Na+/K+ ATPase α1 and ß3 subunits are localized to the basolateral membrane of trophectoderm cells in human blastocysts.

STUDY QUESTION: Is there a relation between specific Na+/K+ ATPase isoform expression and localization in human blastocysts and the developmental behavior of the embryo? SUMMARY ANSWER: Na+/K+ ATPase α1, ß1 and ß3 are the main isoforms expressed in human blastocysts and no association was found between the expression level of their respective mRNAs and the rate of blastocyst expansion. WHAT IS KNOWN ALREADY: In mouse embryos, Na+/K+ ATPase α1 and ß1 are expressed in the basolateral membrane of trophectoderm (TE) cells and are believed to be involved in blastocoel formation (cavitation). STUDY DESIGN, SIZE, DURATION: A total of 20 surplus embryos from 11 patients who underwent IVF and embryo transfer at a university hospital between 2009 and 2018 were analyzed. PARTICIPANTS/MATERIALS, SETTING, METHODS: After freezing and thawing Day 5 human blastocysts, their developmental behavior was observed for 24 h using time-lapse imaging, and the expression of Na+/K+ ATPase isoforms was examined using quantitative RT-PCR (RT-qPCR). The expressed isoforms were then localized in blastocysts using fluorescent immunostaining. MAIN RESULTS AND THE ROLE OF CHANCE: RT-qPCR results demonstrated the expression of Na+/K+ ATPase α1, ß1 and ß3 isoforms in human blastocysts. Isoforms α1 and ß3 were localized to the basolateral membrane of TE cells, and ß1 was localized between TE cells. A high level of ß3 mRNA expression correlated with easier hatching (P = 0.0261). LARGE SCALE DATA: N/A. LIMITATIONS, REASONS FOR CAUTION: The expression of mRNA and the localization of proteins of interest were verified, but we have not been able to perform functional analysis. WIDER IMPLICATIONS OF THE FINDINGS: Of the various Na+/K+ ATPase isoforms, expression levels of the α1, ß1 and ß3 mRNAs were clearly higher than other isoforms in human blastocysts. Since α1 and ß3 were localized to the basolateral membrane via fluorescent immunostaining, we believe that these subunits contribute to the dilation of the blastocoel. The ß1 isoform is localized between TE cells and may be involved in tight junction formation, as previously reported in mouse embryos. STUDY FUNDING/COMPETING INTEREST(S): This work was supported by the JSPS KAKENHI (https://www.jsps.go.jp/english/index.html), grant number 17K11215. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors have no conflicts of interest.

Plasma CD147 reflects histological features in patients with lupus nephritis.

OBJECTIVE: A glycosylated transmembrane protein, CD147, has been implicated in regulating lymphocyte responsiveness and leukocyte recruitment. As lupus nephritis (LN) often follows a relapsing-remitting disease course, accurate understanding of the disease activity would be extremely helpful in improving prognosis. Unfortunately, neither clinical nor serological data can accurately reflect the histological features of LN. The present study investigated whether CD147 can accurately predict pathological features of LN. METHODS: Plasma and spot urine samples were collected from 64 patients who underwent renal biopsy between 2008 and 2011. Disease activity for LN tissues was evaluated using the biopsy activity index, and compared to levels of biomarkers including CD147. RESULTS: In LN tissues, CD147 induction was striking in injured glomeruli and infiltrating inflammatory cells, but not in damaged tubules representing atrophy. Plasma CD147 levels accurately reflected the histological disease activity. However, prediction using a single molecule would be quite difficult because of the complex pathogenesis of LN. The diagnostic accuracy of multiplex parameters indicated that the combination including plasma CD147 might yield excellent diagnostic abilities for guiding ideal LN therapy. CONCLUSION: Plasma CD147 levels might offer useful insights into disease activity as a crucial biomarker in patients with LN.

Cd-content and temperature dependences of hyperfine fields in CdxFe3-xO4.

