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Biomedical subjects

J Xie

Publications and source records attributed to J Xie.

At least 253 records · Page 14Linked to original sources
PubMed1994

[Effect of some drugs on electroacupuncture analgesia and cytosolic free Ca2+ concentration of mice brain].

In this paper, the effects of some analgesic drugs such as corydalis yanhusuo, Angelica dahurica and Analginum on electroacupuncture analgesic function were studied. In the meantime, the concentrations of cytosolic free Ca2+ ([Ca2+]i) in mice hypothalamus (HT) and periaqueductual grey (PAG) were determined by use of the fluorescence dye Fura-2/AM and AR-CM cation measurement system. The results showed that Corydalis yanhusuo obviously strengthened the analgesic function produced by electroacupuncture. Besides, the [Ca2+]i in the two brain regions of mice in these analgesic experiments with electroacupuncture and Corydalis yanhusuo were all decreased (compared with saline control group, P < 0.01), In the same experimental condition, the [Ca2+]i in Angelica dahurica group and Analginum group has no significant difference compared with the control group, the analgesic mechanisms may be different from that of electroacupuncture and Corydalis yanhusuo.

Acupuncture Analgesia↗
PubMed1994

[The effect of Sindbis virus multiplication on gene expression of host cells].

Sindbis virus (SBV) infection mediated a rapid shutoff of host cellular gene expression (mRNA synthesis and protein synthesis); however the synthesis of cellular rRNA remained at the same level as the uninfected cells. Meanwhile a cellular protein P105 was shown to be enriched in the nuclear matrix. Actionmycin D treatment after virus infection resulted in an apparent reduce in the production of viral structural proteins and infectious virions. The results presented here not only demonstrated the complexity of SBV-mediated regulation of host gene expression, but also suggested SBV nonstructural protein nsP2 and capsid protein C were possibly involved in this process.

Animals↗
PubMed1994

Effects of chelating agents on tissue distribution and excretion of nickel in mice.

N-Benzyl-D-glucaminedithiocarbamate (BGD), diethyldithiocarbamate (DDTC), di-hydroxyethyldithiocarbamate (DHED), trans-1,2-cyclohexanediamine N,N,N',N'-tetra-acetic acid (CDTA), and 2,3-dimercaptosuccinic acid (DMSA) were studied for their relative efficacies in the distribution and excretion of nickel in mice exposed to nickel. Mice were injected intraperitoneally with NiCl2 (5mgNi/kg) and 30 min or 24 hr later, they were injected intraperitoneally with chelating agents (400 mumol/kg). At 30 min after treatment with nickel, these chelating agents all significantly enhanced the fecal excretion of nickel, and DMSA significantly increased the urinary excretion of the metal. At 24 hr after nickel treatment, BGD, DDTC, and DHED significantly increased the fecal excretion of nickel and BGD was the most effective on the fecal excretion of nickel. CDTA and DMSA significantly enhanced the urinary excretion of the metal. At 30 min after nickel treatment, chelating agents other than CDTA effectively depressed nickel concentration in the kidney, lung, and testes. BGD, CDTA, and DMSA significantly reduced the nickel concentration in the liver. However, DDTC and DHED caused the redistribution of nickel to the brain. At 24 hr after nickel treatment, these chelating agents were effective in mobilizing nickel from the kidney, and chelating agents other than DHED were effective in mobilizing nickel from the liver, lung, and testes. These results indicate that the injection of BGD or DMSA at both 30 min and 24 hr after treatment with nickel can remove nickel from the body without redistribution of nickel to other tissues, such as brain, more effectively than DDTC, DHED, and CDTA. Furthermore, the pattern of excretion of nickel after treatment with the chelating agents was related to the partition coefficients of the nickel-chelating agent complexes.

Animals↗
PubMed1994

Selective pulmonary and venous smooth muscle relaxation by furosemide: a comparison with morphine.

