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Biomedical subjects

P Fan

Publications and source records attributed to P Fan.

At least 91 records · Page 5Linked to original sources

Transesophageal color Doppler evaluation of obstructive lesions using the new "Quasar" technology.

Due to the unavoidable problem of aliasing, color flow signals from high blood flow velocities cannot be measured directly by conventional color Doppler. A new technology termed Quantitative Un-Aliased Speed Algorithm Recognition (Quasar) has been developed to overcome this limitation. Employing this technology, we used transesophageal color Doppler echocardiography to investigate whether the velocities detected by the Quasar would correlate with those obtained by continuous-wave Doppler both in vitro and in vivo. In the in vitro study, a 5.0 MHz transesophageal transducer of a Kontron Sigma 44 color Doppler flow system was used. Fourteen different peak velocities calculated and recorded by color Doppler-guided continuous-wave Doppler were randomly selected. In the clinical study, intraoperative transesophageal echocardiography was performed using the same transducer 18 adults (13 aortic valve stenosis, 2 aortic and 2 mitral stenosis, 2 hypertrophic obstructive cardiomyopathy and 1 mitral valve stenosis). Following each continuous-wave Doppler measurement, the Quasar was activated, and a small Quasar marker was placed in the brightest area of the color flow jet to obtain the maximum mean velocity readout. The maximum mean velocities measured by Quasar closely correlated with maximum peak velocities obtained by color flow guided continuous-wave Doppler in both in vitro (0.53 to 1.65 m/s, r = 0.99) and in vivo studies (1.50 to 6.01 m/s, r = 0.97). We conclude that the new Quasar technology can accurately measure high blood flow velocities during transesophageal color Doppler echocardiography. This technique has the potential of obviating the need for continuous-wave Doppler.

Adult↗

Cannabinoid agonists inhibit the activation of 5-HT3 receptors in rat nodose ganglion neurons.

1. Effects of cannabinoid agonists on the serotonin (5-HT)3 receptor-mediated current were investigated in rat nodose ganglion neurons. Anandamide, Win 55212-2, and CP55940 inhibited the 5-HT-induced current in a concentration dependent manner. IC50 values were 190, 310, and 94 nM for anandamide, Win 55212-2, and CP55940, respectively, and 1.6 microM for the nonpsychoactive enantiomer CP56667. This inhibition was slowly developing, noncompetitive, not dependent on membrane potential, and not affected by adenosine 3',5'-cyclic monophosphate (cAMP) analogues, guanosine-5'-O-(2-thiodiphosphate) (GDP-beta-S), and opioid receptor antagonist naltrexone. These data suggest that 5-HT3 receptor ion-channel is a site acted upon by cannabinoid agonists in the nervous system, and the action of cannabinoid agonists on 5-HT3 receptors may be a possible mechanism for some of the behavioral effects of cannabinoids, such as antiemesis and analgesia.

Animals↗

[Correlation analysis of lipids and apolipoproteins in plasma HDL, LDL and VLDL of normal subjects and endogenous hypertriglyceridemics].

The linear correlation and multiple stepwise regression analysis of lipids and apolipoproteins in plasma, HDL, LDL and VLDL of 20 normal subjects and 20 patients with endogenous hypertriglyceridemia was made. The result of simple factor analysis showed that there was a positive correlation of TG and VLDL TG with apoC II, C III, E, LDL apoB100 and VLDL apoC II, C III, E, B100; and a negative correlation with HDL apoA I. HDL-C was related positively with apoA I, HDL apoA I, C III and negatively with apoC III, E, LDL apoB100 and VLDL apoB100, C II, C III, E. TC was correlated positively with apoB100 and LDL apoB100. The result of multiple factor analysis showed that apoC III, E, B100/A I, VLDL apoC III and HDL apo C II, E, C II/C III, among 20 factors, were main factors which were related with TG. Apo C III, VLDL apoC III and LDL apoB100 were main factors which affected VLDL TG. ApoB100, and C II were main apolipoproteins which were related with TC; while the main apolipoproteins which affected HDL-C were apoA I, HDL apoA I, C II, VLDL apoE, HDL apoA II, the significance of the results is discussed.

