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Wasting
Kinds of Wasting Terms modified by Wasting Selected AbstractsReduced Nerve Blood Flow In Diabetic Rats Is A Reflection Of Hindlimb Muscle WastingJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Dr Tomlinson We examined the influence of muscle wasting, as a result of streptozotocin-induced diabetes, on sciatic nerve laser Doppler flux (SNLDF), as an index of nerve blood flow, and conduction velocity (NCV). We compared dietary-restricted weight-reduced non-diabetic rats with controls and with diabetic rats and we studied the effects of clenbuterol, an anabolic ,-adrenoceptor agonist, in control and diabetic rats. Dietary restriction reduced the weights of hindlimb muscles,extensor digitorum longus, soleus and gastrocnemius,half as much as did streptozotocin-diabetes and clenbuterol increased muscle weights in control and diabetic rats. This gave a hierarchy of muscle weights in the order,clenbuterol-controls, untreated controls, weight-reduced non-diabetics, clenbuterol-diabetics and untreated diabetics. Diabetes without treatment reduced SNLDF by 51% (p < 0.01); dietary restriction by 25% (p < 0.01) and there were proportional increases associated with clenbuterol treatment. Combined muscle weights regressed closely with SNLDF (r2=0.69; p < 0.001) and, when the latter was expressed relative to muscle weights, a similar value was obtained for all five groups,there were no significant differences. Thus, sciatic nerve blood flow is closely related to hindlimb muscle weight and the effect of diabetes on nerve blood flow may be secondary to muscle wasting. Sciatic/tibialis motor and sensory conduction velocities were also reduced by muscle wasting in the dietary restricted group of non-diabetic rats, but, unlike nerve Doppler flux, it was unaffected by clenbuterol. [source] Neuromuscular Electrical Stimulation As a Possible Means to Prevent Muscle Tissue Wasting in Artificially Ventilated and Sedated Patients in the Intensive Care Unit: A Pilot StudyNEUROMODULATION, Issue 4 2010Raf L.J. Meesen PhD Objective:, The aim of this study was to explore if electrical stimulation could prevent muscle atrophy. Material and Methods:, Patients were hospitalized for postoperative coronary artery bypass graftin, chronic obstructive pulmonary disease, ventilatory failure, or acute cerebro-vascular accident, and were divided into an intervention group or a control group. The intervention group underwent daily 30 minute training with an intermittent neuromuscular electrical stimulation applied to the right quadriceps muscle. Heart rate, respiration rate, systolic and diastolic blood pressure, and oxygen saturation were monitored before, during, and after electrical stimulation. Circumference of both thighs was measured. Results:, The intervention resulted in a significant reduction of muscle atrophy in the stimulated as compared with the non-stimulated limb (p < 0.05), without making any impact on cardiovascular, respiratory and, hemodynamic characteristics. Conclusions:, Muscle atrophy is prevented by intermittent neuromuscular electrical stimulation while this intervention showed no obvious impact on the cardio-respiratory conditions of the patients. [source] Radiographic and Computed Tomographic Studies of Calcium Hydroxylapatite for Treatment of HIV,Associated Facial Lipoatrophy and Correction of Nasolabial FoldsDERMATOLOGIC SURGERY, Issue 2008ALASTAIR CARRUTHERS MD OBJECTIVES This study sought to assess the radiographic appearance produced by calcium hydroxylapatite soft tissue filler (CaHA; Radiesse, BioForm Medical Inc.) following augmentation to correct the nasolabial folds or facial wasting associated with human immunodeficiency virus lipoatrophy. METHODS A total of 58 patients, with either lipoatrophy or pronounced nasolabial folds, were treated with CaHA. Radiographic (X-ray) and computed tomographic (CT) imaging studies were conducted pre- and posttreatment in most patients; the images were sent to an independent laboratory to be analyzed by two evaluators who were board-certified radiologists and blinded to study purpose, product, and patient condition. RESULTS While results for X-ray evaluation showed inconsistencies in visualization of CaHA, CT scans showed consistent visualization in nearly all cases in patients who were imaged immediately after treatment. In addition, the results indicated no obscuration of underlying structures by CaHA and no evidence of CaHA migration. CONCLUSIONS Earlier clinical trials established CaHA as a safe and effective soft tissue filler. This CaHA study shows no overt radiographic safety concerns. CaHA is unlikely to be confused with conventional abnormal and adverse radiographic findings. The product is not always visible on X-ray. Although usually visible on CT scans, its appearance is distinct from surrounding bony structures and does not interfere with normal analysis. In addition, the product does not obscure underlying structures on CT scans. [source] Effects of forest harvesting on the occurrence of landslides and debris flows in steep terrain of central JapanEARTH SURFACE PROCESSES AND LANDFORMS, Issue 6 2008Fumitoshi Imaizumi Abstract Landslides and debris flows associated with forest harvesting can cause much destruction and the influence of the timing of harvesting on these mass wasting processes therefore needs to be assessed in order to protect aquatic ecosystems and develop improved strategies for disaster prevention. We examined the effects of forest harvesting on the frequency of landslides and debris flows in the Sanko catchment (central Japan) using nine aerial photo periods covering 1964 to 2003. These photographs showed a mosaic of different forest ages attributable to the rotational management in this area since 1912. Geology and slope gradient are rather uniformly distributed in the Sanko catchment, facilitating assessment of forest harvesting effects on mass wasting without complication of other factors. Trends of new landslides and debris flows correspond to changes in slope stability explained by root strength decay and recovery; the direct impact of clearcutting on landslide occurrence was greatest in forest stands that were clearcut 1 to 10 yr earlier with progressively lesser impacts continuing up to 25 yr after