Applying spatial regression to evaluate risk factors for microbiological contamination of urban groundwater sources in Juba, South Sudan

This study developed methodology for statistically assessing groundwater contamination mechanisms. It focused on microbial water pollution in low-income regions. Risk factors for faecal contamination of groundwater-fed drinking-water sources were evaluated in a case study in Juba, South Sudan. The study was based on counts of thermotolerant coliforms in water samples from 129 sources, collected by the humanitarian aid organisation M,decins Sans FrontiSres in 2010. The factors included hydrogeological settings, land use and socio-economic characteristics. The results showed that the residuals of a conventional probit regression model had a significant positive spatial autocorrelation (Moran\u27s I = 3.05, I-stat = 9.28); therefore, a spatial model was developed that had better goodness-of-fit to the observations. The most significant factor in this model (p-value 0.005) was the distance from a water source to the nearest Tukul area, an area with informal settlements that lack sanitation services. It is thus recommended that future remediation and monitoring efforts in the city be concentrated in such low-income regions. The spatial model differed from the conventional approach: in contrast with the latter case, lowland topography was not significant at the 5% level, as the p-value was 0.074 in the spatial model and 0.040 in the traditional model. This study showed that statistical risk-factor assessments of groundwater contamination need to consider spatial interactions when the water sources are located close to each other. Future studies might further investigate the cut-off distance that reflects spatial autocorrelation. Particularly, these results advise research on urban groundwater quality

Change in quality of life and their predictors in the long-term follow-up after group cognitive behavioral therapy for social anxiety disorder: a prospective cohort study

<p>Abstract</p> <p>Background</p> <p>Social anxiety disorder (SAD) is one of the most common anxiety disorders. The efficacy of cognitive behaviour therapy (CBT) has been examined but to date its effects on Quality of Life (QoL) have not been appropriately evaluated especially in the long term.</p> <p>The study aimed to examine, in the long term, what aspects of Quality of Life (QoL) changed among social anxiety disorder (SAD) patients treated with group cognitive behaviour therapy (CBT) and what predictors at baseline were associated with QoL.</p> <p>Methods</p> <p>Outpatients diagnosed with SAD were enrolled into group CBT, and assessed at follow-ups for up to 12 months in a typical clinical setting. QoL was evaluated using the Short Form 36. Various aspects of SAD symptomatology were also assessed. Each of the QoL domains and scores on symptomatology were quantified and compared with those at baseline. Baseline predictors of QoL outcomes at follow-up were investigated.</p> <p>Results</p> <p>Fifty-seven outpatients were enrolled into group CBT for SAD, 48 completed the whole program, and 44 and 40 completed assessments at the 3-month and 12-month follow-ups, respectively. All aspects of SAD symptomatology and psychological subscales of the QoL showed statistically significant improvement throughout follow-ups for up to 12 months. In terms of social functioning, no statistically significant improvement was observed at either follow-up point except for post-treatment. No consistently significant pre-treatment predictors were observed.</p> <p>Conclusions</p> <p>After group CBT, SAD symptomatology and some aspects of QoL improved and this improvement was maintained for up to 12 months, but the social functioning domain did not prove any significant change statistically. Considering the limited effects of CBT on QoL, especially for social functioning, more powerful treatments are needed.</p

Hypoxia Due to Cardiac Arrest Induces a Time-Dependent Increase in Serum Amyloid β Levels in Humans

Amyloid β (Aβ) peptides are proteolytic products from amyloid precursor protein (APP) and are thought to play a role in Alzheimer disease (AD) pathogenesis. While much is known about molecular mechanisms underlying cerebral Aβ accumulation in familial AD, less is known about the cause(s) of brain amyloidosis in sporadic disease. Animal and postmortem studies suggest that Aβ secretion can be up-regulated in response to hypoxia. We employed a new technology (Single Molecule Arrays, SiMoA) capable of ultrasensitive protein measurements and developed a novel assay to look for changes in serum Aβ42 concentration in 25 resuscitated patients with severe hypoxia due to cardiac arrest. After a lag period of 10 or more hours, very clear serum Aβ42 elevations were observed in all patients. Elevations ranged from approximately 80% to over 70-fold, with most elevations in the range of 3–10-fold (average approximately 7-fold). The magnitude of the increase correlated with clinical outcome. These data provide the first direct evidence in living humans that ischemia acutely increases Aβ levels in blood. The results point to the possibility that hypoxia may play a role in the amyloidogenic process of AD