Miracle-dz/UniFAR-FTUs huggingface dataset:
Symposium on ‘Intervention policies for deprived households’ Policy initiatives to address low-income households' nutritional needs in the UK

Members of low-income households in the UK are more likely to have patterns of food and nutrient intakes that are less inclined to lead to good health outcomes in the short and long term. Health inequalities, including the likelihood of child and adulthood obesity, have long been documented in the UK and show little sign of improving so far, despite 10 years of attention from a government that has committed itself to addressing them. Following the Acheson Inquiry into Inequalities in Health (1998) in England a number of initiatives to tackle inequalities in food and diet were established, both nationally and within the devolved nations of Scotland, Wales and Northern Ireland. Nevertheless, until recently, there has been no overall strategic policy addressing the food and nutritional needs of low-income households. The present paper reviews how the problems have been constructed and understood and how they have been addressed, briefly drawing on recent evaluations of food and nutrition policies in Scotland and Wales. The contemporary challenge is to frame cross-cutting policy initiatives that move beyond simple targeting and local actions, encompass a life-course approach and recognise both the diversity of households that fall into ‘low-income’ categories and the need for ‘upstream’ intervention.
CAUSES OF DEATH IN ADULTS WITH ACUTE LEUKEMIA

The causes of death were investigated in 315 adults with acute leukemia during a 7-year period (1966-1972). Infection alone or in combination was the most common cause (75%), followed by hemorrhage (24%) and organ failure (9%). Most of the infections were either systemic or pulmonary. Seventy-five percent of the systemic infections and 72% of the pneumonias were caused by bacteria. Klebsiella pneumoniae, Escherichia coli and Pseudomonas aeruginosa were the most frequent organisms isolated. After 1968, there was a sharp decrease in the number of fatal infections caused by Pseudomonas aeruginosa and a marked increase in the incidence of fatal infections caused by Klebsiella spp. and E. coli. Infections caused by Gram-positive cocci occurred in only 3% of the cases. The incidence of systemic fungal infections was 13%; most common fungi causing infection were Candida spp. and Aspergillus spp. Eighty-five percent of 159 patients with a terminal neutrophil count of less than 100/mm3 died of infection, compared to 48% of 62 patients with a terminal neutrophil count of greater than 1000/mm3. Hemorrhage was mostly due to thrombocytopenia (61%) and disseminated intravascular coagulation (12%). This study indicates that infection continues to be the most common cause of death in patients with acute leukemia. Although advances in antibiotic therapy have changed the distribution of causative organisms, ultimate control of infection requires further improvements in supportive care measures which rectify impairments in the patients' host defense mechanisms.
[Plasma homocysteine assay in the exploration of thrombosis in young subjects].

Homocystinuria is a rare inherited metabolic disease transmitted as an autosomal recessive trait. Arterial and venous thromboembolic events are frequent and life-threatening complications in homocystinuric patients. It has been suggested that mild homocysteinemia could be a risk factor for vascular disease. We measured total plasma L-homocysteine concentrations by radioisotopic assay in 32 subjects with arterial (n = 15) or venous (n = 17) thrombosis. Twelve subjects exceeded the upper normal limit (2.70 SD above the mean), i.e. 14.1 mumol/l. Seven had arterial thrombotic disease and five had deep vein thrombosis. In 18 subjects thrombosis developed in the absence of any of the hitherto recognized risk factors; 6 of these subjects had mild homocysteinemia. Thus, homocysteine metabolism must be investigated in patients with thromboembolism. An increase of homocysteinemia could be a risk factor for thromboembolic events, and the possible benefit of vitamin therapy should be discussed.
Focus on the potential effects of treatments for spondylarthritides on cardiovascular risk

The past years have seen the publication of several studies on seronegative spondylarthritides (SpA) and cardiovascular risk as a result of new insights into the connection between inflammation and atherogenesis. Although the overall cardiovascular disease is a complex entity, chronic inflammation of SpA is known to contribute as an independent risk factor, and new therapies are aimed at reducing this persistent inflammatory status. This review provides an overview of the recent advances in understanding the role of the current therapeutic measures of SpA in preventing or accelerating cardiovascular risk.
The Value of Upsloping ST Depression in Diagnosing Myocardial Ischemia

