Sarcopenia is the decline in muscle mass that occurs with normal aging. Sarcopenia is a major cause of frailty, disability, and loss of independence in the elderly [1]. It is not a disease and is seen even in master athletes as they age. However, exercise can reverse many of the effects of sarcopenia, and even make elderly people stronger than sedentary young ones. Exercise is also known to have beneficial effects on mood, which is often depressed in people with sarcopenia, and it may have psychological as well as physiological benefits in this population.
{"title":"Exercise, sarcopenia, cognition, and mood.","authors":"Ronenn Roubenoff","doi":"10.1159/000061864","DOIUrl":"https://doi.org/10.1159/000061864","url":null,"abstract":"Sarcopenia is the decline in muscle mass that occurs with normal aging. Sarcopenia is a major cause of frailty, disability, and loss of independence in the elderly [1]. It is not a disease and is seen even in master athletes as they age. However, exercise can reverse many of the effects of sarcopenia, and even make elderly people stronger than sedentary young ones. Exercise is also known to have beneficial effects on mood, which is often depressed in people with sarcopenia, and it may have psychological as well as physiological benefits in this population.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"151-9; discussion 160-2"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061864","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the struggle for life, humans as every mammal and other living species, have to face two main dangers: (1) the competition against other individuals or other living species, including parasites, bacteria and viruses, and (2) the extreme toxicity of oxygen. The so-called ‘degenerative diseases’, which include the process of aging, are also related to both oxygen toxicity and immune defense against other living species, although some specific genetic characteristics may also be involved. The existence of a family of chemical compounds, called free radicals, has long been recognized as well as their harmful effects on biological molecules [1–5]. But, despite very active research concerning this field of reactive oxygen species (ROS) and extended work in both basic and clinical fields, we are still facing severe morbidity probably related to abnormalities on this pathway [6–12]. Several experimental studies have reported successful attempts to prevent or to counteract the deleterious effects of ROS [13–18] but, aside from important exceptions, the results so far have not produced the degree of evidence we are expecting [6, 19–25]. This relative lack of efficacy of the therapeutic approaches regarding oxidative stress and antioxidant treatments is probably related to the high degree of complexity of the ROS pathway and the antioxidant family, as well as the limitations for investigating oxidative stress and antioxidant status in patients. Besides several pharmacological approaches to such disorders [6, 22–26], which could be very promising, nutritional intake represents the most important way of providing an adequate antioxidant status in daily clinical practice.
{"title":"How valid is the concept of antioxidants and cell injury?","authors":"Xavier M Leverve, Cécile Batandier, Eric Fontaine","doi":"10.1159/000067511","DOIUrl":"https://doi.org/10.1159/000067511","url":null,"abstract":"In the struggle for life, humans as every mammal and other living species, have to face two main dangers: (1) the competition against other individuals or other living species, including parasites, bacteria and viruses, and (2) the extreme toxicity of oxygen. The so-called ‘degenerative diseases’, which include the process of aging, are also related to both oxygen toxicity and immune defense against other living species, although some specific genetic characteristics may also be involved. The existence of a family of chemical compounds, called free radicals, has long been recognized as well as their harmful effects on biological molecules [1–5]. But, despite very active research concerning this field of reactive oxygen species (ROS) and extended work in both basic and clinical fields, we are still facing severe morbidity probably related to abnormalities on this pathway [6–12]. Several experimental studies have reported successful attempts to prevent or to counteract the deleterious effects of ROS [13–18] but, aside from important exceptions, the results so far have not produced the degree of evidence we are expecting [6, 19–25]. This relative lack of efficacy of the therapeutic approaches regarding oxidative stress and antioxidant treatments is probably related to the high degree of complexity of the ROS pathway and the antioxidant family, as well as the limitations for investigating oxidative stress and antioxidant status in patients. Besides several pharmacological approaches to such disorders [6, 22–26], which could be very promising, nutritional intake represents the most important way of providing an adequate antioxidant status in daily clinical practice.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"67-81; discussion 81-5"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067511","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
For the purpose of this article, ‘specialized nutrition support’ means using nutrient formulations that have particular adaptations deemed either to alter the inflammatory response or correct a conditional deficiency. The term ‘immunonutrition’ is widely used. For ‘whom’ requires an understanding of the pathological processes patients are undergoing and ‘when’ implies there is some optimal intervention window. However, implicit in both is the need to understand the objectives of the nutritional intervention and the balance between the benefits and risks involved and how these relate to outcome. The focus will be on the survival of critically ill patients and how we can make decisions that are of practical consequence for the general clinician.
