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Biomedical subjects

H Sun

Publications and source records attributed to H Sun.

At least 217 records · Page 12Linked to original sources
PubMed1999

Ethylenediamine-palladium(II) complexes with pyridine and its derivatives: synthesis, molecular structure and initial antitumor studies.

The synthesis of four mononuclear palladium complexes of general formula [Pd(en)Cl(L)]NO3 (en = ethylenediamine; L = pyridine (I), 4-methylpyridine (II), 4-hydroxypyridine (III) or 4-aminopyridine (IV) has been achieved. The structure of these compounds was studied by elemental analysis, IR, far-IR and 1H NMR; complex I was analyzed by X-ray diffraction. The crystal of [Pd(en)(pyridine)Cl]NO3 is monoclinic, space group P21/c (a = 7.990(2), b = 16.058(3), c = 9.846(2) A, beta = 103.81(3) degrees, Z = 4, R = 0.067, Rw = 0.066). The Pd(II) atom exhibits an approximately square planar coordination with bond lengths in the range 2.017-2.042 A for Pd-N and 2.320 A for Pd-Cl. In order to determine the donor strength of the aromatic pyridine ligands, the stability constants of binary complex ML2+ (M = [Pd(en) (H2O)2]2+; L = pyridine, 4-Me-pyridine, 4-OH-pyridine and 4-NH2-pyridine) were determined by potentiometric pH titration in aqueous solution (T = 25 degrees C, I = 0.1 mol l-1 NaNO3). The results show that the stability constants of the binary complexes systematically increase with increasing pKa of the pyridines. The above four palladium complexes, [Pt(en)(pyridine)Cl]NO3 and cis-diamminedichloroplatinum (II) (cis-DDP) were assayed for cytotoxicity in vitro against the human leukemia cell line HL-60, and compounds I, II, III and cis-DDP show significant cytotoxic activity against HL-60.

Antineoplastic Agents↗
PubMed1999

Electroactive hemoglobin-surfactant-polymer biomembrane-like films.

Polyions complex 2C12N+ PSS- was prepared by reacting poly(sodium styrenesulfonate) (Na+ PSS-) with didodecyldimethylammonium bromide (2Cl2N+ Br-). Stable thin films made from 2C12N+ PSS- with incorporated redox protein hemoglobin (Hb) on pyrolytic graphite (PG) electrodes were then characterized by electrochemistry and other techniques. Cyclic voltammetry (CV) of Hb-2C12N+ PSS- films showed a pair of well-defined and nearly reversible peaks for HbFe(III)/Fe(II) couple at about -0.17 V vs. saturated calomel electrode (SCE) in pH 5.5 buffers. The electron transfer rate between Hb and PG electrode was greatly facilitated in microenvironment of 2C12N+ PSS- films. Positions of Soret absorption band suggest that Hb keeps its secondary structure similar to its native state in 2C12N+ PSS- films at the medium pH. The results of X-ray diffraction and differential scanning calorimetry (DSC) suggest synthesized lipid 2C12N+ PSS- films have an ordered bilayer structure intercalated between PSS- polyion layers, and the incorporated Hb expands the layer spacing of the films. HbFe(I), a highly reduced form of Hb, might also be produced in these films at about -1.09 V, and could be used to catalytically reduce organohalide pollutants.

Calorimetry, Differential Scanning↗
PubMed1999

Evidence for nitric oxide and nitric oxide synthase activity in proximal stumps of transected peripheral nerves.