We evaluated the value of upsloping ST‐segment depression in predicting the severity of myocardial ischemia. Comparison of the exercise electrocardiographic changes was made to myocardial perfusion images and coronary angiograms as the criteria for ischemia. We retrospectively reviewed 621 patients who underwent exercise technetium‐99m tetrofosmin single photon emission computed tomography (SPECT) for the assessment of suspected or known coronary artery disease followed by coronary angiography within a 3‐month period. The test sensitivity and specificity of 1 mm horizontal or downsloping ST depression in predicting reversible ischemia as assessed by gated SPECT imaging (GSI) were 65% and 87%, respectively. The corresponding values were 67% and 94% compared to coronary angiography. The sensitivity and specificity of gated SPECT imaging compared to coronary angiography were 78% and 89%. On the other hand when 1 mm upsloping ST depression at 70 ms past the J‐point was regarded as abnormal, along with horizontal and downsloping, the sensitivity and specificity were 82% and 90% compared to myocardial perfusion imaging, and 77% and 92% as assessed by coronary angiography. We conclude that upsloping ST‐segment depression is associated with an increased risk of coronary artery disease and is a valuable predictor of myocardial ischemia.
Hypermethylation of the p 16 gene promoter in pterygia and its association with the expression of DNA methyltransferase 3 b

A pterygium has long been considered a degenerative disease. However, after p53 protein was found to be abnormally expressed in the epithelium, a pterygium is now considered to be uncontrolled cell proliferation related to exposure to UV light, similar to a tumor [1-7]. Our previous studies revealed that mutations in the p53 gene (TP53) occur in pterygia [8,9]. However, only 15.7% of pterygia had p53 mutations [8]. Several mutations are required for a normal cell to be converted to a tumoral cell, and several oncogenes or tumor suppressor genes are reported to be involved in tumoral formation. Therefore, it is logical to assume that tumor-related genes other than p53 are involved in the formation of pterygia. The oncogene Kiras was recently found to be mutant in 10% of pterygia [10]. Hence, we suggest that tumor suppressor genes or oncogenes besides p53 and Ki-ras genetic mutations are involved in pterygial formation. The p16 gene (CDKN2A) is a tumor suppressor gene, and its product, p16 protein, controls the cell cycle and prevents tumoral formation. This gene is inactivated in many cancers [11-14]. Hence, like p53, p16 is another important gene involved in tumorigenesis. However, unlike p53, which mutations frequently inactivate, p16 is frequently inactivated by hypermethylation of its promoters [15]. Hypermethylation of regulatory elements, a well-know epigenetic change, is an important alternative to genetic alteration for inactivating genes, and it plays an important role in the pathogenesis of human cancers [16]. At least three independently encoded DNA methyltransferases (DNMTs) are known. They are DNMT1, DNMT3a, and DNMT3b, which are involved in hypermethylation [17,18]. Overexpression of DNMT1 and DNMT3b is common in human tumors, but DNMT1 is constitutively expressed in proliferating cells. Therefore, DNMT3b is commonly evaluated in tumors [17,18]. We hypothesized that the p16 gene loses its function in pterygia and that, besides genetic mutations, epigenetic changes (e.g., hypermethylation of genetic regulatory elements) occur. To test these hypotheses, we analyzed hypermethylation of the p16 gene promoter in pterygia and investigated the relationship between this hypermethylation and the expression of p16 and DNMT3b protein. ©2006 Molecular Vision
To Screen or Not to Screen : Is That the Question ? Improving the Outcomes of Depression in Primary Care

• Objective: To review the utility of screening in improving depression outcomes. • Methods: Qualitative review of the literature. • Results: Depression is highly prevalent in the community and in primary care settings and imposes a burden of illness greater than most chronic medical disorders. Standardized screening for depression in primary care has been recommended by a number of practice guidelines, yet there is minimal evidence for an impact of screening on patient outcome. Education of patients and providers has shown equally marginal impact. Improved outcomes for depression in primary care seem to hinge on more systematic depression management systems, involving more integration of specialized mental health services and primary care and more assertive outreach to follow depressed patients. Such interventions have been shown to have good cost-effectiveness. • Conclusion: Efforts to improve outcomes of depression in primary care should move from emphasis on screening and education to the development of depression management systems that involve collaborative care by primary care providers and mental health professionals and active outreach to monitor compliance and response. In recent years the management of depression in primary care settings has received increased attention. The prevalence of major depression in such settings has been estimated at 4.8% to 8.6%, and that of dysthymia (chronic lowergrade depression) at 2.1 to 3.7% [1]. Only 57.7% of patients with major depression receive any treatment [2], and of those who receive treatment, more do so through their primary care physicians (PCPs) than through mental health specialists [3]. In addition, depression has been associated with increased medical comorbidity, higher utilization of medical services, and reduced productivity and quality of life [4]. Despite the prevalence of depression and the magnitude of its associated burdens, the disorder frequently goes undetected. As many as 50% of depressed patients may go undiagnosed in primary care settings [5]. For this reason there has been much interest in using screening tools to improve identification of depressed patients. The appeal of screening—also termed “case-finding”—derives from its potential as a quick, simple, and inexpensive tool for use in busy primary care clinics. The expectation has been that by augmenting detection rates, screening will lead to increased numbers of patients receiving treatment and thus to overall improved outcomes for these patients [6–8]. In this paper, we will review case-finding instruments for depression, current recommendations for their use in primary care settings, and whether screening increases rates of detection and treatment of depression by PCPs. We will also examine which interventions improve outcomes for depressed patients and gaps in the current research on how to optimize primary care management of depression.
Gene expression changes after hypoxic preconditioning in rat hepatocytes.

