Relevant bibliographies by topics / Physiological, Pathological

Academic literature on the topic 'Physiological, Pathological'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Physiological, Pathological"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Physiological, Pathological"

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Embleton, Sally J. "Physiological and pathological human ocular perfusion characteristics." Thesis, Aston University, 2002. http://publications.aston.ac.uk/14558/.

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There were three principle aims to this thesis. Firstly, the acquisition protocols of clinical blood flow apparatus were investigated in order to optimise them for both cross-sectional and longitudinal application. Secondly, the effects of physiological factors including age and systematic circulation on ocular blood flow were investigated. Finally, the ocular perfusion characteristics of patients diagnosed with ocular diseases considered to be of a vascular origin were investigated. The principle findings of this work are:- 1) Optimisation of clinical investigations Photodiode sensitivity of the scanning laser Doppler flowmeter should be kept within a range of 70-150 DC when acquiring images of the retina and optic nerve head in order to optimise the reproducibility of capillary blood flow measures. Account of the physiological spatial variation in retinal blood flow measures can be made using standard analysis protocols of the scanning laser Doppler flowmeter combined with a local search strategy. Measurements of pulsatile ocular blood flow using the ocular blood flow analyser are reproducible, however this reproducibility can be improved when consecutive intraocular pressure pulses are used to calculate pulsatile ocular blood flow. Spectral analysis of the intraocular pressure pulse-wave is viable and identifies the first four harmonic components of the waveform. 2) Physiological variation in ocular perfusion Age results in a significant reduction in perfusion of the retinal microcirculation, which is not evident in larger vessel beds such as the choroid. Despite known asymmetry in the systemic vasculature, no evidence of interocular asymmetry in ocular perfusion is apparent. 3) Pathological variation in ocular perfusion In primary open angle glaucoma, perfusion is reduced in the retinal microcirculation of patients classified as having early to moderate visual field defects. However, ocular pulsatility defects are masked when patients and subjects are matched for systemic variables (pulse rate and mean arterial pressure); differentiation is facilitated by the application of waveform analysis to the continuos intraocular pressure curve even in the early stages of disease. Diabetic patients with adequate glycaemic control, exhibit maintenance of macular blood flow, macular topography and visual function following phacoemulsification.
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Robbie, Linda Ann. "Physiological and pathological role of inhibitors of fibrinolysis." Thesis, University of Aberdeen, 1994. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU539722.

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The activity of the fibrinolytic system is dependent on the activation of plasminogen to plasmin by the activators t-PA and u-PA. These proteases are regulated by plasminogen activator inhibitor 1 (PAI-1); 2-antiplasmin (2-AP) inhibits the plasmin generated by their action. Both PAI-1 and 2-AP occur in plasma and platelets. The relative importance of the plasma and platelet inhibitors of fibrinolysis was examined using a simple microtitre plate system to study fibrin clot lysis in vitro. Cross-linked fibrin clots contained plasminogen, fibrinogen and t-PA at concentrations close to physiological. Purified 2-AP and PAI-1 caused dose-dependent inhibition of clot lysis. The inhibition due to normal plasma, platelet-rich or platelet-poor, was neutralised only by antibodies to 2-AP. Isolated platelets, at a final concentration similar to that in blood, 2.5 x 108 platelets/ml, gave rise to marked inhibition of clot lysis. This inhibition was neutralised only by antibodies to PAI-1. At the normal circulating ratio of platelets to plasma, 2-AP was the dominant inhibitor. When the platelet to plasma ratio was elevated some 20-fold, platelet PAI-1 provided a significant contribution. At a platelet to plasma ratio of 50:1 the balance was shifted such that PAI-1 became the dominant inhibitor. These results indicate that the local concentration of platelet PAI-1 would have to be very high for this inhibitor to achieve a significant regulatory role relative to that of plasma 2-AP. The study was subsequently extended to examine the concentrations of these inhibitors, and other related components of the fibrinolytic system, in human thrombi formed in vivo and normal and diseased arteries.
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Luth, Eric Sloan. "Physiological and Pathological Characterization of Alpha-Synuclein Oligomers." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11513.

