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Journal articles on the topic 'Physiological, Pathological'

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Published: 4 June 2021
Last updated: 19 February 2022

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1

Marchetti, F., G. Tornese, and A. Ventura. "Physiological or pathological?" BMJ 341, sep22 2 (September 22, 2010): c5155. http://dx.doi.org/10.1136/bmj.c5155.

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2

Wales, J. K. "Physiological and pathological auxology." Archives of Disease in Childhood 90, no. 7 (July 1, 2005): 769. http://dx.doi.org/10.1136/adc.2004.070532.

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3

JACOB, R., M. VOGT, and H. RUPP. "Physiological and pathological hypertrophy*." Journal of Molecular and Cellular Cardiology 18 (1986): 35. http://dx.doi.org/10.1016/s0022-2828(86)80135-3.

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4

Michie, CA. "Physiological or pathological chemokines." Lancet 352, no. 9135 (October 1998): 1221. http://dx.doi.org/10.1016/s0140-6736(05)60557-0.

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5

Becroft, David MO. "Physiological or pathological chemokines." Lancet 352, no. 9135 (October 1998): 1221. http://dx.doi.org/10.1016/s0140-6736(05)60558-2.

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6

de Beaufort, AJ. "Physiological or pathological chemokines." Lancet 352, no. 9135 (October 1998): 1221–22. http://dx.doi.org/10.1016/s0140-6736(05)60559-4.

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7

Shimizu, Ippei, and Tohru Minamino. "Physiological and pathological cardiac hypertrophy." Journal of Molecular and Cellular Cardiology 97 (August 2016): 245–62. http://dx.doi.org/10.1016/j.yjmcc.2016.06.001.

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8

Kavazis, Andreas N. "Pathological vs. physiological cardiac hypertrophy." Journal of Physiology 593, no. 17 (September 1, 2015): 3767. http://dx.doi.org/10.1113/jp271161.

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9

Haan, Serge. "SOCS2 physiological and pathological functions." Frontiers in Bioscience 8, no. 1 (2016): 189–204. http://dx.doi.org/10.2741/760.

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10

Haan, Serge. "SOCS2 physiological and pathological functions." Frontiers in Bioscience 8, no. 1 (2016): 189–204. http://dx.doi.org/10.2741/e760.

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11

Yang, William Y., Ying Shao, Jahaira Lopez-Pastrana, Jietang Mai, Hong Wang, and Xiao-feng Yang. "Pathological conditions re-shape physiological Tregs into pathological Tregs." Burns & Trauma 3 (May 28, 2015): 1–11. http://dx.doi.org/10.1186/s41038-015-0001-0.

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Abstract CD4+FOXP3+ regulatory T cells (Tregs) are a subset of CD4 T cells that play an essential role in maintaining peripheral immune tolerance, controlling acute and chronic inflammation, allergy, autoimmune diseases, and anti-cancer immune responses. Over the past 20 years, a significant progress has been made since Tregs were first characterized in 1995. Many concepts and principles regarding Tregs generation, phenotypic features, subsets (tTregs, pTregs, iTregs, and iTreg35), tissue specificity (central Tregs, effector Tregs, and tissue resident Tregs), homeostasis (highly dynamic and apoptotic), regulation of Tregs by receptors for PAMPs and DAMPs, Treg plasticity (re-differentiation to other CD4 T helper cell subsets, Th1, Th2, Tfh, and Th17), and epigenetic regulation of Tregs phenotypes and functions have been innovated. In this concise review, we want to briefly analyze these eight new progresses in the study of Tregs. We have also proposed for the first time a novel concept that “physiological Tregs” have been re-shaped into “pathological Tregs” in various pathological environments. Continuing of the improvement in our understanding on this important cellular component about the immune tolerance and immune suppression would lead to the future development of novel therapeutics approaches for acute and chronic inflammatory diseases, allergy, allogeneic transplantation-related immunity, sepsis, autoimmune diseases, and cancers.
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12

Mrówczyńska, Lucyna, and Włodzimierz Mrówczyński. "Physiological and pathological roles of gangliosides." Postępy Higieny i Medycyny Doświadczalnej 67 (September 10, 2013): 938–49. http://dx.doi.org/10.5604/17322693.1066059.

