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Artykuły w czasopismach na temat "Metabolic disorders"

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Wikiera, Beata, Agnieszka Zubkiewicz-Kucharska, Julita Nocoń-Bohusz i Anna Noczyńska. "Metabolic disorders in polycystic ovary syndrome". Pediatric Endocrinology Diabetes and Metabolism 23, nr 4 (2017): 204–8. http://dx.doi.org/10.18544/pedm-23.04.0094.

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Dora, Esther. "Inherited Metabolic Disorders: A Prospective Study". Endocrinology and Disorders 2, nr 2 (15.02.2018): 01. http://dx.doi.org/10.31579/2640-1045/020.

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Ding, Hui, Mengyuan Ouyang, Jinyi Wang, Minyao Xie, Yanyuan Huang, Fangzheng Yuan, Yunhan Jia, Jun Wang, Na Liu i Ning Zhang. "Obsessive-Compulsive Disorder and Metabolic Disorders". Journal of Nervous & Mental Disease 210, nr 12 (grudzień 2022): 951–59. http://dx.doi.org/10.1097/nmd.0000000000001594.

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Crushell, Ellen, i Mary King. "Metabolic disorders". Journal of Pediatric Neurology 08, nr 01 (30.07.2015): 111–12. http://dx.doi.org/10.3233/jpn-2010-0370.

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&NA;. "METABOLIC DISORDERS". Journal of Pediatric Orthopaedics 5, nr 1 (styczeń 1985): 122. http://dx.doi.org/10.1097/01241398-198501000-00036.

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&NA;. "METABOLIC DISORDERS". Journal of Pediatric Orthopaedics 6, nr 3 (maj 1986): 386. http://dx.doi.org/10.1097/01241398-198605000-00034.

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&NA;. "METABOLIC DISORDERS". Journal of Pediatric Orthopaedics 6, nr 4 (lipiec 1986): 514–15. http://dx.doi.org/10.1097/01241398-198607000-00036.

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&NA;. "METABOLIC DISORDERS". Journal of Pediatric Orthopaedics 7, nr 3 (maj 1987): 374. http://dx.doi.org/10.1097/01241398-198705000-00037.

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Halliwell, Barry. "METABOLIC DISORDERS". Lancet 341, nr 8837 (styczeń 1993): 92. http://dx.doi.org/10.1016/0140-6736(93)92566-c.

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Yu, Zhiping, i Valerie Muehleman. "Eating Disorders and Metabolic Diseases". International Journal of Environmental Research and Public Health 20, nr 3 (30.01.2023): 2446. http://dx.doi.org/10.3390/ijerph20032446.

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Eating disorders are complex diseases with multifactorial causes. According to the Diagnostic and Statistical Manual of Mental Disorders text version (DSM-5-TR) and the WHO International Classification of Diseases and Related Health Problems (ICD-11), the major types of eating disorders include anorexia nervosa, bulimia nervosa, and binge eating disorder. The prevalence of eating disorders is alarmingly increasing globally. Moreover, the COVID-19 pandemic has led to more development and worsening of eating disorders. Patients with eating disorders exhibit high rates of psychiatric comorbidities and medical comorbidities such as obesity, diabetes, and metabolic syndrome. This paper aims to review and discuss the comorbidities of eating disorders with those metabolic diseases. Eating disorder treatment typically includes a combination of some or all approaches such as psychotherapy, nutrition education, and medications. Early detection and intervention are important for the treatment of eating disorders.
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Rozprawy doktorskie na temat "Metabolic disorders"

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Shaham, Oded. "A metabolic profiling approach to human disorders of energy metabolism". Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/54670.