Furosemide and morphine reduce pulmonary edema associated with congestive heart failure. It is uncertain whether furosemide or morphine are direct-acting relaxants of arterial and venous smooth muscle. The authors compared the effect of furosemide and morphine on isolated rings of canine pulmonary artery (PA) and vein (PV) and mesenteric, splenic and anterior tibial arteries and their corresponding veins precontracted with norepinephrine or (15S)-hydroxy-11 alpha, 9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid. Furosemide (10-300 microM) selectively relaxed veins by an endothelium-independent mechanism, with its greatest efficacy on the PV. Morphine (10-1000 microM) relaxed both arteries and veins. The mechanism of relaxation by furosemide and morphine was examined in the PV and PA. Morphine-induced relaxation of the PV and PA was dependent on prostanoid release from endothelium and smooth muscle because it was attenuated in endothelium-rubbed and ibuprofen-treated PV and PA but not in blood vessels treated with inhibitors of nitric oxide system/cyclic GMP system (I-NG-nitroarginine and methylene blue). Furosemide-mediated relaxation of the PV was refractory to each of these interventions. Similarly, furosemide- and morphine-induced relaxation of the PV were unaffected by 4-aminopyridine, tetraethylammonium, glibenclamide, dendrodotoxin and apamin and, thereby, were independent of an action on K+ channels. Reduction of extracellular K+ or Cl- attenuated furosemide-mediated relaxation of, and inhibition of 86Rb+ uptake by, PV even in the presence of ouabain. It was concluded that furosemide relaxes veins by an effect on Na+/K+/Cl- cotransport or chloride-mediated refilling of intracellular calcium stores.

Animals↗
PubMed1994

Secular trends in cerebrovascular mortality.

Since 1950 a marked decrease in cerebrovascular mortality has occurred in most Western countries. To evaluate whether changes in the pharmacological treatment of hypertension, introduced during the period observed (1950-87), have influenced this downward trend the linear time-trends over the period considered were calculated. Mass treatment of hypertension at the population level started in the early 1970s. Before this period a marked decrease in cerebrovascular mortality had already occurred. Moreover, the linear time trends were highly significant over the whole period with several correlation coefficients of > 0.98. The decrease in cerebrovascular mortality can best be explained by a decreased salt and saturated fat intake in the populations considered. In several Eastern European countries cerebrovascular mortality has increased. This runs parallel with an increase in all-cause mortality and an increase in ischaemic heart disease mortality and can be explained by the high saturated fat intake of these populations. The data show that important changes in cerebrovascular mortality are also occurring in the older age groups, e.g. 70-74 and 80-84 years. Epidemiological data point towards nutrition as playing an important role in the evolution of cerebrovascular mortality over the period considered.

Aged↗
PubMed1994

Phenol red is a thromboxane A2/prostaglandin H2 receptor antagonist in canine lingual arteries and human platelets.

Phenol red (PR) is used as a pH indicator in cell culture medium. We found that cell culture medium containing PR relaxed canine lingual arteries (LA) contracted by the thromboxane A2/prostaglandin endoperoxide (TPE) receptor agonist (15S)-hydroxy-11-alpha-9-alpha- (epoxymethano)prosta-5Z,13E-dienoic acid (U46619). We tested the effect of PR and the TPE receptor antagonist ONO-3708 on U46619, prostaglandin F2 alpha (PGF2 alpha), phenylephrine (PE) and potassium chloride (KCl)-induced contraction of the LA and on human platelet aggregation to U46619, ADP, arachidonic acid (AA), A23187 and thrombin. U46619, PGF2 alpha, KCl and PE produced equal tension development of the LA. PR relaxed the LA contracted with U46619 and PGF2 alpha with IC50 concentrations of 18.3 +/- 10 and 37.3 +/- 8.8 microM, respectively. ONO-3708 inhibited the contractions to U46619 and PGF2 alpha with IC50 of 9.4 +/- 2.2 and 12.2 +/- 2.2 nM, respectively. However, PR (300 microM) and ONO-3708 (300 nM) did not affect contraction of the LA to KCl or PE. PR inhibited human platelet aggregation, in vitro, to AA and U46619 and second wave aggregation to ADP but did not affect thrombin or first wave ADP-mediated platelet aggregation. PR inhibited U46619 and AA-induced changes in cyclic AMP and Fura-2 calcium transients in platelets and LA. However, PR did not affect the activation of cyclic AMP or intracellular calcium ion in platelets or calcium influx and the release of intracellular calcium ion in canine LA produced by ryanodine, KCl and PE. The concentration of PR in many culture media is between 40 and 70 microM. The data support the conclusion that PR, in concentrations used as a pH indicator, is a selective antagonist of TPE receptors.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Alcohol administration attenuates LPS-induced expression of inducible nitric oxide synthase in Kupffer and hepatic endothelial cells.