harvesting. Sediment supply rate from landslides in forests clearcut 1 to 10 yr earlier was about 10-fold higher than in control sites. Total landslide volume in forest stands clearcut 0 to 25 yr earlier was 5·8 × 103 m3 km,2 compared with 1·3 × 103 m3 km,2 in clearcuts >25 yr, indicating a fourfold increase compared with control sites during the period when harvesting affected slope stability. Because landslide scars continue to produce sediment after initial failure, sediment supply from landslides continues for 45 yr in the Sanko catchment. To estimate the effect of forest harvesting and subsequent regeneration on the occurrence of mass wasting in other regions, changes in root strength caused by decay and recovery of roots should be investigated for various species and environmental conditions. Copyright © 2007 John Wiley & Sons, Ltd. [source] A unique case of limb-girdle muscular dystrophy type 2A carrying novel compound heterozygous mutations in the human CAPN3 geneEUROPEAN JOURNAL OF NEUROLOGY, Issue 7 2007E. Matsubara A unique sib pair afflicted by limb girdle muscular dystrophy type 2A (LGMD2A) is described showing a slowly progressive autosomal recessive type of muscular dystrophy with onset in the third and fourth decades. The patients had early asymmetric muscle involvement characterized by prominent biceps brachii atrophy with sparing of the knee extensors. Additional findings included elevation of serum creatine kinase level, myopathic EMG changes and dystrophic type of pathology on muscle biopsy. Asymmetrical wasting of muscles in the extremities exhibited uniform and highly selective CT imaging patterns. RNA and DNA analyses confirmed novel compound heterozygous mutations (R147X/L212F) in the human CAPN3 gene. [source] Flail arm syndrome: a clinical variant of amyotrophic lateral sclerosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 8 2004A. Czaplinski We describe a case of a 65-year old patient diagnosed with amyotrophic lateral sclerosis. The clinical findings, with symmetric, predominantly proximal wasting and weakness of both arms (especially of the infra-, supraspinatus and deltoideus) leading to severe functional disability and contrasting with preserved independent ambulation and sparing of bulbar muscles, were consistent with the proposed criteria of the so-called flail arm syndrome. Based on our case we characterize the clinical features of flail arm syndrome and review the literature. [source] Myotonic dystrophy type 2EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2002J. Finsterer Myotonic dystrophy type 2 (DM2) is a clinically but not genetically heterogeneous, multisystem disorder, that is clinically similar to, but distinct from myotonic dystrophy type 1 (DM1). Initially, different phenotypes of DM2 were described by Ricker (proximal myotonic myopathy, PROMM), Ranum (myotonic dystrophy 2, DM2) and Udd (proximal myotonic dystrophy, PDM). Clinical features these three phenotypes had in common were diffuse, proximal or distal weakness, wasting, myotonia, cataract, cerebral, endocrine and cardiac abnormalities. Initially, the clinical differences between DM1 and PROMM seemed unmistakable, but meanwhile it has become apparent that the clinical differences between these entities are blurring. In 1999, Day et al., Meola et al. and Ricker et al. mapped the mutated gene of all three phenotypes to chromosome 3q. In 2001, the three different phenotypes were found to rely on the same mutation in the ZNF9 gene on chromosome 3q21.3. Although DM2 may be clinically heterogeneous, it is by result of a mutation in a single gene. The mutation responsible for DM2 is a CCTG-repeat expansion of 75,11 000 repeats in intron 1 of the ZNF9 gene on chromosome 3q21.3. Because of the clinical heterogeneity, the diagnosis of DM2 should rely on DNA analysis alone. [source] Ulnar neuropathy at the elbow due to unusual sleep positionEUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2000J. Finsterer Abnormal strain of the ulnar nerve over the sulcus due to an unusual sleep position is a rare cause of ulnar neuropathy at the elbow. A 57-year-old patient with Mandelung's deformity developed progressive weakness in the flexion of fingers 4 and 5 and in finger straddling on the left side. Additionally, there was slight wasting of the left hypothenar and the left interossei muscles. Motor and sensory nerve conduction studies of the left ulnar nerve showed delayed conduction velocities over the left ulnar sulcus. He preferred to sleep in a left lateral position with his head lying on a headrest roll, his left forearm being flexed at 110° and his hand lying either under his cheek or placed on the roll. Only three weeks after the patient had been advised to change his sleep position and to sleep without the headrest roll, weakness markedly improved. This case shows that sleeping in a lateral position with the head on a headrest roll and the hand placed on the roll or under the cheek may cause ulnar neuropathy at the elbow. Change of such a habitual sleep position promptly resolves the symptoms. [source] Myotendinous plasticity to ageing and resistance exercise in humansEXPERIMENTAL PHYSIOLOGY, Issue 3 2006N. D. Reeves The age-related loss of muscle mass known as senile sarcopenia is one of the main determinants of frailty in old age. Molecular, cellular, nutritional and hormonal mechanisms are at the basis of sarcopenia and are responsible for a progressive deterioration in skeletal muscle size and function. Both at single-fibre and at whole-muscle level, the loss of force exceeds that predicted by the decrease in muscle size. For single fibres, the loss of intrinsic force is mostly due to a loss in myofibrillar protein content. For whole muscle, in addition to changes in neural drive, alterations in muscle architecture and in tendon mechanical properties, exemplified by a reduction in tendon stiffness, have recently been shown to contribute to this phenomenon. Resistance training can, however, cause substantial gains in muscle mass and strength and provides a protective effect against several of the cellular and molecular changes associated with muscle wasting and weakness. In old age, not only muscles but also tendons are highly responsive to training, since an increase in tendon stiffness has been observed after a period of