Books: 'Active tissue'

1

service), SpringerLink (Online, ed. Active Implants and Scaffolds for Tissue Regeneration. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2011.

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Zilberman, Meital, ed. Active Implants and Scaffolds for Tissue Regeneration. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-18065-1.

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3

Treinen, Moslen Mary, and Smith Charles V, eds. Free radical mechanisms of tissue injury. Boca Raton: CRC Press, 1992.

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4

Cassidy, Nicola Marie. Isolation of extracellular matrix components from dentine active in dental cytodifferentiation and tissue repair. Birmingham: University of Birmingham, 1995.

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5

Nowak, Alicja. Metabolizm tkanki kostnej u aktywnych fizycznie młodych mężczyzn-- wpływ wysiłku fizycznego =: Bone tissue metabolism in active young men--influence of physical exercise. Poznań: Akademia Wychowania Fizycznego im. Eugeniusza Piaseckiego, 2005.

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6

Miller, Franklin G. Death, dying, and organ transplantation: Reconstructing medical ethics at the end of life. Oxford: Oxford University Press, 2011.

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7

Robert, Truog, ed. Causing death: Reconstructing medical ethics at the end of life. Oxford: Oxford University Press, 2011.

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8

Clark, J. Andrew. Scar tissue. [Santa Barbara, CA?]: Lip Think Press in conjunction with Dial R Studios, 2007.

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9

Crasbercu, Corinne. Tout en patch' ...: Plaids, sacs et autres bricoles. [Paris]: Marabout, 2010.

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10

Reid, Helen M. Tissue inhibitors of matrix metalloproteinases are modulated differently by 12-0-Tetradeconoylphorbol-13-actate (TPA) and 1,1,1-Trichoro-2,2-Bis-(p-Chlorophenyl)-ethane (DDT). [S.l: The Author], 1997.

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11

Ontario. Esquisse de cours 12e année: Vie active et santé ppl4o cours ouvert. Vanier, Ont: CFORP, 2002.

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12

E, Bloom Floyd, and Roth Robert H. 1939-, eds. The biochemical basis of neuropharmacology. 8th ed. Oxford: Oxford University Press, 2003.

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13

E, Bloom Floyd, and Roth Robert H. 1939-, eds. The biochemical basis of neuropharmacology. 6th ed. New York: Oxford University Press, 1991.

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14

E, Bloom Floyd, ed. The biochemical basis of neuropharmacology. 7th ed. New York: Oxford University Press, 1996.

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15

E, Bloom Floyd, and Roth Robert H. 1939-, eds. The biochemical basis of neuropharmacology. 5th ed. New York: Oxford University Press, 1986.

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16

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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17

Ontario. Esquisse de cours 12e année: Danse atc4m cours préuniversitaire. Vanier, Ont: CFORP, 2002.

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18

Ontario. Esquisse de cours 12e année: Histoire de l'Occident et du monde chy4c cours précollégial. Vanier, Ont: CFORP, 2002.

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19

Ontario. Esquisse de cours 12e année: English eae4u cours préuniversitaire. Vanier, Ont: CFORP, 2002.

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20

Zilberman, Meital. Active Implants and Scaffolds for Tissue Regeneration. Springer, 2011.

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21

Zilberman, Meital. Active Implants and Scaffolds for Tissue Regeneration. Springer, 2013.

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22

Maibach, Howard I., and Peter Elsner. Cosmeceuticals And Active Cosmetics (Cosmetic Science and Technology). 2nd ed. Crc Pr I Llc, 2005.

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23

B, Matkovics, Karmazsin L, Kalász H. 1941-, and Oxygen Radical Conference (3rd : 1989 : Szeged, Hungary), eds. Radicals, ions, and tissue damage. Budapest: Akadémiai Kadó, 1990.

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24

Oxygen stress and tissue damage. Budapest: Akadémiai Kiadó, 1994.

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25

1940-, Tarr Merrill, and Samson Fred 1918-, eds. Oxygen free radicals in tissue damage. Boston: Birkhäuser, 1993.

