domain-wall trapping. For metallic samples, we find a magnetoresistance up to 8%, which can be understood from spin accumulation. In samples where, due to depletion at the constriction, a tunnel barrier is formed, we observe a magnetoresistance of up to 2000%.

Journal Article↗
PubMed2003

Disrupted circadian rhythms in VIP- and PHI-deficient mice.

The related neuropeptides vasoactive intestinal peptide (VIP) and peptide histidine isoleucine (PHI) are expressed at high levels in the neurons of the suprachiasmatic nucleus (SCN), but their function in the regulation of circadian rhythms is unknown. To study the role of these peptides on the circadian system in vivo, a new mouse model was developed in which both VIP and PHI genes were disrupted by homologous recombination. In a light-dark cycle, these mice exhibited diurnal rhythms in activity which were largely indistinguishable from wild-type controls. In constant darkness, the VIP/PHI-deficient mice exhibited pronounced abnormalities in their circadian system. The activity patterns started approximately 8 h earlier than predicted by the previous light cycle. In addition, lack of VIP/PHI led to a shortened free-running period and a loss of the coherence and precision of the circadian locomotor activity rhythm. In about one-quarter of VIP/PHI mice examined, the wheel-running rhythm became arrhythmic after several weeks in constant darkness. Another striking example of these deficits is seen in the split-activity patterns expressed by the mutant mice when they were exposed to a skeleton photoperiod. In addition, the VIP/PHI-deficient mice exhibited deficits in the response of their circadian system to light. Electrophysiological analysis indicates that VIP enhances inhibitory synaptic transmission within the SCN of wild-type and VIP/PHI-deficient mice. Together, the observations suggest that VIP/PHI peptides are critically involved in both the generation of circadian oscillations as well as the normal synchronization of these rhythms to light.

Animals↗
PubMed2003

Current transients associated with BK channels in human glioma cells.

We have previously demonstrated the expression of BK channels in human glioma cells. There was a curious feature to the whole-cell currents of glioma cells seen during whole-cell patch-clamp: large, outward current transients accompanied repolarization of the cell membrane following an activating voltage step. This transient current, Itransient, activated and inactivated rapidly (approximately 1 ms). The I-V relationship of Itransient had features that were inconsistent with simple ionic current through open ion channels: (i) Itransient amplitude peaked with a -80 mV voltage change and was invariant over a 200 mV range, and (ii) Itransient remained large and outward at -140 mV. We provide evidence for a direct relationship of Itransient to glioma BK currents. They had an identical time course of activation, identical pharmacology, identical voltage-dependence, and small, random variations in the amplitude of the steady-state BK current and Itransient seen over time were often perfectly in phase. Substituting intracellular K+ with Cs+, Li+, or Na+ ions reversibly reduced Itransient and BK currents. Itransient was not observed in recordings of other BK currents (hbr5 expressed in HEK cells and BK currents in rat neurons), suggesting Itransient is unique to BK currents in human glioma cells. We conclude that Itransient is generated by a mechanism related to the deactivation, and level of prior activation, of glioma BK channels. To account for these findings we propose that K+ ions are "trapped" within glioma BK channels during deactivation and are forced to exit to the extracellular side in a manner independent of membrane potential.

Adaptation, Physiological↗
PubMed2003

Magnetic domain structure and magnetic anisotropy in Ga1-xMn(x)As.

Large, well-defined magnetic domains, on the scale of hundreds of micrometers, are observed in Ga1-xMn(x)As epilayers using a high-resolution magneto-optical imaging technique. The orientations of the magnetic moments in the domains clearly show in-plane magnetic anisotropy, which changes through a second-order transition from a biaxial mode (easy axes nearly along [100] and [010]) at low temperatures to an unusual uniaxial mode (easy axis along [110]) as the temperature increases above about T(c)/2. This transition is a result of the interplay between the natural cubic anisotropy of the GaMnAs zinc-blende structure and a uniaxial anisotropy which attribute to the effects of surface reconstruction.

Journal Article↗
PubMed2003

Osmomechanical stress selectively regulates translocation of protein kinase C isoforms.

Osmomechanical stress, resulting in cell swelling and activation/regulation of numerous cellular processes, may play a critical role in cell signaling by selectively regulating translocation of protein kinase C (PKC) isoforms from cytosol to membrane compartments. Western blotting of renal epithelial cell fractions demonstrated the expression of five PKC isoforms. Three of these isoforms (PKCalpha, PKCepsilon, PKCzeta) translocated to the membrane fraction upon exposure of cells to osmomechanical stress (hypotonic medium). Immunohistochemical staining of cells using isoform-specific antibodies further demonstrated translocation of the phorbol ester-sensitive isoforms, PKCalpha and PKCepsilon, to both the plasma membrane and perinuclear sites, reflecting potential initial steps in regulation of specific effector pathways. Indeed, selective inhibition of PKCs indicates a potential role for PKCalpha in modulating a calcium influx channel. It is concluded that osmomechanical stress induces selective translocation of specific PKC isoforms, demonstrating a key role of osmomechanical stress in selectively regulating PKC-dependent signaling pathways.

