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Biomedical subjects

J Xie

Publications and source records attributed to J Xie.

At least 235 records · Page 13Linked to original sources
PubMed1995

Independent suppression of nitric oxide and TNF alpha in the lung of conscious rats by ethanol.

Tumor necrosis factor-alpha (TNF alpha) and nitric oxide (NO) mediate in part the microbicidal response of murine and rodent alveolar macrophages (AM) and recruited neutrophils (PMN) to airborne infections. Ethanol (ETOH) suppresses intrapulmonary TNF alpha and NO release and impairs pulmonary host defense mechanisms. We tested the concept that ETOH down-regulates NO by inhibiting production of TNF alpha. Male rats were given intratracheal (i.t.) saline (PBS), a polyclonal anti-TNF alpha antibody (TNFab) or nonimmune IgG (22 mg/kg, i.m.) 2 h before giving i.t. Escherichia coli endotoxin (LPS) to normal rats or rats pretreated with ETOM (5.5 g/kg, i.p.) 30 min before experimentation. AM and PMN were obtained from the bronchoalveolar lavage fluid (BAL) fluid of rats killed 2 and 4 h after administration of LPS. mRNA for inducible NO synthase (iNOS) and TNF alpha were measured in AM and PMN with competitor equalized RT-PCR techniques. The BAL fluid, AM, and PMN were assayed for TNF alpha and NO2-, and NO3- (RNI) with the L929 bioassay and chemiluminescence, respectively. TNFab abolished LPS-induced increases in TNF alpha but did not suppress the NO content of the BAL fluid or gene expression for iNOS by AM or PMN. ETOH suppressed LPS-induced increases in mRNA for iNOS, production of RNI, and BAL fluid TNF alpha but did not affect LPS-induced increases in mRNA for TNF alpha. ETOH-induced attenuation of LPS-induced up-regulation of the iNOS system did not differ in rats pretreated with TNFab or IgG. Thus, ETOH down-regulates iNOS gene expression and RNI production independent of its effects on TNF alpha. Acute ETOH administration suppresses iNOS at the level of transcription and TNF alpha at the level of translation or release of the peptide.

Amino Acid Oxidoreductases↗
PubMed1995

Ethanol suppresses Mycobacteria tuberculosis-induced mRNA for nitric oxide synthase in alveolar macrophages, in vivo.

Acute ingestion of alcohol [ethanol (ETOH)] adversely affects the immunocompetence of both naive individuals as well as chronic alcohol abusers. An increased incidence and severity of tuberculosis is found in chronic alcohol abusers. Nitric oxide (NO) produced by alveolar macrophages (AMs) may play a role in the in vitro killing of Mycobacterium avium and Mycobacterium tuberculosis (MTB). Moreover, tumor necrosis factor-alpha (TNF-alpha) is believed to be a primary cytokine mediator of NO production by AMs. Recent studies from our laboratory demonstrated that ETOH suppressed endotoxin-induced increases in both TNF-alpha and NO in AMs, in vivo. We tested the postulate that acute ingestion of ETOH can interfere with mycobacteria-induced upregulation of the NO system in AMs, in vivo. We show that heat-killed M. avium complex (MAC) and human virulent MTB instilled into rat lungs rapidly increased mRNA for inducible NO synthase II (iNOS) of AMs in fluid obtained by bronchoalveolar lavage (BAL fluid). This was associated with production of reactive nitrogen intermediates [(RNIs); NO2- and NO3-] in BAL fluid, lung homogenate, and AMs in the absence of a significant increase in BAL fluid TNF-alpha. A single dose of ETOH (5.5 g/kg, ip) administered 30 min before intratracheal administration of MAC or MTB attenuated both MAC and MTB-induced increases in RNI in BAL fluid, lung, and AMs, and the increase in mRNA for iNOS. Thus, mycobacteria upregulate iNOS mRNA and enhance RNI production by AMs without any increase in the production of TNF-alpha. Moreover, ETOH attenuates mycobacteria-induced upregulation of mRNA for iNOS and RNI production in the absence of ETOH-mediated suppression of TNF. Speculatively, ETOH-mediated inhibition of the AM NO system may offer an explanation for the increased severity of mycobacterial infections in alcoholics.