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α-Synuclein (αSyn) is highly abundant cytosolic protein whose conversion into insoluble fibrils is a pathological hallmark of Parkinson's disease (PD) and other synucleinopathies. Despite decades of research, fundamental questions regarding αSyn biology are unresolved. Soluble, prefibrillar oligomers, not their fibrillar end products, are believed to be neurotoxic in humans and in disease models, but their mechanism of action remains unknown. Evidence from our lab and others increasingly suggests that, in healthy cells, αSyn does not exist purely as an unfolded monomer, as the field has long believed, but also as aggregation-resistant, α-helical oligomers; however, their physiological role remains controversial. Thus, my aim was twofold: to characterize toxic αSyn species in the context of mitochondrial dysfunction, a central phenotypic feature of PD; and to purify helical αSyn oligomers from human brain to enable further characterization of physiological αSyn.
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Lai, Duen-mun, and 黎端敏. "The neuropsychological basis of pathological gambling." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46480456.

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Sørhaug, Sveinung. "The Pulmonary Neuroendocrine System : Physiological, pathological and tumourigenic aspects." Doctoral thesis, Norwegian University of Science and Technology, Department of Circulation and Medical Imaging, 2007. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-1760.

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Nevroendokrine (NE) celler er en benevnelse på spesialiserte celler som finnes diffust utbredt i flere organ i kroppen og som har evnen til å produsere og skille ut hormon-liknende substanser. I lungene oppfattes ansamlinger av disse cellene som sanseorgan som monitorerer oksygen-nivået, og de spiller sannsynligvis en viktig rolle for lungenes utvikling, regulering av lungesirkulasjon og luftstrøm, samt immunrespons.

Hovedmålet med avhandlingen har vært å se på ulike sider ved lungenes NE system ved fysiologiske og patologiske tilstander, med fire delarbeider som hver for seg belyser ulike aspekt ved dette.

I det første arbeidet ble den generelle NE markøren kromogranin A (CgA) målt i blodprøver fra personer som deltok i Helseundersøkelsen i Nord-Trøndelag (HUNT 1995-97). Resultatene viste at mannlige deltakere med dårlig lungefunksjon hadde høyere nivå av CgA enn deltakere med normal lungefunksjon, som et uttrykk for NE aktivering.

Det andre arbeidet omhandler et 72 ukers eksponerings-forsøk med inhalasjon av karbon monoksid (CO) hos rotter gitt i konsentrasjoner som tilsvarer blod-verdier hos stor-røykere. Bortsett fra forstørret hjerte, ble det ikke funnet andre røyke-relaterte skader på hjerte/kar-systemet eller lungene. CO hadde ingen effekt på svulstforekomst eller forandringer i antall NE celler.

I det tredje arbeidet ble ulike NE markører undersøkt med immunhistokjemiske, immunelektronmikroskopiske og biokjemiske metoder hos pasienter med ikke-småcellet lungecancer. Hovedfunnet her var et større antall svulster positive for NE markører enn tidligere beskrevet når signalforsterkende teknikker ble brukt ved immunhistokjemi. Dette kan ha betydning for forståelsen av svulstenes biologi, og kan være uttrykk for at lungenes NE celler er opphavsceller for flere slike svulster enn tidligere antatt.

Det siste delarbeidet belyser sekresjon av substanser fra lungenes NE system ved hypoksi i en isolert, ventilert og sirkulert rottelunge-modell. Ved lave oksygennivå falt konsentrasjonen av proteinet bombesin i buffer sirkulert gjennom lungekretsløpet. I tillegg ble det funnet øket antall immunmerkede celler med calcitonin gene-related peptide, noe som tyder på redusert cellulær utskillelse ved eksponering for hypoksi. Resultatene viser at hypoksi er assosiert med raske forandringer i lungenes NE system for å opprettholde en balansert ventilasjon og sirkulasjon.

