The preoperative evaluation included small molecule library screening history taking, physical examination, voiding diary, stress and 1-h

pad tests and a comprehensive urodynamic examination. Postoperative evaluation included a stress test, 1-h pad test, and uroflowmetry with postvoid residuals. Results: After 1 year of follow up, the rates of cure and satisfaction were 93.5 and 93.0%, respectively, in the Sparc group. The rates of cure and satisfaction were 95.2 and 85.7%, respectively, in the Monarc group. After 2 years of follow up, the rates of cure (93.5 vs 92.9%) and satisfaction (84.8 vs 83.3%) were similar between the two groups. No bladder injury occurred in the Monarc group. Bladder injury occurred in 6.5% (n = 3) of the patients in the Sparc group. Vaginal wall perforation occurred in 4.8% (n = 2) of the patients in the Monarc group (P >

0.05). Late complications included de novo urge symptoms (8.7 vs 11.9%) and voiding dysfunction (10.9 vs 9.5%). Conclusions: The transobturator Monarc procedure appears to be as efficient and safe as the retropubic Sparc procedure for the treatment of SUI. “
“To evaluate the effects of chronic hyperlipidemia on bladder function, we examined the functional and histological changes of the bladder in myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHL-MI) rabbits. Two age groups of WHHL-MI rabbits (6–12 months old, young WHHL-MI rabbits; and 20–24 months old, old WHHL-MI rabbits group) and the sex- and age-matched control rabbits were prepared. PTK6 Bladder functions were evaluated using frequency volume charts selleck chemicals and cystometrograms, and functional experiments using isolated bladder specimens. Histological studies of bladder were performed with HE staining and immunohistochemical staining

with mouse monoclonal S-100 protein antibodies and sheep polyclonal calcitonin gene-related peptide (CGRP) antibodies. In cystometrograms, it has been demonstrated that WHHL-MI rabbits showed significantly shorter micturition interval, smaller voided volume with non-voiding contractions compared to control. There was no significant difference in voiding pressure between young WHHL-MI and control rabbits. However, old WHHL-MI rabbits showed a lower voiding pressure than control rabbits. The functional experiments revealed that carbachol- and electrical field stimulation (EFS)-induced contractile responses of isolated bladder strips were significantly increased in young WHHL-MI rabbits than in control rabbits. However, in the bladder strips of old WHHL-MI rabbits, decreased responses to carbachol and EFS were observed. In WHHL-MI rabbits, bladder urothelium became thinner, smooth muscle area decreased and connective tissue area increased gradually with aging. A significant decrease in S-100 protein-positive neurons, and an increased number of CGRP-positive neurons were observed in both young and old WHHL-MI rabbits.

The finding that AMPs were upregulated in colonic ECs in pIgR KO mice suggests that epithelial sensing of bacteria through microbe-associated molecular patterns are increased in mice lacking Alisertib SIgs compared with WT animals, perhaps because live bacteria or microbe-associated molecular patterns can more readily reach the epithelium. This is in agreement with the observation of enhanced epithelial invasion by Salmonella typhimurium in naïve pIgR KO mice [30]. Alternatively, the altered composition of

the intestinal microbiota in pIgR KO mice could provide qualitatively different signals to the epithelium. We found 208 genes that were differentially regulated in colonic ECs of pIgR KO and WT mice when both strains had conventional intestinal microbiota. However, when

both genotypes were treated with antibiotics, this number was reduced to 27, suggesting that most of the observed MK 2206 differences in untreated mice were driven by the endogenous microbiota. Furthermore, we identified 296 genes with more than twofold differential expression between antibiotic-treated and untreated pIgR KO mice (Fig. 1). The same comparison in WT mice revealed a substantially fewer 106 genes altered [17]. Thus, a considerably higher number of genes were regulated by the commensal microbiota in pIgR KO mice than in WT mice, suggesting that the commensals drive epithelial activation in the absence of SIg. This finding is in agreement with a recent study of jejunal responses in B cell and IgA-deficient mice as well as immunocompromised humans [31]. In the absence of B cells or IgA, ECs mounted a commensal microbiota-driven immune response at the cost of reduced metabolic function. We

observed a similar microbiota-driven enhancement of epithelial immune responses in the colon of pIgR KO mice. However, there was little overlap of genes differentially expressed in jejunum of B-cell KO mice compared with WT mice [31] with genes differentially expressed in colonic epithelium of untreated pIgR KO mice compared with WT Methocarbamol mice (this study). These differences are probably due to differences in anatomy and physiological function of the two intestinal sites. We found that several xenobiotic-metabolizing enzymes were downregulated in pIgR KO mice, in agreement with published reports that these enzymes are downregulated by the presence of intestinal bacteria [32]. We conclude that although the biological principle of enhanced epithelial defense in the absence of IgA is conserved between small and large intestine, the host expressed molecules mediating this defense differ. The fine-tuned balance between beneficial intestinal bacteria and the host is important for maintaining a healthy gut [33, 34]. Underlying causes of a perturbed host–microbiota relationship are complex.

