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Summary A 21-year-old neutered female domestic shorthaired cat was presented with a history of inappetence, vomiting and haematuria. The cat was humanely destroyed at the owner's request and a necropsy examination was performed. A 0.8 × 0.5 × 0.5 cm mass was located in the left lobe of the pancreas. The mass was gelatinous in nature and the external and cut surfaces were pale yellow in colour. Microscopically, the mass was non-capsulated and comprised an accumulation of extracellular stromal mucin containing suspended neoplastic columnar epithelial cells forming tubular structures. Immunohistochemically, these cells diffusely expressed cytokeratin (CK) AE1/AE3, CK7 and carcinoembryonic antigen and were partially positive for CK19 and trypsin, but negative for vimentin. The tumour was diagnosed as a colloid carcinoma. The clinical presentation in this case was caused by chronic renal failure complicated by secondary renal hyperparathyroidism and associated metastatic calcinosis. To the best of our knowledge, this is the first report of colloid carcinoma arising from the pancreas in a cat.

Summary Antioxidant activity of symbiotic organisms known as lichens is an intriguing field of research because of its strong contribution to their ability to withstand extremes of physical and biological stress (e.g. desiccation, temperature, UV radiation and microbial infection). We present a comparative study on the antioxidant activities of 76 Icelandic and 41 Hawaiian lichen samples assessed employing the DPPH- and FRAP-based antioxidant assays. Utilizing this unprecedented sample size, we show that while highest individual sample activity is present in the Icelandic dataset, the overall antioxidant activity is higher for lichens found in Hawaii. Furthermore, we report that lichens from the genus Peltigera that have been described as strong antioxidant producers in studies on Chinese, Russian and Turkish lichens also show high antioxidant activities in both Icelandic and Hawaiian lichen samples. Finally, we show that opportunistic sampling of lichens in both Iceland and Hawaii will yield high numbers of lichen species that exclusively include green algae as photobiont.

Background and aims The toll-like receptors (TLRs) are critical participants in vertebrate innate immune recognition of pathogen-associated molecular patterns (PAMPs). Diverse ligands act as “danger signals” detected by this component of the innate immune system. TLR7 and 8 are located in the endosomes of specific immune subpopulations, and are activated by single-stranded RNA from viruses or by autologous RNA fragments bound to immune complexes, inducing the generation of cytokines such as interferons (specifically IFN-alpha) and IL-6. Strong genetic evidence supports variants in TLR7 as contributors to development of systemic lupus erythematosus (SLE). Methods In vitro and in vivo assays were used to guide development of potent and specific small molecule inhibitors. Results We describe novel and selective small molecule non-oligonucleotide TLR7/8 antagonists for the treatment of SLE. They exhibit potent activity in vitro in TLR-specific reporter systems (IC50 of ˜100 nM) and in primary human blood cells (IC50 of 50–500 nM across various ligands and cytokine readouts), suppressing TLR7 and TLR8 but with no activity against TLR9 or other TLRs tested. Exploration of mechanism of action shows direct interaction of the lead compound with the external domain of TLR8. The compounds are orally available and active in a mouse model of R848 challenge. When tested in long-term dosing in pristane-induced or spontaneous NZB/W disease the compounds slow the advance of autoantibody titers and efficiently suppress development of nephritis and associated proteinuria. Conclusions We have identified novel small molecule antagonists of human TLR7 and TLR8 with beneficial activity in mouse models of systemic lupus.

We report here the 6.0-Mb draft genome assembly of Pseudoalteromonas luteoviolacea strain IPB1 that was isolated from the Hawaiian marine sponge Iotrochota protea . Genome mining complemented with bioassay studies will elucidate secondary metabolite biosynthetic pathways and will help explain the ecological interaction between host sponge and microorganism.

This study was prospectively designed to evaluate a phase II study of gefitinib for non-small-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations. Clinical samples were tested for EGFR mutations by peptide nucleic acid-locked nucleic acid PCR clamp, and patients having EGFR mutations were given gefitinib 250 mg daily as the second treatment after chemotherapy. Poor PS patients omitted chemotherapy. Of 107 consecutive patients enrolled, samples from 100 patients were informative, and EGFR mutations were observed in 38 patients. Gefitinib was given to 27 patients with EGFR mutations, and the response rate was 78% (one complete response and 20 partial responses; 95% confidence interval: 58-93%). Median time to progression and median survival time (MST) from gefitinib treatment were 9.4 and 15.4 months, respectively. Grade 3 hepatic toxicity and skin toxicity were observed in one patient each. There were significant differences between EGFR mutations and wild-type patients in response rates (78 vs 14%, P = 0.0017), and MST (15.4 vs 11.1 months, P = 0.0135). A Cox proportional hazards model indicated that negative EGFR mutation was a secondary prognostic factor (hazards ratio: 2.259, P = 0.036). This research showed the need for screening for EGFR mutations in NSCLC patients.

