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Books on the topic 'Iron overload'

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Published: 4 June 2021
Last updated: 11 March 2023

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1

Yehuda, Shlomo, and David I. Mostofsky, eds. Iron Deficiency and Overload. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-59745-462-9.

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2

(undifferentiated), David Smith. Iron overload and birth defects. Leicester: De Montfort University, 1993.

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3

Barton, James C., Corwin Q. Edwards, Pradyumna D. Phatak, Robert S. Britton, and Bruce R. Bacon, eds. Handbook of Iron Overload Disorders. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511777035.

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4

C, Barton James, ed. Handbook of iron overload disorders. Cambridge: Cambridge University Press, 2010.

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5

Christos, Kattamis, and International Conference on Thalassemia and the Hemoglobinopathies (2nd : 1987 : Herakleion, Crete), eds. Iron overload and chelation in thalassaemia. Toronto: H. Huber Publishers, 1989.

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6

Yehuda, Shlomo. Iron deficiency and overload: From basic biology to clinical medicine. New York, N.Y: Humana Press, 2010.

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7

Stobie, Shannon Blaire. The novel oral iron chelator, L1, in acute and chronic iron overload. Ottawa: National Library of Canada, 1993.

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8

1939-, Weinberg Hedy, ed. Living with hemochromatosis: Answers to questions about iron overload. New York: Healthy Living Books, 2003.

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9

The unexpected consequences of iron overload: A fund raiser for the Haemochromatosis Society. England]: James Minter, 2014.

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10

Christos, Kattamis, ed. Iron overload and chelation in thalassaemia: A symposium held during the 2nd International Conference on Thalass[a]emia and the Hemoglobinopathies, Herakleion, Crete, 1987. Toronto: H. Huber Publishers, 1989.

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11

Handelsman, Harry. Hemoperfusion in conjunction with deferoxamine for the treatment of aluminum toxicity or iron overload in patients with end-stage renal disease. Rockville, MD: National Center for Health Services Research and Health Care Technology Assessment, U.S. Dept. of Health and Human Services, Public Health Service, 1987.

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12

Handelsman, Harry. Hemoperfusion in conjunction with deferoxamine for the treatment of aluminum toxicity or iron overload in patients with end-stage renal disease. Rockville, MD: National Center for Health Services Research and Health Care Technology Assessment, U.S. Dept. of Health and Human Services, Public Health Service, 1987.

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13

Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Iron overload cardiomyopathies. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199685288.003.0972_update_001.

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14

Yehuda, Shlomo, and David I. Mostofsky. Iron Deficiency and Overload. Springer, 2011.

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15

Handbook of Iron Overload Disorders. Cambridge University Press, 2008.

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16

Edwards, Corwin Q., Bruce R. Bacon, James C. Barton, Pradyumna D. Phatak, and Robert S. Britton. Handbook of Iron Overload Disorders. Cambridge University Press, 2010.

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17

Edwards, Corwin Q., Bruce R. Bacon, James C. Barton, Pradyumna D. Phatak, and Robert S. Britton. Handbook of Iron Overload Disorders. Cambridge University Press, 2011.

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18

Edwards, Corwin Q., Bruce R. Bacon, James C. Barton, Pradyumna D. Phatak, and Robert S. Britton. Handbook of Iron Overload Disorders. Cambridge University Press, 2010.

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19

Edwards, Corwin Q., Bruce R. Bacon, James C. Barton, Pradyumna D. Phatak, and Robert S. Britton. Handbook of Iron Overload Disorders. Cambridge University Press, 2010.

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20

Hallahan, Lawrence C. Dietary iron and iron overload (hemosiderosis) illness: Index of new information. ABBE Publishers Association of Washington, D.C, 1998.

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21

Yehuda, Shlomo, and David I. Mostofsky. Iron Deficiency and Overload: From Basic Biology to Clinical Medicine. Humana, 2012.

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22

Hershko, Chaim. Iron Chelation Therapy. Springer, 2012.

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23

Hershko, Chaim. Iron Chelation Therapy. Springer London, Limited, 2012.

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24

E.D., Ph.D. Weinberg and Cheryl D. Garrison. Exposing the Hidden Dangers of Iron: What Every Medical Professional Should Know About the Impact of Iron on the Disease Process. Cumberland House Publishing, 2004.

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25

Guo, Feng. Correlations of in vitro and in vivo metabolism and pharmacokinetics of a new iron chelator, APOCP363, in the normal and iron-overload rat. 2001.

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26

Hepatic iron quantitation and liver biopsy in sickle cell disease and thalassemia major: Impact on monitoring and preventing the progression of iron overload due to regular transfusion therapy. Ottawa: National Library of Canada, 2001.

