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  1. Book ; Online ; E-Book: Transition of Care

    Polak, Michel

    From Childhood to Adulthood in Endocrinology, Gynecology, and Diabetes

    (Endocrine Development ; Vol.33)

    2018  

    Author's details editors, Michel Polak, Philippe Touraine
    Series title Endocrine Development ; Vol.33
    Keywords Endocrinology ; Pediatrics ; Andrology ; Diabetes ; Fertility ; Genetics ; Gynecology ; Hospital Care ; Metabolic Diseases ; Metabolism ; Neuroendocrinology ; Obesity ; Pediatric Endocrinology ; Psychology ; Reproduction
    Language English
    Size 1 online resource (VIII + 164 pages), 14 figures, 3 in color, 11 tables
    Publisher S. Karger
    Publishing place Basel
    Document type Book ; Online ; E-Book
    Note Your key source for managing the transition period
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT020068929
    ISBN 9783318061437 ; 9783318061420 ; 3318061433 ; 3318061425
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Paediatric thyroid disease

    Polak, Michel

    (Best practice & research : Clinical endocrinology & metabolism ; 28,2)

    2014  

    Author's details M. Polak, guest ed
    Series title Best practice & research : Clinical endocrinology & metabolism ; 28,2
    Best practice & research
    Best practice & research ; Clinical endocrinology & metabolism
    Collection Best practice & research
    Best practice & research ; Clinical endocrinology & metabolism
    Language English
    Size S. 131 - 277 : zahlr. Ill.
    Publisher Elsevier
    Publishing place Amsterdam u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT018226827
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Se 1075 -28,2- verfügbar in Königswinter Königswinter

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  3. Book: Diabètes sucrés de l'enfant: révolution dans le traitement?

    Polak, Michel

    (Archives de pédiatrie ; 20, Suppl. 4)

    2013  

    Title variant Diabetes in pediatrics: revolution in treatment?
    Author's details nr. coord. par Michel Polak
    Series title Archives de pédiatrie ; 20, Suppl. 4
    Collection
    Language French
    Size S. S109 - S156 : Ill., graph. Darst.
    Publisher Elsevier Masson
    Publishing place Issy-les-Moulineaux
    Publishing country France
    Document type Book
    HBZ-ID HT018134801
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    Zs A 3942 -20,Suppl.4- not available for loan Zeitschriften-Lesesaal

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  4. Book: Paediatric thyroid disorders: new insights

    Polak, Michel / Szinnai, Gabor

    19 tables

    (Hormone resarch in paediatrics ; 83,2)

    2015  

    Author's details guest ed. Michel Polak ; Gabor Szinnai
    Series title Hormone resarch in paediatrics ; 83,2
    Hormone research in paediatrics
    Collection Hormone research in paediatrics
    Language English
    Size S. 76 - 147 : Ill., graph. Darst.
    Publisher Karger
    Publishing place Basel u.a.
    Publishing country Switzerland
    Document type Book
    HBZ-ID HT018594996
    ISBN 978-3-318-03030-3 ; 9783318030310 ; 3-318-03030-9 ; 3318030317
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    Zs A 414 -83- not available for loan Zeitschriften-Lesesaal

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  5. Book ; Conference proceedings: 40th International Symposium on Endocrinology and Metabolism

    Polak, Michel

    Paris, France, May 23 - 24, 2008

    (Hormone research ; 71, Suppl. 1)

    2009  

    Event/congress International Symposium on Endocrinology and Metabolism (40, 2008, Paris)
    Author's details guest ed. Michel Polak
    Series title Hormone research ; 71, Suppl. 1
    Collection
    Language English
    Size IV, 151 S. : Ill., graph. Darst.
    Publisher Karger
    Publishing place Basel u.a.
    Publishing country Switzerland
    Document type Book ; Conference proceedings
    HBZ-ID HT016038805
    ISBN 978-3-8055-9073-0 ; 9783805590747 ; 3-8055-9073-3 ; 3805590741
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    Zs A 414 -71,Suppl.1- not available for loan Zeitschriften-Lesesaal

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  6. Article ; Online: Letter to the Editor From Banigé and Polak: "Population-based TSH Screening of Newborns for Hyperthyroidism: It May Be Feasible, But Is It Justified?"

