Cool and Hot Executive Function Impairments in Violent Offenders with Antisocial Personality Disorder with and without Psychopathy

Background

Impairments in executive function characterize offenders with antisocial personality disorder (ASPD) and offenders with psychopathy. However, the extent to which those impairments are associated with ASPD, psychopathy, or both is unknown.

Methods

The present study examined 17 violent offenders with ASPD and psychopathy (ASPD+P), 28 violent offenders with ASPD without psychopathy (ASPD−P), and 21 healthy non-offenders on tasks assessing cool (verbal working memory and alteration of motor responses to spatial locations) and hot (reversal learning, decision-making under risk, and stimulus-reinforcement-based decision-making) executive function.

Results

In comparison to healthy non-offenders, violent offenders with ASPD+P and those with ASPD−P showed similar impairments in verbal working memory and adaptive decision-making. They failed to learn from punishment cues, to change their behaviour in the face of changing contingencies, and made poorer quality decisions despite longer periods of deliberation. Intriguingly, the two groups of offenders did not differ significantly from the non-offenders in terms of their alteration of motor responses to spatial locations and their levels of risk-taking, indicated by betting, and impulsivity, measured as delay aversion. The performance of the two groups of offenders on the measures of cool and hot executive function did not differ, indicating shared deficits.

Conclusions

These documented impairments may help to explain the persistence of antisocial behaviours despite the known risks of the negative consequences of such behaviours.     

Magno- and Parvocellular Contrast Responses in Varying Degrees of Autistic Trait

Autistic tendency has been associated with altered visual perception, especially impaired visual motion sensitivity and global/local integration, as well as enhanced visual search and local shape recognition. However, the neurophysiological mechanisms underlying these abnormalities remain poorly defined. The current study recruited 29 young adults displaying low, middle or high autistic trait as measured by Baron-Cohen''s Autism spectrum Quotient (AQ), and measured motion coherence thresholds psychophysically, with manipulation of dot lifetime and stimulus contrast, as well as nonlinear cortical visual evoked potentials (VEPs) over a range of temporal luminance contrast levels from 10% to 95%. Contrast response functions extracted from the major first order and second order Wiener kernel peaks of the VEPs showed consistent variation with AQ group, and Naka-Rushton fits enabled contrast gain and semi-saturation contrasts to be elicited for each peak. A short latency second order response (previously associated with magnocellular processing) with high contrast gain and a saturating contrast response function showed higher amplitude for the High AQ (compared with Mid and Low groups) indicating poorer neural recovery after rapid stimulation. A non-linearity evoked at longer interaction times (previously associated with parvocellular processing) with no evidence of contrast saturation and lower contrast gain showed no difference between autism quotient groups across the full range of stimulus contrasts. In addition, the short latency first order response and a small, early second order second slice response showed gain and semi-saturation parameters indicative of magnocellular origin, while the longer latency first order response probably reflects a mixture of inputs (including feedback from higher cortical areas). Significant motion coherence (AQ group) * (dot lifetime) interactions with higher coherence threshold for limited dot lifetime stimuli is consistent with atypical magnocellular functioning, however psychophysical performance for those with High AQ is not explained fully, suggesting that other factors may be involved.     

Big houses and small houses: Doing matriliny in West Sumatra

The big house is a potent symbol of rural Minangkabau life, embodying the centrality of Minangkabau women to the continuity and reproduction of the matrilineage. But big houses are not simply sites of social reproduction. Mothers and daughters negotiate and contest the ties of kinship embodied in the big house. Where big houses represented mother's power to control their daughters, national discourses of domesticity have reoriented daughters’ desires toward a house of their own. Daughters assert the importance of their own nuclear households as a way to resist their mother's control. Yet daughters have not become the housewives and mothers of national fantasy. They are reworking matrilineal ideology to gain the right to control their own small houses, ultimately reconstituting big houses in new forms.     

