Assessing the roles of shape prototypicality and sexual dimorphism in ratings of the trustworthiness of faces

Perceptions of the trustworthiness of faces predict important social outcomes, including economic exchange and criminal sentencing decisions. However, the specific facial characteristics that drive trustworthiness perceptions remain poorly understood. Here we investigated this issue by exploring possible relationships between ratings of the trustworthiness of face images and objective assessments of two aspects of face shape that researchers have previously suggested are important for perceptions of trustworthiness: distinctiveness and sexual dimorphism. We found that faces with more distinctive shapes were rated as less trustworthy. By contrast, sexual dimorphism of face shape was not significantly correlated with trustworthiness ratings. These results suggest that distinctiveness of face shape plays a more important role in trustworthiness perceptions than does sexual dimorphism and suggest that perceptions of trustworthiness may stem, at least in part, from the ‘anomalous-is-bad’ stereotype

Assessing the roles of symmetry, prototypicality, and sexual dimorphism of face shape in health perceptions

Health perceptions are thought to play an important role in human mate preferences. Although many studies have investigated potential relationships between health ratings of faces and facial symmetry, prototypicality, and sexual dimorphism, findings have been mixed across studies. Consequently, we tested for potential relationships between health ratings of faces and the symmetry, prototypicality, and sexual dimorphism of those faces' shapes. When these three shape characteristics were considered in separate regression models, we observed significant positive relationships between health ratings and both shape symmetry and prototypicality. By contrast, health ratings and sexual dimorphism were not significantly correlated in these analyses. However, in analyses in which symmetry, prototypicality, and sexual dimorphism were entered simultaneously as predictors in a single model, prototypicality, but not symmetry, was significantly correlated with health ratings. Moreover, sexual dimorphism predicted health ratings of female, but not male, faces in these analyses. Collectively, these results suggest that the relationship between symmetry and health ratings is, at least partly, driven by the effect of prototypicality on health perceptions and highlight the importance of considering multiple aspects of face shape when investigating factors that predict perceived health

The importance of face-shape masculinity for perceptions of male dominance depends on study design

Dominance perceptions play an important role in social interactions. Although many researchers have proposed that shape masculinity is an important facial cue for dominance perceptions, evidence for this claim has come almost exclusively from studies that assessed perceptions of experimentally manipulated faces using forced-choice paradigms. Consequently, we investigated the role of masculine shape characteristics in perceptions of men’s facial dominance (1) when shape-manipulated stimuli were presented in a forced-choice paradigm and (2) when unmanipulated face images were rated for dominance and shape masculinity was measured from face images. Although we observed large effects of masculinity on dominance perceptions when we used the forced-choice method (Cohen’s ds = 2.51 and 3.28), the effect of masculinity on dominance perceptions was considerably smaller when unmanipulated face images were rated and shape masculinity measured from face images (Cohen’s ds = 0.44 and 0.62). This pattern was observed when faces were rated separately for physical dominance, social dominance, and masculinity, and was seen for two different sets of stimuli. Collectively, these results suggest that shape masculinity may not be a particularly important cue for dominance perceptions when faces vary simultaneously on multiple dimensions, as is the case during everyday social interactions

Posttraumatic growth among suicide-loss survivors : an updated systematic review and meta-analysis protocol

