Endocrine - Thyroid Development - Revision history

Z8600021 at 09:44, 1 Ocak 2020

2020-01-01T09:44:39Z

← Older revision		Revision as of 20:44, 1 Ocak 2020
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	This pathway forms a temporary duct (thyroglossal duct). There are abnormalities of incomplete or excessive descent of these thyroid precursor cells. The thyroid is one of the earliest endocrine organs to differentiate and has an important hormonal role in embryonic development. The early bundle of cells then forms the thyroid by first dividing to form 2 lobes separated by a narrow connecting isthmus.		This pathway forms a temporary duct ({{thyroglossal duct}}). There are abnormalities of incomplete or excessive descent of these thyroid precursor cells. The thyroid is one of the earliest endocrine organs to differentiate and has an important hormonal role in embryonic development. The early bundle of cells then forms the thyroid by first dividing to form 2 lobes separated by a narrow connecting isthmus.

	In the first trimester, the developing fetus is initially dependent upon maternal thyroid hormone crossing the placental barrier.{{#pmid:17574007\|PMID17574007}} Around week 16 ({{GA}} week 18) the fetal thyroid becomes active enough to support the fetal requirements for neural development.		In the first trimester, the developing fetus is initially dependent upon maternal thyroid hormone crossing the placental barrier.{{#pmid:17574007\|PMID17574007}} Around week 16 ({{GA}} week 18) the fetal thyroid becomes active enough to support the fetal requirements for neural development.

Z8600021 at 23:53, 3 Ocak 2019

2019-01-03T23:53:28Z

← Older revision		Revision as of 10:53, 4 Ocak 2019
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	# monocarboxylate transporter		# monocarboxylate transporter

	{\|		<br>
	~~\|+ '''~~Maternal Thyroid~~'''~~		{{Maternal Thyroid Function table}}
	\|-
	~~! Time~~		<br>
	~~! Thyrotropin (TSH)~~
	~~! Free Thyroxine (FT4)~~
	\|-
	~~\| 9-12 weeks~~
	~~\| 0.18 - 2.99 mIU/L~~
	~~\| 11 -19.2 pmol/L~~
	\|-
	~~\| second trimester~~
	~~\| 0.11 - 3.98 mIU/L~~
	~~\| 10.5 - 18.2 pmol/L~~
	\|-
	~~\| third trimester~~
	~~\| 0.48 - 4.71 mIU/L~~
	~~\| 9.0 - 16.1 pmol/L~~
	\|-
	~~\| colspan=3\|Data 95th percentile reference{{#pmid:30595114\|PMID~~}}
	\|}

	A study has identified an association of maternal thyroid function during early pregnancy with child brain morphology and IQ{{#pmid:26497402\|PMID26497402}}		A study has identified an association of maternal thyroid function during early pregnancy with child brain morphology and IQ{{#pmid:26497402\|PMID26497402}}

Z8600021 at 23:51, 3 Ocak 2019

2019-01-03T23:51:13Z

@@ Line 192: / Line 192: @@
 # monocarboxylate transporter
-A recent study has identified an association of maternal thyroid function during early pregnancy with child brain morphology and IQ{{#pmid:26497402|PMID26497402}}
+A study has identified an association of maternal thyroid function during early pregnancy with child brain morphology and IQ{{#pmid:26497402|PMID26497402}}
 * Maternal levels of free T4 during pregnancy correlate with their offspring's IQ, cortex volume and grey matter volume

Z8600021 at 01:25, 18 December 2018

2018-12-18T01:25:46Z

← Older revision		Revision as of 12:25, 18 December 2018
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	\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}		\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}

	Search term: ''Thyroid Embryology''		Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Thyroid+Embryology ''Thyroid Embryology''] \| http://www.ncbi.nlm.nih.gov/pubmed/?term=thyroglossal+duct ''thyroglossal duct'']

