Cuthbertson

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John M Kinney - One of the best experts on this subject based on the ideXlab platform.

  • sir david Cuthbertson and arvid wretlind pillars of espen
    Clinical Nutrition, 2003
    Co-Authors: John M Kinney
    Abstract:

    repair and maintenance. He felt that the protein breakdown was somehow required to maintain a constant level of metabolism. A corollary seemed to be that any increase in heat production was due to the specific dynamic action arising from the increase in protein breakdown. Cuthbertson became interested in the finding that an injured patient had a decrease in heat production and body temperature followed by a subsequent phase of ‘enhanced vitality’ with an increase in heat production and body temperature. The curves of urinary increase in nitrogen and the basal consumption of oxygen generally moved in parallel. The loss of 7–8% of the body’s content of nitrogen was considered to be too great an amount to come from the local area of injury alone. The loss of body tissue could not be fully accounted for by the loss of muscle substance from the site of injury or even the injured limb. There appeared to be a generalized increase in catabolism. These observations lead Cuthbertson to propose what later became known as ‘the metabolic response to injury’, namely that the presence of an injury produced a systemic response which involved tissues throughout the body. Nitrogen balance has been regarded as the hallmark of this response and remained a source of intense curiosity for Cuthbertson throughout his life. This response to injury was further clarified by Cuthbertson during the early years of World War II, a time of renewed interest in traumatic shock. He introduced the term ‘ebb phase’ for the shock phase, followed by the ‘flow phase’ which was characterized by hypermetabolism, nitrogen loss and the other features of the metabolic response which he had been studying. He observed that the flow phase had many of the features of a generalized inflammatory response, and also observed that it was doubtful whether during the early catabollc phase, any dietary measure could effectively suppress the catabolic destruction of body protein.

Robert R Wolfe - One of the best experts on this subject based on the ideXlab platform.

  • the 2017 sir david p Cuthbertson lecture amino acids and muscle protein metabolism in critical care
    Clinical Nutrition, 2017
    Co-Authors: Robert R Wolfe
    Abstract:

    In this short review, our current understanding of key aspects of the catabolic response are presented in the context of the seminal contributions of Sir David Cuthbertson. Studies have confirmed that an increase in resting energy expenditure occurs in almost all forms of critical illness and injury. However, meeting the resulting increase in caloric requirement is not an insurmountable problem. The primary focus of nutritional support should be the net loss of body protein. Increased intake of dietary protein may ameliorate, but usually will not entirely reverse, the accelerated loss of body protein because of anabolic resistance. Anabolic resistance is due, at least in part, to impaired inward transport efficiency of amino acids from blood into muscle. Simultaneous consumption of excess non-protein calories in an anabolic resistant state provides minimal additional benefit, and may cause potentially adverse effects, including accumulation of liver fat and excess production of carbon dioxide. Because of the limited effectiveness of dietary protein and non-protein caloric intake, it is likely that traditional nutritional support alone will not reverse the net loss of body protein in the catabolic state. The reversal of the catabolic response can only be accomplished in many patients by combining reasonable nutritional support with appropriate metabolic control. Metabolic control may be achieved with the use of a number of pharmacological approaches, including propranolol, insulin or testosterone. Regardless of the approach, ensuring an adequate availability of dietary essential amino acids is necessary for pharmacologic therapy to result in an increased rate of protein synthesis.

Andrew Henley - One of the best experts on this subject based on the ideXlab platform.

  • econometric modelling of uk aggregate investment the role of profits and uncertainty
    Social Science Research Network, 2001
    Co-Authors: Alan Carruth, Andrew Dickerson, Andrew Henley
    Abstract:

    This paper focuses on the determinants of aggregate investment spending in the UK for the industrial and commercial companies (ICC) sector. It complements recent work by Cuthbertson and Gasparro, who study an augmented Tobin's q model of investment in the manufacturing sector. Important focal points of our analysis are a role for real profits (internal funds), which allow firms to combat liquidity constraints when access to capital markets is not perfect, and the impact of irreversibility and uncertainty in determining aggregate investment spending. Earlier work on manufacturing investment by Bean developed a dynamic error-correction specification based on the flexible accelerator model. Following Cuthbertson and Gasparro we use multivariate cointegration techniques to discover a parsimonious dynamic model, which can explain the investment experience of the ICC sector in the 1980s and early 1990s. Our results show that a model based on investment and output alone does not cointegrate, and a short-run dynamic model of these variables suffers from heteroscedasticity. This may be consistent with the idea that increased (uncontrolled for) uncertainty has led to increased volatility in investment. The possibility that movements in the real price of gold reflect uncertainty in financial and other traded commodity markets is explored. Investigation of this more general model indicates that real profits and the real price of gold can enhance the explanation of investment spending by the ICC sector.