Samlet gir arbeidene økt kunnskap om det nevroendokrine system ved ulike sykdoms-prosesser som luftveisobstruksjon, inhalasjon av gasser som CO, i svulstutvikling og ved fysiologiske prosesser som hypoksi.


Paper II is reprinted with kind permission of Elsevier, sciencedirect.com
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Crampton, Matthew S., and n/a. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070104.165826.

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Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Determination of the molecular pathways underlying myocardial hypertrophy remains a challenge for cardiovascular research. The objective of the work presented in this thesis was to identify genes differentially expressed during pathological and physiological hypertrophy in order to enhance our knowledge of the mechanistic processes involved. A reverse Northern hybridisation method was applied to profile the expression of specifically selected genes in the hypertrophic models examined. Functional categories represented in the gene panel assembled included cardiac contractile and cytoskeletal markers, matrix metalloproteinases, vasoactive pathway factors, calcium handling genes, ion channels, cardiac regulatory factors, signalling pathway intermediates, apoptotic factors and histone deacetylases. In order to investigate pathological hypertrophy, a deoxycorticosterone acetate-salt (DOCA-salt) rat model was utilised. DOCA-salt treated rats used in this study demonstrated a 1.4-fold increase in heart weight to body weight ratio compared to controls. Impaired cardiac function indicative of a decompensated pathological phenotype in the DOCA-salt treated group was demonstrated by way of decreased chamber size, impaired myocardial compliance and significantly reduced cardiac output. Reverse Northern hybridisation analysis of 95 selected genes identified a number of candidates with differential expression in hearts of DOCA-salt treated rats. Increased gene expression was demonstrated for the collagenase MMP1 and stress-activated signal transduction factor Sin1. In contrast, the sarcoplasmic reticulum calcium ATPase SERCA-2 and anti-apoptotic factor BCL2l-10 genes exhibited decreased expression. To investigate changes in gene expression associated with physiological hypertrophy, use was made of an endurance run-trained rat model. The run-trained rats used in this study demonstrated a 24.1% increase in heart weight to body weight ratio and improvements in performance consistent with physiological cardiac adaptation. These performance indicators included improvements in systolic volume, cardiac output, myocardial compliance and bio-energetic function. Reverse Northern hybridisation expression analysis of 56 genes identified a number of differentially expressed mRNA transcripts in run-trained hypertrophied hearts. Four genes shown to demonstrate reduced expression in the run-trained rat model were interleukin-1 receptor associated kinase (IRAK1) and the developmentally expressed transcription factors Nkx-2.3, dHAND, and IRX-2. Based upon the reverse Northern hybridisation results, four genes were selected for Western blotting analysis of rat cardiac tissue. Of these, MMP1 and a putative isoform of Sin1 exhibited increased levels in DOCA-salt treated hypertrophic left ventricular tissue, results that correlate with the findings of increased mRNA expression for these two genes. Therefore, this study identified MMP1 and Sin1 as candidates involved in pathological but not physiological hypertrophy. This finding is in accord with other recent investigations demonstrating that pathological hypertrophy and physiological hypertrophy are associated with distinct molecular phenotypes. An aside to the major objective of identifying genes differentially regulated in left ventricular hypertrophy involved the application of the P19CL6 cell in vitro model of cardiomyogenesis to compare protein expression during hypertrophy and development. The Sin1 isoform, found to be up-regulated during DOCA-salt induced hypertrophy, was also shown to be more abundant in differentiating, than non-differentiating, P19CL6 cells. This result is consistent with the developing paradigm that implicates 'fetal' genes in the hypertrophic remodelling process.
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Hill, Nathan R. "Analysis of non-steady state physiological and pathological processes." Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:c96c88a6-5dd4-43ce-989b-ac524d2654ea.

