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Release date November 18, 2013
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Eur J Pediatr. 2006 Nov; 165Suppl 1: 1РІ389.
Liggins Institute, University of Auckland, New Zealand
The results of changes in nutrition on body composition with the growing animal be determined by the timing, in addition to severity, duration and nature, from the nutritional insult. In sheep, both maternal undernutrition around any time of conception plus a high plane of nutrition inside a young mother still growing herself end in impaired maternal metabolic adaptation to pregnancy, so because of this greater substrate distribution to maternal for the expense of conceptus tissue accretion. Maternal nutrition at the beginning of pregnancy also determines subsequent growth and the body composition with the offspring, with mild-moderate maternal undernutrition producing offspring of normal weight at birth however with increased weight of fat depots thereafter. Undernutrition in late pregnancy commonly reduces offspring birthweight, and also this in turn affects later growth and the entire body composition. After birth, continuing development of different tissues is strongly affected by both prior and current nutritional experiences. Lambs of lower birthweight more and more difficult to start to find weight after birth. They also need a higher feed intake to realize a given excess weight, and even more of that weight is gained as fat and much less as muscle in comparison with lambs of upper birthweight. However for confirmed birthweight, slower postnatal putting on weight is generally from a proportionately greater muscle growth. Rate of growth also determines other areas of body composition. Muscle fibre number, which limits final muscle size, is usually determined before birth, and even before the last trimester of childbearing in many species. Lambs rapidly expanding either before or after birth generally have proportionately larger livers, whereas chronically slow growth is part of reduced liver size relative to bodyweight. Similar patterns are noticed in the lymphoreticular tissues for example spleen and thymus. It seems likely these variations in body composition may have important functional consequences for later wellbeing.
Ciencias de la Salud, Universidad de Zaragoza, Zaragoza, Spain,
Department of Nutrition and Food Science, University of The Basque Country, Vitoria, Spain
There are critical periods during childhood that influence the introduction of obesity, including gestation and early infancy. Size at birth and early postnatal growth are determinants of adult height and the entire body mass index. The aim of this research was to evaluate if birth weight has any affect on body composition and/or fat distribution in adolescents.
Body composition was assessed by both skinfold thickness measurements and dual energy X-ray absorptiometry DXA in 234 adolescents born at term 140 females and 94 males, now aged 13 18 y and living within the city of Zaragoza AVENA-Zaragoza cohort. Relative fat distribution was estimated together with the ratio in the subscapular to triceps skinfolds S/T. Birth weight and gestational age were assessed by means of an questionnaire, thinking about the paediatric neonatal records.
Birth weight was inversely connected with S/T ratio P 0.05 in men and directly regarding bone mass P 0.01 and free of fat mass P 0.05 in women. This association was separate from age, Tanner stage, gestational age, socioeconomic status, exercising and height.
In adolescents born at term, genetic and/or intrauterine environmental factors that influence foetal growth and therefore are reflected in birth weight have long lasting consequences on bone and muscular mass, measured by DXA, in ladies and in subcutaneous fat distribution of males.
Institute of Life Science, University of Louvain, Louvain-la-Neuve, Belgium
A body of evidence now points too poor intrauterine milieu elicited by maternal nutritional disturbance or placental insufficiency may programme susceptibility inside fetus to later develop chronic degenerative disease like diabetes, obesity, hypertension and cardio-vascular disease. The compatibility of early postnatal nutrition with fetal experience can also be decisive for that rate of occurrence of degenerative disease.
The knowledge of mechanisms underlying the programming in the metabolic syndrome is currently progressing on account of animal studies the place that the fetal and neonatal environment is manipulated.
Similarly to data from epidemiological studies in humans, obesity in rodent models arises principally in offspring published to malnutrition noisy . stages of gestation and which presented an earlier catch-up growth. Four different pathways for programming obesity could possibly be proposed: 1 programming central circuits within the hypothalamic area controlling feeding and metabolism, 2 modification of their time expenditure, 3 generation of any hormonal context favouring adipose tissue development, 4 modification with the pools of fat cell precursors which will lead to hypertrophichyperplastic obesity. These pathways and respective importance according to your time-window of exposure along with the type of malnutrition have become subject to intense study. Studies within the progressive appearance of insulin resistance in rodents which have been growth-retarded in utero revealed a heightened sensitivity of target tissues to insulin in the younger generation, as well as insulin resistance in older age. The insulin resistance was associated with modifications to expression of key components in the insulin-signalling cascade in muscle and adipocytes. The modifications in expression of which molecular markers are already detected also in muscle and fat biopsies of males with the lowest birth weight. Possible molecular mechanisms included in nutritional programming are merely starting to emerge, for instance early definitive modifications to the organelle central to energy utilisation, mitochondria, or epigenetic modifications to nuclear DNA.
