Autophagy is an adaptive, cell survival-promoting mechanism. However, it is also considered a cell death-inducing condition that, if prolonged, can lead to what is known as “nonapoptotic type II programmed cell death.” To study whether the autophagic activation in our model promotes or compromises cell survival, we treated HeLa cells stably expressing mtdsRed with 3MA, a class III PI3K inhibitor often applied as a suppressor of autophagosomal formation.24 Previous reports have shown that EFV exerts an inhibitory effect on cell viability and proliferation in both Hep3B and HeLa, with higher concentrations of this drug promoting apoptosis.13 Our experiments revealed DNA Methyltransferas inhibitor that inhibition

of autophagy worsened the damaging effect of EFV, suggesting that autophagy plays a cell survival-promoting role. Static cytometry showed that exposure to EFV (24

hours) produced a concentration-dependent cell number reduction (92.35 ± 3.50% and 43.04 ± 2.74% in EFV 25 μM and 50 μM, respectively, versus 100% in untreated cells). Importantly, this reduction was more pronounced in the presence of 3MA (76.84 ± 5.22% and 30.36 ± 2.11% in EFV 25 μM and 50 μM, respectively, versus 100% in 3MA-treated controls) (Fig. 7A). When we studied the mitochondrial signal by means of mtdsRed fluorescence, cells treated with EFV 25 μM in the presence of 3MA showed higher mean fluorescence values than those in which autophagy was not inhibited. However, in the case of EFV 50 μM Opaganib the increase in the red signal was modest and without statistical significance.

This provides further confirmation that EFV 50 μM leads to a blockage of the autophagic pathway in our model. Finally, no significant changes were detected with the lowest EFV concentration (10 μM) in the presence of 3MA (Fig. 7A). Similarly, incubation with 3MA alone did not affect cell number or mean mtdsRed fluorescence (data not shown). A similar effect of 3MA regarding cell survival was observed in Hep3B (Fig. 7B) and primary human hepatocytes (Fig. 8E). Moreover, we performed Bivariate Annexin V/PI analysis selleckchem to address the induction of apoptotic cell death in Hep3B cells subjected to EFV in the presence of 3MA. The presence of four cellular subpopulations was evaluated by static cytometry: vital (double negative), apoptotic (Annexin V+/PI−), late apoptotic/necrotic (Annexin V+/PI+), and damaged cells (Annexin V−/PI+) cells. As displayed in Fig. 7B. cotreatment with 3MA enhances the apoptotic effect of EFV but it does not interfere with the action of the common apoptotic inducer STS, thus suggesting a specific role of autophagy in the EFV-induced effect. Autophagy is a cellular self-digestion process crucial for cell differentiation and survival.25 All eukaryotic cells rely on constitutive autophagy to carry out the basal elimination of damaged organelles.

,17 we believe that one case, in which UC developed 4.5 years after IFN-β1a treatment was discontinued, was not caused by IFN, as no evidence was provided to support this assumption of causation. The interval between the initiation of IFN therapy and development or exacerbation of UC was 7.7 ± 9.8 months (mean ± standard deviation) in 14 of the remaining 15 cases (one case lacked a detailed description).

This interval was 4.7 ± 5.2 months for the nine cases reported in Japan (Table 1) and 13.1 ± 14.1 months Doxorubicin cell line for the five cases reported in Europe and the USA (Table 2). Although these intervals appeared to be shorter in the cases reported in Japan, the difference was not significant (unpaired Student’s t-test; P = 0.06, one-tailed). If we divide the reported

cases into three groups, the interval from the initiation of IFN treatment to development of UC was 4.3 ± 4.9 months for patients with type-C chronic hepatitis (n = 11), 9.0 ± 4.2 months for those with renal cell carcinoma (n = 2), and 28.5 ± 20.4 months for those with MS (n = 4). This interval was significantly Sorafenib mw longer for patients with MS (unpaired Student’s t-test; P < 0.01, one-tailed). The number of patients with UC in Japan is reported to be 104 721, and the number of new cases of UC per year is approximately 5000.28 In some of these new cases, patients had long experienced the symptoms of UC, but the condition was only recently diagnosed. In 1995, Morita et al. reported the incidence of UC development as 1.95 cases per 105 person-years, and the incidence is rising in Japan.29 With 5000 new cases per year28 and the Japanese population of 200 million, the incidence of UC is about 2.5 cases per 105 person-years. Asakura et al. reported the UC prevalence in Japan to be 63.6 cases per 105 persons in 2005.30 The frequency and prevalence of UC in Japan are relatively low;29,30 thus, UC could be considered

