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Journal articles on the topic 'Physiopathology'

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1

Rouach, Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France, no. 116 (June 15, 2018): 653–55. http://dx.doi.org/10.4000/annuaire-cdf.13463.

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Rouach, Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France, no. 117 (September 1, 2019): 639–40. http://dx.doi.org/10.4000/annuaire-cdf.14766.

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Rouach, Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France, no. 118 (December 30, 2020): 661–63. http://dx.doi.org/10.4000/annuaire-cdf.16154.

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4

Rouach, Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France 121 (2024): 695–97. http://dx.doi.org/10.4000/12kvr.

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5

Rouach, Responsable :. Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France, no. 120 (February 13, 2023): 544–45. http://dx.doi.org/10.4000/annuaire-cdf.18789.

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6

Jullien, D. "Psoriasis physiopathology." Journal of the European Academy of Dermatology and Venereology 20, s2 (November 2006): 10–23. http://dx.doi.org/10.1111/j.1468-3083.2006.01768.x.

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7

Bonanno, FabrizioGiuseppe. "Physiopathology of shock." Journal of Emergencies, Trauma, and Shock 4, no. 2 (2011): 222. http://dx.doi.org/10.4103/0974-2700.82210.

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8

García Rodríguez, Diego Felipe, and Carlos Abud Mendoza. "Physiopathology of fibromyalgia." Reumatología Clínica (English Edition) 16, no. 3 (May 2020): 191–94. http://dx.doi.org/10.1016/j.reumae.2020.02.004.

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9

Venance, Laurent. "Dynamique et physiopathologie des réseaux neuronaux / Dynamics and physiopathology of neuronal networks." L’annuaire du Collège de France, no. 116 (June 15, 2018): 657–59. http://dx.doi.org/10.4000/annuaire-cdf.13492.

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Venance, Laurent. "Dynamique et physiopathologie des réseaux neuronaux / Dynamics and physiopathology of neuronal networks." L’annuaire du Collège de France, no. 117 (September 1, 2019): 645. http://dx.doi.org/10.4000/annuaire-cdf.14783.

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Venance, Laurent. "Dynamique et physiopathologie des réseaux neuronaux / Dynamics and physiopathology of neuronal networks." L’annuaire du Collège de France, no. 118 (December 30, 2020): 668–69. http://dx.doi.org/10.4000/annuaire-cdf.16178.

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Venance, Laurent. "Dynamique et physiopathologie des réseaux neuronaux / Dynamics and physiopathology of neuronal networks." L’annuaire du Collège de France 121 (2024): 703–4. http://dx.doi.org/10.4000/12kvv.

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13

Venance, Responsable :. Laurent. "Dynamique et physiopathologie des réseaux neuronaux / Dynamics and physiopathology of neuronal networks." L’annuaire du Collège de France, no. 120 (February 13, 2023): 551. http://dx.doi.org/10.4000/annuaire-cdf.18823.

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14

Gaspar, Ana Teresa, and Filipe Antunes. "Síndrome doloroso regional complexo tipo I." Acta Médica Portuguesa 24, no. 6 (June 20, 2012): 1031. http://dx.doi.org/10.20344/amp.1411.

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Type I complex regional pain syndrome is a neurophatic pain syndrome whose physiopathology is not yet fully understood. It mainly affects limb extremities and often occurs after local trauma. There is no consensus on the treatment, but early intervention seems important, particularly in the context of Physical Medicine and Rehabilitation. The authors review physiopathologic mechanisms and point to importance of an early diagnosis, since failure to recognize this clinical picture and the consequent delay in treatment may cause serious functional impairments.
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15

Cohen-Salmon, Martine. "Physiologie et physiopathologie de l’unité gliovasculaire / Physiology and physiopathology of the gliovascular unit." L’annuaire du Collège de France 121 (2024): 681–83. http://dx.doi.org/10.4000/12kvi.

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Martine Cohen-Salmon, Responsable :. "Physiologie et physiopathologie de l’unité gliovasculaire / Physiology and physiopathology of the gliovascular unit." L’annuaire du Collège de France, no. 120 (February 13, 2023): 532–34. http://dx.doi.org/10.4000/annuaire-cdf.18721.

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17

Sgambato, F., S. Prozzo, C. Caporaso, L. Milano, E. Sgambato, and G. L. Piscitelli. "Clinical physiopathology of hypernatremia." Italian Journal of Medicine 1, no. 2 (May 3, 2013): 6. http://dx.doi.org/10.4081/itjm.2007.2.6.

