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Biomedical subjects

Y Qin

Publications and source records attributed to Y Qin.

At least 127 records · Page 7Linked to original sources

[Inotropic effect of novel domestic cardiotonic agent, vesnarinone--test in vitro].

This paper reports the studies on the positive inotropic effect of the novel domestic cardiotonic agent, vesnarinone on isolated papillary muscle and atrium of guinea pigs and rabbits, and on the comparison of the positive inotropic effect and toxicity of vesnarinone with amrinone, milrinone and strophanthin. The result suggests that vesnarinone has an apparent dose-effect relationship on a positive inotropic effect, the strength of which is between amrinone and milrinone. The positive inotropic effect of vesnarinone is higher and the toxicity is lower than that of strophanthin.

Amrinone↗

Tie-1 and tie-2 define another class of putative receptor tyrosine kinase genes expressed in early embryonic vascular system.

We report the molecular cloning and characterization of two structurally related putative receptor tyrosine kinases, encoded by distinct genes (tie-1 and tie-2) on mouse chromosome 4. Both tie-1 and tie-2 encode receptor proteins possessing unique multiple extracellular domains: two immunoglobulin-like loop domains flanking three epidermal growth factor repeats followed by three fibronectin-type III repeats. Both genes are expressed in early embryonic vascular system and in maternal decidual vascular endothelial cells, where the vasculature undergoes an active angiogenesis. tie-2, but not tie-1, expression was also detected in extraembryonic mesoderm of the amnion. tie-1, but not tie-2, is expressed in an acute myelogenic cell line in vitro. tie-1 and tie-2 may form another class within the receptor tyrosine kinase gene family, and further characterization of these genes and identification of their putative ligands should define the nature of the signal-transduction cascades underlying early vascular system development, as well as their differential roles in mesodermal cells of the amniotic and myeloid lineages.

Animals↗

Perforin and tumor necrosis factor alpha in the pathogenesis of experimental allergic encephalomyelitis: comparison of autoantigen induced and transferred disease in Lewis rats.

A cell-mediated cytotoxic reaction is believed to be involved in inflammatory lesion formation of experimental allergic encephalomyelitis (EAE). We compared EAE diseased animals which had either been immunized with myelin basic protein (MBP) or adoptively received MBP specific T-cell lines in order to study whether the different courses of disease induction are reflected by quantitative or qualitative differences in the expression of genes encoding putative mediators of tissue damage, i.e. TNF alpha, and the pore-forming protein perforin. With the appearance of signs of paralysis, both genes are induced in cells within the CNS lesions, whereas drastically reduced numbers of TNF alpha- and perforin gene-expressing cells are observed during recovery, despite the presence of high numbers of mononuclear cells in the CNS. Marked differences, however, exist in the gene expression profiles: during the phase of most severe clinical signs TNF alpha expressing cells are 2 to 3 times more frequent in transferred than immunized animals. In animals with MBP-induced EAE the number of perforin expressing cells represents only 1.6% of the IL2R gene expressing cells, while this fraction represents 25% in mice which received autoaggressive T cells. Thus, the presence of a high number of activated killer cells may accelerate tissue damage and progression of disease in passive EAE whereas in actively induced EAE activation of regulatory mechanisms induced by polyclonal activation after immunization may prevent generation of large amounts of activated cytotoxic T cells.

Animals↗

Dual expression of CD45RA and CD45RO isoforms on myelin basic protein-specific CD4+ T-cell lines in multiple sclerosis.

Myelin basic protein (MBP)-specific T-cell lines from patients with multiple sclerosis (MS) and healthy controls were analyzed for the expression of CD45 isoforms and adhesion molecules. In the multiple sclerosis group, 22 of 24 MBP-specific T-cell lines were CD4+. Two distinct patterns were observed with regard to CD45 isoform expression. Pattern I showed dual expression of CD45 isoforms (CD4+CD45RA+CD45RO+CD29+) and Pattern II included cells with a single CD45 isoform (CD4+CD45RA-CD45RO+CD29+). All 10 cell lines from healthy controls were CD4+ and displayed Pattern II (CD4+CD45RA-CD45RO+CD29+). The dual expression of CD45 isoform in T-cell lines from MS was stable, did not represent a transition stage from CD45RA to CD45RO, and was cell-cycle independent. All cell lines from MS and controls expressed increased levels of LFA-1 (CD11a), LFA-2 (CD2), LFA-3 (CD58), ICAM-1 (CD54), and VLA-4 (CDw49d). These data show the presence of unique MBP-specific T cells (CD4+CD45RA+CD45RO+CD29+) that might play a role in the pathogenesis of MS.

