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Published: 4 June 2021
Last updated: 2 February 2022

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1

Schwartz, Marvin. Recovery of inferior alveolar nerve function following nerve damage. [Toronto: Faculty of Dentistry, University of Toronto], 1990.

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2

Kysela, Boris. Ionizing radiation-induced DNA damage and repair in relation to biological function. Uxbridge: Brunel University, 1994.

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3

Spence, John W. Theoretical damage function for the effects of acid deposition on galvanized steel structures. Research Triangle Park, NC: U.S. Environmental Protection Agency, Atmospheric Sciences Research Laboratory, 1988.

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4

Spence, John W. Theoretical damage function for the effects of acid deposition on galvanized steel structures. Research Triangle Park, NC: U.S. Environmental Protection Agency, Atmospheric Sciences Research Laboratory, 1988.

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5

The healing power of neurofeedback: The revolutionary LENS technique for restoring optimal brain function. Rochester, Vt: Healing Arts Press, 2006.

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6

Brain injury survival kit: 365 tips, tools & tricks to deals with cognitive function loss. New York: Demos Medical Pub., 2009.

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7

Söderback, Ingrid. Intellectual function training and intellectual housework training in patients with acquired brain damage: A study of occupational therapy methods. Stockholm: Folksam, 1988.

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8

Schutz, Larry E. Head injury recovery in real life. San Diego: Plural Pub., 2010.

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9

Brain repair after stroke. Cambridge: Cambridge University Press, 2010.

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10

Abraham, Kenneth S. The forms and functions of tort law. 2nd ed. New York, N.Y: Foundation Press, 2002.

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11

The forms and functions of tort law. 4th ed. New York, N.Y: Foundation Press Thomson/West, 2012.

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12

Murdoch, B. E. Acquired speech and language disorders: A neuroanatomical and functional neurological approach. Cheltenham: Stanley Thornes, 1997.

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13

Abraham, Kenneth S. The forms and functions of tort law: An analytical primer on cases and concepts. Westbury, N.Y: Foundation Press, 1997.

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14

Dasgupta, Purnamita. Valuing health damages from water pollution in urban Delhi, India: A health production function approach. Delhi: Institute of Economic Growth, 2001.

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15

Knoll, Franz, and Thomas Vogel. Design for Robustness. Zurich, Switzerland: International Association for Bridge and Structural Engineering (IABSE), 2009. http://dx.doi.org/10.2749/sed011.

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<p>Robustness is the ability to survive unforeseen circum-stances without undue damage or loss of function. It has become a requirement expressed in modern building codes, mostly without much advice as to how it can be achieved. Engineering has developed some approaches based on tra-ditional practice as well as recent insight. However, know-ledge about robustness remains scattered and ambiguous, making it difficult to apply to many specific cases.<p> The authors' attempt to collect and review elements, methods and strategies toward structural robustness, using a holistic, almost philosophical approach. This leads to a set of consid-erations to guide selection and implementation of measures in specific cases, followed by a collection of applications and examples from the authors practice.<p>The world, engineering and construction are imperfect and not entirely predictable. Robustness provides a measure of structural safety beyond traditional codified design rules.
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16

Dikengil, Angela Tipton. Building functional social skills: Group activities for adults. Tucson, Ariz: Therapy Skill Builders, 1992.

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17

(Editor), Harvey S. Levin, and Jordan Grafman (Editor), eds. Cerebral Reorganization of Function after Brain Damage. Oxford University Press, USA, 2000.

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18

Keeley, Susanne Phillips. The Source for Executive Function Disorders. LinguiSystems, 2003.

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19

Moe, Bergman, Lowenstein Rehabilitation Hospital, and International Congress of Physical Medicine and Rehabilitation (9th : 1984 : Jerusalem, Israel), eds. Restoration of function: An integrated rehabilitation approach. Stockholm: distributed by Almqvist & Wiksell, 1985.

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20

Radiation Damage in DNA: Structure/Function Relationships at Early Times. Battelle Press, 1995.

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21

1960-, Fuciarelli Alfred F., and Zimbrick John D. 1938-, eds. Radiation damage in DNA: Structure/function relationships at early times. Columbus: Battelle Press, 1995.

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22

Irmgard, Marboe. 2 The Function of Compensation and Damages. Oxford University Press, 2017. http://dx.doi.org/10.1093/law/9780198749936.003.0002.