Alcoholic Intoxication↗
PubMed1995

Bonding of composite resin to contaminated human enamel and dentin.

PURPOSE: The purpose of this in vitro study was to evaluate the bond strengths of a bonding agent and composite resin system to human enamel and dentin treated with five contaminants (saliva, plasma, zinc oxide-eugenol cement, noneugenol zinc oxide cement, and handpiece lubricant) using air, moisture, and water as controls. MATERIALS AND METHODS: A commercial bonding agent (Gluma 2000; Bayer AG, Dormagen, Germany) and its composite (Pekafill; Bayer AG) were applied to tooth structure under two conditions (contaminated and re-etched). Samples were debonded in tension after 24 hours using an inverted, truncated cone bond test. RESULTS: Among the controls, the highest bond strengths were obtained to enamel (20 MPa) and dentin (12 MPa) with air drying. Contaminants lowered the bond strength by 20% to 100%. Re-etching without additional mechanical preparation resulted in bond strengths similar to the air control. CONCLUSIONS: Bond strength of Gluma 2000/Pekafill to tooth structure is sensitive to common forms of contamination but can be improved by re-etching after contamination occurs.

Acid Etching, Dental↗
PubMed1995

Bending of blood vessel wall: stress-strain laws of the intima-media and adventitial layers.

In order to determine the stress-strain relationship of the inner (intima and media) and outer (adventitia) layers of blood vessels in the neighborhood of the zero-stress state, bending experiments were performed on aortic strips of rats. In the experiments, one end of a strip was clamped, and a force was applied on the other end. The deflection curves of the strips were measured. By regarding the aortic strip as a curved beam, the classical beam theory was employed to analyze the strain distribution from the experimental data. A computer program dealing with nonlinear equations and nonlinear least squares optimization was developed. Strains were referred to the zero-stress state. The load-deflection relationship was then used to determine the stress-strain relationship. Certain forms of the stress-strain laws were assumed. The linear laws fit the experimental data accurately, probably because the strains during bending are quite small, although the rotations are large. The Young's modulus of the inner layer, which consists of endothelial and smooth muscle cells and elastic lamina, was found to be three to four times larger than that of the outer layer which consists of collagen with a small amount of fibroblasts and elastin. The residual stresses and strains at the no-load state were calculated from the deduced stress-strain relationship. It is shown that large errors (up to 50 percent) in the values of the residual strains will occur if the wall material was treated as homogeneous, i.e., if the layered constitution was ignored.

Animals↗
PubMed1995

Differential effects of in vivo ethanol on LPS-induced TNF and nitric oxide production in the lung.

Alcohol (EtOH) has been shown to suppress lipopolysaccharide (LPS)-induced nitric oxide (NO) generation and tumor necrosis factor (TNF) production in the lung in vivo. We have previously reported that EtOH suppressed gene expression for inducible nitric oxide synthase (iNOS) with a subsequent decrease in release of reactive nitrogen intermediates by alveolar macrophages and recruited lung neutrophils. We hypothesized that a similar mechanism may be involved in EtOH-induced suppression of LPS-stimulated TNF production. In contrast to what we found with iNOS, EtOH had no effect on TNF mRNA in alveolar macrophages or recruited lung neutrophils. However, immunoreactive and bioactive TNF was reduced by 72%. EtOH treatment resulted in an increased level of the membrane-bound 26-kDa form of TNF, which suggested that proteolytic cleavage of this prohormone was affected by EtOH. Experiments with t-butyl alcohol, a tertiary alcohol that is not metabolized to acetaldehyde, yielded similar results. Thus EtOH appears to be the active substance in suppression of TNF in the lung in vivo. Pretreatment with intratracheal interferon-gamma 24 h before intratracheal LPS increased TNF bioactivity partly due to increased TNF mRNA and by increasing TNF processing, as evidenced by a decrease in the 26-kDa TNF prohormone and an increase in immunoreactive and bioactive TNF.

