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  1. Article ; Online: Tenascin-X-Discovery and Early Research.

    Miller, Walter L

    Frontiers in immunology

    2021  Volume 11, Page(s) 612497

    MeSH term(s) Animals ; Ehlers-Danlos Syndrome/genetics ; Humans ; Mutation/genetics ; Tenascin/genetics
    Chemical Substances Tenascin ; tenascin X
    Language English
    Publishing date 2021-01-11
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.612497
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  2. Article: Steroidogenic electron-transfer factors and their diseases.

    Miller, Walter L

    Annals of pediatric endocrinology & metabolism

    2021  Volume 26, Issue 3, Page(s) 138–148

    Abstract: Most steroidogenesis disorders are caused by mutations in genes encoding the steroidogenic enzymes, but work in the past 20 years has identified related disorders caused by mutations in the genes encoding the cofactors that transport electrons from NADPH ...

    Abstract Most steroidogenesis disorders are caused by mutations in genes encoding the steroidogenic enzymes, but work in the past 20 years has identified related disorders caused by mutations in the genes encoding the cofactors that transport electrons from NADPH to P450 enzymes. Most P450s are microsomal and require electron donation by P450 oxidoreductase (POR); by contrast, mitochondrial P450s require electron donation via ferredoxin reductase (FdxR) and ferredoxin (Fdx). POR deficiency is the most common and best-described of these new forms of congenital adrenal hyperplasia. Severe POR deficiency is characterized by the Antley-Bixler skeletal malformation syndrome and genital ambiguity in both sexes, and hence is easily recognized, but mild forms may present only with infertility and subtle disorders of steroidogenesis. The common POR polymorphism A503V reduces catalysis by P450c17 (17-hydroxylase/17,20-lyase) and the principal drugmetabolizing P450 enzymes. The 17,20-lyase activity of P450c17 requires the allosteric action of cytochrome b5, which promotes interaction of P450c17 with POR, with consequent electron transfer. Rare b5 mutations are one of several causes of 17,20-lyase deficiency. In addition to their roles with steroidogenic mitochondrial P450s, Fdx and FdxR participate in the synthesis of iron-sulfur clusters used by many enzymes. Disruptions in the assembly of Fe-S clusters is associated with Friedreich ataxia and Parkinson disease. Recent work has identified mutations in FdxR in patients with neuropathic hearing loss and visual impairment, somewhat resembling the global neurologic disorders seen with mitochondrial diseases. Impaired steroidogenesis is to be expected in such individuals, but this has not yet been studied.
    Language English
    Publishing date 2021-09-30
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 2800460-7
    ISSN 2287-1292 ; 2287-1012
    ISSN (online) 2287-1292
    ISSN 2287-1012
    DOI 10.6065/apem.2142154.077
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  3. Article ; Online: History of Adrenal Research: From Ancient Anatomy to Contemporary Molecular Biology.

    Miller, Walter L / White, Perrin C

    Endocrine reviews

    2022  Volume 44, Issue 1, Page(s) 70–116

    Abstract: The adrenal is a small, anatomically unimposing structure that escaped scientific notice until 1564 and whose existence was doubted by many until the 18th century. Adrenal functions were inferred from the adrenal insufficiency syndrome described by ... ...

