Biomedical subjects

Z Tang

Publications and source records attributed to Z Tang.

At least 73 records · Page 4Linked to original sources

PubMed2000

An Unprecedented (1infinity)

A chain of vertex-linked "bare" nido-Ge(9)(2-) clusters (shown in the picture) is featured by the novel polymeric Zintl anion formed from the binary alloy "KGe(4)", ethylenediamine, and [18]crown-6. The polymerization of nido-Ge(9)(4-) clusters is counterintuitive to known two-electron oxidation behavior of nido clusters and the existence of the isolated closo-Ge(9)(2-) ion. The novel semiconducting cluster "wire" establishes direct structural and mechanistic links between molecular Zintl cluster ions with the extended structures of Zintl phases and elemental nanophase materials.

Journal Article↗

PubMed2000

Coupling immunoassays with chromatographic separation techniques.

Coupling immunoassays with HPLC separation techniques is becoming increasingly useful in the analysis of biological and nonbiological samples of both large and small molecules. This is because it provides both sensitivity and selectivity for molecular analysis at relatively low cost, low maintenance and with excellent potential for automation. This paper reviews application of this hyphenated approach both in the pre-column immunoextraction and post-column immunodetection modes. Systems in which immunoassays are interfaced to chromatographic separations in order to separate bound and free fractions of the immunoassay will not be included since these systems do not provide the enhanced selectivity common to hyphenated systems. Post-column immunodetection is based on various immunoassay formats such as direct detection, one-site, competitive and sandwich immunoassays. Homogeneous immunodetectors are more convenient than heterogeneous immunodectors since there are no separation and column regeneration steps involved in homogeneous immunoassays. On the other hand, heterogeneous immunoassays are generally more sensitive than homogeneous immunoassays since interfering substances are removed prior to immunodetection. Advantages and limitations for the various approaches will be discussed.

Antibodies↗

PubMed2000

Bcl-1 rearrangement and cyclin D1 protein expression in multiple myeloma precursor cells.

The rearrangement of Bcl-1 gene (Bcl-1/IgH rearrangement) and expression of cyclin D1 in multiple myeloma (MM) precursor cells were studied and the role of cyclin D1 in the pathogenesis of MM was investigated. The BCL-1 rearrangement and cyclin D1 protein expression in 15 cases of MM were detected. By using hemi-nested polymerase chain reaction (PCR) the genomic DNA from fresh peripheral blood and bone marrow was amplified and the expression of cyclin D1 in the smears was detected by using immunohistochemical method. Ten volunteer with normal bone marrow served as control group. The results showed Bcl-1 rearrangement was detectable in 3/15 (20%) MM patients and cyclin D, expression in 4/15 (27%) MM patients. Bcl-1 rearrangement and cyclin D1 protein expression were also detected in MM precursor cells. No overexpression of cyclin D1 or the rearrangement of the Bcl-1 gene was found in the 10 volunteers. It was concluded that Bcl-1 rearrangement and cyclin D1 protein overexpression were detected in MM precursor cells, speculating that overexpression of cyclin D1 protein may play an initial (critical) role in the pathogenesis of MM.

Adult↗

PubMed2000

Leukocyte functions in 2 cases of Papillon-Lefèvre syndrome.

AIM: To investigate the rôle of leukocytes in the pathogenesis of Papillon-Lefevre syndrome (PLS). METHODS: Peripheral blood polymorphonuclear neutrophils (PMNs), monocytes (MNs) and gingival crevicular fluid (GCF) were obtained from 2 cases of PLS with typical features. The chemotaxis of PMNs and MNs were evaluated using a modified Boyden chamber. The adherence of PMNs was determined by adherence of PMNs to petri dishes. Interleukin-8 (IL-8) in GCF was detected by sandwich ELISA. Elastase activity in GCF was measured with a low molecular weight substrate (S-2484) specific for granulocyte elastase. RESULTS: PMNs from both patients showed depressed chemotactic response to FMLP and IL-8. Total amounts of IL-8 in GCF from the 2 patients were much higher than those of the normal controls. Elastase activity was not significantly different from that of the controls. The adherence of PMN and the chemotaxis of MN in the 2 patients were normal. CONCLUSION: The depressed chemotactic response of PMN leads to decreased recruitment of PMN and/or release of lysozyme from PMN in the diseased gingival tissue, increasing the susceptibility of PLS patients to periodontal infection.

