However, we also observed a small but significant decrease in Bsep expression in the absence of InsP3R2. This may reflect that the half-life of Bsep in the intracellular compartment is shorter than

in the membrane. Evidence Selleck CHIR 99021 for this comes from studies of rodent liver treated with estrogen, which induces rapid internalization of Bsep.33 In this model, total protein content of the transporter decreases without a change in mRNA levels, suggesting a posttranslational mechanism of Bsep down-regulation such as increased protein turnover.38 Our findings suggest not only that InsP3R2 promotes bile secretion but that canalicular cholestasis (in both estrogen and LPS models) is associated with loss of InsP3R2 expression. Bsep and Mrp2 are mistargeted in both of these models and overall expression of these proteins is reduced secondary to posttranslational mechanisms.33, 34, 38-41 Moreover, in the case of Bsep this defect is reversed by UDCA,40 which increases Ca2+,42 and stimulates exocytosis.19 Considering our current and previous Selleck BMN-673 findings,22 it may be that decreased expression and localization of canalicular transporters seen in canalicular cholestasis is secondary to loss of pericanalicular Ca2+ signaling. This may be analogous to what is observed in cholangiocytes, in which InsP3R3 rather than InsP3R2 is the predominant isoform.11 InsP3R3

expression is concentrated subapically in cholangiocytes and is lost in animal models of ductular cholestasis, as well as in patients with a variety of cholestatic disorders.27 This decreased InsP3R3 expression impairs polarized Ca2+ signaling27 and ductular bicarbonate secretion.43 Therefore, loss or redistribution of apical InsP3Rs may be a common basis for selleckchem impaired secretion in polarized epithelia. Cells in various tissues use raft-based platforms to spatially coordinate membrane proteins with the Ca2+ release machinery that regulates them.44 Rafts can promote physical

and functional interactions between ER channels and membrane proteins,45-48 and also can cluster Ca2+ signaling proteins, including PLC49 and PIP244; downstream effectors such as PKCα49 and store operated Ca2+ entry proteins,44 such as TRPC1 and Orai; and the plasma membrane Ca2+ ATPase.44 Thus, lipid rafts help generate large amplitude localized Ca2+ transients in specific membrane microdomains, and this may be ideal for regulating Bsep insertion. It is interesting to note that InsP3R2 labeling can be punctate, perhaps indicating focal densities of release channels coordinated with sites of exocytosis. The localized nature of Ca2+ signaling microdomains would also help explain the apparent inconsistency between the present results, which support a choleretic effect of Ca2+, and earlier studies, which suggest a cholestatic effect.

However, we also observed a small but significant decrease in Bsep expression in the absence of InsP3R2. This may reflect that the half-life of Bsep in the intracellular compartment is shorter than

in the membrane. Evidence Palbociclib nmr for this comes from studies of rodent liver treated with estrogen, which induces rapid internalization of Bsep.33 In this model, total protein content of the transporter decreases without a change in mRNA levels, suggesting a posttranslational mechanism of Bsep down-regulation such as increased protein turnover.38 Our findings suggest not only that InsP3R2 promotes bile secretion but that canalicular cholestasis (in both estrogen and LPS models) is associated with loss of InsP3R2 expression. Bsep and Mrp2 are mistargeted in both of these models and overall expression of these proteins is reduced secondary to posttranslational mechanisms.33, 34, 38-41 Moreover, in the case of Bsep this defect is reversed by UDCA,40 which increases Ca2+,42 and stimulates exocytosis.19 Considering our current and previous this website findings,22 it may be that decreased expression and localization of canalicular transporters seen in canalicular cholestasis is secondary to loss of pericanalicular Ca2+ signaling. This may be analogous to what is observed in cholangiocytes, in which InsP3R3 rather than InsP3R2 is the predominant isoform.11 InsP3R3

expression is concentrated subapically in cholangiocytes and is lost in animal models of ductular cholestasis, as well as in patients with a variety of cholestatic disorders.27 This decreased InsP3R3 expression impairs polarized Ca2+ signaling27 and ductular bicarbonate secretion.43 Therefore, loss or redistribution of apical InsP3Rs may be a common basis for see more impaired secretion in polarized epithelia. Cells in various tissues use raft-based platforms to spatially coordinate membrane proteins with the Ca2+ release machinery that regulates them.44 Rafts can promote physical