Apolipoproteins↗

Nonopioid mechanism of morphine modulation of the activation of 5-hydroxytryptamine type 3 receptors.

The effect of morphine on the ion current mediated by 5-hydroxytryptamine (5-HT3) receptors was investigated in rat nodose ganglion neurons and in Xenopus oocytes expressing the cloned 5-HT3 receptor. Morphine reversibly inhibited the 5-HT-induced current and shifted the 5-HT concentration-response curve to the right in a parallel fashion, without reducing the maximal 5-HT response. IC50 values for morphine were 0.3 microM in nodose neurons and 0.32 microM in oocytes. The apparent Kd of morphine in nodose neurons was 0.903 microM. This effect of morphine was immediate not dependent on membrane potential, and not prevented by the opioid receptor antagonists naltrexone and beta-chlornaltrexamine. It is concluded that opioid receptors were not involved in the present study and that morphine acted at the agonist recognition site located on the 5-HT3 receptor.

Amino Acid Sequence↗

[Study on lipid and apolipoprotein composition of plasma VLDL, LDL and HDL in endogenous hypertriglyceridemia].

We analysed the lipid and apolipoprotein (apo) composition of plasma VLDL, LDL and HDL including TG, FC, CE, PL and apoA I, A II, B100, C II, C III and E in 20 endogenous HTG patients whose plasma TG levels were > 2.26 mmol/L, TC < 6.74 mmol/L and in 20 normal subjects whose plasma lipid levels were normal (TG < 1.70 mmol/L, TC < 5.96 mmol/L). The results showed that the fasting plasma TG, apoC II, C III and E levels were significantly higher and HDL-C and apo A I levels lower in the HTG group than those in the normal group (P < 0.05). Abnormality of lipid and apolipoprotein composition of plasma VLDL, LDL and HDL in HTG was found. TG, FC, CE, PL and apoB100, C II, C III and E contents in VLDL were significantly increased in HTG (P < 0.01), while CE, apoA I, C II, C III and E in HDL were significantly decreased (P < 0.05) and TG in HDL significantly increased (P < 0.05) in HTG. TG and apoB100 in LDL in the HTG group were higher than those in the normal group (P < 0.05).

Adult↗

High expression of synthetic human interferon-gamma cDNA in E. coli.

Human interferon-gamma (IFN-gamma) cDNA was synthesized, and it makes the usage of favorable codons in E. coli. The authors got 9 different expression plasmids which contain the synthetic IFN-gamma-cDNA and have different spaces between SD sequence and ATG. The free energies G0f298 in the formation of stable secondary structure in the translation initiation region (TIR) are different in various expression plasmids. One of them, pLY4-gamma 5, can highly yield INF-gamma which will be about 60%-80% of the total bacterial proteins, such a high expression was hardly noted in literature. The reasons of high expression in this work are optimal spaces between SD and ATC, favorable delta G0f298, favourable condons usage for E. coli.

Amino Acid Sequence↗

Antagonism by forskolin of the 5-HT3 receptor-mediated current in nodose ganglion neurons is independent of cyclic AMP.

The effect of forskolin on the inward current mediated by 5-HT3 receptors (5-HT current) was investigated in rat nodose ganglion neurons. Forskolin inhibited the peak amplitude of the 5-HT current and increased current desensitization in a dose-dependent manner. Dideoxyforskolin, which does not stimulate adenylate cyclase, had a similar inhibitory effect on the 5-HT current. The effect of forskolin was neither mimicked by intracellular application of exogenous cyclic AMP (0.5 to 4 mM) nor occluded by intracellular forskolin (30 microM) or protein kinase inhibitor H-7 (100 microM). Intracellular applications of forskolin, cyclic AMP or H-7 had no effect on 5-HT current. Data suggest that forskolin acted at an extracellular site on 5-HT3 receptors and this effect of forskolin was not mediated by cyclic AMP-dependent processes.

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

Inhibition of the 5-HT3 receptor-mediated current by the protein kinase inhibitor, H-7.