Adult↗

PubMed2000

Functional haploinsufficiency of the human homeobox gene MSX2 causes defects in skull ossification.

The genetic analysis of congenital skull malformations provides insight into normal mechanisms of calvarial osteogenesis. Enlarged parietal foramina (PFM) are oval defects of the parietal bones caused by deficient ossification around the parietal notch, which is normally obliterated during the fifth fetal month. PFM are usually asymptomatic, but may be associated with headache, scalp defects and structural or vascular malformations of the brain. Inheritance is frequently autosomal dominant, but no causative mutations have been identified in non-syndromic cases. We describe here heterozygous mutations of the homeobox gene MSX2 (located on 5q34-q35) in three unrelated families with PFM. One is a deletion of approximately 206 kb including the entire gene and the others are intragenic mutations of the DNA-binding homeodomain (RK159-160del and R172H) that predict disruption of critical intramolecular and DNA contacts. Mouse Msx2 protein with either of the homeodomain mutations exhibited more than 85% reduction in binding to an optimal Msx2 DNA-binding site. Our findings contrast with the only described MSX2 homeodomain mutation (P148H), associated with craniosynostosis, that binds with enhanced affinity to the same target. This demonstrates that MSX2 dosage is critical for human skull development and suggests that PFM and craniosynostosis result, respectively, from loss and gain of activity in an MSX2-mediated pathway of calvarial osteogenic differentiation.

Adult↗

PubMed2000

Msx2 deficiency in mice causes pleiotropic defects in bone growth and ectodermal organ formation.

The composite structure of the mammalian skull, which forms predominantly via intramembranous ossification, requires precise pre- and post-natal growth regulation of individual calvarial elements. Disturbances of this process frequently cause severe clinical manifestations in humans. Enhanced DNA binding by a mutant MSX2 homeodomain results in a gain of function and produces craniosynostosis in humans. Here we show that Msx2-deficient mice have defects of skull ossification and persistent calvarial foramen. This phenotype results from defective proliferation of osteoprogenitors at the osteogenic front during calvarial morphogenesis, and closely resembles that associated with human MSX2 haploinsufficiency in parietal foramina (PFM). Msx2-/- mice also have defects in endochondral bone formation. In the axial and appendicular skeleton, post-natal deficits in Pth/Pthrp receptor (Pthr) signalling and in expression of marker genes for bone differentiation indicate that Msx2 is required for both chondrogenesis and osteogenesis. Consistent with phenotypes associated with PFM, Msx2-mutant mice also display defective tooth, hair follicle and mammary gland development, and seizures, the latter accompanied by abnormal development of the cerebellum. Most Msx2-mutant phenotypes, including calvarial defects, are enhanced by genetic combination with Msx1 loss of function, indicating that Msx gene dosage can modify expression of the PFM phenotype. Our results provide a developmental basis for PFM and demonstrate that Msx2 is essential at multiple sites during organogenesis.

Abnormalities, Multiple↗

PubMed2000

Oxygen effects on glucose measurements with a reference analyzer and three handheld meters.

Oxygen may affect glucose meter and reference analyzer measurements. We evaluated the effects of changes in blood oxygen tension (Po2) on Accu-Chek Comfort Curve (Roche Diagnostics, Indianapolis, IN), Precision G, (Abbott Laboratories, Bedford, MA) and One Touch II (Lifescan, Milpitas, CA) glucose meter measurements, and on Yellow Springs Instruments (YSI) (Yellow Springs, OH) reference analyzer measurements. Venous blood drawn from healthy volunteers was adjusted to three glucose levels of 80, 200, and 400 mg/dL, each tonometered with six different Po2 levels (40, 80, 160, 240, 320, and 400 torr). To quantitate oxygen effects on reference analyzer measurements, glucose differences between test sample (Po2 changed) and control (Po2 80 torr) were calculated (YSItest-YSIcontrol). The threshold for determination of oxygen effects was +/-2 SD, where 2 SD was fro

Blood Chemical Analysis↗

PubMed2000

Copper deficiency induces hepatic fatty acid synthase gene transcription in rats by increasing the nuclear content of mature sterol regulatory element binding protein 1.