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26

Oxygen free radicals and the tissue injury. Budapest: Akadémiai Kiadó, 1988.

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27

Balasubramaniyam, Lavanya, Brian James Abelson, and Kamali Thara Abelson. Release Your Pain - Resolving Soft Tissue Injuries with Exercise and Active Release Techniques. Rowan Tree Books Ltd., 2012.

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28

Barry, Halliwell, and Upjohn Company, eds. Oxygen radicals and tissue injury: Proceedings of a Brook Lodge symposium, Augusta, Michigan, U.S.A., April 27 to 29, 1987. Bethesda, MD, U.S.A: Published for the Upjohn Company by the Federation of American Societies of Experimental Biology, 1988.

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29

Miller, Franklin G., and Robert D. Truog. Death, Dying, and Organ Transplantation: Reconstructing Medical Ethics at the End of Life. Oxford University Press, Incorporated, 2016.

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30

Miller, Franklin G., and Robert D. Truog. Death, Dying, and Organ Transplantation: Reconstructing Medical Ethics at the End of Life. Oxford University Press, 2012.

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31

Bellingan, Geoffrey, and Brijesh V. Patel. Repair and recovery mechanisms following critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0309.

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Inflammation is the beneficial host response to foreign challenge or tissue injury that ultimately leads to the restoration of tissue structure and function. Critical illness is associated with an overwhelming and prolonged inflammatory activation. Resolution of the inflammatory response is an active process that requires removal of the inciting stimuli, cessation of the pro-inflammatory response, a timely coordinated removal of tissue leukocyte infiltration, a conversion from ‘toxic’ to reparative tissue environment, and restoration of normal tissue structure and function. Mortality may result from deficits in these resolution mechanisms. Improved delivery of critical care through prevention of harm and removal of stimuli has already delivered significant mortality benefits. Most critically-ill patients present with uncontrolled inflammation, hence anti-inflammatory strategies ameliorating this response are likely to be too late and thus futile. Rather, strategies augmenting endogenous pathways involved in the control and appropriate curtailment of such inflammatory responses may promote resolution, repair, and catabasis. Recent evidence showing that inflammation does not simply ‘fizzle out’, but its resolution involves an active and coordinated series of events. Dysfunction of these resolution checkpoints alters the normal inflammatory pathway, and is implicated in the induction and maintenance of states such as ARDS and sepsis. Improved understanding of resolution biology should provide translational pathways to not only improve survival, but also to prevent long-term morbidity resulting from tissue damage.

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32

Rothschild, Bruce, and Ernst Feldtkeller. Spondyloarthritis in antiquity and in history. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0001.

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Spondyloarthropathy has a long history in the fossil record, one that even predates dinosaurs. It is prevalent in contemporary animals, especially apes, bears, rhinoceros, and Komodo dragons. Prevalence in the archaeologic record is predominantly uniform, independent of geology, except in areas where sanitation is compromised. Major advance in its diagnosis came about with the introduction of radiologic techniques, HLA-B27 tissue typing, and recognition that it was not a rheumatoid variant. In spondyloarthritis therapy, immobilization was replaced by active physiotherapy and thorough patient education.

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33

O’Connell, Sue. Lyme borreliosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0009.

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Lyme borreliosis is the most common vector-borne bacterial infection in the temperate northern hemisphere. In the United States of America over 35,000 confirmed or probable cases were reported by state health departments to the Centers for Disease Control and Prevention (CDC) in 2008. It is likely that well over 100,000 cases occur in Europe each year. Lyme borreliosis is caused by several genospecies of Borrelia burgdorferi sensu lato, which are transmitted by ticks of the Ixodes ricinus complex. The infection occurs most commonly in forested, woodland and heathland habitats that support the lifecycles of Ixodes ticks and the small mammals and birds that are reservoir-competent hosts for B burgorferi. The most common presenting feature of Lyme borreliosis is erythema migrans, a slowly spreading rash. The spirochaetes can disseminate through the bloodstream and lymphatics to other organs and tissues and cause later manifestations, most commonly affecting the nervous and musculoskeletal systems. The infection responds to appropriate antibiotic treatment at any stage of disease, with excellent outcomes in most cases, but patients with severe tissue damage from previously untreated late stage disease may recover incompletely. A small proportion of patients can have persistent non-specific symptoms following treatment, without evidence of continuing active infection. This has been termed “post-Lyme syndrome” and appears to be similar to other post-infection syndromes. Prevention relies mainly on personal protection measures against tick bites.

