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Artykuły w czasopismach na temat "Acidose – métabolisme"
Suter. "Metabolisches Syndrom". Praxis 92, nr 15 (1.04.2003): 681–88. http://dx.doi.org/10.1024/0369-8394.92.15.681.
Pełny tekst źródłaBRIERE, S., J. P. BRILLARD, M. PANHELEUX i P. FROMENT. "Alimentation, fertilité et bien-être des oiseaux reproducteurs domestiques : des liens complexes". INRAE Productions Animales 24, nr 2 (7.04.2011): 171–80. http://dx.doi.org/10.20870/productions-animales.2011.24.2.3251.
Pełny tekst źródłaPorras, Miguel C., José N. Lecumberri i José Luis P. Castrillón. "Trimethoprim/Sulfamethoxazole and Metabolic Acidosis in HIV-Infected Patients". Annals of Pharmacotherapy 32, nr 2 (luty 1998): 185–89. http://dx.doi.org/10.1345/aph.17042.
Pełny tekst źródłaFrankfurter, Claudia, Kevin Venus i David Frost. "Minding The Gap: Severe Anion Gap Metabolic Acidosis Associated With 5-Oxoproline Secondary To Chronic Acetaminophen Use". Canadian Journal of General Internal Medicine 14, nr 4 (19.11.2019): e43-e49. http://dx.doi.org/10.22374/cjgim.v14i4.339.
Pełny tekst źródłaHERMIER, D., M. R. SALICHON, G. GUY, R. PERESSON, J. MOUROT i S. LAGARRIGUE. "La stéatose hépatique des palmipèdes gavés : bases métaboliques et sensibilité génétique". INRAE Productions Animales 12, nr 4 (1.09.1999): 265–71. http://dx.doi.org/10.20870/productions-animales.1999.12.4.3887.
Pełny tekst źródłaMarais, Ophélie. "Une acidose métabolique exceptionnelle". Option/Bio 22, nr 460 (październik 2011): 5. http://dx.doi.org/10.1016/s0992-5945(11)70850-9.
Pełny tekst źródłaPreti, Beatrice, Jasna Deluce i Siddhartha Srivastava. "Type B Lactic Acidosis in a Solid-Tumour Malignancy Without Liver Metastases". Canadian Journal of General Internal Medicine 16, nr 2 (21.06.2021): 38–42. http://dx.doi.org/10.22374/cjgim.v16i2.427.
Pełny tekst źródłaSimon, M., T. Baudry, R. Hernu, M. Cour i L. Argaud. "Intoxication à la metformine". Médecine Intensive Réanimation 28, nr 5 (wrzesień 2019): 380–88. http://dx.doi.org/10.3166/rea-2019-0127.
Pełny tekst źródłaDeschênes, G., L. de Parscau i C. Ichai. "Comment réfléchir devant une acidose métabolique". Archives de Pédiatrie 17, nr 6 (czerwiec 2010): 671–72. http://dx.doi.org/10.1016/s0929-693x(10)70053-1.
Pełny tekst źródłaTESSERAUD, S., I. BOUVAREL, P. FRAYSSE, S. MÉTAYERCOUSTARD, A. COLLIN, M. LESSIRE i C. BERRI. "Optimiser la composition corporelle et la qualité des viandes de volailles en modulant le métabolisme par les acides aminés alimentaires". INRAE Productions Animales 27, nr 5 (12.12.2014): 337–46. http://dx.doi.org/10.20870/productions-animales.2014.27.5.3081.
Pełny tekst źródłaRozprawy doktorskie na temat "Acidose – métabolisme"
Remblier-Dejean, Catherine. "Influence d'une acidose lactique sur la concentration extracellulaire de dopamine dans le striatum : études par microdialyse chez le rat vigile". Poitiers, 1999. http://www.theses.fr/1999POIT1802.