Animals↗
PubMed2003

Vasoreactions to acute hypoxia, whole lungs and isolated vessels compared: modulation by NO.

We aimed to explain diverse pulmonary vascular responses to hypoxia in different preparations and their modulation by NO. In rats we compared isolated perfused lungs (IPL), small vessels in vitro (PRVs) and in vivo preparations. In IPL and in vivo, acute and chronic nitric oxide synthase (NOS) blockade with L-NAME left normoxic pulmonary artery pressure unchanged but enhanced hypoxic vasoconstriction, hypoxia-induced pulmonary vasoconstriction (HPV). PRVs in vitro, precontracted with PGF(2alpha), showed four tension changes in acute hypoxia: dilatation, contraction, dilatation, contraction. Acute and chronic NOS blockade reduced the first two phases. In non-precontracted PRVs (from other laboratories), NOS inhibition enhanced HPV as in vivo and IPL; attenuation of HPV seems associated with precontraction. Thus reduced NOS activity does not cause pulmonary hypertension but exaggerates HPV. In IPL, prolonged severe hypoxia caused biphasic vasoconstriction separated by dilatation; the time course resembled that seen in PRVs. We suggest that the sequence of events during hypoxia in PRVs can be detected in whole lung preparations.

Animals↗
PubMed2003

Improved method for measurement of human plasma xanthine oxidoreductase activity.

The XOR activity in human plasma was measured by quantifying the XOR-derived uric acid (UA) in plasma using the high-performance liquid chromatography (HPLC) equipped with a UV detector. Chromatographic separation consisted of the mobile phase (a mixture of 0.1% trifluoroacetic acid in Milli-Q water and 0.085% trifluoroacetic acid in acetonitrile in a mix ratio of 99:1) running through a Zorbax StableBond SB-C(18) column at a flow-rate of 1 ml/min. Deproteinization with heat-treatment of plasma samples after the reaction was used in the assay to avoid splitting of the UA and xanthine peaks caused by acid deproteinization that could interfere the accurate determination of human plasma XOR activity in our case. Based on the examination of the dependence of XOR activity on added amounts of xanthine and reaction times, the amount of xanthine and reaction time for XOR activity assay were determined to prevent the errors caused by the limiting effect of substrates and plateau phase of the reaction. Using this method, human plasma XOR activities of 25 healthy people were measured. The average human plasma XOR activity was 2.1+/-0.8 (x10(-3) U/ml).

Chromatography, High Pressure Liquid↗
PubMed2003

Determination of the subthreshold state contribution in 13C(alpha,n)16O, the main neutron-source reaction for the s process.

The reaction rate of the stellar reaction 13C(alpha,n)16O, which is currently considered to be the main neutron source for the slow (s) process at low energies, has been rederived using the direct alpha-transfer reaction 13C(6Li,d)17O leading to the subthreshold state at 6.356 MeV in 17O. The contribution of the subthreshold state is found to be much smaller than the currently accepted predictions for the main neutron source of the s process, indicating less of a role of this reaction as the neutron source for the s-process scenario in low-mass stars at the asymptotic giant branch.

Journal Article↗
PubMed2003

Infrared response of multiwalled boron nitride nanotubes.

We report the infrared (IR) response of bulk samples of multiwalled boron nitride nanotubes, produced by a substitution reaction from single walled carbon nanotubes, which is dominated by two characteristic BN-vibrations at 800 and 1372 cm-1.

Journal Article↗
PubMed2003

Low dose latrunculin-A inhibits dexamethasone-induced changes in the actin cytoskeleton and alters extracellular matrix protein expression in cultured human trabecular meshwork cells.