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27

Broe, Marc E. De. Aluminum and Iron Overload in Haemodialysis: An International Workshop Held During the Xxvth Congress of the European Dialysis and Transplant Associa. Hans Huber Pub, 1989.

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28

Bartfay, Wally J. increased free radical generation, as measured by aldehyde-derived peroxidation products is observed in the heart with chronic iron-overload. 1999.

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29

E, De Broe M., and European Dialysis and Transplant Association - European Renal Association. Congress, eds. Aluminum and iron overload in haemodialysis: An international workshop held during the XXVth Congress of the European Dialysis and Transplant Association/European Renal Association. Toronto: Hogrefe & Huber Publishers, 1989.

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30

Tuschl, Karin, Peter T. Clayton, and Philippa B. Mills. Disorders of Manganese Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0045.

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Manganese is an essential trace metal for numerous metalloenzymes. Manganese homeostasis requires tight regulation in vivo and disruption of this balance can lead to manganese overload and subsequent accumulation of manganese in brain, liver, and blood. Mutations in SLC30A10, a cell surface-localized manganese efflux transporter, cause an autosomal recessive hypermanganesemia syndrome with two distinct phenotypes: childhood onset dystonia and adult onset Parkinsonism, associated with chronic liver disease, polycythemia and features of iron depletion. MRI brain appearances are characteristic of Mn deposition with hyperintense basal ganglia on T1-weighted images. Chelation therapy with disodium calcium edetate and iron supplementation effectively lower blood manganese levels, halt liver disease progression and improve neurological symptoms.The inherited form of hypermanganesemia can be distinguished from acquired causes of manganese overload including environmental overexposure and acquired hepatocerebral degeneration in cases of end stage liver disease.
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31

Oudit, Gavin Y. Role of L-type Ca2+ channel and oxidative stress in the pathogenesis of iron-overload cardiomyopathy: Calcium channel blockers and taurine as potential therapies. 2005.

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32

Overlords of the Iron Dragon (Kharadron Overlords). Games Workshop, 2018.

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33

Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Red cell disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0002.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia - β thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
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34

Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, Banu Kaya, and Angela Theodoulou. Red cell disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0002_update_001.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α‎ thalassaemia - β‎ thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
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35

Macdougall, Iain C. Clinical aspects and overview of renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0123.

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Anaemia is an almost ubiquitous complication of chronic kidney disease, which has a number of implications for the patient. It is associated with adverse outcomes, an increased rate of red cell transfusions, poor quality of life, and reduced physical capacity. Severe anaemia also impacts on cardiac function, as well as on platelet function, the latter contributing to the bleeding diathesis of uraemia. Renal anaemia occurs mainly in the later stages of chronic kidney disease (stages 3B, 4, and 5), and up to 95% of patients on dialysis suffer from this condition. It is caused largely by inappropriately low erythropoietin levels, but other factors such as a shortened red cell survival also play a part. The anaemia is usually normochromic and normocytic, unless concomitant iron deficiency is present. The latter is also common in renal failure, partly due to low dietary iron intake and absorption, and partly due to increased iron losses. Prior to the 1990s, treatment options were limited, and many patients (particularly those on haemodialysis) required regular blood transfusions, resulting in iron overload and human leucocyte antigen sensitization. Correction of anaemia requires two main treatment strategies: increased stimulation of erythropoiesis, and maintenance of an adequate iron supply to the bone marrow. Ever since the introduction of recombinant human erythropoietin, it has been possible to boost erythropoietic activity, and both oral and intravenous iron products are available to provide supplemental iron. In dialysis patients, oral iron is usually poorly absorbed due to upregulation of hepcidin activity, and intravenous iron is often required. The physiological processes relevant to red cell production are described, as well as the prevalence, characteristics, pathogenesis, and physiological consequences of renal anaemia.
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36

Rees, David. Haemoglobinopathies. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0172.

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Inherited abnormalities of the globin genes are the commonest single-gene disorders in the world and fall into two main groups: thalassaemias and sickle cell disease. Thalassaemias are due to quantitative defects in globin chain synthesis which cause variable anaemia and ineffective erythropoiesis. Thalassaemia was initially thought to be a disease of the bones due to uncontrolled bone marrow expansion causing bony distortion, although this is now unusual with appropriate blood transfusions. Osteopenia, often severe, is a feature of most patients with thalassaemia major and intermedia, caused by bone marrow expansion, iron overload, endocrinopathy, and iron chelation. Treatment with bisphosphonates is generally recommended. Other rheumatological manifestations include arthropathy associated with the use of the iron chelator deferiprone. Sickle cell disease involves a group of conditions caused by polymerization of the abnormal -globin chain, resulting in abnormal erythrocytes which cause vaso-occlusion, vasculopathy, and ischaemic tissue damage. The characteristic symptom is acute bone pain caused by vaso-occlusion; typical episodes require treatment with opiate analgesia and resolve spontaneously by 5 days with no lasting bone damage. The frequency of acute episodes varies widely between patients. The incidence of osteomyelitis is increased, particularly with salmonella, although it is much rarer than acute vaso-occlusion. Avascular necrosis can affect the hips, and less commonly the shoulders and knees. Coincidental rheumatological disease sometimes complicates the condition, particularly systemic lupus erythematosus (SLE) which is more prevalent in populations at increased risk of sickle cell disease.
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37

Rees, David. Haemoglobinopathies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0172_update_001.

