Initial sessions were done for 2 to3 hours daily for 3 days with 2.5 to 3 liters of ultra filtration daily. First two to three sessions Daporinad mouse were done as inpatient and subsequently as outpatients. Results: Around 7 to 10 liter of ascitic fluid was ultra filtered during first two to three sessions. At time of discharge body weight of these patients were reduced by 7 to 8 kg and diuretics were stopped after initiation of AURT. All these patients showed improved quality of life and renal function and first patient also showed improved S. albumin level. Conclusion: We conclude that AURT is safe alternative to repeated paracentesis with albumin infusion. AOKI TATSUYA, IO HIROAKI, NAKATA JUNICHIRO, YANAGAWA HIROYUKI,

KANDA REO, WAKABAYASHI KEIICHI, HAMADA CHIEKO, HORIKOSHI SATOSHI, TOMINO YASUHIKO Division of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine Introduction: Abdominal hernia is serious complication of the peritoneal dialysis (PD) patients. The objective of this study is to

analyze the clinical characteristics of abdominal hernia in PD patients. Methods: We retrospectively evaluated 79 patients (male 61, female 18) who initiated PD in the Juntendo University Hospital from January 2003 to December 2012. Results: Eight out of 79 patients (10.1%: inguinal hernia 7, diaphragmatic hernia 1) which developed abdominal hernia were men. The age was 48.0 ± 16.6 years old at the time of appearance of the abdominal hernia. The PD vintage (onset time) was 16.0 ± 13.5 months. buy Selumetinib Four patients were CAPD and 4 patients were APD. The mean of fluid volume was 1,837 ± 232.6 ml. All patients had hernial radical operation. It was a hernioplasty using mesh for inguinal hernia Amisulpride in 7 patients. We performed thoracoscopic repair in 1 patient for diaphragmatic hernia. All patients were able to restart the PD postoperatively, inguinal hernia patients were not relapsed during the follow-up. However, the diaphragmatic hernia patient was complicated plueroperitoneal communication

1 month after the operation. There was no significant difference in the fluid volume between patients with hernia and those without hernia. However, patients with hernia had tended to more fluid volume than without hernia. The systolic blood pressure of patients with hernia was significantly lower than without hernia at the initiation of PD (p < 0.01). The nPCR levels in patients with hernia were significantly lower than those without hernia (p < 0.05). Area under the curve (AUC) of Receiver Operatorating Characteristic (ROC) curve was high in order of systolic blood pressure, nPCR, fluid volume / body surface area. Conclusion: The complication of abdominal hernia was developed within 2 years from PD induction. History of steroid therapy, hypotension and low nPCR level at the initiation of PD were needed to observe carefully in such patients.

; 2Department of Hospital and Health Care Administration, Chia Nan University of Pharmacy and Science, Tainan, Taiwan; 3Departments of Anesthesiology, Chi-Mei Medical Center, Tainan, Taiwan.; 4Departments of Nephrology, Chi-Mei Medical Center, Tainan, Taiwan.; 5Department of Health Care Management, National Taipei University of Nursing and Health Sciences, Taiwan Introduction: We explored the relationship between

hospital/surgeon volume and postoperative severe sepsis/graft-failure and mortality. Methods: The Taiwan National Health Insurance Research Database claims data for all patients with end-stage renal disease patients who underwent kidney transplantation between mTOR inhibitor January 1, 1999, and December 31, 2007, were reviewed. Surgeons and hospitals were categorized

into two groups based on their patient volume. The two primary outcomes were severe sepsis and graft failure/mortality. The unconditional logistical regressions were done to compute Small molecule library mouse the odds ratios (OR) of outcomes after adjusting for possible confounding factors. Kaplan-Meier analysis was used to calculate the cumulative survival rates of graft failure/death after kidney transplantation during follow-up (1999–2008). Results: The risk of developing severe sepsis in a hospital in which surgeons do few renal transplantations was significant (odds ratio [OR]; p = 0.0115): 1.65 times higher than for a hospital in which surgeons do many. The same trend was true for hospitals with a low volume of renal transplantations (OR = 2.39; p < 0.0001). The likelihood of a graft failure within one year for the low-volume surgeon group was 3.1 times higher than for the high-volume surgeon group (p < 0.0001); the trends were similar for hospital

