This was due to the fact that β-catenin-positive hepatocytes were indeed more apt at expansion and survival in the adverse milieu of chronic DDC exposure exhibited in enhanced atypical ductular reaction and fibrosis. It was interesting to note that hepatic regeneration reflected by hepatocyte proliferation was ongoing in both WT and KO livers at 80 and 150 days when

the hepatocytes lacked terminal differentiation as reflected by decreased expression of HNF4α, C/EBPα, and others. The lack of maturation may be due to ongoing proliferation of the hepatocytes or additional unknown factors due to chronic DDC injury and will need further evaluation. Intriguingly, no atypical ductular proliferation, oval cells, or cholangiocytes were positive for β-catenin in the KO livers at baseline or at the time of initiation of their expansion. The first time when β-catenin-positive cholangiocytes were observed in KO HSP assay livers was at 80 and 150 days after being on the DDC diet, suggesting that some of these cells may have been derived from β-catenin-positive hepatocytes. Transdifferentiation of hepatocytes to biliary epithelial cells has been demonstrated before and might be

an attempt at repairing biliary damage brought about by DDC.22 Does lack of β-catenin in GSK-3 inhibitor review cholangiocytes as well as atypical ductules in KO liver after chronic DDC administration impede optimal bile duct organization, thus also contributing to intrahepatic cholestasis? A role of β-catenin in biliary specification of the hepatoblasts is known.23-26 Furthermore, β-catenin is important in oval cell proliferation in rats and mice, and its role has recently been shown in differentiation of oval cells to hepatocytes.6, 7, 27 β-Catenin may also

have an important role in bile duct homeostasis. Indeed, in a recent collaborative study we have shown an important either role of β-catenin in regulating bile duct morphology.28 Overall, the above findings demonstrate a lack of an optimal reparative response in the absence of β-catenin to DDC-induced chronic liver injury, which is observed as increased atypical ductular proliferation resulting in greater hepatic fibrosis and development of intrahepatic cholestasis. This occurs despite repopulation of the livers with β-catenin-positive hepatocytes, which, however, does improve hepatocyte function in the KO when compared to the WT. These finding support an important role of Wnt/β-catenin signaling in bile duct homeostasis and reiterate its prosurvival and proproliferative role in hepatocyte biology. Additional Supporting Information may be found in the online version of this article. “
“Obesity and associated metabolic disorders have been implicated in liver carcinogenesis; however, there are little data on the role of obesity-related biomarkers on liver cancer risk.

Patients with diabetes at second follow-up did not have

significantly different BMI, waist or hip circumference at baseline compared to those without diabetes. However patients with diabetes at second follow up exhibited a more pronounced hepatic fatty infiltration at baseline compared to those without diabetes (14.3 ± 9.7 % vs. 8.0 ± 9.5 %, P = 0.01). BMI, waist or hip circumference and presence of dyslipidemia at first and second follow-up were not significantly different between patients with and without subsequent development of diabetes. Fibrosis stage at baseline was not significant for the outcome of diabetes at second follow-up. However, severity of fibrosis at baseline predicted the development of end-stage liver disease during follow-up (P = 0.021). Conclusion. The amount of Erlotinib hepatic steatosis in NAFLD is associated with

future risk of developing type 2 diabetes. Severe fibrosis is associated with future development of end-stage liver disease. Disclosures: The following people have nothing to disclose: Patrik S. Nasr, Mattias Ekstedt, Ulrik L. Mathiesen, Stergios Kechagias Non-Alcoholic Fatty Liver Disease (NAFLD) is an emerging forerunning cause of liver transplant (LT) in USA and worldwide. check details With the obesity epidemics on the rise, the incidence of NAFLD/Non-Alcoholic Steato-Hepatitis (NASH) and its complications, such as cirrhosis and hepatocellular carcinoma (HCC), have also increased over the last decades. To date, LT is the last-resort treatment of NASH, yet lack of reliable clinical and biochemical biomarkers limit pre-LT diagnosis of NASH largely on the Ceramide glucosyltransferase basis of liver histology. We aimed to identify clinical and routine biochemical signature features of patients who had undergone LT and had histological findings suggestive of NASH in the explant livers, in order to define predictive parameters of NASH prior to LT. Our cohort includes patients from the University of Florida Liver Transplant database from 1990-2013, for a total 1,646 patients; of those 174 were listed for cryptogenic cirrhosis (CC) or NASH cirrhosis as cause of LT. Eighteen