We determined the effects of a low dose of the actin-disrupting agent latrunculin (LAT)-A on dexamethasone (DEX)-induced changes in actin organization, focal adhesions, and production of extracellular matrix proteins in cultured human trabecular meshwork (HTM) cells. HTM cells were cultured to a highly confluent stage with stable endothelium-like morphology and incubated with 0.1 or 0.2 microM DEX and/or 0.1 microM LAT-A. Changes in the actin cytoskeleton and vinculin-containing focal contacts were evaluated by immunofluorescence microscopy. Expression of thrombospondin-1 (TSP1) and fibronectin (FN) in HTM cells was evaluated by Western blot analysis. The results showed that DEX induced morphological changes and actin reorganization in HTM cells. The cells partly recovered after DEX withdrawal, but the addition of low dose LAT-A hastened the recovery. In addition, DEX failed to induce changes when co-incubated with LAT-A for at least 4 weeks, and for at least 2 weeks when cells were pre-treated with LAT-A for 2 weeks. HTM cells treated with 0.1 microM LAT-A only for 5 days showed mild disorganization of the actin cytoskeleton and focal adhesions, which persisted during the 4 weeks of treatment. DEX stimulated production of FN in HTM cells independent of LAT-A treatment. LAT-A and, to a lesser extent, DEX inhibited production of TSP1 by HTM cells. Although LAT-A is not a DEX receptor antagonist, it is able to prevent the effects of DEX on the actin cytoskeleton in cultured HTM cells at a dose subthreshold for increasing outflow facility in monkeys. This suggests that LAT-A at low doses may be useful in treating steroid and other glaucomas. TSP1 may be an important target of LAT-A in HTM cells and modulation of TSP may influence the actin cytoskeleton of the trabecular meshwork (TM), and consequently, intraocular pressure.

Actins↗
PubMed2003

Suppression of genioglossus muscle tone and activity during reflex hypercapnic stimulation by GABA(A) mechanisms at the hypoglossal motor nucleus in vivo.

The genioglossus muscle is involved in the maintenance of an open airway for effective breathing. Inhibitory neurotransmitters may be responsible for the major suppression of hypoglossal motor output to genioglossus muscle that occurs in certain behaviours such as rapid-eye-movement sleep. There is evidence for GABA(A) receptor-mediated inhibition of hypoglossal motoneurons in vitro. However, comparable studies have not been performed in vivo and the interactions of such mechanisms with integrative reflex respiratory control have also not been determined. Urethane-anaesthetised, tracheotomized and vagotomized rats were studied whilst diaphragm and genioglossus muscle activities, blood pressure and the electroencephalogram were recorded. Microdialysis probes were implanted into the hypoglossal motor nucleus, with sites verified by histology. Genioglossus responses to microdialysis perfusion of muscimol (GABA(A) agonist: 0, 0.1, 1 and 10 microM in artificial cerebrospinal fluid) were recorded at inspired CO(2)s of 0, 5 and 7.5% in six rats. Responses to bicuculline (GABA(A) antagonist, 0, 1, 10, 100 and 1000 microM) were also studied in six rats with and without CO(2) stimulation. Genioglossus activity decreased with muscimol (P<0.0001), with major suppression at 1 and 10 microM during air breathing (decreases=70.2% and 92.8%, P<0.005). Genioglossus activity increased with CO(2) (P=0.003), but genioglossus activation with 5 and 7.5% CO(2) were almost abolished with 10-microM muscimol. Responses were specific to genioglossus muscle as there were no changes in diaphragm, respiratory rate or blood pressure with muscimol (P>0.144). Antagonism of GABA(A) receptors increased genioglossus activity (P<0.001). These results show that GABA(A) receptor stimulation at the hypoglossal motor nucleus suppresses both genioglossus muscle tone and activity in the presence of reflex stimulation produced by hypercapnia. Recruitment of such mechanisms may contribute to the major suppression of genioglossus activity observed with and without CO(2) stimulation in behaviours such as rapid-eye-movement sleep.

Animals↗
PubMed2003

Expression of fibroblast growth factor 2 and its receptor during skeletal muscle development from turkeys with different growth rates.

Fibroblast growth factor 2 (FGF2) is a key regulator of muscle cell proliferation and differentiation. To address how FGF2 and fibroblast growth factor receptor 1 (FGFR1) gene expression influences skeletal muscle development and growth, pectoralis major muscle was isolated at embryonic days (ED) 14, 16, 18, 20, 22, and 24, and at 1-, 8-, 12-, and 16-week posthatch from a turkey line (F) selected only for increased 16-week body weight and its genetic control line (RBC2). The mRNA levels of FGF2 and FGFR1 were measured by semi-quantitative reverse transcription polymerase chain reaction. Compared to the RBC2 line males, the F line males had higher FGF2 mRNA levels at ED 14 and 16, and higher FGFR1 mRNA levels at ED 18, but down-regulated FGF2 and FGFR1 gene expression at ED 22. Although no FGF2 mRNA was detected in posthatch muscle tissue, the F line turkeys had more FGFR1 gene expression at 8-, 12-, and 16-week posthatch than the RBC2 line turkeys. During myogenic satellite cell proliferation, the F line cells had higher FGF2 and FGFR1 mRNA levels than the RBC2 line cells. The satellite cell responsiveness to FGF2 treatment was evaluated by the ability of the cells to proliferate. The male satellite cells were more responsive to FGF2 stimulation than the female cells in both lines. These results suggest that the F line turkeys have increased FGF2 signaling that may affect muscle cell proliferation and differentiation, which may also lead to an enhancement in muscle development and growth rate.