increased loading. Many of the myotendinous factors characterizing ageing can be at least partly reversed by resistance training. [source] Cardiac ankyrin repeat protein is a marker of skeletal muscle pathological remodellingFEBS JOURNAL, Issue 3 2009Lydie Laure In an attempt to identify potential therapeutic targets for the correction of muscle wasting, the gene expression of several pivotal proteins involved in protein metabolism was investigated in experimental atrophy induced by transient or definitive denervation, as well as in four animal models of muscular dystrophies (deficient for calpain 3, dysferlin, ,-sarcoglycan and dystrophin, respectively). The results showed that: (a) the components of the ubiquitin,proteasome pathway are upregulated during the very early phases of atrophy but do not greatly increase in the muscular dystrophy models; (b) forkhead box protein O1 mRNA expression is augmented in the muscles of a limb girdle muscular dystrophy 2A murine model; and (c) the expression of cardiac ankyrin repeat protein (CARP), a regulator of transcription factors, appears to be persistently upregulated in every condition, suggesting that CARP could be a hub protein participating in common pathological molecular pathway(s). Interestingly, the mRNA level of a cell cycle inhibitor known to be upregulated by CARP in other tissues, p21WAF1/CIP1, is consistently increased whenever CARP is upregulated. CARP overexpression in muscle fibres fails to affect their calibre, indicating that CARP per se cannot initiate atrophy. However, a switch towards fast-twitch fibres is observed, suggesting that CARP plays a role in skeletal muscle plasticity. The observation that p21WAF1/CIP1 is upregulated, put in perspective with the effects of CARP on the fibre type, fits well with the idea that the mechanisms at stake might be required to oppose muscle remodelling in skeletal muscle. [source] The kidney disease wasting: Inflammation, oxidative stress, and diet-gene interactionHEMODIALYSIS INTERNATIONAL, Issue 4 2006Kamyar KALANTAR-ZADEH Abstract The 350,000 maintenance hemodialysis (MHD) patients in the United States have an unacceptably high mortality rate of >20%/year. Almost half of all deaths are assumed to be cardiovascular. Markers of kidney disease wasting (KDW) such as hypoalbuminemia, anorexia, body weight and fat loss, rather than traditional cardiovascular risk factors, appear to be the strongest predictors of early death in these patients. The KDW is closely related to oxidative stress (SOX). Such SOX markers as serum myeloperoxidase are associated with pro-inflammatory cytokines and poor survival in MHD patients. Identifying the conditions that modulate the KDW/SOX-axis may be the key to improving outcomes in MHD patients. Dysfunctional lipoproteins such as a higher ratio of the high-density lipoprotein inflammatory index (HII) may engender or aggravate the KDW, whereas functionally intact or larger lipoprotein pools, as in hypercholesterolemia and obesity, may mitigate the KDW in MHD patients. Hence, a reverse epidemiology or "bad-gone-good" phenomenon may be observed. Diet and gene and their complex interaction may lead to higher proportions of pro-inflammatory or oxidative lipoproteins such as HII, resulting in the aggravation of the SOX and inflammatory processes, endothelial dysfunction, and subsequent atherosclerotic cardiovascular disease and death in MHD patients. Understanding the factors that modulate the KDW/SOX complex and their associations with genetic polymorphism, nutrition, and outcomes in MHD patients may lead to developing more effective strategies to improve outcomes in this and the 20 to 30 million Americans with chronic disease states such as individuals with chronic heart failure, advanced age, malignancies, AIDS, or cachexia. [source] Kennedy's disease: pathogenesis and clinical approachesINTERNAL MEDICINE JOURNAL, Issue 5 2004K. J. Greenland Abstract Kennedy's disease, also known as spinal and bulbar muscular atrophy, is a progressive degenerative condition affecting lower motor neurons. It is one of nine neurodegenerative disorders caused by a polyglutamine repeat expansion. Affecting only men, Kennedy's disease is the only one of these conditions that follows an X-linked mode of inheritance. The causative protein in Kennedy's disease, with a polyglutamine expansion residing in the first N-terminal domain, is the androgen receptor. Research in this field has made significant advances in recent years, and with the increased understanding of pathogenic mechanisms, feasible approaches to treatments are being investigated. In Kennedy's disease research, the most significant issue to emerge recently is the role of androgens in exacerbating the disease process. On the basis of animal experiments, a viable hypothesis is that higher circulating levels of androgens in men could trigger the degeneration of motor neurons causing this disease, and that lower levels in heterozygous and homozygous women are protective. This is a major issue, as treatment of individuals affected by Kennedy's disease with testosterone has been considered a reasonable therapy by some neurologists. The rationale behind this approach relates to the fact that Kennedy's disease is accompanied by mild androgen insensitivity. It was therefore believed that treatment with high doses of testosterone might compensate for this loss of androgen action, with the added benefit of preventing muscle wasting. The current review provides an overview of recent advances in the field of Kennedy's disease research, including approaches to treatment. (Intern Med J 2004; 34: 279,286) [source] A concept analysis of malnutrition in the elderlyJOURNAL OF ADVANCED NURSING, Issue 1 2001Cheryl Chia-Hui Chen RN MSN GNP A concept analysis of malnutrition in the elderly Purpose.,Malnutrition is a frequent and serious problem in the elderly. Today there is no doubt that malnutrition contributes significantly to morbidity and mortality in the elderly. Unfortunately, the concept of malnutrition in the elderly is poorly defined. The purpose of this paper is to clarify the meaning of malnutrition in the elderly and to develop the theoretical underpinnings, thereby facilitating communication regarding the phenomenon and enhancing research efforts. Scope, sources used.,Critical