    Abstract The adrenal is a small, anatomically unimposing structure that escaped scientific notice until 1564 and whose existence was doubted by many until the 18th century. Adrenal functions were inferred from the adrenal insufficiency syndrome described by Addison and from the obesity and virilization that accompanied many adrenal malignancies, but early physiologists sometimes confused the roles of the cortex and medulla. Medullary epinephrine was the first hormone to be isolated (in 1901), and numerous cortical steroids were isolated between 1930 and 1949. The treatment of arthritis, Addison's disease, and congenital adrenal hyperplasia (CAH) with cortisone in the 1950s revolutionized clinical endocrinology and steroid research. Cases of CAH had been reported in the 19th century, but a defect in 21-hydroxylation in CAH was not identified until 1957. Other forms of CAH, including deficiencies of 3β-hydroxysteroid dehydrogenase, 11β-hydroxylase, and 17α-hydroxylase were defined hormonally in the 1960s. Cytochrome P450 enzymes were described in 1962-1964, and steroid 21-hydroxylation was the first biosynthetic activity associated with a P450. Understanding of the genetic and biochemical bases of these disorders advanced rapidly from 1984 to 2004. The cloning of genes for steroidogenic enzymes and related factors revealed many mutations causing known diseases and facilitated the discovery of new disorders. Genetics and cell biology have replaced steroid chemistry as the key disciplines for understanding and teaching steroidogenesis and its disorders.
    MeSH term(s) Humans ; Adrenal Hyperplasia, Congenital/genetics ; Hormones ; Mixed Function Oxygenases ; Molecular Biology ; Steroids ; Adrenal Gland Diseases/genetics ; Adrenal Gland Diseases/history ; Adrenal Gland Diseases/pathology ; Adrenal Gland Diseases/therapy ; Adrenal Glands/anatomy & histology ; Biomedical Research/history
    Chemical Substances Hormones ; Mixed Function Oxygenases (EC 1.-) ; Steroids
    Language English
    Publishing date 2022-08-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 603096-8
    ISSN 1945-7189 ; 0163-769X
    ISSN (online) 1945-7189
    ISSN 0163-769X
    DOI 10.1210/endrev/bnac019
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  4. Article ; Online: Rickets, Vitamin D, and Ca/P Metabolism.

    Miller, Walter L / Imel, Erik A

    Hormone research in paediatrics

    2022  Volume 95, Issue 6, Page(s) 579–592

    Abstract: Rickets was a major public health problem dating from Roman times, and medical descriptions of rickets date from the 17th century. Sniadecki first advocated treatment by exposure to sunshine in 1822; contemporaneously, several British physicians ... ...

    Abstract Rickets was a major public health problem dating from Roman times, and medical descriptions of rickets date from the 17th century. Sniadecki first advocated treatment by exposure to sunshine in 1822; contemporaneously, several British physicians advocated use of cod liver oil. Both approaches were successful. Work in 1924 showed that exposure to UV light endowed fats and other foods with antirachitic properties. Vitamins D2 and D3, the antirachitic agent in cod liver oil, were, respectively, produced by UV radiation of ergosterol and 7-dehydrocholesterol. Calcitriol (1,25[OH]2D3) was identified as the biologically active form of vitamin D in the early 1970s. The vitamin D 25-hydroxylase, 24-hydroxylase, and 1α-hydroxylase were cloned in the 1990s and their genetic defects were soon delineated. The vitamin D receptor was also cloned and its mutations identified in vitamin D-resistant rickets. Work with parathyroid hormone (PTH) began much later, as the parathyroids were not identified until the late 19th century. In 1925, James B. Collip (of insulin fame) identified PTH by its ability to correct tetany in parathyroidectomized dogs, but only in the 1970s was it clear that only a small fragment of PTH conveyed its activity. Congenital hypoparathyroidism with immune defects was described in 1968, eventually linked to microdeletions in chromosome 22q11.2. X-linked hypophosphatemic rickets was reported in 1957, and genetic linkage analysis identified the causative PHEX gene in 1997. Autosomal dominant hypophosphatemic rickets similarly led to the discovery of FGF23, a phosphate-wasting humoral factor made in bone, in 2000, revolutionizing our understanding of phosphorus metabolism.
    MeSH term(s) Animals ; Dogs ; Humans ; Cod Liver Oil/therapeutic use ; Familial Hypophosphatemic Rickets/genetics ; Familial Hypophosphatemic Rickets/history ; Parathyroid Hormone ; Rickets/genetics ; Rickets/history ; Rickets/physiopathology ; Rickets/therapy ; Vitamin D/physiology ; Vitamin D/therapeutic use ; Vitamins
    Chemical Substances Cod Liver Oil (8001-69-2) ; Parathyroid Hormone ; Vitamin D (1406-16-2) ; Vitamins
    Language English
    Publishing date 2022-11-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2537278-6
    ISSN 1663-2826 ; 1663-2818
    ISSN (online) 1663-2826
    ISSN 1663-2818
    DOI 10.1159/000527011
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  5. Article ; Online: A Brief History of Congenital Adrenal Hyperplasia.