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Inherited abnormalities of the globin genes are the commonest single-gene disorders in the world and fall into two main groups: thalassaemias and sickle cell disease. Thalassaemias are due to quantitative defects in globin chain synthesis which cause variable anaemia and ineffective erythropoiesis. Thalassaemia was initially thought to be a disease of the bones due to uncontrolled bone marrow expansion causing bony distortion, although this is now unusual with appropriate blood transfusions. Osteopenia, often severe, is a feature of most patients with thalassaemia major and intermedia, caused by bone marrow expansion, iron overload, endocrinopathy, and iron chelation. Treatment with bisphosphonates is generally recommended. Other rheumatological manifestations include arthropathy associated with the use of the iron chelator deferiprone. Sickle cell disease involves a group of conditions caused by polymerization of the abnormal -globin chain, resulting in abnormal erythrocytes which cause vaso-occlusion, vasculopathy, and ischaemic tissue damage. The characteristic symptom is acute bone pain caused by vaso-occlusion; typical episodes require treatment with opiate analgesia and resolve spontaneously by 5 days with no lasting bone damage. The frequency of acute episodes varies widely between patients. The incidence of osteomyelitis is increased, particularly with salmonella, although it is much rarer than acute vaso-occlusion. Avascular necrosis can affect the hips, and less commonly the shoulders and knees. Coincidental rheumatological disease sometimes complicates the condition, particularly systemic lupus erythematosus (SLE) which is more prevalent in populations at increased risk of sickle cell disease.
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38

Rogers, Thomas R., and Elizabeth M. Johnson. Mucoraceous moulds. 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/9780198755388.003.0018.

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The mucoraceous moulds are members of the order Mucorales and comprise a number of genera within which are species that typically cause life-threatening infections in immunocompromised hosts, but are also pathogens of patients with diabetes mellitus or burns, or following traumatic injuries or near-drowning incidents, and in iron overload. Clinical presentations may be of rhinocerebral, pulmonary, cutaneous, or disseminated disease. Once established at its initial focus, the infection can progress rapidly. Diagnosis is challenging because this is a relatively rare disease, cultures from sites of infection may be negative, and few biomarkers exist to aid laboratory diagnosis. Histopathological examination of infected tissue is useful in diagnosis. Clinicians should have a high level of suspicion when immunocompromised patients present with sinus infection, facial swelling, orbital bone erosion, nodular lung infiltration, or necrotic skin eschars. The only currently available antifungal agents with evidence of clinical utility in mucormycosis are amphotericin B, posaconazole, and isavuconazole.
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39

Macdougall, Iain C. Erythropoiesis-stimulating agents in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0124.

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The advent of recombinant human erythropoietin (epoetin) in the late 1980s transformed the management of renal anaemia, liberating many dialysis patients from lifelong regular blood transfusions, in turn causing severe iron overload and human leucocyte antigen sensitization. Epoetin can be administered either intravenously or subcutaneously, but the half-life of the drug is fairly short at around 6–8 hours, necessitating frequent injections. To circumvent this problem, two manipulations to the erythropoietin molecule were engineered. The first of these was to attach an extra two carbohydrate chains to the therapeutic protein hormone (to make darbepoetin alfa), and the second was to attach a large pegylation chain to make continuous erythropoietin receptor activator. Both of these strategies prolonged the circulating half-life of the erythropoietin analogue. The next erythropoietic agent to be produced was peginesatide, a peptide-based agent which had no structural homology with native or recombinant erythropoietin, but shared the same biological and functional characteristics. Future strategies include stabilization of hypoxia-inducible factor, by orally active inhibitors of the prolyl hydroxylase enzyme, and advanced clinical trials are underway. In the meantime, several large randomized controlled trials have highlighted the potential harm in targeting a near normal haemoglobin of 13–14 g/dL (with an increased risk of cardiovascular complications), and sub-normal correction of anaemia is now advised. Some patients may show mild or severe resistance to erythropoiesis-stimulating agent (ESA) therapy, and common causes include iron insufficiency, infection, and underlying inflammation. Very rarely, patients may produce antibodies against their ESA, which neutralize not only the ESA, but also endogenous erythropoietin, causing pure red cell aplasia.
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40

There and Back: Cheap Travel Overland Through Turkey, Iran and Afghanistan. Swiftnick, 2002.