review of literature is the approach used to systematically build and develop the theoretical propositions. Conventional search engines such as Medline, PsyINFO, and CINAHL were used. The bibliography of obtained articles was also reviewed and additional articles identified. Key wards used for searching included malnutrition, geriatric nutrition, nutritional status, nutrition assessment, elderly, ageing, and weight loss. Conclusions.,The definition of malnutrition in the elderly is defined as following: faulty or inadequate nutritional status; undernourishment characterized by insufficient dietary intake, poor appetite, muscle wasting and weight loss. In the elderly, malnutrition is an ominous sign. Without intervention, it presents as a downward trajectory leading to poor health and decreased quality of life. Malnutrition in the elderly is a multidimensional concept encompassing physical and psychological elements. It is precipitated by loss, dependency, loneliness and chronic illness and potentially impacts morbidity, mortality and quality of life. [source] Therapeutic Effects of Anti-FGF23 Antibodies in Hypophosphatemic Rickets/Osteomalacia,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 11 2009Yukiko Aono Abstract X-linked hypophosphatemia (XLH), characterized by renal phosphate wasting, is the most common cause of vitamin D-resistant rickets. It has been postulated that some phosphaturic factor plays a causative role in XLH and its murine homolog, the Hyp mouse. Fibroblast growth factor 23 (FGF23) is a physiological phosphaturic factor; its circulatory level is known to be high in most patients with XLH and Hyp mice, suggesting its pathophysiological role in this disease. To test this hypothesis, we treated Hyp mice with anti-FGF23 antibodies to inhibit endogenous FGF23 action. A single injection of the antibodies corrected the hypophosphatemia and inappropriately normal serum 1,25-dihydroxyvitamin D. These effects were accompanied by increased expressions of type IIa sodium-phosphate cotransporter and 25-hydroxyvitamin-D-1,-hydroxylase and a suppressed expression of 24-hydroxylase in the kidney. Repeated injections during the growth period ameliorated the rachitic bone phenotypes typically observed in Hyp mice, such as impaired longitudinal elongation, defective mineralization, and abnormal cartilage development. Thus, these results indicate that excess actions of FGF23 underlie hypophosphatemic rickets in Hyp mice and suggest a novel therapeutic potential of the FGF23 antibodies for XLH. [source] Sarcopenia is not due to lack of regenerative drive in senescent skeletal muscleAGING CELL, Issue 2 2005Erik Edström Summary Sarcopenia, loss of skeletal muscle mass, is a hallmark of aging commonly attributed to a decreased capacity to maintain muscle tissue in senescence, yet the mechanism behind the muscle wasting remains unresolved. To address these issues we have explored a rodent model of sarcopenia and age-related sensorimotor impairment, allowing us to discriminate between successfully and unsuccessfully aged cohort members. Immunohistochemistry and staining of cell nuclei revealed that senescent muscle has an increased density of cell nuclei, occurrence of aberrant fibers and fibers expressing embryonic myosin. Using real-time PCR we extend the findings of increased myogenic regulatory factor mRNA to show that very high levels are found in unsuccessfully aged cohort members. This pattern is also reflected in the number of embryonic myosin-positive fibers, which increase with the degree of sarcopenia. In addition, we confirm that there is no local down-regulation of IGF-I and IGF-IR mRNA in aged muscle tissue; on the contrary, the most sarcopenic individuals showed significantly higher local expression of IGF-I mRNA. Combined, our results show that the initial drive to regenerate myofibers is most marked in cases with the most advanced loss of muscle mass, a pattern that may have its origin in differences in the rate of tissue deterioration and/or that regenerating myofibers in these cases fail to mature into functional fibers. Importantly, the genetic background is a determinant of the pace of progression of sarcopenia. [source] Malnutrition, a Rare Form of Child Abuse: Diagnostic CriteriaJOURNAL OF FORENSIC SCIENCES, Issue 3 2006Marie-Dominique Piercecchi-Marti M.D., Ph.D. ABSTRACT: Infantile malnutrition is often difficult to diagnose as it is rarely observed in industrialized countries. It may be associated with physical violence or occur in isolation. The essential clinical sign is height and weight retardation, but malnutrition also causes a variety of internal and bone lesions, which lead to neuropsychological sequelae and death. We report a rare case of death by malnutrition in a female child aged 6½ months. The infant presented height and weight growth retardation and internal lesions related to prolonged protein,energy malnutrition (fat and muscle wasting, thymic atrophy, liver steatosis) resulting in a picture of marasmus or kwashiorkor. We detail the positive and negative criteria that established the diagnosis of abuse, whereas the parents had claimed a simple dietary error. [source] A review of nutrition in Duchenne muscular dystrophyJOURNAL OF HUMAN NUTRITION & DIETETICS, Issue 5 2009Z. E. Davidson Abstract Duchenne muscular dystrophy (DMD) is a recessive X linked genetic disorder characterised by progressive muscle weakness and reduced muscle tone. Affecting only boys, it limits life expectancy to approximately 20 years. A literature review was conducted using MEDLINE and the Cochrane Library, employing the term ,Duchenne muscular dystrophy'. A total of 1491 articles in English were recovered. These papers were searched thematically under the headings: body composition (n = 10), energy expenditure (n = 10), nutrition (n = 6), corticosteroid therapy (n = 55) and gene therapy (n = 199). Key dietetic practice points were identified relevant to nutritional management. Papers supporting these key themes were assigned a level of evidence and grade of recommendation. There is limited high-quality evidence to guide the nutritional management of boys with DMD. Currently, the majority of evidence is based on expert opinion and clinical expertise. Delayed growth, short stature, muscle wasting and increased fat mass