Cd-content and temperature dependences of hyperfine fields in CdxFe3-xO4 (0 ≤ x ≤ 0.5) were investigated by means of time-differential perturbed angular correlation spectroscopy with the 111Cd(←111In) probe. It was found that Cd2+ ions selectively occupy the tetrahedral A site in the spinel structure in all the range of the present Cd content x. The magnetic transition temperature TC becomes lower with increasing x due to the interference of the long-range ordering of Fe spins as a result of expansion of the lattice constants by Cd doping. The measurement of room-temperature hyperfine fields at different x shows that the supertransferred magnetic hyperfine field (SMHF) at the probe decreases as x increases in the range of 0 ≤ x ≤ 0.5. Isothermal measurements at 15 K revealed a contrastive phenomenon for the Cd contents up to x = 0.4: the SMHF becomes great with increasing x; however, this increasing trend of the SMHF turns to reduction at x = 0.46. These observations can be explained based on the effect of Cd doping on the antiferromagnetic coupling between Fe ions in the A and B sites.

Charcot-Marie-Tooth neuropathy type 1B is associated with mutations of the myelin P0 gene.

P0, a major structural protein of peripheral myelin, is a homophilic adhesion molecule and maps to chromosome 1q22-q23, in the region of the locus for Charcot-Marie-Tooth neuropathy type 1B (CMT1B). We have investigated P0 as a candidate gene in two pedigrees with CMT1B and found point mutations which are completely linked with the disease (Z = 5.5, theta = 0). The mutations, glutamate substitution for lysine 96 or aspartate 90, are located in the extracellular domain, which plays a significant role in myelin membrane adhesion. Individuals with CMT1B are heterozygous for the normal allele and the mutant allele. Our results indicate that P0 is a gene responsible for CMT1B.

Temperature-dependent thermal behavior of impurity hydrogen trapped in vacancy-type defects in single crystal ZnO.

Interacting nature between impurity hydrogen atoms and vacancy-type defects in single crystal ZnO was investigated by means of positron annihilation lifetime spectroscopy. In order to clarify the observation of their thermal behavior, the sample was implanted with 1H+ using an electrostatic accelerator. After the implantation, the positron lifetime became shorter, which suggests that the hydrogen atoms were captured by zinc vacancies (VZn) to form vacancy-hydrogen complexes (VZn + nH). The complexes decompose by heat treatment: most of the hydrogen atoms gradually dissociate from VZn + nH in the temperature range 393-773 K. It was also suggested that large vacancy clusters were formed by the agglomeration of smaller clusters during the process of stepwise isochronal annealings at temperatures from 773 to 1073 K, and their decomposition took place at 1173-1373 K. Temperature-dependent thermal behaviors of hydrogen atoms and vacancy-type defects in ZnO are discussed.

Circumvention of multidrug resistance by a newly synthesized quinoline derivative, MS-073.

Newly synthesized quinoline derivatives were investigated for their efficacy to reverse multidrug resistance (MDR). In this study, one of the most effective quinoline derivatives, MS-073, was compared with verapamil with regard to its ability to overcome MDR in vitro and in vivo. MS-073 at 0.1 microM almost completely reversed in vitro resistance to vincristine (VCR) in VCR-resistant P388 cells. The compound also reversed in vitro VCR, adriamycin (ADM), etoposide, and actinomycin D resistance in ADM-resistant human myelogenous leukemia K562 (K562/ADM) cells, ADM-resistant human ovarian carcinoma A2780 cells, and colchicine-resistant human KB cells. MS-073 administered i.p. daily for 5 days with VCR enhanced the chemotherapeutic effect of VCR in VCR-resistant P388-bearing mice. Increases in life span of 19-50% were obtained by the combination of 100 micrograms/kg of VCR with 3-100 mg/kg of MS-073, as compared to the control. The ability of MS-073 to reverse MDR was remarkably higher, especially at low MS-073 doses, than that of verapamil, both in vitro and in vivo. MS-073 enhanced accumulation of [3H]VCR in K562/ADM cells. Photolabeling of P-glycoprotein with 200 nM [3H]azidopine in K562/ADM plasma membranes was completely inhibited by 10 microM MS-073, indicating that MS-073 reverses MDR by competitively inhibiting drug binding to P-glycoprotein.

Emotional cognition without awareness after unilateral temporal lobectomy in humans.

To investigate the function of the amygdala in human emotional cognition, we investigated the electrodermal activity (EDA) in response to masked (unseen) visual stimuli. Six epileptic subjects were investigated after unilateral temporal lobectomy. Emotionally valenced photographic slides (10 negative, 10 neutral) from the International Affective Picture System were presented to their unilateral visual fields under either subliminal or supraliminal conditions. An interaction between hemispheres and emotional valences was found only under the subliminal conditions; greater EDA responses to negative stimuli compared with neutral ones were observed when stimuli were presented to the intact hemispheres. The findings suggest that nonconscious emotional processing is reflected in EDA in a different manner from conscious emotional processing. Medial temporal structures, including the amygdala, thus appear to play a critical role in the neural substrates for this automatic processing.

