Picosecond-Scale Ultrafast Many-Body Dynamics in an Ultracold Rydberg-Excited Atomic Mott Insulator.

We report the observation and control of ultrafast many-body dynamics of electrons in ultracold Rydberg-excited atoms, spatially ordered in a three-dimensional Mott insulator (MI) with unity filling in an optical lattice. By mapping out the time-domain Ramsey interferometry in the picosecond timescale, we can deduce entanglement growth indicating the emergence of many-body correlations via dipolar forces. We analyze our observations with different theoretical approaches and find that the semiclassical model breaks down, thus indicating that quantum fluctuations play a decisive role in the observed dynamics. Combining picosecond Rydberg excitation with MI lattice thus provides a platform for simulating nonequilibrium dynamics of strongly correlated systems in synthetic ultracold atomic crystals, such as in a metal-like quantum gas regime.

Ultrafast Creation of Overlapping Rydberg Electrons in an Atomic BEC and Mott-Insulator Lattice.

We study an array of ultracold atoms in an optical lattice (Mott insulator) excited with a coherent ultrashort laser pulse to a state where single-electron wave functions spatially overlap. Beyond a threshold principal quantum number where Rydberg orbitals of neighboring lattice sites overlap with each other, the atoms efficiently undergo spontaneous Penning ionization resulting in a drastic change of ion-counting statistics, sharp increase of avalanche ionization, and the formation of an ultracold plasma. These observations signal the actual creation of electronic states with overlapping wave functions, which is further confirmed by a significant difference in ionization dynamics between a Bose-Einstein condensate and a Mott insulator. This system is a promising platform for simulating electronic many-body phenomena dominated by Coulomb interactions in the condensed phase.

The interaction between Lyn and FcεRIß is indispensable for FcεRI-mediated human mast cell activation.

BACKGROUND: FcεRIß reportedly functions as an amplifier of the FcεRIγ-mediated activation signal using a reconstitution system. However, the amplification mechanisms in human mast cells (MCs) are poorly understood. We previously reported the hyperexpression of FcεRIß of MCs in giant papillae from vernal keratoconjunctivitis patients, compared with that in conjunctivae from nonallergic conjunctivitis patients. Elucidation of the molecular mechanisms of the amplification induced by FcεRIß should provide new targets for novel therapeutic interventions. The aim is to understand in greater details the function of FcεRIß in human MC FcεRI expression and signaling. METHODS: FcεRIß and Lyn expression was reduced using a lentiviral shRNA silencing technique. Localization of Lyn and FcεRIß in cultured MCs was examined by confocal microscopic analysis. Mediators were measured by ELISAs. RESULTS: The diminution of FcεRIß significantly downregulated cell surface FcεRI expression and FcεRI-mediated mediator release/production. The downregulation of FcεRI-mediated degranulation was not only due to the decrease in FcεRI expression. The diminution of FcεRIß inhibited the redistribution of Lyn within the cell membrane following IgE sensitization. The diminution of Lyn in MCs significantly downregulated FcεRI-mediated degranulation. The recombinant cell-penetrating forms of phosphorylated FcεRIß immunoreceptor tyrosine-based activation motif (ITAM) for intracellular delivery disturbed the interaction between Lyn and phosphorylated endogenous FcεRIß ITAM, resulted in inhibiting IgE-dependent histamine release from MCs in vitro and from giant papillae specimens ex vivo. CONCLUSION: The interaction between Lyn and FcεRIß is indispensable for FcεRI-mediated human MC activation, and specific inhibition of the interaction may represent a new therapeutic strategy for the treatment of human allergic diseases.

Dislocation-driven surface dynamics on solids.

Dislocations are line defects that bound plastically deformed regions in crystalline solids. Dislocations terminating on the surface of materials can strongly influence nanostructural and interfacial stability, mechanical properties, chemical reactions, transport phenomena, and other surface processes. While most theoretical and experimental studies have focused on dislocation motion in bulk solids under applied stress and step formation due to dislocations at surfaces during crystal growth, very little is known about the effects of dislocations on surface dynamics and morphological evolution. Here we investigate the near-equilibrium dynamics of surface-terminated dislocations using low-energy electron microscopy. We observe, in real time, the thermally driven nucleation and shape-preserving growth of spiral steps rotating at constant temperature-dependent angular velocities around cores of dislocations terminating on the (111) surface of TiN in the absence of applied external stress or net mass change. We attribute this phenomenon to point-defect migration from the bulk to the surface along dislocation lines. Our results demonstrate that dislocation-mediated surface roughening can occur even in the absence of deposition or evaporation, and provide fundamental insights into mechanisms controlling nanostructural stability.