Background: Losing a loved one to suicide is an event which can have strong and potentially traumatic impacts on the lives of the bereaved survivors, especially regarding their grief which can be complicated. These bereaved individuals are also less likely to receive social support following their bereavement. However, besides these adverse impacts, there is growing evidence to support the concept of posttraumatic growth following suicide bereavement. Posttraumatic growth is personal improvement that occurs as a consequence of experiencing a traumatic or extremely challenging event or crisis. Only one systematic review and meta-analysis on posttraumatic growth following suicide bereavement has been conducted; this protocol is for the planned systematic review and meta-analysis update of the original systematic review and meta-analysis, as the original review collected its data in 2018.Method: This protocol outlines the planned procedures of the updated systematic review and meta-analysis. This review and its protocol have been registered with PROSPERO(Registration Number: CRD42024485421). MEDLINE, PsycINFO, Embase, CINAHL, Scopus, and Web of Science (Core Collection) will be examined, and the search results will be imported to Covidence where title and abstract screenings, full text screenings, and data extraction will occur. The inclusion and exclusion criteria for this updated review match those in the original review: i) the study population must contain participants bereaved by suicide, ii) the study data must be quantitative, iii) the study must report data on posttraumatic or stress-related growth. The original review conducted its search prior to 2019; thus, this updated review searched databases for the timeframe of January 2019 to January 2024. The updated meta-analysis will synthesise data from both the original and updated reviews to examine trends over time. Discussion: The results of this updated systematic review and meta-analysis will be used to examine key relationships and findings regarding posttraumatic growth in individuals bereaved by suicide. The discussion will also investigate the findings of this updated review in comparison to the findings of the original review. Any differences would be highlighted

EBV, HHV8 and HIV in B cell non Hodgkin lymphoma in Kampala, Uganda

<p>Abstract</p> <p>Background</p> <p>B cell non Hodgkin lymphomas account for the majority of lymphomas in Uganda. The commonest is endemic Burkitt lymphoma, followed by diffuse large-B-cell lymphoma (DLBCL). There has been an increase in incidence of malignant lymphoma since the onset of the HIV/AIDS pandemic. However, the possible linkages of HHV8 and EBV to the condition of impaired immunity present in AIDS are still not yet very clearly understood.</p> <p>Objectives</p> <p indent="1">1. To describe the prevalence of Epstein-Barr virus, Human Herpes virus 8 and Human Immunodeficiency Virus-1 in B cell non Hodgkin lymphoma biopsy specimens in Kampala, Uganda.</p> <p indent="1">2. To describe the histopathology of non Hodgkin lymphoma by HIV serology test result in Kampala, Uganda</p> <p>Method</p> <p>Tumour biopsies specimens from 119 patients with B cell non Hodgkin lymphoma were classified according to the WHO classification. Immunohistochemistry was used for detection of HHV8 and in situ hybridization with Epstein Barr virus encoded RNA (EBER) for EBV. Real time and nested PCR were used for the detection of HIV.</p> <p>The patients from whom the 1991-2000 NHL biopsies had been taken did not have HIV serology results therefore 145 patients biopsies where serology results were available were used to describe the association of HIV with non Hodgkin lymphoma type during 2008-2009.</p> <p>Results</p> <p>In this study, the majority (92%) of the Burkitt lymphomas and only 34.8% of the diffuse large B cell lymphomas were EBV positive. None of the precursor B lymphoblastic lymphomas or the mantle cell lymphomas showed EBV integration in the lymphoma cells.</p> <p>None of the Burkitt lymphoma biopsies had HIV by PCR. Of the 121 non Hodgkin B cell lymphoma patients with HIV test results, 19% had HIV. However, only 1(0.04%) case of Burkitt lymphoma had HIV. All the tumours were HHV8 negative.</p> <p>Conclusions</p> <p>The majority of the Burkitt lymphomas and two fifths of the diffuse large B cell lymphomas had EBV. All the tumours were HHV8 negative. Generally, the relationship of NHL and HIV was weaker than what has been reported from the developed countries. We discuss the role of these viruses in lymphomagenesis in light of current knowledge.</p

Microbial Translocation Is Associated with Increased Monocyte Activation and Dementia in AIDS Patients