volume as well. Female patients had a lower risk than did male patients, and patients 55 years old or older, as well as those with a higher Charlson comorbidity index score, had a higher risk of severe sepsis. Conclusion: We conclude that the likelihood of severe sepsis and graft failure/mortality is higher for patients treated in hospitals and by surgeons with a low volume of renal transplantations. Therefore, Isotretinoin we hypothesize that defining and exporting best practices through educational outreach, and, if necessary, regulation, must be part of the health policy. AGARWAL LALIT KUMAR Dr Lalit Kumar Agarwal Introduction: BK virus (BKV) is one of the most common viral pathogens affecting kidney allografts. Indian data indicates an incidence of ∼9% for BKV infection. BKV nephropathy (BKVN) is an important complication of renal transplantation with a reported incidence between 1% and 10% in different parts of the world. To determine associated factors, and outcome of BKV in our kidney transplant population in order to improve identification and management. Methods: Kidney transplants from 2008 to 2012 were retrospectively reviewed.

The activation and inhibition of TCR signaling by costimulation with particular molecules for each consequence have been extensively

studied in T-cell proliferation [[27, 28]]. Therefore, we postulated that the concentration-dependent functional transition by the same ligand would be suitable for the delicate tuning of immune responses according to the intensity of signals from the immunological microenvironment. In this study, the modulatory effects of ephrin-Bs on TCR-mediated activation of murine primary T cells were carefully evaluated. The results revealed certain ephrin-Bs/EphBs as a novel class of costimulatory molecules with a unique action: concentration-dependent switching from costimulation to inhibition. To elucidate the details

of the regulation of primary T-cell function by EphB/ephrin-B Selleck Bortezomib system, 3H-thymidine uptake assay was performed. Interestingly, solid phase ephrin-B1 and ephrin-B2 ligands exhibited unique biphasic effects in T-cell proliferation by the suboptimal solid phase anti-CD3 stimulation: stimulatory effect at lower concentration and inversely suppressive effect at higher concentration (Fig. 1A). On the other hand, ephrin-B3 costimulation showed simply promotional effect as previously reported selleck chemical [[18]]. These unique modulation patterns were background independent (C57BL/6: Fig. 1A, Icr mix: Fig. 1B) and conserved even by the more intense TCR signaling with higher anti-CD3 concentration (Supporting Information Fig. 1). The magnitude of response to the anti-CD3 stimulation depended on the genetic background of mice employed in each experiment. The level of peak promotional effects by each ephrin-B (ephrin-B1/B2: at 2.5–5 μg/mL, ephrin-B3: at 20 μg/mL) were comparable with those by optimal anti-CD28 addition (10 μg/mL) (Fig. 1B). The cytokine production by T cells in this culture system was also assessed. After 48 h incubation, the concentrations of TNF-α, IL-2,

and IFN-γ in culture supernatants were similar to the pattern of T-cell proliferation (Fig. 2). On the other hand, secretion of IL-4 Dolichyl-phosphate-mannose-protein mannosyltransferase was very low and not altered by different ephrin-B-Fc, and IL-5 was under detectable level in all wells. Collectively, the functional consequence of T-cell activation was confirmed to be uniquely modulated by each ephrin-B ligand in cooperation with TCR stimulation. According to the binding studies, EphA receptors bind to ephrin-As and EphB receptors bind to ephrin-Bs [[29]], although some exceptions have been found [[30]], such as, (i) EphA4 binds to ephrin-B2 and ephrin-B3, as well as ephrin-A ligands [[31, 32]] and (ii) EphB2 interacts with ephrin-A5 in addition to ephrin-B ligands [[33]].

4b, upper panel). By BMN 673 supplier contrast, Ku70 staining was faint and nuclear staining was nearly undetectable in CD40L/IL-4-stimulated B cells (Fig. 4b, lower panel), a finding that coincided with the absence of proliferation

(Fig. 1b) and B-cell blast formation under these stimulatory conditions.[17] Full-blown proliferative responses as observed with CpG ODN stimulation might, therefore favour nuclear translocation of Ku70/80, but do not seem to be a prerequisite for RAG re-expression, because RAG-1 was detectable in CD40L/IL-4-stimulated B cells, whereas BCR stimulation failed to trigger RAG-1 expression (Fig. 2d). Having confirmed these molecular prerequisites for receptor revision we sought functional evidence for RAG activity. We postulated that re-expression of RAG in peripheral B cells enables Igκ/Igλ rearrangement in response to TLR9 ligation. To prove this hypothesis we purified Igκ+ B cells, and compared Igκ/Igλ expression in B cells stimulated with CpGPTO or CD40L/rhIL-4,