patients listed with NASH and 116 with CC had electronic records and were included in the analysis. Of 116 patients who have undergone LT for CC, 18 were excluded because they carried dual diagnosis. Of remaining 98 patients listed with sole CC diagnosis as a cause for LT, 3 individuals exhibited histologic evidence of alpha1-antitrypsin deficiency, 7 has strong stains for iron, and 3 have HCC along with cirrhosis in native liver explant, thus were excluded. Based on biopsies of the explant liver, the group was further distributed in a cohort of 24 patients which did not have inflammation or steatosis (True CC), 24 patients which had steatosis and inflammation (NASH) and 28 patients with inflammation but no ste-atosis (Late-stage NASH).

2A and Supporting Fig. 2A). The significant morphological differences in

the initial liver injury between the transgenic and wild-type mice were further confirmed by the measurement of liver injury on day 7, which resulted in average serum ALT levels of 1256 U/L for CD40 transgenic mice and 263 U/L for wild-type animals (Fig. 3A). By using quantitative PCR analysis, we found no significant difference in the viral copy numbers between the CD40 transgenic and wild-type groups on day 7 (P > 0.05; Fig. 3B). Although the viral copy numbers in both groups decreased steadily from day 7 to day 14 (P < 0.01), no statistical difference was found between the two groups on day 14 (P > 0.05). These results demonstrate that increased lymphocyte infiltration and hepatic inflammation are not associated with enhanced viral clearance in the liver. To test how

parenchymal CD40 expression exacerbates ACP-196 in vitro liver injury in viral hepatitis, we examined population dynamics and effector functions of IHLs in all three groups of mice. As expected, the total numbers Palbociclib chemical structure of IHLs in the AdCre-infected mice, regardless of their transgenic status or the point in time, were significantly higher than those in the PBS group (Fig. 4A). The effect of parenchymal CD40 expression on lymphocyte accumulation in the liver was most evident on day 7 because the average number of IHLs rose significantly higher in transgenic animals versus wild-type animals (29.3 versus 18.2 × 105, P < 0.01). Although the increased IHL numbers were sustained in the wild-type mice into the second week (18.5 × 105), the IHL numbers in the transgenic animals declined nearly 3-fold to 10.1 × 105, which was significantly lower

than the value for the nontransgenic animals (P < 0.01). By using flow cytometry, we found that the adenoviral infection resulted in increases in the percentages of intrahepatic CD8+ cells in both groups of mice on day 7 (57.9% and 62.0%; Table 1); these levels were higher than the level of the PBS group (21.4%, P < 0.001). This CTL expansion was more vigorous in the CD40 transgenic mice versus their wild-type Fludarabine in vivo counterparts (18.2 versus 10.5 × 105) and contributed to their more expanded IHL populations (Fig. 4A). Although both AdCre-infected groups maintained high percentages of CD8+ T cells in the liver on day 14 (76.3% and 77.5%), the transgenic mice had far lower numbers of CD8+ cells than the wild-type animals because of their greatly diminished IHL pools on day 14 (7.8 versus 14.1 × 105). In comparison with the wild-type animals, more intrahepatic CD8+ cells in the CD40 transgenic mice entered the apoptosis process [annexin V–positive and 7-aminoactinomycin D (7-AAD)–negative] as early as day 7 (Fig. 4B and Supporting Fig. 6). This accelerated rate of apoptosis occurred only among CD8+ effector cells in the transgenic mice and not in CD8− cells (presumably CD4+, B, and NK cells).

Augmentation of immunosuppression using steroids is dictated by clinical, biochemical and histological severity of AR and represents the main way of treatment. “
“Endoscopic intervention with metallic biliary stenting is increasingly being performed for the management of variety of pancreatic and hepatobiliary disorders. A rare complication of metallic biliary stent insertion is stent embedment. Although a recognized complication, there is limited literature available addressing the treatment

of this complication. This report demonstrates the effectiveness of a “stent-in-stent” technique to remove an embedded biliary metal stents. A 50-year-old man with chronic alcoholism presented with biliary obstruction related to a chronic pancreatitis and a benign biliary stricture. The initial ERCP (Endoscopic Retrograde Cholangio Pancreatography) showed a 5 mm benign biliary stricture that was treated with sequential insertion of plastic buy PD98059 biliary stents. Despite two attempts with plastic stents, the stricture did not improve radiologically. The patient was subsequently treated by insertion of a self-expanding covered metal stent (WallFlex Biliary RX Fully Covered 10 mm × 60 mm, Boston Scientific,