    Banigé, Maïa / Polak, Michel

    The Journal of clinical endocrinology and metabolism

    2022  Volume 107, Issue 8, Page(s) e3536–e3537

    MeSH term(s) Humans ; Hyperthyroidism/diagnosis ; Infant, Newborn ; Mass Screening ; Thyrotropin ; Thyroxine
    Chemical Substances Thyrotropin (9002-71-5) ; Thyroxine (Q51BO43MG4)
    Language English
    Publishing date 2022-05-06
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/clinem/dgac284
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.134: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Génétique de l’hypothyroïdie congénitale.

    Stoupa, Athanasia / Kariyawasam, Dulanjalee / Polak, Michel / Carré, Aurore

    Medecine sciences : M/S

    2022  Volume 38, Issue 3, Page(s) 263–273

    Abstract: Congenital hypothyroidism (CH) is the most frequent neonatal endocrine disorder. CH is due to thyroid development or thyroid function defects (primary) or may be of hypothalamic-pituitary origin (central). Primary CH is caused essentially by abnormal ... ...

    Title translation Genetic of congenital hypothyroidism.
    Abstract Congenital hypothyroidism (CH) is the most frequent neonatal endocrine disorder. CH is due to thyroid development or thyroid function defects (primary) or may be of hypothalamic-pituitary origin (central). Primary CH is caused essentially by abnormal thyroid gland morphogenesis (thyroid dysgenesis, TD) or defective thyroid hormone synthesis (dyshormonogenesis, DH). DH accounts for about 35% of CH and a genetic cause is identified in 50% of patients. However, TD accounts for about 65% of CH, and a genetic cause is identified in less than 5% of patients. The pathogenesis of CH is largely unknown and may include the contribution of individual and environmental factors. During the last years, detailed phenotypic description of patients, next-generation sequence technologies and use of animal models allowed the discovery of novel candidate genes in thyroid development and function. We provide an overview of recent genetic causes of primary and central CH. In addition, mode of inheritance and the oligogenic model of CH are discussed.
    MeSH term(s) Congenital Hypothyroidism/genetics ; Databases, Genetic ; Humans ; Mutation ; Thyroid Dysgenesis/genetics ; Thyroid Hormones
    Chemical Substances Thyroid Hormones
    Language French
    Publishing date 2022-03-25
    Publishing country France
    Document type Journal Article
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/2022028
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 2872: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Genetics of congenital hypothyroidism: Modern concepts.

    Stoupa, Athanasia / Kariyawasam, Dulanjalee / Polak, Michel / Carré, Aurore

    Pediatric investigation

    2022  Volume 6, Issue 2, Page(s) 123–134

    Abstract: Congenital hypothyroidism (CH) is the most common neonatal endocrine disorder and one of the most common preventable causes of intellectual disability in the world. CH may be due to developmental or functional thyroid defects (primary or peripheral CH) ... ...

    Abstract Congenital hypothyroidism (CH) is the most common neonatal endocrine disorder and one of the most common preventable causes of intellectual disability in the world. CH may be due to developmental or functional thyroid defects (primary or peripheral CH) or be hypothalamic-pituitary in origin (central CH). In most cases, primary CH is caused by a developmental malformation of the gland (thyroid dysgenesis, TD) or by a defect in thyroid hormones synthesis (dyshormonogenesis, DH). TD represents about 65% of CH and a genetic cause is currently identified in fewer than 5% of patients. The remaining 35% are cases of DH and are explained with certainty at the molecular level in more than 50% of cases. The etiology of CH is mostly unknown and may include contributions from individual and environmental factors. In recent years, the detailed phenotypic description of patients, high-throughput sequencing technologies, and the use of animal models have made it possible to discover new genes involved in the development or function of the thyroid gland. This paper reviews all the genetic causes of CH. The modes by which CH is transmitted will also be discussed, including a new oligogenic model. CH is no longer simply a dominant disease for cases of CH due to TD and recessive for cases of CH due to DH, but a far more complex disorder.
    Language English
    Publishing date 2022-05-14
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2574-2272
    ISSN (online) 2574-2272
    DOI 10.1002/ped4.12324
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Paediatric thyroid disease. Preface.

