Annexin A2 Promotes Development of Retinal Neovascularization through PI3K/ AKT Pathway

Abstract Background RNV is a pathological characteristic of PDR and ANXA2 play an important role in the process of RNV while the mechanism remains unclear. We explore the role and molecular basis of ANXA2 in the formation of RNV and seek for new potential targets for the prevention and treatment of PDR. Methods Lentivirus containing plasmids which can interfere ANXA2 and overexpress ANXA2 were packaged and infected HRECs, dividing HRECs into 4 groups. Moreover, 1ul SC79 solution was added in shA2 group and 1ul LY294002 solution was added into lentiA2 group. Western Blot was used to detect expression of ANXA2 and changes in phosphorylation degree of major proteins in PI3K/AKT signaling pathway in each group of HRECs. HRECs of all groups were used to perform EDu cell proliferation assay, Transwell cell migration assay and Matrix tube formation assay. C57BL/6J mice were randomly divided into 3 groups. Mice of OIR group were injected intraperitoneally with 0.05ml PBS every day from 7th to 10th day while mice of LY294002 treatment group were injected with 0.05ml LY294002 solution and no treatment in the control group. Lectin GS-IB4 fluorescence staining was used to observe RNV in mice in all groups. The expression of ANXA2 in mouse retinas was detected by Westen-blot. Results The proliferation, immigration and angiogenesis ability of HRECs is lower in shA2 group than shNC and SC79 treatment group while higher in lentiA2 group than lenti-EGFP and LY294002 treatment group. ANXA2 expression is significantly higher in retina of mice in OIR group and LY294002 treatment group. RNV is significantly less severe in LY294002 treatment group than that in OIR group. Conclusions ANXA2 can promote development of RNV through PI3K/ AKT Pathway.

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Prevention and treatment of post-partum depression: a controlled randomized study on women at risk

Psychological Medicine ◽

10.1017/s0033291702006062 ◽

2002 ◽

Vol 32 (6) ◽

pp. 1039-1047 ◽

Cited By ~ 103

Author(s):

H. CHABROL, ◽

F. TEISSEDRE, ◽

M. SAINT-JEAN, ◽

N. TEISSEYRE, ◽

B. ROGÉ ◽

...

Keyword(s):

At Risk ◽

Treatment Group ◽

Rating Scale ◽

Post Partum ◽

Control Group ◽

Post Partum Depression ◽

Cognitive Behavioural ◽

Post Natal Depression ◽

Prevention And Treatment ◽

Probable Depression

Background. Research is needed to evaluate the efficacy of prevention and treatment for post-partum depression.Method. Subjects were screened with the Edinburgh Post-natal Depression Scale (EPDS) at the obstetric clinic. Mothers at risk (N = 258) (EPDS scores [ges ]9) were randomly assigned to a prevention/treatment group or a control group. The prevention group received one cognitive-behavioural prevention session during hospitalization. At 4 to 6 weeks post-partum, subjects were screened again with the EPDS, after drop-out rates (refusals plus no return of the second EPDS) of 25.4% (33/130) in the intervention group and 10.9% (14/128) in the control group. Mothers with probable depression (EPDS scores [ges ]11) were assessed using the Hamilton Depression Rating Scale (HDRS) and the Beck Depression Inventory (BDI). Mothers with major depression continued in the treatment group (N = 18) or in the control group (N = 30). Treated subjects received a cognitive-behavioural programme of between five and eight weekly home-visits.Results. Compared with the control group, women in the prevention group had significant reductions in the frequency of probable depression (30.2% v. 48.2%). Recovery rates based on HDRS scores of <7 and BDI scores of <4 were also significantly greater in the treated group than in the control group.Conclusions. The study suggests that this programme for prevention and treatment of post-partum depression is reasonably well-accepted and efficacious.

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MicroRNA-126 modulates angiogenesis and tube formation through enhancing epidermal growth factor-like domain 7 expression and phosphorylating PI3K/AKT signaling pathway

Archives of Medical Science ◽

10.5114/aoms/127014 ◽

2021 ◽

Author(s):

Qiang Li ◽

Zhong-ming Wang ◽

Ai-yue Wang ◽

Qiong-Guan Xu ◽

Zhou-feng Fu ◽

...

