989 resultados para Growth disorders


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La bursite infectieuse aviaire (IBD) est une des causes majeures de pertes économiques pour l’industrie aviaire. La vaccination est le principal outil de contrôle de cette maladie et les oiseaux susceptibles doivent être vaccinés aussitôt que le niveau des anticorps maternels (MA) anti-IBDV est suffisamment bas. L’estimation du moment de vaccination est habituellement déterminée par la formule de Deventer qui utilise le titre initial de MA anti-IBDV et la demi-vie des anticorps pour prédire l’évolution du titre. Dans la présente étude, l’effet du gain de poids sur la vitesse de disparition des MA a été étudié dans le but de l’utiliser pour prédire la détermination du moment de la vaccination. L’analyse des taux d’anticorps neutralisants par ELISA a montré que les poussins avec une forte croissance avaient un taux de disparition plus rapide des MA que ceux à faible croissance. Une formule pour la prédiction du moment de vaccination contre le IBDV, basée sur le gain de poids et le niveau des MA a été développée et vérifiée. La prédiction du moment de vaccination avec cette formule a montré une haute corrélation avec les titres de MA mesurés par ELISA. Le virus de l’anémie infectieuse aviaire (CIAV) est une cause importante d’immunosuppression chez le poulet augmentant la pathogénicité des infections secondaires et en entraînant une réponse humorale suboptimale et une forte mortalité. D’autre part, l’infections sub-clinique du au CIAV provoque une immunosuppression qui facilite la coinfection par d’autre virus tel que le IBDV. Les effets de la coinfection à J1 avec une souche vaccinale de CIAV CAV-VAC® (Intervet) et à J14 avec une souche faiblement virulente de IBDV isolée au Québec, sur l’état de santé des poussins, sur la persistance virale et sur la réponse immunitaire ont été étudiés autant chez des poussins de 1 jour d’âge exempts d’agents pathogènes specifique (SPF) que ceux provenant d’élevages commerciaux. Les résultats ont montré que l’inoculation de la souche vaccinale du CIAV a entraîné une infection sub-clinique, une persistance virale dans la rate et le thymus, une altération de la thymopoièse et une réponse humorale temporaire chez les poussins SPF. Ces effets ont aussi été mis en évidence chez des poussins d’élevage commerciaux malgré des taux élevés de MA. Lors de l’infection avec la souche de IBDV chez des poussins déjà vaccinés contre le CIAV, la persistance du CIAV dans les organes lymphoïdes a été aggravée par une présence de réponses humorales temporaires contre les deux virus et une altération des populations lymphocytaires dans les organes lymphoïdes. Par contre, la présence des MA contre le CIAV a limité temporairement ces effets. Ces travaux ont mis en évidence des désordres immunitaires cellulaires et humoraux et une persistance virale chez des poussins vaccinés contre le CIAV et co-infectés avec le IBDV.

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Les maladies cardio-vasculaires (MCV), telles que l’hypertension et l’athérosclérose, s’accompagnent de modifications structurales et fonctionnelles au niveau vasculaire. Un fonctionnement aberrant de la migration, l’hypertrophie et la prolifération des cellules musculaires lisses vasculaires (CMLV) sont des évènements cellulaires à l’origine de ces changements. L’endothéline-1 (ET-1) contribue à la pathogénèse des anomalies vasculaires, notamment via l’activation des protéines MAPK et PI3-K/PKB, des composantes clés impliquées dans les voies prolifératives et de croissance cellulaires. Il a été suggéré que le stress oxydant jouerait un rôle intermédiaire dans les effets pathophysiologiques vasculaires de l’ET-1. En conséquence, une modulation de la signalisation induite par l’ET-1 peut servir comme éventuelle stratégie thérapeutique contre le développement des MCV. Il apparaît de nos jours un regain d’intérêt dans l’utilisation des agents phyto-chimiques pour traiter plusieurs maladies. La curcumine, constituant essentiel de l’épice curcuma, est dotée de plusieurs propriétés biologiques parmi lesquelles des propriétés anti-oxydantes, anti-prolifératrices et cardio-protectrices. Cependant, les mécanismes moléculaires de son effet cardio-protecteur demeurent obscurs. Dans cette optique, l’objectif de cette étude a été d’examiner l’efficacité de la curcumine à inhiber la signalisation induite par l’ET-1 dans les CMLV. La curcumine a inhibé la phosphorylation des protéines IGF-1R, PKB, c-Raf et ERK1/2, induite par l’ET-1 et l’IGF-1. De plus, la curcumine a inhibé l’expression du facteur de transcription Egr-1 induite par l’ET-1 et l’IGF-1, dans les CMLV. Ces résultats suggèrent que la capacité de la curcumine à atténuer ces voies de signalisation serait un mécanisme d’action potentiel de ses effets protecteurs au niveau cardiovasculaire.

