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Books on the topic 'Diabetes in childhood'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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1

Coombs, Catherine Anne. Childhood diabetes. Birmingham: University of Birmingham, 1994.

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2

Scaramuzza, Andrea, Carine de Beaufort, and Ragnar Hanas, eds. Research into Childhood-Onset Diabetes. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-40242-0.

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3

Coping with diabetes in childhood and adolescence. London: Sheldon Press, 2008.

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4

Miller, Janette Brand. The new glucose revolution pocket guide to childhood diabetes. New York: Marlowe, 2004.

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5

Pat, Thomas. Why am I so tired?: A first look at childhood diabetes. London: Wayland, 2008.

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6

Asian Symposium on Childhood and Juvenile Diabetes Mellitus (2nd Naha). Childhood and juvenile diabetes mellitus: Proceedings of the Second Asian Symposium on Childhood and Juvenile Diabetes Mellitus, Naha, Nov. 23-25, 1984. Edited by Mimura Gorō. Amsterdam: Excerpta Medica, 1985.

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7

Georgia. General Assembly. Senate. Diabetes and Childhood Obesity Study Committee. Final report of the Senate Diabetes and Childhood Obesity Study Committee. Atlanta, Georgia: Senate Research Office, 2007.

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8

Rytkönen, Mika. Geographical study on childhood Type I diabetes mellitus (TIDM) in Finland. Oulu: Oulu University Press, 2004.

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9

International Symposium on Childhood Diabetes (1993 Siena, Italy). An update on childhood diabetes and short stature: Proceedings of the International Symposium on Childhood Diabetes and the International Workshop on Non-Conventional GH-Treatment : Siena, Italy, May 26-29, 1993. Bologna: Monduzzi, 1993.

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10

Drash, Allan L. Clinical care of the diabetic child. Chicago: Year Book Medical Publishers, 1987.

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11

C, Levy-Marchal, and Czernichow P, eds. Epidemiology and etiology of insulin-dependent diabetes in the young. Basel: Karger, 1992.

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12

Zvi, Laron, and Karp Moshe, eds. Prognosis of diabetes in children: An update on early and late complications : proceedings of the 7th International Beilinson Symposium on Late Prognosis of Juvenile Onset Diabetes, Jerusalem, November 1-7, 1987. Basel: Karger, 1989.

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13

Weber, Bruno, Prof. Dr. med., ed. Early vascular complications in children with diabetes mellitus: Proceedings of an International Workshop on Diabetic Angiopathy in Children, Berlin, September 25-26, 1986. Basel: Karger, 1988.

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14

Randi, Henderson, ed. Clinical management of the child and teenager with diabetes. Baltimore, MD: John Hopkins University Press, 1998.

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15

Dinnage, Rosemary. The child with a chronic medical problem--cardiac disorders, diabetes, haemophilia. Windsor, Berkshire, England: NFER-Nelson, 1986.

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16

Weber, Bruno, Prof. Dr. med., Burger W. 1950-, and Danne T. 1959-, eds. Structural and functional abnormalities in subclinical diabetic angiopathy: International Workshop on Diabetic Angiopathy in Children, Berlin/Gosen, September 2-4, 1991. Basel: Karger, 1992.

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17

Childhood diabetes. London: Baillière Tindall, 1996.

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18

Kelnar, C. Childhood and Adolescent Diabetes. A Hodder Arnold Publication, 1999.

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19

Dr, Court Simon, and Lamb Bill MD, eds. Childhood and adolescent diabetes. Chichester: J. Wiley, 1997.

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20

H, Kelnar C. J., ed. Childhood and adolescent diabetes. London: Chapman & Hall Medical, 1995.

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21

Lamb, Bill, and Simon Court. Childhood and Adolescent Diabetes. Wiley & Sons, Incorporated, John, 2007.

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22

Greydanus, Donald E., Joav Merrick, and Manmohan K. Kamboj. Diabetes Mellitus: Childhood and Adolescence. Nova Science Publishers, Incorporated, 2016.

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23

Kaplan, David W. Diabetes in Childhood and Adolescence. S Karger Pub, 1986.

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24

Diabetes in Childhood and Adolescence. Muenchen: Karger, 2006.

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25

Chiarelli, F., K. Dahl-J�rgensen, and W. Kiess, eds. Diabetes in Childhood and Adolescence. S. Karger AG, 2005. http://dx.doi.org/10.1159/isbn.978-3-318-01099-2.