a rare disease. Furthermore, because development or exacerbation of UC in response to IFN therapy is rare, its occurrence during or after IFN therapy may be due to random causes. Even if the data from recently published studies31,32 are sufficient to support a causal correlation between IFN treatment selleck products and UC (or support its effectiveness for treating UC), we must compare the frequency of UC development or exacerbation between the general population (i.e. those who have not undergone IFN treatment) and patients with chronic hepatitis C, renal cell carcinoma, or multiple sclerosis who have been treated with IFN. However, it is reasonable to suspect that published cases of UC associated with IFN are in fact due to an adverse reaction to IFN for the following reasons: (i) the interval between the development of UC and initiation of IFN treatment is relatively short; (ii) in many cases, acute symptoms (e.g.

Although staining for additional mesenchymal markers check details would have strengthened the conclusions, the data are nonetheless compelling in demonstrating in the CCl4 model that hepatocytes and their derivatives do not express FSP1, type I collagen, or α-SMA and thus do not undergo EMT. Why do the authors of the two lineage tracing articles on hepatocyte EMT reach such different conclusions? Taura et al. propose that technical limitations associated with β-Gal staining yielded false-positive results in the Zeisberg

study. This hypothesis is supported by the observation that detection of β-Gal expression by immunostaining does not coincide with detection of β-Gal activity by X-gal.12 I would suggest that failure to rigorously

define EMT is another reason for the divergent findings. BIBW2992 cost Zeisberg et al. define EMT through expression of the controversial and potentially nonspecific marker FSP1 but do not examine collagen synthesis, the feature ultimately most relevant to fibrosis. Taura et al., although focused on collagen synthesis as a primary marker of EMT, also demonstrate that hepatocytes in the fibrotic liver fail to express α-SMA, a finding of key importance given the many demonstrations (including in their study) that α-SMA–positive cells make up a large percentage of fibrogenic cells. Does the work of Taura et al. lay to rest the concept of hepatocyte EMT? The answer is a qualified yes. There are caveats, including the reality that neither the genetic background of the mice nor the injury model (CCl4) accurately model human disease. Regardless, this study effectively refutes the published selleck products data that support hepatocyte EMT. Although it is still theoretically possible that hepatocyte EMT occurs in human disease,
s of evidence will be required for this to reemerge as a viable concept. Interestingly,

an exhaustive study has recently been published calling into question EMT in the kidney. Using two different epithelial cell–specific drivers, two different reporters, and two different models of renal fibrosis, Humphreys et al. find no evidence that epithelial cells of the kidney contribute to the myofibroblast population in vivo (or express FSP1).16 Like Taura and colleagues, this group suggests that nonspecific methods to detect the β-Gal reporter could have contributed to discordant findings in the literature. Thus, there is now convincing evidence that neither hepatocyte nor renal epithelial cell EMT occurs in fibrosis. Whether cholangiocyte EMT contributes to fibrosis in the liver is still an open question. Several groups, making use of both animal models and human tissue, have reported that cholangiocytes in fibrotic livers (from bile duct–ligated mice as well as humans with primary biliary cirrhosis, biliary atresia, and several other diseases) coexpress multiple epithelial and mesenchymal markers by immunostaining and are therefore likely to be undergoing EMT.

[50] These human studies may support the actual involvement

Raf inhibitor of exogenous NO in the pathogenesis of reflex esophagitis. In this context, another recent study demonstrated a diverse esophageal microbiome in relation to inflammation and metaplasia in the distal esophagus.[51] Further studies are warranted to investigate how the diversity of microbiomes in the oral cavity as well as the esophagus affect the exogenous luminal NO production at the GE junction or at the distal esophagus by modulating the conversion of nitrate to nitrite. One important observation concerning esophageal adenocarcinoma is its strong male predominance (male : female ratios of 3:1 to 12:1).[52, 53] The male-predominant see more gender difference consistently exists across the GERD spectrum,[54-56] although the ratios become higher with progression toward the later stages.[56] Meanwhile, reflux symptoms or non-erosive reflux disease in general affects more women than men.[57] These epidemiological data allow us to hypothesize that the esophageal epithelium is more vulnerable in men, or more resistant in women, to the refluxed gastroduodenal contents, than in their respective counterparts. Identification of the causative luminal factors for inducing the gender-related difference would be clinically relevant to predict the actual etiologic factors involved in the pathogenesis of reflux esophagitis in humans. Employing chronic rat reflux esophagitis