Keyword(s):

Growth Factor ◽

Epidermal Growth Factor ◽

Signaling Pathway ◽

Akt Signaling ◽

Tube Formation ◽

Luciferase Assay ◽

Control Group ◽

Akt Signaling Pathway ◽

Invasive Ability ◽

Epidermal Growth

IntroductionDysregulated angiogenesis is a critical characteristic for endothelial dysfunction disorders. This study aimed to determine functions of microRNA-126 in formation of tube and investigated the potential mechanisms.Material and methodsThe synthesized microRNA-126 control and microRNA-126 inhibitor plasmids were transfected into human umbilical-vein endothelial cells (HUVECs) using lipofectamine 2000 reagent. Cell counting kit-8 (CCK-8) was employed to measure proliferative capability of HUVECs. Transwell analysis was used to evaluate HUVECs invasive ability. Real time PCR (RT-PCR) was utilized to access epidermal growth factor-like domain 7 (EGFL7) and microRNA-126 mRNA transcription. Tube-forming capability in HUVECs was determined. Dual-luciferase assay and linear-regression analysis were conducted to measure interaction between EGFL7 and microRNA-126 molecule. Phosphoinositide-3-kinase/protein kinase-B (PI3K/AKT) signaling pathway associated molecules were evaluated using western blot assay.ResultsSilencing of microRNA-126 significantly enhanced proliferative capability and invasive ability of HUVECs compared to those of microRNA-126 control group (p<0.05). microRNA-126 silencing remarkably promoted tube formation and significantly up-regulated EGFL7 compared to those of microRNA-126 control group (p<0.05). microRNA-126 could interact with EGFL7 molecule. microRNA-126 was also negatively correlated with EGFL7 molecule in HUVECs (p<0.05). Silencing of microRNA-126 significantly enhanced p-PI3K/PI3K ratio compared to that of microRNA-126 control group (p<0.05). microRNA-126 silencing also remarkably increased p-AKT/AKT ratio compared to that of microRNA-126 control group (p<0.05).ConclusionsmicroRNA-126 modulated angiogenesis and tube formation through increasing EGFL7 expression and phosphorylating PI3K/AKT signaling pathway.

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NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma

Open Medicine ◽

10.1515/med-2021-0268 ◽

2021 ◽

Vol 16 (1) ◽

pp. 742-748

Author(s):

Jianlong Wang ◽

Tao Li ◽

Lifeng Ma ◽

Guochao Liu ◽

Guiying Wang ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Tube Formation ◽

Endothelial Cell Proliferation ◽

Hematogenous Metastasis ◽

Control Group ◽

Migration Assay ◽

Assay Tube ◽

Ndrg2 Expression ◽

Huvec Proliferation ◽

Hcc Cells

Abstract Hepatocellular carcinoma (HCC) is an angiogenesis-dependent tumor, and angiogenesis plays pivotal roles in progression and hematogenous metastasis. Upregulating NDRG2 expression could inhibit endothelial cell proliferation and tumor angiogenesis. However, the development of angiogenesis is a complicated and dynamic process, and the specific mechanisms that NDRG2 influences its progression are largely unknown. Conditioned media (CM) was collected from HCC cells. Cell viability, migration assay, tube formation, and western blot were used to evaluate the effect of NDRG2 on angiogenesis in HCC cells. ELISA assay was used to measure the level of VEGFA in CM. CM from NDRG2 knockdown cells significantly promoted HUVECs proliferation, migration, and tube formation compared with control cells. The level of VEGFA in CM was increased by NDRG2 knockdown relative to the control group. The expression of VEGFA, HIF-1α, and p-Akt was significantly increased in NDRG2 knockdown cells. CM from NDRG2 knockdown cells with VEGFA antibody failed to induce HUVEC proliferation, migration, and tube formation. YC-1 significantly inhibited the level of VEGFA in CM from NDRG2 knockdown cells. YC-1 also inhibited the expression of VEGFA and HIF-1α. Therefore, NDRG2 inhibition promoted the angiogenesis of HCC via VEGFA and may be used to be an anti-angiogenesis target.