    Miller, Walter L / White, Perrin C

    Hormone research in paediatrics

    2022  Volume 95, Issue 6, Page(s) 529–545

    Abstract: The adrenal has played a major role in the history of pediatric endocrinology. Cases of congenital adrenal hyperplasia (CAH) were reported in the 19th century, leading to the understanding that the adrenal influenced sexual phenotypes as well as being ... ...

    Abstract The adrenal has played a major role in the history of pediatric endocrinology. Cases of congenital adrenal hyperplasia (CAH) were reported in the 19th century, leading to the understanding that the adrenal influenced sexual phenotypes as well as being mysteriously required for survival. Numerous adrenal steroids were isolated in the early 20th century, and bioassays eventually distinguished glucocorticoids, mineralocorticoids, and androgens. Treatment of CAH with cortisone in 1950 by Wilkins and by Bartter and Albright revolutionized clinical endocrinology and launched a productive era of pediatric adrenal research. Through careful clinical studies, Wilkins established the contemporary approach to treating CAH. Alfred Bongiovanni identified defective 21-hydroxylation in CAH in 1957, followed by deficiencies of 3β-hydroxysteroid dehydrogenase and 11β-hydroxylase. P450 enzymes were described in 1962-1964, and 21-hydroxylation was the first activity ascribed to a P450. Accurate assays for 17OH-progesterone in newborns and in response to ACTH permitted the diagnosis of CAH in children and families. Application of the techniques of molecular genetics elucidated genetic and biochemical bases of these disorders from 1984 to 2004. Pediatric endocrinologists played central roles in identifying the genes responsible for both common and rare forms of congenital adrenal hyperplasia and determining their most appropriate treatments.
    MeSH term(s) Humans ; Adrenal Hyperplasia, Congenital/diagnosis ; Adrenal Hyperplasia, Congenital/genetics ; Mineralocorticoids ; Endocrinology ; Glucocorticoids/therapeutic use ; Androgens
    Chemical Substances Mineralocorticoids ; Glucocorticoids ; Androgens
    Language English
    Publishing date 2022-11-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2537278-6
    ISSN 1663-2826 ; 1663-2818
    ISSN (online) 1663-2826
    ISSN 1663-2818
    DOI 10.1159/000526468
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  6. Article ; Online: Congenital Adrenal Hyperplasia: Time to Replace 17OHP with 21-Deoxycortisol.

    Miller, Walter L

    Hormone research in paediatrics

    2019  Volume 91, Issue 6, Page(s) 416–420

    Abstract: Congenital adrenal hyperplasia (CAH) due to steroid 21-hydroxylase deficiency (21OHD) has a worldwide incidence of 1 in 15-20,000. Affected individuals have adrenal insufficiency and androgen excess; the androgen excess begins during fetal life, ... ...

    Abstract Congenital adrenal hyperplasia (CAH) due to steroid 21-hydroxylase deficiency (21OHD) has a worldwide incidence of 1 in 15-20,000. Affected individuals have adrenal insufficiency and androgen excess; the androgen excess begins during fetal life, typically resulting in 46,XX disordered sexual development. In 21OHD, 17-hydroxyprogesterone (17OHP), the steroid proximal to 21-hydroxylase, accumulates. Most industrialized countries have newborn screening programs that measure 17OHP; such screening has permitted rapid detection of newborns with 21OHD, saving lives previously lost to mineralocorticoid deficiency and salt wasting. However, newborn screening is plagued by false positives. 17OHP is above most "cutoff values" in the first 24 h of life, is high in otherwise normal premature infants, and in many term infants with physiologic stress from unrelated diseases. In addition, newborn 17OHP may be elevated in other forms of CAH, including 11-hydroxylase deficiency, 3β-hydroxysteroid dehydrogenase deficiency, and P450 oxidoreductase deficiency. In 21OHD, some of the accumulated intra-adrenal 17OHP is converted to 21-deoxycortisol (21-deoxy) by 11β-hydroxylase (CYP11B1); 21-deoxy is not elevated in premature infants or in other forms of CAH, and hence is a more specific marker for 21OHD. However, 21-deoxy assays have not been generally available until recently, hence experience is limited. We urge clinical investigators, commercial reference laboratories, and newborn screening programs to investigate replacing 17OHP with 21-deoxy as the analyte of choice for studies of 21OHD.
    MeSH term(s) 17-alpha-Hydroxyprogesterone/metabolism ; Adrenal Hyperplasia, Congenital/diagnosis ; Adrenal Hyperplasia, Congenital/drug therapy ; Adrenal Hyperplasia, Congenital/metabolism ; Adrenal Hyperplasia, Congenital/pathology ; Cortodoxone/therapeutic use ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Neonatal Screening
    Chemical Substances 21-deoxycortisol (641-77-0) ; 17-alpha-Hydroxyprogesterone (68-96-2) ; Cortodoxone (WDT5SLP0HQ)
    Language English
    Publishing date 2019-08-26
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2537278-6
    ISSN 1663-2826 ; 1663-2818
    ISSN (online) 1663-2826
    ISSN 1663-2818
    DOI 10.1159/000501396
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  7. Article ; Online: MECHANISMS IN ENDOCRINOLOGY: Rare defects in adrenal steroidogenesis.

