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How can we impact the immune system with pre- and probiotics? 我们如何用益生菌和益生菌影响免疫系统?
Pub Date : 2005-01-01 DOI: 10.1159/000083307
E J Schiffrin, A Donnet, S Blum
In recent years there has been a growing interest in understanding the influence of intestinal microbiota on the physiology of the body. Moreover, with the available genomic studies, it is now possible to analyze how components of the intestinal microbiota modulate features of human postnatal development and physiology [1]. An area of major interest has been the relationship between the gut bacteria and the immune system, both at the intestinal and systemic level [2]. Changes in the microbiologic content of the intestine can be induced by the administration of selected bacterial inoculums as part of a normal diet or as dietary supplements. The health-promoting microorganisms are called probiotics. The administration of specific fibers in the diet called prebiotics can also modify the intestinal ecology by promoting the growth of some particular components of the intestinal microbiota, such as bifidobacteria. On the one hand, there is an immune activation which is associated with improved mucosal defenses against pathogens and responses to oral vaccines. On the other, a modified immune reactivity which preserves homeostasis in mucosal tissues confronted with a constantly changing environment. Not only does the latter avoid an excessive reaction and inflammatory damage in the local environment, it also influences the homeostasis of the systemic immune system and prevents the development of allergic or autoimmune diseases. It is difficult to provide a simple mechanistic explanation for the underlying cellular and molecular events that support these apparently opposing effects. However, a brief overview of the evolving models that have been postulated to explain basic immune function, may help us understand how intestinal bacteria effect the mucosal and systemic immune systems [3, 4]. The most important of these are the following. Lochs H, Thomas DR (eds): Home Care Enteral Feeding. Nestlé Nutrition Workshop Series Clinical & Performance Program, vol 10, pp 203–217, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2005.
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引用次数: 4
How can we modulate cytokine production and action? 我们如何调节细胞因子的产生和作用?
Pub Date : 2005-01-01 DOI: 10.1159/000083308
Luc Cynober
The loss of body weight and development of cachexia are common signs associated with several diseases. Net muscle protein catabolism is the result of a neuronal and endocrinological response, the main hormone involved in this process being cortisol [1]. Besides this, a number of pathological situations (e.g. cancer, infection, trauma, surgery) lead to activation of the immunological system which, in particular, involves the release of mediators. Among these, cytokines play a preeminent role. Cytokines are now classified according to the cell subset synthesizing them (i.e. Th1 and Th2) and their main action (i.e. proversus anti-inflammatory). The main Th1 cytokines are tumor necrosis factor(TNF), interleukin (IL)-1 and and interferon(IFN). The main Th2 cytokines are IL-4 and IL-10. A notable exception to this classification is IL-6, which is synthesized by Th2 cells but is more a proinflammatory cytokine (PIC) [2]. Th1 cytokines inhibit Th2 cytokine production and vice versa. PICs contribute to protein wasting via several mechanisms, including a direct effect on: (i) protein turnover (i.e. net protein catabolism) increasing protein catabolism through NFB activation [3] and activation of the ubiquitinproteasome system [4, 5], especially activation of E3 ligases atrogin-1 and MURF-1 [6–8], decreasing protein synthesis through inhibition of eIF2B [9] or other factors involved in the translation process such as 4E-BP1 [10], and (ii) amino acid metabolism and oxidation through gluconeogenesis [11]. Also, cytokines potentiate cortisol and glucagon action at the target tissue level (i.e. muscle and liver, respectively) and blunt IGF-1 production and action in muscle [6]. However, the problem is complicated by the fact that each individual PIC has a more or less significant effect on specific aspects of protein Lochs H, Thomas DR (eds): Home Care Enteral Feeding. Nestlé Nutrition Workshop Series Clinical & Performance Program, vol 10, pp 219–232, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2005.