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Efficacy of propylene glycol on prevention and treatment of ketosis for dairy cows in lactation stage

The Journal of Agriculture and Development ◽

10.52997/jad.4.02.2020 ◽

2020 ◽

Vol 19 (02) ◽

pp. 28-35

Author(s):

Hai T. Nguyen

Keyword(s):

Treatment Group ◽

Dairy Cows ◽

Propylene Glycol ◽

Block Design ◽

Treated Group ◽

Control Group ◽

Untreated Control Group ◽

Lactation Stage ◽

Randomized Complete Block Design ◽

Prevention And Treatment

The objective of this study was to evaluate the efficacy of propylene glycol (PG) on prevention and treatment of ketosis in dairy cows from 09/2018 to 03/2019. The study consisted of 2 experiments using a total of 126 multiparous dairy cows in a HF crossbred herd. Cows in both experiments were randomly assigned to treatments in a randomized complete block design. In Exp. 1, 96 cows without ketosis disease (BHBA < 1.4 mmol/L) were assigned to 2 groups (48 cows/group), including (1) untreated control group (no PG) and (2) treatment group (oral PG for 3 consecutive days after parturition). In Exp. 2, 30 ketotic cows (BHBA ≥ 1.4 mmol/L) were divided into 3 groups (10 cows/group), including (1) cows provided with glucose + vitamin B12 + dexamethasone (TT1), (2) cows treated with PG for 3 days (TT2), and (3) combination of TT1 and TT2 (TT3). The results of the Exp. 1 showed that the proportion of ketotic cows was lower (P < 0.01) in the PG-treated group (18.75%) than in the control group (47.92%). The PG treatment also reduced (P < 0.01) the blood ketone concentration of cows as compared with the control without PG use (0.89 vs. 1.22 mmol/L). In the Exp. 2, after treatment the reduction of blood ketone concentration was much greater (P < 0.01) in TT3 cows (1.97 mmol/L) than in TT2 cows (1.30 mmol/L) and TT1 cows (1.23 mmol/L). The percentage of cows recovered from ketosis was greatest in TT3 (90%), followed by TT2 (60%), and then TT1 (50%) (P > 0.05).

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Influences of S100A8 and S100A9 on Proliferation of Nasopharyngeal Carcinoma Cells through PI3K/Akt Signaling Pathway

BioMed Research International ◽

10.1155/2021/9917365 ◽

2021 ◽

Vol 2021 ◽

pp. 1-7

Author(s):

Liting Wen ◽

Yu Ding ◽

Xiaodong Chen ◽

Keyong Tian ◽

Danfeng Li ◽

...

Keyword(s):

Nasopharyngeal Carcinoma ◽

Signaling Pathway ◽

Akt Signaling ◽

Carcinoma Cells ◽

Akt Pathway ◽

Control Group ◽

Akt Signaling Pathway ◽

Protein Levels ◽

Positive Rate ◽

Sirna Group

Objective. To investigate the effects of S100A8 and S100A9 on proliferation in nasopharyngeal carcinoma cells and the regulatory effects of PI3K/Akt signaling pathway. Methods. Nasopharyngeal carcinoma cells (CNE1) were cultured and randomly divided into three groups: control group, S100A8/S100A9 overexpression group, and siRNA S100A8/S100A9 group. CCK-8 method was used to detect the effect of S100A8 and S100A9 on the viability of nasopharyngeal carcinoma cells. The effects of S100A8 and S100A9 on the colony forming ability of nasopharyngeal carcinoma cells were detected by colony forming assay. The effects of S100A8 and S100A9 on the proliferation of nasopharyngeal carcinoma cells were detected by EdU staining. The mRNA levels of PI3K and Akt were detected by RT-PCR. The expression levels of PI3K and Akt in NPC cells were detected by Western blot. Wortmannin, an inhibitor of PI3K/Akt pathway, was used to inhibit the activation of PI3K/Akt pathway. Results. Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were increased in the overexpression group. Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were decreased in the siRNA group. After inhibiting the activation of PI3K/Akt pathway, the viability of NPC cells in the overexpression group decreased significantly at 48 h and 72 h, while that in the siRNA group increased significantly. Conclusion. SiRNA S100A8 and S100A9 could inhibit the proliferation of nasopharyngeal carcinoma cells, and the underlying mechanism may be related to the inhibition of PI3K/Akt signaling pathway.

