Effectiveness of a parenting programme in a public health setting: a randomised controlled trial of the positive parenting programme (Triple P) level 3 versus care as usual provided by the preventive child healthcare (PCH)

BACKGROUND: Considering the high burden of disease of psychosocial problems in children and adolescents, early intervention regarding problem behaviour of young children is very important. The Preventive Child Healthcare (PCH) offers a good setting to detect such problem behaviour and to provide parenting support to the parents concerned. This paper aims to describe the design of an effectiveness study of a parenting programme for parents of children with mild psychosocial problems after an initial, evidence based screening in routine PCH. METHODS/DESIGN: The effects of the intervention will be studied in a randomised controlled trial. Prior to a routine PCH health examination, parents complete a screening questionnaire on psychosocial problems. Parents of children with increased but still subclinical levels of psychosocial problems will be assigned at random to the experimental group (Triple P, level 3) or to the control group (care as usual). Outcome measures, such as problem behaviour in the child and parenting behaviour, will be assessed before, directly after and 6 and 12 months after the intervention. DISCUSSION: Parenting support may be an effective intervention to reduce psychosocial problems in children but evidence-based parenting programmes that fit the needs of the PCH are not available as yet. Although the Triple P programme seems promising and suitable for a universal population approach, evidence on its effectiveness in routine PCH still lacks. TRIAL REGISTRATION: NTR1338

Gut Microbiota, Probiotics and Diabetes

Diabetes is a condition of multifactorial origin, involving several molecular mechanisms related to the intestinal microbiota for its development. In type 2 diabetes, receptor activation and recognition by microorganisms from the intestinal lumen may trigger inflammatory responses, inducing the phosphorylation of serine residues in insulin receptor substrate-1, reducing insulin sensitivity. In type 1 diabetes, the lowered expression of adhesion proteins within the intestinal epithelium favours a greater immune response that may result in destruction of pancreatic β cells by CD8+ T-lymphocytes, and increased expression of interleukin-17, related to autoimmunity. Research in animal models and humans has hypothesized whether the administration of probiotics may improve the prognosis of diabetes through modulation of gut microbiota. We have shown in this review that a large body of evidence suggests probiotics reduce the inflammatory response and oxidative stress, as well as increase the expression of adhesion proteins within the intestinal epithelium, reducing intestinal permeability. Such effects increase insulin sensitivity and reduce autoimmune response. However, further investigations are required to clarify whether the administration of probiotics can be efficiently used for the prevention and management of diabetes

Gut microbiota and diabetes: from pathogenesis to therapeutic perspective

More than several hundreds of millions of people will be diabetic and obese over the next decades in front of which the actual therapeutic approaches aim at treating the consequences rather than causes of the impaired metabolism. This strategy is not efficient and new paradigms should be found. The wide analysis of the genome cannot predict or explain more than 10–20% of the disease, whereas changes in feeding and social behavior have certainly a major impact. However, the molecular mechanisms linking environmental factors and genetic susceptibility were so far not envisioned until the recent discovery of a hidden source of genomic diversity, i.e., the metagenome. More than 3 million genes from several hundreds of species constitute our intestinal microbiome. First key experiments have demonstrated that this biome can by itself transfer metabolic disease. The mechanisms are unknown but could be involved in the modulation of energy harvesting capacity by the host as well as the low-grade inflammation and the corresponding immune response on adipose tissue plasticity, hepatic steatosis, insulin resistance and even the secondary cardiovascular events. Secreted bacterial factors reach the circulating blood, and even full bacteria from intestinal microbiota can reach tissues where inflammation is triggered. The last 5 years have demonstrated that intestinal microbiota, at its molecular level, is a causal factor early in the development of the diseases. Nonetheless, much more need to be uncovered in order to identify first, new predictive biomarkers so that preventive strategies based on pre- and probiotics, and second, new therapeutic strategies against the cause rather than the consequence of hyperglycemia and body weight gain

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

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Multipotent Stromal Cells Induce Human Regulatory T Cells Through a Novel Pathway Involving Skewing of Monocytes Toward Anti-inflammatory Macrophages

Multipotent stromal cells (MSC) have been shown to possess immunomodulatory capacities and are therefore explored as a novel cellular therapy. One of the mechanisms through which MSC modulate immune responses is by the promotion of regulatory T cell (Treg) formation. In this study, we focused on the cellular interactions and secreted factors that are essential in this process. Using an in vitro culture system, we showed that culture-expanded bone marrow-derived MSC promote the generation of CD4(+)CD25(hi)FoxP3(+) T cells in human PBMC populations and that these populations are functionally suppressive. Similar results were obtained with MSC-conditioned medium, indicating that this process is dependent on soluble factors secreted by the MSC. Antibody neutralization studies showed that TGF-1 mediates induction of Tregs. TGF-1 is constitutively secreted by MSC, suggesting that the MSC-induced generation of Tregs by TGF-1 was independent of the interaction between MSC and PBMC. Monocyte-depletion studies showed that monocytes are indispensable for MSC-induced Treg formation. MSC promote the survival of monocytes and induce differentiation toward macrophage type 2 cells that express CD206 and CD163 and secrete high levels of IL-10 and CCL-18, which is mediated by as yet unidentified MSC-derived soluble factors. CCL18 proved to be responsible for the observed Treg induction. These data indicate that MSC promote the generation of Tregs. Both the direct pathway through the constitutive production of TGF-1 and the indirect novel pathway involving the differentiation of monocytes toward CCL18 producing type 2 macrophages are essential for the generation of Tregs induced by MSC. Stem Cells2013;31:1980-199

Analysis of Lower Airway Inflammation in a Rabbit Model of Acute Rhinosinusitis

This study aimed to investigate the association of inflammatory changes of upper and lower airways in a rabbit model of acute rhinosinusitis. The study included six adult albino rabbits. The sinuses of one animal were injected with saline solution and the animal was served as sham control. Other animals were implanted with intranasal S. aureus soaked-absorbable gelatin sponge. Acute rhinosinusitis was induced and subjects were sacrificed at the end of the second week. Tissue samples from all levels of the airway were obtained. They were evaluated for the presence of inflammatory changes histologically. A scoring system for airway inflammation was used for quantitative assessment of the degree of inflammation. Structural changes in the epithelial and stromal layers of the upper and lower airway structures were analyzed, as well. The animal of which the sinuses were injected with saline solution developed neither acute rhinosinusitis nor lower airway inflammation. In contrast, the animals in which acute rhinosinusitis was induced demonstrated significant upper and lower airway inflammation histologically. Inflammatory changes ranged from engorgement of blood vessels and polymorphonuclear cell proliferation within the capillaries, in the perivascular tissue of the epithelium or in the lamina propria and to epithelial disruption. Nasal airway inflammation scores (2.86 ± 1.81) were significantly higher than lower airway scores (1.36 ± 0.77), (P < 0.01). We obtained a generalized mucosal inflammatory response against localized bacterial inflammation in a rabbit model of acute rhinosinusitis, confirming the suggestion of ‘one airway––one disease’ from a bacterial infection point of view