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This chapter analyses the function of compensation and damages in international investment disputes. It shows that compensation upon expropriation serves a different function than damages after an unlawful act, be it breach of a treaty, such as a BIT, or a contract. While the former aims at the restitution of the ‘value’ of the expropriated property, the latter aims at providing “reparation” for the damage caused by the unlawful act. It follows that expropriation compensation should be equivalent to the ‘objective’ value of the expropriated asset while an amount of damages may also include subjective valuation approaches.
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23

Bunch, Chris. Normal blood function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0277.

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This chapter reviews normal blood function and disorders of haemopoiesis. Blood consists of cells of three main types, suspended in plasma. The cellular component comprises about 40%–50% of the total volume and consists of red cells (erythrocytes), white cells (leucocytes), and platelets. Blood cells are formed from progenitor cells in the bone marrow by haemopoiesis, a process of proliferation and differentiation. Failure of haemopoiesis usually results from damage to proliferating marrow cells by cytotoxic drugs or radiation, haemopoietic malignancy, or a combination of the two.
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24

Dinser, Robert, and Ulf Müller-Ladner. Skeletal muscle physiology and damage. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0055.

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This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.
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25

Dinser, Robert, and Ulf Müller-Ladner. Skeletal muscle physiology and damage. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0055_update_001.

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This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.
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26

Coakley, Davis. Minute Eye Movement and Brain Stem Function. Taylor & Francis Group, 2019.

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27

Coakley, Davis. Minute Eye Movement and Brain Stem Function. Taylor & Francis Group, 2019.

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28

Coakley, Davis. Minute Eye Movement and Brain Stem Function. Taylor & Francis Group, 2019.

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29

Coakley, Davis. Minute Eye Movement and Brain Stem Function. Taylor & Francis Group, 2019.

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30

S, Levin Harvey, Eisenberg Howard M, and Benton Arthur Lester 1909-, eds. Frontal lobe function and dysfunction. New York: Oxford University Press, 1991.

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31

Hodges, John R. Testing Cognitive Function at the Bedside. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780192629760.003.0005.

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Chapter 5 covers testing cognitive function at the bedside, and how the first part of the examination should assess distributed cognitive functions; deficits in these indicate damage to particular brain systems, but not to focal areas of one hemisphere. The second part of the assessment should deal with more localized functions, divided into those associated with the dominant (i.e. the left side, in right-handers) and non-dominant hemispheres.
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32

M, Dennis, Boll Thomas J, Bryant Brenda K. 1948-, and American Psychological Association, eds. Clinical neuropsychology and brain function: Research, measurement, and practice. Washington, DC: American Psychological Association, 1988.

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33

Cursi, Floriana. The Scope and Function of Civil Wrongs in Roman Society. Edited by Paul J. du Plessis, Clifford Ando, and Kaius Tuori. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780198728689.013.49.

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The earliest evidence of Roman delicts is to be found in the rules of the XII Tables which introduced the first types of delict and obligation. From these rules the Roman lawyers did not develop a general law of delict governing the delictual liability. The Roman system of delicts was in fact typical: with new delicts emerging until the first century BC. Simultaneously, during the final Republican period, the praetor introduced some actions for reparation of damage, later included by Justinian in quasi delict category. But the Roman system of delicts, was too typical to ensure the total reparation of the private damages deriving from an unlawful conduct. So actio de dolo was introduced to repair the loss caused by dolus, in case of absence of any specific delictual action. This was a subsidiary remedy, which filled the gaps of the typical system of actions.
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34

Hodges, John R. Testing Cognitive Function at the Bedside. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749189.003.0005.

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This chapter explores the second component of assessment in patients with suspected cognitive dysfunction: testing cognitive function at the bedside. The first part of the examination should assess distributed cognitive functions, notably orientation and attention, episodic and semantic memory, and frontal executive function (initiation in the form of verbal fluency, abstraction, response inhibition, and set shifting); deficits in these indicate damage to particular brain systems, but not to focal areas of one hemisphere. The second part of the assessment deals with localized functions, divided into those associated with the dominant (i.e. the left side, in right-handers) and non-dominant hemispheres. The former relates largely to tests of spoken language with supplementary tests of reading, writing, calculation, and praxis when applicable. Testing right hemisphere function focuses on neglect (personal and extrapersonal), visuospatial and constructional abilities, and the agnosias including object and face agnosia.
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35

Kortgen, Andreas, and Michael Bauer. Hepatic function in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0175.