two stimuli that result in comparable cellular survival and autocrine find more IL-6 but that differ in the extent of proliferation. Despite the absence of Igλ+ cells in sorted Igκ+ B cells (Fig. 5a), unstimulated and CD40L/rhIL-4-stimulated B cells, a small population of Igκ-negative Igλ+ B cells became detectable after TLR9 stimulation for 4–6 days (Fig. 5b). Moreover, co-expression of Igκ and Igλ on a subset of B cells (Fig. 5b) was interpreted as indicative for ongoing Igκ/Igλ rearrangement. Staining with the isotype control proved the specificity of the anti-Igλ staining (Fig. 5c). Importantly, the low frequency of the evolving Igλ+ population (Fig. 5b), e.g. for CpGPTO: 0·4 ± 0·2% (n = 6) and for CD40L/IL4: 0·03 ± 0·04% (n = 4) makes Igκ/Igλ rearrangement a rare event, a finding that is compatible with the overall low expression of TLR9-induced RAG-1 and selective accumulation of RAG-1 and Ku70 in a small B-cell subfraction. Taken together, these results provided the notion cAMP that stimulation with TLR9-active ODN triggers RAG re-expression and consecutively catalyses LC rearrangements in a subfraction of B cells, so proving functional

integrity of TLR9-induced RAG proteins in these cells. The current understanding of receptor editing and revision implies that these processes must be initiated by binding of an autoantigen to the BCR. Of note, earlier reports described binding of CpGPTO to the BCR,[22] which raised the notion that CpGPTO could act as unselective BCR stimuli or might even mimic autoantigens. In a previous report we further demonstrated that stimulation of TLR9 with PTO-modified ODN selects IgM+ B cells for proliferation and differentiation.[17] As depicted in Fig. 6(a), CpGPTO-induced B-cell blasts originate from IgM+ CD27+ B cells because blast formation in response to CpGPTO is restricted to CD27+ and IgM+ B-cell fractions and is absent in CD27− and IgM− (class switched) B-cell fractions.

The c.14524G>A change in

exon 101 resulted in a p.Val4842Met substitution that mapped to the M8 trans-membrane fragment of the Ca2+ pore domain [27]. RyR1 expression analysis did not show truncated proteins but instead a major decrease of the mature protein, indicating the residual presence of a low amount (15 ± 8%) of mutated Met4842 Crizotinib cell line protein in the proband’s muscle (Figure 6). Patient 2 was p.[Thr4709Met] + p.[Glu4181Lys] compound heterozygous. The paternal p.Thr4709Met substitution, resulting from a c.14126C>T change in exon 96 that affected a conserved threonyl residue located in the Ca2+ pore domain of the protein, has been previously reported in a case of recessive core myopathy [28]. The maternal p.Glu4181Lys novel substitution that resulted from a c.12541G>A transition in exon 90,

affected a highly conserved glutamyl residue located in a cytoplasmic domain of unknown function (Table 2). Patient 3 was compound heterozygous for the novel p.[Glu4911Lys] and p.[Arg2336Cys] variants. The paternal p.Glu4911Lys (c.14731G>A, exon 102) variant affected selleck compound a highly conserved glutamyl residue that mapped to the M10 trans-membrane fragment of the Ca2+ pore domain [27]. The maternal p.Arg2336Cys (c.7006C>T, exon 43) variant also substituted a very well-conserved arginyl residue located in the MH2 domain of the protein, usually associated with malignant hyperthermia dominant mutations. However, no anaesthetic history has been reported in the patient or relatives harbouring the p.Arg2336Cys variant (Table 2). Patient 4 was p.[Pro3202Leu] + p.[Gly3521Cys] compound heterozygous. Both variants are novel and substituted highly conserved residues among species and RYR isoforms. Ixazomib concentration The paternal p.Pro3202Leu (c.9605C>T, exon 65) variant affected

a prolyl residue located in a central region of the protein of unknown function. The maternal p.Gly3521Cys (c.10561G>T) variant substituted a glycyl residue located within exon 71 adjacent to the alternatively spliced region I (ASI), possibly involved in interdomain interaction (Table 2) [29]. Patient 5 was p.[Pro3138Leu] + p.[Arg3772Trp] compound heterozygous. The paternal p.Pro3138Leu (c.9413C>T) variant affected a highly conserved prolyl residue that mapped to exon 63. This variant has not been reported previously. The maternal p.Arg3772Trp (c.11314C>T, exon 79) variant has been recently reported in an MHS patient [30]. The mutation substituted a highly conserved argininyl residue into a nonconservative tryptophan located in a cytoplasmic domain of unknown function (Table 2). Analysis of patient 6′s cDNA revealed the presence of two abnormal transcripts characterized by insertions of 132 bp and 32 bp between exons 56 and 57, and the presence of a normally spliced transcript. Genomic sequencing of intron 56 identified a homozygous c.