Purification and characterization of a human urine ribonuclease (RNAase 1) showing genetic polymorphism.

A ribonuclease (RNAase) was isolated and purified from the urine of a 45-year-old man by column chromatographies on DEAE-Sepharose CL-6B, cellulose phosphate and CM-cellulose followed by gel filtrations on Bio-Gel P-100 and Sephadex G-75, and finally to a homogeneous state by SDS-polyacrylamide gel electrophoresis. The enzyme was designated RNAase 1. It was possible to detect RNAase 1 isozymes in urine and serum without difficulty using isoelectric focusing electrophoresis followed by immunoblotting with a rabbit antibody specific to RNAase 1. The existence of genetic polymorphism of RNAase 1 was detected in human serum utilizing this technique (Yasuda, T. et al. (1988) Am. J. Hum. Genet., in press). RNAase 1 in serum and urine seemed to exist in multiple forms with regard to molecular weight and pI value. Genetically polymorphic RNAase 1 was a glycoprotein, containing three mannose, one fucose, four glucosamine and no sialic acid residues per molecule, with a molecular weight of 16,000 and 17,500 determined by gel filtration and SDS-polyacrylamide gel electrophoresis, respectively. The enzyme was most active at pH 7.0 on yeast RNA substrate and inhibited remarkably by Cu2+, Hg2+ and Zn2+. It also showed definite substrate preference for poly(C) and poly(U), but much less activity against poly(A) and poly(G). Thus, the enzyme is a pyrimidine-specific RNAase.

Specific amplification of deleted mitochondrial DNA from a myopathic patient and analysis of deleted region with S1 nuclease.

Heteroplasmy of the normal-sized and the deleted mitochondrial genome has been observed in mitochondrial myopathy. The deleted region of the genome in the skeletal muscle of a patient was analyzed both by the conventional Southern blot method and by the novel method of employing the combination of polymerase chain reaction and S1 nuclease digestion. The results obtained by these methods were compared. Southern hybridization using various mitochondrial DNA fragments localized the deletion from at least position 9020 to 14,955, but regions of uncertainty of 1 kb remained on both ends of the deletion. Using the polymerase chain reaction, a fragment from the deleted genome was specifically amplified by choosing a pair of primers surrounding the deletion, and two fragments adjacent to the starting and end of the deletion were amplified from the normal-sized genome. S1 nuclease analysis of the heteroduplexes formed among these fragments demonstrated that the deletion extended from positions 8650 +/- 50 to 15,660 +/- 60. This method does not require radioisotopes and, moreover, can determine the deleted region within 5 h, in contrast to the 2 days required by the conventional Southern blot analysis. These results indicate that the novel method is faster and more accurate than the conventional method for the determination of the deleted region of genome.

MicroRNA-574-3p, identified by microRNA library-based functional screening, modulates tamoxifen response in breast cancer.

Most primary breast cancers express estrogen receptor α and can be treated via endocrine therapy using anti-estrogens such as tamoxifen; however, acquired endocrine resistance is a critical issue. To identify tamoxifen response-related microRNAs (miRNAs) in breast cancer, MCF-7 cells infected with a lentiviral miRNA library were treated with 4-hydroxytamoxifen (OHT) or vehicle for 4 weeks, and the amounts of individual miRNA precursors that had integrated into the genome were evaluated by microarray. Compared to the vehicle-treated cells, 5 'dropout' miRNAs, which were downregulated in OHT-treated cells, and 6 'retained' miRNAs, which were upregulated in OHT-treated cells, were identified. Of the dropout miRNAs, we found that miR-574-3p expression was downregulated in clinical breast cancer tissues as compared with their paired adjacent tissues. In addition, anti-miR-574-3p reversed tamoxifen-mediated suppression of MCF-7 cell growth. Clathrin heavy chain (CLTC) was identified as a miR-574-3p target gene by in silico algorithms and luciferase reporter assay using the 3' untranslated region of CLTC mRNA. Interestingly, loss and gain of miR-574-3p function in MCF-7 cells causes CLTC to be upregulated and downregulated, respectively. These results suggest that functional screening mediated by miRNA libraries can provide new insights into the genes essential for tamoxifen response in breast cancer.