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The analysis of non steady state physiological and pathological processes concerns the abstraction, extraction, formalisation and analysis of information from physiological systems that is obscured, hidden or unable to be assessed using traditional methods. Time Series Analysis (TSA) techniques were developed and built into a software program, Easy TSA, with the aim of examining the oscillations of hormonal concentrations in respect to their temporal aspects – periodicity, phase, pulsatility. The Easy TSA program was validated using constructed data sets and used in a clinical study to examine the relationship between insulin and obesity in people without diabetes. In this study fifty-six non-diabetic subjects (28M, 28F) were examined using data from a number of protocols. Fourier Transform and Autocorrelation techniques determined that there was a critical effect of the level of BMI on the frequency, amplitude and regularity of insulin oscillations. Second, information systems formed the background to the development of an algorithm to examine glycaemic variability and a new methodology termed the Glycaemic Risk in Diabetes Equation (GRADE) was developed. The aim was to report an integrated glycaemic risk score from glucose profiles that would complement summary measures of glycaemia, such as the HbA1c. GRADE was applied retrospectively to blood glucose data sets to determine if it was clinically relevant. Subjects with type 1 and type 2 diabetes had higher GRADE scores than the non-diabetic population and the contribution of hypo- and hyperglycaemic episodes to risk was demonstrated. A prospective study was then designed with the aim to apply GRADE in a clinical context and to measure the statistical reproducibility of using GRADE. Fifty-three (Male 26, Female 27) subjects measured their blood glucose 4 times daily for twenty-one days. The results were that lower HbA1c’s correlated with an increased risk of hypoglycaemia and higher HbA1c’s correlated with an increased risk of hyperglycaemia. Some subjects had HbA1c of 7.0 but had median GRADE values ranging from 2.2 to 10.5. The GRADE score summarized diverse glycaemic profiles into a single assessment of risk. Well-controlled glucose profiles yielded GRADE scores <= 5 and higher GRADE scores represented increased clinical risk from hypo or hyperglycaemia. Third, an information system was developed to analyse data-rich multi-variable retinal images using the concept of assessment of change rather than specific lesion recognition. A fully Automated Retinal Image Differencing (ARID) computer system was developed to highlight change between retinal images over time. ARID was validated using a study and then a retrospective study sought to determine if the use of the ARID software was an aid to the retinal screener. One hundred and sixty images (80 image pairs) were obtained from Gloucestershire Diabetic Eye Screening Programme. Images pairs were graded manually and categorised according to how each type of lesion had progressed, regressed, or not changed between image A and image B. After a 30 day washout period image pairs were graded using ARID and the results compared. The comparison of manual grading to grading using ARID (Table 4.3) demonstrated an increased sensitivity and specificity. The mean sensitivity of ARID (87.9%) was increased significantly in comparison to manually grading sensitivity (84.1%) (p<0.05). The specificity of the automated analysis (87.5%) increased significantly from the specificity (56.3%) achieved by manually grading (p<0.05). The conclusion was that automatic display of an ARID differenced image where sequential photographs are available would allow rapid assessment and appropriate triage. Forth, non-linear dynamic systems analysis methods were utilised to build a system to assess the extent of chaos characteristics within the insulin-glucose feedback domain. Biological systems exist that are deterministic yet are neither predictable nor repeatable. Instead they exhibit chaos, where a small change in the initial conditions produces a wholly different outcome. The glucose regulatory system is a dynamic system that maintains glucose homeostasis through the feedback mechanism of glucose, insulin, and contributory hormones and was ideally suited to chaos analysis. To investigate this system a new algorithm was created to assess the Normalised Area of Attraction (NAA). The NAA was calculated by defining an oval using the 95% CI of glucose & Insulin (the limit cycle) on a phasic plot. Thirty non-diabetic subjects and four subjects with type 2 diabetes were analysed. The NAA indicated a smaller range for glucose and insulin excursions with the non-diabetics subjects (p<0.05). The conclusion was that the evaluation of glucose metabolism in terms of homeostatic integrity and not in term of cut-off values may enable a more realistic approach to the effective treatment and prevention of diabetes and its complications.
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Kenyon, Karla. "The physiological and pathological regulation of apoptotic cell clearance /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Immunology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 177-196). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Aguirre, Gutiérrez Marisa Mayela. "Behavioural and physiological indices of normal and pathological sleepiness." Thesis, University of Ottawa (Canada), 1985. http://hdl.handle.net/10393/4942.