Pełny tekst źródłaMutel, Élodie. "Caractérisation d’un nouveau modèle murin de glycogénose de type 1a : du métabolisme glucidique à la thérapie génique". Thesis, Lyon 1, 2011. http://www.theses.fr/2011LYO10005/document.
Pełny tekst źródłaGlycogen storage disease type 1a (GSD1a) is a rare metabolic disorder due to an absence of glucose‐6 phosphatase (G6Pase) activity. G6Pase is the key enzyme of endogenous glucose production (EGP) and catalyzes the last step before the glucose release into the bloodstream. This function to produce glucose is restricted to the liver, the kidneys and the intestine. GSD1a is characterized by chronic hypoglycemia, hepatomegaly associated with hepatic steatosis and nephromegaly. The longterm complications of G6Pase deficiency include hepatocellular adenomas. The available animal model of GSD1a rarely survive over three months of age and the study of mechanisms of hepatocellular adenomas development cannot be investigated. So, we generated an original mouse model of GSD1a with a liver‐specific invalidation of catalytic subunit of G6Pase gene by an inducible CRE‐LOX strategy (L‐G6pc‐/‐ mice). In this work, we demonstrated that L‐G6pc‐/‐ were viable and totally reproduced the liver pathology of GSD1a, including the late development of hepatocellular adenomas. Then, we have begun liver gene therapy treatment using lentiviral and AAV vectors to correct the hepatic pathology. Finally, concerning glucose homeostasis, we have demonstrated that L‐G6pc‐/‐ were able to regulate blood glucose, during prolonged fast, even in the absence of hepatic glucose production. Rapidly, L‐G6pc‐/‐ mice were able to induce renal and intestinal gluconeogenesis thanks to a key role of glucagon and the development of a metabolic acidosis. These results provide evidence that the major role of the liver for EGP during fasting requires re‐examination
Chatel, Benjamin. "Fonction et métabolisme énergétique musculaires dans un modèle de souris drépanocytaires et identification des mécanismes responsables des échanges des protons entre le muscle et le sang". Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0174.
Pełny tekst źródłaSickle cell disease (SCD) is the most frequent inherited disorder in the world. It is characterized by the synthesis of an abnormal hemoglobin S (HbS) and associated with impairments in oxygen delivery processes. If these abnormalities could impact skeletal muscle, this tissue has been rarely investigated. The aim of this thesis was to investigate muscular function and energetics in response to acute exercise, ischemia – reperfusion and endurance training in a mouse model of SCD, as well as identify the mechanisms involved in proton exchanges between muscle and blood.Sedentary and trained SCD mice were submitted to protocols of rest – stimulation – recovery and rest – ischemia – reperfusion during which muscular force and energetics (by magnetic resonance spectroscopy of phosphorus 31) were measured. Monocarboxylate transporter 1 (MCT1) haploinsufficient mice were also submitted to the stimulation protocol. Several muscles were sampled and permitted to analyze in vitro enzyme activities, content of proteins involved in pH regulation and some markers of oxidative stress.This thesis demonstrated that muscular function and energetics were impaired in SCD mice in response to both exercise and ischemia – reperfusion and that endurance training could alleviate some of these abnormalities, particularly acting on oxidative processes. We have also observed that MCT1 is involved in proton uptake by myocytes at rest, but its action is less important during exercise
Alves, de Oliveira Laurent. "Effets de l'acidose chronique et d'un excès de sulfate sur le métabolisme microbien de la thiamine dans le rumen". Lyon 1, 1997. http://www.theses.fr/1997LYO10226.
Pełny tekst źródłaMutel, Élodie. "Caractérisation d'un nouveau modèle murin de glycogénose de type 1a : du métabolisme glucidique à la thérapie génique". Phd thesis, Université Claude Bernard - Lyon I, 2011. http://tel.archives-ouvertes.fr/tel-00858006.
Pełny tekst źródłaAdam, Clément. "Impact de l’acétoacétate sur la biologie des macrophages humains : analyse phénotypique et métabolique The roles of CSF s on the functional polarization of tumor‐associated macrophages". Thesis, Angers, 2019. http://www.theses.fr/2019ANGE0049.
