However, the level was reduced in the low avidity cells. Averaged data are shown in Fig. 4(b). The total phospho-ERK1/2 level in unstimulated cells was similar between the lines. The kinetics of ERK phosphorylation in high and low avidity CTL suggested that high avidity CTL undergo more rapid phosphorylation of ERK1/2 compared with low avidity CTL. However, at 60 min, the amount of phospho-ERK present in high and low avidity cells was similar when evaluated under conditions where the threshold stimulatory peptide concentration was used (10−6 m for low avidity cells and 10−12 m

for high Acalabrutinib avidity cells). By 6 hr post-stimulation, the phospho-ERK1/2 signal had returned to baseline in both cell types (data not shown). The marked peptide concentration-dependent BMN-673 differences in ERK1/2 phosphorylation and calcium flux between the lines suggested that differences in the peptide sensitivity of high

versus low avidity cells was controlled at a more membrane proximal step in the TCR signal transduction cascade. The transmembrane adaptor protein LAT provides a central signalling nexus for activation through initiation of signalosome formation. This complex controls recruitment and activation of phospholipase C-γ1, phophoinositide 3 kinase, and Ras.6,7 We first determined whether total protein levels of LAT in high and low avidity CTL differed and found that this protein was present at equal levels in both CTL lines (Fig. 5a). To evaluate LAT activation, the high and low avidity CTL were stimulated with titrated concentrations of peptide. Phosphorylation of LAT at tyrosine 191 was quantified by intracellular staining. This analysis revealed a pattern similar to that for other molecules analysed in that high avidity CTL were able to induce phosphorylation at all concentrations of peptide used, whereas low avidity CTL exhibited statistically significant increases in LAT phosphorylation Fludarabine cost compared

with stimulation with APC in the absence of peptide only following exposure to APC pulsed with the highest amount of peptide (Fig. 5b,c, for clarification, the significance (*) shown on figure is comparing −5M and −9MCTL). These data suggested that differences in ERK1/2 signalling in high versus low avidity cells arose at a more membrane proximal step in TCR signalling. Tyrosine phosphorylation of ITAMs on the TCR-associated CD3 chains is one of the initial biochemical events detectable in T cells after TCR ligation.3 Phosphorylation at these sites allows ZAP-70 binding and activation, which then becomes competent for phosphorylation of LAT.37,38 To assess CD3ζ phosphorylation in high or low avidity CTL, cells were stimulated with APC bearing titrated concentrations of Ova257–264 peptide and CD3ζ immunoprecipitated at 10 or 60 min post-stimulation. The immunoprecipitates were subjected to SDS–PAGE and immunoblotted with anti-phosphotyrosine antibody. As evident from Fig.

Moreover, spontaneous T-cell proliferation following stimulation with autologous monocyte-derived dendritic cells (autoDCs) has Navitoclax molecular weight been observed in vitro. In this study, we characterized the nature and immunological basis of the autoDC reactivity in the T-cell repertoire of healthy donors. We show that a minority

of naive and memory CD4+ T cells within the healthy human T-cell repertoire mediates HLA-restricted reactivity against autoDCs which behave like a normal antigen-specific immune response. This reactivity appeared to be primarily directed against myeloid lineage cells. Although cytokine production by the reactive T cells was observed, this did not coincide with overt cytotoxic activity against autoDCs. AutoDC reactivity was also observed in the CD8+ T-cell compartment, but this appeared to be mainly cytokine-induced rather than antigen-driven. In conclusion, we show that the presence of autoreactive T cells harboring the potential to react against autologous and HLA-matched allogeneic myeloid cells is a common phenomenon in healthy individuals. These autoDC-reactive T cells may help the induction of primary T-cell responses at the DC priming site. This article is protected by copyright.

