Moderate exercise training attenuates aging-induced cardiac inflammation,hypertrophy and fibrosis injuries of rat hearts

Aging is the most important risk factor in cardiovascular disease (CVD), which is the leading causes of death worldwide and the second major cause of death in Taiwan. The major factor in heart failure during aging is heart remodeling, including long-term stress-induced cardiac hypertrophy and fibrosis. Exercise is good for aging heart health, but the impact of exercise training on aging is not defined. This study used 3-, 12- and 18-month-old rats and randomly divided each age group into no exercise training control groups (C3, A12 and A18) and moderate gentle swimming exercise training groups (E3, AE12 and AE18). The protocol of exercise training was swimming five times weekly with gradual increases from the first week from 20 to 60 min for 12 weeks. Analyses of protein from rat heart tissues and sections revealed cardiac inflammation, hypertrophy and fibrosis pathway increases in aged rat groups (A12 and A18), which were improved in exercise training groups (AE12 and AE18). There were no heart injuries in young rat hearts in exercise group E3. These data suggest that moderate swimming exercise training attenuated aging-induced cardiac inflammation, hypertrophy and fibrosis injuries of rat hearts.     

HPTN 068: A Randomized Control Trial of a Conditional Cash Transfer to Reduce HIV Infection in Young Women in South Africa—Study Design and Baseline Results

Young women in South Africa are at high risk for HIV infection. Cash transfers offer promise to reduce HIV risk. We present the design and baseline results from HPTN 068, a phase III, individually randomized trial to assess the effect of a conditional cash transfer on HIV acquisition among South African young women. A total of 2533 young women were randomized to receive a monthly cash transfer conditional on school attendance or to a control group. A number of individual-, partner-, household- and school-level factors were associated with HIV and HSV-2 infection. After adjusting for age, all levels were associated with an increased odds of HIV infection with partner-level factors conveying the strongest association (aOR 3.05 95 % CI 1.84–5.06). Interventions like cash transfers that address structural factors such as schooling and poverty have the potential to reduce HIV risk in young women in South Africa.     

Chromosomal DNA damage in APOE ɛ4 carriers and noncarriers does not appear to be different

DNA damage may play a key role in promoting disease‐onset and accelerated disease progression in Alzheimer's disease (AD) by increasing the rates of neuronal cell death. The ?4 allele of the APOE gene is the best characterised genetic risk factor for AD, however, it is unknown if APOE ?4 carriers exhibit increased levels of DNA damage which may contribute to increased AD risk. 175 healthy participants (aged 34–67 years old) from South Australia were recruited into the study and provided a single blood sample for the isolation of peripheral blood lymphocytes, APOE genotyping and lymphocyte chromosomal DNA damage analysis using the Cytokinesis‐Block micronucleus cytome (CBMN‐Cyt) assay with the micronucleus index being the primary outcome measure. When compared to non‐APOE ?4 carriers, APOE ?4 carriers did not exhibit altered rates of i) cell division, represented by the nuclear division index (NDI, P = 0.372), ii) cell death as represented by apoptotic (P = 0.457) and necrotic (P = 0.393) frequencies and iii) chromosomal DNA damage as indicated by the number of micronuclei (MNi, P = 0.795), nucleoplasmic bridges (NPBs, P = 0.221) or nuclear buds (NBUDs, P = 0.293) scored in binucleated cells. In conclusion, although we and others have previously shown that rates of chromosomal DNA damage measured using the CBMN‐Cyt assay are elevated in individuals with cognitive impairment, in this South Australian cohort the frequency of genome instability is not substantially influenced by the presence of the APOE ?4 allele. Environ. Mol. Mutagen. 56:694–708, 2015. © 2015 Wiley Periodicals, Inc.     

Delusions and prediction error: clarifying the roles of behavioural and brain responses

Griffiths and colleagues provided a clear and thoughtful review of the prediction error model of delusion formation [Cognitive Neuropsychiatry, 2014 April 4 (Epub ahead of print)]. As well as reviewing the central ideas and concluding that the existing evidence base is broadly supportive of the model, they provide a detailed critique of some of the experiments that we have performed to study it. Though they conclude that the shortcomings that they identify in these experiments do not fundamentally challenge the prediction error model, we nevertheless respond to these criticisms. We begin by providing a more detailed outline of the model itself as there are certain important aspects of it that were not covered in their review. We then respond to their specific criticisms of the empirical evidence. We defend the neuroimaging contrasts that we used to explore this model of psychosis arguing that, while any single contrast entails some ambiguity, our assumptions have been justified by our extensive background work before and since.