Helicobacter pylori is the most common gastric bacteria of human beings. Animal-borne helicobacter have been associated with gastritis, ulceration, and gastric mucosa-associated lymphoid-tissue lymphoma in people. We attempted to identify the species of Helicobacter spp. that infect human beings in north Parana, Brazil. Samples of gastric mucosa from 38 dyspeptic patients were analyzed by optic microscopy on silver stained slides, polimerase chain reaction (PCR), and enzymatic cleavage. Genus and species-specific primers to H. pylori, H. heilmannii, H. felis, and consensual primers to H. bizzozeronii or H. salomonis were used. The PCR products were submitted to enzymatic cleavage by VspI (Helicobacter spp. product) and HinfI (species products) enzymes. Thirty-two out of 38 patients evaluated had 3.2 to 5 µm long bacteria that resembled H. pylori in Warthin-Starry stained slides and were positive to the genus Helicobacter by PCR. In 30 of these patients the bacteria were identified as H. pylori. Two samples positive by silver stain were negative to all species tested by PCR. None of the 38 samples was positive to animal-origin helicobacter species. These results show that PCR and enzymatic restriction are practical methods to identify the species of helicobacters present in gastric mucosa of human beings. People in north Parana appear to be infected mostly with H. pylori.

From the organic extract of a deep-water Hawaiian sponge Dactylospongia sp., a new potent antioxidant and antimicrobial meroterpenoid, puupehenol (1), was isolated. The structure of 1 was determined using spectroscopic techniques ((1)H and (13)C NMR, MS, IR, UV, [α]D). The known compound puupehenone (2) was also isolated and suggested as a probable artifact of the isolation procedures. Complete unambiguous (1)H and (13)C NMR data are provided for compounds 1 and 2. Bioassays performed with 1 and 2 showed them both to be very effective antioxidants and to have antimicrobial properties.

In this review the reported effects of shade levels on the amounts of reputed biologically active potential key chemical markers l -theanine and caffeine, and the four catechin-polyphenols, (−)-epicatechin (EC), (−)-epicatechin gallate (ECG), (−)-epigallocatechin (EGC), and (−)-epigallocatechin gallate (EGCG) found in the bud and first two leaves during development of tea ( Camellia sinensis ) grown on a Hawaiian plantation are discussed. Also discussed is the antioxidant activity of the overall extract of the tea leaf bud, and first and second leaves, together with the importance of employing 1 H NMR spectroscopy as an analytical tool for the determination of the validity of reference materials.

To identify the molecular mechanism which primarily plays a role in the pathogenesis of Crohn's disease (CD) without prior hypothesis, differential display method was employed to detect differentially expressed genes between the inflamed and uninflamed colonic samples from one patient with CD. The mRNA levels of these genes were subsequently semi-quantitated in affected and unaffected tissues from six patients using reverse transcriptase polymerase chain reaction (RT-PCR). Six genes including long form FLICE inhibitory protein (FLIPL) were found to be consistently overexpressed in the inflamed colonic CD tissues. Immunohistochemical studies revealed that FLIPL expressing cells were lamina propria lymphocytes (LPLs). The present study suggested that overexpression of FLIPL in the LPLs may be involved in the pathogenesis of CD through defective activation-induced cell death. In addition, this study provided evidence for a possible role of several previously unsuspected genes in the pathogenesis of CD.

The complete nucleotide sequences of the double-stranded RNA genome segments 5 (S5) from Bombyx mori cypovirus 1 (BmCPV-1) strains I and H were determined. The segments consisted of 2,852 nucleotides encoding putative proteins of 881 amino acids with molecular masses of approximately 101 kDa (p101). A homology search showed that p101 has high similarity (93%) to foot-and-mouth disease virus (FMDV) 2A protease (2Apro) at amino acid position 219 to 235. These findings suggest the possibility that p101 encoded by BmCPV-1 S5 might be cleaved into two non-structural proteins by post-translational autocleavage involving a 2Apro-like protease.