and functional interactions between ER channels and membrane proteins,45-48 and also can cluster Ca2+ signaling proteins, including PLC49 and PIP244; downstream effectors such as PKCα49 and store operated Ca2+ entry proteins,44 such as TRPC1 and Orai; and the plasma membrane Ca2+ ATPase.44 Thus, lipid rafts help generate large amplitude localized Ca2+ transients in specific membrane microdomains, and this may be ideal for regulating Bsep insertion. It is interesting to note that InsP3R2 labeling can be punctate, perhaps indicating focal densities of release channels coordinated with sites of exocytosis. The localized nature of Ca2+ signaling microdomains would also help explain the apparent inconsistency between the present results, which support a choleretic effect of Ca2+, and earlier studies, which suggest a cholestatic effect.

[1, 2] HCV recurrence after transplantation is universal and represents a major therapeutic challenge as current standard therapy against HCV infection is limited to the combination of pegylated interferon-α and ribavirin (IFN/RBV). However, the therapy has considerable side-effects, and the response rate is less than ideal.[3] Several cellular factors are known to be involved in the hepatocellular entry mechanism of HCV.[4] Tight-junction (TJ) proteins claudin-1 (CLDN1) and occludin (OCLN), CD81, scavenger receptor class B type 1 (SCARB1) have been reported to be part of the internalization complex and are essential for HCV entry both in Kinase Inhibitor Library vitro and in vivo.[2, 5-7] Previous studies have shown discrepancies

between messenger RNA (mRNA) and protein expression levels of these receptors in HCV infected patients, suggesting therefore the role of microRNAs (miRs) in the modulation of gene expression.[2, 4, 5] MiRs are small endogenous non-coding ∼22 nucleotide long RNAs that regulate gene expression at posttranscriptional level. MiRs induce degradation of the mRNA or suppression of protein translation upon binding to the 3′ untranslated regions (UTRs) of an mRNA.[8, 9] One microRNA sequence might interact with several mRNAs. selleck products Therefore, miRs exert negative regulation on mRNA and finally on protein expression. They are essential for maintenance of cellular homeostasis and normal function, serving as key regulators of

various biological processes including cellular stress, steatosis, proliferation, differentiation, and apoptosis.[9-11] Dysregulated expression of miRs might play role in the development of many diseases including viral infections and malignancies.[12-14] MiRs also participate in the control of selleck inhibitor HCV infection as well as in the IFN pathway via several mechanisms.[3, 15] The liver-specific microRNA, miR-122, is known

as a positive cofactor in HCV replication cycle[16] and has been found to be downregulated by α/β IFNs.[17] Besides, IFN-β has been described as modulator of the expression of several miRs having sequence-predicted targets within the HCV genomic RNA, and some of these miRs were shown to actively inhibit HCV replication.[17, 18] In addition, the hepatic microRNA expression pattern existing in chronic HCV-infected patients before antiviral therapy was shown to be associated with therapy response.[3] The aim of the current study was to evaluate the expression of miRs, which either have one of the HCV receptors among their target mRNAs according to target prediction software (such as miR-21, miR-34a, miR-96, miR-125b, miR-194, miR-195, and miR-224), or which may play role in HCV infection or in antiviral treatment response (such as miR-23a, miR-99a*, miR-122, miR-181a-2*, miR-217, and miR-221) in liver transplant recipients. A total of 28 liver needle biopsies of HCV-positive adult liver transplanted patients were included.

Twenty-four out of 33 (73%) cases with Chiari 1 malformation complained of headache, and 9/33 (27%) of those patients (5 with mild and 4 with severe tonsillar ectopia) reported headache attributed to Chiari 1 malformation. In our studied pediatric population, the most common symptom for cases diagnosed with Chiari 1 malformation was headache, and headache attributed to Chiari 1 malformation was the most common headache pattern in patients with Chiari 1 malformation. The presence of headache attributed to Chiari 1 malformation along with 3 other signs or symptoms of Chiari 1 malformation were highly predictive of severe tonsillar ectopia. “
“(Headache 2010;50:420-430)

Background.— The serotonergic system is thought to play an important role for mediating susceptibility to migraine and depression, which is frequently found comorbid in migraine. The functional Trametinib research buy polymorphism in the serotonin transporter gene linked polymorphic region (5-HTTLPR/SLC6A4) was previously associated with attack frequency and, thus, possibly with chronification.

