Books: 'GFR' – Grafiati

1

Zaltzman, Jeffrey Steven. Timed creatinine clearance using oral cimetidine (TCC) an assessment of a novel test of glomerular filtration rate (GFR). National Library of Canada, 1994.

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2

Boon, A. G. Report of a visit by members and staff of WRc to Germany (GFR) to investigate the root zone method for treatment of wastewaters. WRC, 1986.

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3

Saradēśapāṇḍe, Yaśavanta. Gir... gir... girmiṭ. Sāhitya Prakāśana, 2012.

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4

Dyck, Ger van. Ger. SDU Uitgeverij, 1989.

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5

Maĭdar, D. Mongġol ger. Ȯbȯr Mongġol-un Soyul-un Keblel-u̇n Qoriy-a, 1987.

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6

Maio, Luís. Afectivamente GNR. Assírio & Alvim, 1989.

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7

compiler, Baṭ Ḥasām, ed. Bāzī gar. Al-Quresh Pablīkeshanz, 2014.

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8

L, Grima, and University of Toronto. Dept. of Geography., eds. GGR 234S. Custom Publishing Service, University of Toronto Bookstores, 1997.

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9

Raḥmān, Bushrá. Cārah gar. Vat̤an Dost, 1986.

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10

Rahat, M. A. Badshah gar. Maqbool Academy, 2003.

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11

L, Grima, and University of Toronto. Dept. of Geography., eds. GGR 234S. Custom Publishing Service, University of Toronto Bookstores, 1999.

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12

Gökçe, Ramiz. Gir, kapanıyorum. Adam Yayınları, 1992.

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13

Myracle, Lauren. L8r, g8r. Amulet Books, 2007.

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14

L, Grima, and University of Toronto. Dept. of Geography., eds. GGR 234. Custom Publishing Service, University of Toronto Bookstores, 2000.

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15

Eikendal, Ger. Ger Eikendal. Van Spijk, 2001.

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16

Jamie, Thomson, ed. Aven ger! Knight, 1985.

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17

Palevsky, Paul M. Monitoring renal function in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0209.

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Renal function needs to be monitored in critically-ill patients to detect changes in glomerular filtration rate (GFR) and promptly diagnosis acute kidney injury (AKI). In the absence of reliable bedside techniques for the assessment of GFR, continuous monitoring of urine output and frequent assessment of serum creatinine levels remain the cornerstone of renal functional monitoring. Calculated estimations of GFR should not be relied upon in critically-ill patients, particularly if kidney function is not stable. The role of serum cystatin C as a marker of GFR and biomarkers of tubular injury in routine monitoring of kidney function is uncertain.

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18

Dussaule, Jean-Claude, Martin Flamant, and Christos Chatziantoniou. Function of the normal glomerulus. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0044_update_001.

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Glomerular filtration, the first step leading to the formation of primitive urine, is a passive phenomenon. The composition of this primitive urine is the consequence of the ultrafiltration of plasma depending on renal blood flow, on hydrostatic pressure of glomerular capillary, and on glomerular coefficient of ultrafiltration. Glomerular filtration rate (GFR) can be precisely measured by the calculation of the clearance of freely filtrated exogenous substances that are neither metabolized nor reabsorbed nor secreted by tubules: its mean value is 125 mL/min/1.73 m² in men and 110 mL/min/1.73 m² in women, which represents 20% of renal blood flow. In clinical practice, estimates of GFR are obtained by the measurement of creatininaemia followed by the application of various equations (MDRD or CKD-EPI) and more recently by the measurement of plasmatic C-cystatin. Under physiological conditions, GFR is a stable parameter that is regulated by the intrinsic vascular and tubular autoregulation, by the balance between paracrine and endocrine agents acting as vasoconstrictors and vasodilators, and by the effects of renal sympathetic nerves. The mechanisms controlling GFR regulation are complex. This is due to the variety of vasoactive agents and their targets, and multiple interactions between them. Nevertheless, the relative stability of GFR during important variations of systemic haemodynamics and volaemia is due to three major operating mechanisms: autoregulation of the afferent arteriolar resistance, local synthesis and action of angiotensin II, and the sensitivity of renal resistance vessels to respond to NO release.