are characteristics of DMD and impact on nutritional status and energy requirements. The early introduction of steroids has altered the natural history of the disease, but can exacerbate weight gain in a population already susceptible to obesity. Prior to commencing steroids, anticipatory guidance for weight management should be provided. Malnutrition is a feature of end stage disease requiring a multidisciplinary approach, such as texture modification and supplemental feeding. Micronutrient requirements are yet to be determined but, as a result of corticosteroid treatment, vitamin D and calcium should be supplemented. Some evidence exists supporting supplementation with creatine monohydrate to improve muscle strength. More research is needed to provide a higher quality of evidence for dietitians working within this area. [source] A service evaluation to determine the effectiveness of current dietary advice in treating human immunodeficiency virus-associated weight loss and to highlight potential service improvementsJOURNAL OF HUMAN NUTRITION & DIETETICS, Issue 4 2008C.A. Hunt Background:, Weight loss and muscle wasting are experienced by many patients with human immunodeficiency virus (HIV) (Grinspoon et al., 2003). Malnutrition is an important predicator of morbidity and mortality; people who are malnourished who received antiretroviral treatment are six times more likely to die than those who are adequately nourished (Paton et al., 2006). The physical manifestations of muscle wasting can have significant psychosocial implications for HIV patients (Power et al., 2003; Sattler, 2003). The aim of this study to evaluate provision of dietetic care to patients referred for acute weight loss advice and identify areas for potential service improvement. Methods:, The data were gathered from the departmental dietetic activity statistics in 2007, diagnosis code ,HIV , acute weight loss'. Fifty-nine cards were located and baseline weight, height and body mass index (BMI) were recorded (two female, 57 male). Qualitative data on dietetic intervention were extracted from record cards , little and often eating approach, food fortification (FF), high energy high protein oral nutritional supplement (ONS) prescribed. Data were collected on body image, exercise and weight at follow-up visits during 2007. Results:, Forty-three percent of the patients referred for ,HIV-acute weight loss' were lost to follow-up. Forty-seven percent of the remaining patients had a BMI <20 kg m,2. Following their initial dietetic intervention, 81% of these patients had gained weight at the first follow-up. All had received nutritional counselling on little and often eating approach and FF; 75% had ONS prescribed. Average weight gain with nutritional counselling alone was 1.3 kg (2.1 kg) and for nutritional counselling plus supplementation was 2.1 kg (1.8 kg). This represented 2.5% (4.1%) and 3.9% (3.4%) weight gain, respectively. Discussion:, This evaluation has highlighted that patient follow-up frequency is an area for service improvement. Fifty-three per cent of patients (excluding those lost to follow up) had a BMI ,20 kg m,2 and were inaccurately recorded in the statistics as being referred for ,HIV-acute weight loss'. Fifty-two percent of these patients reported lipodystrophy and body image concerns, similar to findings of other studies. Fifty-six percent reported weight improvements following dietetic consultation. Body image is a frequent referral trigger, therefore improvements should be made to identify and treat patients with body shape issues. Conclusions:, Dietitians are effective at achieving weight gain in HIV positive patients with a BMI <20 kg m,2 using nutritional counselling methods with or without oral nutritional supplementation; these patients experienced a 3.3% weight gain. Strategies need to be implemented to reduce the number of patients lost to follow-up, as weight loss is a key morbidity and mortality indicator in HIV. References, Grinspoon, S. & Mulligan, K. (2003) Weight loss and wasting in patients infected with HIV. Clin. Infect. Dis.36 (Suppl. 2): 69,78. Nerad, J., Romeyn, M., Silverman, E., Allen-Reid, J., Dieterich, D., Merchant, J., Pelletier, V., Tinnerello, D. & Fenton, M. (2003) General nutritional management in patients infected with HIV. Clin. Infect. Dis.36 (Suppl. 2): 52,62. Ockenga, J., Grimble, R., Jonkers-Schuitema, C., Macallan, D., Melchior, J.C., Sauerwein, H.P., Schwenk, A. & Suttmann, U. (2006) ESPEN guidelines on enteral nutrition: wasting in HIV and other chronic infectious diseases. Clin. Nutr.25, 319,329. Paton, N.I., Sangeetha, S., Earnest, A. & Bellamy, R. (2006) The impact of malnutrition on survival and the CD4 count response in HIV-infected patients starting antiretroviral therapy. HIV Med.7, 232,330. Power, R., Tate, H.L., McGill, S.M. & Taylor, C. (2003) A qualitative study of the psychosocial implications of lipodystrophy syndrome on HIV positive individuals. Sex. Transm. Infect.79, 137,141. Sattler, F. (2003) Body habitus changes related to lipodystrophy. Clin. Infect. Dis36 (Suppl. 2): 84,90. [source] Clinical and biochemical implications of low thyroid hormone levels (total and free forms) in euthyroid patients with chronic kidney diseaseJOURNAL OF INTERNAL MEDICINE, Issue 6 2007J. J. Carrero Abstract., Carrero JJ, Qureshi AR, Axelsson J, Yilmaz MI, Rehnmark S, Witt MR, Bárány P, Heimbürger O, Suliman ME, Alvestrand A, Lindholm B, Stenvinkel P (Karolinska Institutet, Stockholm; and Karo Bio AB, Novum, Huddinge; Sweden). Clinical and biochemical implications of low thyroid hormone levels (total and free forms) in euthyroid patients with chronic kidney disease. J Intern Med 2007; 262: 690,701. Objectives., In this study, we explore the associations of decreased thyroid hormone levels with inflammation, wasting and survival in biochemically euthyroid patients with end-stage renal disease (ESRD). Design., After exclusion of 23 patients with thyroid-stimulating hormone (TSH) values outside the normal range (0.1,4.5 mIU L,1), 187 clinically and biochemically euthyroid incident ESRD stage 5 patients starting dialysis were followed for a median of 20 (range 1,60) months. Measurements of total and free forms of thyroid hormones, s-albumin, hs-CRP, interleukin (IL)-6, vascular adhesion molecule (VCAM)-1 and insulin-like