Evaluation of the Performance of Routine Information System Management (PRISM) framework: evidence from Uganda

<p>Abstract</p> <p>Background</p> <p>Sound policy, resource allocation and day-to-day management decisions in the health sector require timely information from routine health information systems (RHIS). In most low- and middle-income countries, the RHIS is viewed as being inadequate in providing quality data and continuous information that can be used to help improve health system performance. In addition, there is limited evidence on the effectiveness of RHIS strengthening interventions in improving data quality and use. The purpose of this study is to evaluate the usefulness of the newly developed Performance of Routine Information System Management (PRISM) framework, which consists of a conceptual framework and associated data collection and analysis tools to assess, design, strengthen and evaluate RHIS. The specific objectives of the study are: a) to assess the reliability and validity of the PRISM instruments and b) to assess the validity of the PRISM conceptual framework.</p> <p>Methods</p> <p>Facility- and worker-level data were collected from 110 health care facilities in twelve districts in Uganda in 2004 and 2007 using records reviews, structured interviews and self-administered questionnaires. The analysis procedures include Cronbach's alpha to assess internal consistency of selected instruments, test-retest analysis to assess the reliability and sensitivity of the instruments, and bivariate and multivariate statistical techniques to assess validity of the PRISM instruments and conceptual framework.</p> <p>Results</p> <p>Cronbach's alpha analysis suggests high reliability (0.7 or greater) for the indices measuring a promotion of a culture of information, RHIS tasks self-efficacy and motivation. The study results also suggest that a promotion of a culture of information influences RHIS tasks self-efficacy, RHIS tasks competence and motivation, and that self-efficacy and the presence of RHIS staff have a direct influence on the use of RHIS information, a key aspect of RHIS performance.</p> <p>Conclusions</p> <p>The study results provide some empirical support for the reliability and validity of the PRISM instruments and the validity of the PRISM conceptual framework, suggesting that the PRISM approach can be effectively used by RHIS policy makers and practitioners to assess the RHIS and evaluate RHIS strengthening interventions. However, additional studies with larger sample sizes are needed to further investigate the value of the PRISM instruments in exploring the linkages between RHIS data quality and use, and health systems performance.</p

Retinoic Acid Restores Adult Hippocampal Neurogenesis and Reverses Spatial Memory Deficit in Vitamin A Deprived Rats

A dysfunction of retinoid hippocampal signaling pathway has been involved in the appearance of affective and cognitive disorders. However, the underlying neurobiological mechanisms remain unknown. Hippocampal granule neurons are generated throughout life and are involved in emotion and memory. Here, we investigated the effects of vitamin A deficiency (VAD) on neurogenesis and memory and the ability of retinoic acid (RA) treatment to prevent VAD-induced impairments. Adult retinoid-deficient rats were generated by a vitamin A-free diet from weaning in order to allow a normal development. The effects of VAD and/or RA administration were examined on hippocampal neurogenesis, retinoid target genes such as neurotrophin receptors and spatial reference memory measured in the water maze. Long-term VAD decreased neurogenesis and led to memory deficits. More importantly, these effects were reversed by 4 weeks of RA treatment. These beneficial effects may be in part related to an up-regulation of retinoid-mediated molecular events, such as the expression of the neurotrophin receptor TrkA. We have demonstrated for the first time that the effect of vitamin A deficient diet on the level of hippoccampal neurogenesis is reversible and that RA treatment is important for the maintenance of the hippocampal plasticity and function

Chronic alcohol intoxication in rats leads to a strong but transient increase in NGF levels in distinct brain regions

The original publication can be found at www.springerlink.comNerve growth factor (NGF), a member of the neurotrophin family, is an essential mediator of neuronal activity and synaptic plasticity of basal forebrain cholinergic neurons. In this study NGF-protein levels were determined in areas of the basal forebrain cholinergic system, its projection areas as well as the striatum and the cerebellum after long-term exposure (6 and 9 months) to ethanol and a phase of withdrawal in male Sprague-Dawley rats. 6-month alcohol treatment led to an increase of NGF to 650–850% of controls in the basal forebrain and the septum and to a 210–485% increase in the cholinergic projection areas (anterior cortex, hippocampus and olfactory bulb). After 9 months exposure to ethanol, a decrease of NGF by 16% in the frontal cortex was observed compared to controls. In the other brain regions no differences in NGF expression were detectable at this time-point. These results support the idea of an endogenous neuroprotective mechanism acting through a transient NGF induction followed by a decrease in NGF-levels during the course of further neuronal degeneration.C. A. Gericke, O. Schulte-Herbrüggen, T. Arendt and R. Hellwe

What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer's disease, about the therapeutic strategies in Alzheimer's research

Experimental models that faithfully mimic the developmental pathology of sporadic Alzheimer's disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs' efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated