An Implicit Theory of Self-Esteem: The Consequences of Perceived Self-Esteem for Romantic Desirability

The provision of information appears to be an important property of self-esteem as evidenced by previous research concerning the status-tracking and status-signaling models of self-esteem. The present studies examine whether there is an implicit theory of self-esteem that leads individuals to assume targets with higher levels of self-esteem possess more desirable characteristics than those with lower levels of self-esteem. Across 6 studies, targets with ostensibly higher levels of self-esteem were generally rated as more attractive and as more desirable relationship partners than those with lower levels of self-esteem. It is important to note, however, that this general trend did not consistently emerge for female targets. Rather, female targets with high self-esteem were often evaluated less positively than those with more moderate levels of self-esteem. The present findings are discussed in the context of an extended informational model of self-esteem consisting of both the status-tracking and status-signaling properties of self-esteem

Experiences of women with ovarian cancer during the COVID-19 pandemic: Examining intolerance of uncertainty and fear of COVID-19 in relation to psychological distress

Purpose: Our research aimed to examine the role of intolerance of uncertainty (IU) in psychological distress (PD) among women with ovarian cancer. Fear of COVID-19 (FCOV) was examined as a mediator, and participant health status and the reopening status of their geographic region were examined as moderators. Design: A cross-sectional quantitative design was employed. Participants: Participants (n ¼ 100) were recruited through various online sources and completed the study via Qualtrics. Methods: Moderated mediation models and post-hoc linear regression analyses were used to determine the role of predictor variables in PD. Results: No significant moderators or mediators were found. Despite a strong correlation between FCOV and IU, both variables explained unique variance in the anxiety and stress models, while FCOV was not significant in the depressive symptoms model. Implications for Providers: Both IU and FCOV should be considered in helping women with ovarian cancer manage their PD during the COVID-19 pandemic

Distinguishing personal belief from scientific knowledge for the betterment of killer whale welfare – a commentary

We contest publication of Marino et al. regarding captive killer whale (Orcinus orca) welfare because of misrepresentations of available data and the use of citations that do not support assertions. Marino et al. misrepresent stress response concepts and erroneously cite studies, which appear to support Marino et al.’s philosophical beliefs regarding the cetacean hypothalamic–pituitary–adrenal axis. To be clear, these misrepresentations are not differences of scientific opinion, as the authors’ conclusions lack any scientific basis. More extensive review of Marino et al.’s citations reveal a dearth of empirical evidence to support their assertions. Further, Marino et al.’s approach to animal welfare is not consistent with conventional veterinary approaches to animal welfare, including their apparent opposition to use of preventative and therapeutic veterinary interventions. While Marino et al. argue that killer whales’ cognitive and spatial needs preclude management of this species under human care, misrepresentation of the citations used to support this opinion invalidates their arguments. Misleading interpretations of data relative to killer whales’ cognitive and emotional needs and specious and unsubstantiated comparisons with states experienced by humans with posttraumatic stress disorder and other conditions, represent a number of strategies used to misrepresent knowledge regarding killer whale welfare. These misrepresentations and fallacies are inconsistent with scientific ethical standards for credible, peer-reviewed journals (ICMJE, 2018), and are barriers to rigorous discourse and identification of strategies for optimizing killer whale welfare. Assertions in the paper amount to nothing more than a compilation of conclusory, philosophical statements. We would also like to mention that manuscripts such as Marino et al.’s do great damage to the fields of comparative psychology and to behavioral science as a whole

An examination of the health and wellbeing of childless women: A cross-sectional exploratory study in Victoria, Australia

BackgroundChildlessness among Australian women is increasing. Despite this, little is known about the physical and mental health and wellbeing of childless women, particularly during the reproductive years. The aims of this exploratory study were to: 1) describe the physical and mental health and wellbeing and lifestyle behaviours of childless women who are currently within the latter part of their reproductive years (30 &ndash; 45 years of age); and 2) compare the physical and mental health and wellbeing and lifestyle behaviours of these childless women to Australian population norms.MethodsA convenience sample of 50 women aged between 30 and 45 years were recruited to participate in a computer assisted telephone interview. The SF-36 Health Survey v2 and lifestyle indicators were collected in regards to women&rsquo;s health and wellbeing. Data were analysed using descriptive statistics, t-tests for independent sample means and 95% confidence intervals for the difference between two independent proportions.ResultsChildless women in this study reported statistically significant poorer general health, vitality, social functioning and mental health when compared to the adult female population of Australia. With the exception of vegetable consumption, lifestyle behaviours were similar for the childless sample compared to the adult female population in Australia.ConclusionsChildless women may be at a greater risk of experiencing poor physical and mental health when compared to the Australian population. A woman&rsquo;s health and wellbeing during her reproductive years may have longer term health consequences and as such the health and wellbeing of childless women requires further investigation to identify and address implications for the provision of health (and other social) services for this growing population group.<br /