Nitric oxide may be liberated as an inflammatory mediator within injured peripheral nerve trunks. We evaluated the proximal stumps of injured peripheral nerve stumps that later form neuromas or regenerative nerve sprouts, for evidence of local nitric oxide elaboration and activity. Proximal stumps were created in male Sprague-Dawley rats by sectioning of the sciatic nerve and resection of its distal portions and branches. There was striking physiological evidence of nitric oxide activity at the tips of 48-h and 14-day-old proximal nerve stumps. We detected local nitric oxide-mediated hyperemia of both extrinsic plexus and endoneurial microvessels that was reversible, in a dose-dependent stereospecific fashion, by the broad-spectrum nitric oxide synthase inhibitors, Nomega-nitro-L-arginine-methyl ester or Nomega-nitro-L-arginine, but not by 7-nitroindazole, an inhibitor with relative selectivity for neuronal nitric oxide. Immunohistochemical studies provided evidence for the localization of nitric oxide generators at the same sites. In 48-h but not 14-day stumps increased expression of two isoforms of nitric oxide synthase was detected: endothelial nitric oxide and to a much lesser extent neuronal nitric oxide synthase. Both isoforms appeared in axonal endbulb-like profiles that co-localized with neurofilament immunostaining. Western immunoblots identified a band consistent with endothelial nitric oxide synthase expression. In 14-day stumps with early neuroma formation, but not 48-h stumps, there was staining for immunological nitric oxide synthase in some endoneurial and epineurial macrophages. Total nitric oxide synthase biochemical enzymatic activity, measured by labelled arginine to citrulline conversion, was increased in 14-day but not 48-h stumps. Injured peripheral nerves have evidence of early nitric oxide action, nitric oxide synthase expression and nitric oxide activity in proximal nerve stumps. Nitric oxide may have an important impact on the regenerative milieu.

Animals↗
PubMed1999

Uncertain destination dynamics.

Certain dynamical systems exhibit a sensitivity to initial conditions in which the asymptotic state is selected from an infinite number of possible states. The phase space of such systems is foliated with "attractors," each of which is associated with a particular set of initial conditions. The associated uncertain destination dynamics can be analyzed by an appropriate reduction of the full system to a subsystem that explicitly yields the dynamics.

Journal Article↗
PubMed1999

Molecular genetics of human retinal disease.

The past decade has witnessed extraordinary progress in retinal disease gene identification, the analysis of animal and tissue culture models of disease processes, and the integration of this information with clinical observations and with retinal biochemistry and physiology. During this period over twenty retinal disease genes were identified and for many of these genes there are now significant insights into their role in disease. This review presents an overview of the basic and clinical biology of the retina, summarizes recent progress in understanding the molecular mechanisms of inherited retinal diseases, and offers an assessment of the role that genetics will play in the next phase of research in this area.

Humans↗
PubMed1999

Ca(2+)-activated Cl(-) current can be triggered by Na(+) current-induced SR Ca(2+) release in rabbit ventricle.

The Ca(2+)-activated Cl(-) current [I(Cl(Ca))] contributes to the repolarization of the cardiac action potential under physiological conditions. I(Cl(Ca)) is known to be primarily activated by Ca(2+) release from the sarcoplasmic reticulum (SR). L-type Ca(2+) current [I(Ca(L))] represents the major trigger for Ca(2+) release in the heart. Recent evidence, however, suggests that Ca(2+) entry via reverse-mode Na(+)/Ca(2+) exchange promoted by voltage and/or Na(+) current (I(Na)) may also play a role. The purpose of this study was to test the hypothesis that I(Cl(Ca)) can be induced by I(Na) in the absence of I(Ca(L)). Macroscopic currents and Ca(2+) transients were measured using the whole cell patch-clamp technique in rabbit ventricular myocytes loaded with Indo-1. Nicardipine (10 microM) abolished I(Ca(L)) at a holding potential of -75 mV as tested in Na(+)-free external solution. In the presence of 131 mM external Na(+) and in the absence of I(Ca(L)), a 4-aminopyridine-resistant transient outward current was recorded in 64 of 81 cells accompanying a phasic Ca(2+) transient. The current reversed at -42. 0 +/- 1.3 mV (n = 6) and at +0.3 +/- 1.4 mV (n = 6) with 21 and 141 mM of internal Cl(-), respectively, similar to the predicted reversal potential with low intracellular Cl(-) concentration ([Cl(-)](i)) (-47.8 mV) and high [Cl(-)](i) (-1.2 mV). Niflumic acid (100 microM) inhibited the current without affecting the Ca(2+) signal (n = 8). Both the current and Ca(2+) transient were abolished by 10 mM caffeine (n = 6), 10 microM ryanodine (n = 3), 30 microM tetrodotoxin (n = 9), or removal of extracellular Ca(2+) (n = 6). These properties are consistent with those of I(Cl(Ca)) previously described in mammalian cardiac myocytes. We conclude that 1) I(Cl(Ca)) can be recorded in the absence of I(Ca(L)), and 2) I(Na)-induced SR Ca(2+) release mechanism is also present in the rabbit heart and may play a physiological role in activating the Ca(2+)-sensitive membrane Cl(-) conductance.