models[46] of both sexes, we found that there was a striking find more male-predominant, gender-related difference in esophageal tissue damage in the presence of exogenous NO and that estrogen

attenuated the esophageal tissue damage via the estrogen receptor.[58] Further, we found a potential role of esophageal mast cells in the mediation of the suppression of the immune system under estrogen administration.[58] Interestingly, the gender-related difference in the esophagitis model was more prominently observed when exogenous NO was administered compared with exogenous acid (pH 1.8),[58] suggesting that gender-related differences may be specifically potentiated in the presence of exogenous NO as the aggravating agent. These results indicated that gender-related differences in the susceptibility of the esophageal epithelium to damage by exogenous NO might be at least partially responsible for prominent gender-related disease differences in GERD in humans. The LES is a bundle of muscles at the lower end of the esophagus, and it plays a primary role in preventing reflux of gastric contents into the esophagus. It is well known that NO endogenously derived from cNOS localized to non-adrenergic, non-cholinergic nerves mediates the relaxation of the smooth muscle cells, including those of the LES.[59] An in vitro study using muscle strips from the LES of an opossum demonstrated that a low concentration of NO (nM) was sufficient to induce relaxation of the muscle.

[10] To explore the relevance of this signaling pathway for control of HCV RNA replication in mouse liver-derived cells, we generated stable liver cell lines of WT mice and knockout animals with targeted disruption of MAVS,−/−, IRF3,−/−, or IFNAR−/− by in vivo immortalization as described in detail in the Materials and Methods section. In brief, animals were subjected to hydrodynamic http://www.selleckchem.com/products/ABT-263.html tail vein injection of transposon plasmids for expression of constitutively active Akt1 (myrAkt1), for mutated Kras (Kras-G12V), and a short hairpin RNA (shRNA) targeting mouse p53 (shRp53) together

with a plasmid encoding a sleeping beauty transposase (pPGK-SB13) to facilitate genomic integration of the transferred transposons. This treatment led to the growth of palpable liver tumors ∼6-10 weeks postinjection. At this timepoint, animals were sacrificed and liver tumors were collected to establish individual cell lines by limiting dilution subcloning. Established mouse liver tumor (MLT) cell lines exhibited robust and sustained

cell growth in cell culture (Fig. 1A). Genetic disruption of cognate innate immune signaling molecules was confirmed by PCR (data not shown). Overexpression of myrAkt1 and Kras-G12V induces HCC as well as cholangiocellular carcinomas (CCC), which may originate from hepatocytes.[11, 12] Although hydrodynamic injection mainly targets hepatocytes,[13] we characterized the MLT-MAVS−/− cell line by subcutaneous LEE011 datasheet implantation

and subsequent immunohistochemical analysis of induced tumors growing in recipient mice. Using this approach, we confirmed expression of HCC markers cytokeratine 8 (CK8) and CK18, whereas CK19, a marker of cholangiocarcinoma cells, was not expressed (Supporting Fig. S1). Since miR-122 is check details an important determinant of HCV tissue tropism and enhances HCV RNA-translation/replication in MEFs,[6, 7] we determined endogenous levels of mouse miR-122 in these novel liver cell-derived cell lines (Fig. 1B). The abundance of miR-122 was more than 1,000-fold lower in all generated cell lines compared with primary mouse hepatocytes (PMHs), which expressed high endogenous levels of miR-122 comparable to that observed in primary human hepatocytes and ∼3-5-fold lower compared with the level in mouse and human liver. Next we explored the relevance of innate immune signaling and miR-122 expression for HCV RNA replication in these cells by transfecting them with a JFH1 luciferase reporter replicon (Pol +). A defective replicon with an inactivating mutation of the NS5B RNA-dependent RNA-polymerase (Pol −) served as negative control. As expected, we observed efficient amplification of the replication competent replicon in the highly permissive human hepatocarcinoma cell line Huh-7.