Genetic analysis of hog deer (Axis porcinus) in Victoria, Australia, and its applications to invasive species and game management

Hog deer were introduced to Australia in the 1860s, where they have spread across the Gippsland region of Victoria. Due to its status as an introduced species and an important game animal within Victoria, management of the species is complex. Given this complexity, genetic studies can provide important information regarding population structure and diversity which can assist in controlling problematic populations of hog deer, while also ensuring viable game stock in sites managed as game reserves. The aim of this study was to investigate the population genetic structure and diversity of the Victorian hog deer 150 years after introduction using short tandem repeats (STRs). Hog deer samples were collected across 15 sites of differing management regimes in the Gippsland region of Victoria and genotyped for 13 polymorphic STR loci. Up to four distinct genetic clusters were identified across the sites sampled, suggesting that despite low observed genetic diversity, population structure is present across their range. It was also possible to detect evidence of recent translocations among populations. This study suggests that the presence of distinct genetic clusters may enable management of separate genetic units, considering invasive species and game management objectives

The complete mitochondrial genome of Axis porcinus (Mammalia: Cervidae) from Victoria, Australia, using MiSeq sequencing

The mitochondrial genome of the hog deer (Axis porcinus) was sequenced using an Illumina MiSeq. The assembled genome consists of 16,351 bp, and shared a 99.8% similarity to the published chital deer (Axis axis) genome, suggesting that they belong to the same species. Further research is ongoing to understand why these mitochondrial genomes are highly similar

Evidence for More than One Parkinson's Disease-Associated Variant within the HLA Region

Parkinson's disease (PD) was recently found to be associated with HLA in a genome-wide association study (GWAS). Follow-up GWAS's replicated the PD-HLA association but their top hits differ. Do the different hits tag the same locus or is there more than one PD-associated variant within HLA? We show that the top GWAS hits are not correlated with each other (0.00≤r2≤0.15). Using our GWAS (2000 cases, 1986 controls) we conducted step-wise conditional analysis on 107 SNPs with P<10−3 for PD-association; 103 dropped-out, four remained significant. Each SNP, when conditioned on the other three, yielded PSNP1 = 5×10−4, PSNP2 = 5×10−4, PSNP3 = 4×10−3 and PSNP4 = 0.025. The four SNPs were not correlated (0.01≤r2≤0.20). Haplotype analysis (excluding rare SNP2) revealed increasing PD risk with increasing risk alleles from OR = 1.27, P = 5×10−3 for one risk allele to OR = 1.65, P = 4×10−8 for three. Using additional 843 cases and 856 controls we replicated the independent effects of SNP1 (Pconditioned-on-SNP4 = 0.04) and SNP4 (Pconditioned-on-SNP1 = 0.04); SNP2 and SNP3 could not be replicated. In pooled GWAS and replication, SNP1 had ORconditioned-on-SNP4 = 1.23, Pconditioned-on-SNP4 = 6×10−7; SNP4 had ORconditioned-on-SNP1 = 1.18, Pconditioned-on-SNP1 = 3×10−3; and the haplotype with both risk alleles had OR = 1.48, P = 2×10−12. Genotypic OR increased with the number of risk alleles an individual possessed up to OR = 1.94, P = 2×10−11 for individuals who were homozygous for the risk allele at both SNP1 and SNP4. SNP1 is a variant in HLA-DRA and is associated with HLA-DRA, DRB5 and DQA2 gene expression. SNP4 is correlated (r2 = 0.95) with variants that are associated with HLA-DQA2 expression, and with the top HLA SNP from the IPDGC GWAS (r2 = 0.60). Our findings suggest more than one PD-HLA association; either different alleles of the same gene, or separate loci