All rights reserved “
“Institut Curie, Paris, France National Centre for Cardiovascular Research Carlos III, https://www.selleckchem.com/products/CAL-101.html Madrid, Spain DC NK lectin group receptor-1 (DNGR-1, also known as CLEC9A) is a C-type lectin receptor expressed by mouse CD8α+ DC and by their putative equivalents in human. DNGR-1 senses necrosis and regulates CD8+ T-cell cross-priming to dead-cell-associated antigens. In addition, DNGR-1 is a target for selective in vivo delivery of antigens to DC and the induction of CD8+ T-cell and Ab responses.

In this study, we evaluated whether DNGR-1 targeting can be additionally used to manipulate antigen-specific CD4+ T lymphocytes. Injection of small amounts of antigen-coupled anti-DNGR-1 mAb into mice promoted MHC class II antigen presentation selectively by CD8α+ DC. In the steady state, this was sufficient to induce proliferation of antigen-specific naïve CD4+ T cells and to drive their differentiation into Foxp3+ regulatory lymphocytes. Co-administration of adjuvants prevented this induction of tolerance check and promoted immunity. Notably, distinct adjuvants allowed qualitative modulation of CD4+ T-cell behavior: poly I:C induced a strong IL-12-independent Th1 response, whereas curdlan led to the priming of Th17 cells. Thus, antigen targeting to DNGR-1 is a versatile approach for inducing functionally distinct CD4+ T-cell responses. Given the restricted pattern of expression of DNGR-1 across species, this strategy could prove useful for developing immunotherapy protocols in humans. Regulating the T-cell compartment is the principal function of DC and therefore, manipulation of DC offers great promise for immune intervention 1, 2.

, 2007). Finally, sublingual vaccines require much less of the antigen than is required for intragastric vaccination. Also, sublingual mucosa have been proposed to be more permeable to low-molecular-weight drugs (Zhang

et al., 2002) and small immunogenic peptides than the cheek mucosa (Squier, 1991), a general oral VX-809 mucosa that contains dendritic cells (DCs). DCs take up foreign antigens in the submucosal region, which migrate to the regional lymph nodes, where the antigen is presented to T-lymphocytes by DCs to activate the adaptive immune responses (Song et al., 2009). The simultaneous application of adjuvants with an antigen can efficiently induce an antigen-specific immune response. Maltose-binding protein (MBP) is a high affinity maltose/maltodextrin-binding protein and a periplasmic receptor for the capture and transport of maltodextrins from the periplasmic space in gram-negative

bacteria (Fox et al., 2001; Fernandez et al., 2007). MBP was recently reported to act as an adjuvant that elicits innate immunity through Toll-like receptor 4 (TLR4) (Fernandez et al., 2007). Given that MBP can easily be prepared by taking Rapamycin in vitro advantage of its characteristic binding to maltose (Zhu et al., 2007), as well as the enhanced solubility and stability of fusion proteins, MBP is used to facilitate the production and delivery of subunit vaccines against various pathogenic bacteria and viruses (Fox et al., 2001; Routzahn & Waugh, 2002). Although hagA was originally easy to aggregate as an inclusion body (Fox et al., 2001), even the minimal antigenic region of the 25-kDa protein, the fusion form of the 25k-hagA-MBP protein used in this

study, is drastically easier to dissolve under hydrophilic conditions. Therefore, we analyzed the immune responses induced by the fusion protein 25k-hagA-MBP, which comprises the 25-kDa antigenic region of hagA purified from P. gingivalis, including the Olopatadine hemagglutinin-associated minimum motif ‘PVQNLT’ amino acid sequence in the Ab recognition sites (Shibata et al., 1999) as well as MBP from Escherichia coli, to assess the potential sublingual vaccine for preventing P. gingivalis infection. Female 8–11-week-old BALB/c mice were purchased from Sankyo Laboratory Services (Tokyo, Japan) and maintained under pathogen-free conditions in the experimental facility of Nihon University School of Dentistry at Matsudo. Mice received sterile food and water. All animals were maintained and used in accordance with the Guidelines for the Care and Use of Laboratory Animals (Nihon University School of Dentistry at Matsudo). Plasmid pMD157-expressing 25k-hagA-MBP was kindly provided by Dr Yoshimitsu Abiko (Nihon University). The antigen was purified using a p-MAL4 protein purification kit (Bio-Rad, Hercules, CA) (Riggs, 2000; Suyama et al., 2004; Kobayashi et al., 2006).