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18

Micheletto, G., G. Mariot, and E. Andretta. "Physiopathology of pelvic pain." Urologia Journal 64, no. 1 (February 1997): 96–98. http://dx.doi.org/10.1177/039156039706400122.

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19

Maccauro, Giulio, Maria Silvia Spinelli, Sigismondo Mauro, Carlo Perisano, Calogero Graci, and Michele Attilio Rosa. "Physiopathology of Spine Metastasis." International Journal of Surgical Oncology 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/107969.

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The metastasis is the spread of cancer from one part of the body to another. Two-thirds of patients with cancer will develop bone metastasis. Breast, prostate and lung cancer are responsible for more than 80% of cases of metastatic bone disease. The spine is the most common site of bone metastasis. A spinal metastasis may cause pain, instability and neurological injuries. The diffusion through Batson venous system is the principal process of spinal metastasis, but the dissemination is possible also through arterial and lymphatic system or by contiguity. Once cancer cells have invaded the bone, they produce growth factors that stimulate osteoblastic or osteolytic activity resulting in bone remodeling with release of other growth factors that lead to a vicious cycle of bone destruction and growth of local tumour.
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20

Chappard, D. "Physiopathology of spinal osteoporosis." Annals of Physical and Rehabilitation Medicine 54 (October 2011): e253. http://dx.doi.org/10.1016/j.rehab.2011.07.278.

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21

Martin-du Pan, Rémy C., and Aldo Campana. "Physiopathology of spermatogenic arrest." Fertility and Sterility 60, no. 6 (December 1993): 937–46. http://dx.doi.org/10.1016/s0015-0282(16)56388-2.

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22

Vaira, V., C. Verdelli, I. Forno, and S. Corbetta. "MicroRNAs in parathyroid physiopathology." Molecular and Cellular Endocrinology 456 (November 2017): 9–15. http://dx.doi.org/10.1016/j.mce.2016.10.035.

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23

Visconti, A., S. Santucci, L. Fig� Talamanca, S. Cannoni, G. Ristori, and M. Salvetti. "Physiopathology of multiple sclerosis." Neurological Sciences 24 (December 1, 2003): s287—s290. http://dx.doi.org/10.1007/s10072-003-0176-1.

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24

Rochette, Luc. "Symposium Physiopathology of Reperfusion." Cardiovascular Drugs and Therapy 3, no. 6 (November 1989): 893–96. http://dx.doi.org/10.1007/bf01869578.

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25

Boulet, Louis-Philippe. "Physiopathology of airway hyperresponsiveness." Current Allergy and Asthma Reports 3, no. 2 (March 2003): 166–71. http://dx.doi.org/10.1007/s11882-003-0030-9.

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26

Martindu Pan, R. C., and A. Campana. "Physiopathology of spermatogenic arrest." International Journal of Gynecology & Obstetrics 46, no. 3 (September 1994): 353–54. http://dx.doi.org/10.1016/0020-7292(94)90432-4.

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27

Boissel, Jean-Pierre, Benjamin Ribba, Emmanuel Grenier, Guillemette Chapuisat, and Marie-Aimée Dronne. "Modelling methodology in physiopathology." Progress in Biophysics and Molecular Biology 97, no. 1 (May 2008): 28–39. http://dx.doi.org/10.1016/j.pbiomolbio.2007.10.005.

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28

Mareel, M. M. "Physiopathology of Liver Metastasis." Acta Chirurgica Belgica 103, no. 5 (January 2003): 444–47. http://dx.doi.org/10.1080/00015458.2003.11679464.

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29

LAFEBER, F. P. J. G., P. MIOSSEC, and L. A. VALENTINO. "Physiopathology of haemophilic arthropathy." Haemophilia 14, s4 (July 2008): 3–9. http://dx.doi.org/10.1111/j.1365-2516.2008.01732.x.

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30

Reay, Donald T. "Review ofAsphyxia: The Physiopathology." Journal of Forensic Sciences 47, no. 5 (September 1, 2002): 15540J. http://dx.doi.org/10.1520/jfs15540j.

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31

Miller, Ingrid, Ivano Eberini, and Elisabetta Gianazza. "Proteomics of lung physiopathology." PROTEOMICS 8, no. 23-24 (December 2008): 5053–73. http://dx.doi.org/10.1002/pmic.200800315.