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34

Ali, Ased, and Rob Pickard. Infection of the lower urinary tract. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0176_update_001.

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Lower urinary tract infection is common, distressing, and when recurrent can have a significant impact on quality of life. The normally sterile urinary tract is the site of an ongoing but complex interplay between an evolving pathogen and a highly developed host immune defence system. The development of an active infection generally requires either greater virulence in the pathogen or deficient host immune defence. Nonetheless, even where infection has occurred, the interplay between pathogen and host continues, influencing the extent and level of invasion as well as the duration of infection and extent of tissue damage caused.Asymptomatic bacteriuria is discussed, with implications for treatment (usually not). The risk factors, diagnosis and management of simple cystitis are discussed, with a discussion of approaches to managing recurrent infections. Urethritis requires consideration of sexually transmitted infections and co-infections. Prostatitis requires more prolonged antibiotic treatment.

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35

Cooperberg, Matthew, and Peter Carroll. Prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0064.

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Management of prostate cancer remains controversial, in large part because of its wide heterogeneity in terms of aggressiveness and prognosis. Early detection efforts based on prostate specific antigen (PSA) and aggressive treatment of high-risk cancers have yielded major improvements in mortality rates, but overtreatment of low-risk cancers—those unlikely to cause symptoms or threaten life if they were never detected—is associated with high rates of avoidable toxicity and cost. Prostate cancer can be effectively risk-stratified based on tools (e.g. nomograms, CAPRA score) integrating the PSA level, Gleason grade, clinical stage, and extent of biopsy tissue involvement. Most men with low-risk tumours are eligible for active surveillance, a programme of careful monitoring based on PSA and follow-up biopsies. Men with higher-risk cancers are best served with radical prostatectomy or radiation therapy.

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36

Flanagan, Stuart. Pneumocystis jirovecii. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0019.

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In humans, Pneumocystis pneumonia is caused by a yeast-like fungus Pneumocystis jirovecii. Originally called P. carinii, this organism was thought to be a protozoan; however, the discovery of chitin, β‎-1,3-glucan, and ergosterol in the cell wall confirmed it as a fungus. DNA analysis demonstrated that the human disease was caused by P. jirovecii, while P. carinii was found to infect rats. P. jirovecii resides in mammalian lung tissue, usually without ill effects, but in immunocompromised hosts it becomes pathogenic and causes respiratory infection. P. jirovecii has been isolated from air and pond water samples; pond water is the potential source of infection. Almost 90% of cases of Pneumocystis pneumonia occur in HIV-positive individuals with CD4 T-cell counts below 200 cells per microlitre. The infection is diagnosed by clinical history, assessment of oxygenation levels, and direct microscopy of sputum or bronchoalveolar lavage samples. Treatment requires antibiotics and HAART (highly active antiretroviral therapy) for HIV infection.

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37

Tissue-specific estrogen action: Novel mechanisms, novel ligands, novel therapies. Berlin: Springer, 2007.

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38

S, Korach Kenneth, and Wintermantel Tim, eds. Tissue-specific estrogen action: Novel mechanisms, novel ligands, novel therapies. Berlin: Springer, 2007.

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39

Korach, Kenneth S., and Tim Wintermantel. Tissue-Specific Estrogen Action: Novel Mechanisms, Novel Ligands, Novel Therapies. Springer Berlin / Heidelberg, 2014.

