Biomedical subjects

J L Liu

Publications and source records attributed to J L Liu.

At least 91 records · Page 5Linked to original sources

PubMed1997

Lysophosphatidic acid stimulates proliferation of human retinal pigment epithelial cells.

PURPOSE: Proliferative vitreoretinopathy (PVR) can arise from an exaggerated wound-healing response by retinal pigment epithelial (RPE) cells. Lysophosphatidic acid (LPA) is a simple phospholipid, which is secreted by cells, activates G protein-coupled receptors, and appears to contribute to wound healing in other tissues. The present study examined the effects of LPA on three aspects of the behavior of cultured human RPE cells that are important in the pathogenesis of PVR: proliferation, chemotaxis, and contraction. METHODS: Human RPE cells were harvested from donor eyes and cultured using standard culture techniques. Proliferation was assessed by counting cells, cell migration with a modified Boyden chamber, and contraction by seeding RPE cells in a collagen cell. RESULTS: LPA (10 microM) induced RPE cell proliferation and weak chemotaxis, but no gel contraction. RPE cell proliferation increased in a dose-dependent manner from 0.1-100 microM LPA. Consistent with LPA actions at a receptor, an LPA analogue, lysophosphatidylcholine (LPC), was much less effective than LPA in stimulating proliferation and the proliferative response was blocked by pertussis or cholera toxin. Phosphatidic acid (PA) induced a similar proliferative response as LPA. CONCLUSION: These suggest that LPA can potently stimulate RPE cell proliferation via activation of a G-protein coupled receptor. LPA, which can be released by thrombin-activated platelets and growth factor-activated fibroblasts, might, therefore, play a role in the development of PVR.

Adult↗

PubMed1997

Nucleolar and nuclear localization properties of a herpesvirus bZIP oncoprotein, MEQ.

Marek's disease virus (MDV) is one of the most oncogenic herpesviruses and induces T lymphomas in chickens within weeks after infection. Only a limited number of viral transcripts are detected in MDV tumor samples and cell lines. One of the major transcripts encodes MEQ, a 339-amino-acid bZIP protein which is homologous to the Jun/Fos family of transcription factors. The C-terminal half of MEQ contains proline-rich repeats and, when fused to the DNA-binding domain of a yeast transcription factor, Gal4 (residues 1 to 147), exhibits transactivation function. MEQ can dimerize with itself and with c-Jun. The MEQ-c-Jun heterodimers bind to an AP-1-like enhancer within the MEQ promoter region with greater affinity than do homodimers of either protein, and they transactivate MEQ expression. Here we show that MEQ is expressed in the nucleus but, interestingly, with a predominant fraction in the nucleoli and coiled bodies. This makes MEQ the first bZIP protein to be identified in the nucleoli. MEQ contains two stretches of basic residues, designated basic region 1 (BR1) and basic region 2 (BR2). Using a series of deletion mutants, we have mapped the primary nuclear localization signal (NLS) and the sole nucleolar localization signal (NoLS) to the BR2 region. BR1 was shown to provide an auxiliary signal in nuclear translocation. To demonstrate that BR2 is an authentic NoLS, BR2 was fused to cytoplasmic v-Raf (delta gag) kinase. The BR2-Raf fusion protein was observed to migrate into the nucleoplasm and the nucleolus. The BR2 region can be further divided into two long arginine-lysine stretches, BR2N and BR2C, which are separated by the five amino acids Asn-Arg-Asp-Ala-Ala (NRDAA). We provide evidence that the requirement for nuclear translocation is less stringent than that for nucleolar translocation, as either BR2N or BR2C alone is sufficient to translocate the cytoplasmic v-Raf (delta gag) into the nucleus, but only in combination can they translocate v-Raf (delta gag) into the nucleolus. Our studies demonstrate that MEQ is both a nuclear and nucleolar protein, adding MEQ to the growing list of transactivators which localize to the nucleolus.

Amino Acid Sequence↗

PubMed1997

Factors associated with the utilization of traditional Chinese medicine in a small town in Hong Kong.

The practice of Traditional Chinese Medicine (TCM) is largely unregulated in Hong Kong. Yet, as previous studies have shown, a sizable segment of the population consults TCM practitioners for health problems. This paper uses health care utilization data from a telephone health survey of 847 adult subjects in Tai Po District who had suffered from acute illness in the past month, to examine the profile of TCM users in the District. Women, older residents, unemployed workers, low skill laborers, current smokers and subjects dissatisfied with the quality of private sector clinics were significantly more likely to consult TCM practitioners.