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Whittaker, Roger Graham. "The role of mitochondria in physiological and pathological cortical oscillations." Thesis, University of Newcastle Upon Tyne, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.525023.

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Books on the topic "Physiological, Pathological"

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West, S. H., ed. Physiological-Pathological Interactions Affecting Seed Deterioration. Madison, WI, USA: Crop Science Society of America, 1986. http://dx.doi.org/10.2135/cssaspecpub12.

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Hymes, Ian. Thermal radiation: Physiological and pathological effects. Rugby: Institution of Chemical Engineers, 1996.

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International, Congress on Pediatric Work Physiology (16th 1991 Clermont-Ferrand France). Pediatric work physiology: Methodological, physiological and pathological aspects. Paris: Masson, 1992.

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Jepson, Mark Andrew. Physiological and pathological implications of hepatic parenchymal heterogeneity. Birmingham: University of Birmingham, 1988.

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Riley, P. A., and Jan Borovansky. Melanins and melanosomes: Biosynthesis, biogenesis, physiological, and pathological functions. Weinheim: Wiley-Blackwell, 2011.

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1942-, Dyer Ruthanna, ed. Pathophysiology for the health professions. 4th ed. St. Louis, Mo: Saunders/Elsevier, 2011.

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van de Winkel, Jan G. J., and P. Mark Hogarth, eds. The Immunoglobulin Receptors and their Physiological and Pathological Roles in Immunity. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5018-7.

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1910-, Sweet William Herbert, ed. Neurosurgical treatment of persistent pain: Physiological and pathological mechanisms of human pain. Basel: Karger, 1989.

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Crisafulli, Antonio. New insight into cardiovascular apparatus during exercise: Physiological and physio-pathological aspects. Trivandrum, Kerala, India: Research Signpost, 2007.

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Lazenby, Ramona Browder. Handbook of pathophysiology. 4th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2011.

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Book chapters on the topic "Physiological, Pathological"

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Jacob, R., M. Vogt, and H. Rupp. "Physiological and Pathological Hypertrophy." In Developments in Cardiovascular Medicine, 39–56. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2051-7_2.

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Cuspidi, Cesare, Laura Lonati, Lorena Sampieri, Gastone Leonetti, and Alberto Zanchetti. "Physiological Versus Pathological Hypertrophy." In Advances in Experimental Medicine and Biology, 145–58. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5385-4_16.

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Pitrez, Patrícia R., Helena R. Aires, Inês Tomé, Rita Sá Ferreira, and Lino Ferreira. "Physiological and Pathological Vascular Aging." In Biophysical Regulation of Vascular Differentiation and Assembly, 51–72. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99319-5_3.

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Cain, S. M. "Physiological and Pathological Oxygen Supply Dependency." In Update in Intensive Care and Emergency Medicine, 114–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84169-9_9.

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Cavallucci, Virve, and Marcello D’Amelio. "Physiological and Pathological Role of Apoptosis." In Apoptosome, 1–26. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3415-1_1.

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Borovanský, Jan, and Patrick A. Riley. "Physiological and Pathological Functions of Melanosomes." In Melanins and Melanosomes, 343–81. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527636150.ch12.

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Thorne, John H. "Physiology of Soybean Seed Development." In Physiological-Pathological Interactions Affecting Seed Deterioration, 1–10. Madison, WI, USA: Crop Science Society of America, 2015. http://dx.doi.org/10.2135/cssaspecpub12.c1.

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Harman, G. E., and T. E. Stasz. "Influence of Seed Quality on Soil Microbes and Seed Rots." In Physiological-Pathological Interactions Affecting Seed Deterioration, 11–37. Madison, WI, USA: Crop Science Society of America, 2015. http://dx.doi.org/10.2135/cssaspecpub12.c2.