In the total cohort, the median delay for agammaglobulinaemias from 1991 to 2010 lay between 0·8 and 1·4, and between 1·9 and 2·2 for IgG subclass deficiency. In sIgA deficiency, the median delay lay between 1 and 1·8 years. WAS had a median delay between 0·4 and 0·6 years, AT between 1·8 and 3 years, DGS between 0·2 and 0·3 years and CGD between 0·6 and 1·4 years. SCID had a very short median delay of 0·1 to 0·2 years. Details on therapy were reported for 10 091 (81·8%) of the living patients. Of these, 4555 patients (45·1%) received immunoglobulin replacement, which makes it the most frequently reported long-term medication. A total of 3332 patients (73·2%) received immunoglobulins see more intravenously, while

it was administered subcutaneously in 1217 patients (26·7%). Twelve patients (0·3%) received intramuscular immunoglobulins. Six patients received both intravenous and subcutaneous treatment, which explains why the numbers total more than 100%. The

next most frequently reported medication concerns antibiotics (both prophylactic and therapeutic), which were given in 2703 patients (26·8%). Other frequently reported medications are steroids (548 patients, 5·4%), anti-fungals (509 patients, 5%), bronchodilators (275 patients, 2·7%) PD-0332991 in vivo and immunosuppressants (271 patients, 2·7%); 809 patients (8%) had received a stem cell transplant; and 2375 patients (23·5%) had neither received a stem cell transplant nor were they receiving any long-term medication. Since we last published

data extracted from the ESID database in September 2008, the number of registered patients has almost doubled from 7430 to 13 708 patients. The distribution of patients with respect to the single PID entities has remained relatively stable since 2008. CVID continues to represent more than 20% of all registered patients. SIgA deficiency has replaced IgG subclass deficiency as the GABA Receptor second most frequent entity. This is due mainly to the fact that this disease is reported very frequently in Spain and Hungary, countries that joined the ESID database after 2008. Most individuals with sIgA deficiency are free of infections [19], but are still included in the current ESID diagnostic criteria for PID. However, many centres obviously only report patients presenting with clinical manifestations, which means that reporting of this disease is extremely skewed. The prevalence numbers we calculated also differ strongly between countries. However, with 3240 living patients documented in the heterogeneous population of France, the overall prevalence of PID will not be less than 5:100 000. In general, the prevalence and incidence numbers produced from our data collection have to be interpreted with great caution. They can be seen as an indicator towards the actual numbers that would be calculated if the documentation was 100% complete. We believe that the differences we observed between countries and periods can most probably be attributed to under-reporting.

RoVs were present throughout the year, with two peaks in March/April in the spring and in October/December in winter (Fig. 1). The objectives of this study were to investigate the prevalence and determine the G/P genotypes of RoVs isolated from patients with acute gastroenteritis in Seoul, Korea. Although sanitation conditions have improved globally, the relative

prevalence of RoV diarrhoea may still be increasing in developed countries including Ganetespib mouse Japan and Korea (7,10). In our study, 1423 fecal specimens were collected from children hospitalized with diarrhea, 269 (18.9%) of which were positive for RoVs. RoVs were the most frequently detected viral agent in stool samples from children less than three years of age presenting with acute gastroenteritis, as has been shown in previous global studies and reports from Korea (2,11,12).