The authors concluded that the meta-analysis suggests that combined ACEi + ARB reduces 24 h proteinuria to a greater extent than ACEi alone and that this benefit is associated with small effects on GFR. However, analysis also concludes that the available studies were heterogeneous and mostly of short duration

(only one study greater than 12 weeks) and the few longer term studies have not demonstrated a benefit. Hamilton et al.78 conducted a meta-analysis of RCTs evaluating the efficacy of ACEi in the treatment of nephropathy in individuals with type 2 diabetes. Specifically the meta-analysis addressed the reduction in albuminuria or proteinuria and thus included only those studies that provided either geometric or arithmetic means of albuminuria. Studies reporting geometric means and arithmetic means were analysed Selleckchem Dabrafenib separately. The results of the click here meta-analysis indicated that treatment with ACEi produced significant reductions in albuminuria in people with type 2 diabetes in studies where geometric

means were used to normalize data but less clear where data is reported as arithmetic means (presumed to reflect the skewing of the albuminuria data). While studies were stratified on the basis of the degree of albuminuria and study duration, no distinction between normotensive or hypertensive patients have been made. Studies with ARB’s in people with type 2 diabetes and overt kidney disease have shown that angiotensin receptor blockade with irbesartan attenuates the rate of doubling of serum creatinine by 20–30% over 2.7 years Carbohydrate when compared with placebo or amlodipine, used in equihypotensive doses.19 A study of angiotensin receptor blockade with irbesartan in hypertensive, microalbuminuric people with type 2 diabetes showed a 70% decrease in AER over 2 years.72 However, preservation of GFR over and above the effects of BP lowering was not demonstrated in this relatively short-term study. The ADVANCE study is a multinational randomized control trial undertaken

by 215 centres across 20 countries which, in addition to intensive blood glucose treatment, included a BP treatment study arm.67 Participants were randomized to either fixed combined perindopril indapamide or placebo. Additional antihypertensive agents were allowed for both groups as required with the exception that thiazide diuretics were not allowed and the only open labelled ACEi allowed was perindopril to a maximum dose of 4 mg a day thereby ensuring that the active treatment group did not exceed the maximum recommended dose. The active treatment resulted in a mean reduction after 4.3 years (median) in SBP and DBP of 5.6 and 2.2 mm Hg, respectively, compared with placebo. The relative risk of a major microvascular event was 7.9% in the active treatment group compared with 8.6% in the placebo group, however, this was not significant.

We saw no significant decline in PUFA levels related to immunization or challenge in the DTH model, except for arachidonic acid in the control group, even though footpad swelling in individual animals

correlated positively with reductions in serum EPA levels during the challenge phase. Evidently, the Th1-mediated inflammation did not consume the same amounts of fatty acids as the Th2-mediated inflammation. This could be explained by the difference in the size of the organs assessed in the two models – paws in the DTH model compared with the entire respiratory system in the airway model. Another possibility is that Th2-driven inflammation consumes large amounts of fatty acids because eosinophils are versatile producers of products from unsaturated fatty acids [24]. Further, we observed a reduction of Proteasome purification PUFA levels concomitant with immunization with a Th2-promoting adjuvant (alum), but not alongside Trichostatin A in vivo immunization with a Th1-promoting adjuvant (Freund’s complete adjuvant). Th1 immunity was actually accomplished by an increase in serum arachidonic acid and DHA levels after immunization. The consumption of PUFAs during the Th2- but not the Th1-sensitization phase opens

the possibility that lipid mediators formed from PUFAs participate in producing the outcome of the interaction between the antigen-presenting cell and the naive T cell, in a way leading to Th2 cell maturation. The mechanisms can only be speculated upon and need further investigation. PUFAs affect gene transcription factors [25], production of prostaglandins and related mediators and affect thrombocyte activation and coagulation, processes that are linked intimately to inflammation these and immunity [26]. In conclusion, our results demonstrate clearly the complexity of the immunomodulatory effects of PUFAs and point to the importance of a clear definition of the type of immune reaction involved before testing PUFA supplementation as a preventive or disease-modulatory treatment. PUFA supplementation could probably be of significance to patients suffering from Th1-mediated