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13

Vereecken, R. L. "Physiological and Pathological Urethral Pressure Variations." Urologia Internationalis 57, no. 3 (1996): 145–50. http://dx.doi.org/10.1159/000282900.

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14

Michiels, Carine. "Physiological and Pathological Responses to Hypoxia." American Journal of Pathology 164, no. 6 (June 2004): 1875–82. http://dx.doi.org/10.1016/s0002-9440(10)63747-9.

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15

Lieber, Michael R. "Pathological and Physiological Double-Strand Breaks." American Journal of Pathology 153, no. 5 (November 1998): 1323–32. http://dx.doi.org/10.1016/s0002-9440(10)65716-1.

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16

Cortes, Victor. "Physiological and pathological implications of cholesterol." Frontiers in Bioscience 19, no. 3 (2014): 416. http://dx.doi.org/10.2741/4216.

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17

Staton, CA, I. Kumar, MWR Reed, and NJ Brown. "Neuropilins in physiological and pathological angiogenesis." Journal of Pathology 212, no. 3 (2007): 237–48. http://dx.doi.org/10.1002/path.2182.

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18

Fagioli, Francesca, Alice Dell'Erba, Vanina Migliorini, and Giovanni Stanghellini. "Depersonalization: Physiological or pathological in adolescents?" Comprehensive Psychiatry 59 (May 2015): 68–72. http://dx.doi.org/10.1016/j.comppsych.2015.02.011.

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19

Stoothoff, William H., and Gail V. W. Johnson. "Tau phosphorylation: physiological and pathological consequences." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1739, no. 2-3 (January 2005): 280–97. http://dx.doi.org/10.1016/j.bbadis.2004.06.017.

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20

Dunai, Zsuzsanna, Pal I. Bauer, and Rudolf Mihalik. "Necroptosis: Biochemical, Physiological and Pathological Aspects." Pathology & Oncology Research 17, no. 4 (July 21, 2011): 791–800. http://dx.doi.org/10.1007/s12253-011-9433-4.

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21

Baka, Zsuzsanna, Bence György, Pál Géher, Edit I. Buzás, András Falus, and György Nagy. "Citrullination under physiological and pathological conditions." Joint Bone Spine 79, no. 5 (October 2012): 431–36. http://dx.doi.org/10.1016/j.jbspin.2012.01.008.

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22

Navale, Archana M., and Archana N. Paranjape. "Glucose transporters: physiological and pathological roles." Biophysical Reviews 8, no. 1 (January 19, 2016): 5–9. http://dx.doi.org/10.1007/s12551-015-0186-2.

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23

Matsumoto, Andrew, Benjamin H. Brinkmann, S. Matthew Stead, Joseph Matsumoto, Michal T. Kucewicz, W. Richard Marsh, Frederic Meyer, and Gregory Worrell. "Pathological and physiological high-frequency oscillations in focal human epilepsy." Journal of Neurophysiology 110, no. 8 (October 15, 2013): 1958–64. http://dx.doi.org/10.1152/jn.00341.2013.

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High-frequency oscillations (HFO; gamma: 40–100 Hz, ripples: 100–200 Hz, and fast ripples: 250–500 Hz) have been widely studied in health and disease. These phenomena may serve as biomarkers for epileptic brain; however, a means of differentiating between pathological and normal physiological HFO is essential. We categorized task-induced physiological HFO during periods of HFO induced by a visual or motor task by measuring frequency, duration, and spectral amplitude of each event in single trial time-frequency spectra and compared them to pathological HFO similarly measured. Pathological HFO had higher mean spectral amplitude, longer mean duration, and lower mean frequency than physiological-induced HFO. In individual patients, support vector machine analysis correctly classified pathological HFO with sensitivities ranging from 70–98% and specificities >90% in all but one patient. In this patient, infrequent high-amplitude HFO were observed in the motor cortex just before movement onset in the motor task. This finding raises the possibility that in epileptic brain physiological-induced gamma can assume higher spectral amplitudes similar to those seen in pathologic HFO. This method if automated and validated could provide a step towards differentiating physiological HFO from pathological HFO and improving localization of epileptogenic brain.
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24