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The combined effects of shoot pruning (one or two stems) and inflorescence thinning (five or ten flowers per inflorescence) on greenhouse tomato yield and fruit quality were studied during the dry season (DS) and rainy season (RS) in Central Thailand. Poor fruit set, development of undersized (mostly parthenocarpic) fruits, as well as the physiological disorders blossom-end rot (BER) and fruit cracking (FC) turned out to be the prevailing causes deteriorating fruit yield and quality. The proportion of marketable fruits was less than 10% in the RS and around 65% in the DS. In both seasons, total yield was significantly increased when plants were cultivated with two stems, resulting in higher marketable yields only in the DS. While the fraction of undersized fruits was increased in both seasons when plants were grown with a secondary stem, the proportions of BER and FC were significantly reduced. Restricting the number of flowers per inflorescence invariably resulted in reduced total yield. However, in neither season did fruit load considerably affect quantity or proportion of the marketable yield fraction. Inflorescence thinning tended to promote BER and FC, an effect which was only significant for BER in the RS. In conclusion, for greenhouse tomato production under climate conditions as they are prevalent in Central Thailand, the cultivation with two stems appears to be highly recommendable whereas the measures to control fruit load tested in this study did not proof to be advisable.

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Inhibition of myostatin signalling or its biological activity has recently emerged as a potential remedial approach against muscle wasting and degenerative diseases such as muscular dystrophies. In the present study we systemically administered a recombinant AAV8 vector expressing a mutated myostatin propeptide (AAV8ProMyo) to healthy mice in order to assess its impact on the histological, cellular and physiological properties of the skeletal muscle, exploiting the fact that myostatin is naturally inhibited by its own propeptide. We report that a single intravenous administration of AAV8ProMyo leads to increases in muscle mass of tibialis anterior, extensor digitorum longus and gastrocnemius muscles 8 weeks post-injection and tibialis anterior, gastrocnemius and rectus femoris muscles 17 weeks post-injection. Moreover, treatment resulted in muscle fibre hypertrophy but not hyperplasia, with IIB myofibres responding to the greatest extent following propeptide-induced myostatin inhibition. Additionally, myofibre nuclear: cytoplasmic ratio was decreased in the AAV8ProMyo treated animals. Importantly, the hypertrophic EDL muscle 8 weeks after AAV8ProMyo treatment did not show the dramatic decrease in specific force displayed by the germline myostatin null mice. (C) 2009 Elsevier B.V. All rights reserved.

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The lack of myostatin promotes growth of skeletal muscle, and blockade of its activity has been proposed as a treatment for various muscle-wasting disorders. Here, we have examined two independent mouse lines that harbor mutations in the myostatin gene, constitutive null (Mstn(-/-)) and compact (Berlin High Line, BEH(c/c)). We report that, despite a larger muscle mass relative to age-matched wild types, there was no increase in maximum tetanic force generation, but that when expressed as a function of muscle size (specific force), muscles of myostatin-deficient mice were weaker than wild-type muscles. In addition, Mstn(-/-) muscle contracted and relaxed faster during a single twitch and had a marked increase in the number of type IIb fibers relative to wild-type controls. This change was also accompanied by a significant increase in type IIB fibers containing tubular aggregates. Moreover, the ratio of mitochondrial DNA to nuclear DNA and mitochondria number were decreased in myostatin-deficient muscle, suggesting a mitochondrial depletion. Overall, our results suggest that lack of myostatin compromises force production in association with loss of oxidative characteristics of skeletal muscle.