growth factor 1 (IGF-1) were performed at baseline. Results., In this population, 17 out of 210 patients (8%) were defined as subclinically hypothyroid. Multivariate analysis, according to receiver operating characteristic (ROC) curves, showed that mortality was best predicted by total triiodothyronine (T3). When using the cut-off levels derived from ROC, low T3 levels were associated with increased inflammation (higher hs-CRP, IL-6 and VCAM-1) and lower concentration of both s-albumin and IGF-1. Finally, low T3 but not low free triiodothyronine was associated with worse all-cause (Likelihood ratio = 45.4; P < 0.0001) and cardiovascular mortality (Likelihood ratio = 47.8; P < 0.0001) after adjustment for confounding factors. Conclusion., This study showed that low T3 levels are independent predictors of all-cause and also cardiovascular disease mortality in biochemically euthyroid patients, perhaps due to an intimate association with inflammation. Based on these results, the use of T3 levels in studies assessing the relationship between thyroid dysfunction and mortality risk is recommended. [source] Myotonic dystrophy 1 in the nervous system: From the clinic to molecular mechanismsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2008Mario Bermúdez de León Abstract Myotonic dystrophy type 1 (DM1) is a dominant neuromuscular disorder caused by the expansion of trinucleotide CTG repeats in the 3,-untranslated region (3,-UTR) of the DMPK gene. Prominent features of classical DM1 are muscle wasting and myotonia, whereas mental retardation is distinctive for congenital DM1. The main nervous system symptoms of DM1 are cognitive impairment, neuroendocrine dysfunction, and personality and behavior abnormalities. It is thought that expansion of CTG repeats causes DM1 pathology through different molecular mechanisms; however, a growing body of evidence indicates that an RNA gain-of-function mechanism plays a major role in the disease development. At the skeletal muscle level, three main molecular events can be distinguished in this model: 1) formation of nuclear foci that are composed at least of mutant DMPK mRNA and recruited RNA-binding proteins, such as splicing regulators and transcription factors; 2) disturbance of alternative splicing of specific genes; and 3) impairment of cell differentiation. Contrasting with the substantial advances in understanding DM1 muscle pathology, the molecular basis of DM1 in the nervous system has just started to be revealed. This review focuses in the DM1 nervous system pathology and provides an overview of the genetic and molecular studies analyzing the effects of the DMPK gene CUG expanded repeats on cell function in neuronal systems. A comparison between the molecular mechanisms of DM1 in the skeletal muscle and those identified in DM1 nervous system models is provided. Finally, future directions in the study of DM1 in the nervous system are discussed. © 2007 Wiley-Liss, Inc. [source] Critical appraisal of the management of severe malnutrition: 1.JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 10 2006Epidemiology, treatment guidelines Abstract: Hospital case-fatality rates for severe malnutrition in the developing world remain high, particularly in Africa where they have not changed much over recent decades. In an effort to improve case management, WHO has developed treatment guidelines. The aim of this review is to critically appraise the evidence for the guidelines and review important recent advances in the management of severe malnutrition. We conclude that not only is the evidence base deficient, but also the external generalisability of even good-quality studies is seriously compromised by the great variability in clinical practice between regions and types of health facilities in the developing world, which is much greater than between developed countries. The diagnosis of severe wasting is complicated by the dramatic change in reference standards (from CDC/WHO 1978 to CDC 2000 in EpiNut) and also by difficulties in accurate measurement of length. Although following treatment guidelines has resulted in improved outcomes, there is evidence against the statement that case-fatality rates (particularly in African hospitals) can be reduced below 5% and that higher rates are proof of poor practice, because there is wide variation in severity of illness factors. The practice of prolonged hospital treatment of severe malnutrition until wasting and/or oedema has resolved is being replaced by shorter hospital stays combined with outpatient or community follow-up because of advances in dietary management outside of hospital. [source] Inherited myopathy of great DanesJOURNAL OF SMALL ANIMAL PRACTICE, Issue 5 2006A. Lujan Feliu-Pascual A hereditary, non-inflammatory myopathy occurring in young great Danes with distinctive histological features in muscle biopsy specimens is reviewed. Onset of clinical signs is usually before one year of age and both sexes are affected. Clinical signs are characterised by exercise intolerance, muscle wasting, and an exercise-induced tremor. Although most affected dogs have a severe form of the disease, occasional dogs may have a less pronounced form and survive into adulthood with an acceptable quality of life. Litters containing affected puppies are born to clinically unaffected parents, and an autosomal recessive pattern of inheritance is likely. All recorded cases have had fawn or brindle coat coloration. Elevated serum creatinine kinase concentrations and spontaneous electrical activity in skeletal muscles are frequently found. While originally reported (Targett and others 1994) as a central core myopathy in this breed, the histochemical characteristics of the distinct cytoarchitectural structures differ from those of the well-characterised central core myopathy in human beings. In fact, these structures differ from any known myopathy in human beings and likely represents a unique non-inflammatory myopathy affecting dogs. Until this myopathy is characterised further, the name inherited myopathy in great Danes is suggested. [source] Homozygous Defects In Lmna, Encoding Lamin A/C Nuclear-Envelope Proteins, Cause Autosomal Recessive Axonal Neuropathy In Human (Charcot-Marie-Tooth Disorder Type 2) And MouseJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2002A