Catecholamines increase nerve growth factor mRNA content in both mouse astroglial cells and fibroblast cells.

Previous studies have shown that catecholamines increase the nerve growth factor (NGF) content in medium conditioned by mouse L-M fibroblast cells and mouse astroglial cells. In this study, the NGF mRNA levels in these cells were measured by Northern blot analysis. In astroglial cells treated with epinephrine (EN), the cellular NGF mRNA level increased prior to accumulation of NGF in the culture medium. 3-Hydroxytyramine (DA) and norepinephrine (NE) also increased the cellular NGF mRNA content. An increased level of NGF mRNA elicited by EN was also observed in mouse L-M cells. These results indicate that catecholamines enhance NGF synthesis of L-M fibroblast cells and astroglial cells by increasing the cellular content of NGF mRNA. The present results also indicate that the effects of catecholamines are not mediated by adrenergic receptors.

Structure-activity relationship of newly synthesized quinoline derivatives for reversal of multidrug resistance in cancer.

The effect of 24 newly synthesized quinoline derivatives on tumor cell multidrug resistance (MDR) was examined in vitro. At low concentrations, these compounds enhanced the accumulation of [3H]vincristine in K562/ADM cells and reversed tumor cell MDR. The results of the structure-activity relationship analysis indicate that in highly active compounds the two aryl rings in the hydrophobic moiety deviate from a common plane, so they are capable of interacting with hydrogen bond donors of P-170 glycoprotein (P-gp) via pi-hydrogen-pi interactions. Other major structural features which influence the MDR-reversing activities of these compounds are a quinoline nitrogen atom and a basic nitrogen atom in piperazine. Furthermore, in highly active compounds, the distance between the hydrophobic moiety and the basic nitrogen atom (an atom connected to 2-hydroxypropoxyquinoline) must be at least 5 A. Several compounds were found to reverse vincristine resistance in K562/ADM cells in vitro, and compound 16 (MS-209) was selected for clinical studies.

Guinea pig histocompatibility antigens. I. Serological and genetic characterization of GPLA antigens.

Lymphocytotoxic alloantisera were obtained by cross immunization among outbred guinea pigs from a closed colony. Groups of antisera recognizing the same specificities were established by panel analysis, cross immunization among appropriate phenotypes, and absorption studies. Three antigens designated B1, B2, and B3 (perviously B, C, and D) were detected in our outbred colony and also found to be present in a wide variety of guinea pig strains. These antigens were shown by population and breeding studies to be allelic gene products of a first guinea pig locus (GPLA) (designated locus B). Four new guinea pig families homozygous for their B locus antigens are now in the seventh generation of inbreeding. NIH guinea pig strains 2 and 13, which share the B1 antigen, differ by a number of other antigens which have been designated I1, I2, I3 (previously A), and I4. These antigens differ from the B locus gene products in their molecular size and tissue distribution and it is, therefore, postulated that they represent an equivalent of the Ia antigens in mice (designated I region). Cross immunizations among inbred or outbred guinea pigs identical for currently known B locus and I region antigens yield further antisera, possibly recognizing additional Ia specificities and/or a second GPLA locus designated locus S. Whereas the conventional eosin lymphocytoxicity technique easily permits the detection of the widely distributed antigens (such as the B locus antigens), a more sensitive 51Cr release technique is required to demonstrate the "Ia equivalent" antigens of the guinea pig, possibly due to their restricted presence on the membrane of only some lymphoid cell populations.

Detection of platelet mitochondrial DNA deletions in Kearns-Sayre syndrome.