Natural Product Library high throughput Marlborough, MA, USA). Post-procedure the patient was lost to follow up but re-presented 14 months following the metal stent insertion with cholangitis. Repeat ERCP showed a blocked stent with complete embedment of the distal end due to in-growth of epithelial tissue (Fig. 1a). Stent removal was not possible despite vigorous attempts including the use of Jumbo forceps to remove epithelial in-growth. A new self-expanding covered metal stent (WallFlex

Biliary RX Fully Covered 10 mm × 60 mm, Boston Scientific) was inserted within the embedded stent to induce pressure necrosis of ingrown epithelial tissue (Fig. 1b,c). Repeat ERCP was performed 2 weeks later. At this procedure, the recently inserted inner stent was removed without difficulty and the outer embedded stent could now be removed with minimal resistance. Post-ERCP cholangiogram showed resolution of the stricture. The Carbachol patient has remained asymptomatic post-procedure during 6 months during outpatient follow up. Self-expanding metal stents are safe devices for patients with obstructive jaundice secondary to benign as well as malignant biliary strictures. With their large and prolonged patent lumen, they have superior drainage capacity relative to plastic stents. Despite the good safety profile of fully covered self-expanding covered metal stents, serious complications such as stent embedment may occur, particularly if they are left in for prolonged time periods. The majority of embedded metal stent removal techniques involve mechanical modalities using accessories such as grasping Dormia baskets, forceps and snares as well as YAG laser (Neodymium-doped yttrium aluminum garnet). Most these mechanical techniques carry potential risks of perforation and bleeding.

Upon workshop completion, the six trainees demonstrated improved haemophilia-specific PT knowledge and were fully familiar with the HJHS and its administration. The latter was assessed in a mini-reliability study. The ‘Train-the-Trainer’ model is a very effective education programme designed to accelerate training in haemophilia PT to meet the rapidly increasing need for haemophilia-specific rehabilitation

services in a very large country such as China. It is anticipated Cabozantinib that physiatrists/physiotherapists at newly established Chinese haemophilia treatment centres will receive training in haemophilia care as a result of this unique programme in the immediate future. “
“Summary.  In patients with severe haemophilia and inhibitors, regular this website factor VIII inhibitor bypassing activity (FEIBA) prophylaxis

has been shown to reduce the frequency of bleeding by up to 85% and to improve patient quality of life. FEIBA is well tolerated; the incidence of thrombotic events and of allergic reactions is extremely low. The concept of prophylaxis in haemophilia patients with inhibitors is relatively new and some clinicians may be unsure of how to use FEIBA in this context. These treatment recommendations, based on published evidence plus the collective experience of a group of haematologists (with practical knowledge of managing inhibitor patients with FEIBA prophylaxis), are intended to provide guidance to clinicians considering initiating and maintaining patients on FEIBA prophylaxis with specific focus on practical aspects of patient selection, dosing, monitoring and stop criteria. “
“Atrial fibrillation (AF) is a common health problem in the general population, but data on prevalence or management in patients with haemophilia (PWH) are lacking. The aims of this study were to analyse the prevalence of AF and risk factors for stroke using a cross-sectional pan-European design and to document current anticoagulation practice. The ADVANCE Working Group consists of members from 14 European haemophilia centres. Each centre retrieved data on their PWH with AF.

From the total of 3952 adult ifoxetine PWH, 33 had AF with a mean age of 69 years (IQR 62–76). Haemophilia was severe in seven (21%), moderate in six (18%) and mild in 20 (61%) patients. The overall AF prevalence was 0.84% and increased with age; 0.42% in patients 40–60 years and 3.4% in patients >60 years. The mean CHA2DS2-Vasc score was 1.3 (range 0–4), predominantly determined by age and hypertension. Hypertension was reported in 48% of PWH with AF. In 11 patients (33%), anticoagulation was started of whom nine aspirin and two vitamin K antagonists. Of these 11 patients, nine had mild haemophilia. Anticoagulation was given in 42% of patients with a CHA2DS2-Vasc score ≥2. During follow-up (mean 57 months), there were no thrombotic events reported, nor increases in bleeding severity.