Adolescent↗

[Pharmacokinetics of ciprofloxacin in young healthy volunteers].

Pharmacokinetic studies on ciprofloxacin were carried out in 6 young healthy volunteers. Serum and urine levels of ciprofloxacin were measured by reversed-phase high performance liquid chromatography. The drug obeyed one-compartment model kinetics in serum. The mean peak serum concentration, time to peak concentration and the area under the curve were 4.17 +/- 1.05mg/L, 1.75 +/- 0.40h and 18.09 +/- 2.69mg/L.h respectively after oral administration of 500mg of ciprofloxacin tablet. The elimination half life was 2.34 +/- 0.81h and the apparent volume of distribution was 3.71 +/- 0.75L. The urinary rate of ciprofloxacin over 24h after dosing was 34.22 +/- 6.57%. These data indicate that ciprofloxacin is easily absorbed and its concentration reaches the peak level rapidly. There are high levels of drug both in serum and urine.

Adult↗

[Determination of ciprofloxacin in human serum and urine by reversed-phase HPLC].

A sensitive and rapid method for the determination of ciprofloxacin using enoxacin as the internal standard was reported. High-performance liquid chromatograph model 344 (Beckman, USA) with a variable wavelength UV detector and reversed-phase Ultrasphere-ODS column (5 microns, 250 x 4.6 mm) was used. Serum or urine sample preparation involved addition phosphate buffer (pH 7.5) and aqueous solution of sodium lauryl sulfate, followed by chloroform extraction. The organic layer was removed and evaporated to dryness under an air stream in a 37 degrees C water bath. The residue was dissolved in 50 microliters mobile phase and 20 microliters injected. The mobile phase of 0.02 mol/L acetate buffer (pH 3.0) -acetonitril-dimethylformamide-10% aqueous solution of tetrabutyl ammonium hydroxide (88:6.5:5:0.5) was pumped at 0.9 ml/min through the column. The detector operated at 0.01 aufs and the wavelength was set at 276 nm. The retention times for ciprofloxacin and enoxacin were 7.31 min and 5.59 min, respectively. In serum, standard curve was linear in the concentration range of 0.75 to 24 mumol/L, the detective limit was 0.2 mumol/L, extraction recovery was 69-74%, within-day CV was less than 5%, and inter-day CV was less than 6%.

Chromatography, High Pressure Liquid↗

Treatment of liver metastases of human colon cancers in nude mice with somatostatin analogue RC-160.

Hepatic metastases of colon 320 DM and WidR human colon cancers in nude mice were treated by s.c. injections of somatostatin analogue RC-160 for 4 weeks. Chronic administration of RC-160 significantly inhibited the incidence and growth of liver metastases of these 2 colon-cancer cell lines. After RC-160 treatment, the incidence of liver metastases decreased by 25% for colon 320 DM cells and by 37.5% for WidR cells. The mean number of metastatic tumors in each liver decreased by 47.9% for colon 320 DM and 42.6% for WidR. Survival times of mice with liver tumors of colon 320 DM and WidR cells were prolonged by 20 days and 7 days, respectively. The inhibitory effect of RC-160 on the growth of these 2 colon cancers implanted s.c. was also observed. After administration of RC-160 for 4 weeks, the mean tumor volume in the treated groups was only 39.8% of that of controls for the colon 320 DM line and 58% for the WidR line. Tumor-growth rate and final tumor weight were also significantly decreased, while tumor-volume doubling time and tumor-growth delay time were prolonged. The effect of RC-160 on cellular proliferation in the tumors was studied by in vivo labelling with bromodeoxyuridine and immunoperoxidase staining. The mean labelling index in the treatment group was reduced by 14.9% and 19.5%, respectively, for colon 320 DM and WidR tumors. The cytostatic effect of RC-160 was also evident from the apparent reduction in DNA and protein content in the tumor tissues of these cancer lines. Our findings suggest that somatostatin analogue RC-160 may be useful for the treatment of patients with hepatic metastases of colon cancer.