BACKGROUND Hypoxic preconditioning can protect hepatocytes against hypoxic injury, but its mechanism has not been elucidated. The aim of this study was to profile gene expression patterns involved in hypoxic preconditioning and probable mechanism at the level of gene expression. METHODS Hepatocytes were divided into 2 groups: control group and hypoxic preconditioning group. Biotin-labeled cRNA from the control group and the hypoxic preconditioning group was hybridized by oligonucleotide microarray. Genes that were significantly associated with hypoxic preconditioning were filtered, and validated at the level of transcript expression. RESULTS Forty-three genes with significantly altered expression patterns were discovered and most of them had not been previously reported. Among these genes, genes encoding superoxide dismutase 2 (SOD2) and interleukin 10 (IL-10) in the hypoxic preconditioning group were confirmed to be up-regulated with real-time quantitative PCR. CONCLUSIONS Many cytokines are involved in hypoxic preconditioning and protect hepatocytes from hypoxia-reoxygenation injury, and the increase of oxygen free-radical scavengers and anti-inflammatory factors may play a key role in this phenomenon. Diverse signal pathways are probably involved.
Musical training induces functional and structural auditory‐motor network plasticity in young adults

Playing music requires a strong coupling of perception and action mediated by multimodal integration of brain regions, which can be described as network connections measured by anatomical and functional correlations between regions. However, the structural and functional connectivities within and between the auditory and sensorimotor networks after long‐term musical training remain largely uninvestigated. Here, we compared the structural connectivity (SC) and resting‐state functional connectivity (rs‐FC) within and between the two networks in 29 novice healthy young adults before and after musical training (piano) with those of another 27 novice participants who were evaluated longitudinally but with no intervention. In addition, a correlation analysis was performed between the changes in FC or SC with practice time in the training group. As expected, participants in the training group showed increased FC within the sensorimotor network and increased FC and SC of the auditory‐motor network after musical training. Interestingly, we further found that the changes in FC within the sensorimotor network and SC of the auditory‐motor network were positively correlated with practice time. Our results indicate that musical training could induce enhanced local interaction and global integration between musical performance‐related regions, which provides insights into the mechanism of brain plasticity in young adults.
Imaging of T‐cell interactions with antigen presenting cells in culture and in intact lymphoid tissue

Summary: The development of an effective immune response requires cell–cell contact between T cells and antigen‐bearing cells of several types (dendritic cells, B cells, infected tissue cells). Recent advances in light microscopy have led to intense investigation of the molecular events that accompany these cell interactions, especially the redistribution of membrane proteins into discrete organized subdomains within the zone of cell–cell contact termed the ‘immunological synapse’. Here we discuss two aspects of our own studies in this area. First, we highlight results from our in vitro analysis of the role of the cytoskeletal ezrin, radixin, moesin adapter proteins in the exclusion of CD43 from the well‐defined T cell receptor (TCR) and integrin‐rich zones of the synapse. Based on the molecular mechanism uncovered in this work, we propose a new model for how TCR‐signaled changes in cytoskeletal organization indirectly influence both protein distributions and the efficiency of signaling between T cell and presenting cell. We then discuss the development of a new method for dynamic visualization of T cell – dendritic cell interactions in intact lymphoid tissue. The remarkable longevity of monogamous lymphocyte‐presenting cell interactions is discussed, differences between our observations and those of others are laid out in detail, and prospects for future application of this technical approach to analysis of early immune responses in lymphoid organs and of effector lymphocyte function in tissues are presented.
Composition of Bacterial Communities Associated with Aurelia aurita Changes with Compartment, Life Stage, and Population

ABSTRACT The scyphozoan Aurelia aurita is recognized as a key player in marine ecosystems and a driver of ecosystem change. It is thus intensely studied to address ecological questions, although its associations with microorganisms remain so far undescribed. In the present study, the microbiota associated with A. aurita was visualized with fluorescence in situ hybridization (FISH) analysis, and community structure was analyzed with respect to different life stages, compartments, and populations of A. aurita by 16S rRNA gene amplicon sequencing. We demonstrate that the composition of the A. aurita microbiota is generally highly distinct from the composition of communities present in ambient water. Comparison of microbial communities from different developmental stages reveals evidence for life stage-specific community patterns. Significant restructuring of the microbiota during strobilation from benthic polyp to planktonic life stages is present, arguing for a restructuring during the course of metamorphosis. Furthermore, the microbiota present in different compartments of the adult medusa (exumbrella mucus and gastric cavity) display significant differences, indicating body part-specific colonization. A novel Mycoplasma strain was identified in both compartment-specific microbiota and is most likely present inside the epithelium as indicated by FISH analysis of polyps, indicating potential endosymbiosis. Finally, comparison of polyps of different populations kept under the same controlled laboratory conditions in the same ambient water showed population-specific community patterns, most likely due the genetic background of the host. In conclusion, the presented data indicate that the associated microbiota of A. aurita may play important functional roles, e.g., during the life cycle.
Assessment of adverse reactions within a drug surveillance program.