In hepatocytes,

cell division is complex, because polyploidy and aneuploidy are extremely high in p53+/+ livers from mice3 and humans.4 Nonetheless, disruption of normal Aurka and Lats2—and to a lesser extent Foxm1 and Plk4—expression partially accounts for enrichment in mitotic segregation errors and enhanced polyploidy MAPK Inhibitor Library solubility dmso seen in p53-deficient liver. After PH, transcriptional activity of p53 and how it contributes to activation or repression of mitotic or cell cycle regulators is more difficult to interpret. There may be a partial compensation by TA-p73, which has been shown to play a role in liver tumor suppression in combination with p53.35 A fully delineated story of how hepatocytes survive, and even thrive, in spite of high levels of polyploidy and

aneuploidy is not yet clear. p53 and its downstream effectors contribute to polyploidization and mitotic fidelity, as shown here in vivo. Whether p53 regulation is connected to activation of the insulin receptor and AKT signaling, implicated in cytokinesis failure see more and formation of polyploid hepatic cells,36 is unknown. Further characterization of new hepato-specific cell cycle pathways and definition of regulatory mechanisms are critical to understanding development, homeostasis, regeneration, and pathology of the liver. Additional Supporting Information may be found in the online version of this article. “
“JNK plays science a key role in hepatotoxicity by binding and phos-phorylating Sab on the outer mitochondrial membrane (J Biol Chem 286, 35071-8, 2011, Cell Death Dis; 5:e989, Jan 9, 2014). The mechanism for how this event on the cytoplasmic face of the outer membrane leads to impaired mitochondrial electron transport, increased ROS, and APAP-induced necrosis is unknown. We focused our attention on dysregulation of tyro-sine kinases (Src) because mitochondrial Src activity is known to regulate multiple steps in electron transport in other contexts (Biochem J. 447, 281-9,2012). Methods: Isolated mouse liver mitochondria were exposed to pure activated JNK +/− ATP, with or without Src or protein tyrosine

phosphatase (Ptp) inhibitors. APAP (300mg/kg) or PBS was given by ip injection to C57BL/6N mice; mitochondria and cytoplasm were prepared at 1,2,4 hours and histology and serum ALT were assessed at 24 hours. Knockdown of target genes in liver was by adeno-shRNA. Results: Using resistance to proteinase K digestion, we identified intramitochondrial c-Src mainly in an activated form (P-419-c-Src). Upon exposure of isolated mitochondria to P-JNK plus ATP, P-c-Src levels markedly decreased while total c-Src was unchanged. The decrease of P-c-Src was accompanied by inhibition of oxygen consumption rate (OCR), which depended on Sab expression. Addition of Src inhibitors (PP2 or Src inhibitor 1) to normal mitochondria directly inhibited OCR.

Preoperative planning should incorporate a determination of the specific haemostatic therapies to be used during and after surgery, including dosing regimens and whether continuous selleck or bolus treatment will be used. It is often

helpful for a member of the HTC team to be present in the operating room (OR) to assist in communication between the OR staff and the patient/family and to provide on-site guidance regarding haemostatic management, if needed. The use of high-dose FVIII or FIX concentrates to overcome inhibitors in CHwI undergoing surgery, although ideal and measurable [8, 21], is often restricted to those with low-titre or low-responding inhibitors or those who have successfully achieved tolerance. Both bolus and continuous administration of replacement factor have been 3-deazaneplanocin A effectively used in this setting, although in patients with haemophilia B and inhibitors, the use of high doses of FIX may increase the risk for anaphylaxis [10]. In patients with

haemophilia A receiving FVIII replacement for surgery, an anamnestic increase in inhibitor titre may occur, necessitating a switch to bypassing therapy [22]. Although preoperative attempts to reduce the inhibitor titre using rituximab [9] and ITT [6] have been described, these treatments have limitations, most notably the time required for such regimens to take effect and, with immunosuppressive eliminative agents, the potential for susceptibility to infections. Bypassing agents are the haemostatic products of choice for patients with high-titre or high-responding inhibitors or those with haemophilia B and inhibitors. Each of the commercially available Exoribonuclease bypassing agents – recombinant activated FVII (rFVIIa; NovoSeven® RT; Novo Nordisk A/S, Bagsvaerd, Denmark) and activated

