Biomedical subjects

M Huang

Publications and source records attributed to M Huang.

At least 91 records · Page 5Linked to original sources

PubMed2001

[Alterations in the level of calcitonin gene related peptide and endothelin-1 in the cirrhotic rat heart].

OBJECTIVE: To investigate the role of calcitonin gene related peptide(CGRP) and endothelin-1 (ET-1) in cirrhotic cardiomyopathy (CCM). METHODS: We measured the level of CGRP and ET-1 in the samples of rat heart collected from 15 liver cirrhosis rats and 15 controls by using radio immunoassay. RESULTS: The data showed that the levels of CGRP (74.2130 +/- 10.3776 pg/mg protein) and ET-1 level (1.4780 +/- 0.9235 pg/mg protein) were significantly higher in the cirrhotic rat hearts than those in controls (P < 0.05). The increase of ET-1 in the cirrhotic rat hearts was closely associated with the severity of liver cirrhosis (P = 0.004); whereas no significant association was seen between the CGRP concentration and the severity of liver cirrhosis (P = 0.307). CONCLUSION: We infer that the increasing of CGRP level in the cirrhotic rat heart may be a protective or antagonistic reaction to ET-1 or other pathogenic factors for cardiac dysfunction. The disturbance of the balance between CGRP and ET-1 in the liver cirrhosis rat hearts may contribute to the pathologic process of CCM.

Animals↗

PubMed2001

[TGF beta 1 and ET-1 expression in the peripheral blood of patients with cirrhosis].

OBJECTIVE: The aims of this study were to determine 1. the variation of blood TGF beta 1 and ET-1 in patients with liver cirrhosis; 2. the relationship of the blood TGF beta 1 and ET-1 with Child degree of liver function and the severity of esophageal varices. METHODS: Peripheral blood samples were obtained from 72 patients and 24 normal controls. The blood levels of TGF beta 1 and ET-1 were measured by using a standard bioassay and the radioimmunoassay. RESULTS: TGF beta 1 level (11.77 +/- 1.32 ng/ml) and ET-1 level (78.37 +/- 17.54 pg/ml) were significantly higher in the patients than those in controls(P < 0.05). The increase of the ET-1 in the patients is closely associated with Child degree of liver function (r = 0.94) and the severity of esophageal varices(r = 0.87). TGF beta 1 concentration is not associated with Child degree of liver function (r = 0.11) and the severity of esophageal varices (r = 0.03). CONCLUSION: TGF beta 1 and ET-1 may play an important role in the pathophysiologic process of cirrhosis. ET-1 concentration may reflect portal hypertension development.

Adult↗

PubMed2001

[Effects of transforming growth factor beta 1 on the expression of integrin beta 3 and the activity of focal adhesion kinase on human vascular endothelial cell].

OBJECTIVE: To observe the effects of transforming growth factors beta 1 (TGF beta 1) on the expression of integrin beta 3 and the activity of focal adhesion kinase (FAK). METHODS: This study was performed on cultured human endothelial cells (EC) by using cell-ELISA and immunoprecipitation-tyrosine kinase assay respectively. RESULTS: Under the stimulus of TGF beta 1, there a dose-dependent increase in the expression of integrin beta 3 chain in the surface of EC. And after the cultured EC were treated with 5 ng/ml or 10 ng/ml TGF beta 1 for 6 or 24 hours, the FAK activity in EC increased significantly as compared with the control group (P < 0.05). CONCLUSION: The expression of integrin beta 3 and the activity of FAK on EC were regulated by TGF beta 1, and this regulation may be important in cell adherence, angiogenesis, and in the pathophysiology of atherosclerosis.

Cells, Cultured↗

PubMed2001

[Inflammatory mediator in patients with obstructive jaundice and its effect on renal function].

OBJECTIVE: To investigate the effect of inflammatory transmitter on renal function in obstructive jaundice. METHODS: 15 patients with obstructive jaundice (OJ) as the experimental group and 15 non-joundiced patients as the control group were involved in this study. The plasma ET, LPS, TNF-alpha, IL-6, IL-8 and urine REP, TFR, ALB were measured in 15 patients with OJ before and 1, 4, 7 days after surgery and in 15 patients without jaundice as controls. RESULTS: The levels of plasma ET, LPS, TNF-alpha, IL-6, IL-8 and urine RBP, TFR, ALB increased significantly at multiple time points as compared with those in the non-OJ patients (P < 0.05), and the changes of plasma ET, LPS, TNF-alpha, IL-6, IL-8 are the same as those of urine RBP, TFR, ALB. CONCLUSION: These data suggest that there is interaction between ET, LPS, TNF-alpha, IL-6, IL-8 and the damage to renal function with OJ after surgery.

