Alteration of host cell ubiquitination by the intracellular bacterial pathogen Coxiella burnetii

The intracellular bacterial agent of Q fever, Coxiella burnetii, replicates within a phagolysosomelike parasitophorous vacuole (PV) in human macrophages and delivers effector proteins to the host cytosol via a Dot/Icm type IV secretion system (T4SS). The T4SS effectors are critical for PV formation and prevention of host cell death that allows sufficient time for bacterial replication. Recruitment of ubiquitin-related components to the C. burnetii PV is also predicted to be involved in PV formation and bacterial replication and is likely controlled by effector proteins. In this study, we assessed the role of the Dot/Icm T4SS in regulating ubiquitination by comparing subcellular localization of ubiquitinated proteins between cells infected with C. burnetii and a mutant that lacks a functional T4SS. Fluorescence microscopy showed ubiquitinated proteins surrounding wild-type C. burnetii PV but not phagosomes harboring T4SS-defective organisms. Immunoblot analysis showed altered ubiquitinated protein profiles throughout infection, suggesting C. burnetii impacts post-translational modification of host cell and/or bacterial proteins. Future studies will determine how T4SS-mediated recruitment of ubiquitinated proteins impacts C. burnetii-host cell interactions and eventual development of diseas

Nepotistic patterns of violent psychopathy: evidence for adaptation?

Psychopaths routinely disregard social norms by engaging in selfish, antisocial, often violent behavior. Commonly characterized as mentally disordered, recent evidence suggests that psychopaths are executing a well-functioning, if unscrupulous strategy that historically increased reproductive success at the expense of others. Natural selection ought to have favored strategies that spared close kin from harm, however, because actions affecting the fitness of genetic relatives contribute to an individual’s inclusive fitness. Conversely, there is evidence that mental disorders can disrupt psychological mechanisms designed to protect relatives. Thus, mental disorder and adaptation accounts of psychopathy generate opposing hypotheses: psychopathy should be associated with an increase in the victimization of kin in the former account but not in the latter. Contrary to the mental disorder hypothesis, we show here in a sample of 289 violent offenders that variation in psychopathy predicts a decrease in the genetic relatedness of victims to offenders; that is, psychopathy predicts an increased likelihood of harming non-relatives. Because nepotistic inhibition in violence may be caused by dispersal or kin discrimination, we examined the effects of psychopathy on (1) the dispersal of offenders and their kin and (2) sexual assault frequency (as a window on kin discrimination). Although psychopathy was negatively associated with coresidence with kin and positively associated with the commission of sexual assault, it remained negatively associated with the genetic relatedness of victims to offenders after removing cases of offenders who had coresided with kin and cases of sexual assault from the analyses. These results stand in contrast to models positing psychopathy as a pathology, and provide support for the hypothesis that psychopathy reflects an evolutionary strategy largely favoring the exploitation of non-relatives

L-carnitine attenuates cardiac impairment but not vascular dysfunction in DOCA-salt hypertensive rats

L-Carnitine is an important co-factor in fatty acid metabolism by mitochondria. This study has determined whether oral administration of L-carnitine prevents remodelling and the development of impaired cardiovascular function in deoxycorticosterone acetate (DOCA)-salt hypertensive rats (n = 6–12; #p < 0.05 versus DOCA-salt). Uninephrectomized rats administered DOCA (25 mg every 4th day s.c.) and 1% NaCl in drinking water for 28 days developed cardiovascular remodelling shown as systolic hypertension, left ventricular hypertrophy, increased thoracic aortic and left ventricular wall thickness, increased left ventricular inflammatory cell infiltration together with increased interstitial collagen and increased passive diastolic stiffness and vascular dysfunction with increased plasma malondialdehyde concentrations. Treatment with L-carnitine (1.2% in food; 0.9 mg⁄g⁄day in DOCA-salt rats) decreased blood pressure (DOCA-salt 169 € 2; + L-carnitine 148 € 6# mmHg), decreased left ventricular wet weights (DOCA-salt 3.02 € 0.07; + L-carnitine 2.72 € 0.06# mg⁄ g body-wt), decreased inflammatory cells in the replacement fibrotic areas, reduced left ventricular interstitial collagen content (DOCA-salt 14.4 € 0.2; + L-carnitine 8.7 € 0.5# % area), reduced diastolic stiffness constant (DOCA-salt 26.9 € 0.5; + L-carnitine 23.8 € 0.5# dimensionless) and decreased plasma malondialdehyde concentrations (DOCA-salt 26.9 € 0.8; + L-carnitine 21.2 € 0.4# lmol ⁄ l) without preventing endothelial dysfunction. L-carnitine attenuated the cardiac remodelling and improved cardiac function in DOCA-salt hypertension but produced minimal changes in aortic wall thickness and vascular function. This study suggests that the mitochondrial respiratory chain is a significant source of reactive oxygen species in the heart but less so in the vasculature in DOCA-salt rats, underlying the relatively selective cardiac responses to L-carnitine treatment

Using Google Forms to Track Library Space Usage

This article is a response to the excellent “Using Mobile Technology to Observe Student Study Behaviors and Track Library Space Usage” by Susan Thompson (2015). Thompson reviews the literature regarding user counts on mobile devices, and describes the California State University San Marcos (CSUSM) Library’s evaluation of SUMA, Counter+ and CloudOn. After trialing these mobile technologies, CSUSM selected CloudOn. At New York University Abu Dhabi (NYUAD), we use Google Forms to conduct user counts on an iPad and Google Sheets to evaluate this data. We find that Google Forms are easy to set up, modify as necessary, and present the data in easy-to-manipulate spreadsheets

The Psychological Implications of Obesity in Adolescent High School Students

This research project set to answer the questions: Are obese adolescents at risk for short-term and long-term physical health problems? Are obese adolescents at risk for increased depression, decreased self-esteem, increased suicidal thoughts and/or actions, increased peer victimization and detrimental effects to various psychosocial outcomes? A survey, which included The Rosenberg Self-Esteem Scale and The Center for Epidemiological Studies Depression Scale for Children (CES-DC), was given to male and female students, ages 15-17, currently enrolled in a high school health class. The results of this research project were inconclusive, as this researcher was unable to conduct a comparison study between obese and normal weight students as all students that participated were either normal weight or underweight. However, the findings support the literature that was reviewed in that the importance of obesity as an epidemic, the physical health risks associated with obesity and the association of obesity with psychological aspects of mental health, i.e. depression, self-esteem, increased suicidal thoughts and/or actions, peer victimization and psychosocial outcomes in adolescents were all supported

Psychopathy, adaptation, and disorder

In a recent study, we found a negative association between psychopathy and violence against genetic relatives. We interpreted this result as a form of nepotism and argued that it failed to support the hypothesis that psychopathy is a mental disorder, suggesting instead that it supports the hypothesis that psychopathy is an evolved life history strategy. This interpretation and subsequent arguments have been challenged in a number of ways. Here, we identify several misunderstandings regarding the harmful dysfunction definition of mental disorder as it applies to psychopathy and regarding the meaning of nepotism. Furthermore, we examine the evidence provided by our critics that psychopathy is associated with other disorders, and we offer a comment on their alternative model of psychopathy. We conclude that there remains little evidence that psychopathy is the product of dysfunctional mechanisms