Alcoholic Intoxication↗
PubMed1995

In vivo administration of endotoxin and tumor necrosis factor-alpha produce different effects on constitutive and inducible nitric oxide synthase activity in rat neutrophils and aorta ex vivo.

Tumor necrosis factor-alpha (TNF-alpha) inhibits release of nitric oxide (NO) in vitro by stimulating the degradation of constitutive NO synthase (cNOS III) mRNA. However, TNF-alpha is believed to be the cytokine mediator of the hypotension and upregulation of inducible NO synthase (iNOS II) produced by gram-negative bacterial endotoxin (LPS). Some in vivo effects of TNF-alpha are opposite to those which occur in vitro. This study tested the hypothesis that in vivo administration of exogenous TNF-alpha and endogenously released TNF-alpha induce iNOS II activity and inhibit cNOS III activity, and thereby mediate the acute phase effects of LPS on blood pressure and the NO system in the rat. We show that LPS produces acute phase hypotension in ketamine anesthetized rats. The hypotension was associated with elevation of biologically active TNF-alpha in plasma, increased production of RNI (NO2- and NO3- anion) in rat neutrophils (PMN) and suppression of RNI production by A23187 (1 microM) stimulated thoracic aorta (RTA) ex vivo. TNA-alpha (10(6) U/ml, iv) did not produce acute phase hypotension but initially raised arterial blood pressure and heart rate (HR), did not increase RNI production by PMN, and inhibited RNI production by A23187 stimulated RTA ex vivo. Pretreatment of rats with the immunex monomeric soluble P75 receptor binding protein for TNF-alpha (TNFsr, 0.5 mg/kg, iv) 15 min prior to LPS administration decreased circulating TNF-alpha from 92,137 +/- 12,456 U/ml to undetectable levels as determined by the L929 bioassay. However, LPS-induced increases in RNI in PMN was enhanced and LPS-induced decreases in RNI production by RTA was inhibited by TNFsr. Thus, in vivo administration of TNF-alpha does not mimic the hemodynamic and NO-inducing effects of LPS. However, TNF-alpha mediates in part LPS-induced inhibition of RNI production by RTA. Thus, endogenous TNF-alpha is not required for LPS-induced acute phase hypotension or iNOS II activity. The importance of TNF-alpha in sepsis resides in systems other than iNOSII and blood pressure.

Amino Acid Oxidoreductases↗
PubMed1995

Rapid induction of mRNA for nitric oxide synthase II in rat alveolar macrophages by intratracheal administration of Mycobacterium tuberculosis and Mycobacterium avium.

Mycobacterium avium complex (MAC) organisms are among the most common bacterial cause of disseminated infection in patients with acquired immune deficiency syndrome (AIDS). An increase in the incidence of virulent Mycobacterium tuberculosis (MTB) is also occurring throughout the world. In vitro data suggest that nitric oxide (NO) may be important in restricting the growth of MAC. However, the ability of MTB to stimulate NO production and the susceptibility of MTB to the bactericidal activity of NO produced by murine alveolar macrophages (AM) is controversial. This study tested the hypothesis that in vivo administration of heat-killed MAC (strain 100 and 101) and human virulent MTB (strain F1) to rats stimulated NO production by rat AM, ex vivo. We show that heat-killed MTB instilled into rat lungs rapidly induced mRNA for NO synthase (iNOS) II in AM obtained by bronchoalveolar lavage (BAL). In contrast, expression of AM iNOS mRNA was only found in 40% of the rats given MAC. Moreover, the change in iNOS mRNA in the AM obtained from rats given MTB and MAC correlated with the production of the reactive nitrogen intermediates (RNI) NO2- and NO3- in BAL fluid, lung homogenate, and the spontaneous generation of RNI by isolated AM ex vivo and occurred without measurable increases in BAL fluid tumor necrosis factor-alpha (TNF-alpha). L-NG-monomethylarginine (50 mg/kg, ip) given 30 min before MAC or MTB attenuated the increase in RNI in lung homogenates and BAL fluid. This is the first demonstration that in vivo exposure to MTB results in rapid upregulation of gene expression for iNOS which is associated with functional RNI production by rat AM. These results show that MTB human virulent strain 1 has the ability to rapidly upregulate iNOS mRNA in AM. If human AM generate NO from L-arginine by either iNOS or other NADPH oxidases then NO may play a role in the overall host-defense response of the lung to MAC and MTB.