Gogniashvilli, G., E. Steinmeier, G. Mlynski, and A. G. Beule. "Physiologic and pathologic septal deviations: subjective and objective functional rhinologic findings." Rhinology journal 49, no. 1 (March 1, 2011): 24–29. http://dx.doi.org/10.4193/rhino10.089.

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OBJECTIVE: A high incidence of septal deviation with significant inter-rater variability has been reported. An explanation could be the presence of physiological septal deviation besides pathological ones. We differentiated an unselected cohort by their nasal resistance into groups with physiological normal and pathologically increased resistance to detect differences and analogies in comparison to healthy subjects and a pathological cohort. STUDY DESIGN: Prospective cohort study. SETTING: A total of 356 patients were assessed using rhinoresistometry, acoustic rhinometry, endoscopy and visual analogue scales. After definition of a benchmark between physiological and pathological nasal resistance, group differences were calculated and correlations analysed. RESULTS: The normal one-sided inspiratory nasal resistance was defined as less or equal to 0.35 sPa/cm^3 at a flow-velocity of 250 cm^3/s (R250). Using this benchmark, the unselected group of non-rhinological patients was differentiated into 114 subjects with physiological nasal resistance and 44 with pathological septal deviation. Nasal resistance after decongestion was significantly lower for normal or patients with a physiological septal deviation in comparison to the rhinological one on both nasal sides. Healthy subjects and patients with physiological septal deviation showed similarities in objective rhinological parameters as well as rhinological patients and patients with pathological septal deviation derived from the unselected group of non-rhinological patients. Furthermore, this benchmark of nasal resistance shows significant correlations with subjective assessment of nasal breathing. CONCLUSION: Inspiratory nasal resistance obtained at a flow-velocity of 250 cm^3/s using rhinoresistometry may be useful to distinguish patients with physiological and pathological septal deviation. Correlation with subjective assessment and endoscopic findings is improved.
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25

Cronin, R., M. Li, J. Thompson, A. Gordon, C. Raynes Greenow, A. Heazell, T. Stacey, et al. "Late pregnancy sleep disruption - pathological or physiological?" Sleep Medicine 64 (December 2019): S82—S83. http://dx.doi.org/10.1016/j.sleep.2019.11.226.

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26

Yuana, Yuana, Auguste Sturk, and Rienk Nieuwland. "Extracellular vesicles in physiological and pathological conditions." Blood Reviews 27, no. 1 (January 2013): 31–39. http://dx.doi.org/10.1016/j.blre.2012.12.002.

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27

Hirashima, Mitsuomi, Yumiko Kashio, Nozomu Nishi, Akira Yamauchi, Tada-Atsu Imaizumi, Toshiro Kageshita, Naoki Saita, and Takanori Nakamura. "Galectin-9 in physiological and pathological conditions." Glycoconjugate Journal 19, no. 7-9 (2002): 593–600. http://dx.doi.org/10.1023/b:glyc.0000014090.63206.2f.

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28

Yin, Frank C. P., and Chih-Tai Ting. "Compliance changes in physiological and pathological states." Journal of Hypertension 10, Suppliment (August 1992): S31???S34. http://dx.doi.org/10.1097/00004872-199208001-00009.

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29

Nakamura, Michinari, and Junichi Sadoshima. "Mechanisms of physiological and pathological cardiac hypertrophy." Nature Reviews Cardiology 15, no. 7 (April 19, 2018): 387–407. http://dx.doi.org/10.1038/s41569-018-0007-y.