Adult↗

PubMed1997

Angiotensin II blockade [corrected] enhances baroreflex control of sympathetic outflow in heart failure.

Enhanced sympathetic outflow is seen in both patients with congestive heart failure and animals with experimental heart failure. In a previous study, we demonstrated that the baroreflex control of heart rate was impaired in conscious rabbits with pacing-induced heart failure and that this impairment was partially restored by blockade of angiotensin II type 1 (AT1) receptors. In the present study, we determined the interaction between the renin-angiotensin system and baroreflex control of renal sympathetic nerve activity in normal conscious rabbits and conscious rabbits with pacing-induced heart failure before and after AT1 receptor blockade. Heart failure was induced by rapid ventricular pacing at a rate of 360 to 380 beats per minute for an average of 16.7 +/- 0.6 days. To generate baroreflex curves, we altered arterial pressure by administering phenylephrine and sodium nitroprusside. A sigmoidal logistic function was fit to renal sympathetic nerve activity-mean arterial pressure relationships for analysis of several components of baroreflex function. AT1 receptors were blocked by intravenous administration of the specific antagonist L-158,809. In normal rabbits, there was no significant difference in any parameter of baroreflex function before and after blockade of AT1 receptors. In contrast, blockade of AT1 receptors enhanced baroreflex sensitivity in heart failure rabbits. The maximal gain increased to 5.0 +/- 0.7% renal sympathetic nerve activity/mm Hg from 2.6 +/- 0.3 (P < .05). Although L-158,809 had no effect on baseline renal sympathetic nerve activity in normal rabbits, analysis of the data in the heart failure rabbits indicated that baseline renal sympathetic nerve activity was reduced from 33 +/- 5% to 17 +/- 4% after L-158,809 administration after adjustment for changes in arterial pressure. These data suggest that angiotensin II plays a role in baroreflex impairment in this model of heart failure and may be in part responsible for the depressed baroreflex sensitivity observed in heart failure.

Angiotensin II↗

PubMed1997

Avian leukemias and lymphomas: interplay between retroviruses and herpesviruses.

Avian leukemias and lymphomas are caused primarily by retroviruses and herpesviruses. The protooncogenes activated by avian retroviral insertions in B & T-cell lymphomas will be summarized, with discussion on a new common insertion site, bravo, associated with RAV-O LTR insertion. Two novel interactions between avian retroviruses and Marek's disease herpesvirus (MDV) will be described: one involves direct interactions between putative viral oncoproteins and the other integrative recombination between these two viruses.

Alpharetrovirus↗

PubMed1996

Tissue localization and stage-specific expression of the phospholipid hydroperoxide glutathione peroxidase of Schistosoma mansoni.

The tissue localization and the stage-specific expression of the phospholipid hydroperoxide glutathione peroxidase of Schistosoma mansoni (SmPHGSHpx) have been determined. An antiserum raised against the C-terminal region of the predicted protein sequence was used for immunocytochemical investigations. The native protein is expressed only in female and egg vitelline cells and is practically absent from male worm tissue. Western blot data confirmed these results and showed the complete absence of SmPHGSHpx from cercariae. However, Northern blotting indicated the presence of the corresponding mRNA at all life-cycle stages investigated. The sequence determination of the 5' flanking region of the SmPHGSHpx gene revealed the presence of an extended TATA box (5'-TAAATA-3') at -32, a possible CAAT box at -75 and a putative monomeric estrogen response element 5'-GGTCAA-3' at position -486. In addition, direct and inverted repeat elements are present.

Amino Acid Sequence↗

PubMed1996

Ultrastructural localization of Sm28 GST protective antigen in Schistosoma mansoni adult worms.

The localization of the 28 kDa Schistosoma mansoni glutathione S-transferase (Sm28 GST) has been investigated using immunohistochemistry and electron microscopy and the results compared with previously published data. This study confirms the wide distribution of this antigen in the parasite. In male and female worms, Sm28 GST is localized in the tegument, the parenchyma, the oesophageal epithelium and in genital organs. Sm28 GST was clearly detected in germinal and sustentacular cells. The decrease of staining intensity during the differentiation of germinal cells suggests a down-regulated expression of the molecule. At the ultrastructural level, this antigen was abundant in nuclei and less present in the cytoplasm. The marked heterogeneity observed in the staining of individual worms indicates that Sm28 GST seems to be closely associated with the parasite's metabolism. The results are discussed in relation to the biological and protective functions of the protein.