Objective.— We hypothesized that patients with the “s” allele have higher attack frequency and, paralleling results in depression research, higher scores of depression. Methods.— Genetic analysis of the SLC6A4 44 bp insertion/deletion polymorphism (5-HTTLPR) was performed in 293 patients with migraine with and without aura. Self-rating questionnaires were used for assessment of depression. Results.— Multinomial logistic regression analysis found no evidence for association of the 5-HTTLPR polymorphism

Epacadostat with either depression selleck screening library or migraine attack frequency. Conclusion.— We were not able to demonstrate any influence of the serotonin transporter 5-HTTLPR polymorphism on migraine phenomenology (attack frequency or comorbid depression), thereby excluding this variant to be a common genetic denominator for chronic migraine and depression. “
“Wiley has updated its publishing ethics guidelines, first published in 2006. The new guidelines provide guidance, resources, and practical advice on ethical concerns that arise in academic publishing for editors, authors, and researchers, among other audiences. New guidance is also included on whistle blowers, animal research, clinical research, and clinical trial registration, addressing cultural differences, human rights, and confidentiality. The guidelines are uniquely interdisciplinary, and were reviewed by 24 editors and experts chosen from the wide range of communities that Wiley serves. They are also published in Advanced Materials, International Journal of Clinical Practice, Annals of the New York Academy of Sciences, Social Science Quarterly, and on the website http://exchanges.wiley.com/ethicsguidelines. “
“Objective.

The ITS1 and ITS2 regions of rDNA were similar among populations of G. rostochiensis and

differed in 1–3% of 1000-bp sequence. The analysis of populations polymorphism based on the RAPD technique also showed differences among populations of G. rostochiensis, indicating that climatic conditions of the mountainous area might have influence on genetic variability. “
“In 2012, dark brown spots were Tamoxifen observed on leaves of Ledebouriella seseloides (Fang Feng) in several research plots located at the Goseong Agricultural Research Extension services in Gyeongam Province, Republic of Korea. A fungus was isolated from the infected plants which produced pink-coloured spores in mucilage on PDA and conidial morphology suggested that the causal

agent was Colletotrichum gloeosporioides. Internal transcribed spacer sequences of the pathogen showed 99% identity to those of C. gloeosporioides. Pathogenicity of the isolate was proved by Koch’s postulates. This is the first report of anthracnose in L. seseloides caused by CP-868596 supplier C. gloeosporioides. “
“Some lignivorous hymenomycete fungi are capable of causing both cankers and decay in stemwood of adult trees. Recently in Tuscany (Italy), Platanus x acerifolia trees were found colonized by Sarcodontia pachydon (Polyporales, Meruliaceae), a fungus associated with white rot and stem cankers on different host tree species. Because the relationship S. pachyodon-plane-tree was only preliminary studied, we decided to investigate whether isolates obtained from this host are distinct from those commonly collected from oaks. For this purpose, isolates obtained from plane-tree and from holm oak (Quercus ilex) were compared by in vitro test and molecular markers. Results showed that fungal isolates did not differ in growth nor in wood degradation, also molecular tests revealed see more relative similarity among fungal samples. “
“A stem blight disease was observed on the lower portions of Brassica juncea stems during the cropping season (2010–2011). In advanced stages, the lesions were up to 120 cm in length on the stems and also spread to petioles

and midribs of leaves. The purified fungus was identified as Nigrospora oryzae (Berk. & Br.) Petch (teleomorph Khuskia oryzae), which produced similar symptoms when healthy B. juncea plants were inoculated, thus proving Koch’s postulates. This is the first report of the occurrence of N. oryzae on B. juncea. “
“Aster yellows phytoplasma was detected for the first time in goldenrain tree (Koelreuteria paniculata) growing in Sinpyeong-myeon, Jeollabuk-do, South Korea. DNA was extracted from the infected leaf samples and part of the 16S rDNA, rp operon and tuf gene were amplified using R16F2n/R2 and gene-specific primers. The sequence analysis showed that the phytoplasma was closely related (99%) to members of the Aster Yellows (AY) group, and belonging to 16Sr I, subgroup B.