Results: 

The data demonstrate a severe weakening of the lymphatic pump in aged MLV including diminished lymphatic contraction amplitude, contraction frequency, and as a result, lymphatic pump activity. The data also suggest that the imposed flow gradient-generated shear-dependent relaxation does not exist in aged rat MLV, and the sensitivity of both adult and aged MLV to such shear cannot be eliminated by nitric oxide (NO) synthases HIF inhibitor blockade. Conclusions:  These data provide new evidence of lymphatic regional heterogeneity for both adult and aged MLV. In MLV, a constant interplay between the tonic and phasic components of the myogenic response and the shear-dependent release of NO predominantly determine the level of contractile activity;

the existence of another shear-dependent, but NO-independent regulatory mechanism is probably present. Aging remarkably weakens MLV contractility, which would predispose this lymphatic network to lower total lymph flow in resting conditions and limit the ability to respond to an edemagenic challenge in the elderly. “
“Dynamic changes in intracellular Ca2+ levels in vascular smooth muscle cells are critically important for cardiovascular regulation. This Special Topic Issue highlights a series of expert Selleckchem Hydroxychloroquine opinion articles focused on this important subject. After Immune system a brief overview, novel discoveries surrounding smooth muscle cell Ca2+ influx via L-type and T-type channels are reviewed. Current work revealing the functional importance

of dynamic Ca2+ signaling in the control of the parenchymal microvasculature and the emerging role of mitochondrial Ca2+ signaling and store-operated Ca2+ entry in smooth muscle cells is discussed. Finally, recent data describing a new target of localized Ca2+ signaling in arterial myocytes that is responsible for membrane depolarization is reviewed. Authors were encouraged to write in an opinionated and provocative manner with the hope of stimulating discussion in this area of research. “
“Please cite this paper as: White K, Kane NM, Milligan G, Baker AH. The role of miRNA in stem cell pluripotency and commitment to the vascular endothelial lineage. Microcirculation19: 196–207, 2012. Vascular endothelial cells derived from human pluripotent stem cells have substantial potential for the development of novel vascular therapeutics and cell-based therapies for the repair of ischemic damage. To gain maximum benefit from this source of cells, a complete understanding of the changes in gene expression and how they are regulated is required. miRNAs have been demonstrated to play a critical role in controlling stem cell pluripotency and differentiation and are important for mature endothelial cell function.

Two-way repeated measures ANOVA was used to determine the effects of group, treatment, and group–treatment interactions on measured variables (Sigmastat, Chicago, IL, USA). For all ANOVA procedures, Student–Newman–Keuls post hoc analysis was used to identify pair-wise differences among specific groups. Significance was assessed at p < 0.05. PVNS was performed on arcade bridge arterioles to determine responsiveness to sympathetic nerve stimulation [24]. These arterioles, originating from the thoracodorsal and 11th intercostal arteries, are the site of the majority of vascular resistance in the spinotrapezius muscle and hence of major importance in regulation

of blood flow in the muscle [5]. A beveled micropipette was filled with 0.9% saline, attached to a Grass Stimulator (Model learn more S9; Grass Instruments, Quincy, MA, USA), and the tip was brought to gently rest in the arteriolar adventitia. The Trametinib in vivo perivascular nerves were