Animals↗

PubMed1996

Schistosoma mansoni elastase: an immune target regulated during the parasite life-cycle.

Recombinant Schistosoma mansoni elastase was expressed in Escherichia coli and an antiserum raised against the recombinant protein was used to investigate stage-specific control of elastase in the parasite, and to determine whether the enzyme could form the basis of a strategy to prevent larval invasion of the host. Results showed that the expression of elastase is developmentally regulated, even if the basal promoter activity does not seem to be stage specific. The analysis of mRNA expression showed the presence of elastase transcript in adult worms although we could not detect the protein at this stage, suggesting that S. mansoni employs a form of translational control. The measurement of elastase levels in supernatants of culture schistosomula combined with the localization of elastase in cercarieae invading mouse skin showed that the enzyme is heavily released during penetration. Finally, we studied the cytotoxic activity of rat anti-elastase sera, and the analysis of the isotypic profile suggested that IgG2a anti-elastase may be responsible for the cytotoxic effect.

Animals↗

PubMed1996

Expression of NF-Y nuclear factor in Schistosoma mansoni.

The A subunit of NF-Y nuclear factor from Schistosoma mansoni was expressed in E. coli fused to a histidine tag and purified by affinity chromatography using a Ni(2+)-Agarose matrix. Antibodies against the recombinant protein were prepared and used for Western blot and immunolocalization. The presence of SMNF-YA in all stages of the parasite life-cycle was determined by RT-PCR and Western blot analysis. The immunolocalization of SMNF-YA showed the presence of this factor in a parenchymal cell population of cercariae and adult worms and in embryos within eggs. The expression of SMNF-YA was demonstrated to decrease in maturating spermatozoites whereas an accumulation of this factor was observed in the nucleus from oocytes during their maturation processes.

Animals↗

PubMed1996

Effects of NO on baroreflex control of heart rate and renal nerve activity in conscious rabbits.

Recent data suggest that nitric oxide (NO) plays a role in the modulation of sympathetic nerve activity and baroreflex sensitivity. Most of these studies have been carried out in anesthetized preparations, and little if any comparison has been made on the relative role of NO on the baroreflex control of heart rate and sympathetic nerve activity. In the present studies, the effect of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) on the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in conscious, instrumented rabbits. Intravenous bolus injections of 13 mg/kg of L-NNA decreased baseline HR (from 205.0 +/- 6.0 to 145.5 +/- 8.2 beats/min; P < 0.05) without significant changes in mean arterial pressure (MAP) and RSNA. L-NNA significantly reduced the lower plateau of the HR-MAP curves and increased the sensitivities of baroreflex control of HR and RSNA. L-Arginine (600 mg/kg i.v.) but not D-arginine reversed the above effects. The effects of L-NNA on baseline HR were not completely blocked by metoprolol (2 mg/kg) or by atropine (0.2 mg/kg). After pretreatment with metoprolol, baroreflex sensitivity was reduced and L-NNA increased baroreflex sensitivity back to the control level. After pretreatment with atropine, L-NNA still reduced the lower plateau but did not significantly affect baroreflex sensitivity. L-NNA increased the HR responses but not the RSNA response to electrical stimulation of the aortic nerve in chloralose-anesthetized, sinoaortic-denervated (SAD) rabbits. L-NNA had no effect on the HR response to right vagal stimulation. In both conscious intact and SAD rabbits, L-NNA did not increase baseline RSNA. These results suggest that endogenous NO decreases baroreflex control of HR and RSNA. Both sympathetic and parasympathetic components play a role in the effects of NO on the baroreflex control of HR. The effects of NO in the central nervous system play a more important role in the baroreflex control of HR than of RSNA.

Animals↗

PubMed1996

Blockade of AT1 receptors enhances baroreflex control of heart rate in conscious rabbits with heart failure.