Host factors, such

as age, sex, presence of liver cirrhosis, or the HBeAg status at baseline, had no influence on antiviral response to TDF (data not shown). Among the 113 patients with available serum samples at baseline of TDF therapy, mutations associated with resistance against LAM or ADV were detected in 70 (62%), and in 21 (19%) patients. The remaining 22 patients (19%) had HBV wildtype sequences this website (Table 2). The mean baseline HBV DNA levels in these three patient groups were 8.3 ± 8.8 (range, 4.1–9.7), 8.4 ± 8.7 (range, 4.8–9.4) and 8.3 ± 8.9 (range, 4.1–9.7) log10 copies/mL (P = 0.92, log rank). In patients with HBV wildtype infection suboptimal response to previous ADV treatment was the main reason for switching to TDF (Table 2). A comparison buy PLX4032 between the patient groups with genotypic resistance either against LAM (n = 70) or against ADV (n = 21) and those with wildtype HBV (n = 22) showed that the presence of mutations associated with LAM resistance did not affect the decrease of HBV DNA during TDF treatment (Fig. 2). By contrast, patients with genotypic resistance against ADV had a significantly lower probability of achieving a complete virologic response with HBV DNA levels <400 copies/mL (P < 0.001; Fig.

2). Thus, after 12 months of TDF treatment, 33% of the patients with initial ADV genotypic resistance and 90% of the patients without initial ADV resistance had reached HBV DNA levels below the limit of detection. The mean HBV DNA levels in the three patient groups with LAM resistance, ADV resistance, and HBV wildtype after 12 months of TDF treatment were 3 ± 3.4 (range,

2.6–4.2), 5.6 ± 6.2 (range, 2.6–6.8), and 2.9 ± 3.3 (range, 2.6–4.1) log10 copies/mL (P = 0.001). Overall, during the complete observation period the probability of achieving HBV DNA levels below 400 copies/mL was 52% for patients with ADV-resistant variants and 100% for those without. find more Within the subgroup of ADV-resistant patients the level of HBV DNA at the beginning of TDF treatment was the only factor that significantly influenced the probability of complete virologic response (Fig. 3). In contrast, no other factors like ALT levels, age, gender, treatment history with ADV per se (without genotypic resistance) either as monotherapy or add-on combination therapy with LAM as well as pretreatment duration with either ADV or LAM influenced TDF response (Fig. 3). Additionally, the different HBV polymerase gene mutation patterns within the groups of patients with either LAM or ADV resistance had no influence on subsequent responsiveness to TDF (Fig. 4). One patient who previously had ongoing HBV replication during 36 months of entecavir treatment was found to have the entecavir-resistant HBV variants rtL180M, rtM204V, and rtS202G. Nevertheless, this patient showed an immediate response to TDF, and HBV DNA levels were reduced to <400 copies/mL after 12 weeks.

We found not only that LOXL2 this website was regulated by hypoxia/hypoxia-inducible factor 1 alpha (HIF-1α), but also that TGF-β

activated LOXL2 transcription through mothers against decapentaplegic homolog 4 (Smad4), whereas two frequently underexpressed miRNA families, miR-26 and miR-29, cooperatively suppressed LOXL2 transcription through interacting with the 3′ untranslated region of LOXL2. Third, we demonstrated the imperative roles of LOXL2 in modifying the extracellular matrix components in the tumor microenvironment and metastatic niche of HCC. LOXL2 promoted intrahepatic metastasis by increasing tissue stiffness, thereby enhancing the cytoskeletal reorganization of HCC cells. Furthermore, LOXL2 facilitated extrahepatic metastasis by enhancing recruitment of bone-marrow–derived cells to the metastatic site. Conclusion: These findings integrate the clinical relevance, molecular regulation,

and functional implications of LOXL2 in HCC metastasis. Deforolimus clinical trial (Hepatology 2014;60:1645–1658) “
“Paracetamol is the most frequently used analgesic in Australia and can be purchased without a prescription. We aimed to investigate the epidemiology and outcome of paracetamol overdoses occurring in Victoria, Australia. The Victorian admitted episode dataset was examined for all patients who had a diagnosis of paracetamol poisoning (International Statistical Classification of Diseases and Related Health Problems, Tenth Revision, Australian Modification [ICD-10-AM]: T39.1) or paracetamol adverse effect in therapeutic

