Identifying analogue samples of individuals with clinically significant social anxiety: Updating and combining cutoff scores on the Social Phobia Inventory and Sheehan Disability Scale.

The use of analogue samples, as opposed to clinical groups, is common in mental health research, including research on social anxiety disorder (SAD). Recent observational and statistical evidence has raised doubts about the validity of current methods for establishing analogue samples of individuals with clinically significant social anxiety. Here, we used data from large community samples of clinical and nonclinical participants to determine new cutoff scores on self-report measures of social anxiety symptoms and symptom-related impairment. We then examined whether using these newly determined cutoff scores alone or in combination improves the identification of individuals who have SAD from those who do not, revealing the most ideal cutoff combination to be 34 or above on the Social Phobia Inventory and 11 or above on the Sheehan Disability Scale. Finally, we compared the effects of our new cutoff scores with old cutoff scores by extracting analogue samples of participants with high social anxiety from historical data on seven large groups of undergraduate Psychology research participants from the authors' institution spanning the past 5 years (2018-2023). We observed that the new combined cutoff scores identified markedly fewer students as having high social anxiety, lending credibility to their utility. We also observed a striking increase in levels of social anxiety symptoms in the undergraduate population from before to after the COVID-19 pandemic. Of note, most participants were under 30 and identified as Caucasian or Asian women, indicating that future research is needed to examine whether our findings generalize to diverse populations. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

The moderating effects of reported pre-pandemic social anxiety, symptom impairment, and current stressors on mental health and affiliative adjustment during the first wave of the COVID-19 pandemic.

BACKGROUND AND OBJECTIVES: Individuals with social anxiety (SA) have well-established fears of being negatively evaluated and exposing self-perceived flaws to others. However, the unique impacts of pre-existing SA on well-being and interpersonal outcomes within the stressful context of the pandemic are currently unknown. DESIGN: In a study that took place in May 2020, we surveyed 488 North American community participants online. METHODS: We used multiple linear regression to analyze whether retrospective reports of pre-pandemic SA symptoms predicted current coronavirus anxiety, loneliness, fears of negative evaluation, use of preventive measures, and affiliative outcomes, and whether pre-pandemic functional impairment and recent COVID-related stressors moderated these relations. RESULTS: Results highlighted the negative effects of pre-pandemic SA on current mental health functioning, especially for participants with higher pre-pandemic functional impairment and greater exposure to COVID-related stressors. Although participants with higher pre-pandemic SA reported currently feeling lonelier and more fearful of negative evaluation, they also endorsed greater efforts to affiliate with others. CONCLUSIONS: High SA individuals may have heightened desire for social support within the isolating context of the pandemic, in which COVID-related social restrictions enable greater avoidance of social evaluation but may also mask the enduring impairment associated with pre-pandemic SA.

Fears of receiving compassion from others predict safety behaviour use in social anxiety disorder over and above fears of negative self-portrayal.

Why do people with social anxiety disorder (SAD) engage in the use of safety behaviours? While past research has established that fears of negative self-portrayal are strongly associated with safety behaviour use in SAD, no research to date has investigated the potential role of fears of receiving compassion. Both types of fears could motivate those with SAD to engage in safety behaviours in order to keep others at a distance. In the present study, 150 participants with a clinical diagnosis of SAD completed measures of fears of negative self-portrayal, fears of receiving compassion, and safety behaviour use. Multiple regression analyses revealed that when controlling for self-portrayal fears, fears of receiving compassion significantly predicted increased use of safety behaviours overall, as well as the use of avoidance and impression management subtypes. Furthermore, there was a significant interaction effect in which greater fears of receiving compassion predicted greater use of impression management at lower levels of self-portrayal fears. We discuss the implications of our findings for addressing safety behaviours in the treatment of SAD.

Racial disparities in intensity of smoke exposure and nicotine intake among low-dependence smokers.