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Nogo-B Promotes Angiogenesis in Proliferative Diabetic Retinopathy via VEGF/PI3K/Akt Pathway in an Autocrine Manner

Cellular Physiology and Biochemistry ◽

10.1159/000484061 ◽

2017 ◽

Vol 43 (5) ◽

pp. 1742-1754 ◽

Cited By ~ 12

Author(s):

Yuelu Zhang ◽

Liang Wang ◽

Yuechan Zhang ◽

Mo Wang ◽

Qinglei Sun ◽

...

Keyword(s):

Diabetic Retinopathy ◽

Proliferative Diabetic Retinopathy ◽

High Glucose ◽

Cell Communication ◽

Tube Formation ◽

Negative Control ◽

Akt Pathway ◽

Enzyme Linked Immunosorbent Assay ◽

Control Group ◽

Long Term Memory

Background/Aims: Nogo-B, a conservative protein of endoplasmic reticulum, is a member of the reticulon family of proteins. Proliferative diabetic retinopathy (PDR) is the major concerning problem of diabetic retinopathy. This study explored the role of Nogo-B in the regulation of angiogenesis in PDR patients and primary human retinal endothelial cells (HRMECs). Methods: Nogo-B was down-regulated through the use of Lentivirus-NogoB-RNAi, the effects of Nogo-B on angiogenesis under high glucose stimulation were evaluated via CCK-8 assay, wound closure assay, transwell assay, and tube formation assay. Expression of Nogo-B, VEGF, PI3K and Akt were determined by western blotting, immunofluorescence, enzyme-linked immunosorbent assay (ELISA). Co-culture systerm was used to explore cell communication. Results: Nogo-B was highly enriched in ocular tissues of PDR patients and in HRMECs exposed to high glucose. Down-regulation of Nogo-B attenuated high glucose induced cell migration and tube formation in HRMECs. Mechanistically, in comparison with the negative control group, Lentivirus-NogoB-RNAi group had exhibited reduced VEGF secretion, weakened PI3K and Akt activation. Besides, high glucose treatment promoted the secretion of Nogo-B and presented as a “long-term memory”. Conclusions: These data collectively indicated that Nogo-B promoted angiogenesis in HRMECs via VEGF/PI3K/Akt pathway in an autocrine manner.

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Cyclic Mechanical Stretch Ameliorates the Degeneration of Nucleus Pulposus Cells through Promoting the ITGA2/PI3K/AKT Signaling Pathway

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/6699326 ◽

2021 ◽

Vol 2021 ◽

pp. 1-11

Author(s):

Dandan Wang ◽

Yuanzhen Chen ◽

Shengnan Cao ◽

Pengcheng Ren ◽

Haojun Shi ◽

...

Keyword(s):

Cell Cycle ◽

Tensile Stress ◽

Differentially Expressed Genes ◽

Mechanical Stretch ◽

Akt Signaling ◽

Akt Pathway ◽

Control Group ◽

Akt Signaling Pathway ◽

Stress Group ◽

Col2a1 Expression

Background. Intervertebral disc degeneration (IVDD) is one of the major causes of low back pain and motor deficiency. Nucleus pulposus (NP) degeneration plays a key role in the process of IVDD. The mechanical and biological interactions involved in NP degeneration have not been elucidated. The present study is aimed at investigating the effect and mechanism of cyclic mechanical stretch in regulating the function and degeneration of NP cells. Methods. NP cells were subjected to cyclic tensile stress (10% deformation) of 0.1 Hz for 8640 cycles. Cell proliferation was conducted through the MTT assay. The cell cycle and apoptosis were detected by flow cytometry. A gene expression profile chip was used to analyze the differentially expressed genes between the tensile stress group and the control group. Enrichment analysis of Gene Ontology (GO) annotation and signaling pathways were analyzed. Western blot and RNA interference were carried out to investigate the role of the ITGA2/PI3K/AKT pathway in the effect of cyclic mechanical stretch on NP cells. Results. NP cells exhibited a greater ( P < 0.05 ) growth rate in the tensile stress group compared to the control group. Cyclic mechanical stress significantly promoted the cell cycle transition of NP cells from the S phase to the G2/M phase. A fewer proportion of apoptotic cells were found in the tensile stress group ( P < 0.05 ), indicating that cyclic mechanical stretch inhibits NP cell apoptosis. Microarray analysis revealed 689 significant differentially expressed genes between the two groups ( P < 0.05 ), of which 333 genes were upregulated and another 356 genes were downregulated. Cyclic mechanical stretch altered the expression of 31 genes involved in the ITGA2/PI3K/AKT pathway and remarkably promoted this pathway in NP cells. Downregulation of ITGA2 and AKT further demonstrated that the PI3K/AKT pathway was responsible for the proliferation and COL2A1 expression of NP cells upon cyclic mechanical stretch. Conclusions. Cyclic mechanical stretch promoted the proliferation and cell cycle and reversely inhibited the apoptosis of NP cells. Cyclic mechanical stretch promoted COL2A1 expression and ameliorated the degeneration of NP cells via regulation of the ITGA2/PI3K/AKT signaling pathway. Our results may provide a potential target and a possibility of IVDD disease treatment by ameliorating the degenerative changes.