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32

Krasteva, M. "Physiopathology of contact dermatitis." Journal of the European Academy of Dermatology and Venereology 5, no. 1 (October 1995): S14. http://dx.doi.org/10.1016/0926-9959(95)95788-3.

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33

Portales-Castillo, Ignacio, Timo Rieg, Sheikh B. Khalid, Sagar U. Nigwekar, and Javier A. Neyra. "Physiopathology of Phosphate Disorders." Advances in Kidney Disease and Health 30, no. 2 (March 2023): 177–88. http://dx.doi.org/10.1053/j.akdh.2022.12.011.

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34

Suwa, Tetsuya, and Tomoatsu Mune. "1. Physiopathology of Adrenal Crisis." Nihon Naika Gakkai Zasshi 97, no. 4 (2008): 756–60. http://dx.doi.org/10.2169/naika.97.756.

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35

Cazzola, M., F. Atzeni, L. Boccassini, G. Cassisi, and P. Sarzi-Puttini. "Physiopathology of pain in rheumatology." Reumatismo 66, no. 1 (June 6, 2014): 4. http://dx.doi.org/10.4081/reumatismo.2014.758.

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36

Terada, Norio. "II. Physiopathology and Differential Diagnosis." Nihon Naika Gakkai Zasshi 99, no. 5 (2010): 924–29. http://dx.doi.org/10.2169/naika.99.924.

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37

Kubiak, Jacek Z., and Malgorzata Kloc. "Dissecting Physiopathology of COVID-19." International Journal of Molecular Sciences 23, no. 17 (August 24, 2022): 9602. http://dx.doi.org/10.3390/ijms23179602.

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38

Malaguarnera, Lucia. "The physiopathology of lipoprotein a." Frontiers in Bioscience S2, no. 3 (2010): 866–75. http://dx.doi.org/10.2741/s107.

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39

Visseaux, Benoît, Quentin Le Hingrat, Florence Damond, Charlotte Charpentier, and Diane Descamps. "Physiopathology of HIV-2 infection." Virologie 23, no. 5 (October 2019): 277–91. http://dx.doi.org/10.1684/vir.2019.0789.

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40

Prado, Carla M., Mílton A. Martins, and Iolanda F. L. C. Tibério. "Nitric Oxide in Asthma Physiopathology." ISRN Allergy 2011 (April 19, 2011): 1–13. http://dx.doi.org/10.5402/2011/832560.

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Asthma is a chronic inflammatory airway disease characterized by allergen-induced airway hyperresponsiveness, airway inflammation, and remodeling. Nitric oxide (NO) derived from constitutive and inducible enzymes affects many aspects of asthma physiopathology. Animal in vivo studies have indicated that inhibition of iNOS may play a central role in the modulation of these features, particularly extracellular matrix remodeling. Additionally, increases in iNOS-derived NO, observed in asthmatic patients, may lead to an increase in peroxynitrite and an imbalance of oxidant and antioxidant pathways. In addition, endogenous nitric oxide produced by constitutive enzymes may protect against the remodeling of the lung. Therefore, nitric oxide donors and/or iNOS inhibitors may have therapeutic potential in asthma treatment and can also be used with corticosteroids to counteract airway remodeling. This paper focuses on the pathophysiological role of nitric oxide, mainly derived from inducible isoforms, in the various pathologic mechanisms of allergic asthma and the importance of nitric oxide and/or arginase inhibitors in asthma treatment.
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41

Jurysta, Cédric, Abdullah Sener, and Willy J. Malaisse. "Physiopathology of parotid cell energetics." Advances in Biological Chemistry 03, no. 02 (2013): 159–63. http://dx.doi.org/10.4236/abc.2013.32020.

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42

Barros, Alfredo Carlos Simões Dornellas de, and Marcelo de Castro Moura Sampaio. "Gynecomastia: physiopathology, evaluation and treatment." Sao Paulo Medical Journal 130, no. 3 (2012): 187–97. http://dx.doi.org/10.1590/s1516-31802012000300009.

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Gynecomastia (GM) is characterized by enlargement of the male breast, caused by glandular proliferation and fat deposition. GM is common and occurs in adolescents, adults and in old age. The aim of this review is to discuss the pathophysiology, etiology, evaluation and therapy of GM. A hormonal imbalance between estrogens and androgens is the key hallmark of GM generation. The etiology of GM is attributable to physiological factors, endocrine tumors or dysfunctions, non-endocrine diseases, drug use or idiopathic causes. Clinical evaluation must address diagnostic confirmation, search for an etiological factor and classify GM into severity grades to guide the treatment. A proposal for tailored therapy is presented. Weight loss, reassurance, pharmacotherapy with tamoxifen and surgical correction are the therapeutic options. For long-standing GM, the best results are generally achieved through surgery, combining liposuction and mammary adenectomy.
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43

Tarantino, Mario, Elena Vitale, and Ivo Casagranda. "Metabolic alkalosis: pathogenesis and physiopathology." Emergency Care Journal 4, no. 6 (December 20, 2008): 9. http://dx.doi.org/10.4081/ecj.2008.6.9.