A case of feline gastrointestinal eosinophilic sclerosing fibroplasia limited to the mesentery.

An entire, female, mixed-breed cat of unknown age was presented with a 6-week history of lethargy, anorexia and vomiting. There was an increase in the number of white blood cells in the blood, including neutrophils and eosinophils; moderate anaemia; ascites; and possible mesenteric peritonitis. Exploratory laparotomy revealed firm, multifocal small nodules in the mesentery. As the nodules were surgically unresectable, they were biopsied. Histologically, the nodules were composed of thin trabeculae of dense collagen fibres mixed with plump fibroblasts and numerous eosinophils, consistent with feline gastrointestinal eosinophilic sclerosing fibroplasia. Bacteria were not detected on histological examination of the nodules and cytology of the ascites. Remission of disease occurred following treatment with prednisolone and ciclosporin A for 22 days and antibiotics for 40 days. After remission, ciclosporin A was administered for 236 days and then discontinued. Eosinophilia also resolved after treatment with ciclosporin A. The cat is still alive and in good condition on day 689. This report describes what may be an atypical case of feline gastrointestinal eosinophilic sclerosing fibroplasia, lacking involvement of the gastrointestinal tract, and was apparently cured by treatment that involved ciclosporin A.

Electron microscopy of human factor VIII/Von Willebrand glycoprotein: effect of reducing reagents on structure and function.

The structure of native and progressively reduced human factor VIII/von Willebrand factor (FVIII/vWF) was examined by electron microscopy and SDS gel electrophoresis and then correlated with its biological activities. Highly resolved electron micrographs of well-spaced, rotary-shadowed FVIII/vWF molecules showed their structure to consist of a very flexible filament that contains irregularly spaced small nodules. Filaments ranged from 50 to 1,150 nm with a mean length of 478 nm and lacked fixed, large globular domains as seen in fibrinogen and IgM. A population of multimeric FVIII/vWF species ranging in molecular weight from 1 to 5 million daltons and differing in size alternately by one and two subunits was observed on SDS-2% polyacrylamide-0.5% agarose gel electrophoresis. With progressive reduction of disulfide bonds by dithiothreitol (DTT), the electron microscopic size of FVIII/vWF decreased in parallel with increased electrophoretic mobility on SDS-agarose gels; between 0.1 and 0.5 mM DTT its structure changed from predominantly fibrillar species to large nodular forms. A 50% loss of vWF specific activity and FVIII procoagulant activity occurred at 0.4 mM DTT and 1 mM DTT, respectively, corresponding to the reduction of 4 and 12 disulfide bonds of the 62 disulfides per 200,000-dalton subunit. We conclude that reduction of a few critical disulfide bonds results in a major structural change by electron microscopy and a concomitant loss of approximately 50% of the vWF function.

Identifying pathogenic genetic background of simplex or multiplex retinitis pigmentosa patients: a large scale mutation screening study.

BACKGROUND AND PURPOSE: More than half of the retinitis pigmentosa (RP) cases are genetically simplex or multiplex. To date, 37 causative genes of RP have been identified; however, the elucidation of gene defects in simplex or multiplex RP patients/families remains problematic. The aim of our study was to identify the genetic causes of RP in patients with unknown or non-Mendelian inheritance. METHODS AND RESULTS: Since 2003, 52 simplex RP patients, 151 patients from 141 multiplex RP families, and six sporadic patients with retinal degeneration were studied. A total of 108 exons of 30 RP-causing genes that harboured the reported mutations were screened by an efficient denaturing high performance liquid chromatography (dHPLC) based assay. Aberrant fragments were subsequently analysed by automatic sequencing. Twenty-six mutations, including two frameshift mutations, one single amino acid deletion, and 23 missense mutations, were identified in 28 probands (14.07%). Eighteen mutations have not been reported to date. Three pairs of combined mutations in different genes were identified in two sporadic cases and one multiplex family, indicating the possibility of novel digenic patterns. Of the 23 missense mutations, 21 were predicted as deleterious mutations by computational methods using PolyPhen, SIFT, PANTHER, and PMut programs. CONCLUSION: We elucidated the mutation spectrum in Japanese RP patients and demonstrated the validity of the mutation detection system using dHPLC sequencing for genetic diagnosis in RP patients independent of familial incidence, which may provide a model strategy for identifying genetic causes in other diseases linked to a wide range of genes.