Animals↗

Inhibitory effect of somatostatin analogue RC-160 on the growth of hepatic metastases of colon cancer in rats: a study with magnetic resonance imaging.

The effect of somatostatin analogue RC-160 on the growth of hepatic metastases of colon cancer was investigated in rats using magnetic resonance imaging. Experimental liver metastatic tumors were established in syngeneic BDIX rats after intrasplenic injection of DHD/K12 colon adenocarcinoma cells. Each rat with implanted liver tumors received s.c. injections of somatostatin analogue RC-160 (50 micrograms/kg) or the vehicle (control) twice a day for 4 weeks, starting 3 weeks after tumor inoculation. During the treatment with RC-160, the growth of liver tumors was studied quantitatively by measuring liver tumor volumes in vivo with magnetic resonance imaging at intervals of 7 days. Chronic administration of RC-160 inhibited the growth of hepatic metastases of colon cancer in rats. Significant inhibition of liver tumor growth in RC-160-treated rats was observed throughout the treatment. The final liver tumor volume in the treated rats was decreased by 56.1% as compared to the controls. The treatment with RC-160 reduced the percentage increase in liver tumor volume from 1575 +/- 674% (mean +/- SEM) for the control to 1034 +/- 727% in the treated group. The tumor volume doubling time in treated rats was 3.7 days longer than the controls. The liver tumor growth delay time was 15.1 days. At the end of the treatment, the incidence of ascites and the weights of tumorous livers were also decreased by RC-160 treatment. Administration of RC-160 prolonged the median survival time by 13 days in treated rats. In cell cultures, significant inhibitory effects of somatostatin-14 and RC-160 on the growth of DHD/K12 colon cancer cells were determined by MTT assay and [3H]-thymidine incorporation assay, indicating direct effects of these peptides on the growth of colon cancer cells in vitro. These data suggest that administration of RC-160 could inhibit the growth of colon cancer and their hepatic metastases in rats. Somatostatin analogue RC-160 might be considered as a potential new agent for the treatment of patients with hepatic metastases of colorectal cancers.

Amino Acid Sequence↗

Quantitative study of the growth of experimental hepatic tumors in rats by using magnetic resonance imaging.

Precise estimation of the volume and growth rate of hepatic metastases would represent an important step forward not only in clinical oncology but also for the evaluation of experimental treatments in animal models. In the present study, an original method of volumetry of hepatic metastatic tumors in vivo has been tested in rats using magnetic resonance imaging (MRI). Three different hepatic tumor models mimicking liver metastases were established in syngeneic BDIX rats by injection of DHD/K12 rat colon cancer cells either directly under the liver capsule or via the portal system. The liver tumor volumes were estimated in vivo by using MR imaging of the liver and summing the individual tumor volumes in the sequential MR liver sections. The values of the tumor volumes measured by MRI were compared with those determined by a classical method of water displacement in vitro after killing the animals and excising the tumors. At 3 weeks after tumor implantation, liver tumors as small as 1 mm in diameter could be detected by MRI. The difference between the tumor volumes estimated by MRI in vivo and those measured by water displacement in vitro was 9% for single liver tumors and 16% for multiple liver tumors. Close correlation between the values of the tumor volumes measured by MRI and those determined by water displacement was observed in solitary liver tumors (r = 0.985, p less than 0.01) as well as in multiple liver tumors (r = 0.985, p less than 0.01), indicating the high accuracy of MRI volumetry for liver tumors. Estimation of the liver tumor volumes by MRI in the same animals at successive time intervals made it possible to construct tumor growth curves and to calculate tumor growth parameters. These data suggest that MRI volumetry represents an effective means of evaluating the efficacy of experimental treatments in small animals and may have potentially important applications in clinical patients.

Animals↗

Comparative distribution of messenger RNAs encoding glutamic acid decarboxylases (Mr 65,000 and Mr 67,000) in the basal ganglia of the rat.