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The liver with its parenchymal and non-parenchymal cells plays a key role in the organism with manifold functions of metabolism, synthesis, detoxification, excretion, and host response. This requires a portfolio of different tests to obtain an overview of hepatic function. In the critically ill hepatic dysfunction is common and potentially leading to extrahepatic organ dysfunctions culminating in multi-organ failure. Conventional laboratory measures are used to evaluate hepatocellular damage, cholestasis, or synthesis. They provide valuable (differential) diagnostic data and can yield prognostic information in chronic liver diseases, especially when used in scoring systems such as the ‘model for end-stage liver disease’. However, they have short-comings in the critically ill in assessing rapid changes in hepatic function and liver blood flow. In contrast, dynamic quantitative liver function tests measure current liver function with respect to the ability to eliminate and/or metabolize a specific substance. In addition, they are dependent on sinusoidal blood flow. Liver function tests have prognostic significance in the critically ill and may be used to guide therapy.
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36

(Foreword), Gottfried Jean-Louis, ed. The Mild Traumatic Brain Injury Workbook: Your Program for Regaining Cognitive Function & Overcoming Emotional Pain (New Harbinger Self-Help Workbook). New Harbinger Publications, 2004.

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37

Boll, Thomas. Clinical Neuropsychology and Brain Function: Research, Measurement, and Practice (Master Lectures in Psychology). Amer Psychological Assn, 1988.

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38

Wilsey, Brian J. Factors Maintaining and Regulating Grassland Structure and Function. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198744511.003.0003.

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Intrinsic disturbances are processes that have occurred on an evolutionary time scale, and include fire, wind-damage, digging or burrowing by fossorial mammals, defoliation, and trampling by native large mammals. Grassland species evolved with intrinsic disturbances, and they can be important in maintaining grassland community structure and functioning. Adaptations to fire include short herbaceous stature, high allocation belowground, ability to resprout, and smoke-induced seed germination. Fire interacts with grazing because grazing reduces litter (fuel) load, and fires affect forage quality. Plants can tolerate some level of herbivory in most grasslands. Adaptations that enable grassland plants to resist grazing are similar to plant adaptations to fire. Drought can affect grasslands at a variety of time scales. Vegetative reproduction can allow rapid recolonization after droughts have ended. Plowing is the most common disturbance affecting grasslands, and it has been used to transform native grasslands into crop fields and simplified pasture.
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39

A new merit function for evaluating the flaw tolerance of composite laminates. Hampton, Va: National Aeronautics and Space Administration, Langley Research Center, 1995.

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40

A new merit function for evaluating the flaw tolerance of composite laminates. Hampton, Va: National Aeronautics and Space Administration, Langley Research Center, 2000.

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41

A new merit function for evaluating the flaw tolerance of composite laminates. Hampton, Va: National Aeronautics and Space Administration, Langley Research Center, 1997.

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42

W, Shoesmith D., and Atomic Energy of Canada Limited., eds. Estimating the lifetimes of titanium containers for nuclear fuel waste: A damage function for the crevice corrosion of Grade-2 titanium. Pinawa, Man: AECL, Whiteshell Laboratories, 1995.

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43

W, Shoesmith D., Atomic Energy of Canada Limited., and Whiteshell Laboratories, eds. Estimating the lifetimes of titanium containers for nuclear fuel waste: A damage function for the crevice corrosion of grade-2 titanium. Pinawa, Man: Whiteshell Laboratories, 1995.

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44

1941-, Wilson Barbara A., ed. Neuropsychological rehabilitation: Theory, models, therapy, and outcome. Cambridge: Cambridge University Press, 2009.

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45

Gray, Doug, Carole Proctor, and Tom Kirkwood. Biological aspects of human ageing. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0001.