Reducing Poverty in California…Permanently

If California were to seriously commit to equalizing opportunity and reducing poverty, how might that commitment best be realized? This is of course a hypothetical question, as there is no evidence that California is poised to make such a serious commitment, nor have many other states gone much beyond the usual lip-service proclamations. There are many reasons for California’s complacency, but an important one is that most people think that poverty is intractable and that viable solutions to it simply don’t exist. When Californians know what needs to be done, they tend to go forward and get it done. When, for example, the state’s roads are in disrepair, there are rarely paralyzing debates about exactly how to go about fixing them; instead we proceed with the needed repairs as soon as the funds to do so are appropriated. The same type of sure and certain prescription might appear to be unavailable when it comes to reducing poverty. It is hard not to be overwhelmed by the cacophony of voices yielding a thick stream of narrow-gauge interventions, new evaluations, and piecemeal proposals.1 Although the research literature on poverty is indeed large and may seem confusing, recent advances have in fact been so fundamental that it is now possible to develop a science-based response to poverty. In the past, the causes of poverty were not well understood, and major interventions, such as the War on Poverty, had to be built more on hunch than science. It is an altogether different matter now. The causes of poverty are well established, and the effects of many possible policy responses to poverty are likewise well established. The simple purpose of this essay is to assemble these advances into a coherent plan that would, if implemented, reduce poverty in California substantially

The impact of abnormal glucose tolerance and obesity on fetal growth

Factors linked with insulin resistance were examined for their association with large-for-gestational-age (LGA) infant birth weight and gestational diabetes. Study Design. Data came from a longitudinal cohort study of 2,305 subjects without overt diabetes, analyzed using multinomial logistic and linear regression. Results. High maternal BMI (OR = 1.53 (1.11, 2.12)), height (1.98 (1.62, 2.42)), antidepressant use (1.71 (1.20, 2.44)), pregnancy weight-gain exceeding 40 pounds (1.79 (1.25, 2.57)), and high blood sugar (2.68, (1.53, 5.27)) were all positively associated with LGA birth. Strikingly, the difference in risk from diagnosed and treated gestational diabetes compared to women with a single abnormal glucose tolerance test (but no diagnosis of gestational diabetes) was significant (OR = 0.65, p = 0.12 versus OR = 2.84, p \u3c 0.01). When weight/length ratio was used instead, different factors were found to be significant. BMI and pregnancy weight-gain were found to influence the development of gestational diabetes, through an additive interaction. Conclusions. High prepregnancy BM, height, antidepressant use, pregnancy weight-gain exceeding 40 pounds, and high blood sugar were associated with LGA birth, but not necessarily infant weight/length ratio. An additive interaction between BMI and pregnancy weight-gain influenced gestational diabetes development

KEAP1 Is Required for Artesunate Anticancer Activity in Non-Small-Cell Lung Cancer

Artesunate is the most common treatment for malaria throughout the world. Artesunate has anticancer activity likely through the induction of reactive oxygen species, the same mechanism of action utilized in Plasmodium falciparum infections. Components of the kelch-like ECH-associated protein 1 (KEAP1)/nuclear factor erythroid 2-related factor 2 (NRF2) pathway, which regulates cellular response to oxidative stress, are mutated in approximately 30% of non-small-cell lung cancers (NSCLC); therefore, we tested the hypothesis that KEAP1 is required for artesunate sensitivity in NSCLC. Dose response assays identified A549 cells, which have a G333C-inactivating mutation in KEAP1, as resistant to artesunate, with an IC50 of 23.6 µM, while H1299 and H1563 cells were sensitive to artesunate, with a 10-fold lower IC50. Knockdown of KEAP1 through siRNA caused increased resistance to artesunate in H1299 cells. Alternatively, the pharmacological inhibition of NRF2, which is activated downstream of KEAP1 loss, by ML385 partially restored sensitivity of A549 cells to artesunate, and the combination of artesunate and ML385 was synergistic in both A549 and H1299 cells. These findings demonstrate that KEAP1 is required for the anticancer activity of artesunate and support the further development of NRF2 inhibitors to target patients with mutations in the KEAP1/NRF2 pathway