Dietary copper (Cu) deficiency results in an accelerated rate of hepatic fatty acid synthase gene transcription and an enhanced rate of hepatic lipid synthesis. Because the nuclear transcription factor sterol regulatory element binding protein-1 (SREBP-1) is a strong enhancer of fatty acid synthase promoter activity, it was hypothesized that Cu deficiency induces fatty acid synthase gene transcription by increasing the nuclear localization of mature SREBP-1. Male weanling rats were pair-fed a Cu-adequate (6.0 mg/kg) or Cu-deficient (0.6 mg/kg) diet (AIN-93) for 28 d. DNase I hypersensitivity site mapping of the hepatic fatty acid synthase gene revealed the presence of four major hypersensitivity sites located at -8700 to -8600, -7300 to -6900, -600 to -400 and -100 to +50. Although Cu deficiency did not change the hypersensitivity site pattern or intensity, in vitro footprinting of the region between -100 and +50 indicated that Cu deficiency enhanced DNA protein interactions within this region. The sequence between -68 and -58 contains the DNA recognition sequence for SREBP-1 and upstream stimulatory element-1 (USF-1). Western blot analysis revealed that the dietary Cu deficiency increased the hepatic nuclear content of mature SREBP-1 by 150% (P: < 0.05), and it concomitantly decreased the membrane content of precursor SREBP-1 by 45% (P: < 0.05). Changes in the hepatic distribution of SREBP-1 associated with Cu deficiency were not accompanied by changes in SREBP-1 mRNA. The nuclear content of USF-1 was unaffected by dietary Cu status. The hepatic increase in mature SREBP-1 of Cu-deficient rats was accompanied by a 400% increase and an 80% decrease in the abundance of fatty acid synthase and cholesterol 7-alpha hydroxylase mRNA, respectively. hepatic These data indicate that a Cu deficiency stimulates hepatic lipogenic gene expression by increasing the hepatic translocation of mature SREBP-1.

Animals↗

PubMed2000

Biochemical and genetic conservation of fission yeast Dsk1 and human SR protein-specific kinase 1.

Arginine/serine-rich (RS) domain-containing proteins and their phosphorylation by specific protein kinases constitute control circuits to regulate pre-mRNA splicing and coordinate splicing with transcription in mammalian cells. We present here the finding that similar SR networks exist in Schizosaccharomyces pombe. We previously showed that Dsk1 protein, originally described as a mitotic regulator, displays high activity in phosphorylating S. pombe Prp2 protein (spU2AF59), a homologue of human U2AF65. We now demonstrate that Dsk1 also phosphorylates two recently identified fission yeast proteins with RS repeats, Srp1 and Srp2, in vitro. The phosphorylated proteins bear the same phosphoepitope found in mammalian SR proteins. Consistent with its substrate specificity, Dsk1 forms kinase-competent complexes with those proteins. Furthermore, dsk1(+) gene determines the phenotype of prp2(+) overexpression, providing in vivo evidence that Prp2 is a target for Dsk1. The dsk1-null mutant strain became severely sick with the additional deletion of a related kinase gene. Significantly, human SR protein-specific kinase 1 (SRPK1) complements the growth defect of the double-deletion mutant. In conjunction with the resemblance of dsk1(+) and SRPK1 in sequence homology, biochemical properties, and overexpression phenotypes, the complementation result indicates that SRPK1 is a functional homologue of Dsk1. Collectively, our studies illustrate the conserved SR networks in S. pombe consisting of RS domain-containing proteins and SR protein-specific kinases and thus establish the importance of the networks in eucaryotic organisms.

Amino Acid Sequence↗

PubMed2000

Integration of FGF and TWIST in calvarial bone and suture development.