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Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2009.
Cataloged from PDF version of thesis.
Includes bibliographical references.
The integrated network of biochemical reactions known collectively as metabolism is essential for life, and dysfunction in parts of this network causes human disease - both rare, inherited disorders and common diseases such as diabetes mellitus. The study of metabolic disease depends upon quantitative methods which are traditionally custom-tailored to a given compound. Recent advances in technologies such as mass spectrometry now enable the simultaneous measurement of a diverse metabolite collection spanning multiple biological pathways, an approach known as metabolic profiling or metabolomics. This dissertation describes the development of one such metabolic profiling system and its application to the study of two major topics in human energy metabolism: the fasting:feeding transition and mitochondrial disease. In the first study, we profile human plasma in response to glucose ingestion, detecting dozens of metabolite changes and identifying several distinct effects of insulin. Based on these observations, we propose a multivariate view of insulin sensitivity, and show that individuals at risk for developing diabetes mellitus can differ in their insulin response profile, a concept of potential value for estimating disease risk and progression. In the second study, we elucidate a metabolic signature of human mitochondrial disease that reflects substrate oxidation, biosynthesis and energy charge.
(cont.) We demonstrate that the culture media profile of a cellular disease model of mitochondrial dysfunction reflects the plasma profile of human patients, an approach that could be applicable to other diseases as well. In addition, we show that a combination of metabolites distinguishes individuals with mitochondrial disease from healthy individuals better than the currently used diagnostic markers. Our findings provide insight into human disorders of energy metabolism, and demonstrate the utility of a profiling approach for the understanding of metabolic disease.
by Oded Shaham.
Ph.D.
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Swetye, Michael Harrison. "Monitoring, identification, and intervention for metabolic disorders in veterans with psychotic disorders". [New Haven, Conn. : s.n.], 2008. http://ymtdl.med.yale.edu/theses/available/etd-12092008-164555/.

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Gkrania-Klotsas, Effrossyni. "Infections and metabolic diseases". Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610669.

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Steinberg, Steven Jeffrey. "Biochemical characterisation and genetic complementation analysis of generalised peroxisomal disorders and Niemann-Pick disease type C". Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294755.

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Spathaky, Jane Mary. "A novel method for the isolation of genes encoding peroxisomal matrix proteins". Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361693.

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Grosbellet, Edith. "Reciprocal relationships between circadian disruptions and metabolic disorders". Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ060.

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Tous les organismes présentent des rythmes biologiques sous le contrôle d’horloges internes synchronisées sur le cycle jour-nuit. La perturbation des horloges (travail posté chez l’homme) conduit souvent à des troubles métaboliques. A l’inverse, obésité et diabète sont associés à des perturbations circadiennes. Mon but est de comprendre les mécanismes impliqués dans le lien réciproque entre perturbations circadiennes et troubles métaboliques. Une première partie révèle le rôle de la leptine dans les troubles circadiens de souris génétiquement obèses, au niveau central et périphérique. Dans une seconde partie, nous montrons que l’altération des cycles jour-nuit induit une désynchronisation circadienne chez un rongeur diurne, entraînant un état pré-diabétique et un vieillissement prématuré des cellules hépatiques. Nos résultats ouvrent la voie à des traitements préventifs visant à diminuer les troubles circadiens des patients obèses et les troubles métaboliques des travailleurs postés
Most organisms exhibit biological rhythms, generated endogenously by circadian clocks, which are synchronized on the light-dark cycle. Disrupting circadian clocks (e.g, shiftwork) lead in most cases to the occurrence of metabolic disorders. Conversely, obesity and diabetes are associated with circadian disruptions. The aim of my project is to provide new insights in the understanding of mechanisms underlying the reciprocal relationships between circadian disruptions and metabolic disorders. We show in a first part that leptin is involved in circadian disturbances of genetically obese mice, at both central and peripheral levels. In a second part, by altering the light-dark cycle, we induce the circadian desynchronization of a diurnal rodent, which leads in turn to a pre-diabetic state associated with accelerated aging of hepatic cells. Our results pave the road to preventive treatments aiming at reducing circadian disruptions in obese patients and metabolic disorders in shiftworkers
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Marsland, C. H. "Chirality of urinary metabolites in inherited metabolic disorders". Thesis, Sheffield Hallam University, 1989. http://shura.shu.ac.uk/20019/.