This study investigates the effects of in vivo ethanol (primed infusion, causing 170-190 mg% plasma alcohol for 12 hours) and/or LPS (12 hours after injection of E. coli LPS 1 mg/kg bw.) on the mRNA expression of inducible nitric oxide synthase (NOS II) in hepatic cells measured by competitive PCR technique, and on hepatic release of reactive nitrogen intermediates (RNI, NO2- + NO3-). Perfused livers from alcohol- or saline-infused animals did not release measurable amounts of RNI. Under these conditions small amounts of NOS II mRNA were expressed in Kupffer and endothelial cells, while it was not detectable in parenchymal cells. LPS treatment along with markedly elevating hepatic RNI release increased NOS II mRNA levels by 35- and 200-fold, in endothelial and Kupffer cells, respectively. LPS injection and alcohol infusion to the same animal decreased hepatic RNI release by about 70% and almost completely inhibited the LPS-induced, elevated NOS II mRNA in Kupffer or endothelial cells. No similar changes were observed in the parenchymal cells. These data suggest that the primary target of in vivo LPS in upregulating hepatic NO release are the nonparenchymal cells. Furthermore, alcohol inhibits the LPS-induced response which may influence immune-related hepatic function.

Amino Acid Oxidoreductases↗
PubMed1993

Molecular characterization of a multi-promoter gene encoding a chicken filamin protein.

We report the cloning and sequencing of cDNA encoding a chicken filamin protein. The 2,567 amino acid protein contains an NH2-terminal 267 amino acid actin-binding domain followed by a series of 24 repeating units that are each approximately 95 amino acids in length. The overall primary structure of filamin closely resembles that of human actin-binding protein (ABP). However, filamin lacks a 24-amino-acid insertion prior to repeat 16 that is contained within ABP. This region of human ABP is a site of calpain cleavage and is thought to confer flexibility on the molecule. Hence, it is possible that the properties of actin gels formed with either human ABP or filamin reflect the presence or absence of this insertion. Filamin is encoded within a multi-promoter transcription unit. A downstream filamin promoter (Fil1) resembles those of certain housekeeping genes and has a putative binding site for the transcription factor E2F. Thus, transcription from this promoter may be linked to the cell cycle. A second filamin promoter (Fil2) is located at least 8 kilobases upstream from the Fil1 promoter. This structural arrangement suggests that regulation of filamin gene expression is likely to be complex.

Amino Acid Sequence↗
PubMed1993

New mechanism-based inactivators of trypsin-like proteinases. Selective inactivation of urokinase by functionalized cyclopeptides incorporating a sulfoniomethyl-substituted m-aminobenzoic acid residue.