{"title":"Specialized nutrition support in the critically ill: for whom and when?","authors":"Richard D Griffiths","doi":"10.1159/000067499","DOIUrl":"https://doi.org/10.1159/000067499","url":null,"abstract":"For the purpose of this article, ‘specialized nutrition support’ means using nutrient formulations that have particular adaptations deemed either to alter the inflammatory response or correct a conditional deficiency. The term ‘immunonutrition’ is widely used. For ‘whom’ requires an understanding of the pathological processes patients are undergoing and ‘when’ implies there is some optimal intervention window. However, implicit in both is the need to understand the objectives of the nutritional intervention and the balance between the benefits and risks involved and how these relate to outcome. The focus will be on the survival of critically ill patients and how we can make decisions that are of practical consequence for the general clinician.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"199-214; discussion 214-7"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067499","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In a 70-kg man, skeletal muscle accounts for 40–50% of the total body mass. A loss of the muscle mass due to the net breakdown of muscle proteins is a common feature of many acute and long-term illnesses. During the initial flow phase, patients with an acute critical illness (multiple trauma and sepsis) lose 1–2 kg muscle mass per day and up to half the muscle mass in periods of 1–2 weeks [1]. Many chronic diseases that impair the function of the lungs, liver, kidney and heart including cancer and AIDS (affecting multiple systems) are attended by a generally slower, gradual loss of muscle mass. A very slow, but in the end substantial, loss of muscle mass is also observed during aging (sarcopenia) [2]. The reduction in muscle mass in all these conditions is the major component of the reduction in lean body mass. Impairments are also seen in muscle function, with a reduction in strength and endurance capacity being most evident [2, 3]. This again limits the ability of the patients to walk and perform normal activities of daily living. In some of the chronic diseases, the reduction in muscle function forms a serious disability or even handicap that dramatically reduces their quality of life [3]. This limitation in physical performance and continuous subjective feelings of fatigue are experienced as the most distressing phenomenon of many acquired chronic diseases [3, 4]. In patients with multiple trauma and sepsis, the loss of muscle mass and functions leads to life-threatening complications (e.g. respiratory failure) and is a major cause of death [5]. In clinical nutrition practice, the traditional approach to try and combat excessive rates of muscle protein breakdown is to give the patient more
{"title":"The primary target of nutritional support: body composition or muscle function?","authors":"Anton J M Wagenmakers","doi":"10.1159/000067500","DOIUrl":"https://doi.org/10.1159/000067500","url":null,"abstract":"In a 70-kg man, skeletal muscle accounts for 40–50% of the total body mass. A loss of the muscle mass due to the net breakdown of muscle proteins is a common feature of many acute and long-term illnesses. During the initial flow phase, patients with an acute critical illness (multiple trauma and sepsis) lose 1–2 kg muscle mass per day and up to half the muscle mass in periods of 1–2 weeks [1]. Many chronic diseases that impair the function of the lungs, liver, kidney and heart including cancer and AIDS (affecting multiple systems) are attended by a generally slower, gradual loss of muscle mass. A very slow, but in the end substantial, loss of muscle mass is also observed during aging (sarcopenia) [2]. The reduction in muscle mass in all these conditions is the major component of the reduction in lean body mass. Impairments are also seen in muscle function, with a reduction in strength and endurance capacity being most evident [2, 3]. This again limits the ability of the patients to walk and perform normal activities of daily living. In some of the chronic diseases, the reduction in muscle function forms a serious disability or even handicap that dramatically reduces their quality of life [3]. This limitation in physical performance and continuous subjective feelings of fatigue are experienced as the most distressing phenomenon of many acquired chronic diseases [3, 4]. In patients with multiple trauma and sepsis, the loss of muscle mass and functions leads to life-threatening complications (e.g. respiratory failure) and is a major cause of death [5]. In clinical nutrition practice, the traditional approach to try and combat excessive rates of muscle protein breakdown is to give the patient more","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"219-34; discussion 234-8"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067500","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mitochondria contain the only extra-nuclear source of DNA. Under evolutionary pressure mitochondrial DNA (mtDNA) has adapted from genomes containing over 1,000 kb containing significant quantities of non-coding DNA to the highly compact mammalian mtDNA. In humans, the mitochondrial genome consists of a small (16.5 kb) double-stranded circular genome constituting less than 1% of the total cellular nucleic acid, yet its role is essential for the survival and function of the mitochondria and hence the cell (Fig. 1). Human mtDNA is a highly efficient structure in terms of expressed DNA containing no introns. It encodes for 37 genes, all of which are involved in synthesising subunits of the respiratory chain complex, either directly as 13 essential polypeptide components, or indirectly as the 22 transfer RNAs and the 2 ribosomal RNAs of the mitochondrial protein synthesis machinery (Fig. 1b). Human cells contain several hundred to many thousand mitochondria, with each mitochondrion having 2–10 copies of mtDNA [1]. Therefore several thousand copies of mtDNA can be present within a single cell. Both mutated and wild-type (normal) mtDNA can co-exist in any proportion, a situation termed heteroplasmy. The level of mutant mtDNA can vary considerably between mitochondria, cells and even tissues within the same individual. The mitochondrial genome mutates at a faster rate than its nuclear counterpart for several reasons. Firstly mitochondria lack nucleotide excision and recombination DNA repair mechanisms [2]. Secondly mtDNA lacks the structurally DNA stabilising proteins known as histones. Thirdly mtDNAs reside and replicate close to the inner mitochondrial membrane and hence are exposed