Adult↗

PubMed2000

Profilin enhances Cdc42-induced nucleation of actin polymerization.

We find that profilin contributes in several ways to Cdc42-induced nucleation of actin filaments in high speed supernatant of lysed neutrophils. Depletion of profilin inhibited Cdc42-induced nucleation; re-addition of profilin restored much of the activity. Mutant profilins with a decreased affinity for either actin or poly-l-proline were less effective at restoring activity. Whereas Cdc42 must activate Wiskott-Aldrich Syndrome protein (WASP) to stimulate nucleation by the Arp2/3 complex, VCA (verpolin homology, cofilin, and acidic domain contained in the COOH-terminal fragment of N-WASP) constitutively activates the Arp2/3 complex. Nucleation by VCA was not inhibited by profilin depletion. With purified N-WASP and Arp2/3 complex, Cdc42-induced nucleation did not require profilin but was enhanced by profilin, wild-type profilin being more effective than mutant profilin with reduced affinity for poly-l-proline. Nucleation by the Arp2/3 complex is a function of the free G-actin concentration. Thus, when profilin addition decreased the free G-actin concentration, it inhibited Cdc42- and VCA-induced nucleation. However, when profilin was added with G-actin in a ratio that maintained the initial free G-actin concentration, it increased the rate of both Cdc42- and VCA-induced nucleation. This enhancement, also seen with purified proteins, was greatest when the free G-actin concentration was low. These data suggest that under conditions present in intact cells, profilin enhances nucleation by activated Arp2/3 complex.

Actins↗

PubMed2000

Novel interactions between urokinase and its receptor.

Urokinase-type plasminogen activator (uPA) binds to its receptor (uPAR) with a K(d) of about 1 nm. The catalytic activity of the complex is apparent at uPA concentrations close to K(d). Other functions of the complex, such as signal transduction, are apparent at much higher concentrations (35-60 nm). In the present study, we show that uPA and recombinant soluble uPAR (suPAR), at concentrations that exceed the K(d) and the theoretical saturation levels (10-80 nm), establish novel interactions that lead to a further increase in the activity of the single-chain uPA (scuPA)/suPAR and two-chain uPA (tcuPA)/suPAR complexes. Experiments performed using dynamic light scattering, gel filtration, and electron microscopy techniques indicate that suPAR forms dimers and oligomers. The three techniques provide evidence that the addition of an equimolar concentration of scuPA leads to the dissociation of these dimers and oligomers. Biacore data show that suPAR dimers and oligomers bind scuPA with decreased affinity when compared with monomers. We postulate that uPAR is present in equilibrium between oligomer/dimer/monomer forms. The binding of uPA to suPAR dimers and oligomers occurs with lower affinity than the binding to monomer. These novel interactions regulate the activity of the resultant complexes and may be involved in uPA/uPAR mediated signal transduction.

Fibrinolysis↗

PubMed2000

Corticotropin-releasing factor receptor type I mediates stress-induced relapse to opiate dependence in rats.

The possible effect of different corticotropin-releasing factor receptor (CRFR) antagonists (alpha-helical CRF, CP-154,526 and AS-30) on the maintenance and reactivation of morphine-conditioned place preference (CPP) induced by morphine or footshock stress, respectively, were investigated in rats. The results show that morphine-induced maintenance of CPP was not affected by pretreatment with any CRFR antagonists. However, morphine-induced the reactivation of CPP was significantly attenuated by pre-administration of 10 microg alpha-helical CRF (i.c.v.). The maintenance of morphine CPP could be induced by repeated footshock and this effect was significantly attenuated by pretreatment of 10 microg alpha-helical CRF (i.c.v.) and 10 mg CP-154,526 (i.p.). Furthermore, following a 28-day extinction of morphine CPP, a single footshock could again elicit the reactivation of place preference that was blocked by pretreatment with 10 microg alpha-helical CRF (i.c.v.) and 1 or 10 mg CP-154,526 (i.p.). The present study demonstrates that CRFR type 1, but not CRFR type 2, mediates the stress-induced maintenance and reactivation of morphine CPP. These findings suggest that CRFR type 1 antagonists might be of some value in the treatment and prevention of stress-induced relapse to drug dependence long after detoxification.

