Biomedical subjects

J Fan

Publications and source records attributed to J Fan.

At least 235 records · Page 13Linked to original sources

PubMed1997

[Correlation between hepatic fat, lipid peroxidation and hepatic fibrosis in rats chronically fed with ethanol and/or high fat diet].

UNLABELLED: To explore the correlation between hepatic fat and fibrosis and the possible causative mechanism. 40 Wistar rats were randomized into 4 groups i.e. low fat diet (group I), high fat diet (group II), low fat diet plus ethanol (group III), high fat diet plus ethanol (group IV). Rats were sacrificed at 3 and 6 months after experiment. Triglyceride (TG), malonaldehyde (MDA) and hydroproline (Hyp) content in the liver were measured with biochemical analysis. The degree of steatosis and fibrosis and the amount of alpha-smooth muscle actin (alpha-SMA) positive cells in the liver were determined by HE, van Giesson and immunohistochemical ABC stain, respectively. RESULTS: Steatosis was observed in most of the group II, III, IV animals including those sacrificed at 3 months after experiment, but increased amount of alpha-SMA positive cells and hepatic fibrosis was only shown in group III and IV. As compared with group I, hepatic TG content was increased significantly in the group II, III, IV animals, and hepatic MDA and Hyp content were increased significantly in the group III, IV animals. Moreover, changes of these biochemical and histological indexes in group IV were the most outstanding. There was no significant correlation between hepatic TG content and amount of alpha-SMA positive cells in group II, III, IV and no correlation between hepatic TG and Hyp content in group II, IV, and there was significant correlation between hepatic MDA content and Hyp content and the number of alpha-SMA positive cells in group III, IV. CONCLUSIONS: There is no direct relationship between steatosis and initiation of lipocyte activation and resulting fibrogenesis, but hepatic fat per se may promote the initiation and development of hepatic fibrosis induced by the injurious factors of increasing lipid peroxidation.

Animals↗

PubMed1997

[Liver resection after transcatheter hepatic arterial chemoembolization for hepatocellular carcinoma and curative effect analysis].

To study the therapeutic result of hepatic resection for those hepatocellular carcinoma (HCC) shrunked after transcatheter hepatic arterial chemoembolization (TACE) in the patients with unresectable HCC, authors reported 59 patients with HCC. Among the 59 patients, the maximum diameter of the tumor was 5.6 to 20.0 cm prior to the first TACE, mean 9.43 cm. The patients underwent 1 to 6 times of TACE, mean 2.9 times. The tumor diameters were reduced to 3.29 cm prior to operations. The duration between the last TACE treatment and sequential resection varied from 1 to 7 months, mean 2.53 months. Of the 59 patients, 35 patients' serum alpha-fetoprotein (AFP) levels were elevated. AFP levels returned to normal after TACE treatment in 13 patients. Of the patients, liver segmentectomy, combined liver segmentectomy or partial liver resection was performed in 56 patients, left trilobectomy in 2 and left hemihepatectomy in 1. Tumor necrosis ranged from 40% to 100% pathologically and complete tumor necrosis occurred in 9 patients. Of the 13 patients with AFP levels decreased to normal, 9 still had microscopic living tumor foci. The 1-, 3- and 5- year survival rates were 79.7%, 65% and 56%, respectively. These results indicated that TACE treatment can provide chance of tumor resection for those patients with unresectable HCC and good results can be obtained.

Adult↗

PubMed1997

[Endoscopic and CT evaluation of three types of intranasal ethmoidectomies].

To evaluate the curative effects and complications of conventional, microscopic and endoscopic intranasal ethmoidectomuies, 130 cases of sinusitis and polys (stage II) were operated on with intranasal ethmoidectomies. There were 40 conventional, 40 microscopic, and 50 endoscopic ethmoidectomies, followed-up with endoscopy and CT scanning. The results showed that 1. the relieve of symptoms in the endoscopic group(94.0%) was obviously better than the conventional (60.0%) and the microscopic groups (70.0%, P < 0.01): 2. the clinical cure rate in the endoscopic group (86.0%) was obviously higher than the conventional (40.0%) and the microscopic groups (52.5%, P < 0.01); the CT scans showed a normal ratio in the endoscopic group(82.0%) obviously higher than those in the conventional (22.5%) and microscopic groups (37.5%, P < 0.01); 3. the complication ratio in the endoscopic group(12.0%) was slightly higher than those in the conventional(5.0%) and the microscopic groups (2.5%, P > 0.05). The intranasal endoscopic ethmoidectomy was more successful than the conventional and microscopic ethmoidectomies, but attention should be paid to the possibility of complications.