food allergies. However, at present we cannot draw conclusions concerning effects of PUFA supplementation on patients suffering from allergies that are complex mixtures of Th1 and Th2 immune reactions. This work was supported by the Swedish Research Council for Environmental, Agricultural Sciences and Spatial Planning (FORMAS), Food and Health Concept Center, Swedish Nutrition Foundation and Swedish Research Council, Gothenburg, Sweden. The authors declare no financial or commercial conflicts of interest. “
“Department of Clinical Research, Hamdard University, New Delhi, India In T-cell-mediated autoimmune diseases of the CNS, apoptosis of Fas+ T cells by FasL contributes to resolution of disease. However, the apoptosis-inducing cell population still remains to be identified.

However, in autoimmune-prone individuals these control mechanisms can fail and autoimmune disease ensues. As autoimmune diseases BI 6727 supplier progress, intra- and inter-molecular determinant spreading occurs 1 and populations

of effector and memory T cells become established. Therefore, unlike strategies directed at preventing the development of autoimmune disease, where induction of tolerance in naïve T cells may be all that is required, therapies aimed at terminating ongoing autoimmune disease must be capable of inactivating established populations of memory or activated effector T cells. Although naïve T cells are highly dependent on the presence or absence of costimulatory AZD1152-HQPA molecular weight signals to determine the outcome of activation, costimulation appears to play little role in controlling the responses of memory and

effector T cells 2, 3 and these cells are considered costimulation independent. Because of this, in contrast to naïve T cells which are readily deleted or inactivated in the absence of costimulation memory T cells are widely regarded as potentially resistant to tolerance induction. If this were indeed the case, then effector and memory T cells represent a significant hurdle to therapeutic strategies aimed at treating autoimmune diseases. However, we have recently shown that memory and effector CD8+ T cells are susceptible to tolerance induction when cognate antigen is expressed in DC and other APC types 4. The relative roles of CD4+ and CD8+ Calpain T cells in disease progression differ depending on the autoimmune disease but in some diseases, exemplified by autoimmune diabetes, both cells types appear to play

key roles 5. Although CD8+ T cells are primarily considered to play a role as effectors of target cell killing, they may also be important in disease establishment 6, 7. CD4+ T cells, on the other hand, contribute to autoimmune and inflammatory diseases in a wide variety of ways. Effector CD4+ T cells produce molecules that promote local inflammatory reactions or act to kill target cells either directly or by “licensing” intermediate cell types 8. In addition to their direct effector functions, CD4+ T cells also act as key regulators of adaptive immunity by, for instance, providing help to CD8+ T cells and B cells. Indeed, evidence suggests that CD8+ T-cell immunity or tolerance is directly regulated by the presence or absence of CD4+ T-cell help 9–11. Therefore, understanding how to control or inactivate established populations of memory and effector CD4+ T-cells is a key requirement for therapeutic approaches to established autoimmune and inflammatory diseases. Here, we describe studies in which we use an adoptive transfer system to investigate whether the expression of cognate antigen in steady-state DC silences memory CD4+ T cells.

We thank Professor Caroline Sabin and Doctor Pedro Coutinho for support in statistical analysis. We are also grateful to all the blood donors who took part AZD1208 in this study. The authors declare no financial conflicts of interest. Figure S1. High frequency

of cytomegalovirus (CMV) – specific CD4+ T cells. Peripheral blood mononuclear cells were stimulated with CMV, Epstein–Barr virus (EBV), herpes simplex virus (HSV), varicella zoster virus (VZV) or purified protein derivative (PPD) lysate and the percentage of interferon-γ (IFN-γ) secreting antigen-specific CD4+ T cells was assessed by flow cytometry (a). The frequency of CD4+ T cells that were specific for CMV, EBV, HSV, VZV or PPD was determined in individuals who were seropositive for these agents (b). Only responses >0.02% above background (unstimulated cells) were considered positive. Horizontal lines depict median values. Significantly increased frequency of CMV specific CD4+ T cells relative to the other antigens is indicated (Wilcoxon rank test, GraphPad Prism). Figure S2. Multiparameter flow cytometric analysis. Cytoskeletal Signaling inhibitor Representative dot plots from