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19

Speeckaert, Marijn, and Jopis Delanghe. Assessment of renal function. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0007.

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Glomerular filtration rate (GFR) can be measured as the clearance of exogenous or endogenous filtration markers. Practical formulas permit estimation of creatinine clearance or GFR without timed urine collections in many stable patients with CKD. Standardization of serum creatinine is important for all of these estimation methods and implementing traceability of the assays to the new global SRM 967 standard has led to changes in clinical decision-making criteria. Calibration to an IDMS reference produces a lowering of serum creatinine values by 10–30% for most methods. Serum creatinine concentration depends on age, gender and muscle mass. Cystatin C is an alternative marker of GFR, but estimation is more expensive and it is not clear that it has a useful place in routine practice. The MDRD Study equation was validated in the framework of the Modification of Diet in Renal Diseases study. It is superior to the Cockcroft and Gault formula for estimating Creatinine Clearance in most people. In 2009, the CKD Epidemiology Collaboration (CKD-EPI) formula was introduced, which provides a more accurate estimation for patients with GFR values between 60 and 90 mL/min. In children, the Schwartz formula is frequently used. Some urinary markers of kidney disease are also discussed.

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20

Upadhyay, Ashish, Lesley A. Inker, and Andrew S. Levey. Chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0094.

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The conceptual model, definition, and classification of chronic kidney disease (CKD) were first described in the National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines in 2002 and have had a major impact on patient care and research. Since this publication there has been an increased recognition that the cause of CKD influences progression and complications. In addition, epidemiologic reports from diverse populations have consistently shown graded relations between higher albuminuria and adverse kidney outcomes and complications, in addition to, and independent of, low GFR. Given these new understanding in risk relationships, Kidney Disease Improving Global Outcomes (KDIGO) updated the original guidelines in 2012. The updated guidelines retain the KDOQI definition of CKD, but recommend classifying CKD by the cause, level of GFR, and level of urinary albumin to creatinine ratio. Specialized nephrology care is recommended for severe reduction in GFR or high albuminuria, uncertain diagnosis, or difficult to manage complications.

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21

Radović, Milan, and Adalbert Schiller. Balkan endemic nephropathy. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0090_update_001.

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Balkan endemic nephropathy (BEN) is a chronic, slowly progressive tubulointerstitial nephritis, with familial clustering, occurring in several endemic rural regions in countries of the Balkan Peninsula. BEN is characterized by anaemia, tubular proteinuria, renal shrinkage, and slowly declining glomerular filtration rate (GFR). Up to one-third of patients may also develop upper urothelial tumours. The aetiology of BEN is unclear; chronic exposure to aristolochic acid and a polygenic predisposition are the most likely contributing factors. The major pathological characteristics of BEN are symmetrically shrunken, smooth-shaped kidneys, with interstitial fibrosis, mild interstitial inflammation, and tubular atrophy. Diagnosis is usually based upon positive family history of BEN, past or current residence in endemic regions, tubular proteinuria, tubular dysfunctions (such as urine acidification defects, salt wasting, and impaired excretion of ammonia, uric acid, and phosphate), scant urinary sediment, bilateral and symmetrically reduced kidney size, accompanied by severe anaemia, disproportionate to the degree of GFR reduction. There is no specific therapy for BEN; patients should therefore be treated as all patients with chronic kidney disease, in general. The use of distant water supplies or moving to another residence area should be advised to affected families. Careful evaluation for urothelial cancers is mandatory in patients with haematuria.

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22

Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0068_update_001.

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Immunoglobulin A nephropathy is characteristically slowly evolving, and studies from autopsies and kidney donors show that deposition of immunoglobulin A is quite common and not necessarily associated with overt disease. However, series of biopsy-diagnosed patients that extend to 20 or 30 years report rates of end-stage renal failure of up to 40–50%. A very approximate overall rate of end-stage renal disease of 1% per year has been suggested. Proteinuria, glomerular filtration rate (GFR), and possibly some features on renal biopsies enable risk stratification, but all patients need long-term monitoring. Treatment is based on the use of angiotensin converting-enzyme inhibitors for patients with proteinuria, and blood pressure control, and of course during most of the previous long-term studies patients would not have been treated with these agents or to modern blood pressure standards. For patients who show loss of GFR despite this, or other markers of high risk, the best evidence is for treatment with high-dose corticosteroids over a limited period of months. There is little convincing evidence for additional benefit from cytotoxic or other immunomodulatory agents, except possibly in the most aggressive disease, when there is weak evidence for cyclophosphamide. Some studies claim benefit from tonsillectomy, but this is not clear, and most nephrologists only recommend this for patients with recurrent tonsillitis.