The effect of the protein kinase inhibitor, H-7, on the inward current mediated by 5-HT3 receptors was investigated with the whole-cell patch-clamp technique. H-7 inhibited the peak 5-HT current with an IC50 of 1.79 microM. The inhibition was quick, reversible and not blocked by the presence of 50 microM intracellular H-7. It is concluded that the effect of H-7 was independent of protein kinase activity.

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

Inhibition of a 5-HT3 receptor-mediated current by the selective serotonin uptake inhibitor, fluoxetine.

The effect of the selective serotonin uptake inhibitor, fluoxetine, on the inward current mediated by 5-HT3 receptors was investigated with the whole-cell patch-clamp technique. Fluoxetine inhibited the peak 5-HT current with an IC50 value of 1.2 microM. During continuous application of fluoxetine at concentrations of < or = 1 microM, there was a transient decrease in the fluoxetine-induced inhibition of 5-HT current. It is suggested that fluoxetine may have a short-lived action on 5-HT current and that the 5-HT3 receptor is a possible acting site for the therapeutic use of fluoxetine.

Animals↗

Crystal structure and NMR conformation of a cyclic pseudotetrapeptide containing urethane backbone linkages.

Urethane bonds, derived from the hydroxyl group of the tyrosine side chain, have been investigated as a new type of amide bond mimetic in the design of pseudopeptides. The structure of a representative cyclic pseudotetrapeptide that consists of an -Ala-Tyr(urethane)Ala-Tyr(urethane) sequence fused into a rigid ring has been studied in the solid state by x-ray crystallography and in solution by two-dimensional nmr techniques. The cyclic pseudotetrapeptide has an oblong shape. The backbone urethane bonds assume a trans-trans conformation. The carbonyl groups in the ring have an alternating pattern of down, up, down, up with respect to the average ring plane. Solution nmr studies give observed nuclear Overhauser effects and coupling constants largely in agreement with the crystal structure. However, in solution the observed structure is likely to be conformationally averaged, and in the averaged structure, the urethane bond is perpendicular to the plane of the aromatic ring of the tyrosine, while in the crystal it is close to this plane. These differences may be explained by intermolecular hydrogen-bonding interactions. Four aspects of the conformation of the cyclic pseudotetrapeptide were investigated in detail: the tyrosine residue with the attached side-chain urethane bond (the tyrosine-urethane unit), the conformation of the two urethane backbone linkages, the conformation of the two conventional peptide bonds within this unusual ring structure, and the tight turns within the cyclic pseudotetrapeptide. The conformation of the tight turns present in the cyclic pseudotetrapeptide is very similar to that of a beta-bend of type II. Intermolecular hydrogen bonding, joining adjacent layers of the cyclic pseudotetrapeptide in the solid state, resemble a parallel beta-pleated sheet. The presence of these structural motifs in the cyclic pseudotetrapeptide indicates that the tyrosine urethane unit may find applications in peptide and protein engineering.

Amino Acid Sequence↗

Procaine impairs the function of 5-HT3 receptor-ion channel complex in rat sensory ganglion neurons.

Previous studies have shown that local anesthetics block voltage-dependent Na+ channels and nicotinic acetylcholine receptors. The present study investigated the effect of the local anesthetic, procaine on another ligand-gated ion channel, the 5-HT3 receptor, in rat nodose ganglion neurons. Procaine (0.01-100 microM) inhibited the 5-HT3 receptor-mediated inward current in the whole-cell patch clamp recording. The inhibition was fully reversible, concentration-dependent but not sensitive to changes in membrane potential. Concentration-response curves indicated that procaine appears to produce a competitive inhibition on 5-HT3 receptors with a KD of 1.7 microM. These observations suggest that one of the actions of procaine in nervous system is on 5-HT3 receptors.

Animals↗

The effect of atropine on the activation of 5-hydroxytryptamine3 channels in rat nodose ganglion neurons.