Static bone cavity in the condylar neck and mandibular notch of the mandible.

This study presents the radiographic findings of two cases of static bone cavity in the inferior aspect of the condylar neck and mandibular notch of the mandible. On plain CT, a soft tissue mass was observed in each cavity. The submandibular gland and the other glands were not found in each cavity. On contrast-enhanced CT, the soft tissue in the cavity in the inferior aspect of the condylar neck had marked linear enhancement and dilated vasculature structure was observed in the cavity. On the contrast-enhanced MRI, the soft tissue in the cavity of the mandibular notch had marked enhancement and flow void was detected in the cavity. In the inferior aspect of the condylar neck, the cavity size had enlarged radiographically over a period of three years. Vascular lesions were found in the cavity located in the inferior aspect of the condylar neck and mandibular notch of the mandible by both CT and MRI. The vascular lesion might explain the enlargement of the static bone cavity.

Green tea consumption and lung cancer risk: the Ohsaki study.

We examined the risk of lung cancer in relation to green tea consumption in a population-based cohort study in Japan among 41,440 men and women, aged 40-79 years, who completed a questionnaire in 1994 regarding green tea consumption and other health-related lifestyle factors. During the follow-up period of 7 years (from 1995 to 2001), 302 cases of lung cancer were identified, and the Cox proportional hazards regression model was used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs). The multivariable-adjusted HRs of lung cancer incidence for green tea consumption of 1 or 2, 3 or 4, and 5 or more cups/day as compared to less than 1 cup/day were 1.14 (95% CI: 0.80-1.62), 1.18 (95% CI: 0.83-1.66), and 1.17 (95% CI: 0.85-1.61), respectively (P for trend=0.48). This cohort study has found no evidence that green tea consumption is associated with lung cancer.

Sleep duration and the risk of prostate cancer: the Ohsaki Cohort Study.

In a prospective study of prostate cancer incidence (127 cases), among 22 320 Japanese men, sleep duration was associated with lower risk; the multivariate hazard ratio of men who slept >or=9 h per day compared with those who slept less was 0.48 (95% confidence interval: 0.29-0.79, P for trend=0.02).

Degenerative lumbosacral spondylolisthesis: possible factors which predispose the fifth lumbar vertebra to slip.

We have analysed a number of radiological measurements in an attempt to clarify the predisposing factors for degenerative spondylolisthesis of the lumbosacral junction. We identified 57 patients with a slip and a control group of 293 patients without any radiological abnormality apart from age-related changes. The relative thickness of the L5 transverse process, the sacral table angle and the height of the iliac crest were measured and evaluated. The difference in these measurements between men and women was analysed in the control group. We found that the transverse process of L5 was extremely slender, the sacral table more inclined, and the L5 vertebra was less deeply placed in the pelvis in patients with a slip compared with the control group. The differences in these three parameters were statistically significant. We believe that the L5 vertebra is predisposed to slip when these factors act together on a rigidly-stabilised sacrum. This occurs more commonly in women, probably as a result of constitutional differences in the development of the male and female spine.

Giant cell reparative granuloma of the proximal tibia: a case report.

Giant cell reparative granulomas (GCRGs) are non-neoplastic inflammatory lesions, usually of the jaw or gingiva or small bones of the hands and feet. We report one such case in the right proximal tibia of a 45-year-old man. Radiological studies showed a lytic lesion with marginal sclerosis in the epiphysis and metaphysis. After open biopsy, a preliminary diagnosis of a benign giant cell tumour was made. One month after admission, the lesion was curetted and filled with cancellous bone and hydroxyapatite. Based on the histology of the curetted lesion, the diagnosis was changed to a GCRG. The patient had an uneventful postoperative course, with no evidence of local recurrence and metastasis. He died from gastric cancer 2 years later.

Immunological abnormalities of aging: an analysis of T lymphocyte subpopulations of Werner's syndrome.

Two T lymphocyte-specific antisera, i.e. naturally-occurring auto-antibody to T cells of systemic lupus erythematosus patients (natural T cell toxic autoantibody) and heterologous antiserum against human brain tissue (antibrain-associated T-cell antigen), were used to detect cell surface antigens of human peripheral T lymphocytes. Nylon column-purified T cells from normal aged individuals and patients with Werner's syndrome (a premature aging syndrome) were reacted with these auto- and heterologous antibodies followed by staining with appropriate fluorescence reagents. The cells were subjected to the automated analysis with fluorescence-activated cell sorter. Fluorescence profiles to T cells of both aged individuals of over 90 yr and Werner's syndrome showed a very similar pattern, with a drastic decrease in the population that had high fluorescence intensity stained with either antiserum accompanied by the relative increase in the cell population that had low fluorescence intensity. Natural T cell toxic autoantibody comparable to that detected in systemic lupus erythematosus patients was found in the serum of six out of seven patients with Werner's syndrome, whereas normal aged individuals produced no such an autoantibody. The results suggest that Werner's syndrome has a change in the lymphocyte population very similar to old individuals, and that such a change is caused by the production of autoantibodies reactive to T lymphocytes.