Adult↗

PubMed1997

[Human tolerance to landing impact (+Gz) in sitting position].

The study showed that macaca mulatta selected can be used as a substitute for human in studying tolerance to landing impact. Based on the data of the experiments, the revisional coefficient from macaca mulatta to humans was calculated, and curves of human tolerance to landing impact in sitting position were given. Tolerance limits for different injuries such as safe, slight injury, medium injury and serious injury are also given in this paper. The results might be useful for setting human tolerance standards to landing impact in sitting position.

Acceleration↗

PubMed1997

Suppression of mammalian K+ channel family by ebastine.

Nonsedating H1 receptor (H1-R) antagonists exert variable effects on QT interval, most likely mediated through modulation of cardiac K+ channels. We examined the effects of a novel H1-R antagonist, ebastine, on a family of K+ currents in isolated rat and guinea pig ventricular cardiomyocytes as well as on HERG-induced rapidly delayed rectifier K+ current (I(Kr)) in Xenopus laevis oocytes. The effect of ebastine was compared with that of two other H1-R antagonists, terfenadine and loratadine, with and without reported cardiotoxicity, respectively. In guinea pig ventricular myocytes, ebastine at concentrations approximating those found in plasma under certain conditions suppressed in a voltage-independent manner the I(Kr) (Kd = 0.14 microM, maximum block 74%) more effectively than the slowly delayed rectifier K+ current (I(Ks)) (Kd = 0.8 microM, maximum block 60%). Ebastine also suppressed I(Kr) in HERG-expressing X. laevis oocytes with the Kd value of 0.3 microM and a maximal block of 46% at 3 microM. The block of the rapidly activating delayed rectifier channel in rat myocytes (Iped) (Kd = 1.7 microM, maximum block 58%) had a small voltage dependence. Ebastine only minimally suppressed rat transient K+ current (Ito) (Kd = 1.1 microM, maximum block 10%). The drug was also not a very potent blocker of the inwardly rectifier K+ current (I(K1)) of rat and guinea pig (15 +/- 3% block at 3 microM). At concentrations of <100 nM, ebastine produced negligible effect on all K+ currents. We conclude that ebastine blocks various cardiac K+ channels with different potencies. The group of delayed rectifier K+ currents appeared to be most susceptible to ebastine with the order of sensitivity of I(Kr) > I(Ks) > Iped. Ebastine-induced inhibition of all K+ current types was always weaker than that observed with similar concentrations of terfenadine.

Animals↗

PubMed1997

Hepatic lipase is abundant on both hepatocyte and endothelial cell surfaces in the liver.

The cellular location of hepatic lipase was investigated in transgenic rabbits that expressed human hepatic lipase in the liver. The binding of monoclonal antibodies to human hepatic lipase, as detected by either fluorescence-tagged or gold-conjugated secondary antibodies, showed that hepatic lipase was concentrated at the surfaces of hepatic sinusoids. This distribution was the same as observed in the human liver. At the ultrastructural level, immunogold labeling of the space of Disse showed hepatic lipase on both lumenal and sublumenal surfaces of rabbit liver sinusoidal endothelial cells. An equivalent amount of hepatic lipase also was found on the external surfaces of hepatocyte microvilli in the space of Disse, as well as in the interhepatocyte spaces. The distribution suggests that a majority of the hepatic lipase produced by the liver is associated with hepatocyte surfaces, consistent with the functions of this enzyme in lipoprotein metabolism.

Animals↗

PubMed1997

Inhibition of mononuclear cell recruitment in aortic intima by treatment with anti-ICAM-1 and anti-LFA-1 monoclonal antibodies in hypercholesterolemic rats: implications of the ICAM-1 and LFA-1 pathway in atherogenesis.

