Log in

Relevant bibliographies by topics / Acute phase proteins / Books

To see the other types of publications on this topic, follow the link: Acute phase proteins.

Books on the topic 'Acute phase proteins'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 32 books for your research on the topic 'Acute phase proteins.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse books on a wide variety of disciplines and organise your bibliography correctly.

1

Pepys, M. B., ed. Acute Phase Proteins in the Acute Phase Response. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1739-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

B, Pepys M., ed. Acute phase proteins in the acute phase response. London: Springer-Verlag, 1989.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

3

Andrzej, Mackiewicz, Kushner Irving 1929-, and Baumann Heinz 1947-, eds. Acute phase proteins: Molecular biology, biochemistry, and clinical applications. Boca Raton: CRC Press, 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

4

Some aspects of induced protein synthesis in liver cells: Regulatory effects of interleukin-6, insulin, glicated proteins and polyglucans. Kraków: Wydawn. Uniwersytetu Jasgiellońskiego, 1997.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

5

T, Whicher J., and Evans S. W, eds. Biochemistry of inflammation. Dordrecht: Kluwer Academic Publishers, 1992.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

6

B, Sehgal Pravinkumar, Grieninger Gerd, Tosato Giovanna, New York Academy of Sciences., and National Foundation for Cancer Research., eds. Regulation of the acute phase and immune responses: Interleukin-6. New York, N.Y: New York Academy of Sciences, 1989.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

7

H, Gordon A., and Koj A, eds. The Acute-phase response to injury and infection: The roles of interleukin I and other mediators. Amsterdam: Elsevier, 1985.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

8

E, Sim, ed. Humoral factors. Oxford: IRL Press at Oxford University Press, 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

9

Janciauskiene, Sabina, ed. Acute Phase Proteins. InTech, 2013. http://dx.doi.org/10.5772/46063.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Acute Phase Proteins. CRC Press, 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

11

Veas, Francisco, ed. Acute Phase Proteins - Regulation and Functions of Acute Phase Proteins. InTech, 2011. http://dx.doi.org/10.5772/756.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Pepys, Mark B. Acute Phase Proteins in the Acute Phase Response. Springer, 2012.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

13

Pepys, Mark B. Acute Phase Proteins in the Acute Phase Response. Springer, 2012.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

14

Herdman, Jacqueline. Selenium containing proteins: Acute phase reactants? 1996.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

15

Baumann, Heinz, Andrzej Mackiewicz, and Irving Kushner. Acute Phase Proteins Molecular Biology, Biochemistry, and Clinical Applications. CRC, 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

16

S. Nawaz, M. Asif, Z.A. Bhutta, M.F. Kulyar, R. Hussain, A. Ramzan, S. Shafeeq, M.Z. Shakir, M.T. Sarfaraz, and K. Li*. A comprehensive review on acute phase proteins in chicken. Verlag Eugen Ulmer, 2021. http://dx.doi.org/10.1399/eps.2021.344.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Mackiewicz, Andrzej, Irving Kushner, and Heinz Baumann. Acute Phase Proteins Molecular Biology, Biochemistry, and Clinical Applications. Taylor & Francis Group, 2020.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

18

Mackiewicz, Andrzej, Irving Kushner, and Heinz Baumann. Acute Phase Proteins Molecular Biology, Biochemistry, and Clinical Applications. Taylor & Francis Group, 2020.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

19

Mackiewicz, Andrzej, Irving Kushner, and Heinz Baumann. Acute Phase Proteins Molecular Biology, Biochemistry, and Clinical Applications. Taylor & Francis Group, 2020.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

20

Mackiewicz, Andrzej, Irving Kushner, and Heinz Baumann. Acute Phase Proteins Molecular Biology, Biochemistry, and Clinical Applications. Taylor & Francis Group, 2020.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

21

Mackiewicz, Andrzej, Irving Kushner, and Heinz Baumann. Acute Phase Proteins Molecular Biology Biochemistry and Clinical Applications. Taylor & Francis Group, 2019.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

22

Whicher, J., and S. W. Evans. Biochemistry of Inflammation. Springer, 2012.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

23

Veas, Francisco, ed. Acute Phase Proteins as Early Non-Specific Biomarkers of Human and Veterinary Diseases. InTech, 2011. http://dx.doi.org/10.5772/1045.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Sehgal, Pravinkumar B., and Gerd Grieninger. Regulation of the Acute Phase and Immune Responses: Interleukin-6 (Annals of the New York Academy of Sciences, Vol. 557). New York Academy of Sciences, 1989.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

25

Kortgen, Andreas, and Michael Bauer. The effect of acute hepatic failure on drug handling in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0197.