As part of a comprehensive drug surveillance program, we devised a system for identifying and characterizing adverse reactions to drugs. The overall program includes measurements of drug efficacy and a description of the patient population being studied. The data collected thus far suggest that drug reactions represent a major health hazard. Adverse reaction information on any drug must be evaluated for careful consideration of total drug usage, the reasons for prescribing the drug, and its overall efficacy.
The Effect of Increased Temperatures of QMix and EDTA on the Push-out Bond Strength of an Epoxy-resin Based Sealer.

BACKGROUND Bond strength of root canal sealers is mainly influenced by the surface tension of the root canal wall. Heat, or the use of a surfactant might reduce surface tension and it is known that surface tension of an EDTA solution significantly affected from temperature rise. QMix is a novel endodontic irrigant for smear layer removal containing EDTA, chlorhexidine and a detergent. There is no data regarding the influence of the temperature of the EDTA and QMix on the push-out bond strength of root canal sealers. AIM To evaluate effect of temperatures of QMix and EDTA on the bond-strength of AH Plus. MATERIALS AND METHODS Sixty premolars were prepared with ProTaper F4. During preparation 3% NaOCl was performed. Specimens were divided into 4 groups as follows: 5-mL 17% EDTA at 22°C and 37°C; 5-mL QMix at 22°C and 37°C. Three specimens from each group were prepared for observation using SEM. Remaining roots were obturated and prepared for a push-out test. Data was analysed using Anova and Bonferroni tests (p<0.05). RESULTS Samples irrigated with QMix had higher push-out bond strength values than those irrigated with EDTA (p=0.01), regardless of temperature. Samples irrigated with 37°C EDTA resulted in higher bond-strength values than those irrigated with 22°C EDTA (p<0.001). CONCLUSION Temperature of the final irrigant does affect the bond strength values of AH plus to root dentin irrigated with EDTA. Bond strength of AH Plus sealer to root canal dentin may improve with QMix.
The Sense of Presence within Auditory Virtual Environments

Two studies were performed to investigate the sense of presence within stereoscopic virtual environments as a function of the addition or absence of auditory cues. The first study examined the presence or absence of spatialized sound, while the second study compared the use of nonspatialized sound to spatialized sound. Sixteen subjects were allowed to navigate freely throughout several virtual environments and for each virtual environment, their level of presence, the virtual world realism, and interactivity between the participant and virtual environment were evaluated using survey questions. The results indicated that the addition of spatialized sound significantly increased the sense of presence but not the realism of the virtual environment. Despite this outcome, the addition of a spatialized sound source significantly increased the realism with which the subjects interacted with the sound source, and significantly increased the sense that sounds emanated from specific locations within the virtual environment. The results suggest that, in the context of a navigation task, while presence in virtual environments can be improved by the addition of auditory cues, the perceived realism of a virtual environment may be influenced more by changes in the visual rather than auditory display media. Implications of these results for presence within auditory virtual environments are discussed.
Ouro proteins are not essential to tail regression during Xenopus tropicalis metamorphosis

Tail regression is one of the most prominent transformations observed during anuran metamorphosis. A tadpole tail that is twice as long as the tadpole trunk nearly disappears within 3 days in Xenopus tropicalis. Several years ago, it was proposed that this phenomenon is driven by an immunological rejection of larval‐skin‐specific antigens, Ouro proteins. We generated ouro‐knockout tadpoles using the TALEN method to reexamine this immunological rejection model. Both the ouro1‐ and ouro2‐knockout tadpoles expressed a very low level of mRNA transcribed from a targeted ouro gene, an undetectable level of Ouro protein encoded by a target gene and a scarcely detectable level of the other Ouro protein from the untargeted ouro gene in tail skin. Furthermore, congenital athymic frogs were produced by Foxn1 gene modification. Flow cytometry analysis showed that mutant frogs lacked splenic CD8+ T cells, which play a major role in cytotoxic reaction. Furthermore, T‐cell‐dependent skin allograft rejection was dramatically impaired in mutant frogs. None of the knockout tadpoles showed any significant delay in the process of tail shortening during the climax of metamorphosis, which shows that Ouro proteins are not essential to tail regression at least in Xenopus tropicalis and argues against the immunological rejection model.