4-Aminopyridine↗
PubMed1999

Effects of tirilazad mesylate on vasospasm and phospholipid hydroperoxides in a primate model of subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Tirilazad mesylate has been used in the attempt to prevent cerebral vasospasm after subarachnoid hemorrhage (SAH), although the actual targets of this agent in vivo have thus far been controversial. Chemiluminescence/high-performance liquid chromatography provided a new method for direct measurements of phosphatidylcholine hydroperoxide (PCOOH) and phosphatidylethanolamine hydroperoxide (PEOOH) in vivo and showed that phosphatidylcholine is the lipid class most susceptible to lipid peroxidation. In the present study we measured those levels in a primate model of SAH for determination of the effects of tirilazad on vasospasm. METHODS: Fourteen Macaca monkeys of both sexes were randomly assigned into 2 groups: a tirilazad group receiving a dosage of 0.3 mg/kg and a placebo group receiving only the vehicle in which tirilazad was delivered. After the induction of experimental SAH around the right middle cerebral artery on day 0, tirilazad or vehicle was administered intravenously every 8 hours for 6 days. On day 7, the animals were killed after angiography and regional cerebral blood flow measurements were performed. The levels of PCOOH and PEOOH were measured in the clots, bilateral parietal cortices, right frontal cortex contact with clots, cerebellar hemispheres, bilateral middle cerebral arteries, and basilar arteries. RESULTS: In the placebo group, a significant vasospasm occurred in the cerebral arteries on both sides, but most prominently on the right side. The degree of vasospasm in the cerebral arteries was significantly attenuated in the tirilazad group (P<0.005). There were no significant differences in regional cerebral blood flow, PCOOH, and PEOOH levels in the clots, cerebral cortices, and cerebellar hemispheres between the 2 groups. In contrast, the levels of PCOOH in the cerebral arteries were significantly higher in the placebo group than in the tirilazad group (P<0.025). It was remarkable that the tirilazad treatments eliminated PCOOH in any vascular territory after SAH. CONCLUSIONS: PCOOH in the artery wall may be an important indicator for vasospasm, and the inhibition of PCOOH may explain the efficacy of tirilazad on vasospasm.

Animals↗
PubMed1999

Heme oxygenase-1 gene induction as an intrinsic regulation against delayed cerebral vasospasm in rats.

Delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) causes cerebral ischemia and infarction. To date, the pathogenesis and gene expression associated with vasospasm remain poorly understood. The present study used fluorescent differential display to identify differentially expressed genes in a rat model of SAH. By using quantitative RT-PCR, we found that heme oxygenase-1 (HO-1) mRNA was prominently induced in the basilar artery and modestly in brain tissue in a rat vasospasm model. A significant correlation was observed between the degree of vasospasm and HO-1 mRNA levels in the basilar arteries exhibiting vasospasm. Intracisternal injection of antisense HO-1 oligodeoxynucleotide (ODN) significantly delayed the clearance of oxyhemoglobin and deoxyhemoglobin from the subarachnoid space and aggravated angiographic vasospasm. Antisense HO-1 ODN inhibited HO-1 induction in the basilar arteries but not in the whole brain tissue. This phenomenon was not observed in the nontreated, sense HO-1 ODN-treated, or scrambled ODN-treated arteries. We report the protective effects of HO-1 gene induction in cerebral vasospasm after SAH, a finding that should provide a novel therapeutic approach for cerebral vasospasm.

Animals↗
PubMed1999

PTEN affects cell size, cell proliferation and apoptosis during Drosophila eye development.

Mutations in the tumor suppressor gene PTEN (MMAC1/TEP1) are associated with a large number of human cancers and several autosomal-dominant disorders. Mice mutant for PTEN die at early embryonic stages and the mutant embryonic fibroblasts display decreased sensitivity to cell death. Overexpression of PTEN in different mammalian tissue culture cells affects various processes including cell proliferation, cell death and cell migration. We have characterized the Drosophila PTEN gene and present evidence that both inactivation and overexpression of PTEN affect cell size, while overexpression of PTEN also inhibits cell cycle progression at early mitosis and promotes cell death during eye development in a context-dependent manner. Furthermore, we have shown that PTEN acts in the insulin signaling pathway and all signals from the insulin receptor can be antagonized by either Drosophila or human PTEN, suggesting a potential means for alleviating symptoms associated with altered insulin signaling.