To investigate the mechanism(s) for mononuclear cell recruitment in the arterial wall during the development of atherosclerosis, we studied intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) expression in aortic intima from diet-induced hypercholesterolemic rats. ICAM-1 was barely found in the aortic walls from rats fed a normal chow diet; however, in rats on a cholesterol-rich diet for 4 weeks, ICAM-1 expression was markedly enhanced in the intimal endothelial cells of aortas. Enhanced expression of ICAM-1 on endothelial cells especially along the cellular borders in the abdominal aorta was almost invariably associated with increased adherence of mononuclear cells. Compared to control animals, in hypercholesterolemic rats, the numbers of intimal macrophages and T lymphocytes adhering to the "lesion-prone" areas of the abdominal aorta were significantly increased by 5.9-fold (p < 0.001) and 2.2-fold (p < 0.001), respectively. More than 85% of adherent macrophages exhibited LFA-1 antigen on the cellular membrane surface as assessed by immunostaining. To examine the participation of ICAM-1 and LFA-1 in adherence and migration of mononuclear cells, we administered monoclonal antibodies (mAb) against either ICAM-1 or LFA-1 into hypercholesterolemic rats after they were fed a cholesterol-rich diet for 2 weeks. Two weeks after the mAb treatment, the number of macrophages adhering to the intima was significantly inhibited by 42% (p < 0.001) with anti-ICAM-1 mAb and by 31% (p < 0.001) with anti-LFA-1 mAb compared to controls injected with mouse IgG. Combined injection with these two mAb increased the reduction of the number of macrophages in the intima to 58%. Furthermore, we found that the decrease in the number of macrophages that adhered to the intima was almost exclusively due to the reduction of LFA-1-positive macrophages. These results suggest that the ICAM-1 and LFA-1 pathway is involved in mononuclear-endothelial cell interaction during cholesterol-rich diet-induced atherogenesis.

Animals↗

PubMed1997

[Intranasal endoscopic ethmoidectomy and the analysis of curative effect].

Forty cases of intranasal endoscopic ethmoidectomy were analyzed. In this series, 28 males and 12 females were included. Hard endoscopes with diameter of 4 mm, visual angle 30 and 70 were used. All patients were followed-up for 3 to 12 months. The surgical results were that twenty percent of patients were completely relieved of symptoms, 10% symptom-free with additional therapy, 40% improved without additional therapy, 20% improved with additional therapy, 10% no improvement and the total effective rate was 90%. No operative complications happened. Some factors affecting operative effects were discussed.

Adult↗

PubMed1997

[The development of a laser back-scattering erythrocyte-aggregometer].

In this paper, an erythrocyte-aggregometer based on the analysis of the light intensity back-scattered by a blood suspension is presented and described in detail. It allows to approach aggregation phenomenon in terms of kinetics, structural and rheological parameters. A personal computer and a microcomputer are applied to automate the system's sampling, data-processing and data-restoring procedure.

Equipment Design↗

PubMed1997

[Comparison of sequences of hepatitis B virus S gene fragment in eight cities of China].

Sequencing and comparative analysis of 52nd to 512th nucleotide of S gene in hepatitis B virus (HBV) were conducted in 43 cases of sero-positive and 52 cases of sero-negative HB from eight cities, including Changchun, Datong, Hangzhou, Shenzhen, Qingtao, Xi'an, Kunming and Lahsa, to study the relationship between focal variation of HBV S gene and seronegative HB. It was found that sequences of HBV S gene fragment in the same genotype were more conservative, most of its mutation happened randomly, and no insertion, deletion or null mutation occurred. There were three and five hypervariable nucleotide points in HBV isolated from two different HB groups with identical genotype and serotype (C genotype/adr serotype and C genotype/ayw1 serotype), respectively, and there were five hypervariable nucleotide points in HBV of D genotype/ayw1 serotype (five strains of sero-positive HBV) and D genotype/ayw3 serotype (ten strains of sero-negative HBV), respectively. It suggests that most cases of sero-negative HB may correlate with low level of HBV in their blood, and a small number of cases may be caused by HBV S gene mutation.