Human Fc gamma receptor (Fc gamma R) genes form a clustered gene family on chromosome 1q21-24. Although the association of Fc gamma R polymorphisms with systemic lupus erythematosus (SLE) has been extensively studied, the results are often contradictory. In this study, Fc gamma RIIA-131H/R, Fc gamma RIIIA-176F/V and Fc gamma RIIIB-NA1/2 genotypes were determined in the Japanese patients with SLE (n = 81) or rheumatoid arthritis (RA, n = 115) as well as in healthy individuals (n = 217), and possible association with the disease was tested using case-control analysis. Unlike in other populations, significant difference was not observed in the frequencies of Fc gamma RIIA and Fc gamma RIIIA genotypes between patients with SLE and healthy individuals. However, significant difference was detected in the frequencies of Fc gamma RIIIB genotypes between SLE and healthy individuals (P = 0.008). The odds ratio [OR] of the Fc gamma RIIIB-NA2/NA2 homozygotes for the development of SLE was 2.52 (95% confidence interval [CI]: 1.33-4.79). Among the patients with SLE, individuals with NA2/2 were significantly more likely to have lupus nephritis (P = 0.007). No association was observed between any of the Fc gamma R polymorphisms and RA. Significant linkage disequilibrium was detected between Fc gamma RIIIA and IIIB, but neither between IIA and IIIA, nor between IIA and IIIB. These observations may underscore the relevance of defective immune complex handling in the pathogenesis of SLE, or may suggest the presence of primarily associated gene(s) in linkage disequilibrium with Fc gamma R genes.

Objectives The purpose of this study was to elucidate the existence of the experience of and the frequency and severity of related concerns of distressful ethical situations encountered by nursing professionals in organ transplantation. Methods An anonymous self-administered questionnaire was mailed to 569 nurses in 79 facilities that performed organ transplantation with living or brain-dead donors who provided approval for this study. The questionnaire, developed according to the Likert method, was composed of 12 items referring to the basic attributes of nursing professionals based on the results of previous studies and the scientific literature, as well as 27 items referring to the presence or absence and the frequency and severity of concerns regarding ethical situations. The data were analyzed using descriptive statistics. Results The questionnaire was distributed to 569 nursing professionals working in 79 facilities that had provided consent for study participation. Responses were obtained from 218 participants (recovery rate: 38.3%). Among the 3 highest-ranking items, those in the first and second positions in terms of the presence or absence and the frequency of worries were the same as those in the second and third positions in terms of the severity of concerns. In addition, the 3 lower-ranking items also were the same. Among the ethical situations encountered by nursing professionals, the ones most often experienced that caused the most concern were the following: “I have questioned whether it was better for the recipient, who could not do self-care after the transplant, to undergo transplantation”, and “I have felt that a recipient decided to receive a transplant without considering the importance of posttransplant self-management when making a decision about transplant surgery.” Conclusions The results indicate that most of the ethical issues related to organ transplantation in nursing practice were experienced because recipients, their families, and donors could not foresee the various problems that might occur after transplantation.

We developed an enzyme-linked immunosorbent assay (ELISA) for human serum mannose binding protein (MBP), an animal lectin known to function as opsonin and complement activator. A total of 1085 normal Japanese sera from individuals ranging in age from 3 to 100 years old and additional body fluids were measured for the MBP level. Individual serum MBP levels ranged from 0.07 to 6.40 micrograms/ml with a frequency distribution profile of the log-normal type. Arithmetic mean +/- standard deviation (M +/- SD) of serum MBP as a whole was 1.72 +/- 1.15 micrograms/ml, whereas those of cerebrospinal fluid and urine were 1/100 and 1/1000 of serum levels, respectively. When the M +/- SD of serum MBP was calculated for each age group (10-year intervals) and compared, the value declined from age group of 3-9 years old (2.42 +/- 1.31 micrograms/ml) to that of 20-29 years old (1.72 +/- 1.03 micrograms/ml), and thereafter it remained almost constant. Comparing the frequency distribution profile among each group, that of young group revealed a distinct bimodal pattern, one peak at around 1 micrograms/ml and the other at 3 micrograms/ml. The latter peak was gradually depressed with advance of age and finally a typical log-normal type appeared after the age of 30. There was a high age dependency in serum MBP level as well as in distribution profile. It should be stressed that care should be taken with age in the evaluation of MBP level.