Mutations in the FGFR1-FGFR3 and TWIST genes are known to cause craniosynostosis, the former by constitutive activation and the latter by haploinsufficiency. Although clinically achieving the same end result, the premature fusion of the calvarial bones, it is not known whether these genes lie in the same or independent pathways during calvarial bone development and later in suture closure. We have previously shown that Fgfr2c is expressed at the osteogenic fronts of the developing calvarial bones and that, when FGF is applied via beads to the osteogenic fronts, suture closure is accelerated (Kim, H.-J., Rice, D. P. C., Kettunen, P. J. and Thesleff, I. (1998) Development 125, 1241-1251). In order to investigate further the role of FGF signalling during mouse calvarial bone and suture development, we have performed detailed expression analysis of the splicing variants of Fgfr1-Fgfr3 and Fgfr4, as well as their potential ligand Fgf2. The IIIc splice variants of Fgfr1-Fgfr3 as well as the IIIb variant of Fgfr2 being expressed by differentiating osteoblasts at the osteogenic fronts (E15). In comparison to Fgf9, Fgf2 showed a more restricted expression pattern being primarily expressed in the sutural mesenchyme between the osteogenic fronts. We also carried out a detailed expression analysis of the helix-loop-helix factors (HLH) Twist and Id1 during calvaria and suture development (E10-P6). Twist and Id1 were expressed by early preosteoblasts, in patterns that overlapped those of the FGF ligands, but as these cells differentiated their expression dramatically decreased. Signalling pathways were further studied in vitro, in E15 mouse calvarial explants. Beads soaked in FGF2 induced Twist and inhibited Bsp, a marker of functioning osteoblasts. Meanwhile, BMP2 upregulated Id1. Id1 is a dominant negative HLH thought to inhibit basic HLH such as Twist. In Drosophila, the FGF receptor FR1 is known to be downstream of Twist. We demonstrated that in Twist(+/)(-) mice, FGFR2 protein expression was altered. We propose a model of osteoblast differentiation integrating Twist and FGF in the same pathway, in which FGF acts both at early and late stages. Disruption of this pathway may lead to craniosynostosis.

Acrocephalosyndactylia↗

PubMed2000

Effects of drugs on glucose measurements with handheld glucose meters and a portable glucose analyzer.

Thirty drugs used primarily in critical care and hospital settings were tested in vitro to observe interference on glucose measurements with 6 hand-held glucose meters and a portable glucose analyzer. Paired differences of glucose measurements between drug-spiked samples and unspiked control samples were calculated to determine bias. A criterion of +/- 6 mg/dL was used as the cutoff for interference. Ascorbic acid interfered with the measurements on all glucose devices evaluated. Acetaminophen, dopamine, and mannitol interfered with glucose measurements on some devices. Dose-response relationships help assessment of drug interference in clinical use. High dosages of these drugs may be given to critically ill patients or self-administered by patients without medical supervision. Package inserts for the glucose devices may not provide adequate warning information. Hence, we recommend that clinicians choose glucose devices carefully and interpret results cautiously when glucose measurements are performed during or after drug interventions.

Blood Glucose↗

PubMed2000

Functional influences on orienting a reference frame.

Spatial relational terms like above are defined with respect to a reference frame. Reference frames are imposed on reference objects and define the space in which to search for a located object. Reference frames have a number of parameters that must be set during spatial term assignment, including origin, scale, and orientation. Previous research has shown that a functional relationship between objects in the scene influences the selection of a reference frame (Carlson-Radvansky & Radvansky, 1996). However, because this work operated at the level of the reference frame, generalizing across various spatial terms, it is unclear how function had its influence. One possibility is that function influences how the parameters of a reference frame are set. Consistent with this idea, Carlson-Radvansky, Covey, and Lattanzi (1999) showed an influence of function on where the origin of a reference frame was imposed. The present paper demonstrates that function also influences how the orientation of the axes of a reference frame is set. The implications for setting multiple parameters of a reference frame are discussed.

Humans↗

PubMed2000

Point-of-care glucose testing: effects of critical care variables, influence of reference instruments, and a modular glucose meter design.

OBJECTIVE: To assess the clinical performance of glucose meter systems when used with critically ill patients. DESIGN: Two glucose meter systems (SureStepPro and Precision G) and a modular adaptation (Immediate Response Mobile Analysis-SureStepPro) were assessed clinically using arterial samples from critically ill patients. A biosensor-based analyzer (YSI 2700) and a hospital chemistry analyzer (Synchron CX-7) were the primary and secondary reference instruments, respectively. PATIENTS AND SETTING: Two hundred forty-seven critical care patients at the University of California, Davis, Medical Center participated in this study. OUTCOME MEASURES: Error tolerances of +/-15 mg/dL for glucose levels </=100 mg/dL and +/-15% for glucose levels >100 mg/dL were used to evaluate glucose meter performance; 95% of glucose meter measurements should fall within these tolerances. RESULTS: Compared to the primary reference method, 98% to 100% of SureStepPro and 91% to 95% of Precision G measurements fell within the error tolerances. Paired differences of glucose measurements versus critical care variables (Po(2), pH, Pco(2), and hematocrit) were analyzed to determine the effects of these variables on meter measurements. Po(2) and Pco(2) decreased Precision G and SureStepPro measurements, respectively, but not enough to be clinically significant based on the error tolerance criteria. Hematocrit levels affected glucose measurements on both meter systems. Modular adaptation did not affect test strip performance. CONCLUSIONS: Glucose meter measurements correlated best with primary reference instrument measurements. Overall, both glucose meter systems showed acceptable performance for point-of-care testing. However, the effects of some critical care variables, especially low and high hematocrit values, could cause overestimated or underestimated glucose measurements.