use (Y45.5) from July 1, 2000 to June 30, 2007. Data extracted included all ICD-10 codes related to their admissions, gender, age range, date of admission, and cause of death (if applicable). Over 7 years, there was a total of 14 662 hospital admissions for paracetamol overdose with a mean of 2095 cases per year. Accidental overdoses comprised 15% (n = 2149) of cases. The overdose rate fell from 46 cases per 100 000 in 2001 to 39 cases per 100 000 in 2006 (P < 0.001). Most check details overdoses occurred in women (71%), and patients between 15 and 50 years old comprised 78% of all cases. Complications and mortality were relatively uncommon, with only 26 deaths directly attributable to paracetamol overdose over the 7 years. No child under 15 years old died from their overdose. Admission to Victorian hospitals with paracetamol overdose presents an enormous and in many cases preventable health-care burden. Fortunately, there has been a gradual fall in admissions, and most cases appear relatively benign. Further reductions in overdose could be achieved with increased awareness by physicians and the general public regarding the potential for accidental overdose, and increasing funding for mental health initiatives. “
“The body’s requirement for iron is different at different developmental stages. However, the molecular mechanisms of age-dependent iron metabolism are poorly understood.

The results of the base case analysis for the three competing strategies showing total costs, benefits (LYS) and cost per QALY gained are shown in Table 4. Lifestyle modification as a baseline strategy cost $46,000 for the cohort with a total average benefit of 6.2 LYS. Pioglitazone in addition to lifestyle modification was more costly than lifestyle modification alone, but delivered greater health benefits and was cost-effective,

with an incremental benefit of an additional 4.7 LYS and an ICER of $2748/QALY gained. Vitamin E in addition to lifestyle modification was also cost-effective, with additional benefit of 0.6 LYS, resulting in an ICER of $8475/QALY gained. A direct comparison of the two pharmacological strategies indicated that pioglitazone was more cost-effective, with an ICER of $2056/QALY gained

compared with vitamin E. The results of a one-way sensitivity analysis that tested Venetoclax supplier for influential variables in the pioglitazone strategy are shown in Fig. 2. The vertical line represents the ICER for the base case estimate. The arrows show the direction of movement of the ICER across the range that the variable was tested. There were four key variables (represented as horizontal bars) that had a meaningful effect on the ICER. For example, if the annual probability of death in decompensated NASH was 15%, the ICER was more than $7000/QALY gained; however, if the probability was 38%, the ICER was less than $1000, indicating pioglitazone was more cost-effective when the risk of death in decompensated disease increased. learn more Similarly, as the benefit of pioglitazone in preventing progression to cirrhosis increased, the cost-benefit ratio improved. A one-way sensitivity analysis testing variables in the vitamin E strategy indicated that the ability of vitamin E

to prevent decompensation, and the probability of death due to decompensated disease, were the most influential variables. Nevertheless, the ICER remained cost-effective across the ranges tested for these probabilities, likely reflecting the cheap cost of vitamin E. The model was tested over a discounting rate that varied from 3%-8%. At the highest rate of discounting (8%), the ICER for both strategies became more cost-effective (ICERs of $945/QALY selleck compound gained for pioglitazone and $5475/QALY gained for vitamin E). Two-way sensitivity analyses were performed to assess the change in the ICER when two variables were varied simultaneously, in order to find thresholds at which the drugs were no longer cost-effective. Two-way sensitivity analyses in the pioglitazone strategy indicated that if the likelihood of developing cirrhosis for people with advanced fibrosis was less than 2% per year, then lifestyle modification was the more cost-effective option. At probabilities equal or greater than 2%, pioglitazone was more cost-effective.

Plasma IP-10 levels ≥150 pg/mL occurred more often in non-Aboriginals (51% versus 20%, P = 0.014), those with HCV RNA >6 log IU/mL (76% versus 41% in those <4 log IU/mL, P

= 0.002) and those with HIV infection (70% versus 42%, P = 0.002). No differences were observed in the proportions with plasma IP-10 level ≥150 pg/mL by sex, age, or estimated duration of HCV infection. In adjusted logistic regression Trametinib datasheet analyses (Table 2), HCV RNA >6 log IU/mL (versus <4 log adjusted odds ratio [AOR] 6.11; 95% CI: 2.11, 17.69) and HIV infection (AOR 2.11; 95% CI: 0.96, 4.61) were independently associated with plasma IP-10 levels ≥150 pg/mL, while individuals of Aboriginal ethnicity were less likely to have plasma IP-10 levels ≥150 pg/mL at the time of acute HCV detection (AOR 0.17; 95% CI: 0.05, 0.58). No difference was observed in the frequency of IL28B rs12979860 CC genotype among http://www.selleckchem.com/products/MK-2206.html Aboriginals and non-Aboriginals (39% versus 53%, P = 0.254). Plasma IP-10 levels were monitored longitudinally in 20 untreated individuals with acute HCV (eight with clearance, Fig. 3; Supporting Fig. 2). Although