Evolutionary analysis of glycosyl hydrolase family 28 (GH28) suggests lineage-specific expansions in necrotrophic fungal pathogens

Glycosyl hydrolase family 28 (GH28) is a set of structurally related enzymes that hydrolyze glycosidic bonds in pectin, and are important extracellular enzymes for both pathogenic and saprotrophic fungi. Yet, very little is understood about the evolutionary forces driving the diversification of GH28s in fungal genomes. We reconstructed the evolutionary history of family GH28 in fungi by examining the distribution of GH28 copy number across the phylogeny of fungi, and by reconstructing the phylogeny of GH28 genes. We also examined the relationship between lineage-specific GH28 expansions and fungal ecological strategy, testing the hypothesis that GH28 evolution in fungi is driven by ecological strategy (pathogenic vs. non-pathogenic) and pathogenic niche (necrotrophic vs. biotrophic). Our results showed that GH28 phylogeny of Ascomycota and Basidiomycota sequences was structured by specific biochemical function, with endo-polygalacturonases and endo-rhamnogalacturonases forming distinct, apparently ancient clades, while exo-polygalacturonases are more widely distributed. In contrast, Mucoromycotina and Stramenopile sequences formed taxonomically-distinct clades. Large, lineage-specific variation in GH28 copy number indicates that the evolution of this gene family is consistent with the birth-and-death model of gene family evolution, where diversity of GH28 loci within genomes was generated through multiple rounds of gene duplication followed by functional diversification and loss of some gene family members. Although GH28 copy number was correlated with genome size, our findings suggest that ecological strategy also plays an important role in determining the GH28 repertoire of fungi. Both necrotrophic and biotrophic fungi have larger genomes than non-pathogens, yet only necrotrophs possess more GH28 enzymes than non-pathogens. Hence, lineage-specific GH28 expansion is the result of both variation in genome size across fungal species and diversifying selection within the necrotrophic plant pathogen ecological niche. GH28 evolution among necrotrophs has likely been driven by a co-evolutionary arms race with plants, whereas the need to avoid plant immune responses has resulted in purifying selection within biotrophic fungi.     

Characterization of the genetic diversity of <Emphasis Type="Italic">Mycobacterium tuberculosis</Emphasis> in São Paulo city,Brazil

Background

Tuberculosis is a major health problem in São Paulo, Brazil, which is the most populous and one of the most cosmopolitan cities in South America. To characterize the genetic diversity of Mycobacterium tuberculosis in the population of this city, the genotyping techniques of spoligotyping and MIRU were applied to 93 isolates collected in two consecutive years from 93 different tuberculosis patients residing in São Paulo city and attending the Clemente Ferreira Institute (the reference clinic for the treatment of tuberculosis).

Findings

Spoligotyping generated 53 different spoligotype patterns. Fifty-one isolates (54.8%) were grouped into 13 spoligotyping clusters. Seventy- two strains (77.4%) showed spoligotypes described in the international databases (SpolDB4, SITVIT), and 21 (22.6%) showed unidentified patterns. The most frequent spoligotype families were Latin American Mediterranean (LAM) (26 isolates), followed by the T family (24 isolates) and Haarlem (H) (11 isolates), which together accounted for 65.4% of all the isolates. These three families represent the major genotypes found in Africa, Central America, South America and Europe. Six Spoligo-International-types (designated SITs by the database) comprised 51.8% (37/72) of all the identified spoligotypes (SIT53, SIT50, SIT42, SIT60, SIT17 and SIT1). Other SITs found in this study indicated the great genetic diversity of M. tuberculosis, reflecting the remarkable ethnic diversity of São Paulo city inhabitants. The MIRU technique was more discriminatory and did not identify any genetic clusters with 100% similarity among the 93 isolates. The allelic analysis showed that MIRU loci 26, 40, 23 and 10 were the most discriminatory. When MIRU and spoligotyping techniques were combined, all isolates grouped in the 13 spoligotyping clusters were separated.

Conclusions

Our data indicated the genomic stability of over 50% of spoligotypes identified in São Paulo and the great genetic diversity of M. tuberculosis isolates in the remaining SITs, reflecting the large ethnic mix of the São Paulo city inhabitants. The results also indicated that in this city, M. tuberculosis isolates acquired drug resistance independently of genotype and that resistance was more dependent on the selective pressure of treatment failure and the environmental circumstances of patients.

     

Low sclerostin levels: a predictive marker of persistent inflammation in ankylosing spondylitis during anti-tumor necrosis factor therapy?