    Miller, Walter L

    European journal of endocrinology

    2018  Volume 179, Issue 3, Page(s) R125–R141

    Abstract: Congenital adrenal hyperplasia (CAH) is a group of genetic disorders of adrenal steroidogenesis that impair cortisol synthesis, with compensatory increases in ACTH leading to hyperplastic adrenals. The term 'CAH' is generally used to mean 'steroid 21- ... ...

    Abstract Congenital adrenal hyperplasia (CAH) is a group of genetic disorders of adrenal steroidogenesis that impair cortisol synthesis, with compensatory increases in ACTH leading to hyperplastic adrenals. The term 'CAH' is generally used to mean 'steroid 21-hydroxylase deficiency' (21OHD) as 21OHD accounts for about 95% of CAH in most populations; the incidences of the rare forms of CAH vary with ethnicity and geography. These forms of CAH are easily understood on the basis of the biochemistry of steroidogenesis. Defects in the steroidogenic acute regulatory protein, StAR, disrupt all steroidogenesis and are the second-most common form of CAH in Japan and Korea; very rare defects in the cholesterol side-chain cleavage enzyme, P450scc, are clinically indistinguishable from StAR defects. Defects in 3β-hydroxysteroid dehydrogenase, which also causes disordered sexual development, were once thought to be fairly common, but genetic analyses show that steroid measurements are generally unreliable for this disorder. Defects in 17-hydroxylase/17,20-lyase ablate synthesis of sex steroids and also cause mineralocorticoid hypertension; these are common in Brazil and in China. Isolated 17,20-lyase deficiency can be caused by rare mutations in at least three different proteins. P450 oxidoreductase (POR) is a co-factor used by 21-hydroxylase, 17-hydroxylase/17,20-lyase and aromatase; various POR defects, found in different populations, affect these enzymes differently. 11-Hydroxylase deficiency is the second-most common form of CAH in European populations but the retention of aldosterone synthesis distinguishes it from 21OHD. Aldosterone synthase deficiency is a rare salt-losing disorder. Mild, 'non-classic' defects in all of these factors have been described. Both the severe and non-classic disorders can be treated if recognized.
    MeSH term(s) Adrenal Hyperplasia, Congenital/enzymology ; Adrenal Hyperplasia, Congenital/epidemiology ; Adrenal Hyperplasia, Congenital/genetics ; Adrenal Hyperplasia, Congenital/metabolism ; Brazil/epidemiology ; China/epidemiology ; Cholesterol Side-Chain Cleavage Enzyme/genetics ; Humans ; Hydrocortisone/biosynthesis ; Japan/epidemiology ; Mutation ; Phosphoproteins/genetics ; Republic of Korea/epidemiology ; Steroid 17-alpha-Hydroxylase/genetics ; Steroids/biosynthesis
    Chemical Substances Phosphoproteins ; Steroids ; steroidogenic acute regulatory protein ; Steroid 17-alpha-Hydroxylase (EC 1.14.14.19) ; Cholesterol Side-Chain Cleavage Enzyme (EC 1.14.15.6) ; Hydrocortisone (WI4X0X7BPJ)
    Language English
    Publishing date 2018-06-07
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1183856-5
    ISSN 1479-683X ; 0804-4643
    ISSN (online) 1479-683X
    ISSN 0804-4643
    DOI 10.1530/EJE-18-0279
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    Uh III Zs.147: Show issues Location:
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  8. Article ; Online: The Hypothalamic-Pituitary-Adrenal Axis: A Brief History.

