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Figure 3 Childhood craniopharyngioma

Figure 1 Framework for variant interpretation of phaeochromocytomas and/or paragangliomas (PPGLs) susceptibility genes into five classes based on the likelihood.

Figure 1 Number of somatic mutation rates across The Cancer Genome Atlas (TCGA) projects Figure 1 | Number of somatic mutation rates across The Cancer.

Figure 2 Regions of Africa exposed to undernutrition

Figure 3 Life expectancy at birth in all countries included

Figure 2 Pathophysiology of hyperglycaemia in T2DM

with undiagnosed diabetes mellitus by three diagnostic criteria

Figure 4 Amino acid structure of short-acting and long-acting insulins

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Figure 5 Schematic illustration of different clinical trial designs

Figure 1 Mendelian randomization study

Figure 1 Adverse effects in women treated with HRT

Figure 1 Monogenic forms of diabetes mellitus

Figure 1 Current treatments for PNETs

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Figure 1 The Beckwith–Wiedemann spectrum

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Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Figure 1 The burden of chronic kidney disease (CKD)

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Nat. Rev. Endocrinol. doi: /nrendo

Figure 2 Haematoxylin and eosin staining

Figure 1 Regulation of the ‘metabolically healthy obese’ phenotype

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Nat. Rev. Endocrinol. doi: /nrendo

Figure 1 Osteosarcoma epidemiology

Nat. Rev. Endocrinol. doi: /nrendo

Figure 1 Challenges and opportunities of using omics in EDC research

Figure 1 Oestrogen biosynthesis and production sites in the body

Figure 2 Differences between MC and AC

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Figure 2 Pharmacokinetic action profiles of rapid-acting insulins

Figure 4 Tracheal endoscopy in two patients

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Figure 2 Serum levels of TSH and free T4 in a large series

Figure 3 Statistical approaches for the analysis of metabolomic data

Figure 2 Endocrine dysfunction in mitochondrial disease and their associated gene defects Figure 2 | Endocrine dysfunction in mitochondrial disease and.

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Figure 3 Genetic pleiotropy in ALS

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Nat. Rev. Endocrinol. doi: /nrendo

Figure 3 Mutations and epimutations of the imprinted

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Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Endocrinol. doi: /nrendo

Figure 1 Regulation of hepatic glucose metabolism by the gut, brain and liver Figure 1 | Regulation of hepatic glucose metabolism by the gut, brain and.

Figure 2 Frequency and overlap of alterations

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Figure 2 Flowchart for investigation and diagnosis of Beckwith– Wiedemann syndrome Figure 2 | Flowchart for investigation and diagnosis of Beckwith– Wiedemann.

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Figure 1 Sites of action of glucose-lowering agents

Figure 2 Gut microbial gene content and development of T1DM

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Figure 4 Radiogenomics analysis can reveal relationships

Figure 1 Timeline of pancreatic islet transplantation

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Figure 3 Determination of the primary site

Figure 3 Global iodine status and mandatory salt iodization

Figure 1 Relationships between genetic variants, quantitative traits and diseases Figure 1 | Relationships between genetic variants, quantitative traits.

Nat. Rev. Endocrinol. doi: /nrendo

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Nat. Rev. Endocrinol. doi:10.1038/nrendo.2017.76 Figure 3 Distribution of oncogenic alterations in anaplastic thyroid carcinoma Figure 3 | Distribution of oncogenic alterations in anaplastic thyroid carcinoma. Data from Landa et al.45 showing the distribution of oncogenic alterations in anaplastic thyroid carcinoma (ATC). a | The prevalence of the number of different oncogenic alterations in ATC. b | The prevalence of the distribution of multiple single-nucleotide variants (SNVs) in ATC, including SNVs in BRAF, TERT, RAS and other genes. Molinaro, E. et al. (2017) Anaplastic thyroid carcinoma: from clinicopathology to genetics and advanced therapies Nat. Rev. Endocrinol. doi:10.1038/nrendo.2017.76