China↗

PubMed1997

[A study on the inhibitory effects of several chemicals on the production of nitrogen oxide in alveolar macrophage induced by asbestos].

Induction of chrysotile produced in Mang ai to the production of nitrogen oxide (NO) and effects of mixed rare earths (MRE), sodium selenite (SS) and aluminium citrate on the production of NO in alveolar macrophage (AM) induced by asbestos fiber were observed by in vitro cell culture technique and determination of nitrite ion content in the culture medium. Results showed that chrysotile fiber could increase nitrite ion content in the culture medium, with an obvious dose-dependent relationship. MRE, selenite, and aluminium citrate all could inhibit the production of NO in AM induced by asbestos, and its inhibitiory effects increased with the concentration of the above-mentioned chemicals. It suggests antagonism of MRE and selenite to pathogenicity of asbestos may be used in practice.

Aluminum Compounds↗

PubMed1996

Variant GPI structure in relation to membrane-associated functions of a murine folate receptor.

Two variant sublines of murine L1210 leukemia cells (L1210A and L1210JF) overexpress the cell surface folate receptor (FR). The membrane bound FR in L1210A cells exhibited significantly (up to 17-fold) greater relative affinities for (6S)-N5-methyltetrahydrofolate, (6S)-N5-formyltetrahydrofolate and methotrexate compared to the FR in L1210JF cells. Furthermore, receptor-mediated transport of [3H]-(6S)-N5-methyltetrahydrofolate was much more efficient in L1210A cells compared to L1210JF cells. When solubilized with Triton X-100, the ligand binding characteristics of FR from both sublines resembled those of the receptor associated with L1210 JF cell membranes. N-terminal amino acid sequence analysis as well as RT-PCR analysis of the entire coding region revealed a single species of FR in both cells, identical to murine FR-alpha. The FR in L1210JF cells was sensitive to phosphatidylinositol specific phospholipase C (PI-PLC) indicating the presence of a glycosyl-phosphatidylinositol (GPI) membrane anchor while the FR in L1210A cells was resistant to PI-PLC; however, the FR in L1210A cells was released from plasma membranes by nitrous acid, as expected for GPI and its PI-PLC resistant structural variants. Treatment of L1210A cell membranes with mild base rendered the protein PI-PLC sensitive as expected for GPI anchors acylated in the inositol ring and also decreased the affinities of the membrane associated FR for reduced folates. When the cDNA for murine FR-alpha was expressed in parental L1210 cells the protein was PI-PLC resistant but was sensitive to PI-PLC when the cDNA was expressed in human 293 fibroblasts. In L1210JF, L1210A, and parental L1210 cells, several cell surface proteins, including FR, incorporated [3H]ethanolamine, a component of the GPI membrane anchor; however, the labeled proteins were released by PI-PLC only in L1210JF cells. The above results preclude any peculiarity of the FR polypeptide in either L1210 subline as the basis for the observed differences in PI-PLC sensitivity and membrane-associated functions of FR. Partial deglycosylation of membrane associated FR from either cell with N-glycanase did not influence its ligand binding characteristics. The results of this study lead to the hypothesis that variant GPI structures may modulate the function of a protein by influencing its conformation/topography in the membrane. Such effects may be identified by their disappearance/reduction upon detergent solubilization or mild base treatment of the membrane.

Amino Acid Sequence↗

PubMed1996

IL-6 stimulation of insulin-like growth factor binding protein (IGFBP)-1 production.

TNF alpha and IL-1 beta have previously been shown to increase the IGFBP-1 concentration in plasma and liver under in vivo conditions. The present study demonstrates that another inflammatory cytokine, IL-6, also elevates a 30- to 32-kDa IGF binding protein in the plasma of mice. Moreover, IL-6 produced dose- and time-dependent increases in IGFBP-1 production by HepG2 cells. The maximal IL-6-induced increase in IGFBP-1 was comparable to that observed with dexamethasone, and this increase was attenuated by diltiazem or dantrolene, both of which are known to reduce the cytosolic Ca2+ concentration. Finally, incubation of HepG2 cells with TNF alpha or IL-1 beta also increased IGFBP-1 in a dose-dependent manner. These results demonstrate that IGFBP-1 production is mediated directly by proinflammatory cytokines and suggest that this mechanism may be important for the upregulation of IGFBP-1 seen in catabolic conditions associated with overexpression of these cytokines.

