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The purpose of this study is to examine whether theory of mind (ToM) is an endophenotypic marker of borderline personality disorder (BPD), thus constituting an etiopathogenic factor of the disease. This would suggest familial vulnerability to BPD. This was a case-control study involving 146 individuals with 57 BPD patients, 32 first-degree relatives, and 57 controls (median age of BPD and control = 33.4 years, relatives = 52.9 years, BPD females and controls = 91.2%, female relatives = 62.5%). All the participants completed the Spanish version of the Movie for the Assessment of Social Cognition test to evaluate the ToM subclassification: interpretation of emotions, thoughts and intentions. BPD patients and their healthy first-degree relatives exhibited significant deficits in the correct interpretation of emotions and intentions compared to healthy controls. Both patients with BPD and their healthy first-degree relatives exhibited significant deficits in ToM, which suggests that it may be an etiopathogenic factor of BPD, and ToM (interpretation of emotions, thoughts and intentions) is a possible endophenotypic marker of BPD, suggesting a genetic predisposition to the disorder. Therefore, ToM could be considered as an indicator for the early detection of the disorder of and intervention for BPD.

Reparations for human rights violations in the form of rehabilitation can include social services such as education. This can be a particularly appropriate form of reparation for victims who have experienced abuses that result in missed education as a lost opportunity. Reparations can be rehabilitative by directly responding to harms suffered by victims and their ensuing needs, thereby helping to reintegrate those victims into society and restoring to them a functional life. Education can be provided through an administrative program or policy as individual reparations, such as scholarships to victims, as collective reparations, such as the rebuilding of schools in communities hard hit by abuses, and as symbolic reparations, such as naming schools. Court decisions awarding education as a form of reparation have also contributed significantly to our understanding of education as rehabilitation. This article examines the contributions that education as rehabilitation can make to redress as well as the implementation challenges faced by initiatives that have attempted to do so.

We aimed to study whether worsening in markers of kidney function parallels the progression in cerebral small vessel disease (cSVD) and cognitive decline.Data from the ISSYS (Investigating Silent Strokes in Hypertensives Study), a longitudinal population-based study in hypertensives aged 50-70 and dementia and stroke-free at baseline. At both visits, patients underwent a brain MRI, a cognitive diagnosis (normal aging or mild cognitive impairment, [MCI]) and urine and blood sampling collection. We assessed the incidence of infarcts and cerebral microbleeds, and the progression of white matter hyperintensities at periventricular (PVH) and deep areas. We determined changes in albumin-creatinine ratio and estimated glomerular filtration rate (eGFR). These changes were dichotomized into microalbuminuria at follow-up -either in subjects with or without baseline microalbuminuria- and significant decline in eGFR -lowest quintile of eGFR change (-10.57 mL/min/1.73m360 patients were followed-up for 4 years. 80 (23%) patients presented microalbuminuria at follow-up and 68 (20.1%) experienced a significant eGFR decline. Considering cSVD change, we found a relationship between microalbuminuria at follow-up and progression in PVH (β = 0.31, P-value = .01). Regarding cognitive decline, presence of microalbuminuria at follow-up related to a steeper decrease in memory function (β = -0.36, P-value.01). Moreover, patients with significant decline in eGFR were at higher risk of incident MCI (OR = 3.54, P-value = .02). These associations were independent of progression of cSVD.The worsening in markers of kidney function paralleled the decrease in cognition and the progression of cSVD, and this may be explained by common shared underlying risk factors.

Homeless people are highly susceptible to tuberculosis. It has been suggested that this population have high rates of mental disorders associated with tuberculosis. We assessed tuberculosis incidence, its transmission patterns and association with socio-demographic factors and mental disorders in Colombian homeless people. Prospective study which socio-demographic characteristics and mental disorders were assessed through interviews. Sputa from patients with respiratory symptoms were processed and clinical isolates analyzed by IS6110-RFLP. Multivariate analysis performed by logistic regression model. From 426 homeless studied, tuberculosis incidence found was 7.9 %. 44 % of isolates were clustering. It was found high risk of having tuberculosis associated with income from drugs trade (OR: 3.40 [95 % CI: 1.28–9.05]), dysthymia (OR: 2.54 [95 % CI: 1.10–5.86]) and receiving food from other homeless (OR: 2.47 [95 % CI: 1.16–5.25]). Tuberculosis incidence and degree of transmission are high in homeless studied. Implementing programs to better control tuberculosis among homeless population must consider socio-demographic factors and mental disorders associated with the disease.

In this study, the reliability and reproducibility of viral quasispecies quantification by three ultra-deep pyrosequencing (UDPS) methods (FLX+, FLX, and Junior) were investigated and results compared with the conventional cloning technique. Hepatitis B virus (HBV) infection was selected as the model. The preCore/Core region, the least overlapped HBV region, was analyzed in samples from a chronic hepatitis B patient by cloning and by UDPS. After computation filtering of the UDPS results, samples A1 and A2 (FLX+) and sample B (FLX) yielded the same 20 polymorphic positions. Junior yielded 18 polymorphic positions that coincided with the FLX results. In contrast, 50 polymorphic positions were detected by cloning. Quasispecies complexity plotted on graphs showed superimposed patterns and the quantitative parameters were similar between FLX+, FLX, Junior, and the cloning sequences. Twenty-two haplotypes were detected by Junior, and 37, 40, and 39 were detected by FLX A1, A2, and B, respectively. These differences may be attributable to methodological differences between FLX and Junior. By cloning, 47 haplotypes were detected. Eight clones with insertions and deletions that induced de novo stop codons were not observed by UDPS because the UDPS filter discarded them. Our results indicate that UDPS is an optimal alternative to molecular cloning for quantitative study of the viral quasispecies. Nonetheless, specific mutations, such as insertions and deletions, were only detected by cloning. A filter should be designed to analyze cloning sequences, and UDPS filters should be improved to include the specific mutations.

Brain magnetic resonance (MR) study has shown metabolic abnormalities and changes in water distribution of the brain tissue that may relate to the pathogenesis of hepatic encephalopathy (HE). We designed a study to investigate the disturbances in brain water and metabolites during episodic HE using a 3-T MR scanner. Cirrhotic patients with different grades of HE underwent MR during hospitalization ( n = 18). The MR was repeated at 6 weeks' follow-up ( n = 14). The results were compared with those of a group of healthy volunteers ( n = 8). During episodic HE, brain diffusion-weighted imaging showed a high apparent diffusion coefficient (ADC) (12% to 14%) that decreased during follow-up (–1% to −4%). These disturbances were accompanied by high glutamine (581%), low choline (–31%), and low myo-inositol (–86%) peaks on MR spectroscopy. In overt HE, patients showed high glutamine that decreased during follow-up (–22%). In addition, these patients exhibited a rise in plasma S100 beta and enlargement of brain white-matter lesions. In conclusion, several disturbances detected by MR support the presence of impaired brain water homeostasis during episodic HE. Although astrocytes have a major role in this condition, brain edema during episodic HE may be extracellular and does not appear to be directly responsible for the development of neurologic manifestations.