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41

Ansari, Ali M. 3. Iran and Islam. Oxford University Press, 2014. http://dx.doi.org/10.1093/actrade/9780199669349.003.0003.

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In 1979 the Islamic Revolution overthrew the monarchy and transformed Iran’s relations with the outside world. Iranian history was reassessed along with the importance of Islam to Iranian identity. ‘Iran and Islam’ outlines the history of Iranians beginning with the wars between Sasanian Iran and its western Roman/Byzantine rival in the 6th century ce. It charts the fall of the Sasanian Empire to the Muslim Caliphate; the new Umayyad overlords; the Abbasid revolution in the 8th century ce; the rise of the New Persian language; the Mongol invasions of the 13th and 14th centuries and integration with Turanians; and the importance of Shi’ism to the Iranian people.
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42

Accardo, Jennifer. Restless Legs Syndrome and Periodic Limb Movement Disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0172.

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Restless legs syndrome (RLS), also known as Willis Ekbom disease (WED), is a sensory disorder with a circadian component. An irresistible urge to move the legs disrupts sleep onset and maintenance. Periodic limb movements in sleep, semirhythmic in nature, often overlap with RLS, though periodic limb movement disorder can be diagnosed in the absence of RLS’s distinctive sensory symptoms. Disruptions in dopaminergic pathways, iron metabolism, and the opioid system have all been implicated in pathogenesis, and there is a strong genetic component. RLS is common, affecting 5% to 10% of adults. Its best-known treatments are dopamine agonists; however, other treatments are effective.
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43

Howland, John. Hearing Luxe Pop. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199985227.003.0009.

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This chapter examines the concept of the “luxe pop” production practices and their evolution over the last several decades. It traces the connection between modern luxe pop, 1970s symphonic soul, and 1920s symphonic jazz. Each case features the timbre of a lush string orchestra as a stand-in for highbrow or elevated culture, while the overlaid genres of jazz, soul, and hip-hop function as a symbol of lowbrow culture. This juxtaposition of black/white, lowbrow/highbrow, street/luxury functions as musical irony and subversive sarcasm. This chapter traces specifically the connection between Jay-Z’s symphonic hip-hop production “Can I Live,” which samples Isaac Hayes’s cover of Burt Bacharach’s “The Look of Love,” a recording that was featured in the movie Casino Royale (1967). Pop music’s tendency to borrow samples from its own history (“retromania”) leads to an interconnected web of artists spanning decades of popular music.
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44

Randle, John, Miriam Macgregor, Whittington Press Staff, and Fine Book Bindery (Firm) Staff. Slow Ride to India: 128 Photographs Taken During an Overland Journey to India in 1968 Via Romania, Turkey, Iran, Afghanistan, Pakistan, Nepal and Ceylon. Whittington Press, 2017.

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45

Asia Overland : a Pictorial Guide: Europe, Greece, Turkey, Middle East, Syria, Lebanon, Jordan, Saudi Arabia, Bahrain, Kuwait, Iran, South Asia, Afghanistan, Pakistan, India, Nepal. Independently Published, 2020.

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46

Radner, Karen, Nadine Moeller, and D. T. Potts, eds. The Oxford History of the Ancient Near East: Volume II. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/oso/9780190687571.001.0001.

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Abstract This groundbreaking, five-volume series offers a comprehensive, fully illustrated history of Egypt and Western Asia (the Levant, Anatolia, Mesopotamia, and Iran), from the emergence of complex states to the conquest of Alexander the Great. Written by a highly diverse, international team of leading scholars, the volumes in this series focus firmly on the political and social histories of the states and communities of the ancient Near East. The second volume covers broadly the first half of the second millennium BC or, in archaeological terms, the Middle Bronze Age. Eleven chapters present the history of the Near East from the end of the third millennium BC to the fall of Babylon and discuss the First Intermediate Period and Middle Kingdom Egypt, the Mesopotamian kingdom of Ur under the rule of the so-called Third Dynasty of Ur and its successor states centered on the cities of Isin and Larsa. Also included are the subsequent mosaic of states of various sizes and complexity attested from the Eastern Mediterranean shore and the Anatolian highlands to the mountains of Iran, and finally the kingdom of Babylon. Key topics include the absolute chronology of the Middle Bronze Age, the formation, consolidation, and disintegration of complex states, the role of kingship, cult, and material culture in creating and managing social hierarchies, and the overland and maritime trade networks, and the political interactions that bridged deserts, oceans, and mountain ranges to bring together diverse people and polities in the vast area between Sub-Saharan Africa and Central Asia.
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