Animals↗

PubMed1996

Effect of cyclin D1 overexpression on drug sensitivity in a human fibrosarcoma cell line.

BACKGROUND: Alterations in the expression of genes that control the cell cycle may be of critical importance in determining the sensitivity of cells and tumors to drugs (chemosensitivity) and radiation. Mutations and deletions of the p53 tumor suppressor gene in cell lines and tumors are associated with resistance to a variety of DNA-damaging agents. The effects of alterations in the cyclin genes and their products on drug action have not been studied. One of these genes, cyclin D1, is expressed in early G1 phase, and its protein product, together with the cyclin-dependent kinases CDK4 and CDK6, mediates the phosphorylation and functional inactivation of the retinoblastoma protein (pRb). Elevated levels of expression of cyclin D1 protein have been found in a variety of cancers, including breast cancer, head and neck cancer, non-small-cell lung cancer, and mantle cell lymphomas. PURPOSE: This study was conducted to investigate the effect of increased expression of cyclin D1 protein on the chemosensitivity profile of a human fibrosarcoma cell line. METHODS: Expression plasmids containing either the neomycin-resistance gene and the complementary DNA sequence encoding human cyclin D1 or the neomycin-resistance gene only (control) were transfected by lipofection into the human HT1080 fibrosarcoma cell line, and cell colonies resistant to the antibiotic neomycin (G418) were isolated. Cyclin D1 messenger RNA (mRNA) and protein levels were measured by ribonuclease protection and western blot analyses, respectively. Dihydrofolate reductase (DHFR) mRNA and protein levels were measured by northern blot and western blot analyses, respectively. The phosphorylation status of pRb was assessed by western blot analysis. Cell cycle analysis was performed by use of the technique of fluorescence-activated cell sorting. Cytotoxicity assays were carried out by use of the sulforhodamine blue assay. RESULTS: Of the 16 cyclin D1-transfected cell clones that were isolated, four were randomly selected for further study. Two cell clones expressed high levels of cyclin D1 mRNA and protein as compared with control cells transfected with plasmids containing the neomycin-resistance gene only. A relative increase in the phosphorylated form of pRb in cells expressing high versus low levels of cyclin D1 was also revealed by western blot analysis. There was an increased fraction of cells in the S and G2 phases of the cell cycle among cells expressing higher levels of cyclin D1. Transfectants with increased cyclin D1 expression also had increased DHFR mRNA and protein expression. Cytotoxicity assays revealed a statistically significant (P < .01) increase in resistance to methotrexate in cells expressing high levels of cyclin D1 compared with cells expressing lower levels. There was no difference in resistance to doxorubicin, paclitaxel (Taxol), and cytarabine. CONCLUSION: Alterations in the expression of cyclin D1 led to altered cell cycle distribution in a human sarcoma cell line. The associated increase in DHFR expression resulted in increased resistance to methotrexate but had no effect on other classes of anticancer agents. IMPLICATIONS: These results indicate that alterations in cell cycle genes may differ in their effects on cytotoxicity. It will be important to determine the effects of alterations of other cell cycle regulatory genes on the responses of cells to specific classes of drugs. Tumors with overexpression of cyclin D1 may be relatively refractory to methotrexate treatment.

Antimetabolites, Antineoplastic↗

PubMed1996

Microtubule minus ends can be labelled with a phage display antibody specific to alpha-tubulin.