Bile salts present in gallbladder of wild and cultured red seabream, Pagrosomus major, a marine teleost were analyzed. The bile from wild red seabream was found to contain two previously unknown bile salts along with two known bile salts, taurocholate and taurochenodeoxycholate. Isolation of each bile salt was performed by column chromatography. Fast atom bombardment mass spectra of the unknown bile salts showed the molecular ions (M-H)- of m/z 544 and 528 which are shifted 30 mass units upfield compared to those (m/z 514 and 498) of taurocholate and taurochendeoxycholate, respectively; this is consistent with the presence of cysteinolic acid (mol wt 155) instead of taurine (mol wt 125). Enzymatic hydrolysis of the bile salts released cholic acid and chenodeoxycholic acid, respectively, and an amino acid that was identified as D-cysteinolic acid by direct comparison with an authentic sample. From these results, the bile salts in the bile of wild red seabream were identified as the conjugates of cholic acid and chenodeoxycholic acid with cysteinolic acid. 1H- and 13C-magnetic resonance spectra of the bile salts were also consistent with the proposed structure. The cysteinolic acid conjugates were found only in wild and not in cultured red seabream; this distinction seems to result from differences in dietary cysteinolic acid.

SEMA3B, a member of class 3 semaphorins, is a tumor suppressor. Competition with vascular endothelial growth factor (VEGF)165 explains a portion of the activity, whereas the VEGF-independent mechanism was not elucidated. We employed a microarray and screened for the genes whose expression was increased by SEMA3B in NCI-H1299 cells. Insulin-like growth factor-binding protein-6 (IGFBP-6), a tumor suppressor, showed greatest difference in the expression level. Introduction of IGFBP-6 cDNA reduced colony formation both on the dish surface and in soft agar. Insulin-like growth factor II, which antagonizes IGFBP-6, partly abrogated the effect. Inhibition of IGFBP-6 by small interfering RNA diminished the sub-G0/G1 population that was induced by SEMA3B and abrogated the growth suppressive effect of SEMA3B. We concluded that IGFBP-6 is the effector of tumor suppressor activity of SEMA3B in NCI-H1299 cells. It has been reported that beta-catenin suppresses the expression of IGFBP-6. Introduction of beta-catenin into the cells partly abrogated the growth suppressive effect of SEMA3B. Our result indicates that semaphorin signaling and beta-catenin signaling converge on IGFBP-6 and antithetically affect their functions.

CD22, a member of the immunoglobulin superfamily, is a B-cell transmembrane glycoprotein that acts as an accessory-signaling component of the B-cell antigen receptor (BCR). Recent evidence indicating the role of CD22 as a negative regulator of BCR signal transduction prompted us to test the possibility that genetic variations of human CD22 may be associated with autoimmune diseases. In this study, variation screening of the entire CD22 coding region was performed, and possible association with rheumatic diseases was tested, using the genomic DNA from 207 healthy Japanese individuals, 68 patients with systemic lupus erythematosus (SLE), and 119 patients with rheumatoid arthritis (RA). Through the variation screening, seven non-synonymous and four synonymous substitutions were identified. In addition, single base substitutions were found in two introns flanking exon-intron junctions. Among these variations, Q152E substitution within the second extracellular domain was observed with a marginally higher frequency in the patients with SLE (3/68, 4.4%) than that in healthy individuals (1/207, 0.5%) (P=0.048. SLE vs healthy individuals), although this difference was no longer significant after correction for the number of comparisons (Pc=0.62). No significant association was observed between any of the variations and RA. These findings indicate that a number of genetic variants are present in CD22, and suggest that CD22 could be considered a candidate for the susceptibility genes to autoimmune diseases.