Amino Acid Sequence↗
PubMed1999

Population pharmacokinetics. A regulatory perspective.

The application of population approaches to drug development is recommended in several US Food and Drug Administration (FDA) guidance documents. Population pharmacokinetic (and pharmacodynamic) techniques enable identification of the sources of inter- and intra-individual variability that impinge upon drug safety and efficacy. This article briefly discusses the 2-stage approach to the estimation of population pharmacokinetic parameters, which requires serial multiple measurements on each participant, and comprehensively reviews the nonlinear mixed-effects modelling approach, which can be applied in situations where extensive sampling is not done on all or any of the participants. Certain preliminary information, such as the compartment model used in describing the pharmacokinetics of the drug, is required for a population pharmacokinetic study. The practical design considerations of the location of sampling times, number of samples/participants and the need to sample an individual more than once should be borne in mind. Simulation may be useful for choosing the study design that will best meet study objectives. The objectives of the population pharmacokinetic study can be secondary to the objectives of the primary clinical study (in which case an add-on population pharmacokinetic protocol may be needed) or primary (when a stand-alone protocol is required). Having protocols for population pharmacokinetic studies is an integral part of 'good pharmacometric practice'. Real-time data assembly and analysis permit an ongoing evaluation of site compliance with the study protocol and provide the opportunity to correct violations of study procedures. Adequate policies and procedures should be in place for study blind maintenance. Real-time data assembly creates the opportunity for detecting and correcting errors in concentration-time data, drug administration history and covariate data. Population pharmacokinetic analyses may be undertaken in 3 interwoven steps: exploratory data analysis, model development and model validation (i.e. predictive performance). Documentation for regulatory purposes should include a complete inventory of key runs in the analyses undertaken (with flow diagrams if possible), accompanied by articulation of objectives, assumptions and hypotheses. Use of diagnostic analyses of goodness of fit as evidence of reliability of results is advised. Finally, the use of stability testing or model validation may be warranted to support label claims. The opinions expressed in this article were revised by incorporating comments from various sources and published by the FDA as 'Guidance for Industry: Population Pharmacokinetics' (see the FDA home page http:/(/)www.fda.gov for further information).

Data Interpretation, Statistical↗
PubMed1999

[The sequence analysis of the 3' end of intron 15 from human LDL receptor gene and its application in the study of gene diagnosis for familial hypercholesterolaemia].

To understand intron 15 of human LDL receptor gene, the DNA fragments from exon 15 to exon 16 and the 3' end of intron 15 were amplified with long chain PCR and anchored PCR. The 3' end of intron 15 was sequenced with Dynalbeads-Streptavidin Solid Phase technique. The sequence analysis showed that the 3' end of intron 15 contained the 3' splicing site and the branch site at 31 nucleotides upstream of the 3' end. Besides the authentic branch site, it is possible that the 3' end of intron 15 contains a cryptic site (GCCTCAC) at 20 nucleotides upstream of the 3' end. The sequences suggest that the PvuII polymorphism at Intron 15 is caused by the T-C substitution. According to the sequences of the 3' end, the new PCR-RFLP protocol for detection of PvuII polymorphism at intron 15 was developed. Using this protocol a representative familial hypercholesterolaemia family was identified with linkage analysis of PvuII polymorphism at intron 15.

Base Sequence↗
PubMed1999

Competitive antagonism of the mouse 5-hydroxytryptamine3 receptor by bisindolylmaleimide I, a "selective" protein kinase C inhibitor.

We examined the effects of several protein kinase C (PKC) inhibitors on the murine 5-hydroxytryptamine3 (5-HT3) receptor to determine whether they acted directly on the receptor. The 5-HT-evoked currents in Xenopus laevis oocytes expressing the recombinant 5-HT3 receptor were measured with the two-electrode voltage-clamp technique. The PKC inhibitors bisindolylmaleimide I (BIM, GF109203x) and staurosporine, but not calphostin C or chelerythrine, decreased the 5-HT3 receptor-mediated currents when coapplied with 5-HT. BIM blocked 0.5 microM 5-HT-elicited currents with an IC50 value of 7 nM, whereas in the presence of 5 microM staurosporine, 42% inhibition of 0.5 microM 5-HT-mediated currents was observed. Increasing concentrations of BIM resulted in a rightward shift of the 5-HT concentration-response curve, without altering efficacy. A Schild plot was generated, which had a slope of -1.01, suggesting competitive antagonism. The Ki value of BIM was determined to be 29 nM. To confirm competitive antagonism, a competitive binding assay was performed on Sf21 insect cells infected with the mouse 5-HT3 receptor cDNA in a baculovirus expression vector. BIM completely displaced binding of the selective 5-HT3 receptor antagonist [3H]GR65630. BIM bound to the 5-HT3 receptor with a Ki value of 61 nM, which was slightly less potent than that of the selective 5-HT3 receptor antagonist MDL72222 (27 nM). The PKC inhibitor BIM is a potent competitive antagonist at the 5-HT3 receptor.