In order to obtain selective suicide substrates of trypsin-like proteases including plasminogen activators, plasmin, and thrombin, a series of cyclopeptides cyclo[Arg or Lys-aB(CH2X)-Gly4], in which a substituted o- or m-aminobenzoyl group constitutes a latent electrophile, have been prepared. Treatment of the corresponding phenyl ethers cyclo[P1-aB(CH2OC6H5)-Gly4] with HBr/HOAc or R1R2S/TFA gives the bromides (X = Br) or the sulfonium salts (X = +SR1R2 with R1 = R2 = Me or R1 = Me and R2 = C6H5), respectively. These water-soluble cyclopeptides behave as time-dependent inhibitors of bovine trypsin and human urokinase (u-PA) but have no effect on tissue plasminogen activator (t-PA) and no or poor effect on plasmin and thrombin. The compounds containing a m-aminobenzoic acid residue are more efficient inactivators than their anthranilic analogues. The kinetic criteria expected for a suicide inhibition are met. A mechanism of inhibition involving the formation of a quinonimmonium methide intermediate is proposed. The activity of the inhibitors is very sensitive to the nature of the X benzylic substituent. An increased efficiency for the inactivation of human urokinase is observed with the sulfonium salts. The selectivity of the inactivation of u-PA compared to t-PA could be of therapeutical significance in controlling cell proliferation and invasion.

Aminobenzoates↗
PubMed1993

In vitro bond strength of two adhesives to enamel and dentin under normal and contaminated conditions.

In vitro bond strengths of human enamel and dentin treated with five contaminants were measured with air, water and damp conditions as controls. Two commercial bonding agents (a lower-viscosity, solvent-containing type, AB, and a higher-viscosity, hydrophilic monomer type, SB) and their composites were applied to tooth structure under two conditions (contaminated and re-etched). Samples were debonded in tension after 24 h using an inverted, truncated cone test. Among the controls, the highest bond strengths were obtained with damp conditions for AB (24 MPa) and damp conditions or air for SB (22 MPa) with small differences between enamel and dentin. Most contaminants lowered the bond strength. Re-etching without additional mechanical preparation resulted in bond strengths similar to controls. Bond strengths to tooth structure with the bonding agents tested may be less sensitive to common forms of contamination than typically assumed.

Acid Etching, Dental↗
PubMed1993

Co-stimulation with IL-2, but not via CD28, overcomes immunosuppression by breast tumour-derived factors on the in vitro stimulation of human T-cells.

In order to investigate the mode of action of tumour-derived immunosuppressive factor from breast cancer (TDS) we examined its function on human T-cells stimulated via CD3 and co-stimulated via CD28 or the IL-2 receptor. When added at the initiation of culture, TDS inhibited anti-CD3 stimulation and co-stimulation by anti-CD28. In contrast, co-stimulation with IL-2 greatly diminished the TDS inhibition of anti-CD3 stimulated cells. Activation by IL-2 alone was also inhibited at the initiation of culture. When PBMC were activated with IL-2 or anti-CD3 for three days and then exposed to TDS for a further 3 days, only the proliferation of the cells pre-activated with IL-2 was inhibited; the cells pre-activated via CD3 were refractory to TDS inhibition. Pre-activation with anti-CD3 for 48 h was required for this to develop. The cytotoxicity of cells pre-activated with anti-CD3 was lower than that of cells exposed to IL-2, but killing obtained from cultures pre-activated with anti-CD3 plus IL-2 was equivalent to that obtained with IL-2 alone and additionally, these pre-activated cells were not subject to inhibition upon subsequent exposure to TDS.

Breast Neoplasms↗
PubMed1993

Ouabain enhances basal release of nitric oxide from carotid artery.