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Mills, J. T. "Postharvest Insect-Fungus Associations Affecting Seed Deterioration." In Physiological-Pathological Interactions Affecting Seed Deterioration, 39–51. Madison, WI, USA: Crop Science Society of America, 2015. http://dx.doi.org/10.2135/cssaspecpub12.c3.

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McGee, D. C. "Environmental Factors Associated with Preharvest Deterioration of Seeds." In Physiological-Pathological Interactions Affecting Seed Deterioration, 53–63. Madison, WI, USA: Crop Science Society of America, 2015. http://dx.doi.org/10.2135/cssaspecpub12.c4.

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Conference papers on the topic "Physiological, Pathological"

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Tolokonnikov, G. K. "PATHOLOGICAL AND FUNCTIONAL SYSTEMS. CATEGORICAL ASPECT." In MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-75.

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CAZZULLO, CARLO LORENZO. "COGNITIVE IMPAIRMENT IN PHYSIOLOGICAL AND PATHOLOGICAL AGING." In IX World Congress of Psychiatry. WORLD SCIENTIFIC, 1994. http://dx.doi.org/10.1142/9789814440912_0020.

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Umarova, Bella. "MAST CELLS: ROLE IN PHYSIOLOGICAL AND PATHOLOGICAL PROCESSES." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m586.sudak.ns2019-15/416-417.

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Rusu, LD, Laura Poanta, Cristina Hotoleanu, Lucica Coldea Agoston, D. Zdrenghea, and DL Dumitrascu. "Heart rate variability assessment — physiological and pathological aspects." In 2008 IEEE International Conference on Automation, Quality and Testing, Robotics. IEEE, 2008. http://dx.doi.org/10.1109/aqtr.2008.4588882.

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Killian, Megan L., and Tammy L. Haut Donahue. "Effect of Pathological and Physiological Loads on Interleukin-1α Protein Production in Porcine Menisci." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192145.

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The meniscus performs several functions for the maintenance of knee joint health, such as load transmission and joint stability. Meniscal lesions have been suggested as a precursor to the onset of osteoarthritis (OA)[1]. Such lesions often lead to surgical removal of the torn portion of the meniscus, increasing cartilage to cartilage contact area. Partial meniscectomies have been shown using finite element analysis and histology to lead to altered and increased mechanical loading on the remaining meniscus and underlying articular cartilage[2,3]. Consequently, pathological compressive strains of more than 15% have been shown to increase proteoglycan breakdown and meniscal matrix degradation[4]. Preliminary investigations in our laboratory have demonstrated an increase in interleukin-1α (IL-1α) gene expression of meniscal explants subjected to pathological levels of dynamic compressive strain [6,7]. This inflammatory cytokine has been attributed to apoptosis and matrix degradation[5]. However, gene expression measurements merely suggest possible matrix remodeling mechanisms and do not necessarily result in protein syntheses from which matrix changes occur. Therefore, the purpose of this study was to quantify protein synthesis of IL-1α in porcine meniscal implants after compressive strain exercises. It was hypothesized that, similar to mRNA expression, protein synthesis for pathologically loaded (0 or 20% dynamic strain) samples would be greater than samples loaded to physiological levels (10% strain).
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Abraham, Adam C., Kenton R. Kaufman, and Tammy L. Haut Donahue. "Internal Pressure of the Human Meniscal Attachments During Physiological and Pathological Loading." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80742.