Genetic analysis of high-metastatic clone of RCT sarcoma in mice, and its growth regression in vivo in response to angiogenesis inhibitor TNP-470.

Genetic analysis of a high-metastatic clone of RCT sarcoma (HM-RCT) was the aim of the study. HM-RCT was developed by the lung passage as well as limiting dilution method from the original RCT sarcoma, in which a tumor was spontaneously developed in a C3H/He mouse. HM-RCT expressed enhanced POU domain (class 2, associating factor 1), adenylate cyclase 7, procollagen type III (alpha), A kinase anchor protein 4 and Ehm (expressed on high-metastatic cells) and 11 expressed sequence tags (ESTs). compared with the original clone of RCT. Eighteen specific genes and 14 ESTs were underexpressed in HM-RCT. We investigated the effects of angiogenesis inhibitor TNP-470 on tumor growth and metastasis of this HM-RCT in vivo. In an experimental group, mice received TNP-470 (30 mg/kg) intraperitoneally every other day. After 5 weeks, the growth of the TNP-470-treated tumor was significantly suppressed in vivo, but did not affect the metastasis. The proportion of positive PCNA-stained cells and cellular telomerase activity was significantly low in response to TNP-470.

Coexpression of an unusual form of the EWS-WT1 fusion transcript and interleukin 2/15 receptor betamRNA in a desmoplastic small round cell tumour.

BACKGROUND: The beta chain of the interleukin 2/15 receptor (IL-2/15Rbeta) is induced by the expression of the EWS-WT1. A case of desmoplastic small round cell tumour (DSRCT) expressing only an unusual EWS-WT1 treated by us is reported here. AIM: To characterise an unusual form of EWS-WT1. METHODS: Frozen tissue sections of the axillary tumour were examined using a laser-assisted microdissection technique and reverse transcriptase polymerase chain reaction. RESULTS: The novel fusion of exon 8 of EWS and the defective exon 10 of WT1 (-KTS) was detected. Although it was an unusual form, the coexpression of the present EWS-WT1, IL-2/15Rbeta and Janus kinase (JAK1) mRNA was detected in the tumour cells. IL-2 and signal transducers and activators of transcription (STAT5) mRNA were detected in both tumour and stromal cells. CONCLUSION: The induction of the IL-2/15 receptor signalling pathway may contribute to tumorigenesis in DSRCT through a paracrine or an autocrine system, even though the EWS-WT1 was an unusual form.

Pattern of local relapse of maxillary sinus carcinoma.

Maxillary sinus carcinoma (MSC) is a rare disease with a variety of treatment options. The present study was undertaken to review the outcome of patients with treated MSC in order to clarify the factors related to local recurrence by analyzing CT findings. The study group comprised of 47 cases, 40 males and 7 females with a median age of 61 years (range, 40- 84 years) treated between 1988 to 1996 at the department of radiotherapy. CT was taken with a slice thickness of 5 mm and contrast material was routinely used. The mean follow-up period for the group was 45.0 months (range, 3-125 months). The treatment policy was either preoperative radiotherapy of 40Gy/16fr followed by maxillectomy or radical radiotherapy of 65Gy/26fr with partial maxillectomy during the course of radiotherapy. By using CT-simulation, wedge pair techniques were used in most patients with Cobalt or 6MV X-ray machines as treatment sources. Tumor extension was categorized into the following anatomical sites: orbital contents, other paranasal sinuses, posterior wall of the maxillary sinus, pterygoid plate/muscle, nasopharynx, infra-temporal fossa, base of the skull, anterior wall of the maxillary sinus, subcutaneous tissue, cheek mucosa, hard palate and alveolar bone. Local control was computed by using the Kaplan-Meier method and p value was measured by using Chi-squared test. The 5-year overall local control rates for all patients were 56%. The local recurrence was found in 19 of 47 patients (40.4%). Tumors extending to pterygoid plates (n=13) and pterygoid muscles (n=10) showed higher rate of local recurrences as compared to those without extensions (9/13 [69%] vs 10/34 [29%], p<0.02 and 7/10 [70%] vs 12/37 [32%], p<0.05, respectively). Extensions to nasopharynx (6/9, 66%) and base of skull (4/6, 66%) also showed higher rates of recurrence; however, those were not statistically significant. More than 80% of the relapse became manifest within 12 months of diagnosis and isolated local failure was the most common pattern. This analysis indicates that tumor extension to pterygoid plate/muscles, results in higher rates of recurrences. This may due to the difficult surgical accessibility of the tumor. During radiotherapy planning, special emphasis should be given to this sites of tumor extension to avoid possible local recurrence.