We produced VSVg pseudotyped lentiviral vectors expressing the murine Fah complementary DNA (cDNA)

from an internal SFFV promoter. The enhanced green fluorescence protein (eGFP) was coexpressed either by an internal ribosomal entry site (IRES) or by a 2A proteolytic cleveage site (RRL.PPT.SFFV.eGFP.pre*, RRL.PPT.SFFV.Fah.ires.eGFP.pre*, RRL.PPT.SFFV.Fah.2a.eGFP.pre*).29 The vector supernatants were produced by 293T cells, concentrated with Centricon Plus-70 filter units http://www.selleckchem.com/products/Adriamycin.html (Millipore, Schwalbach, Germany) and titrated on HepA1.6 cells.30 Viral titers were in the range of 107 to 108 IU/mL. Hepatocytes were isolated from 3 to 6-month-old mice as described.6 For further enrichment of hepatocytes we used discontinuous Percoll (GE Healthcare) gradients. A 25% phase prevented dead cells and debris from entering the gradient. A lower 50% phase facilitated the enrichment of small, highly viable, and robust hepatocytes. For depletion of nonparenchymal liver cells, we used PE (Phycoerythrin)-labeled anti-CD45 and anti-CD31 antibodies (BD Pharmingen), anti-PE MicroBeads on an automated MACS Separator (Miltenyi Biotech, Bergisch Gladbach). Analysis of eGFP expression was performed on day 5 after in vitro transduction of primary murine hepatocytes

or directly after hepatocyte isolation during serial transplantations by FACS. For in vitro experiments, hepatocytes were cultured on Primaria dishes (1.1 × 106 cells/35 cm2) in HCM medium (Lonza). Fah(-/-) hepatocytes isolated from C57Bl/6-Fahtm1Mgo were cultured in the presence of NTBC (9.6 ng/mL) BTK inhibitors high throughput screening (Swedish Orphan). Transduction (multiplicity of infection [MOI] 10) was performed as previously described by our group.6 RNA from hepatocytes was hybridized on the Affymetrix Mouse 430 2.0 GeneChip.

Data can be found at Geo link http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE34731. LM-PCR was performed and analyzed as described.31, 32 (See also Supporting Material and Methods.) C57Bl/6-Fahtm1Mgo (Fah(-/-)) mice are defective for the Fah gene, which encodes the enzyme fumaryacetoacetate hydrolase (Fah).25 Mice were maintained by supplementation of drinking water with NTBC (4 mg mL-1, Swedish Orphan International).26, selleckchem 27 To allow engraftment of hepatocytes the medication was discontinued For in vivo gene transfer, lentiviral particles were injected in 250 μL phosphate-buffered saline (PBS) intrasplenically (∼1 infectious particle / parenchymal liver cell). For ex vivo gene therapy 1 × 106 cultured Fah(-/-) hepatocytes were transduced overnight (MOI 10). For serial hepatocyte transplantation the livers from gene-corrected mice were perfused with collagenase. Aliquots of 0.5 × 106 liver cells were injected in 250 μL PBS into the next generation of Fah(-/-) mice.

A total of 8 of 11 (73%) nitrofurantoin cases had jaundice at presentation (Table 5), whereas only 3 of 11 (27%) of the minocycline cases had jaundice at presentation (Table 6). All patients with nitrofurantoin-induced AIH were treated with immunosuppression (Table 5), whereas two minocycline patients were not treated (Table 6). In one case attributable to rapidly improving jaundice, liver tests before therapy were instituted, and BMS-777607 cost not in another case attributable to mild liver enzyme abnormalities (Table 6). All cases with all parameters available to make a score for the likelihood of AIH received at least a “probable” score; however, in three cases, information about gamma globulins was not available for