De Sandre-Giovannoli The Charcot-Marie-Tooth (CMT) disorders comprise a group of clinically and genetically heterogeneous hereditary motor and sensory neuropathies, which are mainly characterized by muscle weakness and wasting, foot deformities, and electrophysiological, as well as histological, changes. A subtype, CMT2, is defined by a slight or absent reduction of nerve-conduction velocities together with the loss of large myelinated fibers and axonal degeneration. CMT2 phenotypes are also characterized by a large genetic heterogeneity, although only two genes-NF-L and KIF1Bbeta-have been identified to date. Homozygosity mapping in inbred Algerian families with autosomal recessive CMT2 (AR-CMT2) provided evidence of linkage to chromosome 1q21.2-q21.3 in two families (Z(max) = 4.14). All patients shared a common homozygous ancestral haplotype that was suggestive of a founder mutation as the cause of the phenotype. A unique homozygous mutation in LMNA (which encodes lamin A/C, a component of the nuclear envelope) was identified in all affected members and in additional patients with CMT2 from a third, unrelated family. Ultrastructural explor- ation of sciatic nerves of LMNA null (i.e., ,/,) mice was performed and revealed a strong reduction of axon density, axonal enlargement, and the presence of nonmyelinated axons, all of which were highly similar to the phenotypes of human peripheral axonopathies. The finding of site-specific amino acid substitutions in limb-girdle muscular dystrophy type 1B, autosomal dominant Emery-Dreifuss muscular dystrophy, dilated cardiomyopathy type 1A, autosomal dominant partial lipodystrophy, and, now, AR-CMT2 suggests the existence of distinct functional domains in lamin A/C that are essential for the maintenance and integrity of different cell lineages. To our knowledge, this report constitutes the first evidence of the recessive inheritance of a mutation that causes CMT2; additionally, we suggest that mutations in LMNA may also be the cause of the genetically overlapping disorder CMT2B1. [source] AUTOMIC FAILURE AND NORMAL PRESSURE HYDROCEPHALUS IN A PATIENT WITH CHRONIC DEMYELINATING INFLAMMATORY NEUROPATHYJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002M. Laurà A 75-year-old man with HCV hepatitis developed at the age of 70 presented with rest and action tremor localized at both hands and progressive cognitive impairment with memory loss. Four years later he begun to complain of progressive fatigue, occasional falls, numbness at the extremities and orthostatic hypotension. One month after admission, he rapidly worsened with inability to walk, mainly because of autonomic failure. Neurological examination revealed gait disturbances, including a wide base of support and short stride, slurred speech, reduction of upward gaze, rest and action tremor at both hands, intrinsic hand muscle and anterior tibialis muscle wasting and weakness on both sides, absent deep tendon reflexes, loss of vibration sense at lower limbs, and bilateral pes cavus. Routine laboratory studies, autoantibodies, thyroid function, neoplastic markers and immunoelectrophoresis were normal. Cryoglobulins were absent, whereas CSF protein content was increased (142 mg/dl). Autonomic nervous system investigation detected severe orthostatic hypotension. Nerve conduction studies showed absent sensory potentials and a marked reduction of compound motor action potential amplitudes and of motor conduction velocities. A sural nerve biopsy revealed remarkable onion bulb-like changes, endoneurial and perivascular infiltrations of inflammatory cells. Psychometric tests showed mild cognitive impairment. Brain MRI was consistent with normotensive hydrocephalus. The findings indicated the presence of chronic inflammatory demyelinating polyneuropathy, autonomic nervous system involvement and normal pressure hydrocephalus. A condition of multiple system atrophy (MSA) might be taken into account, even if somatic peripheral nerve involvement may rarely occur in MSA. Moreover the normal pressure hydrocephalus could be due to the high protein content in CSF (Fukatsu R et al., 1997). [source] Reduced Nerve Blood Flow In Diabetic Rats Is A Reflection Of Hindlimb Muscle WastingJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Dr Tomlinson We examined the influence of muscle wasting, as a result of streptozotocin-induced diabetes, on sciatic nerve laser Doppler flux (SNLDF), as an index of nerve blood flow, and conduction velocity (NCV). We compared dietary-restricted weight-reduced non-diabetic rats with controls and with diabetic rats and we studied the effects of clenbuterol, an anabolic ,-adrenoceptor agonist, in control and diabetic rats. Dietary restriction reduced the weights of hindlimb muscles,extensor digitorum longus, soleus and gastrocnemius,half as much as did streptozotocin-diabetes and clenbuterol increased muscle weights in control and diabetic rats. This gave a hierarchy of muscle weights in the order,clenbuterol-controls, untreated controls, weight-reduced non-diabetics, clenbuterol-diabetics and untreated diabetics. Diabetes without treatment reduced SNLDF by 51% (p < 0.01); dietary restriction by 25% (p < 0.01) and there were proportional increases associated with clenbuterol treatment. Combined muscle weights regressed closely with SNLDF (r2=0.69; p < 0.001) and, when the latter was expressed relative to muscle weights, a similar value was obtained for all five groups,there were no significant differences. Thus, sciatic nerve blood flow is closely related to hindlimb muscle weight and the effect of diabetes on nerve blood flow may be secondary to muscle wasting. Sciatic/tibialis motor and sensory conduction velocities were also reduced by muscle wasting in the dietary restricted group of non-diabetic rats, but, unlike nerve Doppler flux, it was unaffected by clenbuterol. [source] Tuberculosis Caused by Mycobacterium microti in South American CamelidsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2009P. Zanolari Background: Infection with Mycobacterium microti can cause chronic disease in animals and threaten human health through its zoonotic potential. Objective: To describe clinical findings, diagnostic investigations, necropsy, and epidemiology results in South American camelids (SAC) infected with M. microti, member