Alkaloids↗
PubMed1999

Characterization of interaction of 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester with Torpedo californica nicotinic acetylcholine receptor and 5-hydroxytryptamine3 receptor.

The widely used calcium channel antagonist 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8) has been identified as a noncompetitive antagonist (NCA) and open-channel blocker of both muscle- and neuronal-type nicotinic acetylcholine receptors (AChRs). To further examine the interaction of TMB-8 with the AChR, the compound was tested as a competitor for the binding of two NCAs of the Torpedo californica AChR, phencyclidine and 3-trifluoromethyl-3-(m[125I]iodophenyl)diazirine, for which the binding to the AChR has been pharmacologically well characterized and a channel binding loci has been established. TMB-8 fully inhibited specific photoincorporation of 3-trifluoromethyl-3-(m[125I]iodophenyl)diazirine into the resting AChR channel (IC50 = 3.1 microM) and inhibited high-affinity [3H]phencyclidine binding to the desensitized AChR (IC50 = 2.4 microM). We conclude that TMB-8 is a potent NCA of the nicotinic AChR, interacting with the resting, open-channel, and desensitized channel conformations. TMB-8 was next tested as an inhibitor of the structurally homologous 5-hydroxytryptamine (5-HT)3 receptor (5-HT3R). Using 5-HT3R containing Sf21 cell membranes, TMB-8 completely inhibited specific binding of the radiolabeled 5-HT3R antagonist [3H]GR65630 (Ki = 2.5 microM). Furthermore, TMB-8 antagonized 5-HT-evoked currents of both mouse and human 5-HT3Rs expressed in Xenopus laevis oocytes, and additional analysis was consistent with a competitive antagonistic mechanism of action. These results, taken together, indicate that TMB-8 antagonizes the function of the AChR and 5-HT3R by different mechanisms. Given the sequence similarity and emerging evidence of structural homology in the channels of these two receptors, these results underscore the existence of subtle yet important structural differences in each channel.

Amino Acid Sequence↗
PubMed1999

[Preliminary studies on gene therapy for lysosomal alpha-mannosidosis].

OBJECTIVE: Exploration of the feasibility of treating human lysosomal alpha-mannosidosis by gene therapy. METHODS: Retroviral vector-mediated transfer of human lysosomal alpha-mannosidase cDNA into the diseased cat skin fibroblasts. Detection of the enzymatic activity in the cells and their culture media at different pH conditions. Localization of the recombinant enzyme in the cells by chemical staining. Cross-correction of untransduced cat cells by incubation in medium containing the secreted enzyme in the absence and presence of mannose-6-phosphate or fetal calf serum. In vivo expression of the recombinant enzyme in organoids containing the vector-transduced cells. RESULTS: Among the two human cDNAs tested, only one encoded high levels of alpha-mannosidase activity in the cat cells, which shared the same pH profile and lysosomal localization with the normal enzyme. The recombinant enzyme was proportionally secreted into the medium of the cell culture and taken up by untransduced cells via mannose-6-phosphate receptor-mediated endocytosis. The uptake was partially inhibited in the presence of fetal calf serum, which was dose-dependent. In vivo, organoids containing the vector-transduced cells expressed detectable alpha-mannosidase activity for up to 6 weeks. CONCLUSION: The human cDNA was functional in the cat cells and the expression system could be used for development of gene therapy for lysosomal alpha-mannosidosis.

Animals↗
PubMed1999

Interactive navigation and bronchial tube tracking in virtual bronchoscopy.