Background Previously well-known “rheumatoid-lung” has been assumed as interstitial pneumonitis (IP). It is not so prevalent in female-majority of rheumatoid arthritis (RA) patients, but rather observed much more in male patients. We have had an impression that IP in male RA patients has a unique feature of concurrent emphysema development. Objectives To study how frequently, and which pulmonary diseases develop in male RA patients. The background and associated laboratory features were also focused on. Methods Male RA patients who visited our hospital from Jan., 2006 to Apr., 2011 are included. The similar number of female patients visited us in the same duration was included as the controls. Lung diseases were diagnosed mainly based on the medical records, XP/HRCT findings, and pulmonary function tests results. As the major disease entities, usual interstitial pneumonia (UIP), nonspecific interstitial pneumonia (NSIP), organizing pneumonia (OP), emphysema and pleuritis were intended. Brinkman Index (BI, smoking index), and serum levels of RF, KL-6 and CRP were evaluated. Results Lung diseases were observed in 27/72 (37.5%) in male and 5/70 (7.1%) in female patients. In male patients, UIP/NSIP was in 20, OP in 3, emphysema in 18, and pleuritis in 1; 12 had both IP and emphysema. In female, UIP was in 2, OP in 2, emphysema in 1, and pleuritis in 1; 1 had both IP and emphysema. The male patients with lung diseases were older than those without them (72.2±10.3 vs. 63.7±12.9 yr.), had a higher serum RF level (511±390 vs.140±141 U/mL), a higher KL-6 level (801±735 vs. 277±179 U/mL), and a higher Brinkman index. Among the cases with stable arthritis, patients with UIP/NSIP/emphysema showed a low CRP level, while those with OP/pleuritis did a high level. Conclusions Male RA patients had lung diseases at a high rate of over 30%. UIP/NSIP was observed the most, which was frequently combined with emphysema. The male RA patients having a high RF level and a high smoking index might develop UIP/NSIP and the combined emphysema with a high prevalence rate. Such patients showed a high KL-6 level but a low CRP level. Disclosure of Interest None Declared

SRPX2 (Sushi repeat-containing protein, X-linked 2) has recently emerged as a multifunctional protein that is involved in seizure disorders, angiogenesis and cellular adhesion. Here, we analyzed this protein biochemically. SRPX2 protein was secreted with a highly post-translational modification. Chondroitinase ABC treatment completely decreased the molecular mass of purified SRPX2 protein to its predicted size, whereas heparitinase, keratanase and hyaluroinidase did not. Secreted SRPX2 protein was also detected using an anti-chondroitin sulfate antibody. These results indicate that SRPX2 is a novel chondroitin sulfate proteoglycan (CSPG). Furthermore, a binding assay revealed that hepatocyte growth factor dose-dependently binds to SRPX2 protein, and a ligand–glycosaminoglycans interaction was speculated to be likely in proteoglycans. Regarding its molecular architecture, SRPX2 has sushi repeat modules similar to four other CSPGs/lecticans; however, the molecular architecture of SRPX2 seems to be quite different from that of the lecticans. Taken together, we found that SRPX2 is a novel CSPG that is overexpressed in gastrointestinal cancer cells. Our findings provide key glycobiological insight into SRPX2 in cancer cells and demonstrate that SRPX2 is a new member of the cancer-related proteoglycan family.

Reports on the efficacy of intravenous immunoglobulin (IVIG) prophylaxis againstcytomegalovirus (CMV) infection after allogeneic hematopoietic cell transplantation (HCT) have often sparked controversy. In addition, we are not aware of any study thathas examined whether prophylaxis with IVIG affects the incidence of CMV infection inpatients who are at high risk of infection; those who are elderly or have receivedHLA-mismatched HCT. In the present open-label, phase II study, we addressed thisquestion. A total of 106 patients were enrolled on the study. The cumulative incidences of CMVinfection 100 days after HCT were similar in the intervention and control groups (68 and 64%, P = .89; 89 and 87%, P = .79, respectively for older patients and those who received HLA-mismatched HCT). In those who receivedHLA-mismatched HCT, 1-year overall survival after HCT was 46% in the interventionand 40% in the control group (P = 0.31); for age >55 years, the corresponding valueswere 46 and 40% (P = 0.27). Our data show that prophylaxis with regular polyvalent IVIG did not affect theincidence of CMV infection or survival in older patients or those who receivedHLA-mismatched HCT.

A 1-year-old girl was admitted to our University Hospital with a history of fever, vomiting, left-sided hemiconvulsion, gait disturbance, and drowsiness. The cerebrospinal fluid (CSF) on the 9th day of illness revealed 157 white blood cells/mm 3 (68 % monocytes), 64 mg/dl of protein, 59 mg/dl of glucose, and 4.2 ng/ml ( < 4.0 ng/ml) of myelin basic protein. Herpes simplex virus (HSV) DNA was detected in the CSF on the 9th day by the use of polymerase chain reaction method [4]. A high Ig M titer against to HSV type I was also detected in the CSE Periodic slow and sharp wave discharges were recorded in the right fronto-temporal region on the electroencephalogram. Intravenous acyclovir was given atadoseofl0 mg/kg8 hourly for 10 days.The T2-weighted MRI on the 15th day showed increased signal intensities in the white matter of the right temporal lobe (Fig. 1 a). No HSV DNA was detected in the CSF on day 23. The patient's symptoms had resolved by day 37. T2-weighted MRI follow-up on day 71 revealed widespread involvement of the right temporal lobe (Fig. 1 b). MRI on day 92 demonstrated no progression of the lesions. A mild left hemiparesis was still present when she was discharged on day 109.

