150 research outputs found
Improving child protection : a systematic review of training and procedural interventions
Aim: To synthesise published evidence regarding the effectiveness of training and procedural interventions
aimed at improving the identification and management of child abuse and neglect by health professionals.
Methods: Systematic review for the period 1994 to 2005 of studies that evaluated child protection training
and procedural interventions. Main outcome measures were learning achievement, attitudinal change,
and clinical behaviour.
Results: Seven papers that examined the effectiveness of procedural interventions and 15 papers that
evaluated training programmes met the inclusion criteria. Critical appraisal showed that evaluation of
interventions was on the whole poor. It was found that certain procedural interventions (such as the use of
checklists and structured forms) can result in improved recording of important clinical information and may
also alert clinical staff to the possibility of abuse. While a variety of innovative training programmes were
identified, there was an absence of rigorous evaluation of their impact. However a small number of onegroup
pre- and post-studies suggest improvements in a range of attitudes necessary for successful
engagement in the child protection process.
Conclusion: Current evidence supports the use of procedural changes that improve the documentation of
suspected child maltreatment and that enhance professional awareness. The lack of an evidence based
approach to the implementation of child protection training may restrict the ability of all health
professionals to fulfil their role in the child protection process. Formal evaluation of a variety of models for
the delivery of this training is urgently needed with subsequent dissemination of results that highlight those
found to be most effective
The Transcription Factor NURR1 Exerts Concentration-Dependent Effects on Target Genes Mediating Distinct Biological Processes
The transcription factor NURR1 plays a pivotal role in the development and maintenance of neurotransmitter phenotype in midbrain dopamine neurons. Conversely, decreased NURR1 expression is associated with a number of dopamine-related CNS disorders, including Parkinson’s disease and drug addiction. In order to better understand the nature of NURR1-responsive genes and their potential roles in dopamine neuron differentiation and survival, we used a human neural cellular background (SK-N-AS cells) in which to generate a number of stable clonal lines with graded NURR1 gene expression that approximated that seen in DA cell-rich human substantia nigra. Gene expression profiling data from these NURR1-expressing clonal lines were validated by quantitative RT-PCR and subjected to bioinformatic analyses. The present study identified a large number of NURR1-responsive genes and demonstrated the potential importance of concentration-dependent NURR1 effects in the differential regulation of distinct NURR1 target genes and biological pathways. These data support the promise of NURR1-based CNS therapeutics for the neuroprotection and/or functional restoration of DA neurons
Authors' Response
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/97166/1/jfo12080.pd
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Ventral midbrain correlation between genetic variation and expression of the dopamine transporter gene in cocaine-abusing versus non-abusing subjects
Altered activity of the human dopamine transporter gene (hDAT) is asssociated with several common and severe brain disorders including cocaine abuse. However, there is little a priori information on whether such alteration was due to nature (genetic variantion) or nurture (human behaviors such as cocaine abuse). This study investigated the correlation between seven markers throughout hDAT and its mRNA levels in postmortem ventral midbrain tissues from 18 cocaine abusers and 18 strictly matched drug-free controls in the African American population. Here we show that one major haplotype with same frequency in cocaine abusers versus drug-free controls displays a 37.1%-reduction of expression levels in cocaine abusers, compared to matched controls (P = 0.0057). The most studied genetic marker, variable number tandem repeats (VNTR) located in Exon 15 (3′VNTR), is not correlated with hDAT mRNA levels. A 5′ upstream VNTR (rs70957367) has repeat numbers positively correlated with expression levels in controls (r2 0.9536, P = 0.0235) but this positive correlation disappears in cocaine abusers. The findings suggest that varying hDAT activity is attributed to both genetics and cocaine abuse