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引用次数: 5
Physiological vs. pathological changes of nutritional status over life time. 一生中营养状况的生理与病理变化。
Pub Date : 2005-01-01 DOI: 10.1159/000083262
Manfred J Müller, Anja Bosy-Westphal, Corinna Geisler, Simone Onur
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引用次数: 4
What are the goals of nutritional support? The example of home enteral nutrition. 营养支持的目标是什么?家庭肠内营养的例子。
Pub Date : 2005-01-01 DOI: 10.1159/000083300
Xavier Hébuterne, Stéphane M Schneider
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引用次数: 6
Psychoimmunology of nutrition. 营养心理免疫学。
Pub Date : 2005-01-01 DOI: 10.1159/000083306
Bruno Lesourd
The relationships between behavior and immune responses have been studied for a long time. It is well recognized that persons under psychological stresses, such as depression, marital problems, bereavement or alcoholism, are more susceptible to infections. Nevertheless only a few studies were conducted before the 1970s. Since then, progress in knowledge of the immune system, improvement in questionnaires assessing the characterization and quantification of different moods, and very recently the link between a psychological approach and brain neuron cell functions (neuroimmunology) have pushed to extend research in this new field, called psychoneuroimmunology. This review will briefly describe the immune system and its roles. Thereafter the most important findings linking psychological stresses and immune responses will be discussed. Recent research at the neuron cell level is reported in order to present the current hypotheses being investigated.
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引用次数: 0
Under- and overnutrition: a global perspective. 营养不足和营养过剩:全球视角。
Pub Date : 2004-01-01 DOI: 10.1159/000080618
W Philip T James, Rachel Leach
The world is now confronted with a set of medical problems of nutritional origin with which it has never previously had to contend, i.e. both undernutrition of various types and a huge and rapidly escalating burden of diseases crudely classified as relating to overnutrition. The problems of malnutrition, particularly affecting young children, were highlighted in the developing world in the 1950s by a remarkable series of studies emanating from first-class nutrition research centers in Africa, Asia and Latin America, e.g. in Chile, India, Jamaica, the Lebanon, Mexico, Peru, Thailand and Uganda. In nutritional circles, for example, malnutrition was often considered to be a practical problem of improving children’s nutrition with multifaceted approaches to improve the maternal and nutritional care of the young child. The promotion of breast-feeding followed by appropriate weaning was vital, together with a recognition of the fundamental human right of poor families to have adequate support. The World Health Organization (WHO) continued to encourage the monitoring of individual children’s growth by means of national statistics while other UN agencies such as UNHCR and WFP, as well as non-governmental organizations, coped with the mounting crises of refugees and displaced persons fleeing from a multitude of wars, or attempting to survive the effects of droughts, floods and consequent crop failures. Support for the steady improvement in agricultural production, on which the escalating numbers of the world’s poor depend, was universally accepted and was the responsibility of FAO and the CGIARs, funded by Western governments, the World Bank and the IMF. More recently, in response to the drive by Grant, the former Director General of UNICEF, the world’s Presidents and Prime Ministers expressed their commitment to tackling the continuing burden of childhood malnutrition at a Children’s Summit [1]. This led to the development of the Millennium Goals [2] Allison SP, Go VLW (eds): Metabolic Issues of Clinical Nutrition. Nestlé Nutrition Workshop Series Clinical & Performance Program, vol 9, pp 1–17, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2004.