Because the renin-angiotensin system is activated in heart failure, we hypothesized that angiotensin II (ANG II) plays a role in altering baroreflex sensitivity in the setting of heart failure. Accordingly, we evaluated the baroreflex control of heart rate (HR) in conscious, chronically instrumented rabbits in the normal state and after the establishment of heart failure. Heart failure was induced by rapid ventricular pacing at a rate of 360-380 beats/min for an average of 14.5 +/- 1.4 days. The data were compared with normal rabbits instrumented in a similar fashion. Baroreflex curves were generated by inflation of implanted hydraulic occluders on the vena cava and aortic arch or by administration of phenylephrine and sodium nitroprusside. Experiments were carried out before and after intravenous administration of the AT1 antagonist L-158,809. Rabbits with heart failure exhibited significantly lower arterial pressure (81 +/- 3 vs. 69 +/- 4 mmHg, P < 0.05), elevated resting HR (230 +/- 5 vs. 260 +/- 10 beats/min, P < 0.05), and elevated left atrial pressure (3.6 +/- 0.7 vs. 13.1 +/- 0.7 mmHg, P < 0.05). ANG II blockade had little effect on resting or baroreflex parameters in normal rabbits. However, in rabbits with heart failure, L-158,809 enhanced baroreflex sensitivity (2.7 +/- 0.5 vs. 4.7 +/- 0.8 beats.min-1.mmHg-1; P < 0.05), primarily by increasing the minimum HR evoked during baroreceptor activation. beta 1-Blockade had no effect on any baroreflex parameter after L-158,809 in rabbits with heart failure. However, L-158,809 significantly reduced the minimum HR after pretreatment with atropine in rabbits with heart failure. These data suggest that ANG II plays a role in modulation of cardiac sympathetic tone in this model of heart failure and may be responsible for the depressed baroreflex sensitivity observed in heart failure.

Angiotensin Receptor Antagonists↗

PubMed1996

Sex differences in the determination of abdominal leak point pressure in patients with intrinsic sphincter deficiency.

PURPOSE: We determined the effect of a urethral catheter on abdominal leak point pressure in men and women with intrinsic sphincter deficiency. MATERIALS AND METHODS: A total of 21 consecutive men treated with prostatectomy and 19 women with intrinsic sphincter deficiency underwent abdominal leak point pressure measurements with a rectal catheter before and after removal of a 10F urethral catheter. RESULTS: Of the 19 women 2 had leakage only when the urethral catheter was removed, while 17 had excellent correlation between abdominal leak point pressures before and after catheter removal (r = 0.83). In contrast, 10 of 21 men had leakage only when the urethral catheter was removed and 11 had weak correlation between abdominal leak point pressures before and after catheter removal (r = 0.46). CONCLUSIONS: An indwelling 10F urethral catheter is much more likely to invalidate abdominal leak point pressure measurement in men than in women with intrinsic sphincter deficiency.

Aged↗

PubMed1996

Internalization of human lactoferrin by the Jurkat human lymphoblastic T-cell line.

Binding of either iron-saturated or iron-free lactoferrin to the Jurkat human lymphoblastic T-cell line was saturable with a dissociation constant Kd of 40 nM. The total number of binding sites was estimated to be approximately 300,000. Non-specific binding did not exceed 30% of the total binding. Removal of the 4 clustered arginine residues of lactoferrin at position 2 to 5, which are involved in the interactions with heparan sulfate, did not modify the binding parameters. Therefore, the high number of low affinity binding sites previously described as responsible for the interaction of lactoferrin with either hepatocytes, enterocytes or the U937 monocytic cell line, is not involved in the binding of lactoferrin to Jurkat cells. After binding at 4 degrees C, a shift to 37 degrees C causes cell to internalize lactoferrin, with the maximum intracellular concentration found at 3 to 8 and 5 to 15 min for iron-saturated and iron-free forms, respectively. Addition of colchicine had no effect on binding or internalization. These results suggest that endocytosis of lactoferrin by Jurkat cells occurs through a receptor-mediated process. Jurkat cells internalize lactoferrin monophasically with a first-order endocytic constant K(in) of 0.060 min-1 at 37 degrees C. Confocal microscopic analysis, using fluorescein-carbohydrate-labeled lactoferrin showed that lactoferrin was mainly localized in intracellular vesicles. Following uptake, the endocytic path utilized by fluorescein-carbohydrate-labeled lactoferrin was shown to diverge from that of rhodamine-labeled serum transferrin; after internalization, lactoferrin and serum transferrin did not fully colocalize. Intracellular lactoferrin was found in endosome vesicles as assessed by electron microscopy. Raising the pH in endosomes using chloroquine led to the accumulation of lactoferrin into endosomes (acidic compartment). After internalization, Jurkat cells released both degraded and intact lactoferrin into the culture medium, suggesting that a fraction (30-40%) of the ligand is degraded at each round of endocytosis.