Full text

Abstract:

Impaired hepatic function is a common event in intensive care unit patients and as the liver plays a central role in drug metabolism and excretion this may lead to profound changes in pharmacokinetics. Underlying mechanisms are altered enzyme function of phase I and phase II metabolism, altered transporter protein function together with cholestasis and hepatic perfusion disorders. Moreover, multidrug therapy may lead to induction and inhibition of these enzymes and transporter proteins. In addition, changes in plasma protein binding and volumes of distribution of drugs are common. Altogether, these changes may not only lead to sometimes unpredictable plasma levels of xenobiotics, but also to drug-induced liver injury when hepatocellular accumulation of noxious substances occurs. Concomitant renal dysfunction may further complicate this situation. Pharmacodynamic alterations might also occur. In conclusion, the clinician must carefully evaluate medication given to patients with hepatic failure. Therapeutic drug monitoring should be performed wherever available to guide therapy.

APA, Harvard, Vancouver, ISO, and other styles

26

Rheumatoid arthritis: The role of acute-phase proteins : proceedings of a satellite meeting held at the VIIth EULAR Symposium, 23 July 1992, Barbican Centre, London, United Kingdom. London: Bailliere Tindall, 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

27

Lachmann, Helen J., and Giampaolo Merlini. The patient with amyloidosis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0152.

Full text

Abstract:

Amyloidosis is a disorder of protein folding in which normally soluble plasma proteins are deposited in the extracellular space in an abnormal insoluble fibrillar form. The process of amyloid formation and deposition causes cytotoxicity and progressive organ dysfunction. Amyloid is remarkably diverse and can be hereditary or acquired, localized or systemic, and lethal or merely an incidental finding. The most important numerically are AL amyloidosis, in which the fibrils are composed of monoclonal immunoglobulin light chains, and AA amyloidosis, in which the acute phase reactant Serum Amyloid A component forms the fibrils.The kidney is involved in 75% of patients with systemic amyloidosis. Heavy proteinuria or nephrotic syndrome is characteristic of most amyloid variants.Without treatment, systemic disease is usually fatal but measures that reduce the supply of amyloid fibril precursor proteins can result in regression of amyloid deposits, prevention of organ failure, and improved quality of life and survival. Early diagnosis, before irreversible organ damage has occurred, is the key to effective treatment. Recent advances in diagnosis and therapy have much improved the outlook of patients with AL amyloidosis, but agents with broader promise are under investigation.

APA, Harvard, Vancouver, ISO, and other styles

28

Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.

Full text

Abstract:

Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.

APA, Harvard, Vancouver, ISO, and other styles

29

Dionisi-Vici, Carlo, Diego Martinelli, Enrico Bertini, and Claude Bachmann. HHH Syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0020.

Full text

Abstract:

Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is an autosomal recessive disorder of the urea cycle characterized by impaired transport of ornithine across the inner mitochondrial membrane. As seen in other urea cycle defects, in the acute phase the disease is characterized by intermittent episodes of hyperammonemia accompanied by vomiting, lethargy, and coma, with or without signs of acute liver failure. The disease course is characterized by a pyramidal tract dysfunction associated with myoclonic seizures and cerebellar symptoms. Most patients reaching adulthood manifest variable degrees of cognitive impairment and abnormal behavior. Long-term treatment consists of a low-protein diet supplemented with citrulline, arginine, or ornithine. Protein restriction may be combined with sodium benzoate. If plasma creatine levels are low, creatine supplementation should be instituted. Acute treatment is similar to other urea cycle defects.

APA, Harvard, Vancouver, ISO, and other styles

30

Wilson, Deanna. Hepatitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0035.