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The COL-4A1 polypeptide destroy endothelial cells through the TGF-β/PI3K/AKT pathway

Scientific Reports ◽

10.1038/s41598-021-94801-5 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Ting Li ◽

Zhonghui Ling ◽

Kaipeng Xie ◽

Yixiao Wang ◽

Zhijing Miao ◽

...

Keyword(s):

Endothelial Cells ◽

Rat Model ◽

Vascular Endothelial Cells ◽

Underlying Mechanism ◽

Tube Formation ◽

Cell Counting ◽

Akt Pathway ◽

Control Group

AbstractPreeclampsia (PE) is commonly considered as a placental disorder in pregnancy. Until now, the etiology and pathological mechanism of PE have remained ambiguous. Although PE can lead to a variety of maternal and infant complications, there are still no effective treatments. This study aimed to explore the correlation between the novel polypeptide COL-4A1 and PE, and to identify the underlying mechanism by which this polypeptide may function and to explore new therapeutic targets for PE. A rat model of PE was established and used to verify the function of the polypeptide COL-4A1 in vivo. Additionally, human umbilical vascular endothelial cells (HUVECs) were cultured with or without COL-4A1 and TNF-α (20 ng/ml). Cell Counting Kit-8 (CCK-8), wound-healing, Transwell and tube formation assays were used to evaluate cell proliferation, migration and angiopoiesis. RNA sequencing and mass spectrometry were conducted to explore the underlying downstream mechanism of COL-4A1. In vivo, COL-4A1 increased blood pressure and elevated the risk of fetal growth restriction (FGR) which was induced by lipopolysaccharide (LPS) in the rat model. In vitro, COL-4A1 significantly inhibited the proliferation and migration of HUVECs. After culture with COL-4A1, compared to control group the adhesive ability and level of reactive oxygen species (ROS) were enhanced and tube formation ability was decreased. Furthermore, Western blotting (WB) and pull-down assays were conducted to explore the underlying mechanism by which COL-4A1 functions, and the TGF-β/PI3K/AKT pathway was identified as the potential pathway involved in its effects. In summary, these results revealed that the polypeptide COL-4A1 caused PE-like symptoms in cells and a rat model. Through the TGF-β/PI3K/AKT pathway, COL-4A1 interferes with the pathogenesis of PE. Thus COL-4A1 is expected to become a potential target of PE, providing a basis for exploring the treatment of PE.

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Exosome-mediated miR-21 promotes angiogenesis within esophageal tumor microenvironment by activating PTEN/Akt signaling pathway in Vascular Endothelial Cells

10.21203/rs.3.rs-31065/v1 ◽

2020 ◽

Author(s):

Tian Wang ◽

Juan Liao ◽

Zijie Yang ◽

Weitao Shen ◽

Zhi kui Gao ◽

...