Introduction

Sclerostin levels have been reported to be low in ankylosing spondylitis (AS), but there is no data regarding the possible role of this Wnt inhibitor during anti-tumor necrosis factor (TNF) therapy. The present study longitudinally evaluated sclerostin levels, inflammatory markers and bone mineral density (BMD) in AS patients under anti-TNF therapy.

Methods

Thirty active AS patients were assessed at baseline, 6 and 12 months after anti-TNF therapy regarding clinical parameters, inflammatory markers, BMD and baseline radiographic damage (mSASSS). Thirty age- and sex-matched healthy individuals comprised the control group. Patients'' sclerostin levels, sclerostin binding low-density lipoprotein receptor-related protein 6 (LRP6) and BMD were evaluated at the same time points and compared to controls.

Results

At baseline, AS patients had lower sclerostin levels (60.5 ± 32.7 vs. 96.7 ± 52.9 pmol/L, P = 0.002) and comparable sclerostin binding to LRP6 (P = 0.387) than controls. Improvement of Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI), Bath Ankylosing Spondylitis Metrology Index (BASMI), Ankylosing Spondylitis quality of life (ASQoL) was observed at baseline vs. 6 vs. 12 months (P < 0.01). Concomitantly, a gradual increase in spine BMD (P < 0.001) and a positive correlation between baseline mSASSS and spine BMD was found (r = 0.468, P < 0.01). Inflammatory parameters reduction was observed comparing baseline vs. 6 vs. 12 months (P <0.01). Sclerostin levels progressively increased [baseline (60.5 ± 32.7) vs. 6 months (67.1 ± 31.9) vs. 12 months (72.7 ± 32.3) pmol/L, P <0.001]. At 12 months, the sclerostin levels remained significantly lower in patients compared to controls (72.7 ± 32.3 vs. 96.70 ± 52.85 pmol/L, P = 0.038). Moreover, sclerostin serum levels at 12 months were lower in the 10 patients with high C reactive protein (CRP) (≥ 5 mg/l) compared to the other 20 patients with normal CRP (P = 0.004). Of note, these 10 patients with persistent inflammation also had lower sclerostin serum levels at baseline compared to the other patients (P = 0.023). Univariate logistic regression analysis demonstrated that AS patients with lower sclerostin serum levels had an increased risk to have high CRP at 12 months (odds ratio = 7.43, 95% CI 1.23 to 45.01, P = 0.020) than those with higher sclerostin values.

Conclusions

Persistent low sclerostin levels may underlie continuous inflammation in AS patients under anti-TNF therapy.     

The response to oestrogen deprivation of the cartilage collagen degradation marker, CTX-II, is unique compared with other markers of collagen turnover

Introduction  

The urinary level of the type II collagen degradation marker CTX-II is increased in postmenopausal women and in ovariectomised rats, suggesting that oestrogen deprivation induces cartilage breakdown. Here we investigate whether this response to oestrogen is also true for other type II collagen turnover markers known to be affected in osteoarthritis, and whether it relates to its presence in specific areas of cartilage tissue.     

Quantitative PCR for Detection and Enumeration of Genetic Markers of Bovine Fecal Pollution

Accurate assessment of health risks associated with bovine (cattle) fecal pollution requires a reliable host-specific genetic marker and a rapid quantification method. We report the development of quantitative PCR assays for the detection of two recently described bovine feces-specific genetic markers and a method for the enumeration of these markers using a Markov chain Monte Carlo approach. Both assays exhibited a range of quantification from 25 to 2 × 10⁶ copies of target DNA, with a coefficient of variation of <2.1%. One of these assays can be multiplexed with an internal amplification control to simultaneously detect the bovine-specific genetic target and presence of amplification inhibitors. The assays detected only cattle fecal specimens when tested against 204 fecal DNA extracts from 16 different animal species and also demonstrated a broad distribution among individual bovine samples (98 to 100%) collected from five geographically distinct locations. The abundance of each bovine-specific genetic marker was measured in 48 individual samples and compared to quantitative PCR-enumerated quantities of rRNA gene sequences representing total Bacteroidetes, Bacteroides thetaiotaomicron, and enterococci in the same specimens. Acceptable assay performance combined with the prevalence of DNA targets across different cattle populations provides experimental evidence that these quantitative assays will be useful in monitoring bovine fecal pollution in ambient waters.