stimulated between 20 and 60 seconds to develop stable constriction at a random frequency of 2–16 Hz. The observation site was distal to the stimulation site by 2–5 mm in the direction of flow. Microvascular reactivity was assessed first under normal superfusate conditions, then in the presence of phentolamine (1 μm). Arterioles were allowed to recover greater than two minutes between stimulations to return to baseline diameter. AH was induced in a separate set of rats through the stimulation of muscular contraction to determine the impact of PMMTM exposure on metabolically induced vasodilation as previously described [24]. Briefly, electrodes were attached to the rostral and caudal ends of the muscle and attached to a Grass Stimulator. Muscular contraction was induced at a frequency of 2–12 Hz randomly for one minute. The l-NMMA was added following normal superfusate responses. Arterioles were allowed to recover greater than two minutes between stimulations to return to baseline diameter.

Intraluminal infusion was performed on a separate set of rats as previously described [35]. Briefly, a micropipette was positioned in line with the stream of blood within an arcade bridge arteriole. Following an acclimation period, ejection of A23187 was performed for three minutes at 10–40 PSI via a Picospritzer II (World Precision Instruments Inc., Sarasota, FL, USA). Isolated mesenteric PAK5 or coronary arteries were equilibrated until the vessels achieved spontaneous tone, then myogenic responsiveness was determined from 0–90 mmHg (coronary) and 0–105 mmHg (mesenteric) in 15 mmHg increments as previously described [26, 27]. Endothelium-dependent arteriolar dilation was assessed with ACh and A23187. NO sensitivity was assessed with the NO donor Spermine NONOate. Adrenergic sensitivity was assessed with PE. Following the addition of each agent, a washout period was performed to allow the vessel to return to basal tone prior to the addition of the next vasoactive agent.

Candida albicans is affected by alpha defensins, LL-37, calprotectin, and HBD1.107,109 In addition, C. albicans is inhibited by both SLPI and Elafin.28 Bacterial vaginosis has been described as a co-factor for HIV

acquisition. Cu-Uvin et al.110 have shown BV to be significantly associated with genital tract shedding of HIV. BV is characterized by loss of the normal protective Lactobacilli and overgrowth of Selleck Opaganib diverse anaerobes.111 The microorganisms involved in BV are many, but include Gardnerella vaginalis, Mobiluncus, Bacteroides, and Mycoplasma. Low levels of SLPI and an increase in lactoferrin in cervicovaginal fluid have been associated with BV,59,112 The increase in lactoferrin could be attributed to higher levels of neutrophil activation and degranulation, but was not sufficient to protect against HIV infection.59 Elafin decreases in CVL from women with BV.61 Trichomonas is an extracellular protozoa

that adheres to and damages vaginal epithelial cells.113T. vaginalis infection predisposes women to HIV infection and increases HIV shedding in the FRT.114,115Trichomonas vaginalis CHIR 99021 lipophosphoglycans induce a dose-dependent upregulation of IL-8 and MIP3α in vaginal, ectocervical, and endocervical epithelial cells.116 TV Infection by T. vaginalis results in significantly higher concentrations of vaginal fluid neutrophil defensins and cervical IL-8 in women with asymptomatic trichomoniasis compared to uninfected counterparts.55 Multiple distinct species of Lactobacilli colonize the lower genital tract of women. In healthy Quisqualic acid women of reproductive age, major phylotypes of Lactobacillus includes L. crispatus, L. iners, L. gasseri, L. jensenii, L. gallinarum, and L. vaginialis.117 These commensals play a very important role in maintaining a healthy vaginal ecosystem that protects

women against sexually transmitted pathogens. The presence of Lactobacilli creates an acidic environment that is detrimental to pathogens. In addition, they secrete bacteriocins that directly kill pathogens. Loss of Lactobacilli through illness or antibiotics intake increases a woman’s chance of getting infected by a sexually transmitted pathogen.117 However, in one study, lactobacilli were reported to enhance HIV infection.118 We and others have shown that FRT secretions contain antimicrobials that act either alone or in synergy to inhibit a number of sexually transmitted pathogens (J. V. Fahey, R. M. Rossoll, C. R. Wira, unpublished observation).40,82,84,92,119 Recently, we tested FRT secretions against L. crispatus and found no effects.92 This suggests an intricate balance in which constitutive secretions containing endogenous antimicrobials can affect pathogens but not commensals, which maintain a healthy vaginal ecosystem. Given the number of proteins with antimicrobial properties found in the FRT, it is likely there are many others yet to be discovered. Several promising candidates are shown in Table II.