To investigate the orientation of alpha- and beta-tubulin heterodimers within microtubules, we cloned a phage display antibody to alpha-tubulin. The N-terminal 100 residues of alpha-tubulin were bacterially expressed and used to select clones from a large repertoire of antibody-expressing phagemid particles. One clone reacted with the expressed alpha-tubulin N terminus and native tubulin dimer but not with the expressed beta-tubulin N terminus. Electron microscopy showed 30 nm gold beads coated with the antibody binding to one end of brain microtubules. The beads bound to the minus ends of axonemes but not to the brain tubulin extensions from their plus ends. In sliding motility assays with a plus end directed motor, beads were pushed ahead of the microtubules. Our results indicate that an N-terminal epitope of alpha-tubulin is exposed only at the minus ends of microtubules.

Animals↗

PubMed1996

Regulation of cardiac sodium-calcium exchanger by beta-adrenergic agonists.

Na+-Ca2+ exchanger and Ca2+ channel are two major sarcolemmal Ca2+-transporting proteins of cardiac myocytes. Although the Ca2+ channel is effectively regulated by protein kinase A-dependent phosphorylation, no enzymatic regulation of the exchanger protein has been identified as yet. Here we report that in frog ventricular myocytes, isoproterenol down-regulates the Na+-Ca2+ exchanger, independent of intracellular Ca2+ and membrane potential, by activation of the beta-receptor/adenylate-cyclase/cAMP-dependent cascade, resulting in suppression of transmembrane Ca2+ transport via the exchanger and providing for the well-documented contracture-suppressant effect of the hormone on frog heart. The beta-blocker propranolol blocks the isoproterenol effect, whereas forskolin, cAMP, and theophylline mimic it. In the frog heart where contractile Ca2+ is transported primarily by the Na+-Ca2+ exchanger, the beta-agonists' simultaneous enhancement of Ca2+ current, ICa, and suppression of Na+-Ca2+ exchanger current, INa-Ca would enable the myocyte to develop force rapidly at the onset of depolarization (enhancement of ICa) and to decrease Ca2+ influx (suppression of INa-Ca) later in the action potential. This unique adrenergically induced shift in the Ca2+ influx pathways may have evolved in response to paucity of the sarcoplasmic reticulum Ca2+-ATPase/phospholamban complex and absence of significant intracellular Ca2+ release pools in the frog heart.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1996

Central opiate modulation of growth hormone and insulin-like growth factor-I.

The effects of central administration of morphine-sulfate (MOR:80 micrograms) and morphine-6-glucuronide (M6G:1 microgram) on the growth hormone (GH)/insulin-like growth factor (IGF) system were assessed. MOR and M6G were injected intracerebroventricularly (ICV) in chronically catheterized 24 h fasted rats; time-matched control animals received H2O (5 microliters). MOR increased plasma GH concentrations 3-fold 2 h after i.c.v. injection, and transiently increased the plasma concentration and liver content of IGF-I (60% and 90%, respectively) 30 min after i.c.v injection. M6G did not produce any significant alterations in plasma GH and IGF-I levels at the time-points measured. Both MOR and M6G increased the concentration of IGF binding protein-1 (IGFBP-1) in plasma and liver 2 h after injection. However, MOR showed 2- to 2.5-fold greater effect than M6G in stimulating plasma and liver IGFBP-1. MOR and M6G produced similar increases in plasma epinephrine (5-fold), norepinephrine (3-fold) and corticosterone (1.5-fold). Neither opiate significantly altered circulating insulin levels. These findings suggest that opiate modulation of GH and IGF may be hormone-independent and centrally modulated. We speculate that differential affinities of MOR and M6G to the different opiate receptor subtypes might be responsible for their distinct effects on GH/IGF-I system.

Animals↗

PubMed1996

An unusually avulsed penis successfully replanted by using microsurgical technique.

An unusually avulsed penis and its successful microsurgical replantation is reported. The penis was self-avulsed between the superficial fascia of the shaft, and the shaft was cut distally, just proximal to the glans, with the whole glans and a short part of the shaft hanging in the avulsed skin of the penis. According to our search in the literature, this is the first successful replantation of such a case by microsurgery. The blood circulation of the replant was reestablished, after 15 hours of tissue ischemia, by means of microsurgical vascular anastomosing of the minimal subcutaneous vessels in the skin. Both the skin and the glans survived, indicating the alternative possibility of replantation of avulsed penile skin by microsurgery, rather than by skin grafting.

Adult↗