To establish a noninvasive genetic diagnosing method for Kearns-Sayre syndrome, the authors used the polymerase chain reaction (PCR) technique for detecting mitochondrial DNA (mtDNA) deletions in the platelets and directly sequenced the crossover regions of the deleted mtDNA using the fluorescence-based automated sequencing system. The mtDNA deletions were identified in the platelets of three of four patients. The sizes and locations of deletions were determined by the nesting primer PCR method, in which the primary PCR products derived from deleted mtDNAs undergo reamplification using a series of nesting primers. With the fluorescence-based sequencing of templates amplified by the asymmetric PCR method, deleted mtDNA was sequenced directly without cloning. In patient 1, guanine (G) was found at the boundaries of a deleted segment spanning 8400 base pairs (bp) between the CO1 and ND6 genes. In patient 2, a 9-bp directly repeated sequence of 5'-ACCTCCCTC-3' (where A = adenine, C = cytosine, and T = thymine) was found at the boundaries of a deleted segment spanning 7221 bp between the CO1 and ND5 genes. In patient 3, an 8-bp sequence of 5'-TCGCTGTC-3' was found at the boundaries of a deleted segment spanning 4664 bp between the ATPase6 and ND5 genes. Deletions were not detected in the mtDNA of patient 4 or in that of the mothers of the patients. Previously, the genetic diagnosis of this syndrome required muscle biopsy specimens and the use of Southern blot analysis. However, this method requires neither muscle biopsy nor isotopes and is more rapid than the Southern blot method.(ABSTRACT TRUNCATED AT 250 WORDS)

Cimetidine reduces impairment of cellular immunity after cardiac operations with cardiopulmonary bypass.

OBJECTIVE: Depressive effects of cardiopulmonary bypass on cell-mediated immune responses may lead to postoperative infectious complications. We previously reported that cimetidine reduced postbypass depression of the cytotoxic activity of natural killer cells. This study evaluated cimetidine as an agent to preserve cellular immunity after cardiac operations. METHODS: In a prospective randomized study, 20 patients were divided into two groups of equal size. Cimetidine-group patients received 400 mg of cimetidine intravenously before bypass and a 33 mg/hr intravenous infusion of cimetidine after the operation, continuing until the fifth postoperative day. Control-group patients received conventional perioperative therapy. Lymphocyte subsets, natural killer cell activity, percentage of CD56+CD16+ (percentage of natural killer cells), and percentage of CD11b+CD8+ (percentage of suppressor T lymphocytes) were measured perioperatively. RESULTS: Although temporary postoperative reductions in percentages of CD3+, CD4+, and CD56+CD16+ cells were observed in both groups, CD8+ percentages on postoperative day 1 and CD11b+CD8+ percentages on postoperative days 1 and 3 in the cimetidine group were significantly lower compared with those in the control group (p = 0.01,p = 0.004, andp = 0.02, respectively). Temporary postoperative reduction of natural killer cell activity was also observed in both groups, but the natural killer cell activity on postoperative day 1 in the cimetidine group (17.1%) was significantly higher (p = 0.02) than that in the control group (8.20%). CONCLUSIONS: Cimetidine counteracts depressive effects of cardiopulmonary bypass on cell-mediated immunity and may possibly reduce postoperative susceptibility to infection.

Human genetically polymorphic deoxyribonuclease: purification, characterization, and multiplicity of urine deoxyribonuclease I.

A deoxyribonuclease I was purified from the urine of a 46-year-old male (a single individual) by using a series of column chromatographies to a homogeneous state as judged by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The enzyme was found to be a glycoprotein, containing 1 fucose, 7 galactose, 10 mannose, 6 glucosamine, and 2 sialic acid residues per molecule. The N-terminal amino acid sequence up to the 27th residue of the enzyme was similar to that of pancreatic deoxyribonuclease I from bovine and other species. The catalytic properties of the enzyme derived from a single individual closely resembled those of deoxyribonuclease I purified from human urine collected from several volunteers [Ito, K. et al. (1984) J. Biochem. 95, 1399-1406]. The purified enzyme was found to consist of multiple forms with different pI values. These findings are compatible with the existence of genetic polymorphism of deoxyribonuclease I in human urine previously reported [Kishi, K. et al. (1989) Hum. Genet. 81, 295-297]. This multiplicity of the urine enzyme might be due to variations in the primary structure and/or differences in the content of sialic acid.

Facial affect recognition in pre-lingually deaf people with schizophrenia.

The present study examined facial affect recognition in pre-lingually deaf individuals with schizophrenia. Affective facial-labeling task and the control task of face feature processing (the Benton facial recognition test) were performed by deaf subjects with schizophrenia using French sign language (FSL), hearing subjects with schizophrenia, and hearing healthy controls. Deaf subjects with schizophrenia performed more poorly than hearing clinical controls with schizophrenia or healthy controls on the affective facial-labeling task. No differences were found on the control task between deaf subjects with schizophrenia and hearing clinical or healthy controls. The results showed that facial affect recognition and face feature processing were differently impaired in pre-lingually deaf individuals with schizophrenia, suggesting that neurocognitive backgrounds of impaired affective facial processing may be distinct from those of general impairment in face processing.