IP-10 levels generally mirrored HCV RNA levels, there was no clear pattern that could predict clearance or persistence. Among the 245 participants who were positive for HCV RNA at the time of acute HCV detection, 214 were either untreated (n = 137) or had chronic infection (persistent HCV RNA and estimated duration of infection ≥26 weeks) at the time of treatment initiation (n = 77) and formed the study population for assessment of spontaneous clearance (Fig. 1). In this group who were HCV RNA-positive at acute HCV detection (n = 214), spontaneous clearance occurred in 14% (29 of 214) of individuals. Among those with available plasma IP-10 levels at acute HCV

detection (n = 187), individuals who failed to clear HCV spontaneously had significantly higher mean plasma IP-10 levels at acute HCV detection than those with spontaneous viral clearance (248 ± 32 versus 142 ± 22 pg/mL, P = 0.008; Fig. 4A); however, the median plasma IP-10 levels did not differ (133 versus 103 pg/mL, P = 0.430). Although one individual had a very high IP-10 value (3,071 pg/mL), mean IP-10 levels remained significantly higher in those without clearance excluding this individual (230 ± 27 versus selleck screening library 142 ± 21, P = 0.010). ROC curve analysis identified an IP-10 level of 380 pg/mL as the most useful threshold associated with spontaneous clearance. No patients with a baseline IP-10 ≥380 pg/mL (0 of 22) achieved spontaneous clearance, compared to 16% (27 of 165) of those with IP-10 levels <380 pg/mL (P = 0.048; Fig. 4B). There was no significant difference in the proportion with spontaneous clearance stratified by plasma IP-10 levels above and below 150 pg/mL (15%, <150 pg/mL, versus 13%, ≥150 pg/mL; P = 0.835). Other factors associated with spontaneous viral clearance were also examined (Table 3).

The key difference from the LMR hypothesis is that, because mimicry is the source of frequency dependence, there is no equivalent frequency-dependent advantage for heteromorphs when they

are rare – they are assumed always to be readily identifiable as mates. Instead, the MM hypothesis assumes that there is some frequency-independent cost borne by the andromorphs: either they are more likely to be attacked by predators than heteromorphs because they are less cryptic (Robertson, 1985), or they are more likely than heteromorphs to be encountered by males, because they are more conspicuous or behave more like males (Sherratt, 2001). Several studies have found evidence that appears

to support the MM hypothesis (Sirot et al., 2003; Rivera & Sánchez-Guillén, 2007; Hammers click here & Van Gossum, 2008; Van Gossum et al., 2011), but in some cases, the reported data are also consistent with the LMR hypothesis (Ting et al., 2009). Hence, the need for predictions that are unique to one or the other hypothesis, and experimental studies, which can test those predictions, has been highlighted (Sherratt, 2001; Van Gossum & Sherratt, 2008). Because LMR is based on males learning to recognize the common female morph as a mate, this morph should always receive a higher number of mating attempts. In contrast, this website the MM hypothesis does not predict that the common morph will always receive more mating attempts, but instead, it predicts (uniquely) that andromorphs should be less harassed when they are rare relative to males, and hence that under equilibrium conditions andromorphs should be relatively more common in populations where the sex

see more ratio is male biased (Sherratt, 2001; Van Gossum & Sherratt, 2008). Although both of these predictions have some empirical support (Hinnekint, 1987; Cordero, 1992; Forbes, Richarson & Baker, 1995; Hammers & Van Gossum, 2008), the problem with testing them in real populations is that female morph frequency may correlate with sex ratio in the wild (e.g. Hammers & Van Gossum, 2008), making it difficult to disentangle cause and effect. A more fruitful line of enquiry may be to examine male behaviour in more detail. There are two studies where andromorph females have been observed to behave similarly to males, and males have responded to them as if they were other males, suggesting that they might actually be fooled by andromorphs (Andrés, Sánchez-Guillén & Cordero-Rivera, 2002; Sirot et al., 2003).