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An important group of inherited metabolic disorders in man produce abnormal excretion of organic acids in the urine. Diagnosis is usually based on identification of the abnormal metabolites, working back from there to characterise the defect at enzymatic level. The chirality of these metabolites may be significant in that the different enantiomers of a substance usually have different metabolic origins. Thus, knowledge of the chirality of a metabolite aids in the understanding of the mechanism of the disorder. The chirality of a number of urinary metabolites in inherited metabolic disease was examined using gas chromatography-mass spectrometry, most of the analyses being performed using single ion monitoring. This analytical method requires the use of chiral reference compounds of known configuration. Chiral lactic and glyceric acids are available commercially, but a range of chiral beta-hydroxy acids were prepared by the reduction of the corresponding beta-ketocarboxylic acid esters with fermenting baker's yeast. After hydrolysis of the esters, separation of the enantiomers is based on their reaction with a suitable chiral reagent to form a volatile mixture of the diastereoisomers which are resolved by gas-liquid chromatography using a capillary column with a non-chiral stationary phase. Information from the analysis of the chiral standards was used to assign the absolute configuration of the following urinary metabolites; lactic acid in an unusual case of lactic aciduria, glyceric acid in the glyceric acidurias, beta-hydroxybutyrate in ketonuria, beta-hydroxyvalerate in propionic acidaemia, 2-methyl beta-hydroxybutyrate in beta-ketothiolase deficiency and beta-hydroxyadipic acid in hydroxydicarboxylic aciduria. The biochemical significance of the chirality of each of these metabolites is discussed. The assigning of configuration to urinary beta-hydroxyvalerate in propionic acidaemia, 2-methyl beta-hydroxybutyrate in beta-ketothiolase deficiency and beta-hydroxyadipic acid in hydroxydicarboxylic aciduria represents original work and has helped to elucidate the metabolic origins of these compounds.
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Kaushanska, O. V. "Peculiarities of gout in patients with metabolic disorders". Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18590.

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Lorbeer, Roberto [Verfasser]. "Endocrine-metabolic markers and subclinical cardiovascular disorders / Roberto Lorbeer". Greifswald : Universitätsbibliothek Greifswald, 2012. http://d-nb.info/1022132911/34.

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Foletti, Mara. "Role of metabolic disorders in estrogen induced reproductive cancer". kostenfrei, 2007. http://e-collection.ethbib.ethz.ch/view/eth:30023.

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Książki na temat "Metabolic disorders"

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H, Herdt Thomas, red. Metabolic disorders of ruminants. Philadelphia: Saunders, 2000.

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Kellum, John A., i Jorge Cerdá. Renal and metabolic disorders. Oxford: Oxford University Press, 2013.

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J, Antel, red. Obesity and metabolic disorders. Amsterdam: IOS Press, 2005.

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The metabolic syndrome. Wyd. 2. Chichester, West Sussex: Wiley-Blackwell, 2011.

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C, Manolagas Stavros, i Olefsky Jerrold M, red. Metabolic bone and mineral disorders. New York: Churchill Livingstone, 1988.

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Farooqui, Tahira, i Akhlaq A. Farooqui, red. Metabolic Syndrome and Neurological Disorders. Chichester, UK: John Wiley & Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118395318.

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Brennfleck, Shannon Joyce, red. Endocrine and metabolic disorders sourcebook. Wyd. 2. Detroit, MI: Omnigraphics, 2007.

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Nyhan, William L. Atlas of metabolic diseases. Wyd. 3. London: Hodder Arnold, 2012.

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1941-, McCandless David W., red. Cerebral energy metabolism and metabolic encephalopathy. New York: Plenum Press, 1985.

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H, Glew Robert, red. Textbook of human metabolism in health and disease. Hoboken, N.J: John Wiley & Sons, 2009.

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Części książek na temat "Metabolic disorders"

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Tappy, Luc, i Jean-Marc Schwarz. "Metabolic Disorders". W Clinical Nutrition, 97–107. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781119211945.ch6.

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Lundholm, K. "Metabolic Disorders". W Surgical Oncology, 320–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-72646-0_30.

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Carroll, Mary, L. Jane Brue i Brian Booth. "Metabolic disorders". W Caring for Older People, 105–8. London: Macmillan Education UK, 1993. http://dx.doi.org/10.1007/978-1-349-12879-2_11.

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Patay, Zoltán. "Metabolic Disorders". W Pediatric Neuroradiology, 543–721. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-26398-5_13.

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Rhodes, Jonathan. "Metabolic Disorders". W Exercise Physiology for the Pediatric and Congenital Cardiologist, 187–93. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16818-6_25.