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At the molecular and cellular levels human ageing is characterized by the accumulation of unrepaired random damage, and an accompanying loss of function. A major source of damage is oxidative stress caused by the generation of reactive oxygen species as a by-product of respiration. DNA and proteins are both susceptible to damage but whereas DNA damage repair systems exist, faulty proteins are generally removed by protein degradation systems. During ageing these systems become less efficient and the subsequent accumulation of damaged protein promotes protein aggregation, a process which is especially problematic in the ageing brain. Other aspects of ageing include genetic and epigenetic changes, mitochondrial dysfunction, telomere shortening, and cellular senescence, all subject to stochasticity. The complexity of the biology of ageing has led to an increase in the use of systems biology approaches whereby the use of mathematical modelling and bioinformatic tools complement the more traditional experimental approaches.
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46

Neuropsychosological Rehabilitation. Springer Publishing Company, 2012.

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47

Turner, Neil. Mechanisms of progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0136.

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Three major hypotheses attempt to explain progressive kidney disease following diverse diseases and injuries. To varying degrees they can explain the observed risk factors for progression and the ability of interventions to lower risk. The hyperfiltration hypothesis argues that progression is due to stress on residual nephrons leading to injury and damage to remaining glomeruli. The toxicity of proteinuria hypothesis proposes that serum proteins or bound substances are toxic to tubular or tubulointerstitial cells. This sets up cycles of damage which lead to tubulointerstitial scarring. The podocyte loss hypothesis contends that proteinuria is simply a biomarker for damaged or dying podocytes, and that it is further podocyte loss that leads to progressive glomerulosclerosis. Renoprotective strategies might have direct effects on podocytes. Importantly these different hypotheses suggest different therapeutic approaches to protecting the function of damaged kidneys. Differences between repair mechanisms may explain why some injuries lead to recovery and others to progressive disease, and may suggest new targets for protective therapy.
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48

Salvatori, Daniela, Harsha D. Devalla, and Robert Passier. Cells to repair the infarcted myocardium. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0030.

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The adult mammalian heart has poor regenerative capacity. Loss of functional cardiomyocytes following myocardial infarction leads to the replacement of functional muscle by scar tissue. This has a detrimental effect on cardiac function and may lead to heart failure. Potential regeneration of severe cardiac damage would require replacement of dead and damaged cardiomyocytes by transplantation, recruitment of endogenous progenitor cells, or induction of cardiomyocyte proliferation. For more than a decade, clinical trials to ameliorate the injured heart have been under way. However, after evaluation of the outcome of these trials it is evident that the beneficial effects of these cell-based transplantations are only marginal, and beneficial effects, if any, are not caused by regeneration of cardiomyocytes. In recent years, alternative approaches and various cell sources have been studied and suggested for cardiac repair. Recent advances in these cell-based therapies or strategies to activate endogenous cardiac repair are discussed.
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49

Eder, Lihi. The clinical course and outcome of psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0021.

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In contrast to early reports, it is now appreciated that psoriatic arthritis (PsA) can present as a destructive, progressive, and disabling arthritis with consequences as severe as those of rheumatoid arthritis. Longitudinal cohort studies of PsA patients contributed important knowledge about long-term outcomes, such as development of structural joint damage, remission achievement, and physical function. These studies identified predictors for improved outcomes including male gender and lower burden of inflammation at presentation while delayed diagnosis, disability, and joint damage are associated with worse long-term outcomes. These findings suggest early diagnosis and aggressive control of inflammation are important as they may prevent the occurrence of subsequent joint damage. The latter is strongly correlated with long-term outcomes, such as reduced physical function and increased mortality. Development of prediction models using clinical measures, laboratory biomarkers, and imaging is warranted to stratify patients with early disease into risk groups for long-term outcomes.
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50

Levy, Barry S. Liver Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0030.

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This chapter describes occupational and environmental liver disorders. It describes the types of liver function and types of liver damage, and how these functions and this damage can be assessed. Workers in healthcare and solid waste management are at increased risk hepatitis B virus and hepatitis C virus infections. Occupational exposure to swine is associated with hepatitis E virus infection. More than 100 industrial chemicals can be acutely hepatotoxic in experimental animals or humans. Metabolic reactions may affect the hepatotoxicity of chemicals. Occupational exposure to organic solvents can cause toxic hepatitis. Occupational exposure to vinyl chloride monomer has been causally associated with toxicant-associated fatty liver disease as well as a form of non-cirrhotic portal hypertension. Several agents can cause cancer of the liver or bile ducts. Vinyl chloride monomer is causally associated with angiosacoma of the liver. Arsenic causes liver cancer. Dietary exposure to aflatoxins can cause hepatoceulluar carcinoma.
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