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23

Gft Bag-Natures Gar. C.R. Gibson Company, 1997.

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24

Flittner, Chr Gfr. Chr. Gfr. Flittner: Die Feier der Liebe Oder Beschreibung der Verlobungs- und Hochzeits-Ceremonieen Aller Nationen. Teil 1. de Gruyter GmbH, Walter, 2021.

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25

Flittner, Chr Gfr. Chr. Gfr. Flittner: Die Feier der Liebe Oder Beschreibung der Verlobungs- und Hochzeits-Ceremonieen Aller Nationen. Teil 2. de Gruyter GmbH, Walter, 2021.

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26

Carrero, Juan Jesús, Hong Xu, and Bengt Lindholm. Diet and the progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0101.

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The dietary management of non-dialysed CKD patients has focused on limiting the intake of substances which lead to accumulation of urea, potassium, phosphorus, and sodium. Recent advances in nutritional epidemiology have given us the opportunity to examine the relationships between diet and CKD. This chapter focuses on evidence relating to retarding progression of renal impairment in the early to mid stages of CKD. Limits may need to change if GFR falls. The hypothesis that a high dietary protein intake leads to progressive CKD through a mechanism of glomerular hyperfiltration has been taught for decades, and it appears effective in animals. However, the evidence that low-protein diets (LPDs) halt CKD progression in patients is weak. Their management is of course likely to include other interventions such as blood pressure control. There is risk to low-protein diets. There is some evidence that high protein intakes are harmful. We therefore recommend moderate protein intake (not low; not high – no protein supplements; around 1g/kg/day). Salt handling is impaired in most patients with CKD, probably even early stages, and hypertension is an early feature, except in salt-losing patients, to whom different rules apply. Salt intake tends to raise blood pressure, worsen proteinuria, and reduce the effects of angiotensin converting enzyme inhibitors on blood pressure and proteinuria. Very low salt intakes are difficult to comply with and limit diet. In early stages of CKD we therefore recommend restriction to moderately low levels (below 6g/day of salt; 100 mmol of sodium). Lower levels may have additional benefits, and these limits may need to be reduced as GFR declines. Potassium is associated with healthy, desirable foods such as fruit and vegetables. It should only be restricted if high serum values make this necessary.

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27

Renal Diet Cookbook: The Complete Guide with 100+ Healthy Recipes to Improve Your GFR and Your Kidney Function, Manage Chronic Kidney Disease to Avoid Dialysis. Independently Published, 2020.

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28

Renal Diet Cookbook: The Complete Guide with 100+ Healthy Recipes to Improve Your GFR and Your Kidney Function, Manage Chronic Kidney Disease to Avoid Dialysis. Independently Published, 2020.

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29

Schiller, Adalbert, Adrian Covic, and Liviu Segall. Chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.

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Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably reduced glomerular filtration rate (GFR), whereas the blood pressure is usually normal or moderately increased. Tubular abnormalities are common, including type 2 (proximal) renal tubular acidosis, Fanconi syndrome, nephrogenic diabetes insipidus, and type 1 (distal) renal tubular acidosis, with hypokalaemia and nephrolithiasis. Radiology exams reveal shrunken kidneys, sometimes with irregular outlines. A renal biopsy is often required for the diagnosis of CTIN and its aetiology. The treatment of CTIN mainly involves discontinuation of exposure to nephrotoxins and specific therapy of renal infections, urinary tract obstruction, or underlying systemic diseases. Agents like ACE inhibitors and pirfenidone, which might reduce interstitial inflammation and fibrosis, are still under clinical evaluation.

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30

Conlan, Charlotte. Atkins Diet and Renal Diet for Beginners 2020-2021. 2 BOOKS IN 1: The Ultimate Guide to Improve your GFR & your Kidney Function. Regain Confidence & Live Healthier in 4 Weeks. Unlucky Ltd, 2020.