Animals↗

PubMed2000

Retinoic acid induces sodium/iodide symporter gene expression and radioiodide uptake in the MCF-7 breast cancer cell line.

The sodium/iodide symporter (NIS) stimulates iodide uptake in normal lactating breast, but is not known to be active in nonlactating breast or breast cancer. We studied NIS gene regulation and iodide uptake in MCF-7 cells, an estrogen receptor (ER)-positive human breast cancer cell line. All-trans retinoic acid (tRA) treatment stimulated iodide uptake in a time- and dose-dependent fashion up to approximately 9.4-fold above baseline. Stimulation with selective retinoid compounds indicated that the induction of iodide uptake was mediated by retinoic acid receptor. Treatment with tRA markedly stimulated NIS mRNA and immunoreactive protein ( approximately 68 kDa). tRA stimulated NIS gene transcription approximately 4-fold, as shown by nuclear run-on assay. No induction of iodide uptake was observed with RA treatment of an ER-negative human breast cancer cell line, MDA-MB 231, or a normal human breast cell line, MCF-12A. The iodide efflux rate of tRA-treated MCF-7 cells was slow (t(1/2) = 24 min), compared with that in FRTL-5 thyroid cells (t(1/2) = 3.9 min), favoring iodide retention in MCF-7 cells. An in vitro clonogenic assay demonstrated selective cytotoxicity with (131)I after tRA stimulation of MCF-7 cells. tRA up-regulates NIS gene expression and iodide uptake in an ER-positive breast cancer cell line. Stimulation of radioiodide uptake after systemic retinoid treatment may be useful for diagnosis and treatment of some differentiated breast cancers.

Alitretinoin↗

PubMed2000

Opposite effects of sulpiride and SCH 23390 on ethanol-induced striatal ascorbic acid release in intact and 6-hydroxydopamine lesioned rats.

The effects of L-sulpiride and SCH 23390 on ethanol-induced striatal ascorbic acid (AA) release in normal and 6-hydroxydopamine-lesioned rats were studied by using microdialysis coupled to high performance liquid chromatography with electrochemical detection. Ethanol (3.0 g/kg i.p.) significantly stimulated striatal AA release by 200% above the baseline in normal, 6-hydroxydopamine-lesioned, and reserpine-treated rats. L-Sulpiride, a dopamine D(2) antagonist, at the dose of 100 mg/kg i.p., decreased basal ascorbic acid release and showed an inhibitory tendency on ethanol-induced ascorbic acid release. However, at the higher dose of 200 mg/kg i.p., L-sulpiride significantly inhibited ethanol-induced ascorbic acid release in both normal and 6-hydroxydopamine-treated rats. SCH 23390, a dopamine D(1) antagonist, at the doses of 0.5 and 1.0 mg/kg i.p., potentiated ethanol-induced ascorbic acid release in normal rats. However, the potentiation of SCH 23390 on ethanol effect was not significant in 6-hydroxydopamine-treated rats at the dose of 1.0 mg/kg i.p. The present study demonstrates that opposite actions exist in the regulation of ethanol-induced ascorbic acid release in the striatum by dopamine D(1) and D(2) receptor blockade. It also suggests that the postsynaptic dopamine receptors are involved in mediation of ethanol-induced ascorbic acid release in rat striatum.

Animals↗

PubMed2000

Differential effects of acute administration of haloperidol and clozapine on ethanol-induced ascorbic acid release in rat striatum.