An interactive virtual environment for simulation of bronchoscopy is developed. Medical doctor can safely plan their surgical bronchoscopy using the virtual environment without any invasive diagnosis which may risk the patient's health. The 3D pen input device of the system allows the doctor to navigate and visualize the bronchial tree of the patient naturally and interactively. To navigate the patient's bronchial tree, a vessel tracking process is required. While manual tracking is tedious and labor-intensive, fully automatic tracking may not be reliable. We propose a semi-automatic tracking technique called Intelligent Path Tracker which provides automation and enough user control during the vessel tracking. To support an interactive frame rate, we also introduce a new volume rendering acceleration technique, named as IsoRegion Leaping. The volume rendering is further accelerated by distributed rendering on a TCP/IP-based network of low-cost PCs. With these approaches, a 256 x 256 x 256 volume data of human lung, can be navigated and visualized at a frame rate of over 10 Hz in our virtual bronchoscopy system.

Bronchoscopy↗
PubMed1999

[Study on the effect of ligustrazine on adherent molecule expression of bone marrow cells in immune-mediated aplastic anemia mice].

OBJECTIVE: To explore the effect of ligustrazine on the expression of adherent molecule of bone marrow cells in immune-mediated aplastic anemia(AA) mice. METHODS: Each immune-mediated AA mouse was intraperitoneally injected with 5 mg ligustrazine twice a day. On the 14th day, expressions of CD49d and CD49c in bone marrow mononuclear cells(MNC) were detected by flow cytometry, and VCAM-1 on stromal cells by immunohistochemistry SABC. RESULTS: Expressions of CD49d, CD49e and VCAM-1 were significantly lower in AA group than in normal group(t = 11.96, 17.18 and 7.09 respectively, P < 0.001), and were much higher in ligustrazine treated group than in non-treated group(t = 9.05, 14.61 and 6.91 respctively, P < 0.001). Expressions of CD49d and VCAM-1 were in the normal range in ligustrazine group. CONCLUSIONS: Ligustrazine can increase the expression of adherent molecule of bone marrow cells in immune-mediated AA mice, thus promote the growth of hematopoietic cells.

Anemia, Aplastic↗
PubMed1999

Surgical treatment of hepatocellular carcinoma and related basic research with special reference to recurrence and metastasis.

OBJECTIVE: To summarize the progress of surgical treatment of hepatocellular carcinoma (HCC) and related basic research at the Liver Cancer Institute of Shanghai Medical University in the recent years, with special reference to recurrence and metastasis. METHODS: Published and unpublished update clinical and experimental data in the above-mentioned areas are summarized. RESULTS: Surgical resection has played an important role in improving prognosis of HCC, the 5-year survival were 63.4% for small HCC resection (n = 806), 39.6% for large HCC resection (n = 1061), 64.7% for cytoreduction (using hepatic artery cannulation and ligation) and sequential resection of initially unresectable HCC (n = 93), 56.0% for cytoreduction using transcatheter arterial chemoembolization (TACE) and followed by resection (n = 65), and 22.4% for hepatic resection with removal of tumor thrombi in portal vein (n = 103). Unfortunately, the 5-year recurrent rate after curative resection of HCC was up to 61.5%, which was mainly a result of intrahepatic "metastasis" and multicentric origin of HCC. Clinically, re-resection of subclinical recurrence yielded 56% of 5-year survival (n = 202); prevention of recurrence by transcatheter arterial chemoembolization (TACE) + Interferon, or LAK/IL-2 therapy have decreased 3-year recurrent rate from 33% to 11%-18%. In experimental aspect, metastatic human HCC model in nude mice (LCI-D20) and HCC cell line with metastatic potential (MHCC97) have been established; studies on HCC invasiveness in the molecular level revealed similar results that reported in other solid cancers, and small HCC showed slightly better biological characteristics as compared with large HCC; microvessel density (MVD) that reflecting angiogenesis adversely correlated with 5-year survival of small HCC; experimental interventions using antisense H-ras, bispecific antibody, BB94, as well as anti-angiogenic agents (TNP470, suramin, CAI, heparin, antisense VEGF, etc.) have been demonstrated to inhibit tumor growth and lung metastasis in nude mice model. CONCLUSIONS: Recurrence and metastasis are the major obstacle to further improve prognosis of HCC, studies should be conducted both in clinical and experimental aspects, "HCC invasiveness" will be the major target to be studied, particularly in the molecular level, and anti-angiogenesis will be one of the important approach.

Angiogenesis Inhibitors↗