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26

Walker, J., Joseph E. Raine, Malcolm Donaldson, John Gregory, and Martin Savage. Practical Endocrinology and Diabetes in Childhood. Blackwell Publishing, Incorporated, 2001.

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27

Foster-Powell, Kaye, Jennie Brand-Miller, and Dr Heather Gilbertson. Childhood Diabetes (The New Glucose Revolution). Hodder, 2003.

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28

Type 2 Diabetes in Childhood and Adolescence. London: Taylor & Francis Group Plc, 2004.

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29

Childhood Diabetes (Balliere's International Practice and Research Paediatrics). Elsevier, 1996.

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30

Diabetes In Childhood And Adolescence (Pediatric and Adolescent Medicine). S. Karger AG (Switzerland), 2005.

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31

Hanas, Ragnar, Andrea Scaramuzza, and Carine de Beaufort. Research into Childhood-Onset Diabetes: From Study Design to Improved Management. Springer, 2016.

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32

Hanas, Ragnar, Andrea Scaramuzza, and Carine de Beaufort. Research into Childhood-Onset Diabetes: From Study Design to Improved Management. Springer, 2018.

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33

Martin, Silink, Kida Kaichi, and Rosenbloom Arlan L, eds. Type 2 diabetes in childhood and adolescence: A global perspective. London: Martin Dunitz, 2003.

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34

Childhood and Juvenile Diabetes Mellitus (Current Clinical Practice, No 27). Elsevier Science Ltd, 1987.

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35

Plunkett, Laura, and Linda Weltner. The Challenge of Childhood Diabetes: Family Strategies for Raising a Healthy Child. iUniverse, Inc., 2006.

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36

T, Lawlor Margaret, and Joslin Diabetes Center, eds. Caring for young children living with diabetes: Professional manual. Boston, MA: Joslin Diabetes Center, 1996.

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37

Caring for Young Children Living With Diabetes: Professional Manual. Joslin Diabetes Center, 1996.

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38

Laron, Zvi, and M. Karp. Prognosis of Diabetes in Children: An Update on Early and Late Complications (Beilinson Symposium on Juvenile Diabetes// Proceedings). S Karger Pub, 1989.

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39

Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.

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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM2) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM2 are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM2 and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM2, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM2 in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.
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40

Ismail, Khalida, Calum D. Moulton, Andrea Danese, and Brenda W. Penninx. A life course approach to understanding the association between depression and type 2 diabetes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0002.

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The relationship between depression and type 2 diabetes is bidirectional and poorly explained by behavioural factors alone. Chronic activation of the innate immune system provides a promising mechanism by which both conditions could develop concurrently across the life course. Genetically, overlap between depression and type 2 diabetes has been reported by twin studies, although not yet at the genome-wide significance level. In utero, activation of inflammatory processes may impact on neurodevelopment of appetite and mood regulation. In early childhood, prolonged adversity is associated with subsequent elevated inflammation, depression, and obesity, which may be amplified by unhealthy lifestyle choices in adolescence. Finally, prolonged low socioeconomic status into adulthood is associated with chronically elevated inflammation and incident type 2 diabetes. In sum, a lifespan approach to the comorbidity of depression and type 2 diabetes offers novel opportunities for timely intervention and even for the primary prevention of type 2 diabetes.
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41

Glasper, Edward Alan, Gillian McEwing, and Jim Richardson, eds. Endocrine and metabolic disorders. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780198569572.003.0019.

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The endocrine system: related anatomy and physiology 632Type 1 diabetes mellitus in childhood and adolescence 634Diabetic ketoacidosis (DKA) 636Management of DKA 638Type 2 diabetes mellitus 640Maturity-onset diabetes mellitus of the young (MODY) 642Hypothyroidism 644Short stature 646Tall stature ...
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42

(Editor), M. Silink, S. Arslanian (Editor), T. Danne (Editor), K. Kida (Editor), M. Knip (Editor), and P. Swift (Editor), eds. The Second International Novo Nordisk Symposium on Diabetes in Childhood and Adolescence: Copenhagen, Denmark, May 31-June2, 2001 (Supplement Issue: Hormone Research 2002, 1). S Karger Pub, 2002.

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43

Clark, Cindy Dell. In Sickness and in Play: Children Coping With Chronic Illness (Rutgers Series in Childhood Studies). Rutgers University Press, 2003.