7076 Background: The responsiveness to gefitinib has been reported to closely link to the presence of EGFR gene mutations. We developed a method, PNA-LNA PCR clamp, capable of detecting EGFR mutations in the presence of 100-fold background of wild type EGFR from normal cells (Can Res. 2005;65:7276). This study was prospectively designed to evaluate 1) the sensitivity and the specificity of the PNA-LNA PCR clamp (sample size > 100 pts) and 2) a phase II study of gefitinib for NSCLC patients (pts) with EGFR gene mutations (sample size > 25 pts to show the lower limit of 95% CI > 50%). Methods: Clinical samples (sputum, pleural effusion, bronchial fluid and paraffin tissue) were obtained from consecutive NSCLC pts with informed consent in our institution, and were tested by the PNA-LNA PCR clamp. After the second informed consent, for PS 0–2, inoperable stage III and IV pts with EGFR mutations, gefitinib (250mg P.O. daily) was given as the second treatment after docetaxel containing chemotherapy. In case of poor PS pts, the first line chemotherapy was omitted. Results: From Sept. ’04 to Oct. ’05, samples from 100 of a total of 107 pts were informative of EGFR mutation status. PNA-LNA PCR clamp detected EGFR mutations in 38 pts (38%) (15 males/23 females; median age:62; adenoca.:33 pts). Exon 19 deletions, L858R and L861Q were found in 25 (66%), 12 (32%) and 1 (2%) patients, respectively. But 62 pts (51 males/11 females; median age:66; Ad:43 pts) were judged to have wild type EGFR. Between positive and negative pts in EGFR mutation, there was significant difference in the distinction of sex (p = 0.00001). Gefitinib was given to 26 pts with EGFR mutations as the first line (4 pts) or the second line treatment (22 pts). One patient and 20 patients showed CR and PRs, respectively, and the response rate was 81% (95% CI: 61–94%). For patients with wild EGFR genes, gefitinib was given to 5 patients and one patient (20%) showed PR. The response rate was significantly different between wild and mutant EGFR genes detected by the PNA-LNA PCR clamp (p = 0.017). Conclusions: PNA-LNA PCR clamp could reliably detect EGFR mutations, indicating the method is useful to detect EGFR mutations in clinical specimens. Updated data will be presented at the meeting. No significant financial relationships to disclose.

3072 Background: Gefitinib, an inhibitor of the tyrosine kinase activity of EGFR,was introduced in the treatment of advanced non-small lung cancers (NSCLC). The responsiveness to gefitinib has been...

Rationale There is increasing evidence that leukotriene receptor antagonist (LTRA) possesses anti-inflammatory effects on the airway disease of asthma. Although cysteinyl-leukotrienes (Cys LTs) by themselves regulates the development of eosinophilic inflammation, LTRA may modulate the eosinophilic response to another inflammatory molecules involved in allergic inflammation. The objective of this study is to evaluate whether pranlukast, a LTRA which has been widely used in Japan, modifies eosinophil transendothelial migration (TEM) in response to chemoattractants including C-C chemokines. Methods Eosinophils were isolated from the peripheral blood of healthy subjects and incubated in the presence or absence of pranlukast. Following the pretreatment, eosinophil TEM across human umbilical vein endothelial cells was examined by an EPO assay. Results Pranlukast did not modify the spontaneous TEM of eosinophils (P>0.1; n=5). As previously reported, the eosinophil TEM was significantly augmented by 0.1 μM LTD4 and this enhancement was blocked by 1μM pranlukast (p 0.1; n=5). Conclusions The inhibitory effect of pranlukast on eosinophil TEM is highly specific for Cys-LT1-dependent pathway and LTRA is unlikely to modulate TEM elicited by C-C chemokines. Such selectivity on eosinophil migrative response may determine the individual response to LTRA in reduction of eosinophil accumulation in the asthmatic airways.