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Hoffman, Richard, i Mariette Gerber. "Metabolic Disorders". W The Mediterranean Diet, 234–57. West Sussex, UK: John Wiley & Sons, Ltd., 2013. http://dx.doi.org/10.1002/9781118785027.ch10.

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Kocaoglu, Mehmet, I. Levent Eralp i F. Erkal Bilen. "Metabolic Disorders". W Pediatric Lower Limb Deformities, 231–53. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-17097-8_15.

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Goltra, Peter S. "Metabolic Disorders". W Medcin, 477–79. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-2286-6_66.

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Cecil, Kim M., i Diana M. Lindquist. "Metabolic Disorders". W MR Spectroscopy of Pediatric Brain Disorders, 123–48. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-5864-8_11.

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Harwood, David, i Karin Mueller. "Metabolic Disorders". W Goat Medicine and Surgery, 299–304. Boca Raton : CRC Press, [2018]: CRC Press, 2018. http://dx.doi.org/10.4324/9781315152233-14.

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Streszczenia konferencji na temat "Metabolic disorders"

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Krželj, Vjekoslav, i Ivana Čulo Čagalj. "INHERITED METABOLIC DISORDERS AND HEART DISEASES". W Symposium with International Participation HEART AND … Akademija nauka i umjetnosti Bosne i Hercegovine, 2019. http://dx.doi.org/10.5644/pi2019.181.02.

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Inherited metabolic disorders can cause heart diseases, cardiomyopathy in particular, as well as cardiac arrhythmias, valvular and coronary diseases. More than 40 different inherited metabolic disorders can provoke cardiomyopathy, including lysosomal storage disorders, fatty acid oxidation defects, organic acidemias, amino acidopathies, glycogen storage diseases, congenital disorders of glycosylation as well as peroxisomal and mitochondrial disorders. If identified and diagnosed on time, some of congenital metabolic diseases could be successfully treated. It is important to assume them in cases when heart diseases are etiologically undefined. Rapid technological development has made it easier to establish the diagnosis of these diseases. This article will focus on common inherited metabolic disorders that cause heart diseases, as well as on diseases that might be possible to treat.
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Thabet, Farouq. "Metabolic Myopathies: Diagnosis and Treatment". W Congenital Dystrophies - Neuromuscular Disorders Precision Medicine: Genomics to Care and Cure. Hamad bin Khalifa University Press (HBKU Press), 2020. http://dx.doi.org/10.5339/qproc.2020.nmd.20.

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Machado, Luiza, Camila Santos, Bianca Leonardi, Andréia Rocha, Igor Fontana, Bruna Bellaver, Gianina Venturin i in. "ACUTE PERIPHERAL INFLAMMATION IMPACT ON CEREBRAL GLUCOSE METABOLISM". W XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda072.

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Background: Neuroinflammation is a phenomenon already described in Alzheimer’s disease (AD). However, the effect of peripheral inflammation in AD is less understood. We recently demonstrated that severe sepsis causes acute brain metabolic disturbances. Nevertheless, whether mild acute peripheral inflammation affects brain metabolism remains unclear. Objective: We aimed at investigating the impact of mild acute peritonitis on glucose brain metabolism. Methods: Adult male wistar rats (n=6, per group) received a single intraperitoneal injection of 500 ml of carrageenan (CG, 500 µg of carrageenan i.p.) or saline (CO). Brain glucose metabolism was assessed using (18F) FDG-PET 4h after i.p. injections, which represents the first peak of inflammation. The peripheral inflammatory process was evaluated by analyzing the peritoneal lavage in a flow cytometer 48h after the injections, during the second peak of inflammation. Results: The CG animals presented a 5-fold increase in macrophages numbers (p0,05). However, carrageenan-induced inflammation did not cause acute changes in brain glucose metabolism (p>0,05). Conclusion: Mild acute peripheral inflammation does not change brain glucose metabolism. Further evaluations aiming to investigate long-term consequences of sustained mild inflammation are needed.
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Kisljakova, A. A. "ASSESSMENT OF INDICATORS OF METABOLIC DISORDERS IN WORKERS OCCUPATIONALLY EXPOSED BY POWER FREQUENCY ELECTRIC AND MAGNETIC FIELDS". W The 4th «OCCUPATION and HEALTH» International Youth Forum (OHIYF-2022). FSBSI «IRIOH», 2022. http://dx.doi.org/10.31089/978-5-6042929-6-9-2022-1-110-114.