    Polak, Michel

    Best practice & research. Clinical endocrinology & metabolism

    2014  Volume 28, Issue 2, Page(s) 131–132

    MeSH term(s) Adolescent ; Adult ; Child ; Child, Preschool ; Female ; Humans ; Hydrolases/genetics ; Infant ; Infant, Newborn ; Membrane Proteins/genetics ; Monocarboxylic Acid Transporters/genetics ; Pregnancy ; Symporters ; Thyroid Diseases/embryology ; Thyroid Gland/embryology ; Thyroid Gland/physiology ; Thyroid Neoplasms/diagnosis
    Chemical Substances Membrane Proteins ; Monocarboxylic Acid Transporters ; SLC16A2 protein, human ; Symporters ; Hydrolases (EC 3.-) ; IYD protein, human (EC 3.8.1.2)
    Language English
    Publishing date 2014-01-15
    Publishing country Netherlands
    Document type Introductory Journal Article
    ZDB-ID 2052339-7
    ISSN 1878-1594 ; 1532-1908 ; 1521-690X
    ISSN (online) 1878-1594 ; 1532-1908
    ISSN 1521-690X
    DOI 10.1016/j.beem.2014.01.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Se 1075: Show issues Location:
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  10. Article ; Online: Human fetal thyroid function.

    Polak, Michel

    Endocrine development

    2014  Volume 26, Page(s) 17–25

    Abstract: The early steps of thyroid development that lead to its function in the human fetus and subsequently the further maturation that allows the human fetus to secrete thyroxine (T4) in a significant amount are reviewed here. We underline the importance of ... ...

    Abstract The early steps of thyroid development that lead to its function in the human fetus and subsequently the further maturation that allows the human fetus to secrete thyroxine (T4) in a significant amount are reviewed here. We underline the importance of the transfer of T4 from the pregnant woman to her fetus, which contributes at all stages of the pregnancy to fetal thyroid function and development. In the first trimester of pregnancy, the temporal and structural correlation of thyroid hormone synthesis with folliculogenesis supported the concept that structural and functional maturations are closely related. Human thyroid terminal differentiation follows a precisely timed gene expression program. The crucial role of the sodium/iodine symporter for the onset of thyroid function in the human fetus is shown. Fetal T4 is detected by the eleventh week of gestation and progressively increases throughout. The pattern of thyroid hormones and thyroid-stimulating hormone levels in the course of pregnancy is given from fetal blood sampling data, and the mechanisms governing this maturation in the human fetus are discussed. Finally an example of primary human fetal thyroid dysfunction, such as in Down syndrome, is given. The understanding of the physiology of the human fetal thyroid function is the basis for fetal medicine in the field of thyroidology.
    MeSH term(s) Female ; Fetal Development/physiology ; Humans ; Pregnancy ; Thyroid Gland/embryology ; Thyroid Gland/physiology ; Thyroid Hormones/physiology
    Chemical Substances Thyroid Hormones
    Language English
    Publishing date 2014
    Publishing country Switzerland
    Document type Journal Article ; Review
    ISSN 1662-2979 ; 1421-7082
    ISSN (online) 1662-2979
    ISSN 1421-7082
    DOI 10.1159/000363152
    Database MEDical Literature Analysis and Retrieval System OnLINE

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