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30

Lopes, Joao P., and Paula Agostinho. "Cdk5: Multitasking between physiological and pathological conditions." Progress in Neurobiology 94, no. 1 (June 2011): 49–63. http://dx.doi.org/10.1016/j.pneurobio.2011.03.006.

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31

Tedgui, A. "Endothelial permeability under physiological and pathological conditions." Prostaglandins, Leukotrienes and Essential Fatty Acids 54, no. 1 (January 1996): 27–29. http://dx.doi.org/10.1016/s0952-3278(96)90077-0.

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32

Njälsson, Runa, and Svante Norgren. "Physiological and pathological aspects of GSH metabolism." Acta Paediatrica 94, no. 2 (January 2, 2007): 132–37. http://dx.doi.org/10.1111/j.1651-2227.2005.tb01878.x.

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33

Blatteis, Clark M. "Fever: pathological or physiological, injurious or beneficial?" Journal of Thermal Biology 28, no. 1 (January 2003): 1–13. http://dx.doi.org/10.1016/s0306-4565(02)00034-7.

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34

Kiyatkin, Eugene A. "Brain hyperthermia as physiological and pathological phenomena." Brain Research Reviews 50, no. 1 (December 2005): 27–56. http://dx.doi.org/10.1016/j.brainresrev.2005.04.001.

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35

Salazar, Juan, Eliana Luzardo, José Carlos Mejías, Joselyn Rojas, Antonio Ferreira, José Ramón Rivas-Ríos, and Valmore Bermúdez. "Epicardial Fat: Physiological, Pathological, and Therapeutic Implications." Cardiology Research and Practice 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/1291537.

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Epicardial fat is closely related to blood supply vessels, both anatomically and functionally, which is why any change in this adipose tissue’s behavior is considered a potential risk factor for cardiovascular disease development. When proinflammatory adipokines are released from the epicardial fat, this can lead to a decrease in insulin sensitivity, low adiponectin production, and an increased proliferation of vascular smooth muscle cells. These adipokines move from one compartment to another by either transcellular passing or diffusion, thus having the ability to regulate cardiac muscle activity, a phenomenon called vasocrine regulation. The participation of these adipokines generates a state of persistent vasoconstriction, increased stiffness, and weakening of the coronary wall, consequently contributing to the formation of atherosclerotic plaques. Therefore, epicardial adipose tissue thickening should be considered a risk factor in the development of cardiovascular disease, a potential therapeutic target for cardiovascular pathology and a molecular point of contact for “endocrine-cardiology.”
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36

Peters, T. "Calcium in Physiological and Pathological Cell Function." European Neurology 25, no. 1 (1986): 27–44. http://dx.doi.org/10.1159/000116059.

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37

Shimada, Atsuyoshi, and Takanori Yokota. "Physiological and pathological brain‐immune system interactions." Clinical and Experimental Neuroimmunology 11, no. 1 (February 2020): 3–4. http://dx.doi.org/10.1111/cen3.12561.

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38

Chang, Yao-Ming. "Vascular sphingolipids in physiological and pathological adaptation." Frontiers in Bioscience 21, no. 6 (2016): 1168–86. http://dx.doi.org/10.2741/4448.

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39

Naglova, H., and M. Bucova. "HMGB1 and its physiological and pathological roles." Bratislava Medical Journal 113, no. 03 (2012): 163–71. http://dx.doi.org/10.4149/bll_2012_039.

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40

Gunter, T. E., K. K. Gunter, S. S. Sheu, and C. E. Gavin. "Mitochondrial calcium transport: physiological and pathological relevance." American Journal of Physiology-Cell Physiology 267, no. 2 (August 1, 1994): C313—C339. http://dx.doi.org/10.1152/ajpcell.1994.267.2.c313.