Full text

Abstract:

Hepatitis A (HAV) and E (HEV) viruses are spread via the fecal-oral route. Hepatitis B virus (HBV) exposure is via occupational or recreational activities. Hepatitis D virus (HDV; also spread parentally) can only coinfect or superinfect those with chronic HBV. Hepatitis C (HCV) transmission is predominantly parenteral; the highest risk group is injection drug users. Prodromal-period patients with acute hepatitis present with vague constitutional symptoms when serum transaminases peak, with elevated serum bilirubin and varying levels of hepatic protein synthesis impairment; during the icteric phase, patients develop abdominal pain, hepatomegaly, and jaundice. Acute hepatitis has limited therapy; treatment is predominantly supportive. However, most adults with acute phase HAV, HBV, HDV, and HEV spontaneously clear the virus. Most individuals with HCV develop chronic hepatitis. Patients with known HAV, HBV, or HEV exposures may be eligible for post-exposure prophylaxis to reduce their risk of infection.

APA, Harvard, Vancouver, ISO, and other styles

31

Abhishek, Abhishek, and Michael Doherty. Investigations of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0051.

Full text

Abstract:

Joint aspiration and microscopic examination of the aspirated synovial fluid remains the gold standard for the diagnosis of calcium pyrophosphate crystal deposition (CPPD). If synovial fluid aspiration is not feasible, plain radiography and/or ultrasound scanning may be used to detect chondrocalcinosis (CC) which predominantly occurs due to calcium pyrophosphate (CPP) crystals, and this can be used as a diagnostic surrogate for CPPD as suggested by the EULAR Task Force. Acute CPP crystal arthritis often associates with a brisk acute phase response (elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), plasma viscosity) and neutrophilia. A mildly raised CRP and/or ESR may be present in chronic CPP crystal inflammatory arthritis. On the contrary, asymptomatic CC, or CPPD with osteoarthritis does not cause raised acute phase reactants. As CPPD most commonly occurs due to increasing age and osteoarthritis, investigations to screen for underlying metabolic abnormalities should be carried out in those with early-onset CPPD (under 55 years), or in those with florid polyarticular CC. As hyperparathyroidism gets more common with ageing its presence should be specifically sought in all age groups. Tests for other predisposing metabolic conditions should only be carried out in the presence of specific clinical features. Genotyping for mutations, especially in the ANKH gene, may be warranted in those with a family history of premature CPPD and no evidence of inherited metabolic predisposition, but such testing is unavailable to most clinicians.

APA, Harvard, Vancouver, ISO, and other styles

32

Compston, Alastair. Multiple sclerosis and other demyelinating diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0871.

Full text

Abstract:

The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflammation, as a generic process, and autoimmunity in which rather a specific set of aetiological and mechanistic conditions pertain. And there are differences between disorders that are driven primarily by immune processes and those in which inflammation occurs in response to pre-existing tissue damage.With these provisos, the pathological processes of demyelination and associated axonal dysfunction often account for episodic neurological symptoms and signs referable to white matter tracts of the brain, optic nerves, or spinal cord when these occur in young people. This is the clinical context in which the possibility of ‘demyelinating disease’ is usually considered by physicians and, increasingly, the informed patient. Neurologists will, with appropriate cautions, also be prepared to diagnose demyelinating disease in older patients presenting with progressive symptoms implicating these same pathways even when there is no suggestive past history. Both in its typical and atypical forms multiple sclerosis remains by far the commonest demyelinating disease. But acute disseminated encephalomyelitis, the leucodystrophies, and central pontine myelinolysis also need to be considered in particular circumstances; and multiple sclerosis itself has a differential diagnosis in which the relapsing-remitting course is mimicked by conditions not associated with direct injury to the axon–glial unit. Since our understanding of the cause, pathogenesis and features of demyelinating disease remains incomplete, classification combines aspects of the aetiology, clinical features, pathology, and laboratory components. Whether the designation ‘multiple sclerosis’ encapsulates one or more conditions is now much debated. We anticipate that a major part of future studies in demyelinating disease will be further to resolve this question of disease heterogeneity leading to a new taxonomy based on mechanisms rather than clinical empiricism. But, for now, the variable ages of onset, unpredictable clinical course, protean clinical manifestations, and non-specific laboratory investigations continue to make demyelinating disease one of the more challenging diagnostic areas in clinical neurology.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!