Blood Glucose↗

PubMed2000

Effects of pH on glucose measurements with handheld glucose meters and a portable glucose analyzer for point-of-care testing.

OBJECTIVES: To determine pH effects on glucose measurements obtained with the latest generation of glucose devices, to quantitate changes in glucose measurements obtained over a wide pH range, and to assess the potential clinical risks of pH effects with use of point-of-care glucose testing. DESIGN: Paired differences of glucose measurements between pH-altered and parallel control samples with target pH 7.40 were calculated. SETTING: A pH range of 6.94 to 7.84 was used to evaluate pH effects on glucose measurements in vitro with 6 handheld glucose meters and a portable glucose analyzer at both normal, 4.81 mmol/L (86.6 mg/dL), and high, 11.16 mmol/L (201 mg/dL), glucose levels. MAIN OUTCOME MEASURES: Glucose measurements obtained from test samples and control samples were compared by calculating paired differences, which were plotted against pH to show pH effects on glucose meter measurements. RESULTS: At the normal glucose level, different pH levels did not interfere significantly with glucose measurements. At the high glucose level, a trend whereby low pH decreased and high pH increased glucose measurements was observed on the Precision G and the Precision QID glucose meters. CONCLUSION: Because of potential risk in diabetic patients with ketoacidosis and in other patients with acid-base disorders, we recommend that clinicians choose glucose devices carefully and interpret the measurements cautiously when point-of-care glucose testing is performed in critically ill patients with acidemia, alkalemia, or changing acid-base status.

Blood Chemical Analysis↗

PubMed2000

Whole-blood glucose and lactate. Trilayer biosensors, drug interference, metabolism, and practice guidelines.

OBJECTIVE: To assess the effects of 30 of the most commonly used critical care drugs on measurements obtained with trilayer electrochemical biosensors on a reference analyzer (ABL625-GL), to determine metabolic changes in glucose and lactate in vitro, and to formulate guidelines for whole-blood analysis of these 2 analytes. DESIGN: Serial measurements were taken of changes in glucose and lactate levels caused by metabolism in whole blood in vitro over time. A parallel control study of drug interference with measurements of glucose and lactate in whole blood and of dose-response relationships in whole-blood samples and in plasma samples also was conducted. RESULTS: At room temperature, whole-blood metabolism decreased glucose levels -2.3% at 15 minutes, -4.6% at 30 minutes, and -6.4% at 45 minutes. Metabolism increased lactate levels 11.4% at 15 minutes, 20.6% at 30 minutes, and 26.7% at 45 minutes in vitro. Paired differences between drug-spiked and control samples were calculated to determine interference (corrected for metabolism). The threshold for determination of interference was +/-2 SD from within-day precision, equal to +/-0.18 and +/-0.10 mmol/L for glucose and lactate, respectively. Only mannitol (C(6)H(14)O(6)) interfered with glucose and lactate measurements. At a concentration of 24 mg/mL, mannitol decreased whole-blood glucose levels by an average of 0.711 mmol/L (12.8 mg/dL) and whole-blood lactate levels by 0.16 mmol/L (1.4 mg/dL). Mannitol interference with measurements may have resulted from suppression of hydrogen peroxide formation in the enzymatic reactions in the biosensors, repartitioning of water between erythrocytes and plasma, or from other mechanisms. CONCLUSIONS: Most critical care drugs had no significant effects on the trilayer electrochemical biosensors. Whole-blood analysis should be performed within 15 minutes for lactate and within 30 minutes for glucose because of metabolism in vitro. Mannitol effects on glucose measurements may be clinically significant in mannitol-induced acute renal failure and therefore should be considered for appropriate diagnosis and treatment of critically ill patients.