RoV is the leading cause of acute gastroenteritis world wide, the incidence of RoV gastroenteritis being higher than of Norovirus gastroenteritis (2,13). Studies in Asia have demonstrated RoV in 45%–66.7% of diarrheal cases (11,14,15). In this study most of the globally common RoVs (G1, G2, G3, and G4) and other types (G8 and G9) were detected. Genotype G1 was observed to be broadly circulating in Korea, with overall incidences of  54.3%. This result is in agreement with the earlier findings that G1 was the most prevalent strain (45–81%) regardless of geographical area or season CDK inhibitor in Korea (16). Human G9 RoVs have recently been highlighted as the fifth most common strain in circulation. In this study, G9s

were infrequently identified (1%); much less than in reports from other Asian (54.8%–91.6%) and European (7.4%) countries (14,17,18). Analysis of P types indicated that P[8] was predominant, followed by P[6], P[4], P[9], and P[10]. This result is consistent with previous data that the most prevalent P type was P[8] in Korea and other countries (29,21,20). Genotype P[9] and P[10] were detected less frequently and have also been detected in previous studies in the region (11,20,23). In fact, More than 42 G/P combinations have been observed in at least one RoV case. Only a relatively small number of these combinations have been frequently reported in humans mafosfamide and genotypes G1P[8], G2P[4], G3P[8] and G4P[8] comprise nearly half of all the RoV infections in the world (7,23). In this study, G1P[8], G2P[4], and G3P[8] made up 47.6% of RoV genotypes, which suggests there were many kinds of RoV strains circulating in this region and period in Korea. Characterization of >2700 stool specimens world-wide for which both G and P types have been determined has revealed that the most prevalent strain is G1P[8], followed by strains G4P[8], G2P[4], and G3P[8][30]. G9P[8], G9P[4], G9P[9], and G9P[6] were also detected in 10.4%, 1.1%, 0.4%, and 0.4% of specimens, respectively.

09 fold vs. 0.78 ± 0.07 fold, 0.69 ± 0.01 fold; *p < 0.05 vs. 2 M) and SOD2 (1 ± 0.21 fold Small molecule library chemical structure vs. 0.73 ± 0.03 fold, 0.56 ± 0.09 fold; **p < 0.01 vs. 2 M) were decreased in 24-month-old mice. In our study, expression of Nrf2 in total protein (1 ± 0.2 fold vs. 1.02 ± 0.12 fold, 1.31 ± 0.24 fold) was not decreased in 24-month-old mice. However, Nrf2 expression in nuclear (1 ± 0.44 fold vs. 1.94 ± 0.7 fold, 1.61 ± 0.46 fold; *p < 0.05 vs. 2 M) and in nuclear/total protein ratio (1 ± 0.82 fold vs. 1.83 ± 0.6 fold, 1.08 ± 0.38 fold; *p < 0.05

vs. 2 M) were decreased with 24-month-old mice. Keap1 expression (1 ± 0.16 fold vs. 0.93 ± 0.12 fold, 1.15 ± 0.35 fold) was increased in 24-month-old mice compared with 2-, 12-month-old mice. HO-1 (1 ± 0.08 fold vs. 9.39 ± 0.81 fold, 8.87 ± 0.51 fold; **p < 0.01 vs. 2 M) and NQO-1 (1 ± 0.01 fold vs. 0.87 ± 0.19 fold, 0.93 ± 0.24 fold) were decreased in 24-month-old mice compared with 12-month-old mice, although this was not statistically significant. Conclusion: Nrf2 was decreased with aging and may relate to antioxidant pathway. Nrf2 suppression and Keap1 activation with aging could induce oxidative stress, leading to decrease in antioxidant gene expression such as HO-1 and NQO-1. Pharmacologically targeting these signaling molecules Belnacasan cost may reduce the pathologic changes of aging in the kidney. HOSOE YOSHIKO1, ASANUMA KATSUHIKO1,2, SASAKI YU1, NONAKA KANAE1,

SEKI TAKUTO1, ASAO RIN1, OLICA TREJO JUAN ALEJANDRO1, TAKAGI MIYUKI1, HIDAKA TERUO1, TANAKA ERIKO3, UENO TAKASHI4, NISHINAKAMURA RYUICHI5, TOMINO YASUHIKO1 1Division of Nephrology, Department of Internal Medicine, Juntendo

University Faculty of Medicine; 2Laboratory for Kidney Research (TMK project), Medical Innovation Center, Kyoto University Graduate School of Medicine; 3Department of Pediatrics, Tokyo Medical and Dental University; 4Laboratory of Proteomics and Medical Science, Research Support Center, Juntendo University Faculty of Medicine; 5Department of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan Introduction: It has been reported that Sall1 homozygous knockout mice died within 24 hours after birth with kidney agenesis or severe dysgenesis. Loss of Sall1 leads to a failure of metanephros Fossariinae development. We have already reported on ADR injected mice as nephrosis and glomerulosclerosis model. To elucidate the role of Sall1 in the injured podocytes, we used adriamycin (ADR) induced nephrosis and glomerulosclerosis model in podocyte specific Sall1 knockout (pSall1 KO) mice. Methods: Sall1 floxed mice were crossed with Podocin Cre mice to generate pSall1 KO mice. ADR was injected to both groups of Wild-type (WT) and pSall1 KO mice for inducing podocyte injury.To further examine the role of Sall1 in podocytes, we created a stable cell line of Sall1 knockdown (KD) podocytes.