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Since the initiation of work on mitochondrial Ca2+ transport in the early 1960s, the relationship between experimental observations and physiological function has often seemed enigmatic. Why, for example, should an organelle dedicated to the crucial task of producing approximately 95% of the cell's ATP sequester Ca2+, sometimes in preference to phosphorylating ADP? Why should there be two separate efflux mechanisms, the Na+ independent and the Na+ dependent, both thought until recently to be driven exclusively either directly or indirectly by the energy of the pH gradient? Does intramitochondrial free Ca2+ concentration control metabolism? Is there evidence for any separate function of the mitochondrial Ca2+ transport mechanisms under pathological conditions? What is the relationship between mitochondrial Ca2+ transport, the mitochondrial membrane permeability transition, and irreversible cell damage under pathological conditions? First, we review what is known about control of metabolism, evidence for a role for intramitochondrial Ca2+ in control of metabolism, the cellular conditions under which mitochondria are exposed to Ca2+, characteristics of the mitochondrial Ca2+ transport mechanisms including the permeability transition, and evidence for and against mitochondrial Ca2+ uptake in vivo. Then the questions listed above and others are addressed from the perspective of the characteristics of the mechanisms of mitochondrial Ca2+ transport.
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41

Roos, Maria Augusta, Luisa Gennero, Tetyana Denysenko, Stefano Reguzzi, Giovanni Cavallo, Gian Piero Pescarmona, and Antonio Ponzetto. "Microparticles in physiological and in pathological conditions." Cell Biochemistry and Function 28, no. 7 (October 2010): 539–48. http://dx.doi.org/10.1002/cbf.1695.

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42

Ertekin, Cumhur. "Physiological and pathological aspects of oropharyngeal swallowing." Movement Disorders 17, S2 (January 31, 2002): S86—S89. http://dx.doi.org/10.1002/mds.10068.

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43

Njälsson, Runa, and Svante Norgren. "Physiological and pathological aspects of GSH metabolism." Acta Paediatrica 94, no. 2 (February 1, 2005): 132–37. http://dx.doi.org/10.1080/08035250410025285.

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44

Kazatchkine, Michael D. "Delineating Physiological (Natural) Autoreactivity from Pathological Autoimmunity." Vox Sanguinis 70, no. 1 (1996): 24–29. http://dx.doi.org/10.1159/000462138.

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45

VIRCHOW, RUDOLF. "As Based upon Physiological and Pathological Histology." Nutrition Reviews 47, no. 1 (April 27, 2009): 23–25. http://dx.doi.org/10.1111/j.1753-4887.1989.tb02747.x.

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46

Kazatchkine, Michel D. "Delineating Physiological (Natural) Autoreactivity from Pathological Autoimmunity." Vox Sanguinis 70 (February 1996): 24–29. http://dx.doi.org/10.1111/j.1423-0410.1996.tb01345.x.

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47

Peng, X., and M. A. Frohman. "Mammalian phospholipase D physiological and pathological roles." Acta Physiologica 204, no. 2 (May 28, 2011): 219–26. http://dx.doi.org/10.1111/j.1748-1716.2011.02298.x.

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48

Fujii, Junichi, Yoshitaka Ikeda, Toshihiro Kurahashi, and Takujiro Homma. "Physiological and pathological views of peroxiredoxin 4." Free Radical Biology and Medicine 83 (June 2015): 373–79. http://dx.doi.org/10.1016/j.freeradbiomed.2015.01.025.

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49

Seaman, Steven, Janine Stevens, Mi Young Yang, Daniel Logsdon, Cari Graff-Cherry, and Brad St. Croix. "Genes that Distinguish Physiological and Pathological Angiogenesis." Cancer Cell 11, no. 6 (June 2007): 539–54. http://dx.doi.org/10.1016/j.ccr.2007.04.017.

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50

Tofaris, G. K., and M. G. Spillantini. "Physiological and pathological properties of α-synuclein." Cellular and Molecular Life Sciences 64, no. 17 (July 2, 2007): 2194–201. http://dx.doi.org/10.1007/s00018-007-7217-5.

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