Antipsychotic drugs were initially considered to act predominantly through their antagonism at dopamine D(2)-like receptors. However, reports have demonstrated that the typical neuroleptic drug haloperidol and the atypical neuroleptic drug clozapine showed differential actions in clinical, behavioral and biochemical studies. Since ascorbic acid has a potential usefulness in psychological therapeutics, the present study investigates the actions of these two drugs on ethanol-induced ascorbic acid release in the striatum in order to help explain the different mechanisms of these drugs. The results showed that clozapine, at the doses of 15 and 30 mg/kg, i.p., had no effect on basal ascorbic acid release. However, a synergistic tendency at a dose of 15 mg/kg and a significant synergism at a dose of 30 mg/kg were observed on ascorbic acid release when clozapine was used with ethanol. In contrast, haloperidol, at the doses of 0.5, 1.0 and 2.0 mg/kg, i.p., administered alone did not affect the basal release of striatal ascorbic acid, and when used together with ethanol had neither a potentiating nor an antagonizing effect on ethanol-induced ascorbic acid release. Chlorpromazine, a nonselective dopamine receptor antagonist, at the dose of 5 mg/kg, i.p., affected neither the basal nor the ethanol-induced ascorbic acid release. Ritanserin, a 5-HT(2) receptor antagonist, at the dose of 1 mg/kg, s.c., significantly antagonized ethanol-induced ascorbic acid release. These results demonstrate that clozapine dose-dependently potentiates the stimulatory effect of ethanol on striatal ascorbic acid release and this effect of clozapine may not be related to its dopamine D(2) receptor antagonism.

Animals↗

PubMed2000

A multimicrospray nebulizer for microwave-induced plasma mass spectrometry

We have developed a nebulizer, called a multimicrospray nebulizer (MMSN), that efficiently introduces analytes for plasma mass spectrometry and plasma emission spectrometry. In this nebulizer, both the sample solution and the nebulizer gas are divided into several streams to produce a multispray. That is, the MMSN is a nebulizer that contains several micronebulization units, each unit including an orifice for passing the nebulizer gas and a capillary for introducing a sample solution. The microspray from each micronebulization unit can be operated at a microliter per minute sample uptake rate to achieve high nebulization efficiency. The multimicrospray nebulizer is capable of introducing more analyte to the plasma compared with a single-orifice micronebulizer, which has a very low sample uptake rate. In this work, an MMSN with three orifices was found to be suitable for microwave-induced plasma mass spectrometry (MIP-MS). The sample uptake rate can be varied within a range of 5-250 microL/min. Therefore, the nebulizer is unique in its ability to deal with various sample volumes and provide high nebulization efficiency. The sensitivity for all elements obtained with the MMSN was higher than that obtained with a conventional concentric nebulizer (CCN), which is difficult to achieve with other types of microintroduction nebulizers. For most elements, the MIP-MS sensitivity was improved about 2-fold at a sample uptake rate of 150 microL/min, a much lower rate than that for the CCN (usually 0.5-1.5 mL/min). The sensitivity for arsenic was improved by a factor of 5. The relative standard deviation was found to be less than 2.0%.

Journal Article↗

PubMed2000

Cholecystokinin-B receptor antagonists attenuate morphine dependence and withdrawal in rats.

The possible effect of a cholecystokinin-8 agonist (caerulein) and antagonists (MK-329 and L365,260) on the development of morphine dependence and withdrawal were investigated in rats. Caerulein treatment (0.01 and 0.1 mg/kg) increased the incidence of naloxone-induced withdrawal syndromes and delayed the extinction of morphine-conditioned place preference in morphine-dependent animals. The signs of the morphine withdrawal syndromes and the formation of morphine-conditioned place preference were suppressed by pretreatment with L365,260 (0.1 and 1 mg/kg) and not affected by pretreatment with MK-329 (0.1 and 1 mg/kg). The present study demonstrated CCK, acting on CCK-B receptors, participates in the development of the opiate dependence. These findings suggest that CCK-B receptor antagonists might be of some value in the treatment and prevention the relapse of opiate addicts.

Animals↗

PubMed2000

Induction of apoptotic cell death and in vivo growth inhibition of human cancer cells by a saturated branched-chain fatty acid, 13-methyltetradecanoic acid.

A saturated branched-chain fatty acid, 13-methyltetradecanoic acid (13-MTD), was purified from a soy fermentation product, which was used by many cancer patients as a treatment supplement. Our preliminary study indicated that 13-MTD could induce cell death in human cancer cell lines K-562, MCF7, DU 145, NCI-SNU-1, SNU-423, NCI-H1688, BxPC3, and HCT 116. The ID50 dosage of 13-MTD for these tumor cells ranged from 10 to 25 microg/ml. Further investigation revealed that 13-MTD caused tumor cell death through rapid induction of apoptosis, which could be detected 2 h after the treatment of tumor cells with 13-MTD. Xenograft tumors of prostate carcinoma cell line DU 145 and hepatocarcinoma LCI-D35 were orthotopically implanted into nude mouse prostate and liver, respectively. 13-MTD was administered p.o. once daily to the implanted mice for approximately 40 days. Our results showed that 13-MTD could effectively inhibit the growth of orthotopic tumor implants of both cell lines compared with control groups. The average inhibition rate was 84.6% for DU 145 and 65.2% for LCI-D35 (P < 0.01). LD50 test results showed that mice could well sustain the oral feeding of 5 g/kg/day without observable anomaly. Our preliminary data demonstrated that 13-MTD could effectively inhibit in vitro and in vivo growth of various cancer cell lines by inducing apoptosis without significant toxic side effects, suggesting 13-MTD as a potential candidate for chemotherapy of human cancers.