Thus, ATP may be acting to allow inflammasome-activating TLR ligands (or other inflammasome activators) to enter the cell. Support for this idea comes from the fact that downregulation of Panx1 or inhibition of its binding to P2X7R

by an inhibitory peptide, 10Panx1, downregulates LPS in the presence of ATP induction of NLRP3 inflammasome activity 13. Another proposed mechanism is based on the fact that the ATP interaction CP-690550 price with P2X7R leads to K+ efflux; thus, ATP may be acting to cause an intracellular cation change necessary for inflammasome activation 14, 15. This idea is supported by the fact that inhibition of K+ efflux by increased extracellular K+ concentrations suppresses NLRP3 inflammasome activation 16, 17. When reconciling these two mechanisms, one should note that inhibition of K+ efflux does not affect Panx1 channel formation and that, conversely, 10Panx1 peptide BGB324 order inhibition of Panx1-mediated pore formation does not inhibit potassium efflux 12, 18. Thus, it is possible that channel formation and potassium efflux are independent functions of the P2X7R/Panx1 complex that are both necessary for NLRP3 inflammasome activation. In initial studies to determine why ATP is not necessary for inflammasome activation in R258W KI mice, it was found that the lack

of ATP dependence occurred in spite of inhibition of K+ efflux. Therefore, the mutation did not cause MYO10 a defect in the intracellular cation balance. In addition, there was no difference between KI and WT cells in their ability to generate endogenous extracellular ATP, hence the ATP independence was not the result of excessive ATP production from KI cells either 9. Further insight

into ATP function in R258W KI and WT cells came from studies of inflammasome activation (IL-1β release) in the presence of 10Panx1 peptide. We found that the presence of 10Panx1 decreased the inflammasome activity of WT cells by about 50% when added up to 4 h prior to the ATP pulse but had no effect on KI cells. This indicated that WT cells were dependent on the rapid Panx1 channel formation, whereas KI cells were not; however, residual inflammasome activation in WT cells in the presence of the Panx1 channel blockade was still dependent on the presence of ATP (perhaps acting via another cellular entry mechanism, depicted in Fig. 1 as the P2X7R/X channel). When 10Panx1 was added together with LPS (24 h prior to the ATP pulse), even the inflammasome activation of KI cells was substantially inhibited. This indicated that Panx1-mediated entry also occurs in KI cells, although that this route of entry is not absolutely critical as inflammasome activation occurs at least partially in the absence of ATP (perhaps due to LPS entry via other cellular mechanism; indicated as channel X in Fig. 1) 9.

IGF-I gene expression was localized in glomerular podocytes, whereas the IGF-IR gene was expressed in glomerular podocytes and cortical tubular cells. In nephrotic rats, the expression of the IGFBP-10 gene was increased in glomerular podocytes; however, the expression levels of IGFBP-2, -7 and -8 did not change. Conclusion:  IGFBP-2, -7, -8 and -10 are produced by normal and injured glomerular podocytes and may regulate local IGF-I actions in podocytes and/or cortical tubular

cells in the kidney. “
“Long-term haemodialysis patients may selleck products be at risk of hydrosoluble vitamin deficiencies. This study aimed to test the hypothesis that in patients with serum B12 < 300 pmol/L, intramuscular hydroxocobalamin reduces erythropoietin requirements whilst maintaining haemoglobin concentrations (Hb). Study design was prospective, non-randomized, open label, with single group assignment. In 61 patients hydroxocobalamin 1000 μg was given weekly for 3 weeks and erythropoietin dose adjusted to target a Hb of 11–12 g/L. The primary outcome was the change in erythropoietin requirements at 2 years. Secondary outcomes included assessment of change in biochemical or clinical parameters. The erythropoietin dose reduced from 11 000 ± 7000