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Background Recent research provides evidence for specific disturbance in feeding and growth in children of mothers with eating disorders. Aim To investigate the impact of maternal eating disorders during the post-natal year on the internal world of children, as expressed in children's representations of self and their mother in pretend mealtime play at 5 years of age. Methods Children of mothers with eating disorders (n = 33) and a comparison group (n = 24) were videotaped enacting a family mealtime in pretend play. Specific classes of children's play representations were coded blind to group membership. Univariate analyses compared the groups on representations of mother and self. Logistic regression explored factors predicting pretend play representations. Results Positive representations of the mother expressed as feeding, eating or body shape themes were more frequent in the index group. There were no other significant group differences in representations. In a logistic regression analysis, current maternal eating psychopathology was the principal predictor of these positive maternal representations. Marital criticism was associated with negative representations of the mother. Conclusions These findings suggest that maternal eating disorders may influence the development of a child's internal world, such that they are more preoccupied with maternal eating concerns. However, more extensive research on larger samples is required to replicate these preliminary findings.

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Objectives: To clarify the role of growth monitoring in primary school children, including obesity, and to examine issues that might impact on the effectiveness and cost-effectiveness of such programmes. Data sources: Electronic databases were searched up to July 2005. Experts in the field were also consulted. Review methods: Data extraction and quality assessment were performed on studies meeting the review's inclusion criteria. The performance of growth monitoring to detect disorders of stature and obesity was evaluated against National Screening Committee (NSC) criteria. Results: In the 31 studies that were included in the review, there were no controlled trials of the impact of growth monitoring and no studies of the diagnostic accuracy of different methods for growth monitoring. Analysis of the studies that presented a 'diagnostic yield' of growth monitoring suggested that one-off screening might identify between 1: 545 and 1: 1793 new cases of potentially treatable conditions. Economic modelling suggested that growth monitoring is associated with health improvements [ incremental cost per quality-adjusted life-year (QALY) of pound 9500] and indicated that monitoring was cost-effective 100% of the time over the given probability distributions for a willingness to pay threshold of pound 30,000 per QALY. Studies of obesity focused on the performance of body mass index against measures of body fat. A number of issues relating to human resources required for growth monitoring were identified, but data on attitudes to growth monitoring were extremely sparse. Preliminary findings from economic modelling suggested that primary prevention may be the most cost-effective approach to obesity management, but the model incorporated a great deal of uncertainty. Conclusions: This review has indicated the potential utility and cost-effectiveness of growth monitoring in terms of increased detection of stature-related disorders. It has also pointed strongly to the need for further research. Growth monitoring does not currently meet all NSC criteria. However, it is questionable whether some of these criteria can be meaningfully applied to growth monitoring given that short stature is not a disease in itself, but is used as a marker for a range of pathologies and as an indicator of general health status. Identification of effective interventions for the treatment of obesity is likely to be considered a prerequisite to any move from monitoring to a screening programme designed to identify individual overweight and obese children. Similarly, further long-term studies of the predictors of obesity-related co-morbidities in adulthood are warranted. A cluster randomised trial comparing growth monitoring strategies with no growth monitoring in the general population would most reliably determine the clinical effectiveness of growth monitoring. Studies of diagnostic accuracy, alongside evidence of effective treatment strategies, could provide an alternative approach. In this context, careful consideration would need to be given to target conditions and intervention thresholds. Diagnostic accuracy studies would require long-term follow-up of both short and normal children to determine sensitivity and specificity of growth monitoring.