Animals↗

PubMed2000

Regulation of carbamoyl phosphate synthetase by MAP kinase.

The de novo synthesis of pyrimidine nucleotides is required for mammalian cells to proliferate. The rate-limiting step in this pathway is catalysed by carbamoyl phosphate synthetase (CPS II), part of the multifunctional enzyme CAD. Here we describe the regulation of CAD by the mitogen-activated protein (MAP) kinase cascade. When phosphorylated by MAP kinase in vitro or activated by epidermal growth factor in vivo, CAD lost its feedback inhibition (which is dependent on uridine triphosphate) and became more sensitive to activation (which depends upon phosphoribosyl pyrophosphate). Both these allosteric regulatory changes favour biosynthesis of pyrimidines for growth. They were accompanied by increased epidermal growth factor-dependent phosphorylation of CAD in vivo and were prevented by inhibition of MAP kinase. Mutation of a consensus MAP kinase phosphorylation site abolished the changes in CAD allosteric regulation that were stimulated by growth factors. Finally, consistent with an effect of MAP kinase signalling on CPS II activity, epidermal growth factor increased cellular uridine triphosphate and this increase was reversed by inhibition of MAP kinase. Hence these studies may indicate a direct link between activation of the MAP kinase cascade and de novo biosynthesis of pyrimidine nucleotides.

Allosteric Regulation↗

PubMed2000

Liquid chromatography/electrospray tandem mass spectrometry method for the quantitation of fosinoprilat in human serum using automated 96-well solid-phase extraction for sample preparation.

A sensitive, specific, accurate and reproducible liquid chromatography/electrospray tandem mass spectrometry method was developed and validated for the quantitation of fosinoprilat in 0.2 mL of human serum. The method employed acidification (with pH 4.0 sodium acetate buffer) of the serum samples to minimize the hydrolysis of the prodrug fosinopril to fosinoprilat prior to purification by automated 96-well solid-phase extraction. The required chromatographic separation of fosinoprilat and fosinopril was achieved isocratically on a Luna C8 analytical column (2 x 50 mm, 3 microm). The total run time was 2 min. The mobile phase contained methanol and water with 10 mM ammonium acetate. Detection was by positive ion electrospray tandem mass spectrometry. The standard curve, which ranged from 2.00 to 500 ng/mL, was fitted to a 1/x(2) weighted linear regression model. Fosinoprilat quality control (QC) samples used to determine the accuracy and precision of the method were prepared in human serum at concentrations of 5.00, 200, 400 and 1000 ng/mL. The assay accuracy was within 8% (dev). The intra- and inter-assay precisions were within 6 and 3% (RSD), respectively. Fosinopril QC samples used to gauge the rate of hydrolysis of fosinopril to fosinoprilat during the assay procedure were prepared in human serum at 500 ng/mL. The hydrolysis of fosinopril to fosinoprilat was </=1%. This degree of conversion would cause little error in the analysis of post-dose serum samples since such samples are known to contain low levels of the prodrug compared with the drug.

Analysis of Variance↗

PubMed2000

Constitutive activation of stat 3 oncogene product in human ovarian carcinoma cells.