Biosensing Techniques↗

PubMed2000

Effects of different hematocrit levels on glucose measurements with handheld meters for point-of-care testing.

OBJECTIVES: To determine the effects of low, normal, and high hematocrit levels on glucose meter measurements and to assess the clinical risks of hematocrit errors. DESIGN: Changes in glucose measurements between low and high hematocrit levels were calculated to determine hematocrit effects. The differences between glucose measured with meters and with a plasma glucose method (YSI 2300) also were compared. SETTING: Six hand-held glucose meters were assessed in vitro at low (19.1%), normal (38.5%), and high (58.3%) hematocrit levels, and at 6 glucose concentrations ranging from 2.06 mmol/L (37.1 mg/dL) to 30.24 mmol/L (544.7 mg/dL). RESULTS: Most systems, regardless of the reference to which they were calibrated, demonstrated positive bias at lower hematocrit levels and negative bias at higher hematocrit levels. Low, normal, and high hematocrit levels progressively lowered Precision G and Precision QID glucose measurements. Hematocrit effects on the other systems were more dependent on the glucose concentration. Overall, Accu-Chek Comfort Curve showed the least sensitivity to hematocrit changes, except at the lowest glucose concentration. CONCLUSIONS: We strongly recommend that clinical professionals choose glucose systems carefully and interpret glucose measurements with extreme caution when the patient's hematocrit value changes, particularly if there is a simultaneous change in glucose level.

Biosensing Techniques↗

PubMed2000

[The expression and localization of wild-type p53-GFP fused gene on human high-metastasis hepatocellular carcinoma cell line].

OBJECTIVE: To study the normal expression and location of wt-p53 protein on human high-metastasis hepatocellular carcinoma (HCC) cell line. METHODS: According to the sequence of human wild-type p53, the mp53 cDNA in which stopped codon TGA was mutated to TGG, was amplified by PCR, ligated to EGFP gene, of pEGFP-N1. The recombinant plasmid was transfected into MHCC97, in which p53 gene was mutated. The expression of human p53 protein was observed by fluorescence microscopy. RESULTS: There was a p53 mutation on 249 codon in human high-metastasis hepatocellular carcinoma cell line MHCC97, but no mutation in low-metastasis HCC cells LD20. The two genes of wt-p53 and GFP were fused in codon frame by DNA sequencing. The fluorescence microscopy showed that fluorescence light was spread in all of MHCC97 cells transfected with pEGFP-N1, but fluorescence light was focused on the nucleus of MHCC97 cells transfected with pEGFP-53. CONCLUSION: The p53 mutation on 249 codon may be related to the character of metastasis of HCC cells. The human wild-type p53-GFP fusion protein is expressed in MHCC97 cell line and located in cell nucleus, which is similar to the expression of wt-p53 protein.

Artificial Gene Fusion↗

PubMed2000

Differential diagnosis between hepatic focal nodular hyperplasia and hepatocellular carcinoma with negative alhpa-fetoprotein.

OBJECTIVE: To study the differential diagnosis between hepatic focal nodular hyperplasia (FNH) and hepatocellular carcinoma (HCC) with negative alpha-feto protein. METHODS: To analyse retrospectively the clinical and imaging materials of 18 patients with FNH and 254 patients with AFP negative HCC proven by operation and pathology during March 1996 to March 1999 in our institute. RESULTS: Patients with FNH were largely younger (66.7% under 40 years), discovered accidentally (66.7%), and without hepatitis background (83.3%). Majority of them had a normal liver function (72.0%). A big central artery was found in the lesion with high velocity and low resistant index in 71.4% of patients by color Doppler ultrasound. CT scan showed transient immediate enhancement in 85.7% of patients after bolus injection, being homogeneous (53.3%) and isodensity (73.3%) in the portal vein phase. MR imaging demonstrated early vigorous enhancement (83.3%) and homogenous (66.7%) lesion. In contrast, patients with AFP negative HCC were generally older (85.8% over 40 years), with symptoms (74.0%). A color flow with high velocity and high resistant index was found by color Doppler ultrasound. CT scan showed early heterogenous enhancement (96.6%) after bolus injection and being hypodensity in portal vein phase. MR imaging indicated early heterogeneous enhancement (91.7%). CONCLUSION: FNH shows some typical clinical and imaging features. Therefore, it is feasible to be differentiated from HCC with negative AFP in some of the patients.

Adolescent↗