The present work presents evidence that a progressively growing, endogenous tumor indeed fails to activate NK-cell effector functions. Escape from NK-cell surveillance seems

to be more complex than the hypothesis of failing priming or failing triggering might suggest. Possibly, NK cells are exhausted as a consequence of prolonged activation, as it was described for T cells 44. Alternately, developing tumors might actively paralyze NK cells. These observations should be considered when establishing, e.g. approaches BTK inhibitor library of adoptive NK-cell transfer. All cell lines were cultured in RPMI 1640 (Invitrogen, Karlsruhe, Germany) medium supplemented with 5% heat-inactivated FBS, 2 mM L-Glutamine, 100 U/mL penicillin and streptomycin, non essential aa, and 50 μM 2-ME. Cells were kept

at 37°C in a humidified 5% CO2 atmosphere. A20 and MPC11 are BALB/c-derived B-cell lymphoma cell lines 45, 46. The variant A20low expressing reduced levels of MHC class I was generated by transfection of A20 with an mCMV-derived gene 6. The murine lymphoma cell line YAC-1 served as a target for NK-cell killing in cytotoxicity assays 47. DC were generated exactly as previously described 22. λ-myc cell lines myc-B, myc-E and 291S were generated by seeding primary lymphoma cells from λ-myc mice on irradiated MRC-5 fibroblasts as a feeding layer. After about 2 wk of culture, cells were able Epigenetics Compound Library manufacturer to grow independently. All animals were kept under specific pathogen-free conditions in our animal facility. C57BL/6 and BALB/c WT mice were purchased from Bommice (Ry, Denmark). λ-myc mice 29 are of C57BL/6 origin and were bred in our own facility. All animal experiments were in accordance with relevant regulations and had been approved by the Regierung von Oberbayern. Groups of at least six age-matched mice were used for experiments. Animals were treated with 10 nMol

CpG-ODN 1668 (Metabion, Martinsried, Germany) that was injected i.p. in 1- to 2-wk intervals 6 or received 5×105 DC subcutaneously as described earlier 22. NK-cell depletion was done by using anti-asialo GM1 Ab (Wako, Neuβ, Germany). 100–300 μL were administered i.v. and i.p. 1 day before each CpG-ODN injection pheromone in λ-myc mice; 300 μL were given i.p. 1 day before as well as 2 and 9 days after challenge with myc-B tumor cells in WT mice. NKT cells were not affected by treatment with anti-asialo GM1. In total, 104 to 105 myc-B, myc-E, 291S or MPC11 cells or 106 A20 or A20low cells were injected i.v. Phenotyping of NK cells was done by labeling with the following mAb: CD49b (DX5, BD Pharmingen, Heidelberg, Germany), CD45R (RA3-6B2, BD Pharmingen), NKG2D (CX5, eBioscience, San Diego, USA), Ly49D (4E5, BD Pharmingen), Ly49I (YLI-90, BD Pharmingen), CD69 (H1.

Another model to be considered is for the development of a small number of Units such as this described above, to become so-called ‘Centres of Excellence’

– probably a better term would be ‘RSC training centres’. In this way, existing staff in a Renal Unit could spend time in one of these centres to learn about management of patients on a non-dialysis Renal Supportive learn more Care programme and take that knowledge back with them to their Unit. In such cases it is likely that a Renal Supportive Care CNC position would still be required in each large Renal Unit to ensure the success of such a programme. Other models will undoubtedly be developed and will be successful. The importance is that whatever model is used the focus should be on ensuring optimum nephrology care while adding a focus on symptom control, holistic physical and spiritual care and, when appropriate, the facilitation of a ‘good deaths’, all of this underpinned by assessment of service performance as outlined above. A Katalin Urban Resuscitation status and Advance Care Plans need to be discussed and clearly documented The Liverpool Care Pathway is a recognized model of end-of-life (EOL) care, and has been adapted for patients with end-stage renal disease Recognition of a dying patient allows initiation of a multidisciplinary EOL pathway such as the Liverpool Care Pathway