Amino Acid Oxidoreductases↗
PubMed1995

Hydroxocobalamin (vitamin B12a) prevents and reverses endotoxin-induced hypotension and mortality in rodents: role of nitric oxide.

The cobalt atom of hydroxocobalamin (OHC) binds cyanide and nitric oxide (NO) and OHC attenuates vascular responses to NO in vitro. NO mediates the hypotension of endotoxemia. Thus, we tested the postulate that OHC may attenuate the acute phase hypotension and toxicity associated with administration of Escherichia coli endotoxin (LPS). Rats were given OHC (20 mg/kg i.v.) or phosphate-buffered saline (PBS, 1 ml/kg i.v.) 30 min before or 15 min after giving LPS (0.8 mg/kg i.v.). Administration of OHC to PBS-treated control rats did not affect mean arterial pressure (MAP), heart rate or the plasma or urine content of the reactive nitrogen intermediates nitrate and nitrite (RNI). LPS decreased MAP by 50 mm Hg in PBS-treated rats and increased the plasma and urinary content of RNI. Administration of OHC to PBS-treated rats did not affect MAP or RNI. However, treatment with OHC before or after giving LPS attenuated LPS-induced hypotension and increases in plasma RNI and enhanced LPS-induced urinary excretion of RNI. OHC (20 mg/kg i.p.) or cyanocobalamin (10 mg/kg i.p.) given to Swiss-Webster mice 30 min before giving LPS (16 mg/kg i.p.) decreased the 24-hr mortality of LPS from 80 to 50% and the 36- and 96-hr mortality from 100 to 60% (OHC) or 70% (cyanocobalamin). Urine obtained from conscious rats given LPS (5 mg/kg i.p.) and OHC (20 mg/kg i.p.) exhibited a UV-visible absorbance spectrum with absorbance peaks characteristic of that formed after coincubation of NO and OHC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

V-J junctional sequences of T cell receptor gamma gene in acute lymphocytic leukemia.

T cell receptor TCR gamma gene rearrangement in a series of acute lymphocytic leukemia (ALL) patients was studied using PCR technique. 18 V-J junctional sequences (designated by N sequence) of TCR gamma gene were amplified with the V gamma and J gamma primers, using an unsymmetrical PCR and analysed by direct sequencing, demonstrating that in Chinese ALLs, the N sequences of TCR gamma gene are indeed clone-specific. Based on the known N sequences, several oligo-nucleotides were synthesized as probes, which were specific for the leukemic clone, and were used to detect the minimal residual disease (MRD) in 4 ALL cases. The sensitivity of this method was 0.1%-0.01%.

Adult↗
PubMed1995

A study of growth kinetics of the flocs from Schizosaccharomyces pombe.

Inducing yeast cells to self-flocculate could be considered a cell immobilization method. The growth kinetics of the flocs from Schizosaccharomyces pombe was studied in an experimental suspended-bed bioreactor with starch hydrolysate obtained by two-stage enzymatic hydrolysis. It was discovered that a limited oxygen supply was necessary during continuous ethanol fermentation with yeast flocs. The oxygen supplied was a kind of limited substrate effecting on the floc growth. Further, a kinetic model describing this floc growth was proposed.