Animal models provide efficient tools to show the time windows of nutritional experience at the begining of life favouring later obesity, and also to decipher progressively physiological and molecular mechanisms linked to such metabolic programming.
Center for Human Genetics, University of Leuven, Belgium
The complete and detailed sequence of your representative sample of human DNA is actually fully known, apart from a few stretches of not easy to sequence DNA. This historic achievement has recently generated a number of surprises. The number of genes about 25, 000 hidden inside the 3 billion nucleotides that define the human genome is quite a bit smaller than initially expected and is particularly only slightly more than in flies, as the total protein coding sequence is just about 3% with the genome. The OMIM register at /Omim/lists over 12, 000 entries for monogenic or Mendelian diseases, including 60 mitochondrial diseases. More than 7, 000 of these have already been already mapped to a specific chromosomal region, while another 2, 000 employ a definite gene locus. The remaining entries are just phenotypic descriptions or any other entries. The molecular basis of such diseases is rapidly being uncovered. In some genes one or some defects are responsible for a certain phenotype; in other business owners, mutations could be scattered throughout the gene the a lot more than 1000 different mutations from the CFTR gene in cystic fibrosis. The majority of our normal traits and diseases are inherited in the multifactorial fashion. This means that some genes usually tens of genes could happen, caused by either normal variation into their sequence or real dysfunctional mutations. In addition, environmental factors modulate the best way these genes influence a final phenotype. Traits inherited within this fashion are mostly quantitative measurable traits for instance height, weight, IQ etc. and show an ordinary Gaussian distribution inside the population. Lamarck, who within the 19th century claimed that acquired traits is usually inherited, has a little revenge lately. Some examples have already been found of how nutritional factors can condition DNA and affect generations to come. As our understanding in the human genome increases, it is now increasingly clear which our knowledge is in present largely insufficient to explain every one of the phenotypic variability observed between individuals troubled by the same disease. It is gradually that people will unravel every one of the genetic and environmental factors accountable for this variability. Nevertheless, many families can already be helped by genetic testing so as to identify with precision just what the nature from the disease is and what are the recurrence risks are. Even fairly precise prediction in the risk to cultivate a disease in life presymptomatic diagnosis or with the susceptibility to formulate serious multifactorial diseases, for example hereditary breast or colorectal cancer, is accessible. Nevertheless we've got to guarantee our clients why these tests are done with all the best quality available and inside the context of appropriate genetic counseling.
Department of Pediatric Pneumology and Immunology, Charit, Berlin, Germany
Despite a robust genetic cause asthma and atopy, no genetic markers unambiguously regarding atopy-related traits has yet been identified. Variants in 100 candidate genes were linked to atopy-related traits. However, replication at least two times was reported for under 30 genes. Discrepant results may partly be attributed type 1 and type 2 errors caused by small sample sizes or no correction for multiple tests. Also, different ethnicities of study populations have to get considered. There is growing evidence that gene-by-gene- and gene-byenvironment interactions strongly influence disease susceptibility knowning that single variant association studies are not sufficient to name the genetic cause for atopic disorders. With regard on the development of asthma and atopy, environmental factors factors linked to living on the farm, allergen exposure, infections appear for being particularly important very at the beginning of life.
Therefore, many gene-by-environment-interaction studies are actually performed in pediatric populations and birth cohorts.