OBJECTIVE: Stat 3 functions in transducing signals from the cell's surface to its nucleus and activation of gene transcription. Aberrations of Stat 3 in breast cancer have raised the possibility of its contribution to oncogenesis. Our goal was to examine ovarian cancer cell lines to determine whether Stat 3 plays a relevant role in ovarian carcinogenesis. METHODS: Protein lysates were extracted from normal ovarian surface epithelial cells and malignant cells. Western blotting techniques were performed with phosphorylation-independent or phosphorylation-specific Stat 3 (tyrosine 705) antibody. Confirmation of Stat 3 activation was determined by a luciferase reporter driven by a promoter containing Stat 3-specific binding sites. Bcl-x(L) and cyclin D(1) were also analyzed by Western blotting. RESULTS: MDAH 2774, OV-1063, Caov-3, and O.C. 22819 expressed high levels of phosphorylated Stat 3. In contrast, A2780 and normal ovarian surface epithelial cells had little Stat 3 phosphorylation recognized. Confirmation of persistent activation of Stat 3 activity was shown by transfection of cells with a Stat 3 luciferase reporter. Potential downstream mediators of Stat 3 including Bcl-x(L) and cyclin D(1) were also evaluated. In cells expressing activated Stat 3, high levels of both Bcl-x(L) and cyclin D(1) were detected, whereas in A2780 cells, which did not express activated Stat 3, only low levels of Bcl-x(L) and cyclin D(1) were expressed. CONCLUSIONS: Constitutive activation of Stat 3 is present in ovarian cancer lines but not in normal ovarian surface epithelial cells. Activation of Stat 3 is a common event during oncogenic transformation upstream to both Bcl-x(L) and cyclin D(1). The relationship of this aberrancy of ovarian carcinoma harboring activated Stat 3 deserves further investigation.

Cell Transformation, Neoplastic↗

PubMed2000

Multistart algorithms for MEG empirical data analysis reliably characterize locations and time courses of multiple sources.

We applied our newly developed Multistart algorithm (M. Huang et al., 1998, Electroencephalogr. Clin. Neurophysiol. 108, 32-44) to high signal-to-noise ratio (SNR) somatosensory responses and low SNR visual data to demonstrate the reliability of this analysis tool for determining source locations and time courses of empirical multisource neuromagnetic data. This algorithm performs a downhill simplex search hundreds to thousands of times with multiple, randomly selected initial starting parameters from within the head volume, in order to avoid problems of local minima. Two subjects participated in two studies: (1) somatosensory (left and right median nerves were stimulated using a square wave pulse of 0.2 ms duration) and (2) visual (small black and white bull's-eye patterns were presented to central and peripheral locations in four quadrants of the visual field). One subject participated in both of the studies mentioned above and in a third study (i.e., simultaneous somatosensory/visual stimulation). The best-fitting solutions were tightly clustered in high SNR somatosensory data and all dominant regions of activity could be identified in some instances by using a single model order (e.g., six dipoles) applied to a single interval of time (e.g., 15-250 ms) that captured the entire somatosensory response. In low SNR visual data, solutions were obtained from several different model orders and time intervals in order to capture the dominant activity across the entire visual response (e.g. , 60-300 ms). Our results demonstrate that Multistart MEG analysis procedures can localize multiple regions of activity and characterize their time courses in a reliable fashion. Sources for visual data were determined by comparing results across several different models, each of which was based on hundreds to thousands of different fits to the data.

Algorithms↗

PubMed2000

Alterations of basement membrane in di-isopropanolnitrosamine-induced carcinogenesis of the rat thyroid gland: an immunohistochemical study.

Alterations of basement membrane (BM) in di-isopropanolnitrosamine (DIPN)-induced carcinogenesis of the rat thyroid gland were examined by means of immunohistochemical localization of collagen type IV (CN-IV), laminin (LN), and fibronectin (FN) in prenodular and nodular thyroid lesions, correlating with the morphogenesis and proliferative activity of these lesions. Adult male rats of the Wistar strain were injected s.c. in the back with DIPN, and the thyroid glands were removed at the 15th and 30th week of treatment. Each of 133 thyroid lesions was histochemically analyzed. The follicular epithelial BM as revealed by CN-IV and LN was discontinued or completely lost during the progression of thyroid lesions from pre-nodular to nodular lesions and finally overt carcinomas. At the same time, the BM of vascular endothelial cells demonstrated a loss of dense capillary networks of follicles, a sinusoidal dilatation and, predominantly in carcinomas, development of interstitial-type blood vessels. However, FN, which was hardly stained in the normal thyroid tissue, was remarkably deposited in the interstitium of invasive carcinomas. These observations strongly suggested that alterations of BM structure play a key role in the morphogenesis of rat thyroid tumors, and that the expression of FN is an important step in the invasive growth of thyroid tumors.

Animals↗