Cell Line↗

PubMed1995

Structure-function analysis of human glucose-6-phosphatase, the enzyme deficient in glycogen storage disease type 1a.

Glucose-6-phosphatase (G6Pase) is the enzyme deficient in glycogen storage disease type 1a, an autosomal recessive disorder. We have previously identified six mutations in the G6Pase gene of glycogen storage disease type 1a patients and demonstrated that these mutations abolished or greatly reduced enzymatic activity of G6Pase, a hydrophobic protein of 357 amino acids. Of these, four mutations (R83C, R295C, G222R, and Q347X) are missense and one (Q347X) generates a truncated G6Pase of 346 residues. To further understand the roles and structural requirements of amino acids 83, 222, 295, and those at the carboxyl terminus in G6Pase catalysis, we characterized mutant G6Pases generated by near-saturation mutagenesis of the aforementioned amino acids. Substitution of Arg-83 with amino acids of diverse structures including Lys, a conservative change, yielded mutant G6Pase with no enzymatic activity. On the other hand, substitution of Arg-295 with Lys (R295K) retained high activity, and R295N, R295S, and R295Q exhibited moderate activity. All other substitutions of Arg-295 had no G6Pase activity, suggesting that the role of Arg-295 is to stabilize the protein either by salt bridge or hydrogen-bond formation. Substitution of Gly-222, however, remained functional unless a basic (Arg or Lys), acidic (Asp), or large polar (Gln) residue was introduced, consistent with the hydrophobic requirement of codon 222, which is predicted to be in the fourth membrane-spanning domain. It is possible that Arg-83 is involved in stabilizing the enzyme (His)-phosphate intermediate formed during G6Pase catalysis. There exist 9 conserved His residues in human G6Pase. His-9, His-119, His-252, and His-353 reside on the same side of the endoplasmic reticulum membrane as Arg-83. Whereas H119A mutant G6Pase had no enzymatic activity, H9A, H252A, and H353A mutant G6Pases retained significant activity. Substitution of His-119 with amino acids of diverse structures also yielded mutant G6Pase with no activity, suggesting that His-119 is the phosphate acceptor in G6Pase catalysis. We also present data demonstrating that the carboxyl-terminal 8 residues in human G6Pase are not essential for G6Pase catalysis.

Amino Acid Sequence↗

PubMed1995

Differential stimulation of somatostatin but not neuropeptide Y gene expression by quinolinic acid in cultured cortical neurons.

Somatostatin (SS) and neuropeptide Y (NPY) are coproduced in a subpopulation of neurons that are selectively resistant to NMDA neurotoxicity. We have previously reported that quinolinic acid (QUIN), an NMDA receptor agonist, augments SS mRNA in cultured fetal rat cortical neurons. This study examines coregulation of SS and NPY by QUIN and NMDA in cultured cortical neurons and compares the effects of these agents with those of forskolin and phorbol 12-myristate 13-acetate (PMA), known to activate SS and NPY gene transcription by protein kinase A- and protein kinase C-dependent mechanisms. In addition, transcriptional regulation of the SS gene was investigated by acute transfection of cortical cultures with an SS promoter-chloramphenicol acetyltransferase (CAT) construct. QUIN and NMDA displayed dose-dependent fourfold augmentation of levels of mRNA for SS but not for NPY. In contrast, forskolin and PMA increased both SS and NPY mRNA levels. QUIN- and NMDA-mediated induction of SS mRNA was blocked by the NMDA receptor antagonist (-)-2-amino-5-phosphonovaleric acid and displayed regional brain specificity because it was not observed in fetal hypothalamic cell cultures. In time course studies, the effects of QUIN/NMDA on SS mRNA occurred after a latency of 8 h, indicating a delayed effect. Cortical cells transfected with pSS-750 CAT showed three- to fourfold stimulation of CAT activity with forskolin but not by QUIN or NMDA. These data reveal a dose-dependent, tissue-specific, NMDA receptor-mediated stimulation of SS but not NPY mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Glucocorticoids inhibit somatostatin gene expression through accelerated degradation of somatostatin messenger ribonucleic acid in human thyroid medullary carcinoma (TT) cells.