Strong evidence for interactions may be presented for genes included in LPS lipopoly-saccharide binding and signalling: One of by far the most extensively examined candidate gene for atopy is CD14, coding for any receptor for LPS. A CD14 promoter variant was regarding both, low and high total serum IgE levels tIgE, other studies showed no affect on tIgE. Recent studies that devoted to CD14 genotypes and endotoxin exposure suggest strong gene-by-environment interactions using the CD14 variant being either protective or even a risk factor for asthma or increased tIgE determined by low or high endotoxin exposure. Toll like receptor TLR genes seemed to be investigated in asthma and atopy. TLRs are important for recognition of microbial pattern associated molecules. A TLR2 variant was of a decreased risk for asthma, but this effect was exclusively affecting children living on the farm, also implying a gene-by-environment interaction. Environmental cigarette ETS exposure may be intensely investigated in gene-by-environment interaction studies. An example is studies connected with an IL13 variant inside of a large German birth cohort. Significant associations with tIgE as well as a common promoter variant were observed at ages young and old from 1 to many years. ETS exposure in utero and/or infancy led to even higher tIgE in kids homozygous with the variant, though no relation to tIgE within the remaining children.
ETS-, endotoxin- and allergen exposure are very important environmental factors with regards to asthma and atopy. Exposure could be assessed and quantified in standardized procedures. Other factors which will contribute on the increased prevalence of atopy and as a consequence of interest for gene-by-environment interaction studies are harder to assess in the standardized fashion diet, infections, medication, stress, which can be an ongoing effort of current birth cohort studies in your division. Taken together, genetic studies of asthma and atopy not merely require large carefully characterized, ethnically homogeneous study populations, and also data on environmental exposure for example endotoxin, ETS and allergens. Birth cohorts are particularly valuable for gene-by-environment interaction studies since exposure may be assessed noisy . infancy, a most vulnerable time period of life with regard towards the development of asthma and atopy.
Department of Pediatrics, Queen Silvia Childrens Hospital, Gothenburg, Sweden
Complex diseases like diabetes, allergy and cancer be determined by multiple interacting genes. It is probably extremely hard to find a key gene in these diseases, a silver bullet that may be used for diagnostic or therapeutic purposes. New technologies, like DNA microarrays allow simultaneous analysis of expression of most human genes. We have applied these technologies and systems biology to allergic rhinitis. The clinical aim is to name markers for treatment response. It is possible that similar principles are usually applicable to complex diseases.
DNA microarrays, clique-based graph algorithms, pathway analysis, real-time PCR, immunohistochemistry, flow cytometry, SNP analysis
Getting a practical understanding on the large datasets generated by DNA microarray studies of complex diseases is usually a significant challenge. One such study may identify tons of genes that differ in expression between patients and controls. While this might be seen as discouraging it lets you do reflect the complexity on the diseases that people study. Moreover, whenever we can get yourself a grip for this complexity this could possibly be used for clinical purposes, by way of example to find combinations of markers for individualized therapy. Systems biology is undoubtedly an emerging discipline that aims to comprehend how complex systems refer to biological effects. One important theoretical framework is network-based analysis. In the context of DNA microarray studies, genes that differ in expression between patients and controls are organized in gene interaction networks. Such networks could be analyzed inside a top-down fashion. The idea could be the same like a microscopic examination. You start having a low magnification to recognize general features on the sample then proceed to detailed studies of human cells. A gene interaction network might be analyzed to locate sub-networks or pathways with distinct functions, for example cell proliferation or apoptosis. These sub-networks might be further dissected to seek out upstream genes with putative key regulatory functions. Typically, several sub-networks or pathways are involved with complex diseases. However, a top-down analysis may cause identification of combinations of key genes that may be used for clinical purposes, like to find markers for personalized medication. In this presentation examples from own research in allergic disease will be provided, together with from oncological research. In the latter case customized DNA microarrays are tried to seek out gene expression signatures for personalized medication in breast cancers.
High-throughput studies and systems biology may contribute to idea of complex diseases. A clinical implication could possibly be identification of markers for personalized medication.
University from the West of England, Bristol, UK
Nurses, whether as academics or practitioners are increasingly necessary to disseminate the findings of research or share ideas and degrees of best practice through publication. Lack of confidence, some time to familiarity with different journal house-styles are sometimes cited as barriers. These issues are going to be considered. Moreover, writing informatively as well as in an accessible format is difficult, but it might be learned through following certain principles, commitment, serious amounts of enthusiasm 1 2. Aim: The purpose of this workshop is perfect for delegates to understand the best way to develop a successful strategy that will produce publication inside a peer-reviewed journal.