BACKGROUND: Compared to white smokers, Black smokers are at disproportionately higher risk for smoking-related disease, despite consuming fewer cigarettes per day (CPD). To examine racial disparities in biobehavioral influences on smoking and disease risk, we analyzed the relationship between self-reported tobacco dependence and intensity of tobacco smoke exposure per cigarette, on the one hand, and intensity of nicotine intake per cigarette, on the other. METHODS: In 270 Black and 516 white smokers, smoke exposure was measured by expired carbon monoxide (CO), and nicotine intake was measured by plasma cotinine (COT) and cotinine+3'-hydroxycotinine ([COT + 3HC]). Using linear regression analyses, we analyzed how the Fagerström Test for Cigarette Dependence (FTCD) predicted intensity of smoke exposure per cigarette (CO/CPD) and intensity of nicotine intake per cigarette (COT/CPD; [COT + 3HC]/CPD), and how race moderated these relations. RESULTS: Overall, Black smokers consumed fewer CPD than white smokers and had higher levels of CO/CPD, COT/CPD, and [COT + 3HC]/CPD. These elevations were most pronounced at lower levels of dependence: amongst Black smokers, FTCD negatively predicted intensity of smoke exposure as measured by CO/CPD (B = -0.12, 95% CI = -0.18, -0.05, p = 0.0003) and intensity of nicotine intake as measured by [COT + 3HC]/CPD (B = -1.31, 95% CI = -2.15, -0.46, p = 0.002). CONCLUSIONS: Low-dependence Black smokers had higher intensities of both smoke exposure and nicotine intake per cigarette compared to similarly dependent white smokers, suggesting that measures of dependence, exposure, and intake underestimate incremental risk of each cigarette to Black smokers.

Deferiprone inhibits iron overload-induced tissue factor bearing endothelial microparticle generation by inhibition oxidative stress induced mitochondrial injury, and apoptosis.

Iron overload-induced cardiovascular toxicity is one of the most common causes of morbidity and mortality in beta-thalassemia major patients. We have previously shown that iron overload-induced systemic arterial changes characterized by endothelial dysfunction are associated with increased endothelial microparticle (EMP) release. In this study, we further demonstrate how EMP release is associated with iron-induced mitochondrial injury and apoptosis of endothelial cells. Iron increased the production of reactive oxygen species (ROS) and calcium influx into mitochondria [Ca2+]m. Iron also disturbed mitochondrial respiration function and eventually led to loss of mitochondrial membrane potential (ΔΨm). A significant increase in apoptotic cells and EMPs were found under iron treatment. EMPs contained tissue factor (TF), which has potential clinical impact on thromboembolic phenomenon. Then, we investigated the salvaging effect of deferiprone (L1) on endothelial cell damage and EMP release. We found that L1 could inhibit iron-induced ROS generation, and decrease mitochondrial damage with the resultant effect of less endothelial cell apoptosis and EMP release. L1 could protect endothelial cells from iron-induced toxic effects and minimize EMP release, which could be potentially helpful in a subgroup of thalassemia patients who have increased thromboembolic complications.

Human definitive hematopoietic specification from pluripotent stem cells is regulated by mesodermal expression of CDX4.

The generation of hematopoietic stem cells from human pluripotent stem cells (hPSCs) is a major goal for regenerative medicine. Achieving this goal is complicated by our incomplete understanding of the mechanism regulating definitive hematopoietic specification. We used our stage-specific hPSC differentiation method to obtain and identify, via CD235a expression, mesoderm harboring exclusively primitive or definitive hematopoietic potential to understand the genetic regulation of definitive hematopoietic specification. Whole-transcriptome gene expression analyses on WNT-dependent KDR+CD235a- definitive hematopoietic mesoderm and WNT-independent KDR+CD235a+ primitive hematopoietic mesoderm revealed strong CDX gene expression within definitive hematopoietic mesoderm. Temporal expression analyses revealed that CDX4 was expressed exclusively within definitive hematopoietic KDR+CD235a- mesoderm in a WNT- and fibroblast growth factor-dependent manner. We found that exogenous CDX4 expression exclusively during mesoderm specification resulted in a >90% repression in primitive hematopoietic potential, but conferred fivefold greater definitive hematopoietic potential, similar to that observed following WNT stimulation. In contrast, CDX4 knockout hPSCs had intact primitive hematopoietic potential, but exhibited a fivefold decrease in multilineage definitive hematopoietic potential. Taken together, these findings indicate that CDX4 is a critical transcription factor in the regulation of human definitive hematopoietic specification, and provides a mechanistic basis for WNT-mediated definitive hematopoietic specification from hPSCs.

Systemic effects of gut microbiota and its relationship with disease and modulation.

The gut microbiota makes up the majority of the human bacterial population, and although the gut microbiota resides in the intestines, it is able to exert systemic effects. Therefore, many diseases and conditions could be impacted by the gut microbiota when its composition is imbalanced, otherwise known as dysbiosis. However, apart from understanding the illnesses, we must also try to understand the intestinal flora itself to move forward and develop potential treatments.