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31

Martin, Christine Ann. International tourism demand forecasting: A comparison of the accuracy of various quantitive forecasting techniques as applied to the main outward tourism flows from the GFR, France, the UK and the USA.. 1987.

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32

Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0338_update_001.

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Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide (Gb3), which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic. Proteinuria and estimated glomerular filtration rate (eGFR) are strongly associated with risk of progression, but this may be reduced by treatment with angiotensin-converting enzyme inhibitors as well as by enzyme replacement therapy (ERT). ERT was approved in 2001; it improves pain and other neuropathic symptoms, and well-being, and has been proven to clear deposits of Gb3 from tissues, at variable speeds. There is limited randomized controlled trial data but protective effects have been proven for renal outcomes, death, and better outcomes in some other organ systems. Renal function may be protected if ERT is commenced before there is heavy proteinuria or substantial loss of GFR. It is recommended to start ERT as soon as the diagnosis is made in those with very low or absent enzyme. For those with intermediate levels it is recommended to commence treatment only when signs or symptoms appear. Proteinuria and eGFR give most information from a renal point of view, but renal biopsy is also useful for confirming the renal diagnosis and staging the disease as well as monitoring progress in selected cases. Management should include regular screening for complications including myocardial and neurological assessments. It is likely that registries will show progressive rises in median survival with this condition.

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33

Lopez, Berenice, and Patrick J. Twomey. Biochemical investigation of rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0062.

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It is important for rheumatologists to have an understanding of biochemical tests including an awareness of their limitations. The biological variability of an analyte both within and between individuals, the limitations of the measurement technology, the sensitivity of laboratory internal quality control and external quality assurance procedures, as well as interlaboratory variations in practices including sample collection procedures, may all impact on the interpretation of a result. Biochemical tests are often requested to monitor organ-specific dysfunction arising as an adverse consequence of pharmacotherapy or as a component of a systemic rheumatic disease, although dysfunction may also reflect infection or coincidental pathology. Patients with rheumatic diseases are at high risk of renal and hepatic disease. Serum creatinine and its derivative estimated glomerular filtration rate (eGFR) are the most readily available surrogate markers of GFR and are used to assess renal impairment and monitor its course. However, the use of creatinine alone lacks sensitivity and a substantial loss of function must occur before creatinine levels are increased. Additional biochemical screening for kidney damage can be performed by assessment of glomerular integrity, including proteinuria or albuminuria and haematuria. A wide spectrum of rheumatic diseases can affect the liver with various degrees of involvement and hepatic pathology. These often present with cholestatic or hepatitic biochemical profiles. The medical management of rheumatic diseases also involves medications that are hepatotoxic, and routine monitoring of liver function is recommended. This approach is not problem-free and may be improved by quantitative determinations of non-invasive markers of liver fibrosis in the future. Together with imaging techniques, biochemical tests play an important role in the assessment and differential diagnosis of metabolic bone disease.

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34

Gnudi, Luigi, Giorgio Gentile, and Piero Ruggenenti. The patient with diabetes mellitus. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0149_update_001.

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About one third of patients with type 1 diabetes develop diabetic nephropathy long-term (usually not before at least 10 years of diabetes), though this proportion is falling as standards of care have risen. Nephropathy is strongly associated with other microvascular complications of diabetes, so that some degree of retinopathy is to be expected, and evidence of neuropathy is common. Patients with type 2 diabetes are equally susceptible, but this is an older group in which vascular disease and other pathologies are also more likely. The rise in type 2 diabetes accounts for diabetes being the most common recorded cause of end stage renal disease (ESRD) in the developed world.Diabetic nephropathy is characterized by a progression through hyperfiltration, microalbuminuria, hypertension, overt proteinuria, nephrotic syndrome, loss of GFR, to ESRD. Risk factors for developing it include genetic factors (though no major single gene effects have been identified), and quality of glycaemic control.The risk of progression can at early stages be reduced by improved glycaemic control, and control of hypertension also slows progression. However angiotensin converting enzyme inhibitors or receptor blockers (ACEi, ARB) are the standard of care for patients with microalbuminuria or overt proteinuria, as they have been shown to reduce the risk of renal endpoints. Combination therapy with both ACEi and ARB together has been associated with a high risk of AKI, hyperkalaemia and other adverse effects so is not generally recommended. Other promising agents in combination are under investigation but none adequately proven at this stage.Patients who reach ESRD have reduced survival on all modalities compared to age-matched patients with other diagnoses. Best rehabilitation and survival for those who are suitable is through renal transplantation, though combined pancreas-renal transplantation may offer still better outcomes for selected patients.