Cell Division↗
PubMed1995

Controlling cancerous pain with analgesic powder for cancers.

Analgesic powder for cancers, composed of more than 20 Chinese drugs, was applied externally to 91 patients with various kinds of cancers for management of cancerous pain. The results showed that it was remarkably effective in 42 cases, fairly effective in 22, effective in 22, and ineffective in 5, the total effective rate being 94.51%. Animal experiments indicated that the pain threshold was evidently higher in mice treated with this powder on the site of femoral artery of the hind limbs than that of the controls without application of this powder.

Administration, Cutaneous↗
PubMed1995

[Effect of buspirone, a serotonergic 5-HT-1A agonist in cerebellar ataxia: a pilot study. Preliminary communication].

We propose a serotonergic hypothesis for cerebellar ataxia. The levorotatory form of 5 hydroxytryptophan has been shown to be partially active in subtypes of cerebellar ataxia, including cerebellar cortical atrophy (CCA). Buspirone, a 5-HT1A agonist usable in human medicine, has been studied in a group of 14 patients with cerebellar cortical atrophy. Patients were given Buspirone for 2 months. The evaluation of cerebellar ataxia was made by a semi-quantitative scale, 10 fully quantitative measures and measurements of the sway path and sway area of the center of gravity at posturography. The primary endpoints were the modifications of the ataxia scores. At 2 months, the decrease of the ataxia scores was significant, both in the intention-to-treat (14 cases) and target (11 cases) populations. In the target population, secondary endpoints like the time measurements for pronouncing a standard sentence, the time for drawing a ladder and posturographic parameters were significantly improved; the mean global ataxia score was improved by 37.4%. These preliminary data might confirm a link between cerebellar ataxia and the metabolism of serotonin.

Adult↗
PubMed1994

Golgi coatomer binds, and forms K(+)-selective channels gated by, inositol polyphosphates.

Coatomer is a distinct type of coat protein complex involved in the formation of specific Golgi intercisternal transport vesicles. Direct binding studies using purified coatomer isolated from bovine liver cytosol show that coatomer specifically binds both inositol 1,3,4,5-tetrakisphosphate ((1,3,4,5)IP4) and inositol hexakisphosphate (IP6) with subnanomolar affinities (0.1 and 0.2 nM, respectively). Diphosphoinositol pentakisphosphate (PP-IP5) is an efficient competitor for both (1,3,4,5)IP4 and IP6 binding to coatomer. Inositol 1,3,4,5,6-pentakisphosphate ((1,3,4,5,6)IP5) is a poor inhibitor of IP6 binding, whereas little or no competition is detected with inositol 1,4,5-trisphosphate ((1,4,5)I-P3). Coatomer displays ion channel activity when reconstituted into planar bilayers which is preferentially permeable to K+. Permeability ratios of the channel are PK+/PCl- approximately 8.0 and PK+/PNa+ approximately 7.1, indicating a cation-selective channel with selectivity of K+ over Na+. In symmetrical 500 mM KCl, the smallest observable unitary channel conductance is 8.3 picosiemens. The coatomer channel activity is normally active with long open times (0.1 to several seconds) and is selectively blocked by 10 microM (1,3,4,5)IP4, 1 microM IP6, and 0.27 microM PP-IP5; even lower concentrations are sufficient to induce channel flicker. The channel activity is not affected by (1,4,5)IP3, or (1,3,4,5,6)IP5. Thus, the channel activity of coatomer is modulated by the inositol polyphosphates which exhibit tight binding to the complex.

Animals↗
PubMed1994

Isolation and characterization of a novel inositol hexakisphosphate binding protein from mammalian cell cytosol.