    Miller, Walter L

    Hormone research in paediatrics

    2018  Volume 89, Issue 4, Page(s) 212–223

    Abstract: The hypothalamic-pituitary-adrenal (HPA) axis is central to homeostasis, stress responses, energy metabolism, and neuropsychiatric function. The history of this complex system involves discovery of the relevant glands (adrenal, pituitary, hypothalamus), ... ...

    Abstract The hypothalamic-pituitary-adrenal (HPA) axis is central to homeostasis, stress responses, energy metabolism, and neuropsychiatric function. The history of this complex system involves discovery of the relevant glands (adrenal, pituitary, hypothalamus), hormones (cortisol, corticotropin, corticotropin-releasing hormone), and the receptors for these hormones. The adrenal and pituitary were identified by classical anatomists, but most of this history has taken place rather recently, and has involved complex chemistry, biochemistry, genetics, and clinical investigation. The integration of the HPA axis with modern neurology and psychiatry has cemented the role of endocrinology in contemporary studies of behavior.
    MeSH term(s) Adrenocorticotropic Hormone/history ; Adrenocorticotropic Hormone/metabolism ; Animals ; Corticotropin-Releasing Hormone/history ; Corticotropin-Releasing Hormone/metabolism ; Endocrinology/history ; History, 16th Century ; History, 17th Century ; History, 18th Century ; History, 19th Century ; History, 20th Century ; Humans ; Hydrocortisone/history ; Hydrocortisone/metabolism ; Hypothalamo-Hypophyseal System/metabolism ; Pituitary-Adrenal System/metabolism ; Receptors, Cell Surface/history ; Receptors, Cell Surface/metabolism
    Chemical Substances Receptors, Cell Surface ; Adrenocorticotropic Hormone (9002-60-2) ; Corticotropin-Releasing Hormone (9015-71-8) ; Hydrocortisone (WI4X0X7BPJ)
    Language English
    Publishing date 2018-05-02
    Publishing country Switzerland
    Document type Historical Article ; Journal Article ; Review
    ZDB-ID 2537278-6
    ISSN 1663-2826 ; 1663-2818
    ISSN (online) 1663-2826
    ISSN 1663-2818
    DOI 10.1159/000487755
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  9. Book ; Conference proceedings: 2nd International Symposium on Molecular Steroiodogenesis

    Miller, Walter L.

    Monterey, California, June 7 - 11, 1996 ; [papers]

    (Steroids ; Vol. 62, no. 1)

    1997  

    Event/congress International Symposium on Molecular Steroidogenesis (2, 1996, MontereyCalif.)
    Author's details guest ed.: Walter L. Miller
    Series title Steroids ; Vol. 62, no. 1
    Collection
    Keywords Steroids / biosynthesis / congresses ; Gene Expression Regulation / congresses
    Language English
    Size 211 S. : Ill., graph. Darst.
    Publisher Elsevier
    Publishing place New York, NY
    Publishing country United States
    Document type Book ; Conference proceedings
    HBZ-ID HT007467537
    Database Catalogue ZB MED Medicine, Health

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    Zs A 87 -62- not available for loan Zeitschriften-Lesesaal

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  10. Article: In Memoriam: Melvin M. Grumbach, MD, (1925-2016) Pediatric Endocrinologist, Scientist, Educator, Leader.

    Miller, Walter L

    Pediatric endocrinology reviews : PER

    2017  Volume 14, Issue 3, Page(s) 96–102

    Language English
    Publishing date 2017-05-08
    Publishing country Israel
    Document type Editorial
    ZDB-ID 2434390-0
    ISSN 1565-4753
    ISSN 1565-4753
    DOI 10.17458/per.vol14.2017.WM.IM.grumbach
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