of the Mycobacterium tuberculosis complex. Animals: Eleven SAC with tuberculous lesions. Methods: Description of 10 llamas and 1 alpaca, aged 4,18 years, from 6 herds with a history of wasting and weakness admitted to the Vetsuisse-Faculty of Berne over 8 years. Results: Clinical signs included weight loss, recumbency, and anorexia in late stages of the disease. Respiratory problems were seen in 6 animals of 11. No consistent hematologic abnormalities were identified. Suspect animals were examined in detail by abdominal ultrasonography and thoracic radiology. Abnormal findings such as enlarged mediastinal, mesenteric, or hepatic lymph nodes were seen only in animals with advanced disease. Single comparative intradermal tuberculin test with bovine protein purified derivate (PPD) and avian PPD was negative in all animals. At necropsy, typical tuberculous lesions were found, and confirmed by bacteriological smear and culture, molecular methods, or both. Conclusions and Clinical Importance: Infection caused by M. microti should be considered a differential diagnosis in chronic debilitating disease with or without respiratory signs in SAC. Antemortem confirmation of the diagnosis remains challenging at any stage of infection. Because cases of M. microti infection have been reported in immunocompromized human patients, the zoonotic potential of the organism should be kept in mind when dealing with this disease in SAC. [source] Muscular Dystrophy in female DogsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 3 2001G. Diane Shelton The most common form of muscular dystrophy in dogs and humans is caused by mutations in the dystrophin gene. The dystrophin gene is located on the X chromosome, and, therefore, disease-causing mutations in dystrophin occur most often in males. Therefore, females with dystrophin deficiency or other forms of muscular dystrophy may be undiagnosed or misdiagnosed. Immunohisto-chemistry was used to analyze dystrophin and a number of other muscle proteins associated with muscular dystrophy in humans, including sarcoglycans and laminin ,2, in muscle biopsy specimens from 5 female dogs with pathologic changes consistent with muscular dystrophy. The female dogs were presented with a variety of clinical signs including generalized weakness, muscle wasting, tremors, exercise intolerance, gait abnormalities, and limb deformity. Serum creatine kinase activity was variably high. One dog had no detectable dystrophin in the muscle; another was mosaic, with some fibers normal and others partly dystrophin-deficient. A 3rd dog had normal dystrophin but no detectable laminin ,2. Two dogs could not be classified. This study demonstrates the occurrence of dystrophin- and laminin ,2-associated muscular dystrophy and the difficulty in clinical diagnosis of these disorders in female dogs. [source] Altered mRNA splicing of dystrophin in type 1 myotonic dystrophyMUSCLE AND NERVE, Issue 2 2007Masayuki Nakamori MD Abstract Myotonic dystrophy type1 (DM1) is a multisystemic disorder caused by a CTG repeat expansion in the DMPK gene. Aberrant mRNA splicing of several genes has been reported to contribute to some of the symptoms, including myotonia and insulin resistance, but the cause of muscle wasting is unknown. Dystrophin is a cytoskeletal protein that is required for structural stability and signaling at the sarcolemma and has several spliced isoforms. We investigated the alternative splicing of dystrophin in skeletal and cardiac muscle of DM1 patients by using reverse transcriptase,polymerase chain reaction and found that dystrophin isoforms lacking exon 71 or 78, which is suggested to encode an important region for protein binding and hydrophobicity, were significantly increased. We suggest that the aberrantly spliced dystrophin is responsible for the muscle wasting in DM1. Muscle Nerve, 2007 [source] Oxidative stress, chronic disease, and muscle wastingMUSCLE AND NERVE, Issue 4 2007Jennifer S. Moylan PhD Abstract Underlying the pathogenesis of chronic disease is the state of oxidative stress. Oxidative stress is an imbalance in oxidant and antioxidant levels. If an overproduction of oxidants overwhelms the antioxidant defenses, oxidative damage of cells, tissues, and organs ensues. In some cases, oxidative stress is assigned a causal role in disease pathogenesis, whereas in others the link is less certain. Along with underlying oxidative stress, chronic disease is often accompanied by muscle wasting. It has been hypothesized that catabolic programs leading to muscle wasting are mediated by oxidative stress. In cases where disease is localized to the muscle, this concept is easy to appreciate. Transmission of oxidative stress from diseased remote organs to skeletal muscle is thought to be mediated by humoral factors such as inflammatory cytokines. This review examines the relationship between oxidative stress, chronic disease, and muscle wasting, and the mechanisms by which oxidative stress acts as a catabolic signal. Muscle Nerve, 2007 [source] Effect of transcranial magnetic stimulation on voluntary activation in patients with quadriceps weaknessMUSCLE AND NERVE, Issue 2 2005Dietmar Urbach MD Abstract Joint disease causes weakness and wasting of adjacent muscles, in part because of inability to fully activate these muscles voluntarily. Previous findings suggest that transcranial magnetic stimulation (TMS) paired with muscle contractions enhances maximal voluntary contraction force (MVC) in healthy subjects by improving voluntary activation (VA). The aim of the present study was to evaluate whether such an effect is also present in subjects suffering from diminished muscle force due to decreased VA. Three single TMS over resting motor threshold were applied in 10 patients with a mean age of 62 years after total-knee arthroplasty either during MVC or during muscle relaxation (control experiment) in a blinded randomized crossover study. MVC and VA were determined using a twitch-interpolation technique at 1, 15, 30, and 60 min after stimulation. There was a significant effect of TMS on MVC if applied in synchrony with muscle contraction, and this persisted for at least 60 min beyond stimulation. In patients suffering from joint disease, TMS might make physiotherapy more effective. 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