We previously reported that dexamethasone (DEX) induces dose-dependent biphasic effects on steady state somatostatin (SS) messenger RNA (mRNA) levels in normal rat islet and islet SS-producing tumor cells (1027B2), characterized by stimulation at low doses and marked inhibition at high doses. The stimulatory effect is transcriptionally mediated, whereas the molecular mechanism underlying DEX-induced suppression of SS mRNA levels is unknown. In the present study, we investigated these mechanisms in human thyroid medullary carcinoma (TT) cells, which exhibit only inhibition of SS mRNA with DEX. Cultured TT cells synthesized and secreted large quantities of SS-like immunoreactivity (content, 90 ng/10(6) cells; release, 18 ng/10(6) cells/24h). DEX produced a dose-dependent reduction of both SS-like immunoreactivity secretion and SS mRNA levels, with a maximum inhibition of 60% at 10(-6) M at 48 h. In time-course studies, DEX inhibition of SS function occurred after a lag period of about 12 h, suggesting a posttranscriptional mechanism. To exclude a transcriptional effect of DEX on the SS gene, chloramphenicol acetyltransferase (CAT) activity was determined in TT cells acutely transfected with SS promoter (-750 base pairs) ligated to the receptor CAT gene. No inhibition of CAT activity occurred with DEX (10(-6) M) for 48 h. Furthermore, DEX did not influence the rate of SS gene transcription determined by nuclear run-on assay compared to approximately 2-fold stimulation by cAMP. Actinomycin D (inhibitor of mRNA synthesis) reduced the size of the SS mRNA transcript and rendered it resistant to DEX-induced degradation when coincubated with DEX, but not when it was added after a delay of 12 h, indicating that DEX destabilizes SS mRNA by an active process requiring ongoing gene transcription. Cycloheximide (inhibitor of protein synthesis) reduced SS mRNA levels to the same level as DEX, suggesting that the two agents promote SS mRNA degradation through a common pathway. We conclude that glucocorticoids inhibit steady state SS mRNA levels in TT cells. This effect is not mediated through direct transcriptional inhibition of the SS gene. It requires transcription of another gene(s) whose product(s) accelerates SS mRNA degradation.

Carcinoma, Medullary↗

PubMed1995

Genetic basis of glycogen storage disease type 1a: prevalent mutations at the glucose-6-phosphatase locus.

Diagnosis of glycogen storage disease (GSD) type 1a currently is established by demonstrating the lack of glucose-6-phosphatase (G6Pase) activity in the patient's biopsied liver specimen. Recent cloning of the G6Pase gene and identification of mutations within the gene that causes GSD type 1a allow for the development of a DNA-based diagnostic method. Using SSCP analysis and DNA sequencing, we characterized the G6Pase gene of 70 unrelated patients with enzymatically confirmed diagnosis of GSD type 1a and detected mutations in all except 17 alleles (88%). Sixteen mutations were uncovered that were shown by expression to abolish or greatly reduce G6Pase activity and that therefore are responsible for the GSD type 1a disorder. R83C and Q347X are the most prevalent mutations found in Caucasians, 130X and R83C are most prevalent in Hispanics, and R83H is most prevalent in Chinese. The Q347X mutation has thus far been identified only in Caucasian patients, and the 130X mutation has been identified only in Hispanic patients. Our results demonstrate that the DNA-based analysis can accurately, rapidly, and noninvasively detect the majority of mutations in GSD type 1a. This DNA-based diagnosis now permits prenatal diagnosis among at-risk patients and serves as a database in screening and counseling patients clinically suspected of having this disease.

Alleles↗

PubMed1995

DNA cytometric abnormalities in human esophageal squamous intraepithelial and invasive carcinomas.

DNA ploidy abnormalities of 21 archival human esophageal intraepithelial neoplasia samples were assessed, using image cytometry of deparaffinized samples, with reference to invasive squamous cell carcinoma and corresponding uninvolved squamous epithelium. Cytometric parameters investigated were proportion of G0G1 aneuploid cell population, histogram typing, proportion of G0G1 diploid nuclei, coefficient of variation, mean DNA content, crude 5c exceeding proportion, 2c deviation index, malignancy index and grade, and entropy. The distributions of the above parameters were compared using the paired t test and Fisher's exact test. Among 10 parameters used, Auer typing of DNA histograms, crude 5c exceeding rate, 2c deviation index and malignancy grade according to Böcking allowed discrimination between uninvolved epithelium and invasive squamous cell carcinoma as well as intraepithelial neoplasia. In particular, the distribution of 2c deviation index in the uninvolved epithelium did not overlap that of intraepithelial and invasive carcinomas. The above four parameters, however, were unable to discriminate intraepithelial neoplasia from invasive carcinoma.

Aneuploidy↗