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Knee menisci are semi-lunar, fibrocartilaginous structures that convert applied compressive loads to circumferential hoop stresses which are attenuated at the tibial plateau via the meniscal attachments [1]. These specialized interfaces, located at the lateral anterior (LA), lateral posterior (LP), medial anterior (MA), and medial posterior (MP) horns, are crucial to maintaining mechanical functionality of menisci, thereby preventing osteoarthritis [2]. Soft-tissues subjected to compression and shear loads are known to possess proteoglycans, which aid in resisting these applied stresses by retaining interstitial fluid [1]. Interestingly, proteoglycans are also known to be present at the meniscus to bone interface [3]. Despite the presence of these biphasic attachments and their important role in joint load transfer, there have been no quantitative investigations of the mechanical environment within these attachments under physiological and pathological loads. Recent development of a novel pressure microsensor now allows direct observation of fluid pressure, which will aid in understanding the internal mechanical environment within the attachment sites. Previous work indicates that the attachment sites are geometrically, mechanically, and histologically different [4], thus it is hypothesized that the fluid pressures would likewise differ.
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Murai, Toshiyuki, and Hiroto Kawashima. "Tools for analysis of cell adhesion molecules under physiological and pathological conditions." In 2008 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2008. http://dx.doi.org/10.1109/mhs.2008.4752473.

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Bark, David L., Andrea N. Para, and David N. Ku. "Thrombus Initiation With Subsequent Growth Measured for Physiological Shear and High Pathological Shear." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53865.

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Arterial thrombosis is often found near an atheroma in atherosclerotic disease, which can lead to acute myocardial infarction, i.e. a heart attack. Thrombus typically grows in regions of exposed subendothelium, which can exist when the plaque cap of the atheroma ruptures or erodes. The subendothelium creates an adherent surface to platelets and other thrombus constituents. Furthermore, an atheroma alters the normal physiological hemodynamics, which has been reported to correspond to local thrombus growth, despite equally adherent surfaces in undisturbed flow regions [1,2]. However, there has been some disagreement about which hemodynamics, specifically shear, may play the most influential role of localizing thrombus. Low shear and high shear have both resulted in thrombus growth [1,2]. Shear in the region of an atheroma can get over 100,000 s−1 [3].
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Chen, Wei, Jizhong Lou, Jen Hsin, Klaus Schulten, and Cheng Zhu. "In Silico Force-Induced Unbending of αVβ3 Integrin." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206205.

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Integrins are type I transmembrane heterodimers that consist of two noncovalently associated α- and β-subunits. They mediate cell-cell, cell-extracellular matrix, and cell-pathogen adhesions in a wide variety of physiological and pathological processes [1].
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10

Ackermann, Marko. "A Novel Optimization Approach to Generate Physiological Human Walking Patterns." In ASME 2007 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/detc2007-35014.

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Dynamic simulation of the musculoskeletal system is increasingly being used to study human normal and pathological walking. The common approach to predict walking patterns is based on the assumption that the central nervous system minimizes an intrinsic performance criterion. For instance, during walking, the energy expenditure per unit of distance traveled was shown to play a key role. The resulting optimal control problem is almost exclusively solved by the so-called dynamic optimization. Dynamic optimization relies on the parameterization of neural excitations using nodal values serving as optimization variables. The reconstructed neural excitations are then used to numerically integrate the differential equations describing the dynamics of the musculoskeletal system. This approach has been successfully applied to predict salient normal walking patterns, including muscle coordination and energy expenditure. In spite of the growing use of dynamic optimization, the extremely high computational effort arising from the several numerical integrations of the large-scale state equations required prevents it from being more widely applied, e.g., for bioassistive devices. Approaches based on inverse dynamics have the potential to reduce the high computation effort by avoiding the necessity of numerically integrating the state equations, but have been poorly explored in biomechanics. The development of an inverse dynamics-based approach to generate near-optimal human walking patterns that deals with the overdeterminacy of muscle actuation in conjunction with Hill-type muscle models widely used in biomechanics is proposed in this paper. The approach is based on the parameterization of the motion and muscle forces. The neural excitations are obtained by inverting the muscle contraction and activation dynamics. The compatibility between motion and muscle forces is guaranteed by checking the fulfillment of the equations of motion of the skeletal system at control points. The approach is implemented and human normal and pathological gaits are generated and applied to the design of transtibial prostheses.
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