Pełny tekst źródłaIn case of inflammation or injury, macrophages must adapt and function in a hostile environment, such as an acidic environment. Indeed, excessive production and local accumulation of lactic acid, is a characteristic of inflammatory process and tissue damage. Currently, the metabolic adaptation of human monocytes and macrophages to acidosis and the nature of the factors that enable them to acquire a repair profile are poorly understood. In this study, we show that monocytes differentiated in vitro into macrophages in the presence of the acetoacetate, aketone body produced by the liver, show an increase in oxidative phosphorylation associated with the acquisition of a pronounced repair profile. In addition, ketone bodies and acetoacetate accelerate the rate of healing in an in vivo healing model. From a mechanistic point of view, monocytes differentiated into lactic acidosis accumulate depolarized mitochondria and show signs of mitophagy as well as a significant reduction in nutrient absorption making their survival dependent on autophagy. Interestingly, acetoacetate prevents the consequences of acid stress (maintaining integrity and mitochondrial function), allowing cells to survive without resorting to autophagy. Acetoacetate therefore appears as a unique metabolite to improve the tolerance of cells and tissues to damage induced by acidosis and a local factor promoting the generation of macrophages with a repair profile
Daher, Raed. "Implication de BMP6, GLRX5 et la H+/K+ ATPase dans les troubles du métabolisme de fer : de la physiologie à la pathologie". Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC280.
Pełny tekst źródłaIron is an essential element for many biological processes. Its homeostasis is maintained by a closed mechanism based on its absorption in the intestine, its usage by the erythroid precursors for hemoglobin production, and its recycling and storage in the liver and spleen macrophages. Iron metabolism is under the negative control of hepcidin, a small peptide mainly synthesized by the liver. Hepcidin inhibits the intestinal absorption of iron and its release from macrophages. The deregulation of iron balance leads to the appearance of multiple pathological situations. Indeed, iron deficiency is the most frequent cause of anemia which can be sideroblastic or not, and the excess of iron leads to hemochromatosis which may be either primary (hereditary) or secondary. This thesis project consists of studying the functional mechanisms of some abnormalities, inherited or acquired, resulting in iron overload
Guelzim, Najoua. "Régulation du métabolisme secondaire de l'arginine et de la cystéine par l'acide alpha-linolénique. Implication dans la physiopathologie du syndrome métabolique". Phd thesis, AgroParisTech, 2011. http://pastel.archives-ouvertes.fr/pastel-00781861.
Pełny tekst źródłaBurthier, Jean Michel. "Les déficits en pyruvate déshydrogénase". Paris 5, 1990. http://www.theses.fr/1990PA05P176.
Pełny tekst źródłaRimbaud, Stéphanie. "Métabolisme énergétique dans l'hypertrophie de l'insuffisance cardiaque : évaluation d'une thérapie métabolique". Paris 11, 2010. http://www.theses.fr/2010PA114843.
Pełny tekst źródłaWhen the heart is submitted to an increase in workload, it adapts its mass resulting in cardiac hypertrophy (CH) which can progress towards heart failure (HF), characterized by important energetic disorders. Cardiac phenotype was assessed in different models of CH, with a physiological (gestation, training) or a pathological (hypertension) origin and revealed a harmonious increase in mitochondrial mass and function, in line with maintained cardiac function. Therefore energy metabolism disturbances appear to be a marker of HF and could be considered as a relevant therapeutic target in HF. Eight weeks treatment with resveratrol, a polyphenol with known metabolic effects, of Dahl salt-sensitive rats, an experimental model of cardiovascular dysfunction, induced multiple beneficial effects on survival, endothelial and cardiac function, and cardiac energy metabolism. Thus resveratrol could be an interesting candidate for an adjuvant metabolic therapy in HF
Książki na temat "Acidose – métabolisme"
Riadh, Jazrawi, Northfield Tim i Zentler-Munro Patrick, red. Bile acids in health and disease: Update on cholesterol gallstones and bile acid diarrhoea. Dordrecht: Kluwer Academic, 1988.