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40

Sempert, Mattie-Martha. Sweet Spots: Writing the Connective Tissue of Relation. punctum books, 2021. http://dx.doi.org/10.53288/0340.1.00.

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Sweet Spots thinks transversally across language and body, and between text and tissue. This assemblage of essays collectively proposes that words—that is, language that lands as written text—are more-than-human material. And, these materials, composed of forces and flows and tendencies, are capable of generating text-flesh that grows into a thinking in the making. The practice of acupuncture—and its relational thinking—often makes its presence felt to twirl the text-tissue of the bodying essays. Ficto-critical thinking is threaded throughout to activate concepts from process philosophy and use the work of other thinkers (William James, Félix Guattari and Gilles Deleuze, Baruch Spinoza, and Virginia Woolf, to name a few) to forge imaginative connections. Entangled in the text-tissue are an assortment of entities, such as bickering body parts, quivering jellyfish, heart pacemaker cells, a narwhal tooth, Taoist parables, always with ubiquitous, stretchy connective tissue — from gooey interstitial fluid to thick planes of fascia — ever present to ensure that the essaying bodies become, what Alfred North Whitehead calls the one-which-includes-the-many-includes-the-one. The essaying bodies orient towards the sweetest sweet spot which is found, not in the center, but slightly askew, felt in the reverbing more-than that carries their potential. Crucially, this produces a shift in perspective away from self-enclosed bodies and experts toward a care for the connective tissue of relation.

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41

Uwe, Lendeckel, and Hooper N. M, eds. Proteases in tissue remodelling of lung and heart. New York: Kluwer Academic/Plenum Publishers, 2003.

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42

Proteases in tissue remodeling of lung and heart. New York, NY: Kluwer Academic/Plenum Publishers, 2004.

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43

Clarke, Andrew. Water. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199551668.003.0005.

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Liquid water is essential for life, and a metabolically active cell is ~70% water. The physical properties of liquid water, and their temperature dependence, are dictated to a significant extent by the properties of hydrogen bonds. From an ecological perspective, the important properties of liquid water include its high latent heats of fusion and vapourisation, its high specific heat, the ionisation, low dynamic viscosity and high surface tension. The solubility in water of oxygen, carbon dioxide and the calcium carbonate used to build skeletons in many invertebrates groups all increase with decreasing temperature. The hydrophobic interaction is important in the formation of cellular membranes and the folding of proteins; its strength increases with temperature, which may be a factor in the cold-denaturation of cellular macromolecules. The cell is extremely crowded with macromolecules. Coupled with the highly structured water close to membranes or protein surfaces and the hydration shells around ions, this means that the behaviour of water in cells is different from that of bulk water. The thermal behaviour of isolated cellular components studied in dilute aqueous buffers many not reflect accurately their behaviour in the intact cell or tissue.

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44

(Editor), K. S. Korach, and Tim Wintermantel (Editor), eds. Tissue-Specific Estrogen Action: Novel Mechanisms, Novel Ligands, Novel Therapies (Ernst Schering Foundation Symposium Proceedings). Springer, 2007.

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45

Dixon, Sharon. Principles of biomechanics and their use in the analysis of injuries and technique. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199533909.003.0008.

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Biomechanics, defined literally, is the mechanics of living systems. Human biomechanics involves the study of mechanical aspects of human movement. It is the science studying the internal and external forces experienced by the human and the effects of such forces. Nigg and Herzog (2007) highlight that forces may result in movement of body segments, deformation of biological materials, or biological changes in the tissue(s) on which they act. Thus biomechanics can involve the study of human movement and factors that affect this movement, deformation of biological structures and factors that influence this, and the biological effects of locally acting forces on living tissue (e.g. effects on growth development or injuries)....

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46

Rich, Mark M. Critical Illness Neuropathy, Myopathy, and Sodium Channelopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0033.