Variant type of sialyl Lewis X antigen expressed on adult T cell leukemia cells is associated with skin involvement.

Expression of a variant type of sialyl Le(x) antigen defined by 2F3 monoclonal antibody on leukemia cells was studied in 15 adult T cell leukemia (ATL) patients. The expression of 2F3-defined sialyl Le(x) antigen on CD4+CD45+ cells, which is an ATL cell-rich population, was higher in patients with skin involvement (50.1 +/- 23.1% were positive) than in patients without skin involvement (18.1 +/- 12.5%) (P < 0.01). The other surface markers including classical sialyl Le(x) antigen defined by SNH3 or FH6 and LFA-1, VLA-4, CD4, CD25, ICAM-1, Leu8, and HLA-DR did not show a significant difference regardless of skin involvement. In the skin lesion of four patients that we could examine, infiltrating leukemia cells strongly expressed 2F3-defined sialyl Le(x) antigen. In one patient, we could also examine the expression of classical sialyl Le(x) antigen defined by SNH-3 and CSLEX-1, but this was almost negligible. Both skin and lymph node biopsy specimens were examined in two patients. Leukemia cells in the skin strongly expressed 2F3-defined sialyl Le(x) antigen, while its expression was almost negligible on the leukemia cells in the lymph node. These findings suggest that the expression of 2F3-defined sialyl Le(x) antigen on ATL cells is associated with skin involvement of ATL.

Contribution of carbohydrate antigens sialyl Lewis A and sialyl Lewis X to adhesion of human cancer cells to vascular endothelium.

The carbohydrate antigen, sialyl Lex, is known to be a ligand for the cell adhesion molecule called ELAM-1 (E-selectin, endothelial cell leukocyte adhesion molecule-1), which is present on cytokine-activated human endothelial cells. Recently, we reported that another carbohydrate antigen, sialyl Lea, can also serve as a ligand for ELAM-1 (A. Takada, K. Ohmori, N. Takahashi, K. Tsuyuoka, K. Yago, K. Zenita, A. Hasegawa, and R. Kannagi, Biochem. Biophys. Res. Commun., 179: 713-719, 1991). Both sialyl Lex and sialyl Lea are expressed in many human malignant cells. In order to assess the contribution of these carbohydrate antigens to the adhesion of human malignant cells to vascular endothelium, we selected a panel of 12 cultured human epithelial cancer cell lines and a panel of 12 human leukemia cell lines which express sialyl Lex and/or sialyl Lea antigens. All 12 epithelial cancer cell lines exhibited a clearly ELAM-1-dependent adhesion to cytokine-activated human umbilical vein endothelial cells, while only 3 of the 12 leukemia cell lines exhibited significant participation of ELAM-1 in the adhesion. With regard to epithelial cancer cells, the adhesion of 6 cancer cell lines, mostly of colon and pancreas origin, was dependent almost exclusively on sialyl Lea. A significant contribution of the sialyl Lex antigen was noted in the adhesion of the other 6 cell lines, including cancers of lung and liver origin. These results imply that the sialyl Lea/ELAM-1 adhesion system, as well as the sialyl Lex/ELAM-1 adhesion system, plays an important role in the adhesion of human cancer cells to human umbilical vein endothelial cells. With regard to leukemia cells, on the other hand, adhesion of the 3 leukemia cell lines that showed ELAM-1-dependent adhesion was mediated by the sialyl Lex antigen, and none of these leukemia cell lines expressed sialyl Lea or exhibited sialyl Lea-dependent adhesion.

Expression of alpha-(1,3)-fucosyltransferases which synthesize sialyl Le(x) and sialyl Le(a), the carbohydrate ligands for E- and P-selectins,in human malignant cell lines.