Keyword(s):

Endothelial Cells ◽

Tumor Microenvironment ◽

Signaling Pathway ◽

Akt Signaling ◽

Tube Formation ◽

Luciferase Reporter ◽

Control Group ◽

Esophageal Tumor ◽

Akt Signaling Pathway ◽

Transwell Assay

Abstract Background Angiogenesis, a pivotal component in the tumor microenvironment (TME), boosts tumor growth and metastasis. Cancer-derived exosomes, which have been widely reported to play a crucial role in the establishment of TME can be effective angiogenic modulators. We aim to investigate the contribution of microRNA-21 (miR-21) for angiogenesis which was packaged in cancer-derived exosomes in esophageal squamous cell carcinoma (ESCC). Methods The co-cultivation model was constructed to mimic the tumor microenvironment based at a physical level to explore the effects of cancer-derived exosomes on angiogenesis of human umbilical vein endothelial cells (HUVECs). EdU assay, transwell assay and tube formation assay formation experiments were conducted for the evaluation of HUVECs proliferation, migration, and angiogenesis, respectively. In addition, Dual-luciferase reporter (DLR) assay was performed to validate the relationship between miR-21 and its target gene PTEN. Similarly, miR-21 inhibitors and LY294002 was applied to evaluate the regulation of miR-21 via pro-angiogenesis in recipient HUVECs by PTEN/Akt signaling pathway. Results After 24 h co-cultivation with EC9706 cells, miR-21 levels in recipient HUVECs was raised. The results from EdU assay, transwell assay and blood vessel formation experiment showed that exosomes which were secreted from EC9706 cells (EC9706-Exo) delivered miR-21 stimulated proliferation, migration and tube formation of HUVECs. DLR assay indicated that miR-21 could directly bind to the 3'-untranslated region (UTR) of PTEN genes, real-time PCR and western blot analysis for PTEN showed it was inhibited by EC9706-Exo shuttled miR-21. Meanwhile, phospho-Akt (p-Akt) (Ser473), one of the downstream genes of PTEN, was significantly increased in recipient HUVECs compared to the control group, while inhibiting miR-21 and PI3K/Akt pathway respectively both led to a sharp decrease in p-Akt levels, suggesting that exosomal miR-21 promote angiogenesis via activating PTEN/Akt signaling pathway. Conclusion Exosomal miR-21 acts as a driver of pro-angiogenesis by activating PTEN/Akt signaling pathway, it might serve as a blood-based biomarker for ESCC metastasis. Suppressing the expression or blocking the transmission of these exosome-derived miR-21 might be a novel antiangiogenic therapeutic strategy for ESCC.

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A Newspaper’s Effect on the Strength of Automatic Associations in Memory

Journal of Media Psychology Theories Methods and Applications ◽

10.1027/1864-1105/a000057 ◽

2012 ◽

Vol 24 (1) ◽

pp. 1-8 ◽

Cited By ~ 12

Author(s):

Florian Arendt

Keyword(s):

Treatment Group ◽

Term Effect ◽

Control Group ◽

Implicit Measure ◽

Short Term ◽

Short Term Treatment ◽

Short Term Effect ◽

Automatic Associations ◽

Foreign Nationality ◽

The Impact

A test was done to see if reading a newspaper which consistently overrepresents foreigners as criminals strengthens the automatic association between foreign country and criminal in memory (i.e., implicit cultivation). Further, an investigation was done to find out if reading articles from the same newspaper produces a short-term effect on the same measure and if (1) emotionalization of the newspaper texts, (2) emotional reactions of the reader (indicated by arousal), and (3) attributed text credibility moderate the short-term treatment effect. Eighty-five participants were assigned to one of three experimental conditions. Participants in the control group received short factual crime texts, where the nationality of the offender was not mentioned. Participants in the factual treatment group received the same texts, but the foreign nationality was mentioned. Participants in the emotionalized treatment group received emotionalized articles (i.e., texts which are high in vividness and frequency) covering the same crimes, with the foreign nationality mentioned. Supporting empirical evidence for implicit cultivation and a short-term effect was found. However, only emotionalized articles produced a short-term effect on the strength of the automatic association, indicating that newspaper texts must have a minimum of stimulus intensity to overcome an effect threshold. There were no moderating effects of arousal or credibility pertaining to the impact on the implicit measure. However, credibility moderated the short-term effect on a first-order judgment (i.e., estimated frequency of foreigners of all criminals). This indicates that a newspaper’s effect on the strength of automatic associations is relatively independent from processes of propositional reasoning.

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