	~~<pubmed limit=5>Thyroid Embryology</pubmed>~~
	\|}		\|}
	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"
	! Older papers		! Older papers
	\|-		\|-
	\|		\| {{Older papers}}
	* '''Pyramidal lobe of the thyroid gland and the thyroglossal duct remnant: a study using human fetal sections'''{{#pmid:25458181\|PMID25458181}} "To investigate developmental changes in the thyroglossal duct, we observed serial sagittal sections of eight embryos (crown-rump length (CRL) 6-12 mm; approximately 5-6 weeks of gestation) as well as serial horizontal or cross-sections of 70 embryos and fetuses (CRL 15-110 mm; 6-15 weeks). In the sagittal sections, the thyroglossal duct was identified as a small sheet or mass of relatively large cells with vacuolization anterior, superior or inferior to the fourth pharyngeal arch artery. However, we found no continuous duct-like structure that reached the thyroid gland. Thus, previous classical schemes might have overestimated the continuity of the duct. ...Descent of the thyroid gland was not evident after the CRL 20 mm stage (6 weeks): the gland appeared to retain its position at the level of the third-sixth cervical vertebrae."		* '''Pyramidal lobe of the thyroid gland and the thyroglossal duct remnant: a study using human fetal sections'''{{#pmid:25458181\|PMID25458181}} "To investigate developmental changes in the thyroglossal duct, we observed serial sagittal sections of eight embryos (crown-rump length (CRL) 6-12 mm; approximately 5-6 weeks of gestation) as well as serial horizontal or cross-sections of 70 embryos and fetuses (CRL 15-110 mm; 6-15 weeks). In the sagittal sections, the thyroglossal duct was identified as a small sheet or mass of relatively large cells with vacuolization anterior, superior or inferior to the fourth pharyngeal arch artery. However, we found no continuous duct-like structure that reached the thyroid gland. Thus, previous classical schemes might have overestimated the continuity of the duct. ...Descent of the thyroid gland was not evident after the CRL 20 mm stage (6 weeks): the gland appeared to retain its position at the level of the third-sixth cervical vertebrae."

Z8600021 at 00:15, 3 July 2018

2018-07-03T00:15:07Z

← Older revision		Revision as of 11:15, 3 July 2018
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	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
	* '''A branching morphogenesis program governs embryonic growth of the thyroid gland'''{{#pmid:29361553\|PMID29361553}} "Here, we show that branching-like morphogenesis is a driving force to attain final size of the embryonic thyroid gland in mice. ~~{{Sox}}9~~, a key factor in branching organ development, distinguishes Nkx2-1+ cells in the thyroid bud from the progenitors that originally form the thyroid placode in anterior endoderm. As lobes develop the thyroid primordial tissue branches several generations. Sox9 and Fgfr2b are co-expressed distally in the branching epithelium prior to folliculogenesis. The thyroid in Fgf10 null mutants has a normal shape but is severely hypoplastic. Absence of Fgf10 leads to defective branching and disorganized angiofollicular units although Sox9/Fgfr2b expression and the ability of cells to differentiate and form nascent follicles are not impaired." {{SOX}} \| {{FGF}}		* '''A branching morphogenesis program governs embryonic growth of the thyroid gland'''{{#pmid:29361553\|PMID29361553}} "Here, we show that branching-like morphogenesis is a driving force to attain final size of the embryonic thyroid gland in mice. Sox9, a key factor in branching organ development, distinguishes Nkx2-1+ cells in the thyroid bud from the progenitors that originally form the thyroid placode in anterior endoderm. As lobes develop the thyroid primordial tissue branches several generations. Sox9 and Fgfr2b are co-expressed distally in the branching epithelium prior to folliculogenesis. The thyroid in Fgf10 null mutants has a normal shape but is severely hypoplastic. Absence of Fgf10 leads to defective branching and disorganized angiofollicular units although Sox9/Fgfr2b expression and the ability of cells to differentiate and form nascent follicles are not impaired." {{SOX}} \| {{FGF}}