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The aim of this review article is to provide an overview of the role of pigs as a biomedical model for humans. The usefulness and limitations of porcine models have been discussed in terms of metabolic, cardiovascular, digestive and bone diseases in humans. Domestic pigs and minipigs are the main categories of pigs used as biomedical models. One drawback of minipigs is that they are in short supply and expensive compared with domestic pigs, which in contrast cost more to house, feed and medicate. Different porcine breeds show different responses to the induction of specific diseases. For example, ossabaw minipigs provide a better model than Yucatan for the metabolic syndrome as they exhibit obesity, insulin resistance and hypertension, all of which are absent in the Yucatan. Similar metabolic/physiological differences exist between domestic breeds (e.g. Meishan v. Pietrain). The modern commercial (e.g. Large White) domestic pig has been the preferred model for developmental programming due to the 2- to 3-fold variation in body weight among littermates providing a natural form of foetal growth retardation not observed in ancient (e.g. Meishan) domestic breeds. Pigs have been increasingly used to study chronic ischaemia, therapeutic angiogenesis, hypertrophic cardiomyopathy and abdominal aortic aneurysm as their coronary anatomy and physiology are similar to humans. Type 1 and II diabetes can be induced in swine using dietary regimes and/or administration of streptozotocin. Pigs are a good and extensively used model for specific nutritional studies as their protein and lipid metabolism is comparable with humans, although pigs are not as sensitive to protein restriction as rodents. Neonatal and weanling pigs have been used to examine the pathophysiology and prevention/treatment of microbial-associated diseases and immune system disorders. A porcine model mimicking various degrees of prematurity in infants receiving total parenteral nutrition has been established to investigate gut development, amino acid metabolism and non-alcoholic fatty liver disease. Endoscopic therapeutic methods for upper gastrointestinal tract bleeding are being developed. Bone remodelling cycle in pigs is histologically more similar to humans than that of rats or mice, and is used to examine the relationship between menopause and osteoporosis. Work has also been conducted on dental implants in pigs to consider loading; however with caution as porcine bone remodels slightly faster than human bone. We conclude that pigs are a valuable translational model to bridge the gap between classical rodent models and humans in developing new therapies to aid human health.

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Background. Within a therapeutic gene by environment (GxE) framework, we recently demonstrated that variation in the Serotonin Transporter Promoter Polymorphism; 5HTTLPR and marker rs6330 in Nerve Growth Factor gene; NGF is associated with poorer outcomes following cognitive behaviour therapy (CBT) for child anxiety disorders. The aim of this study was to explore one potential means of extending the translational reach of G×E data in a way that may be clinically informative. We describe a ‘risk-index’ approach combining genetic, demographic and clinical data and test its ability to predict diagnostic outcome following CBT in anxious children. Method. DNA and clinical data were collected from 384 children with a primary anxiety disorder undergoing CBT. We tested our risk model in five cross-validation training sets. Results. In predicting treatment outcome, six variables had a minimum mean beta value of 0.5: 5HTTLPR, NGF rs6330, gender, primary anxiety severity, comorbid mood disorder and comorbid externalising disorder. A risk index (range 0-8) constructed from these variables had moderate predictive ability (AUC = .62-.69) in this study. Children scoring high on this index (5-8) were approximately three times as likely to retain their primary anxiety disorder at follow-up as compared to those children scoring 2 or less. Conclusion. Significant genetic, demographic and clinical predictors of outcome following CBT for anxiety-disordered children were identified. Combining these predictors within a risk-index could be used to identify which children are less likely to be diagnosis free following CBT alone or thus require longer or enhanced treatment. The ‘risk-index’ approach represents one means of harnessing the translational potential of G×E data.

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Objective
To investigate tenocyte regulatory events during the development of overuse supraspinatus tendinosis in rats.

Methods
Supraspinatus tendinosis was induced by running rats downhill at 1 km/hour for 1 hour a day. Tendons were harvested at 4, 8, 12, and 16 weeks and processed for brightfield, polarized light, or transmission electron microscopy. The development of tendinosis was assessed semiquantitatively using a modified Bonar histopathologic scale. Apoptosis and proliferation were examined using antibodies against fragmented DNA or proliferating cell nuclear antigen, respectively. Insulin-like growth factor 1 (IGF-1) expression was determined by computer-assisted quantification of immunohistochemical reaction. Local IGF-1 signaling was probed using antibodies to phosphorylated insulin receptor substrate 1 (IRS-1) and ERK-1/2.