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Study is directed to power frequency (PF) electric and magnetic field (EF and PF) occupational exposure possible effects to carbohydrate and lipid metabolism. As part of the periodic medical examination based in the FSBI «Izmerov Research Institute of Occupational Health», 144 men occupationally exposed by PF electromagnetic field (EMF) were examined. The control group consisted of 40 practically healthy men who were not in contact with the studied harmful factor. Based on the results of therapeutic examination and the results of a biochemical blood test, a metabolic syndrome (MS) was established in some of the persons. It was revealed that 55.5% of the employees of the main group have MS, more than 80% of men have a violation of lipid metabolism, and 43% of the subjects - carbohydrate metabolism. Higher indicators of carbohydrate metabolism were revealed in the group of primary exposure PF EMF magnetic component. Only. The group of primary exposure to both components of PF EMF (EF and MF) had higher levels of lipid metabolism. Obtained results indicate a negative effect of PF EMF occupational exposure to lipid and carbohydrate metabolism.
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Chyzheuskaya, Iryna, Ludmila Byelyaeva, Tatyana Matsushko i Tamara Yuraga. "SAT0491 METABOLIC DISORDERS IN CHILDREN WITH JUVENILE IDIOPATHIC ARTHRITIS". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7633.

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Florentina, Nechita. "The Role Of Primary Kinetoprophilaxy In Metabolic Disorders – Exogenous Obesity". W EduWorld 2018 - 8th International Conference. Cognitive-Crcs, 2019. http://dx.doi.org/10.15405/epsbs.2019.08.03.109.

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Radoi, Ion, i Cristina Tudoran. "Aspects of metabolic disorders in pigs fed exclusively with barley". W First International Symposium on the Ecology of Salmonella in Pork Production. Iowa State University, Digital Press, 2007. http://dx.doi.org/10.31274/safepork-180809-62.

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Nekrasova, Julia, i Mikhail Kanarskii. "METABOLIC ADAPTATION SYNDROME IN PATIENTS WITH CHRONIC DISORDERS OF CONSCIOUSNESS". W XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2252.sudak.ns2021-17/279-280.

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Ming Chen i R. Hofestadt. "Integrative Analysis of Metabolic Disorders by Means of Medical Bioinformatics". W 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616385.

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Kapilevich, L., S. Orlov i A. Kabachkova. "Myokines as a promising marker of metabolic disorders and physical activity". W NEW OPERATIONAL TECHNOLOGIES (NEWOT’2015): Proceedings of the 5th International Scientific Conference «New Operational Technologies». AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4936025.

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Raporty organizacyjne na temat "Metabolic disorders"

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Moskalenko, O. L., O. V. Smirnova, E. V. Kasparov i I. E. Kasparova. STRUCTURE OF PSYCHOLOGICAL DISORDERS IN PATIENTS WITH METABOLIC SYNDROME AND NON-ALCOHOLIC FAT LIVER DISEASE. Science and Innovation Center Publishing House, 2021. http://dx.doi.org/10.12731/2658-4034-2021-12-4-2-340-348.

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The article is devoted to the study of the psychological characteristics of the behavior of patients with non-alcoholic fatty liver disease (NAFLD). The manifestations of NAFLD are a powerful frustrating factor for patients, negatively affect the quality of life, hinder psychosocial adaptation and serve as the basis for the formation of chronic stress from the disease, which blocks the actual needs of the individual. Psychological factors are an important component in the clinical assessment of patients in connection with the individualization of the treatment process and secondary psychoprophylaxis, including methods of somato-centered and personality-centered psychotherapy.
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Aleksandrov, V. A., A. V. Aleksandrov, L. N. Shilova, G. Y. Osmanova i N. V. Aleksandrova. EFFECT OF ANGIOPOIETIN-LIKE PROTEIN TYPE 4 ON OSTEOPOROTIC DISORDERS IN RHEUMATOID ARTHRITIS PATIENTS WITH METABOLIC SYNDROME. DOI CODE, 2021. http://dx.doi.org/10.18411/wco-iof-esceo-2021-460.