(10 000) IU to 5000 ± 6000 (3000) IU per week (P < 0.001) with no change in Hb 116 ± 16 (117) g/L before and after 114 ± 15 (113) g/L (P = 0.488) hydroxocobalamin supplementation. Serum albumin rose from 35 ± 4 (35) g/L to 36 ± 4 (36) g/L (P = 0.03). A significant LY2109761 rise in red cell folate (RCF) and serum vitamin B12 levels was observed. Serum ferritin rose despite a reduction

in intravenous iron usage and no significant change in c-reactive protein or transferrin saturation. In HD patients with B12 < 300 pmol/L, following treatment with hydroxocobalamin there was reduced erythropoietin requirements, maintained Hb and a small but significant rise in the serum albumin. RCF may be low in haemodialysis patients with metabolic cobalamin deficiency and rises significantly after supplementation. Hydroxocobalamin supplementation may have the potential to reduce the cost Liothyronine Sodium of anaemia management. “
“Insomnia is an important problem in dialysis patients. A greater prevalence of insomnia in chronic kidney disease compared with non-renal patients suggests a role for uraemic toxins in contributing to insomnia. The aim of this study was to examine if dialysis modality and membrane permeability is associated with the frequency and severity of insomnia in haemodialysis patients. In our cross-sectional study, we evaluated 122 patients who were divided into three groups: on-line haemodiafiltration, high flux haemodialysis and low flux haemodialysis. The frequency and severity of insomnia was evaluated with the Insomnia Severity Index. Insomnia was present in 47.5% of all patients.

2A). In this experimental setting, we also observed a significant increase this website in the expression of the activation marker CD38 on B-cell surface after IFN-β treatment (Supporting Information Fig. 2B). Given that this protein is notoriously type I IFN inducible

[20], this result clearly shows that B lymphocytes are target of the IFN-β therapy confirming previous study by Zula et al. [21] who described a rapid activation of IFN signal transduction pathways in B cells present in unseparated blood from RRMS patients soon after IFN-β injection. In the past, we dissected the regulation of TLR7 in maturing monocyte-derived DCs and observed that its transcription was dependent on the endogenous IFN-β release [22]. Thus, to evaluate whether IFN-β therapy would modulate TLR7 expression in MS patients, we first monitored by real-time RT-PCR TLR7 level of transcription, together with that of TLR9, in MS patients versus HDs. It was of great interest to find that PBMCs obtained from MS patients display a clear defect, as compared with those of HDs, in TLR7 expression that was statistically significant (25 HDs and 45 MS patients analyzed) (Fig. 2A). This difference was not observed in the transcription

of TLR9 gene (Fig. 2B), demonstrating that in MS patients, the defective TLR7 expression is specific. Furthermore, we observed that in PBMCs isolated from the same MS patients U0126 clinical trial following 1 month of IFN-β therapy, the level of TLR7 mRNA was restored to the level observed in HDs, while that of TLR9 was not modulated (Fig. 2A and B). In the attempt to investigate which TLR7-expressing cell types in the peripheral blood might be responsible for this defect in MS patients, B cells and monocytes were purified from both HDs and MS patients at baseline and 1 month after the beginning of IFN-β therapy, since these two leukocyte populations express TLR7. Data on TLR7 expression in B cells isolated from HDs or MS (7 and 13 individuals, respectively) did not mirror the impairment observed in the context of the