  • econometric modelling of uk aggregate investment the role of profits and uncertainty
    Studies in Economics, 1997
    Co-Authors: Alan Carruth, Andrew Dickerson, Andrew Henley
    Abstract:

    This paper focuses on the determinants of aggregate investment spending in the UK for the industrial and commercial company (ICC) sector. It complements recent work by Cuthbertson and Gasparro (1995), who study an augmented Tobin's q model of investment in the manufacturing sector. Important focal points of our analysis are a role for real profits (internal funds), which allow firms to combat liquidity constraints when access to capital markets is not perfect, Chirinko (1987), and the impact of irreversibility and uncertainty in determining aggregate investment spending. Earlier work on manufacturing investment by Bean (1981a) developed a dynamic, error correction specification based on the flexible accelerator model. Following Cuthbertson and Gasparro we use multivariate cointegration techniques to discover a parsimonious dynamic model, which can explain the 1980s and early 1990s investment experience of the ICC sector. Our results show that a model based on investment and output alone does not cointegrate, and a short-run dynamic model of these variables suffers from heteroscedasticity. This may be consistent with the idea that increased (uncontrolled for) uncertainty has led to increased volatility in investment. The possibility that movements in the real price of gold reflect uncertainty in financial and other traded commodity markets is explored. Investigation of this more general model indicates that real profits and the real price of gold can enhance the explanation of investment spending by the ICC sector.

Gema Fruhbeck - One of the best experts on this subject based on the ideXlab platform.

  • the sir david Cuthbertson medal lecture hunting for new pieces to the complex puzzle of obesity
    Proceedings of the Nutrition Society, 2006
    Co-Authors: Gema Fruhbeck
    Abstract:

    Disentangling the neuroendocrine systems that regulate energy homeostasis and adiposity has been a long-standing challenge in pathophysiology, with obesity being an increasingly important public health problem. Adipose tissue is no longer considered a passive bystander in body-weight regulation. It actively secretes a large number of hormones, growth factors, enzymes, cytokines, complement factors and matrix proteins, at the same time as expressing receptors for most of these elements, which influence fuel storage, mobilisation and utilisation at both central and peripheral sites. Thus, an extensive cross talk at a local and systemic level in response to specific external stimuli or metabolic changes underpins the multifunctional characteristics of adipose tissue. In addition to the already-known adipokines, such as IL, TNFalpha, leptin, resistin and adiponectin, more recently attention has been devoted to 'newcomers' to the 'adipose tissue arena', which include aquaporin, caveolin, visfatin, serum amyloid A and vascular endothelial growth factor. While in vitro and in vivo experiments have provided extremely valuable information, the advances in genomics, proteomics and metabolomics are offering a level of information not previously attainable to help unlock the molecular basis of obesity. The potential and power of combining pathophysiological observations with the wealth of information provided by the human genome, knock-out models, transgenesis, DNA microarrays, RNA silencing and other emerging technologies offer a new and unprecedented view of a complex disease, conferring novel insights into old questions by identifying new pieces to the unfinished jigsaw puzzle of obesity.

Nicolaas E P Deutz - One of the best experts on this subject based on the ideXlab platform.

  • the 2007 espen sir david Cuthbertson lecture amino acids between and within organs the glutamate glutamine citrulline arginine pathway
    Clinical Nutrition, 2008
    Co-Authors: Nicolaas E P Deutz
    Abstract:

    Summary In daily practice, the plasma concentration of amino acids is usually viewed as a parameter of production. However, both a high production and/or a reduced disposal capacity can result in an increased plasma concentration. In this presentation, I will discuss my research on interorgan relationships of the amino acids glutamate, glutamine, citrulline and arginine to explain the regulation of the plasma arginine level. The reduced glutamine disposal during liver failure is related to enhanced plasma glutamine level without any change in muscle and gut production or consumption rate. In contrast during sepsis, a small reduction in plasma glutamine is related to a substantially enhanced organ glutamate and glutamine production or consumption rate. These observations are a good example that plasma levels are directly related to production or consumption rates. Because glutamine breakdown in the gut produces citrulline, there is a good relation between the amount of metabolically active gut tissue and gut and whole body citrulline production. Arginine is produces from citrulline in the kidney and a reduced gut glutamine to citrulline conversion during sepsis explains the reduced de novo arginine production that is related to the reduced plasma arginine level. The interorgan route between muscle, gut, liver and kidney of the amino acids glutamate, glutamine, citrulline and arginine is a very good example of how complicated the regulation of plasma amino acid levels can be. However, in-depth research is necessary and will give us important clues to new nutritional strategies.