Comparison of a nurse initiated insulin infusion protocol for intensive insulin therapy between adult surgical trauma, medical and coronary care intensive care patients
<p>Abstract</p> <p>Background</p> <p>Sustained hyperglycemia is a known risk factor for adverse outcomes in critically ill patients. The specific aim was to determine if a nurse initiated insulin infusion protocol (IIP) was effective in maintaining blood glucose values (BG) within a target goal of 100–150 mg/dL across different intensive care units (ICUs) and to describe glycemic control during the 48 hours after protocol discontinuation.</p> <p>Methods</p> <p>A descriptive, retrospective review of 366 patients having 28,192 blood glucose values in three intensive care units, Surgical Trauma Intensive Care Unit (STICU), Medical (MICU) and Coronary Care Unit (CCU) in a quaternary care hospital was conducted. Patients were > 15 years of age, admitted to STICU (n = 162), MICU (n = 110) or CCU (n = 94) over 8 months; October 2003-June 2004 and who had an initial blood glucose level > 150 mg/dL. We summarized the effectiveness and safety of a nurse initiated IIP, and compared these endpoints among STICU, MICU and CCU patients.</p> <p>Results</p> <p>The median blood glucose values (mg/dL) at initiation of insulin infusion protocol were lower in STICU (188; IQR, 162–217) than in MICU, (201; IQR, 170–268) and CCU (227; IQR, 178–313); <it>p </it>< 0.0001. Mean time to achieving a target glucose level (100–150 mg/dL) was similar between the three units: 4.6 hours in STICU, 4.7 hours in MICU and 4.9 hours in CCU (<it>p </it>= 0.27). Hypoglycemia (BG < 60 mg/dL) occurred in 7% of STICU, 5% of MICU, and 5% of CCU patients (<it>p </it>= 0.85). Protocol violations were uncommon in all three ICUs. Mean blood glucose 48 hours following IIP discontinuation was significantly different for each population: 142 mg/dL in STICU, 167 mg/dL in MICU, and 160 mg/dL in CCU (<it>p </it>< 0.0001).</p> <p>Conclusion</p> <p>The safety and effectiveness of nurse initiated IIP was similar across different ICUs in our hospital. Marked variability in glucose control after the protocol discontinuation suggests the need for further research regarding glucose control in patients transitioning out of the ICU.</p
Translational Model for External Volume Expansion in Irradiated Skin
Introduction: External Volume Expansion (EVE) treatment has gained popularity in breast reconstruction, enriching recipient sites for fat grafting. For patients receiving radiotherapy (XRT), results of EVE use vary, partly because the effects of EVE on irradiated tissue are not well understood. Based on our previous work with EVE and XRT, we developed a new translational model to investigate the effects of EVE in the setting of chronic radiation skin injury. Methods: Twenty-Eight SKH1-E mice received 50Gy of beta-radiation to each flank. Animals were monitored until chronic radiation fibrosis developed (8 weeks). EVE was then applied to one side for 6hrs on 5 consecutive days. The opposite side served as control. Hyperspectral Imaging (HSI) was used to assess perfusion changes before and after EVE. Mice were sacrificed at 5 days (n=14) and 15 days (n=14) after last application for histological analysis. Tissue samples were stained for vascularity (CD31) and collagen composition (Picro-Sirius red). Results: All animals developed skin fibrosis 8 weeks post-radiation, and changes in perfusion verified skin damage. EVE application induced edema on treated sides. Five days post-application, both sides were hypo-perfused as seen by HSI; with the EVE side 13% more ischemic than the untreated side (p\u3c0.001). Perfusion returned to control side levels by day 15. Blood vessels increased 20% by day 5 in EVE versus control. Collagen composition showed no difference in scar index analysis. Conclusion: EVE temporarily augments radiation-induced hypo-perfusion, likely due to transient edema. Fibrosis remained unchanged after EVE, possibly accounting for the limited expansion seen in patients. It appears that EVE induces angiogenic effect but does not affect dermal collagen composition. Future efforts should focus on reducing fibrosis post radiation to allow EVE to achieve its full potential, to benefit irradiated patients
Synaptic Zn2+ potentiates the effects of cocaine on striatal dopamine neurotransmission and behavior