prothrombin complex concentrate (aPCC; FEIBA®, Factor Eight Inhibitor Bypassing Agent); Baxter Healthcare Corporation (Westlake Village, CA, USA) – have been successfully used for haemostatic coverage for surgery in both children and adults with CHwI, with comparable efficacy and safety. However, there are no evidence-based guidelines for the use of either agent in this setting. Recombinant FVIIa has a relatively short half-life of 2.7 h in adults and 1.3 h in children [23]. Optimal dosing remains uncertain. The choice of product for those with high-titre inhibitors is dependent on the age of the patient, prior exposure to plasma products, type of bleeding episode, volume-of-reconstitution cost, efficacy and safety. At most institutions, for patients who are plasma-naïve or for those with haemophilia B and inhibitors, rFVIIa is used to achieve rapid haemostasis (recombinant porcine FVIII may likewise be used for the same purpose in patients with haemophilia A and inhibitors who are plasma-naïve, when it becomes available). However, for patients with haemophilia A who have been previously exposed to plasma products, either aPCC or rFVIIa may be used [24].

Swet, Iain H. McKillop OBJECTIVE: There are few studies that have examined the relationship between specific single-nucleotide polymorphisms (SNPs) and VX-770 nmr the development of liver disease in Latinos. A genome-wide association study that was conducted in the multi-ethnic population-based Dallas Heart Study identified rs738409 (I148M) in PNPLA3 as the only variant that was strongly associated with hepatic fat. The prevalence of I148M was 49% among Latinos, 23% among Caucasians, and 17% among African Americans. For this study, we evaluated the prevalence and association between nine SNPs in or near the following genes: IRS1, PNPLA3,

GCKR, PPPR3B, NCAN, ADI-POR2, LYPLA1 and PPARG and the presence of persistently elevated levels of alanine aminotranseras (ALT) or aspartate aminotransferase (AST) in a sample of Mexican adults. All the SNPs we examined have been associated with hepatic steato-sis in non-Latino populations, but only PNPLA3 (rs738409) has

been investigated in Latinos. METHODS: Samples and data were obtained from the Mexican Health Worker Cohort Study, https://www.selleckchem.com/products/BMS-777607.html in Cuernavaca, Mexico. A total of 207 cases were found to have persistently elevated levels of ALT or AST (>40 IU/L) and 534 controls had at least two consecutive normal ALT and AST measurements over a period of 6 months, during 2006-2010 and 2011-2013. Genotyping of the SNPs was performed using the TaqMan allelic discrimination assay. RESULTS: The most prevalent SNPs were: rs2943634 (84.4%) and rs2972146 (83.3%) (IRS1); rs738409 CYTH4 (57.8%) (PNPLA3); rs780094

(33.2%) (GCKR ); and rs4240624 (27.9%) (PPP1R3B). The least prevalent SNPs were: rs2228603 (2.7%) (NCAN); rs767870 (10.6%) (ADIPOR2); rs12137855 (11.5%) (LYPLAL1); and rs1801282 (13.7%) (PPARG). The following SNPs were significantly associated with persistently elevated ALT or AST levels, after adjusting for age, sex and BMI: PNPLA3 (OR=1.62, 95%CI=1.25-2.09), LYPLA1 (OR=1.46, 95%CI=1.02-2.10), and NCAN (OR=2.19, 95% CI=1.09-4.40). CONCLUSIONS: Our results confirm those of other studies that report a high prevalence of the PNPLA3 “G” allele among Latino populations. We found that PNPLA3 (rs738409), LYPLA1 (rs12137855), and NCAN (rs2228603) were significantly associated with the presence of persistently elevated transaminase levels in this sample of Mexican adults. To the extent that elevated aminotransferase levels may reflect sub-clinical liver inflammation, these results suggest that the presence of these polymorphisms could be indicative of an increased risk of developing chronic liver disease. To the best of our knowledge, this is the first study to examine these SNPs in a large sample of adults in Mexico. Disclosures: The following people have nothing to disclose: Yvonne N. Flores, Manuel Bahue-los, Manuel Quiterio, Hal F.