{"title":"The mitochondrial genome, aging and neurodegenerative disorders.","authors":"D A Cottrell, D M Turnbull","doi":"10.1159/000061856","DOIUrl":"https://doi.org/10.1159/000061856","url":null,"abstract":"Mitochondria contain the only extra-nuclear source of DNA. Under evolutionary pressure mitochondrial DNA (mtDNA) has adapted from genomes containing over 1,000 kb containing significant quantities of non-coding DNA to the highly compact mammalian mtDNA. In humans, the mitochondrial genome consists of a small (16.5 kb) double-stranded circular genome constituting less than 1% of the total cellular nucleic acid, yet its role is essential for the survival and function of the mitochondria and hence the cell (Fig. 1). Human mtDNA is a highly efficient structure in terms of expressed DNA containing no introns. It encodes for 37 genes, all of which are involved in synthesising subunits of the respiratory chain complex, either directly as 13 essential polypeptide components, or indirectly as the 22 transfer RNAs and the 2 ribosomal RNAs of the mitochondrial protein synthesis machinery (Fig. 1b). Human cells contain several hundred to many thousand mitochondria, with each mitochondrion having 2–10 copies of mtDNA [1]. Therefore several thousand copies of mtDNA can be present within a single cell. Both mutated and wild-type (normal) mtDNA can co-exist in any proportion, a situation termed heteroplasmy. The level of mutant mtDNA can vary considerably between mitochondria, cells and even tissues within the same individual. The mitochondrial genome mutates at a faster rate than its nuclear counterpart for several reasons. Firstly mitochondria lack nucleotide excision and recombination DNA repair mechanisms [2]. Secondly mtDNA lacks the structurally DNA stabilising proteins known as histones. Thirdly mtDNAs reside and replicate close to the inner mitochondrial membrane and hence are exposed","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"1-13; discussion 13-6"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061856","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
It is becoming increasingly apparent that the early environment both before birth and in infancy has profound effects on aging and long-term health. This is due to environmental programming whereby influences acting at critical periods of growth and development can permanently change structure and function with lifelong consequences. Many biological characteristics of the adult can be affected including the maximum size attained, the structure and function of different systems and the response to stimuli [1]. Nutrition is the most widely researched cause of environmental programming but other agents include physical factors such as temperature, light and noise.
{"title":"Early life effects on aging.","authors":"Avan Aihie Sayer, Cyrus Cooper","doi":"10.1159/000061857","DOIUrl":"https://doi.org/10.1159/000061857","url":null,"abstract":"It is becoming increasingly apparent that the early environment both before birth and in infancy has profound effects on aging and long-term health. This is due to environmental programming whereby influences acting at critical periods of growth and development can permanently change structure and function with lifelong consequences. Many biological characteristics of the adult can be affected including the maximum size attained, the structure and function of different systems and the response to stimuli [1]. Nutrition is the most widely researched cause of environmental programming but other agents include physical factors such as temperature, light and noise.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"33-44; discussion 44-8"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061857","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Normal aging is often described as a continuous process characterized by a decrease in lean body mass, an increase in fat, and a decrease in total body water. However, it has been pointed out that many older people, especially those aged 75 years and over, may feel healthy in spite of a chronic illness [1]. Thus, both nutrition and hydration may be altered by chronic diseases, infection, as well as by changes in functional status, mobility disorders, confusion, impaired sensory perception, medication effects and difficulties in drinking, swallowing and eating because of the absence of teeth or ill-fitting dentures. For water balance, two factors place the elderly at risk for dehydration: a decreased fluid intake and an increased fluid loss. In the human, the normal pattern of drinking is intermittent while water is continuously lost by various routes so that dehydration occurs. Dehydration is the most common cause of fluid and electrolyte imbalance and is frequently reported in residents, hospitalized and community-dwelling elderly people. It has been stated that one of the greatest threats to the survival of any terrestrial animal, including man, is that of dehydration [2]. In this chapter we review the factors which may disturb fluid balance and predispose elderly to dehydration, the mechanisms involved and the changes in body water compartments. The possible health consequences of dehydration and the new recommendations of fluid intake in elderly populations are also discussed.