PLX-4720 cell line the AIH score. At the end of follow-up, among those who had at least 6 months’ follow-up at the Mayo clinic, 22 of 23 (96%) of the DIAIH patients were in biochemical remission, as were 159 of 177 (90%) of the other AIH patients (NS). None of the DIAIH patients developed cirrhosis during follow-up, and all were alive at last follow-up, whereas 18 of 257 (7%) AIH patients had developed cirrhosis clinically (P = NS). Overall, five of these patients had decompensated

liver cirrhosis with mild ascites in most, and 13 patients had nonbleeding esophageal varices. Among the seven patients who died during the study period, only two deaths were liver related. One patient died of fulminant hepatic failure on the liver transplantation list a few months after presentation, and one other patient died in chronic liver failure and with a disseminated breast cancer. Others died of stroke, heart failure, and colon cancer, and two had unknown causes of death. At the end of follow-up, one of the above-mentioned patients with cirrhosis had undergone liver transplantation, two were listed, and one was evaluated for transplantation. The results of the current study suggest that among consecutive patients with click here well-characterized AIH, drug-induced AIH makes up a significant proportion, approximately 9%, of AIH cases. More than 90% of these DIAIH cases were associated with two drugs, nitrofurantoin and minocycline. Overall, the histological features of DIAIH seem to be identical

to those of AIH. Severe imaging abnormalities with liver lobe and general liver atrophy were also commonly observed in nitrofurantoin but not in minocycline cases, indicating postnecrotic scarring. None of the patients with DIAIH developed cirrhosis during follow-up, and these patients seem to have a generally favorable prognosis. All patients with DIAIH in whom discontinuation of immunosuppressive therapy was tried could withdraw drug therapy without a relapse, whereas only approximately one third of the other AIH patients did not experience a relapse after withdrawal of immunosuppression. Taken together, our results suggest that DIAIH is a distinct phenomenon, and a trial of withdrawal of immunosuppression should be undertaken in these patients.

Hepatocyte apoptosis is a characteristic

feature of NASH as opposed to simple steatosis.92,93 Recently, a prospective study in Chinese patients with paired liver biopsies confirmed that alterations in serum cytokeratin-18 fragment level correlated well with changes in the NAFLD activity score.79 Likewise, serum levels of adipokines have been tested in NAFLD subjects. In general, patients with NASH tend to have lower serum levels of adiponectin and higher tumor necrosis factor-alpha and interleukin-6 level.24,65 However, the overall accuracy of these markers has not been fully evaluated and is probably limited by their variability with time. As the hepatic manifestation of the MetS, it is expected that coronary artery disease (CAD) will be an important cause of Neratinib chemical structure morbidity and mortality in longitudinal studies. This has been borne out PI3K inhibitor in both population-based as well as clinic-based studies. However, data are accruing that the CAD risk with NAFLD may be greater than that expected through its association with the MetS.94 Possible mechanisms include

the contributions of NAFLD-related pathogenetic processes and epiphenomena such as oxidative stress, inflammatory cytokine alterations, changes in blood coagulation and an unfavorable atherogenic lipid profile. In a study of 317 adult Iranian patients undergoing coronary angiography, the detection of fatty liver by ultrasound scan increased 8-fold the risk of significant coronary artery disease.95 In addition, there are several studies showing an association with other markers of general cardiovascular risk such as carotid intima-media thickness,96,97 and total

Framingham risk score98 as well as those specific to CAD (coronary artery calcium score).99 However, since prospective data linking NAFLD and hard cardiovascular outcomes are not consistent among studies, routine workup for coronary selleck chemical artery disease cannot be recommended at this stage. Nevertheless, clinicians should be alert for symptoms and signs of vascular diseases. Lifestyle modification is the cornerstone of management of NAFLD. In observational studies, even modest weight loss (2–3 kg) is associated with reduction in hepatic steatosis and other histological improvement.79,100 Lifestyle programs emphasizing calorie and fat restriction and regular exercise have been successfully implemented both in adults101–103 and also children.104 Aerobic exercise training has been shown to reduce intrahepatic triglycerides and visceral fat even in the absence of significant weight changes. In a randomized controlled trial conducted in Australia, 19 NAFLD patients were randomized to aerobic exercise training or usual treatment for 4 weeks.105 Using magnetic resonance spectroscopy, patients undergoing aerobic exercise training showed a 21% reduction in hepatic triglyceride content and a 12% reduction in visceral fat. However, a combination of diet and exercise appears to be superior to either diet or exercise alone.