Animals↗
PubMed2003

Association of autism severity with a monoamine oxidase A functional polymorphism.

A functional polymorphism (the upstream variable-number tandem repeat region, or uVNTR) in the monoamine oxidase A (MAOA) promoter region has been reported to be associated with behavioral abnormalities as well as increased serotonergic responsivity. We examined the relation between MAOA-uVNTR alleles and the phenotypic expression of autism in 41 males younger than 12.6 years of age. Children with the low-activity MAOA allele had both lower intelligence quotients (IQ) and more severe autistic behavior than children with the high-activity allele. In follow-up testing of 34 of the males at the 1-year time-point, those with the low-activity allele showed a worsening in IQ but no change in the severity of their autistic behavior. We conclude that functional MAOA-uVNTR alleles may act as a genetic modifier of the severity of autism in males.

Activities of Daily Living↗
PubMed2003

Presence of functional vasopressin receptors in spinal ventral horn neurons of young rats: a morphological and electrophysiological study.

The objective of the present work was double. (i) Light microscopic autoradiography was used to determine the distribution of vasopressin and oxytocin binding sites in the spinal cord of rats. (ii) Whole-cell recordings were performed in lumbar spinal cord slices in order to assess whether these receptors are functional, whether they are located pre- or postsynaptically and whether they are present in motoneurons. In newborns, vasopressin binding sites of the V1a type were present in all laminae of the central gray at all segmental levels, whereas oxytocin binding sites were found only in the superficial layers of the dorsal horn. In adults, binding sites for both neuropeptides were also present, but were less dense. The dissociation constants for vasopressin were similar in newborns and adults. Whole-cell recordings showed that in identified motoneurons vasopressin exerted a direct effect, by inducing a membrane depolarization or by generating a sustained inward current, and an indirect effect, by enhancing glycinergic and GABAergic inhibitory transmission. Vasopressin-induced facilitation of inhibitory transmission could also be demonstrated in unidentified ventral horn neurons. All these effects were mediated by V1a but not V1b receptors. In some neurons, glycinergic transmission was also facilitated by a selective oxytocin receptor agonist. Our data, together with data obtained previously in brainstem motor nuclei, suggest that vasopressin of hypothalamic origin could play a role in motricity. The neuropeptide could act as a neuromodulator, because it would not directly activate motoneurons, but rather render them more responsive to incoming excitatory inputs. Vasopressin may thus act as a regulator of muscular force.

Animals↗
PubMed2003

E-Selectin mediates pathogenic effects of antiphospholipid antibodies.

Antiphospholipid (aPL) antibodies, detected in patients with antiphospholipid syndrome (APS) are associated with thrombosis, pregnancy loss and thrombocytopenia. Studies have shown that aPL are thrombogenic in vivo, but the mechanism(s) involved are not completely understood. Several studies have demonstrated that aPL antibodies activate endothelial cells (ECs) in vitro, as determined by up-regulation of adhesion molecules: E-selectin (E-sel); intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and in vivo. The objectives of these study were to determine the effects of aPL antibodies on the expression of E-selectin on ECs, on the adhesion of monocytes to ECs and to study the role of E-selectin on aPL antibodies enhanced thrombus formation and activation of ECs in vivo. We demonstrated that the surface expression of E-selectin on HUVEC by ELISA was increased 400-fold when treated with tumor necrosis factor-alpha (TNF-alpha) and 421-fold when treated with aPL antibodies during 4 h. APL antibodies also induced activation of the nuclear factor-kappa B (NF-kappaB). APL antibodies increased significantly the number of adhering leukocytes to ECs in vivo in C57BL/6 J mice when compared to IgG-NHS treated mice. This effect was abrogated in E-selectin-deficient mice. The thrombus size was significantly increased in C57BL/6 J mice treated with aPL antibodies when compared to mice treated with IgG-NHS. This enhancement in thrombus size by aPL antibodies was abrogated in E-selectin-deficient mice treated with aPL antibodies.

Animals↗
PubMed2003

CoMFA of the acute toxicity of phenylsulfonyl carboxylates to Vibrio fischeri.

From the Comparative Molecular Field Analysis (CoMFA) method, the paper describes a three-dimentional quantitative structure-activity relationship (3D-QSAR) model for the acute toxicity logEC50 (15min-EC50 in micromol l(-1)) of 56 phenylsulfonyl carboxylates on Vibrio fischeri. The achievement of a high leave-one-out (LOO) cross-validated correlation coefficient q2 of 0.790 with four optimum components indicates the significance of the correlation of the steric and electrostatic fields with the biological activities. The key features in the CoMFA contour maps are critical to trace the important properties and gain insight into the toxic mechanism of the tested phenylsulfonyl carboxylates.

Carboxylic Acids↗