for hospital inpatients, and for support for families Selleckchem BGJ398 if a home death is planned. A fall in performance status is an indicator of decline. End-stage kidney disease (ESKD) is associated with high levels of morbidity and poor prognosis. Despite this, end

of life care for these patients is variable. An essential part of caring for these patients (especially on the conservative management pathway) should include ensuring a good death. End of life care incorporates four key domains of care, physical, psychological, social and spiritual (Table 1) and supports the family at that time and into bereavement. The Liverpool Care Pathway (LCP) was developed for patients dying of terminal cancer (mainly in the acute hospital setting – Uroporphyrinogen III synthase although also transferable to the community) and has been shown to be transferable to patients dying from cerebrovascular accident or heart failure.[1] The LCP is an integrated care pathway designed for the care of patients who are in the last days/hours of their life, to facilitate effective planning and provision of care during this critical time. The challenge is to ensure best practice in end of life care in the renal failure setting. In the UK, a Steering Group was set up to determine if the LCP was transferable to patients with chronic kidney disease (CKD), and a Renal LCP document was formulated with prescribing guidelines.

CNVs are frequent in higher eukaryotes and associated with a substantial portion of inherited and acquired risk for various human diseases. CNVs are distributed widely in the genomes of apparently healthy individuals and thus constitute significant amounts of population-based genomic variation. Human CNV loci are Proteases inhibitor enriched for immune genes and one of the most striking examples of CNV in humans involves a genomic region containing the chemokine genes CCL3L and CCL4L. The CCL3L–CCL4L copy number

variable region (CNVR) shows extensive architectural complexity, with smaller CNVs within the larger ones and with interindividual variation in breakpoints. Furthermore, the individual genes embedded in this CNVR account for an additional level of genetic and mRNA complexity: CCL4L1 and www.selleckchem.com/products/epz-6438.html CCL4L2 have identical exonic sequences but produce a different pattern of mRNAs. CCL3L2 was considered previously as a CCL3L1 pseudogene, but is actually transcribed. Since 2005, CCL3L-CCL4L CNV has been associated extensively with various human immunodeficiency virus-related outcomes, but some recent studies called these associations into question. This controversy may be due

in part to the differences in alternative methods for quantifying gene copy number and differentiating the individual genes. This review summarizes and discusses the current knowledge about CCL3L–CCL4L CNV and points out that elucidating their complete phenotypic impact requires dissecting Y-27632 2HCl the combinatorial genomic complexity posed by various proportions of distinct CCL3L and CCL4L genes among individuals. In the last decade, many studies showed

that a major component of the differences between individuals is variation in the copy number of segments of the genome [copy number variation (CNV) or copy number polymorphism (CNP)]. CNVs are distributed widely in the genomes of healthy individuals and thus constitute significant amounts of population-based genomic variation [1–7]. CNV seems to be at least as important as single nucleotide polymorphisms (SNPs) in determining the differences between individual humans [8]. CNV also seems to be a major driving force in evolution, especially in the rapid evolution that has occurred, and continues to occur, within the human and great ape lineage. Compared with other mammals, the genomes of humans and other primates show an enrichment of CNVs. Primate lineage-specific gene CNV studies reveal that almost one-third of all human genes exhibit a copy-number change in one or more primate species [9–12]. To date, almost 58 000 human CNVs from approximately 14 500 regions (CNVRs) have been identified (data from Database of Genomic Variants, http://projects.tcag.ca/variation/). These CNVRs may cover 5–15% of the human genome and encompass hundreds of genes [4,13], and their abundance underscores their substantial contribution to genetic variation and genome evolution [14].

[12] In contrast, a randomised phase III study evaluating granulocyte transfusions in neutropaenic cancer patients with febrile neutropaenia

and pulmonary or soft-tissue infiltrates after conventional or high-dose chemotherapy demonstrated no impact on the course and outcome of infection.[13] Unfortunately, no sub-analyses are available for patients suffering from mucormycosis, which is most likely due to the low number of patients included with these infections. Beside neutrophils, lymphocytes, in particular CD4+ T cells, may also provide critical defence mechanisms against mucormycosis (Fig. 2). This hypothesis is supported by the clinical this website observation that mucormycoses often occur several months after allogeneic HSCT, at a time, when neutropaenia and mucositis have already resolved, but adaptive immune responses are still hampered. A recent study reported that the median time of diagnosis of mucormycosis was 173 days (range, 7–2254) after transplantation; this time frame is comparable to the findings in invasive aspergillosis, which occurs at a median of 82 days (3–6542) after allogeneic HSCT.[14]