one donor show the distribution of stimulated CD4 T cells within each CD45RA/CD27 subset. Panels show CD4 plotted against: CD40 ligand (CD40L; upper right), interferon-γ (IFN-γ; upper left), interleukin-2 (IL-2; lower right) and tumour necrosis factor-α (TNF-α; lower left), each for unstimulated and anti-CD3 stimulated T cells. Figure S3. Cell recovery. Purified CD45RA/CD27 CD4+ T-cell subsets were activated with anti-CD3

and irradiated antigen-presenting cells and irradiated antigen-presenting cells. At the indicated time-points, the cell number was determined on a haemocytometer. Results are expressed as a percentage of the initial number of cells placed in culture; results for one donor are shown. (b,c) Apoptosis was assessed by Annexin V staining and propidium iodide (PI) incorporation. The percentage of early apoptotic (Annexin V+ PI–) and late apoptotic/necrotic (Annexin V+ PI+) cells was assessed in the indicated days. Representative pseudocolour plots are 17-DMAG (Alvespimycin) HCl shown (b). Figure S4. CD4+ CD45RA– CD27+ cells were purified by FACS sorting and analysed for the expression of CD45RA and CD45RO before culture. Cells were stimulated with interleukin-2 (IL-2) or IL-15 and CD45RA/CD45RO expression was assessed by flow cytometry at the indicated time-points. The results shown are representative of four experiments. Figure S5. CD4+ CD45RA– CD27– cells were purified by FACS sorting and analysed for the expression of CD45RA and CD45RO before culture. Cells were stimulated with interleukin-7 (IL-7), IL-2 or IL-15 and CD45RA/CD45RO expression was assessed by flow cytometry at the indicated time-points. The results shown are representative of three experiments. Figure S6. CD4+ CD45RA– CD27+ cells were purified by FACS sorting.

In addition, as specific IgE antibodies to helminths

persist for a long time (153), serology allows the identification of previous contacts with Ascaris, even in egg-negative adolescents and adults; yet, this diagnostic tool also has the potential problem of the lack of specificity because of cross-reactivity. In the search for useful serological markers to diagnose ascariasis, selleck kinase inhibitor various antigen sources have been tested (154). Some have evaluated whole nematode extracts and others the pseudocoelomic fluid or preparations of excretory/secretory antigens. Currently, different reagents are under investigation including recombinant or purified antigens such as one of 24 kDa (155) and a specific somatic antigen of 34 kDa from adult A. lumbricoides (156). Because now it is clear that a high degree of cross-reactivity exists between Ascaris and mite extracts (24), this has to be added to the recognized problem of cross-reactivity between some proteins of

Ascaris and other nematodes (156–159) and should be taken into account when assessing see more ascariasis using specific IgE or IgG against whole Ascaris extracts. In this circumstance, it is also necessary to start using component-resolved diagnosis, what means further basic research to isolate useful diagnostic components from Ascaris and mites. One important step has been achieved by M. Kennedy et al. who identified and cloned the abundant Ascaris allergen called ABA-1 (160). ABA-1 (Asc s 1) is a member of the nematode polyprotein allergen/antigens (161–163). Studies support that immune

responses (IgG and IgE) to ABA-1 are associated with previous infection and immunity to Ascaris (152). In endemic regions, the antibodies isotypes to ABA-1 correlate with the severity of infection, being IgE associated with low infection levels and IgG4 or seronegativity with higher susceptibility to the infection (88). This protein of 15 kDa has only been found in nematodes, has fatty acid-binding properties (164) and is synthesized as a polyprotein in gut of the worms and released into the pseudocoelomic fluid of the parasite Adenylyl cyclase (161,165). We found no cross-reactivity between ABA-1 and any component of the D. pteronyssinus and B. tropicalis extracts, confirming its usefulness as a more specific marker of Ascaris infection, avoiding the bias of cross-reacting mite allergens. However, the sensitivity and specificity of tests with ABA-1 should be further evaluated because homologous molecules like gp15/400 ladder protein of Brugia malayi (166) and TBA-1 from Toxocara ssp. (167) may affect the utility of the assay. Another aspect of this problem is the impact of cross-reactivity in the diagnosis of mite allergy. It is generally accepted that total IgE is not a good diagnostic parameter for allergy in the tropics because parasite infections increase serum levels of this immunoglobulin (168).