The authors tested the postulate that ouabain releases nitric oxide (NO) from the vascular endothelium of porcine carotid arteries (PCAs) with the technique of perfusion-superfusion bioassay, in which the perfused PCA with endothelium served as the source of NO and superfused left circumflex coronary artery (CMFX) rings with rubbed endothelium served as the bioassay tissue. Selective exposure of the PCA to ouabain (10 microM) enhanced the basal release of NO but did not affect bradykinin-stimulated (BK; 0.1-100 picomoles) release of NO. The effect of ouabain on basal release of NO from PCA persisted after pretreatment of either PCA or circumflex coronary artery with propranolol (1 microM); ibuprofen (1 microM); and hydrocortisone (10 microM). Finally, selective pretreatment of the PCA with L-NG-monomethylarginine (LNMMA; 100 microM) to inhibit 1-arginine-derived NO synthesis inhibited the relaxation of the circumflex coronary artery to basal, BK, and ouabain-stimulated effluent. Since a nonspecific increase in intracellular calcium ion will enhance both basal and agonist-induced release of NO, the authors conclude that a ouabain-sensitive ATPase is involved in basal release of NO from the endothelium of the PCA. Alternatively, ouabain may act on an isozyme of NO synthase in the vascular endothelium. Speculatively, ouabain-induced stimulation of NO release from vascular endothelium may contribute to the beneficial effect of ouabain in congestive heart failure.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Tumor necrosis factor-alpha inhibits endothelium-dependent relaxation.

Tumor necrosis factor-alpha (TNF-alpha) stimulates nitric oxide (NO) in vascular endothelium by induction of the enzyme NO synthase II (NOS II). We examined the effects of TNF-alpha on 1) endothelium-dependent (EDR) and endothelium-independent (EIR) relaxation and 2) contraction of bovine intralobar pulmonary arteries (BPA) and veins (BPV) in vitro. Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-NMMA; 300 microM). TNF-alpha (0.00417, 0.0417, 0.417, and 1.25 micrograms/ml) incubated with BPA for 60 min inhibited EDR of the BPA to ACh, BK, and histamine. The effects of TNF required 30 min for onset. Recovery of EDR occurred 3-4 h after washout of TNF-alpha. Pentoxifylline (1 microM) did not affect ACh-induced EDR but selectively reversed TNF-alpha-mediated inhibition of ACh-induced EDR. TNF-alpha-mediated inhibition of EDR was not reversible by L-NMMA, an inhibitor of NOS I and NOS II, the cyclooxygenase inhibitor ibuprofen, or CV-3908 (1 microM), a platelet-activating factor antagonist. The inhibitory effect of TNF-alpha on EDR was not mediated by nonspecific sensitization of the endothelium to human protein because recombinant human granulocyte colony-stimulating factor (10, 50, and 500 x 10(3) U/ml) did not affect EDR of BPA. The effect of TNF-alpha was specific for release of NO from the endothelium of BPA because TNF-alpha did not affect 1) EDR of BPV to ACh, BK, or ATP; 2) EIR of BPA or BPV to nitroprusside; and 3) contraction of either BPA or BPV to KCl, U-46619, histamine, norepinephrine, or serotonin. Thus TNF-alpha appears to selectively inhibit receptor-mediated EDR and NO release in BPA. TNF-alpha-mediated inhibition of EDR differs from that of L-arginine-based inhibitors and may represent an endogenous physiological mechanism of regulation of NO in the endothelium.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Tumor necrosis factor inhibits stimulated but not basal release of nitric oxide.

Tumor necrosis factor alpha (TNF alpha) increases nitric oxide (NO) synthase in vascular endothelium, but it inhibits endothelium-dependent relaxation (EDR) of vascular smooth muscle. We tested whether TNF alpha inhibits the response to, or release of, NO in bovine pulmonary artery (BPA) using the technique of perfusion-superfusion bioassay and ozone chemiluminescence. Effluent from the perfused BPA with endothelium (donor)-relaxed endothelium-rubbed bovine coronary artery (BCA) (detector). Moreover, effluent from the donor stimulated with acetylcholine (ACh) or bradykinin (BK) (0.001 to 100 nmol) relaxed the detector. Direct application of these agonists to the detector failed to produce relaxation. Basal and agonist-stimulated effluent from the donor treated with L-NG-monomethylarginine (LNMMA) (100 microM) suppressed effluent-mediated relaxation of the detector. ACh and BK released LNMMA-inhibitable nitrite and nitrate from the BPA. Thus, the effluent contained NO. Exposure of the donor to TNF alpha (1.25 micrograms/ml) for 60 min did not affect basal release of NO, but it attenuated bioassayable and chemiluminescence-detectable NO release by ACh and BK. The inhibition of NO release was directly related to the magnitude of inhibition of EDR by ACh and BK. Thus, TNF alpha selectively inhibits receptor-mediated release of NO without affecting basal release of NO. This effect differs from that of L-arginine-based inhibitors of NO and represents a unique physiologic mechanism of regulation of NO in the endothelium.