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35

Gft. Independent Publisher, 2009.

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36

ger. gerrge, 2000.

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37

Blaisian, Luke. Gar. Independently Published, 2018.

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38

Norman, John. Captive of Gor . Gor #7. Star, 1988.

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39

Dirnberger, Donald aka Azure. Dances of Gor: Gor Volumes. Independently Published, 2019.

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40

Norman, John. Hunters of Gor (The Gor Series). Masquerade Books, 1998.

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41

Norman, John. Swordsmen of Gor: Gor Book 29. Orion Publishing Group, Limited, 2012.

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42

Gar yād rahe: Gar yaad rahay. Buk Kārnar, 2019.

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43

Norman, John. Mariners of Gor: Gor Book 30. Orion Publishing Group, Limited, 2012.

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44

Norman, John. Savages of Gor: Gor Book 17. Orion Publishing Group, Limited, 2011.

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45

Norman, John. Prize of Gor: Gor Book 27. Orion Publishing Group, Limited, 2012.

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46

Norman, John. Tarnsman of Gor: Gor Book 1. Orion Publishing Group, Limited, 2011.

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47

Norman, John. Magicians of Gor: Gor Book 25. Orion Publishing Group, Limited, 2011.

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48

Bergwik, Staffan, Linn Holmberg, and Karin Dirke, eds. Konsten att kontextualisera: Om historisk förståelse och meningsskapande. Stockholm University Press, 2022. http://dx.doi.org/10.16993/bbt.

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Denna bok handlar om historievetenskaperna sätt att producera kunskap genom att kontextualisera. Den vänder sig primärt till studenter och forskare inom de humanistiska discipliner som arbetar med historiska perspektiv. Bokens ambition är ta med läsaren in i själva görandet och visa hur kontextualisering är ett viktigt moment i historiska studier på alla nivåer. Boken hoppas därmed stimulera till ökad reflektion och diskussion om hur vi går till väga när vi tolkar, skapar eller omtolkar historiska, kulturella och samhälleliga sammanhang. Boken ger för det första en introduktion till vad kontextualisering kan vara och göra när vi möter det förflutna i form av texter, bilder eller artefakter. Redan från första dagen på universitetet hamnar studenter inom historiska discipliner i sådana möten. Därför vänder sig bokens fyra första kapitel i första hand till studenter på de inledande terminerna. Vad innebär det egentligen att analysera, syntetisera, kontextualisera eller kritisera – och hur förhåller sig de sätten att arbeta med det förflutna till varandra? Och vidare, vilka historiska tider arbetar vi med: läser vi källmaterial från vår egen horisont eller från de historiska aktörernas? Är källmaterialet del av en lång historia eller en kort? Och vem bestämmer svaret på sådana frågor? För det andra ger boken en fördjupad diskussion om kontextualiserings roll när vi skapar ny historisk kunskap. Bokens senare kapitlen ställer frågor om hur kontextualisering förhåller sig till historievetenskaplig teori och metod, och riktar strålkastarljuset mot aktiviteten att skapa, argumentera för, och ompröva de sammanhang som ger mening och betydelse åt historiska källmaterial. Den mest centrala lärdom boken vill förmedla är att kontextualisering är en pågående aktivitet. Mänskliga förståelsehorisonter rör sig ständigt i takt med samtidens kunskapsintressen. Det kommer alltid finnas nya sätt att förstå historiska uttryck, och det är en anledning till att historiska studier utgör en viktig del av samhällets gemensamma kunskapsbas.

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49

Villaruel, Luis. Rey Gor. Villaruel, Luis, 2022.

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50

Jackson, Allen. GER Route. Amberley Publishing, 2017.

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Books on the topic 'GFR'

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