Vitamin D homeostasis is maintained by the synthetic activity of 1a-hydroxylase and catabolic activity of 24-hydroxylase (CYP24A1). 1,25(OH)2D3 regulates 1a-hydroxylase activity both directly through negative feedback but also by way of inhibition of parathyroid hormone (PTH) activity. Conversely, in response to hypocalcemia, PTH increases 1a-hydroxylase transcription and, therefore, 1,25(OH)2D3 synthesis through a cyclic adenosine monophosphate (cAMP)-dependent pathway. Another mediator of vitamin D homeostasis is fibroblast growth factor 23 (FGF23) which is produced primarily by osteoblasts and

osteocytes and influences vitamin D metabolism through down-regulation of 1a-hydroxylase activity and promotion of 24-hydroxylase activity.[3] Sex hormones, calcitonin, and prolactin

can also affect vitamin D homeostasis, though 1a-hydroxylase activity remains INCB024360 the primary factor Romidepsin manufacturer in vitamin D homeostasis.[4] In addition to sun exposure and diet, vitamin D levels may also be affected by genetic factors and high heritability of VDD has been shown in several epidemiologic studies.[5, 6] The exact genes involved have only recently been investigated, with the most substantial study to date showing single nucleotide polymorphisms (SNPs) in the genes encoding CYPR21 and DBP were associated with vitamin D status in an initial cohort of 156 unrelated healthy Caucasians and a similar replication cohort of 340 patients.[7] Given the essential role of CYPR21 and DBP in vitamin D homeostasis, these findings are not surprising and have been replicated in other studies.[8] Interestingly, the study by Ramos-Lopez et al.[8] associated the CYP2R1 gene with both vitamin D levels and type 1 diabetes, although no data exist evaluating the SNPs associated with vitamin D levels in NAFLD patients. Conversely, the genes associated with a high incidence of NAFLD have not been evaluated Bay 11-7085 for a putative role in vitamin D metabolism. The primary mediator of vitamin D is the vitamin D nuclear

receptor (VDR), which is a member of the superfamily of nuclear hormone receptors. VDR has four major domains that interact to confer ligand-activated transcription factor activity: a ligand-binding domain, a retinoid X receptor (RXR) heterodimerization domain, a DNA binding domain to vitamin D response elements, and a recruitment domain of VDR coregulators.[9] VDR bound to RXR forms a heterodimer that interacts with vitamin D response elements (VDRE) located within promoter regions of target genes and leads to activation or repression of transcription.[10] Target genes of the VDR are broad and include functions of hormone secretion, immune regulation, cellular proliferation, and differentiation. The nonclassic actions of vitamin D can be grouped into three primary categories to include modulation of immunologic function, hormone secretion, and cellular proliferation and differentiation (Fig. 1).

Specialized working memory may be especially important for aggressive mimics that express flexibility in their use of signals.

We have seen flexibility already when, for example, we considered the strategies of bolas https://www.selleckchem.com/products/gsk126.html spiders that use different chemical signals at different stages in their lives and with different prey. However, it is especially with Portia that the cognitive character of aggressive mimicry is strikingly expressed in conjunction with extreme predatory versatility and flexibility. Especially many of Portia’s tactics are based on invading the webs of non-salticid spiders and, for understanding these tactics, we need an understanding of the web spider’s unusual sensory system. We may be predisposed to think of sense organs as being part of an animal’s anatomy, but the web in conjunction with setae and slit sensilla on the spider’s body is the primary sense organ of the web spiders on which Portia preys (Witt,

1975; Barth, 2001). It is particularly interesting that this sense organ is extended out into the environment because this means that Portia can walk directly into it. In another spider’s web, Portia’s intimacy with its prey’s sensory world gives especially literal meaning to the expression ‘sensory exploitation’. By invading a web, Portia enters into intimate and often dangerous contact with its prey’s sensory world – dangerous because the tables may be turned, and Portia’s intended dinner may Pexidartinib become the diner (e.g. Jackson et al., 2002). After entering

a web, instead of simply stalking or chasing down the resident spider, Portia communicates using web signals (Tarsitano, Jackson & Kirchner, 2000), ‘web DNA Damage inhibitor signals’ referring to the vibratory and tension patterns Portia generates by using any one or any combination of its 10 appendages (eight legs and two palps). Each appendage can be moved independently and in a variety of ways, with the net effect being that Portia has at its disposal virtually an unlimited assortment of different signals for potential use when in other spiders’ webs (Jackson & Blest, 1982). This is relevant because, instead of targeting only one or only a few web-building spider species, Portia appears to be ready to take on almost any spider it finds in a web, as long as the other spider is similar to Portia’s own size. However, each of these prey spiders has its own refined ability to acquire and process sensory information (Barth, 2001). Many variables, including the resident spider’s species, sex–age class, feeding state and previous experience (Jackson, 1986; Masters, Markl & Moffat, 1986; Landolfa & Barth, 1996), influence response to signals.