In this model, the parietal lobe is thought to play a pivotal role in binding together the synaesthetic perceptions (hyperbinding). In addition, we hypothesized that the auditory cortex and the fusiform gyrus would qualify as strong hubs in synaesthetes. Although synaesthetes and non-synaesthetes demonstrated a similar small-world network topology, the parietal lobe turned out to be a stronger hub in synaesthetes

than in non-synaesthetes supporting the two-stage model. The auditory cortex was also identified as a strong hub in these coloured-hearing synaesthetes (for the alpha2 band). Thus, our a priori hypotheses receive strong support. Several additional hubs (for which no a priori hypothesis has been formulated) were found to be different in terms of the R788 clinical trial degree measure selleck chemicals llc in synaesthetes, with synaesthetes demonstrating stronger degree measures indicating stronger interconnectedness. These hubs were found in brain areas known to be involved in controlling memory processes (alpha1: hippocampus and retrosplenial area), executive functions (alpha1 and alpha2: ventrolateral prefrontal cortex; theta: inferior frontal cortex), and the generation of perceptions (theta: extrastriate cortex; beta: subcentral area). Taken together this graph-theoretical analysis of the resting state EEG supports

the two-stage model in demonstrating that this website the left-sided parietal

lobe is a strong hub region, which is stronger functionally interconnected in synaesthetes than in non-synaesthetes. The right-sided auditory cortex is also a strong hub supporting the idea that coloured-hearing synaesthetes demonstrate a specific auditory cortex. A further important point is that these hub regions are even differently operating at rest supporting the idea that these hub characteristics are predetermining factors of coloured-hearing synaesthesia. “
“Impaired social cognition has been claimed to be a mechanism underlying the development and maintenance of borderline personality disorder (BPD). One important aspect of social cognition is the theory of mind (ToM), a complex skill that seems to be influenced by more basic processes, such as executive functions (EF) and emotion recognition. Previous ToM studies in BPD have yielded inconsistent results. This study assessed the performance of BPD adults on ToM, emotion recognition, and EF tasks. We also examined whether EF and emotion recognition could predict the performance on ToM tasks. We evaluated 15 adults with BPD and 15 matched healthy controls using different tasks of EF, emotion recognition, and ToM. The results showed that BPD adults exhibited deficits in the three domains, which seem to be task-dependent. Furthermore, we found that EF and emotion recognition predicted the performance on ToM.

In this model, the parietal lobe is thought to play a pivotal role in binding together the synaesthetic perceptions (hyperbinding). In addition, we hypothesized that the auditory cortex and the fusiform gyrus would qualify as strong hubs in synaesthetes. Although synaesthetes and non-synaesthetes demonstrated a similar small-world network topology, the parietal lobe turned out to be a stronger hub in synaesthetes

than in non-synaesthetes supporting the two-stage model. The auditory cortex was also identified as a strong hub in these coloured-hearing synaesthetes (for the alpha2 band). Thus, our a priori hypotheses receive strong support. Several additional hubs (for which no a priori hypothesis has been formulated) were found to be different in terms of the PLX-4720 research buy degree measure selleck inhibitor in synaesthetes, with synaesthetes demonstrating stronger degree measures indicating stronger interconnectedness. These hubs were found in brain areas known to be involved in controlling memory processes (alpha1: hippocampus and retrosplenial area), executive functions (alpha1 and alpha2: ventrolateral prefrontal cortex; theta: inferior frontal cortex), and the generation of perceptions (theta: extrastriate cortex; beta: subcentral area). Taken together this graph-theoretical analysis of the resting state EEG supports

the two-stage model in demonstrating that this website the left-sided parietal

lobe is a strong hub region, which is stronger functionally interconnected in synaesthetes than in non-synaesthetes. The right-sided auditory cortex is also a strong hub supporting the idea that coloured-hearing synaesthetes demonstrate a specific auditory cortex. A further important point is that these hub regions are even differently operating at rest supporting the idea that these hub characteristics are predetermining factors of coloured-hearing synaesthesia. “
“Impaired social cognition has been claimed to be a mechanism underlying the development and maintenance of borderline personality disorder (BPD). One important aspect of social cognition is the theory of mind (ToM), a complex skill that seems to be influenced by more basic processes, such as executive functions (EF) and emotion recognition. Previous ToM studies in BPD have yielded inconsistent results. This study assessed the performance of BPD adults on ToM, emotion recognition, and EF tasks. We also examined whether EF and emotion recognition could predict the performance on ToM tasks. We evaluated 15 adults with BPD and 15 matched healthy controls using different tasks of EF, emotion recognition, and ToM. The results showed that BPD adults exhibited deficits in the three domains, which seem to be task-dependent. Furthermore, we found that EF and emotion recognition predicted the performance on ToM.