Frontal midline theta rhythm is correlated with cardiac autonomic activities during the performance of an attention demanding meditation procedure.

Frontal midline theta rhythm (Fm theta), recognized as distinct theta activity on EEG in the frontal midline area, reflects mental concentration as well as meditative state or relief from anxiety. Attentional network in anterior frontal lobes including anterior cingulate cortex is suspected to be the generator of this activity, and the regulative function of the frontal neural network over autonomic nervous system (ANS) during cognitive process is suggested. However no studies have examined peripheral autonomic activities during Fm theta induction, and interaction of central and peripheral mechanism associated with Fm theta remains unclear. In the present study, a standard procedure of Zen meditation requiring sustained attention and breath control was employed as the task to provoke Fm theta, and simultaneous EEG and ECG recordings were performed. For the subjects in which Fm theta activities were provoked (six men, six women, 48% of the total subjects), peripheral autonomic activities were evaluated during the appearance of Fm theta as well as during control periods. Successive inter-beat intervals were measured from the ECG, and a recently developed method of analysis by Toichi et al. (J. Auton. Nerv. Syst. 62 (1997) 79-84) based on heart rate variability was used to assess cardiac sympathetic and parasympathetic functions separately. Both sympathetic and parasympathetic indices were increased during the appearance of Fm theta compared with control periods. Theta band activities in the frontal area were correlated negatively with sympathetic activation. The results suggest a close relationship between cardiac autonomic function and activity of medial frontal neural circuitry.

Improvement by the insulin-sensitizing agent, troglitazone, of abnormal fibrinolysis in type 2 diabetes mellitus.

This study evaluated abnormal fibrinolysis in diabetic patients in terms of the pathophysiological significance and reversibility by oral hypoglycemic agents. Forty-seven patients with type 2 diabetes mellitus were randomly treated for 4 weeks with glibenclamide (n = 23) or troglitazone (n = 24). Before and after treatment, glycemic control, steady-state plasma glucose and insulin (SSPG and SSPI, respectively), and markers of fibrinolysis (tissue plasminogen activator [tPA] and plasminogen activator inhibitor-1 [PAI-1]) were analyzed in each patient. Pretreatment plasma PAI-1 in diabetic patients, but not tPA, was well correlated with the severity of retinopathy assessed by the fluorescence technique. Four weeks of treatment with troglitazone significantly decreased hemoglobin A1c (HbA1c), SSPG, and PAI-1 without an alteration of tPA. The troglitazone-induced decrease in plasma PAI-1 (50.3 v28.8 micromol/L; P < .05) was correlated with HbA1c (8.80% v7.21%, r = .539, P < .01) and SSPG (16.2 v 8.97 mmol/L, r = .562, P < .01) but not with SSPI. In contrast, treatment with glibenclamide for 4 weeks also reduced the HbA1c titer to almost the same extent as troglitazone (1.38% v 1.59%), but did not change the plasma PAI-1 or SSPG titer. These results suggest that an abnormal fibrinolytic state, especially overproduction of PAI-1, may be a pathogenic factor in the development of diabetic complications such as retinopathy, which may be improved by correction of the insulin resistance with troglitazone.

Emotional expression boosts early visual processing of the face: ERP recording and its decomposition by independent component analysis.

To investigate the hypothesis that early visual processing of stimuli might be boosted by signals of emotionality, we analyzed event related potentials (ERPs) of twelve right-handed normal subjects. Gray-scale still images of faces with emotional (fearful and happy) or neutral expressions were presented randomly while the subjects performed gender discrimination of the faces. The results demonstrated that the faces with emotion (both fear and happiness) elicited a larger negative peak at about 270 ms (N270) over the posterior temporal areas, covering a broad range of posterior visual areas. The result of independent component analysis (ICA) on the ERP data suggested that this posterior N270 had a synchronized positive activity at the frontal-midline electrode. These findings confirm that the emotional signal boosts early visual processing of the stimuli. This enhanced activity might be implemented by the amygdalar re-entrant projections.