Notably, allogeneic HSCT transplant recipients have a low number of anti-Aspergillus TH1 cells for months after transplantation,[15] and it has been demonstrated that TH1-biased immunity correlates with protection and a better outcome in invasive aspergillosis.[16] These observations formed the rationale of transferring functionally active Aspergillus-specific HIF-1 pathway TH1 cells to allogeneic HSCT recipients at high-risk for or suffering from invasive

aspergillosis. In fact, a proof of principle study in 10 patients after haploidentical HSCT with evidence of invasive aspergillosis demonstrated that transfusion of anti-Aspergillus TH1 cells resulted in a clinical benefit.[17] In patients receiving adoptive immunotherapy, galactomannan as a surrogate marker for the invasive fungal disease cAMP decreased significantly earlier as compared to patients not receiving immunotherapy, and only one of 10 patients receiving immunotherapy died as compared to six of the 13 controls. This observation might be transferred to invasive mucormycosis and suggests that the reconstitution of the cellular immunity by the administration of donor-derived antifungal-TH1 cells against mucormycetes could improve the prognosis of allogeneic HSCT recipients suffering from mucormycosis. Our in vitro studies showed that in all healthy individuals tested, a cellular immune response against Rhizopus oryzae could be detected.[18] These interferon (IFN)-γ producing T cells could be enriched and cultivated, and according to the phenotype and cytokine secretion upon restimulation with R.

Morning fasting blood samples were taken from all the BP patients and the 20 normal subjects in vacutainer tubes (Beckton & Dickinson, Rutherford, NJ, USA) by means of the clean puncture of an antecubital vein with minimal stasis, using sodium citrate 3·8% as anti-coagulant. The samples were centrifuged at 2000 g at 4°C to obtain plasma, which was then divided into aliquots, frozen and stored at −80°C until testing. Plasminogen activator inhibitor type 1 (PAI-1) antigen was measured using a commercially available ELISA (Innotest

PAI-1; Byk Gulden, Konstanz, Germany). The intra- and interassay coefficients of variation (CVs) were, respectively, 8 and 13%. PAI-1 activity was measured using a commercially available bioimmunoassay (Zymutest PAI-1 activity; Hyphen BioMed, Neuville-sur-Oise, France) with intra- and interassay CVs of 3·5 and 5·6%. TAFI antigen was measured using a commercially available ELISA (Zymutest TAFI antigen; Hyphen BioMed) with intra- PD0325901 supplier and interassay CVs of 7 and 14%. t-PA antigen was measured using a commercially available ELISA (Imunolyse tPA; Biopool, Umea, Sweden), in accordance with the manufacturer’s instructions. The intra- and interassay CVs were, respectively, 6·5 and 8%. d-dimer levels were measured by means of an ELISA (Zymutest d-dimer; Hyphen BioMed), in accordance with the manufacturer’s instructions. The intra- and inter-assay CVs were, respectively,

this website find more 10 and 15%. Prothrombin fragment F1+2 levels were measured using a sandwich ELISA (Enzygnost F1+2; Behring Diagnostic GmbH, Frankfurt, Germany), with intra- and interassay CVs of, respectively, 5 and 8%. CRP was measured by means of an ELISA (Zymutest CRP; Hyphen BioMed, Andresy, France) with intra-

and inter-assay coefficients of variation (CVs) of 7–11%. As the data were positively skewed, they were log-transformed before analysis and are given as the anti-log values of the mean values and standard deviations (SDs). Student’s t-test for unpaired data was used to assess the statistical significance of the differences between the normal controls and the patients with active BP. The effect of treatment was analysed using Student’s t-test for paired samples. Correlations were assessed by means of least-square linear regression. The significance level was set at P < 0·05. Data were analysed using the spss PC statistical package, version 17·00 (SPSS Inc., Chicago, IL, USA). Figure 1 shows that PAI-1 antigen and active PAI-1 levels were significantly higher in the 20 BP patients with active disease (25·06 ± 8·88 ng/ml and 15·65 ± 5·75 ng/ml) than in the 20 healthy controls (10·04 ± 7·80 ng/ml and 7·25 ± 5·49 ng/ml) (P = 0·0001 for both). Figure 2 shows that plasma t-PA levels were also significantly higher in the patients (34·70 ± 33·22 ng/ml versus 6·60 ± 6·78 ng/ml; P = 0·0001), whereas there was no significant between-group difference in TAFI levels (91·58 ± 23·93% versus 92·73 ± 20·61%). As shown in Fig.