Transcripts of alpha-(1,3)-fucosyltransferases in human epithelial cancer and leukemia cell lines were analyzed by Northern blotting and reverse transcriptase mediated-polymerase chain reaction using specific probes and primers which can discriminate between the transcripts derived from the four alpha-(1,3)-fucosyltransferase genes Fuc-TIII, IV, V, and VI. Flow cytometric analysis of the sialyl Le(x) and sialyl Le(a) antigens was also performed on the same cell lines. The sialyl Le(x) antigen was expressed on 14 of 15 epithelial cancer cell lines, and the sialyl Le(a) antigen was detected on 8 of them. The message of Fuc-TIII was detected in most of the epithelial cancer cell lines (14 of 15), which correlated with the surface expression of these carbohydrate determinants. In addition, the messages of Fuc-TIV and Fuc-TVI were detected in most epithelial cancer cell lines, while the message of Fuc-TV was undetectable in most of them. On the other hand, all leukemia cell lines were positively stained for sialyl Le(x), but none of them was stained for sialyl Le(a) in flow cytometry. The messages of Fuc-TIV++ were detected in all leukemia cell lines tested. Small quantities of Fuc-TIII, V, and/or VI messages were also detected in some leukemia cell lines in reverse transcriptase mediated-polymerase chain reaction analysis. These studies indicate that alpha-(1,3)-fucosyltransferase activities in epithelial cancer and leukemia cell lines are mixtures of multiple molecular species of alpha-(1,3)-fucosyltransferases. It is natural that epithelial cancer cells contain a significant amount of Fuc-TIII mRNA and leukemia cell lines contain Fuc-TIV mRNA, since their normal counterparts, normal epithelial cells and leukocytes, respectively, are known to contain these fucosyltransferases. The unexpectedly frequent occurrence of Fuc-TIV mRNA in epithelial cancer cell lines may be related to their retro-differentiation associated with tumorigenesis. Another unexpected finding was a weak but significant expression of the alpha-(1,3)-fucosyltransferases Fuc-TIII, V, and/or VI in leukemia cell lines detected by reverse transcriptase mediated-polymerase chain reaction analysis. Since these enzymes are known to be capable of synthesizing the sialyl Le(x) determinant, this finding implies a possibility that some of them may be involved in the synthesis of sialyl Le(x) in leukemia cells.

Expression of sialyl 6-sulfo Lewis X is inversely correlated with conventional sialyl Lewis X expression in human colorectal cancer.

Sialyl 6-sulfo Lewis X determinant has been described recently as a major ligand for L-selectin on high endothelial venules of human peripheral lymph nodes. From our investigation of its distribution in human colorectal cancer tissues and cultured colon cancer cells, the sialyl 6-sulfo Lewis X determinant was preferentially expressed in the nonmalignant colonic epithelia rather than cancer cells (P < 0.001; n = 23). This was in contrast to the distribution of conventional sialyl Lewis X, which was preferentially expressed in cancer tissues rather than nonmalignant epithelia (P = 0.007; n = 23), indicating that 6-sulfation predominantly occurs in nonmalignant tissues and is suppressed upon malignant transformation. In confirmation of this, a nonsialylated determinant 6-sulfo Lewis X was also found to be preferentially localized in the nonmalignant epithelia. Significant expression of sialyl 6-sulfo Lewis X was observed in only 2 lines, whereas 8 were positive for conventional sialyl Lewis X, among 13 cultured colon cancer cell lines. Transfection of cells with fucosyltransferase (Fuc-T) VI induced expression of sialyl 6-sulfo Lewis X, whereas transfection of Fuc-T III did not, suggesting that the determinant was synthesized mainly by Fuc-T VI in colonic epithelia. Members of the sialic acid cyclase pathway, the de-N-acetyl sialyl 6-sulfo Lewis X and cyclic sialyl 6-sulfo Lewis X determinants, were also preferentially expressed in the nonmalignant epithelia rather than colonic cancer cells (P < 0.001; n = 23). Stimulation of the sialyl 6-sulfo Lewis X-positive colon cancer cell line with a calcium ionophore ionomycin markedly reduced sialyl 6-sulfo Lewis X and induced cyclic sialyl 6-sulfo Lewis X expression. These results suggested that the metabolic conversion of sialyl 6-sulfo Lewis X into cyclic sialyl 6-sulfo Lewis X by a calcium-dependent enzyme, sialic acid cyclase, as we hypothesized for human leukocytes previously (C. Mitsuoka et al., Proc. Natl. Acad. Sci. USA, 96: 1597-1602, 1999), also occurs in nonmalignant colonic epithelia.