Results
Tendinosis was present after 12 weeks of downhill running and was characterized by tenocyte rounding and proliferation as well as by glycosaminoglycan accumulation and collagen fragmentation. The proliferation index was elevated in CD90+ tenocytes in association with tendinosis and correlated with increased local IGF-1 expression by tenocytes and phosphorylation of IRS-1 and ERK-1/2. Both apoptosis and cellular inflammation were absent at all time points.

Conclusion
In this animal model, early tendinosis was associated with local stimulation of tenocytes rather than with extrinsic inflammation or apoptosis. Our data suggest a role for IGF-1 in the load-induced tenocyte responses during the pathogenesis of overuse tendon disorders.

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There is growing recognition of the important role of mental health in the workforce and in the workplace. At the same time, there has been a rapid growth of studies linking job stress and other psychosocial working conditions to common mental disorders, and a corresponding increase in public concern media attention to job stress and its impact upon worker health and well-being. This article provides a summary of the relevant scientific and medical literature on this topic for practitioners and policy-makers. It presents a primer on job stress concepts, an overview of the evidence linking job stress and common mental disorders, a summary of the intervention research on ways to prevent and control job stress, and a discussion of the strengths and weakness of the evidence base. We conclude that there is strong evidence linking job stress and common mental disorders, and that it is a substantial problem on the population level. On a positive note, however, the job stress intervention evidence also shows that the problem is preventable and can be effectively addressed by a combination of work- and worker-directed intervention.

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The circadian system regulates 24 hour rhythms in biological creatures. It impacts mood regulation. The disruptions of circadian rhythms cause destabilization in individuals with affective disorders, such as depression and bipolar disorders. Previous work has examined the role of the circadian system on effects of light interactions on mood-related systems, the effects of light manipulation on brain, the impact of chronic stress on rhythms. However, such studies have been conducted in small, preselected populations. The deluge of data is now changing the landscape of research practice. The unprecedented growth of social media data allows one to study individual behavior across large and diverse populations. In particular, individuals with affective disorders from online communities have not been examined rigorously. In this paper, we aim to use social media as a sensor to identify circadian patterns for individuals with affective disorders in online communities.We use a large scale study cohort of data collecting from online affective disorder communities. We analyze changes in hourly, daily, weekly and seasonal affect of these clinical groups in contrast with control groups of general communities. By comparing the behaviors between the clinical groups and the control groups, our findings show that individuals with affective disorders show a significant distinction in their circadian rhythms across the online activity. The results shed light on the potential of using social media for identifying diurnal individual variation in affective state, providing key indicators and risk factors for noninvasive wellbeing monitoring and prediction.

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While it is understood that body composition impacts on physical conditions, such as diabetes and cardiovascular disease, it is only now apparent that body composition might play a role in the genesis of common mental disorders, depression and anxiety. Sarcopenia occurs in ageing and comprises a progressive decline in muscle mass, strength and function, leading to frailty, decreased independence and poorer quality of life. This review presents an emerging body of evidence to support the hypothesis that shared pathophysiological pathways for sarcopenia and the common mental disorders constitute links between skeletal muscle and brain function. Contracting skeletal muscle secretes neurotrophic factors that are known to play a role in mood and anxiety, and have the dual role of nourishing neuronal growth and differentiation, while protecting the size and number of motor units in skeletal muscle. Furthermore, skeletal muscle activity has important immune and redox effects that impact behaviour and reduce muscle catabolism.

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Acromegalia é doença crônica rara, insidiosa, decorrente da hipersecreção de hormônio do crescimento, cujos efeitos tróficos e metabólicos frequentemente incorrem em manifestações cutâneas, que podem ser precoces. Os autores avaliaram 15 pacientes portadores de acromegalia e evidenciaram alterações dermatológicas em todos, principalmente espessamento da pele, acrocórdons, cistos epidérmicos, pseudoacantose nigricante, queratoses seborreicas, nevos melanocíticos e manchas lentiginosas.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)