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44

Sacco, Emilio. "Physiopathology of Overactive Bladder Syndrome." Urologia Journal 79, no. 1 (January 2012): 24–35. http://dx.doi.org/10.5301/ru.2012.8972.

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The pathophysiology of OAB is complex, multifactorial and still largely unknown. Several pathophysiological mechanisms have been highlighted that may play a different role in different patient groups. There are now experimental evidences that support both the myogenic and neurogenic hypothesis, but in recent years the “integrative” hypothesis has been gaining more and more acceptance, where a disruption in the multiple interactions between different cell types (neurons, urothelium, interstitial cells, myocytes) and network functions represent a central element of lower urinary tract dysfunctions. Of utmost importance, a disorder in the urothelial sensory function and in the urothelial/suburothelial non-neural cholinergic system, favored by age and comorbidities, appears to be crucial for the development of the OAB. Neuroplastic and detrusor changes in OAB are broadly similar to those observed in bladders exposed to outlet obstruction, neuropathies, inflammation or aging, and may be driven by a common urothelial dysfunction. Several signaling substances and their receptors were found to be involved in central pathways of bidirectional communication between the different cell types in the bladder, and were shown to be modified in several animal models of OAB as well as in human models, indicating new potential therapeutic targets.
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45

Redington, Andrew N. "Physiopathology of Right Ventricular Failure." Seminars in Thoracic and Cardiovascular Surgery: Pediatric Cardiac Surgery Annual 9, no. 1 (January 2006): 3–10. http://dx.doi.org/10.1053/j.pcsu.2006.02.005.

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46

Cormier, Catherine. "Physiopathology and etiology of osteoporosis." Current Opinion in Rheumatology 3, no. 3 (June 1991): 457–62. http://dx.doi.org/10.1097/00002281-199106000-00019.

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47

Maseri, A., L. M. Biasucci, and G. Liuzzo. "Physiopathology of Acute Coronary Syndromes." Platelets 4, sup1 (January 1993): 5–7. http://dx.doi.org/10.3109/09537109309013243.

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48

Cerletti, C., and G. De Gaetano. "Current Concepts of Platelet Physiopathology." International Journal of Artificial Organs 16, no. 5_suppl (May 1993): 205–8. http://dx.doi.org/10.1177/039139889301605s46.

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The genesis of the modern concept of platelet physiopathology can be traced historically to many individuals and developments, including the pioneering work of Giulio Bizzozero over 100 years ago. Much knowledge has since been gained to the point that we can now define many of the elements of the platelet function in relation to the hemostatic process in terms of their molecular biology. This presentation will attempt to synthesize a simple, understandable, yet global perspective of platelet function and of its participation to the pathogenesis of arterial thrombosis. Focus will be placed on the crucial importance of cell-cell interaction. A symbolic representation of platelet plug formation using simple mathematical figures like the line, point, and triangle is helpful. The line represents the vascular system with intact endothelial cell linings. The irritation/disruption of vascular endothelium can be viewed as a point on the line representative of a localized event. From this initial (often small) stimulus, amplification occurs rapidly to produce an appropriate cellular and humoral response, represented by a triangle. Each component (vessel wall, platelets, leukocytes, coagulation and fibrinolysis systems) of this complicated response has biological characteristics which localize and amplify subsequent reactions to the site of primary injury until bleeding is arrested and the wound is healed or arterial thrombosis progresses to vascular occlusion.
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49

Cademartiri, Filippo, Ludovico La Grutta, Pim J. de Feyter, and Gabriel P. Krestin. "Physiopathology of the Aging Heart." Radiologic Clinics of North America 46, no. 4 (July 2008): 653–62. http://dx.doi.org/10.1016/j.rcl.2008.04.011.

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50

Fike, J. R. "Physiopathology of radiation-induced neurotoxicity." Revue Neurologique 167, no. 10 (October 2011): 746–50. http://dx.doi.org/10.1016/j.neurol.2011.07.005.

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