It has been suggested that changes in brain 5-hydroxytryptamine3 receptor function may contribute to some behavior disorders, such as anxiety, schizophrenia and drug abuse. We are using the whole-cell version of the patch-clamp technique to study the function of 5-hydroxytryptamine3 channels in neurons freshly dissociated from rat nodose ganglion. In these cells, 5-hydroxytryptamine elicits an inward current over the concentration range of 0.25-100 microM (EC50 = 2.62 microM) by activating 5-hydroxytryptamine3 receptors. The muscarinic cholinergic antagonist atropine reduced the amplitude of 5-hydroxytryptamine activated inward current in a concentration-dependent manner. Other muscarinic antagonists, scopolamine, dexetimide, the M1 muscarinic receptor antagonist pirenzepine, the M2 receptor antagonist methoctramine and the M3 receptor antagonist 4-DAMP methiodide also inhibited 5-hydroxytryptamine-induced inward current. Atropine did not appear to change the reversal potential of this current. In the presence of 5 microM atropine, the concentration-response curve for 5-hydroxytryptamine current was shifted to the right in a parallel fashion. The EC50 value for 5-hydroxytryptamine was increased from 2.62 to 8.76 microM. Schild plots of increasing atropine and 5-hydroxytryptamine concentrations revealed a pA2 value of 5.74 for atropine (apparent KD = 1.8 microM). These observations suggest that atropine competitively antagonizes the activation of a receptor for the neurotransmitter serotonin, a novel action of muscarinic antagonists in the nervous system. This effect of atropine may contribute to the clinical symptoms seen in severe atropine intoxication.

Animals↗

Facilitation of 5-hydroxytryptamine3 receptor desensitization by fluoxetine.

Effect of fluoxetine on the desensitization of the inward current mediated by 5-hydroxytryptamine3 receptors in rat nodose ganglion neurons was investigated with whole cell patch-clamp recording. 5-Hydroxytryptamine3 current desensitization was best fitted in most experiments by a single exponential function and showed little dependence on membrane potential. Fluoxetine greatly facilitated the rate of 5-hydroxytryptamine3 current desensitization in a dose-dependent manner. The effect of fluoxetine was gradual, long-lasting, voltage-independent and the recovery was incomplete. The IC50 value for the decrease of the desensitization time-constant by fluoxetine was 0.171 microM and the Hill coefficient was 1.1. Fluoxetine also inhibited the peak and steady-state 5-hydroxytryptamine3 current with the latter being more sensitive to fluoxetine. The IC50 value for the effect of fluoxetine on peak current was 1.27 microM and that on steady-state current was 0.172 microM. There is a highly significant correlation between the two effects of fluoxetine on current desensitization and on current amplitudes: r-values for the correlation between the decrease in time-constant and the reduction in peak and steady-state current amplitudes were 0.82 and 0.88, respectively (P < 0.001). This action of fluoxetine on 5-hydroxytryptamine3 receptors may be involved in the behavioral effects of fluoxetine.

Animals↗

Effects of antidepressants on the inward current mediated by 5-HT3 receptors in rat nodose ganglion neurones.

1. Effects of three different categories of antidepressants, imipramine (tricyclic), fluoxetine (selective 5-hydroxytryptamine (5-HT) uptake inhibitor), phenelzine and iproniazid (monoamine oxidase (MAO) inhibitor) on the inward current mediated by 5-HT3 receptors were investigated in rat nodose ganglion neurones. The whole-cell patch-clamp technique was used for recording the 5-HT current. 2. All the antidepressants tested inhibited the peak 5-HT current. The inhibition gradually reached a steady level and the recovery was incomplete when antidepressants were removed. IC50 values for imipramine, fluoxetine and phenelzine were 0.54 microM, 1.3 microM and 4.2 microM respectively. The correspondent Hill coefficients were 0.9, 0.87 and 0.92. 3. The antidepressants examined increased the rate of 5-HT current desensitization. IC50 values for imipramine, fluoxetine and phenelzine on the decrease in desensitization time constant were 0.11 microM, 0.18 microM and 2.4 microM respectively. The correspondent Hill coefficients were 0.9, 1.14 and 1.06. 4. Intracellular applications of the protein kinase inhibitor, H-7 (100 microM), GDP-beta-S (2 mM) and the calcium chelator BAPTA (20 mM) did not affect the 5-HT current and the actions of antidepressants on 5-HT current. 5. These results suggest that the 5-HT3 receptor is an acting site for the therapeutic use of antidepressants. The present observation is also helpful in explaining the analgesic effect of antidepressants seen in pain clinics.