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Tedla, Jaya Shanker, Devika Rani Sangadala, Debjani Mukherjee, Ravi Shanker Reddy, Venkata Nagaraj Kakaraparthi, Kumar Gular i Snehil Dixit. Quality of life among children with special needs in the Kingdom of Saudi Arabia. A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, marzec 2023. http://dx.doi.org/10.37766/inplasy2023.3.0016.

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Review question / Objective: The purpose of this systematic review is to find the details of the quality of life among children with disabilities in the Kingdom of Saudi Arabia. Condition being studied: Quality of life is a holistic concept that goes beyond the health dimension. Quality of life is not affected by disability alone but also by the person's experiences. Different disorders affect neurological, sensory, respiratory, metabolic, cardiac, musculoskeletal, hematological, and autoimmune disorders, either prenatal, perinatal, post-natal or during the development of the children. These disorders affect any of the physical, emotional, social, and spiritual domains of the life of children. If any one aspect of domains of life is affected, which in turn influences the quality of life in these children. There is a prevalence of disability in children due to different disorders in the Kingdom of Saudi Arabia. In the current systematic review, we intended to review the quality of life of children with different disorders in Saudi Arabia.
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Hu, Yang Yang, Xing Zhang, Yue Luo i Yadong Wang. Systematic review and Meta analysis of the efficacy and safety of rifaximin in the prevention and treatment of hepatic encephalopathy. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, luty 2023. http://dx.doi.org/10.37766/inplasy2023.2.0061.

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Review question / Objective: P:Liver cirrhosis patients with risk factors associated with HE attack;HE patients caused by chronic liver diseases represented by cirrhosis. I: Rifaximin treatment. C: Other drugs or placebo. O:HE incidence; HE improvement; All-cause mortality; Blood ammonia level; PSE index; mental state; NCT-A; NCT-B; Adverse events. Condition being studied: Hepatic encephalopathy(HE) is a neuropsychiatric disorder syndrome based on metabolic disorders, which is caused by severe acute and chronic liver dysfunction or various abnormalities of portosystemic shunt (hereinafter referred to as portosystemic shunt). The research data shows that the prevalence of OHE in patients with cirrhosis is 10-14%, and the prevalence of HE in patients with decompensated cirrhosis is 16-21%. HE can lead to 60-80% of patients with liver cirrhosis with mild cognitive impairment, affecting their ability of daily life and quality of life. When OHE occurs, the one-year mortality rate of patients with liver cirrhosis is 64%, which brings a heavy economic burden to patients and public health resources. Therefore, the prevention and early management of HE is very important.
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Paul, Satashree. Autism Spectrum Disorder. Science Repository, luty 2021. http://dx.doi.org/10.31487/sr.blog.26.

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Jin, Dachuan, Gao Peng, Shunqin Jin, Tao Zhou, Baoqiang Guo i Guangming Li. Comparison of therapeutic effects of anti-diabetic drugs on non-alcoholic fatty liver disease patients without diabetes: A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, listopad 2022. http://dx.doi.org/10.37766/inplasy2022.11.0014.

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Review question / Objective: To evaluate the efficacy of different anti-diabetic drugs in the treatment of non-diabetic non-alcoholic disease by network meta-analysis, and find the best intervention. Condition being studied: Non-alcoholic fatty liver disease (NAFLD) refers to the disease in which the liver fat content exceeds 5%, and excludes the secondary causes of alcohol, infection, drugs or other specific metabolic diseases. As a spectrum of disorders, it includes hepatocyte steatosis and steatohepatitis at the initial stage, liver fibrosis at the later stage, cirrhosis at the final stage, and even liver cancer. Nowadays Non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the world with an incidence rate as high as 25% which has been rising steadily worldwide in the past 30 years. Currently there are still no approved specific therapeutic agents and global treatment guidelines for NAFLD. For non-diabetic NAFLD, there is far from a consensus, too.
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Spitsina, S. S. Lipid metabolism disorders in patients with rheumatoid arthritis. Actual problems of experimental and clinical medicine: Materials 77th International Scientific and Practical Conference of Young Scientists and students, 2019. http://dx.doi.org/10.18411/makarenko-e-p.