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引用次数: 1
The role of minerals and trace elements in relation to long-term health and chronic disease. 矿物质和微量元素在长期健康和慢性疾病中的作用。
Pub Date : 2004-01-01 DOI: 10.1159/000080662
Alan Shenkin
By definition, all of the major minerals and essential trace elements are necessary for health, and the range of these elements implies that they are part of all aspects of cellular function. They are involved as structural components, such as calcium or phosphorus in bone, as cofactors for enzyme activity or as an integral part of enzyme or protein structure (metalloproteins). They influence all metabolic pathways, are part of the antioxidant systems to prevent oxidative damage to cells, and are part of control mechanisms in the cell such as the zinc finger transcription factors. The breadth of this topic is extremely wide, and hence the current discussion will be limited only to nutritional deficiency states and their effects, and to examples selected from three key minerals (calcium, phosphorus, and magnesium), and from the well-established trace elements (iron, zinc, copper, selenium, chromium, molybdenum, manganese, cobalt and iodine). The ‘classical’ way of describing the progressive development of a nutritional deficiency state is shown in figure 1. When dietary supply is inadequate, the body will first mobilize any stores, if available, e.g. calcium will be mobilized from bone. Thereafter there will be an attempt to compensate either by increasing absorption from the gut, e.g. for iron, or reducing urinary excretion, e.g. for magnesium or phosphate. If the inadequate supply continues, or if there is no effective homeostatic mechanism, cellular deficiencies will occur which will have a wide range of effects on metabolism, depending on the element and the tissues mainly involved. These cellular effects may be apparent in some change in metabolism, e.g. chromium deficiency and glucose intolerance in type-2 diabetes, or magnesium deficiency and hypocalcemia. Signs and symptoms may be fairly nonspecific at this time – fatigue, mental and cognition changes, Allison SP, Go VLW (eds): Metabolic Issues of Clinical Nutrition. Nestlé Nutrition Workshop Series Clinical & Performance Program, vol 9, pp 169–185, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2004.
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引用次数: 3
Mechanisms of insulin-induced alterations in metabolism during critical illness. 危重疾病期间胰岛素诱导代谢改变的机制。
Pub Date : 2004-01-01 DOI: 10.1159/000080624
Dieter Mesotten
Through the explosion of therapeutic possibilities within the setting of intensive care medicine, patients can nowadays survive previously lethal disease states. Specific endocrine approaches to critical illness have always been limited to sporadic trials and isolated schools advocating rigorous metabolic control. This is in stark contrast with the boom of therapeutic possibilities for diabetes mellitus and coronary artery disease, where tight glycemic and lipemic control are now common practice. The Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) [1] showed an improved outcome of diabetic patients with myocardial infarction upon ‘moderate’ blood glucose control. As a further step, a large prospective, randomized, controlled trial was set up to examine the effect of ‘strict’ glycemic control below 6.1 mmol/l (110 mg/dl) with exogenous insulin on the mortality and morbidity of critically ill patients [2], both diabetic and nondiabetic. Over a 1-year period, 1,548 mechanically ventilated patients admitted to the intensive care unit (ICU), predominantly after extensive surgery or trauma, were randomly allocated to either intensive insulin therapy with blood glucose levels kept tightly between 4.5 and 6.1 mmol/l (80–110 mg/dl), or the conventional approach which only recommended insulin therapy when blood glucose levels exceeded 12 mmol/l. Strict blood glucose control reduced the intensive care mortality of critically ill patients by more than 40%. Even patients in the conventional insulin treatment schedule with only moderate hyperglycemia (6.1–11.1 mmol/l), the equivalent of the therapeutic arm in the DIGAMI study, showed higher mortality compared to the patients in the strict glycemic control schedule [3]. Intensive insulin therapy also had a major effect on morbidity. It decreased the duration of ventilatory support and intensive care stay, Allison SP, Go VLW (eds): Metabolic Issues of Clinical Nutrition. Nestlé Nutrition Workshop Series Clinical & Performance Program, vol 9, pp 69–75, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2004.
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引用次数: 6
Fatty acid isomers in lipid metabolism. 脂质代谢中的脂肪酸异构体。
Pub Date : 2004-01-01 DOI: 10.1159/000080649
J L Sébédio, L Bretillon, J M Chardigny
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引用次数: 0
Insulin resistance in catabolic diseases. 分解代谢疾病中的胰岛素抵抗。
Pub Date : 2004-01-01 DOI: 10.1159/000080623
Simon P Allison
With remarkable intuition, John Hunter [1] in 1794 described the response to injury as follows: ‘Impressions are capable of producing or increasing natural actions and are then called stimuli: they are likewise capable of producing too much action as well as depraved, unnatural or what we commonly called diseased actions’. Scientific studies over the last century have lent support to this hypothesis in which the neuroendocrine, cytokine and consequent metabolic responses to injury are essential to survival, but when carried to extreme may put survival in jeopardy.
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Nestle Nutrition workshop series. Clinical & performance programme
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