Cocaine binds to the dopamine (DA) transporter (DAT) to regulate cocaine reward and seeking behavior. Zinc (Zn2+) also binds to the DAT, but the in vivo relevance of this interaction is unknown. We found that Zn2+ concentrations in postmortem brain (caudate) tissue from humans who died of cocaine overdose were significantly lower than in control subjects. Moreover, the level of striatal Zn2+ content in these subjects negatively correlated with plasma levels of benzoylecgonine, a cocaine metabolite indicative of recent use. In mice, repeated cocaine exposure increased synaptic Zn2+ concentrations in the caudate putamen (CPu) and nucleus accumbens (NAc). Cocaine-induced increases in Zn2+ were dependent on the Zn2+ transporter 3 (ZnT3), a neuronal Zn2+ transporter localized to synaptic vesicle membranes, as ZnT3 knockout (KO) mice were insensitive to cocaine-induced increases in striatal Zn2+. ZnT3 KO mice showed significantly lower electrically evoked DA release and greater DA clearance when exposed to cocaine compared to controls. ZnT3 KO mice also displayed significant reductions in cocaine locomotor sensitization, conditioned place preference (CPP), self-administration, and reinstatement compared to control mice and were insensitive to cocaine-induced increases in striatal DAT binding. Finally, dietary Zn2+ deficiency in mice resulted in decreased striatal Zn2+ content, cocaine locomotor sensitization, CPP, and striatal DAT binding. These results indicate that cocaine increases synaptic Zn2+ release and turnover/metabolism in the striatum, and that synaptically released Zn2+ potentiates the effects of cocaine on striatal DA neurotransmission and behavior and is required for cocaine-primed reinstatement. In sum, these findings reveal new insights into cocaine's pharmacological mechanism of action and suggest that Zn2+ may serve as an environmentally derived regulator of DA neurotransmission, cocaine pharmacodynamics, and vulnerability to cocaine use disorders
Reduction in BACE1 decreases body weight, protects against diet-induced obesity and enhances insulin sensitivity in mice
Insulin resistance and impaired glucose homoeostasis are important indicators of Type 2 diabetes and are early risk factors of AD (Alzheimer's disease). An essential feature of AD pathology is the presence of BACE1 (β-site amyloid precursor protein-cleaving enzyme 1), which regulates production of toxic amyloid peptides. However, whether BACE1 also plays a role in glucose homoeostasis is presently unknown. We have used transgenic mice to analyse the effects of loss of BACE1 on body weight, and lipid and glucose homoeostasis. BACE1−/− mice are lean, with decreased adiposity, higher energy expenditure, and improved glucose disposal and peripheral insulin sensitivity than wild-type littermates. BACE1−/− mice are also protected from diet-induced obesity. BACE1-deficient skeletal muscle and liver exhibit improved insulin sensitivity. In a skeletal muscle cell line, BACE1 inhibition increased glucose uptake and enhanced insulin sensitivity. The loss of BACE1 is associated with increased levels of UCP1 (uncoupling protein 1) in BAT (brown adipose tissue) and UCP2 and UCP3 mRNA in skeletal muscle, indicative of increased uncoupled respiration and metabolic inefficiency. Thus BACE1 levels may play a critical role in glucose and lipid homoeostasis in conditions of chronic nutrient excess. Therefore strategies that ameliorate BACE1 activity may be important novel approaches for the treatment of diabetes
ScreenTrack: Using a Visual History of a Computer Screen to Retrieve Documents and Web Pages
Computers are used for various purposes, so frequent context switching is
inevitable. In this setting, retrieving the documents, files, and web pages
that have been used for a task can be a challenge. While modern applications
provide a history of recent documents for users to resume work, this is not
sufficient to retrieve all the digital resources relevant to a given primary
document. The histories currently available do not take into account the
complex dependencies among resources across applications. To address this
problem, we tested the idea of using a visual history of a computer screen to
retrieve digital resources within a few days of their use through the
development of ScreenTrack. ScreenTrack is software that captures screenshots
of a computer at regular intervals. It then generates a time-lapse video from
the captured screenshots and lets users retrieve a recently opened document or
web page from a screenshot after recognizing the resource by its appearance. A
controlled user study found that participants were able to retrieve requested
information more quickly with ScreenTrack than under the baseline condition
with existing tools. A follow-up study showed that the participants used
ScreenTrack to retrieve previously used resources and to recover the context
for task resumption.Comment: CHI 2020, 10 pages, 7 figure
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