Znajdź pełny tekst źródłaA, Drevon C., Baksaas I i Krokan Hans, red. Omega-3 fatty acids: Metabolism and biological effects. Basel: Birkhäuser Verlag, 1993.
Znajdź pełny tekst źródłaMendel, Friedman, red. Absorption and utilization of amino acids. Boca Raton, Fla: CRC Press, 1989.
Znajdź pełny tekst źródłaSimon, Eaton, i Fatty Acid Oxidation and Ketogenesis Conference (4th : 1998 : London, England), red. Current views of fatty acid oxidation and ketogenesis: From organelles to point mutations. New York: Kluwer Academic/Plenum Publishers, 1999.
Znajdź pełny tekst źródłaSimon, Eaton, i Fatty Acid Oxidation and Ketogenesis Conference (4th : 1998 : London, England), red. Current views of fatty acid oxidation and ketogenesis: From organelles to point mutations. New York: Kluwer Academic/Plenum Publishers, 1999.
Znajdź pełny tekst źródłaXian, Xu, red. Suan ti nai bai bing zhi yuan: Shan shi suan jian ping heng zhi nan. Tianjin Shi: Tianjin ke ji fan yi chu ban gong si, 2005.
Znajdź pełny tekst źródłaTadao, Yasugi, Hakamura Haruo i Soma Masayoshi, red. Advances in polyunsaturated fatty acid research: Proceedings of the 5th Scientific Meeting of the Society for Research on Polyunsaturated Fatty Acids (PUFA), Tokyo, 11-14 November 1992. Amsterdam: Excerpta Medica, 1993.
Znajdź pełny tekst źródłaA, Cynober Luc, red. Metabolic and therapeutic aspects of amino acids in clinical nutrition. Wyd. 2. Boca Raton: CRC Press, 2004.
Znajdź pełny tekst źródłaG, Hardie D., red. Protein phosphorylation: A practical approach. Oxford: Oxford University Press, 1993.
Znajdź pełny tekst źródłaInternational, Symposium on Metabolism and Enzymology of Nucleic Acids Including Gene Manipulations (6th 1987 Smolenice Slovakia). Metabolism and enzymology of nucleic acids including gene manipulations. New York: Plenum Press, 1988.
Znajdź pełny tekst źródłaCzęści książek na temat "Acidose – métabolisme"
De Lonlay, Pascale, Sandrine Dubois, Vassili Valayannopoulos, Eliane Depondt, Chris Ottolenghi i Daniel Rabier. "Déficits de l’oxydation des acides gras". W Prise en charge médicale et diététique des maladies héréditaires du métabolisme, 259–80. Paris: Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0046-2_16.
Pełny tekst źródłaChaïb, Aurès. "Acidose métabolique". W Urgences-Réanimation-Transfusion, 60–62. Elsevier, 2015. http://dx.doi.org/10.1016/b978-2-294-74374-0.00021-9.
Pełny tekst źródła"Acidose métabolique". W Méga Guide STAGES IFSI, 1815–17. Elsevier, 2015. http://dx.doi.org/10.1016/b978-2-294-74529-4.00593-0.
Pełny tekst źródłaAlexandre, J., A. Balian, L. Bensoussan, A. Chaïb, G. Gridel, K. Kinugawa, F. Lamazou i in. "Acidose métabolique". W Le tout en un révisions IFSI, 1638–40. Elsevier, 2009. http://dx.doi.org/10.1016/b978-2-294-70633-2.50575-8.
Pełny tekst źródłaGONTERO, Brigitte, i Stephen Christopher MABERLY. "Mécanismes biochimiques de concentration du dioxyde de carbone". W Planète bleue, photosynthèse rouge et verte, 135–68. ISTE Group, 2023. http://dx.doi.org/10.51926/iste.9082.ch5.
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