Elevated plasma lipopolysaccharide (LPS), an indicator of microbial translocation from the gut, is a likely cause of systemic immune activation in chronic HIV infection. LPS induces monocyte activation and trafficking into brain, which are key mechanisms in the pathogenesis of HIV-associated dementia (HAD). To determine whether high LPS levels are associated with increased monocyte activation and HAD, we obtained peripheral blood samples from AIDS patients and examined plasma LPS by Limulus amebocyte lysate (LAL) assay, peripheral blood monocytes by FACS, and soluble markers of monocyte activation by ELISA. Purified monocytes were isolated by FACS sorting, and HIV DNA and RNA levels were quantified by real time PCR. Circulating monocytes expressed high levels of the activation markers CD69 and HLA-DR, and harbored low levels of HIV compared to CD4+ T-cells. High plasma LPS levels were associated with increased plasma sCD14 and LPS-binding protein (LBP) levels, and low endotoxin core antibody levels. LPS levels were higher in HAD patients compared to control groups, and were associated with HAD independently of plasma viral load and CD4 counts. LPS levels were higher in AIDS patients using intravenous heroin and/or ethanol, or with Hepatitis C virus (HCV) co-infection, compared to control groups. These results suggest a role for elevated LPS levels in driving monocyte activation in AIDS, thereby contributing to the pathogenesis of HAD, and provide evidence that cofactors linked to substance abuse and HCV co-infection influence these processes

Minocycline Inhibition of Monocyte Activation Correlates with Neuronal Protection in SIV NeuroAIDS

Background: Minocycline is a tetracycline antibiotic that has been proposed as a potential conjunctive therapy for HIV-1 associated cognitive disorders. Precise mechanism(s) of minocycline’s functions are not well defined. Methods: Fourteen rhesus macaques were SIV infected and neuronal metabolites measured by proton magnetic resonance spectroscopy (1H MRS). Seven received minocycline (4 mg/kg) daily starting at day 28 post-infection (pi). Monocyte expansion and activation were assessed by flow cytometry, cell traffic to lymph nodes, CD16 regulation, viral replication, and cytokine production were studied. Results: Minocycline treatment decreased plasma virus and pro-inflammatory CD14+CD16+ and CD14loCD16+ monocytes, and reduced their expression of CD11b, CD163, CD64, CCR2 and HLA-DR. There was reduced recruitment of monocyte/ macrophages and productively infected cells in axillary lymph nodes. There was an inverse correlation between brain NAA/ Cr (neuronal injury) and circulating CD14+CD16+ and CD14loCD16+ monocytes. Minocycline treatment in vitro reduced SIV replication CD16 expression on activated CD14+CD16+ monocytes, and IL-6 production by monocytes following LPS stimulation. Conclusion: Neuroprotective effects of minocycline are due in part to reduction of activated monocytes, monocyte traffic. Mechanisms for these effects include CD16 regulation, reduced viral replication, and inhibited immune activation. Citation: Campbell JH, Burdo TH, Autissier P, Bombardier JP, Westmoreland SV, et al. (2011) Minocycline Inhibition of Monocyte Activation Correlate

Single Nucleotide Polymorphism in Gene Encoding Transcription Factor Prep1 Is Associated with HIV-1-Associated Dementia

BACKGROUND: Infection with HIV-1 may result in severe cognitive and motor impairment, referred to as HIV-1-associated dementia (HAD). While its prevalence has dropped significantly in the era of combination antiretroviral therapy, milder neurocognitive disorders persist with a high prevalence. To identify additional therapeutic targets for treating HIV-associated neurocognitive disorders, several candidate gene polymorphisms have been evaluated, but few have been replicated across multiple studies. METHODS: We here tested 7 candidate gene polymorphisms for association with HAD in a case-control study consisting of 86 HAD cases and 246 non-HAD AIDS patients as controls. Since infected monocytes and macrophages are thought to play an important role in the infection of the brain, 5 recently identified single nucleotide polymorphisms (SNPs) affecting HIV-1 replication in macrophages in vitro were also tested. RESULTS: The CCR5 wt/Δ32 genotype was only associated with HAD in individuals who developed AIDS prior to 1991, in agreement with the observed fading effect of this genotype on viral load set point. A significant difference in genotype distribution among all cases and controls irrespective of year of AIDS diagnosis was found only for a SNP in candidate gene PREP1 (p = 1.2 × 10(-5)). Prep1 has recently been identified as a transcription factor preferentially binding the -2,518 G allele in the promoter of the gene encoding MCP-1, a protein with a well established role in the etiology of HAD. CONCLUSION: These results support previous findings suggesting an important role for MCP-1 in the onset of HIV-1-associated neurocognitive disorders