The workshop is going to be based using a power-point presentation but delegates will probably be expected to participate through open discussion and questions to explore an array of other related issues.
The conclusion will summarise the seven key stages on preparing a paper for publication like the importance of considering international readers.
Paediatric and Neonatal Intensive Care Unit, Great Ormond Street Hospital, London, UK
Play therapy has become part in the intensive care service in your hospital since 1996. Hospital Play Specialists HPS be part from the multidisciplinary and psychosocial team in the intensive care unit. We reviewed our experience with play therapy in long-term patients whilst on intensive care.
We performed overview of long-term ventilated patients on our intensive care unit, between 2002-2006 by which we routinely devised play programmes. The average stay was 1 year. Reason for contact and outcome were reviewed.
The HPS assessed the childs needs and devised appropriate programmes for him or her, which fit an everyday routine. The programme ensured appropriate stimulation together with establishing periods respite and sleep, whilst still appreciating the childs medical and nursing input. The programmes changed to match the childs development and looked in the psychosocial needs from the child and also the family whilst requiring intensive care. Examples are shown.
A play specialist may become an integral part in the intensive care unit working alongside the medical and nursing staff to enhance the long-term patients development. The HPS teaches nurses and parents to play inside the intensive care environment. The HPS works together with the long-term patient, their family along with the intensive care staff to beat issues for instance behaviour, eating, and communication problems. The Play Specialist meets the patients needs through play; they supply fun and stimulation wanting to provide some normality in the otherwise stressful and frightening environment.
University of Southampton,
Southampton University Hospitals Trust, Southampton, UK
The by using humour being a therapy is receiving increasing attention from physicians. This study discusses the views of The English Theodora Childrens Trust Clown Doctors with the items works best and least well throughout a clown encounter having a sick child in hospital.
Nominal group technique NGT. Sample size 12.
What is best suited when a clown doctor visits a sick child?
Listening, watching then responding
Changing atmosphere: What works least well every time a clown doctor visits a sick child?
Bad communication, devoid of enough time, utilizing no feeling and ignoring the childs feelings
Not judging your situation, whenever a child is diagnosed because terminally ill/dying, deficiency of information within the childs status rather than feeling in your best
This report in the perceptions of Clown Doctors has revealed that there are numerous elements which enhance a clown doctor encounter that has a sick child.
Department of Respiratory and Sleep Medicine, Royal Hospital for Sick Children, Edinburgh, UK
Cystic Fibrosis, first described in 1938, was quickly recognised, like a great number of other conditions to be of autosomal recessive inheritance. There was understandable great excitement around the discovery in 1989 of DeltaF508, one of the most common gene mutation for cystic fibrosis. As a recessive single gene defect disease the opportunity of replacing the defective gene would have been a stimulating prospect. Seventeen years later, whilst other single gene defects happen to be corrected, a solution towards the cystic fibrosis gene defect remains unresolved. The reasons with this lack of resolution are frustrating to patients and clinicians, but have opened novel and fruitful research directions. What is usually so complex about it single gene defect? Firstly, there isnt one gene defect, there are no over 1000 genes identified linked to cystic fibrosis, falling into five functional classes. Secondly, we have now become increasingly aware the interplay of ancillary modifier genes play a crucial but to date poorly quantified relation to the principle gene defect. Thirdly, like with other diseases, the complex evolving phenotype of cystic fibrosis, incorporates the interplay of genotype and environment, together with all the possible role of epigenetics heritable modifications to gene function that occur without having a change within the DNA sequence. Together these factors convey a substantial complexity from what was considered a straightforward model of disease. Into this environment, the next generation of pulmonary trials for correction in the cystic fibrosis gene defect are being planned. The first pulmonary trials were successful for the reason that gene transfer occurred, yet not enough and unwanted side effects too many. Important lessons were learnt, and using a hiatus to reform the entire infrastructure with the gene delivery systems further trials have become planned. There are expected additional problems in youngsters, including of which can be how will any of us know if gene transfer works. Yet youngsters are considered the linchpin on the success of which studies repairing the defect before major pulmonary injury has occurred and principals are underway to make sure that children mustn't be disenfranchised out of this major biotechnological advance.
Laboratoire dAntibiologie, CHU Nantes, France