Inositol hexakisphosphate (IP6) is present in most mammalian cells, although its intracellular function is as yet undefined. We find that the total protein fraction from bovine brain cytosol contains a significant level of specific binding for IP6 precipitable with 40% saturated ammonium sulfate. A protein complex has been isolated from this fraction that specifically binds IP6 and is purified about 500-fold over the cytosol. The IP6 binding protein (IP6BP) chromatographs as a single peak of binding activity on a gel exclusion column, with a Stokes radius equivalent to 266 +/- 14 kDa. The IP6BP is a heterooligomeric complex composed of a number of subunits with molecular weights varying from 23,000 to 60,000, as determined by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate (SDS-PAGE). Scatchard analyses of IP6 binding of both the crude ammonium sulfate fraction and the purified complex show the presence of a similar high-affinity binding site (Kd approximately 6.0 nM). Bmax for the purified fraction is 1.8 nmol of IP6/mg of protein or 0.48 mol of IP6 bound/mol of complex. Other inositol polyphosphates, such as inositol 1,3,4,5,6-pentakisphosphate, inositol 1,3,4,5-tetrakisphosphate, and inositol 1,4,5-trisphosphate, are poor competitors for IP6 binding to the purified complex. The purification scheme, when applied to a rat liver cytosol fraction, yields a similar IP6BP. This complex has an apparent size of 512,000 using gel exclusion chromatography and contains an additional protein band with M(r) = 97,000 by SDS-PAGE.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Magnetic resonance imaging of radiation dose distributions using a polymer-gel dosimeter.

A new formulation of a tissue-equivalent polymer-gel dosimeter for the measurement of three-dimensional dose distributions of ionizing radiation has been developed. It is composed of aqueous gelatin infused with acrylamide and N, N'-methylene-bisacrylamide monomers, and made hypoxic by nitrogen saturation. Irradiation of the gel, referred to as BANG, causes localized polymerization of the monomers, which, in turn, reduces the transverse NMR relaxation times of water protons. The dose dependence of the NMR transverse relaxation rate, R2, is reproducible (less than 2% variation) and is linear up to about 8 Gy, with a slope of 0.25 s(-1)Gy(-1) at 1.5 T. Magnetic resonance imaging may be used to obtain accurate three-dimensional dose distributions with high spatial resolution. Since the radiation-induced polymers do not diffuse through the gelatin matrix, the dose distributions recorded by BANG gels are stable for long periods of time, and may be used to measure low-activity radioactive sources. Since the light-scattering properties of the polymerized regions are different from those of the clear, non-irradiated regions, the dose distributions are visible, and their optical densities are dependent on dose.

Acrylic Resins↗
PubMed1994

Rapid induction of messenger RNA for nitric oxide synthase II in rat neutrophils in vivo by endotoxin and its suppression by prednisolone.

Nitric oxide is believed to participate in nonspecific cellular immunity. Gram negative bacterial endotoxins increase the production of reactive nitrogen intermediates (RNI) in phagocytic cells by inducing the enzyme nitric oxide synthase II (NOS II). Anti-inflammatory glucocorticoids attenuate endotoxin-induced increases in RNI. This study evaluated the effect of in vivo administration of prednisolone on Escherichia coli lipopolysaccharide endotoxin (LPS)-induced increases in plasma RNI and neutrophil mRNA for NOS II and production of RNI in the rat. We show that LPS rapidly induces mRNA for NOS II and production of RNI (NO2- and NO3- anion) in rat neutrophils within 2 hr after in vivo administration of a sublethal dose of 0.5 mg/kg, i.v. A pharmacologic dose of prednisolone (50 micrograms/kg, im) given 15 min before LPS-attenuated production of NO2- and NO3- by neutrophils and suppressed LPS-stimulated mRNA for NOS II. 3-Amino, 1,2,4-triazine inhibited NO2- and NO3- production without affecting gene expression for NOS II. These data demonstrate that LPS rapidly induces functional gene expression for NOS II and prednisolone prevents induction of NOS II activity by inhibiting transcription of its mRNA.

Amino Acid Oxidoreductases↗