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Skeletal muscle weakness is a common problem that complicates recovery from critical illness. The primary causes of weakness include neuropathic disorders, myopathic disorders, and mixed disorders. Recent studies have demonstrated that reduced excitability of the nerve and muscle cell membranes might contribute to weakness during the acute stages of the polyneuropathy and myopathy encountered in critically ill patients. In both tissues, an acquired sodium channelopathy can lead to increased inactivation of channels, leading to inexcitability an paralysis. Experimental sepsis models have demonstrated a similar reduction in excitability in myocardial cells as well as in motor neurons within the spinal cord. The presence of a channelopathy in multiple tissues raises the possibility that reduced excitability of neurons within the CNS might contribute to septic encephalopathy. If this is the case, a single therapy to improve excitability might treat failure of a number of electrically active tissues.

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47

Hutson, Mike. Assessment and management. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199533909.003.0011.

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Individuals undertaking exercise include those engaged in aerobic activities as part of a healthy lifestyle, those engaged in an active fitness or rehabilitation programme relevant to acute or chronic conditions such as cardiovascular disease, respiratory problems, and musculoskeletal disorders, and the committed competitive athlete with high performance targets. Accordingly, those injured as a consequence of exercise or sport attend medical practitioners in diverse circumstances. Urgency of assessment of the full impact of injury clearly varies across the spectrum from the life-threatening situation on the field of play (or other sports/recreational exercise location, for instance poolside or roadside) to one in which a chronic condition can be evaluated in the relative comfort of the clinician’s consulting room. Irrespective of the circumstances, the primary requirement is the establishment of an accurate diagnosis. The process of assessment is aided when relevant by an appropriate index of suspicion with respect to those injuries that are not often seen outside sporting and recreational activity (e.g. throwers’ elbow and shin splints). Diagnosis of tissue injury is followed by a full assessment of its impact on the function of the surrounding structures, and subsequently assessment of impairment of sporting capacity in general. Evaluation is made of the aetiological factors associated with the development of injury, the behavioural responses, including motivation and health prioritization, and the individual’s standard of performance (actual and potential). Clinical assessment (and reassessment) is a constant theme throughout the text....

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48

Poppinga, Simon, Ulrike Bauer, Thomas Speck, and Alexander G. Volkov. Motile traps. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198779841.003.0014.

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We review the biomechanics, functional morphology, and physiology of motile traps. The movements of snap traps in Aldrovanda and Dionaea, motile adhesive traps in Drosera and Pinguicula, and suction traps in Utricularia are driven by active water displacement processes leading to reversible turgor changes of motor cells, irreversible growth, or mechanical pre-stressing of tissues. In some cases, the motion is amplified by the release of elastic energy stored in these tissues. The only known case of a passive motile trapping movement is the ‘springboard’ trapping mechanism of Nepenthes gracilis, in which a rapid vibration of the pitcher lid is actuated by the impact force of raindrops. Open research questions are summarized and future studies are suggested.

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49

Wainger, Brian J. Drug Discovery and Neuropathic Pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0117.

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Pain is one of the most common causes of physician visits and disability. Pain has been classified into specific subtypes. We refer to baseline or nociceptive pain as pain that results from an ongoing, high-threshold stimulus acting on an unenhanced somatosensory system. Inflammatory pain refers to pain in the setting of tissue damage and specifically the release of inflammatory molecules that activate and sensitize the nociceptive machinery. Hyperalgesia, or increased pain in response to a noxious stimulus, results from nociceptor sensitization whereas neuropathic pain results from a lesion or disease of the somatosensory system. Pain can have spontaneous, stimulus-independent components as well as evoked components such as hyperalgesia or allodynia, pain that is elicited by a normally innocuous stimulus. This chapter describes the research strategy for discovering new drugs to relieve these different kinds of pain.

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50

van Mil, Edgar G. A. H. Exercise, sport, and diabetes mellitus. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0036.

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Diabetes mellitus is a group of metabolic diseases characterized by chronic hyperglycaemia, resulting from defects in insulin secretion, insulin action, or both. The abnormalities in carbohydrate, fat, and protein metabolism that are found in diabetes are due to deficient action of insulin on target tissues (www.ispad.org)....

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Books on the topic 'Active tissue'

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