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Blumwald, Eduardo, i Avi Sadka. Sugar and Acid Homeostasis in Citrus Fruit. United States Department of Agriculture, styczeń 2012. http://dx.doi.org/10.32747/2012.7697109.bard.

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Citrus fruit quality standards have been determined empirically, depending on species and on the particular growing regions. In general, the TSS (total soluble solids) to total acidity (TA) ratio determines whether citrus fruit can be marketed. Soluble sugars account for most of the TSS during harvest while TA is determined almost solely by the citric acid content, which reaches levels of 1-5% by weight in many cultivated varieties. Acid and sugar homeostasis in the fruit is critical for the management of existing cultivars, the development of new cultivars, the improvement of pre- and post-harvest strategies and the control of fruit quality and disorders. The current proposal (a continuation of a previous proposal) aimed at: (1) completing the citrus fruit proteome and metabolome, and establish a citrus fruit functional database, (2) further characterization of the control of fruit acidity by studying the regulation of key steps affecting citrate metabolism, and determine the fate of citrate during acid decline stage, and (3) Studying acid and sugar homeostasis in citrus fruits by characterizing transport mechanisms across membranes. These aims were completed as the following: (1) Our initial efforts were aimed at the characterization and identification of citric acid transporters in citrus juice cells. The identification of citrate transporters at the vacuole of the citrus juice cell indicated that the steady-state citrate cytosolic concentration and the action of the cytosolic aconitase were key elements in establishing the pH homeostat in the cell that regulates the metabolic shift towards carbon usage in the fruit during the later stages of fruit development. We focused on the action of aconitase, the enzyme mediating the metabolic use of citric acid in the cells, and identified processes that control carbon fluxes in developing citrus fruits that control the fruit acid load; (2) The regulation of aconitase, catalyzing a key step in citrate metabolism, was further characterized by using two inhibitors, citramalte and oxalomalte. These compounds significantly increased citrate content and reduced the enzyme’s activity. Metabolite profiling and changes of amino-acid metabolizing enzymes in oxalomalate- treated cells suggested that the increase in citrate, caused by aconitase inhibition, induces amino acid synthesis and the GABA shunt, in accordance with the suggested fate of citrate during the acid decline stage in citrus fruit. (3) We have placed a considerable amount of time on the development of a citrus fruit proteome that will serve to identify all of the proteins in the juice cells and will also serve as an aid to the genomics efforts of the citrus research community (validating the annotation of the fruit genes and the different ESTs). Initially, we identified more than 2,500 specific fruit proteins and were able to assign a function to more than 2,100 proteins (Katz et al., 2007). We have now developed a novel Differential Quantitative LC-MS/MS Proteomics Methodology for the identification and quantitation of key biochemical pathways in fruits (Katz et al., 2010) and applied this methodology to identify determinants of key traits for fruit quality (Katz et al., 2011). We built “biosynthesis maps” that will aid in defining key pathways associated with the development of key fruit quality traits. In addition, we constructed iCitrus (http://wiki.bioinformatics.ucdavis.edu/index.php/ICitrus), a “functional database” that is essentially a web interface to a look-up table that allows users to use functional annotations in the web to identify poorly annotated citrus proteins. This resource will serve as a tool for growers and field extension specialists.
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Kravtsov, V. I., L. E. Sivordova, J. V. Polyakova, Y. R. Akhverdyan i B. V. Zavodovsky. DISORDERS OF LIPID METABOLISM IN PATIENTS WITH OSTEOARTHRITIS. CLINICAL-PATHOGENIC VALUE. Планета, 2018. http://dx.doi.org/10.18411/978-5-907109-24-7-2018-xxxv-192-196.

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Sharma, Pushpa, Neil Grunberg, He Li, Erin Berry i Brandi Benford. Mitochondrial Damage: A Diagnostic and Metabolic Approach in Traumatic Brain Injury and Post-Traumatic Disorder. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2013. http://dx.doi.org/10.21236/ada579698.

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