Acetylcholine↗
PubMed1993

Tumor necrosis factor alpha inhibits contractions to sympathetic nerve stimulation by a nitric oxide-dependent mechanism.

Gram-negative sepsis and administration of tumor necrosis factor alpha (TNF alpha) are associated with hypotension and peripheral neuropathies suggestive of impaired sympathetic neurotransmission. We examined the effect of TNF alpha on the responses of the bovine pulmonary artery (BPA) to transmural sympathetic nerve stimulation (SNS). BPA contracted to SNS (0.5-32 Hz, 5-10 V, 2-msec duration, 2-msec delay) in a frequency-dependent manner. The contractions of the BPA to SNS were mediated by norepinephrine and activation of postsynaptic alpha 1-adrenoceptors, since they were attenuated by prazosin. Maximum contraction of the BPA to SNS was significantly enhanced (148 +/- 37% increase, n = 6) after inhibition of nitric oxide synthase with L-NG-monomethylarginine (LNMMA, 500 microM), an effect abrogated by L-arginine (1 mM). TNF alpha (0.0042, 0.042, and 0.42 micrograms/ml) selectively inhibited contractions of the BPA to SNS without affecting the contraction of the BPA to exogenous norepinephrine. In BPA incubated with LNMMA (5-500 microM), TNF alpha facilitated rather than inhibited SNS. TNF alpha increased the formation of amperiometrically measured free nitric oxide in bovine adrenal chromaffin cells in primary culture. The data show that in the absence of LNMMA, TNF alpha releases free nitric oxide from a sympathetic neuron and selectively inhibits the contractions of the BPA to SNS. In BPA in which nitric oxide synthase I is inhibited by LNMMA, TNF alpha amplifies the contractions to SNS, even in the absence of endothelium. Thus, TNF alpha can modify vascular smooth muscle tone by affecting SNS. TNF alpha inhibits SNS at the level of the neuron by a mechanism involving the L-arginine-nitric oxide pathway. TNF alpha-induced suppression of SNS and neurotransmission may contribute to the hypotension and peripheral neuropathy of sepsis.

Acetylcholine↗
PubMed1993

[The multiplication of Sindbis virus in BHK-21 cell].

One step growth curve of Sindbis virus (SbV) in BHK-21 cells showed that a lot of progeny viruses could be observed at 2 hr. after infection. The titer of virus reached the highest about 10(9)TCID50/ml at 6hr. post infection. The viral morphological characters and morphogenetic process in BHK-21 cells were examined by electron microscopic techniques. The dynamics of viral proteins synthesis and the effect on host cell were studied and discussed in this paper.

Animals↗
PubMed1993

[A cephalometric study on determining the orientation of occlusal plane].

A study of the parallel relationship between the occlusal plane and the line connecting nasal alar and tragus was made in 90 dentulous cases by using cephalometry. The results show that the line connecting the inferior point of nasal alar and the mid-point of tragus runs much more parallel with the occlusal plane. The regression equation reveals a "line of closest fitting". It was used in the prosthetic treatment for 50 edentulous patients with good clinical results. The line connecting the inferior point of nasal alar and the mid-point of tragus therefore represents a proper reference plane for determining occlusal plane and hence should be still a valuable index in clinical dentistry.

Adolescent↗