Glutamic acid decarboxylase, the enzyme required for GABA synthesis, exists as distinct isoforms, which have recently been found to be encoded by different genes. The relative expression of messenger RNAs encoding two isoforms of glutamic acid decarboxylase (Mr 67,000 and Mr 65,000) was measured at the single-cell level in neurons of the rat basal ganglia with in situ hybridization histochemistry. Both messenger RNAs were expressed in neurons of the striatum, pallidum, and substantia nigra pars reticulata, but marked differences in the relative level of labelling were observed with the two probes. In striatum, efferent neurons were more densely labelled for the messenger RNA encoding glutamic acid decarboxylase (Mr 65,000) than for the messenger RNA encoding glutamic acid decarboxylase (Mr 67,000), whereas the reverse was observed for GABA-ergic interneurons. Neurons of the entopeduncular nucleus were much more densely labelled for messenger RNA encoding glutamic acid decarboxylase (Mr 65,000) than for messenger RNA encoding glutamic acid decarboxylase (Mr 67,000). In addition, labelling for messenger RNA encoding glutamic acid decarboxylase (Mr 65,000) was higher in the entopeduncular nucleus (internal pallidum) than in the globus pallidus (external pallidum), a structure which expressed similar levels of both mRNAs. In contrast to neurons of the internal pallidum, efferent neurons of the substantia nigra pars reticulata expressed slightly more messenger RNA encoding glutamic acid decarboxylase (Mr 67,000) than that encoding the other isoform of the enzyme. The results suggest a differential expression of the messenger RNAs encoding the two isoforms of glutamic acid decarboxylase in subpopulations of basal ganglia neurons in rats.

Animals↗

Immune regulation in self tolerance: functional elimination of a self-reactive, counterregulatory CD8+ T lymphocyte circuit by neonatal transfer of encephalitogenic CD4+ T cells lines.

Transfer of encephalitogenic, CD4+ T lymphocyte lines into syngeneic adult Lewis rats not only leads to the development of experimental autoimmune encephalomyelitis (EAE), but, in addition, to the expansion of counterregulatory, CD8+ T lymphocyte clones which are able to lyse specifically the encephalitogenic T cells in vitro and to neutralize their encephalitogenic capacity in vivo. In striking contrast, in neonatal rats, which still lack myelin (autoantigens), injection of the same encephalitogenic lines neither mediates EAE, nor confers protection in later life against the myelin-specific T cells. In fact, this treatment results in the life-long functional elimination of counterregulatory, clonotypic CD8+ T lymphocytes, which cannot even be reinduced by repeated injections of the relevant CD4+ T line. These data seem to point to a self-protective T cell control mechanism which is developed within the immune system prior to, and thus independent of the appearance of the appropriate self antigen.

Animals↗

Effects of quinolinic acid on messenger RNAs encoding somatostatin and glutamic acid decarboxylases in the striatum of adult rats.

The level of expression of mRNAs encoding somatostatin and two isoforms of glutamic acid decarboxylase (Mr 65,000, GAD65 and 67,000, GAD67) was examined by quantitative in situ hybridization histochemistry in the striatum of adult rats after local injections of quinolinic acid. After a 2-week survival period, Nissl strains showed a profound loss of neurons in the injected striata. With a dose of 120 nmol quinolinic acid, the lesioned area was completely devoid of somatostatin mRNA-positive neurons but contained cells expressing nicotinamide adenine dinucleotide-diaphorase activity (a marker of somatostatinergic interneurons in striatum). After 60 nmol of quinolinic acid, the number of neurons expressing somatostatin mRNA in the lesioned area was similar to controls but the level of labeling per neuron was increased. In the lesioned area, labeling for GAD65 mRNA was abolished and labeling for GAD67 mRNA markedly reduced. However, scattered neurons expressing GAD67 mRNA could still be detected. The majority of surviving GABA-ergic neurons expressed immunoreactivity to parvalbumin, a marker for striatal GABA-ergic interneurons. The results show that quinolinic acid induces dose-dependent alterations in the expression of striatal somatostatin mRNA and reveal a relative sparing of GABA-ergic interneurons in the quinolinic acid-lesioned rat striatum.

Acetylcholinesterase↗

Indoor air pollution and pulmonary function in children.

Pulmonary function in winter time in 1,343 school children aged 10-13 years was measured in four cities located in northern and southern part of China. The results showed that FVC, FEV1, PEF, V75, V50 and V25 in children living in homes with coal stoves were decreased by 1.5-10.7% compared with children living in homes with gas or LPG stoves in Chengde and Shanghai. In contrast to this, no significant difference in pulmonary function was found in Shenyang and Wuhan. It suggested that this phenomenon was related to indoor air pollution, and partly related to passive smoking or outdoor air pollution.

Air Pollution, Indoor↗