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

Mepacrine-induced inhibition of the inward current mediated by 5-HT3 receptors in rat nodose ganglion neurones.

1. With the whole-cell patch clamp technique, the effect of the antimalarial drug, mepacrine (quinacrine) on the inward current mediated by 5-HT3 receptors (5-hydroxytryptamine (5-HT)-induced current) was investigated in isolated nodose ganglion neurones of the rat. 2. 5-HT and the selective 5-HT3 receptor agonists, 2-methyl-5-HT and m-chlorophenylbiguanide elicited an inward current which reversed at around 0 mV and quickly desensitized to a steady state level. 3. Mepacrine dose-dependently inhibited the peak current induced by 5-HT with an IC50 of 2.1 microM and an apparent Hill coefficient of 0.99. 4. Mepacrine increased the decay rate of the 5-HT-induced current. 5. The effect of mepacrine on the 5-HT-induced current was reversible and not dependent on membrane potential. The reversal potential of the 5-HT-induced current was not affected. 6. Intracellular mepacrine had no significant effect on the 5-HT-induced current and did not block the extracellular action of mepacrine. 7. Concentration-response curves in the presence and absence of mepacrine suggest a non-competitive inhibition of 5-HT-induced current by mepacrine.

Animals↗

[The spectral characters of pulsed Doppler in fetal arrhythmia].

Blood flow spectra of left ventricular inflow and outflow of the fetus were measured by pulsed Doppler echocardiography in 82 cases who were diagnosed as fetal arrhythmia clinically. By analysing the order of atrio- ventricular excitation, the spectral characters and the relationship of time- phase, the classification of fetal arrhythmia was confirmed. Among the 82 cases, there were 17 cases of sinus bradycardia, 16 cases of sinus tachycardia, 28 cases of atrial premature beats, 16 cases of ventricular premature beats, 3 cases of II degrees atrioventricular conduction block, 2 cases of atrial fibrillation. These common spectral characters of fetal arrhythmia were confirmed by the examination of neonatal Doppler echocardiography and ECG. This study indicated that this method could be used as one of the diagnostic methods for fetal arrhythmia.

Arrhythmias, Cardiac↗

[Clinical significance of increased serum soluble interleukin-2 receptor levels in patients with pulmonary tuberculosis].

The serum soluble interleukin-2 receptor (sIL-2R) was measured in 40 patients with pulmonary tuberculosis by using sandwich enzyme linked immunosorbent assay. The results show that the levels of sIL-2R in sera of the various stage patients are markedly higher than that of the normal controls and the serum levels of sIL-2R were associated significantly with the patients' conditions. These findings suggest that sIL-2R may be an useful referential indicator for diagnosing, monitoring and predicting pulmonary tuberculosis.

Adolescent↗

Effects of cocaine on the serotonin-induced inward current in rat nodose ganglion neurons.

Application of 5-hydroxytryptamine (5-HT) to freshly isolated rat nodose ganglion neurons produced a fast inward current when measured using the whole-cell patch-clamp technique. This current was blocked by the 5-HT3 receptor antagonist MDL72222. The selective 5-HT3 receptor agonist 2-methyl-5-HT induced a similar current. Cocaine (0.1-300 microM) applied simultaneously with 5-HT (0.25-50 microM) inhibited the 5-HT-induced current. The inhibition did not appear to be voltage dependent. If cocaine was preapplied for about 30 sec, the effect of cocaine on 5-HT current was increased. Both the peak and the steady-state 5-HT current was depressed by cocaine. However, the peak current was more sensitive to cocaine than the steady-state current. The concentration-response curves of cocaine in different agonist concentrations revealed that cocaine competitively inhibited the 5-HT3 receptor-mediated current with a pA2 value of 5.8 and an apparent KD of 1.6 microM. These results suggest that in addition to the other well known mechanisms, the 5-HT3 receptor-ion channel complex is another site for cocaine action.

Animals↗