mixed cell population of PBMCs (Fig. 2C and D), although a slightly enhanced level of TLR7 transcription in response to IFN-β Phosphoprotein phosphatase occurred also in this experimental setting. As observed in unseparated PBMCs, TLR9 levels of B cells did not differ in HDs and MS patients irrespective of IFN-β treatment. Interestingly, when the expression of TLR7 was analyzed in monocytes of MS patients (13 individuals), a different picture appeared. Indeed, a lower TLR7 mRNA level was highlighted in monocytes from MS patients than that obtained from HD (8 individuals) and, moreover, also a robust induction was observed in response to IFN-β therapy (longitudinal analysis of 5 patients at baseline and 1 month after IFN-β treatment) (Fig. 2E). TLR9 expression was absent in monocytes (data not shown). These data for the first time indicated a defect in TLR7 signaling in monocytes of MS patients.

40, SD = 4.13; t(21) = 3.98, p = .001, d = 1.91; see Figure 5). The middle

region also showed significantly greater PSW PD-0332991 in vitro amplitude than the right region (t(21) = 3.32, p = .003, d = 1.59). To examine the mean amplitude of the Nc component in the temporal region, a 3 (condition: VPC, recent familiar, novel) × 2 (region: Left, right) × 2 (group: CON, HII) repeated-measures ANOVA was run using condition and region as the within-subjects factors and group as the between-subjects factor. This analysis revealed a significant interaction between condition and group (F(2, 40) = 4.12, p < .024, ηp2 = .17). Follow-up t tests revealed that for CON, mean amplitude of the Nc did not differ across the three conditions (VPC: M = −3.98, SD = 3.93; recent familiar: M = −4.86, SD = 4.01; Novel: M = −3.59, SD = 2.92; all ps > .14). For HII, the Nc response to the VPC face (M = −5.03, SD = 3.64) was significantly greater (more negative) than to the recent familiar face (M = −.58, SD = 3.00; t(5) = 2.62, p = .047, d = 1.46) and marginally greater than to the novel face (M = −2.93, SD = 3.63; t(5) = 2.02, p = .099, d = .63); Nc responses to recent

familiar and novel faces did not differ for HII (p = .29). No other main effects or interactions were significant. A 3 (condition: VPC, recent familiar, novel) × 2 (region: Left, right) × 2 PD0325901 (group: CON, HII) repeated-measures ANOVA with condition and region as the within-subjects factors and group as the between-subjects factor examined the mean amplitude of Resveratrol the PSW component for the temporal electrode sites and, consistent with results at frontocentral electrode sites, found a main effect of region (F(1, 20) = 11.15, p = .003, ηp2 = .36), with PSW mean amplitude greater (more positive) over the left region (M = 5.11, SD = 4.12) as compared to the right (M = −1.42, SD = 5.17), A main

effect of condition was also revealed (F(2, 40) = 8.84, p = .001, ηp2 = .31), with a significantly greater PSW for the recent familiar condition (M = 3.15, SD = 3.67) as compared to the VPC condition (M = .93, SD = 3.05; t(21) = 2.94, p = .008, d = .67) and marginally greater responding to the recent familiar as compared to novel (M = 1.45, SD = 2.94; t(21) = 1.97, p = .063, d = .52). PSW responses to VPC and novel faces did not significantly differ (p = .5). A significant interaction between condition and group (F(2, 40) = 8.84, p = .001, ηp2 = .31) was also found. Follow-up t tests revealed that for HII, PSW to the recent familiar condition (M = 5.56, SD = 3.42) was significantly greater as compared to the VPC (M = −.10, SD = 3.59; t(5) = 3.03, p = .029, d = 1.77) and marginally greater as compared to novel (M = 1.13, SD = 3.04; t(5) = 2.40, p = .06, d = 1.5); for CON, PSW to recent familiar (M = 2.25, SD = 3.43) was marginally greater than to VPC (M = 1.32, SD = 2.85; t(15) = 1.86, p = .08, d = .3), while there was no difference between PSW to novel (M = 1.57, SD = 2.