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44

Clark, Cindy Dell. In Sickness and in Play: Children Coping With Chronic Illness (Rutgers Series in Childhood Studies). Rutgers University Press, 2003.

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45

Levy, David. Adolescence and emerging adulthood. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198766452.003.0009.

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Adolescence and emerging childhood forms an increasing proportion of the lifespan of urbanized individuals. Glycaemic control worsens during adolescence; physiology and psychology contribute. A1C levels peak around 9% (75 mmol/mol) before declining from late teens onwards. However, unchanging glycaemia (tracking) is common. Glycaemia has generally improved in the past 10–15 years, but significant differences between and within countries persist. Microvascular complications are prevalent at this stage, but have probably also decreased with time. During this important period, the stage can be set for premature macrovascular disease (early onset hypertension, arterial stiffening, dyslipidaemia, and smoking). Exercise reduces the risk of microvascular complications. Smoking is as common in young Type 1 patients than in the general population. Efforts at smoking cessation need reinforcing. Glycaemic control during university does not improve. Transition from paediatric to adult diabetes services is often unsatisfactory; clinics should implement simple procedures focusing on accessibility, flexibility, and improved communications.
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46

Modena, Alejandro, and Colin Ingram. Yalla!: A Wandering Jew Survives Palestine, Cuba, Jamaica, And America. Robert D. Reed Publishers, 2006.

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47

Landrigan, Philip J., and Mary M. Landrigan. Children and Environmental Toxins. Oxford University Press, 2018. http://dx.doi.org/10.1093/wentk/9780190662646.001.0001.

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Over the past four decades, the prevalence of autism, asthma, ADHD, obesity, diabetes, and birth defects has increased substantially among children throughout the world. Not coincidentally, more than 80,000 new chemicals have been developed and released into the global environment during this same period. Today the World Health Organization attributes more than one third of all childhood deaths to environmental causes. Children’s environmental health is a new and growing discipline that responds to the expanding threat of chemical and environmental hazards to child health. Amid mounting evidence that children are especially sensitive to their environment-and that exposure during their developmental “windows of susceptibility” can trigger cellular changes that lead to lifelong disease and disability-there is a compelling need for continued scientific study of the relationship between children’s health and their environment. Children and Environmental Toxins: What Everyone Needs to Know® offers an authoritative yet accessible question-and-answer guide to the "silent spring" of threats in our collective backyard. As the burdens of environmental toxins and chronic disease continue to defy borders, this book will be an invaluable addition to the conspicuously sparse literature in this area.
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48

Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.

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Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal phenotype in mitochondrial disease is proximal tubulopathy (Fanconi syndrome in the severest cases); however, as all regions of the nephron can be affected, from the glomerulus to the collecting duct, patients may also present with proteinuria, decreased glomerular filtration rate, nephrotic syndrome, water and electrolyte disorders, and renal tubular acidosis. Understanding of the relationship between underlying genotype and clinical phenotype remains incomplete in mitochondrial disease. Proximal tubulopathy typically occurs in children with severe multisystem disease due to mtDNA deletion or mutations in nDNA affecting mitochondrial function. In contrast, glomerular disease (focal segmental glomerulosclerosis) has been reported more commonly in adults, mainly in association with the m.3243A<G point mutation. Co-enzyme Q10 (CoQ10) deficiency has been particularly associated with podocyte dysfunction and nephrotic syndrome in children. Underlying mitochondrial disease should be considered as a potential cause of unexplained renal dysfunction; clinical clues include lack of response to conventional therapy, abnormal mitochondrial morphology on kidney biopsy, involvement of other organs (e.g. diabetes, cardiomyopathy, and deafness) and a maternal family history, although none of these features are specific. The diagnostic approach involves acquiring tissue (typically skeletal muscle) for histological analysis, mtDNA screening and oxidative phosphorylation (OXPHOS) complex function tests. A number of nDNA mutations causing mitochondrial disease have now been identified and can also be screened for if clinically indicated. Management of mitochondrial disease requires a multidisciplinary approach, and treatment is largely supportive as there are currently very few evidence-based interventions. Electrolyte deficiencies should be corrected in patients with urinary wasting due to tubulopathy, and CoQ10 supplementation may be of benefit in individuals with CoQ10 deficiency. Nephrotic syndrome in mitochondrial disease is not typically responsive to steroid therapy. Transplantation has been performed in patients with end-stage kidney disease; however, immunosuppressive agents such as steroids and tacrolimus should be used with care given the high incidence of diabetes in mitochondrial disease.
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