{"title":"Age-related changes in hydration.","authors":"Maurice J Arnaud","doi":"10.1159/000061866","DOIUrl":"https://doi.org/10.1159/000061866","url":null,"abstract":"Normal aging is often described as a continuous process characterized by a decrease in lean body mass, an increase in fat, and a decrease in total body water. However, it has been pointed out that many older people, especially those aged 75 years and over, may feel healthy in spite of a chronic illness [1]. Thus, both nutrition and hydration may be altered by chronic diseases, infection, as well as by changes in functional status, mobility disorders, confusion, impaired sensory perception, medication effects and difficulties in drinking, swallowing and eating because of the absence of teeth or ill-fitting dentures. For water balance, two factors place the elderly at risk for dehydration: a decreased fluid intake and an increased fluid loss. In the human, the normal pattern of drinking is intermittent while water is continuously lost by various routes so that dehydration occurs. Dehydration is the most common cause of fluid and electrolyte imbalance and is frequently reported in residents, hospitalized and community-dwelling elderly people. It has been stated that one of the greatest threats to the survival of any terrestrial animal, including man, is that of dehydration [2]. In this chapter we review the factors which may disturb fluid balance and predispose elderly to dehydration, the mechanisms involved and the changes in body water compartments. The possible health consequences of dehydration and the new recommendations of fluid intake in elderly populations are also discussed.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"193-205; discussion 205-6"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061866","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Efficacy of nutritional support can be defined in two main ways: the first relates to the production of new body tissue or the prevention of loss of existing tissue, this could either be growth in a child or repair or maintenance in an adult, and the second relates to how well the various body tissues are functioning. So the issue raised in the title of this chapter can be crystallized into ‘How do trace elements affect the amount and function of body tissues?’
{"title":"Trace elements: contribution to the efficacy of nutritional support.","authors":"Alan Shenkin","doi":"10.1159/000067515","DOIUrl":"https://doi.org/10.1159/000067515","url":null,"abstract":"Efficacy of nutritional support can be defined in two main ways: the first relates to the production of new body tissue or the prevention of loss of existing tissue, this could either be growth in a child or repair or maintenance in an adult, and the second relates to how well the various body tissues are functioning. So the issue raised in the title of this chapter can be crystallized into ‘How do trace elements affect the amount and function of body tissues?’","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"133-45; discussion 145-9"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067515","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The aims of nutritional support administered to acutely ill patients have markedly evolved with time, from supplying huge amounts of calories and nitrogen (in an attempt to abolish the catabolic response and to guarantee weight gain) to providing a limited and balanced intake of macroand micronutrients in order to maintain or restore an adequate composition of different body compartments [1]. Currently, the focus is to improve the function of those organs, which are critical for the survival of acutely ill patients by quickly supplying conditionally essential substrates. Again, priorities have changed from protecting skeletal muscle to maintaining or improving immune defenses, intestinal integrity and barrier function, as well as cardiac work. Still, little attention has so far been paid to protecting other important functions, namely those performed by the endothelium including tissue microperfusion. It has also taken some time to realize that acute phase conditions are associated with marked changes in the priorities for substrate requirements, and that the pharmacological effects of given nutrients could be used to optimize metabolic support and ultimately clinical outcome. This requires an improved knowledge of the metabolic pathways involved in the delivery of active agents, as well as of the action of such agents in key tissues and organs. In this chapter, we will consider ways of optimizing the delivery of essential fatty acids from the n-3 family to the endothelium in an attempt to maintain or optimize its functions.
{"title":"Optimizing intravenous supply of functional lipid components.","authors":"Yvon A Carpentier, Isabelle E Dupont","doi":"10.1159/000067512","DOIUrl":"https://doi.org/10.1159/000067512","url":null,"abstract":"The aims of nutritional support administered to acutely ill patients have markedly evolved with time, from supplying huge amounts of calories and nitrogen (in an attempt to abolish the catabolic response and to guarantee weight gain) to providing a limited and balanced intake of macroand micronutrients in order to maintain or restore an adequate composition of different body compartments [1]. Currently, the focus is to improve the function of those organs, which are critical for the survival of acutely ill patients by quickly supplying conditionally essential substrates. Again, priorities have changed from protecting skeletal muscle to maintaining or improving immune defenses, intestinal integrity and barrier function, as well as cardiac work. Still, little attention has so far been paid to protecting other important functions, namely those performed by the endothelium including tissue microperfusion. It has also taken some time to realize that acute phase conditions are associated with marked changes in the priorities for substrate requirements, and that the pharmacological effects of given nutrients could be used to optimize metabolic support and ultimately clinical outcome. This requires an improved knowledge of the metabolic pathways involved in the delivery of active agents, as well as of the action of such agents in key tissues and organs. In this chapter, we will consider ways of optimizing the delivery of essential fatty acids from the n-3 family to the endothelium in an attempt to maintain or optimize its functions.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"87-98; discussion 98-102"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067512","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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