	* '''Review - Development of the thyroid gland'''{{#pmid:28634271\|PMID28634271}} "Thyroid hormones are crucial for organismal development and homeostasis. ...Here, we review the principal mechanisms involved in thyroid organogenesis and functional differentiation, highlighting how the thyroid forerunner evolved from the endostyle in protochordates to the endocrine gland found in vertebrates. New findings on the specification and fate decisions of thyroid progenitors, and the morphogenesis of precursor cells into hormone-producing follicular units, are also discussed."		* '''Review - Development of the thyroid gland'''{{#pmid:28634271\|PMID28634271}} "Thyroid hormones are crucial for organismal development and homeostasis. ...Here, we review the principal mechanisms involved in thyroid organogenesis and functional differentiation, highlighting how the thyroid forerunner evolved from the endostyle in protochordates to the endocrine gland found in vertebrates. New findings on the specification and fate decisions of thyroid progenitors, and the morphogenesis of precursor cells into hormone-producing follicular units, are also discussed."

Z8600021 at 00:14, 3 July 2018

2018-07-03T00:14:25Z

← Older revision		Revision as of 11:14, 3 July 2018
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	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
	* '''A branching morphogenesis program governs embryonic growth of the thyroid gland'''{{#pmid:29361553\|PMID29361553}} "Here, we show that branching-like morphogenesis is a driving force to attain final size of the embryonic thyroid gland in mice. ~~Sox9~~, a key factor in branching organ development, distinguishes Nkx2-1+ cells in the thyroid bud from the progenitors that originally form the thyroid placode in anterior endoderm. As lobes develop the thyroid primordial tissue branches several generations. Sox9 and Fgfr2b are co-expressed distally in the branching epithelium prior to folliculogenesis. The thyroid in Fgf10 null mutants has a normal shape but is severely hypoplastic. Absence of Fgf10 leads to defective branching and disorganized angiofollicular units although Sox9/Fgfr2b expression and the ability of cells to differentiate and form nascent follicles are not impaired." {{SOX}} \| {{FGF}}		* '''A branching morphogenesis program governs embryonic growth of the thyroid gland'''{{#pmid:29361553\|PMID29361553}} "Here, we show that branching-like morphogenesis is a driving force to attain final size of the embryonic thyroid gland in mice. {{Sox}}9, a key factor in branching organ development, distinguishes Nkx2-1+ cells in the thyroid bud from the progenitors that originally form the thyroid placode in anterior endoderm. As lobes develop the thyroid primordial tissue branches several generations. Sox9 and Fgfr2b are co-expressed distally in the branching epithelium prior to folliculogenesis. The thyroid in Fgf10 null mutants has a normal shape but is severely hypoplastic. Absence of Fgf10 leads to defective branching and disorganized angiofollicular units although Sox9/Fgfr2b expression and the ability of cells to differentiate and form nascent follicles are not impaired." {{SOX}} \| {{FGF}}

	* '''Review - Development of the thyroid gland'''{{#pmid:28634271\|PMID28634271}} "Thyroid hormones are crucial for organismal development and homeostasis. ...Here, we review the principal mechanisms involved in thyroid organogenesis and functional differentiation, highlighting how the thyroid forerunner evolved from the endostyle in protochordates to the endocrine gland found in vertebrates. New findings on the specification and fate decisions of thyroid progenitors, and the morphogenesis of precursor cells into hormone-producing follicular units, are also discussed."		* '''Review - Development of the thyroid gland'''{{#pmid:28634271\|PMID28634271}} "Thyroid hormones are crucial for organismal development and homeostasis. ...Here, we review the principal mechanisms involved in thyroid organogenesis and functional differentiation, highlighting how the thyroid forerunner evolved from the endostyle in protochordates to the endocrine gland found in vertebrates. New findings on the specification and fate decisions of thyroid progenitors, and the morphogenesis of precursor cells into hormone-producing follicular units, are also discussed."

	* '''Thyroid follicle development requires Smad1/Smad5- and endothelial-dependent basement membrane assembly'''{{#pmid:27068110\|PMID27068110}} "Thyroid follicles, the functional units of the thyroid gland, are delineated by a monolayer of thyrocytes resting on a continuous basement membrane. Developmental mechanisms whereby follicles are formed by reorganization of a non-structured mass of non-polarized epithelial cells (folliculogenesis) largely unknown. Here we show that assembly of the epithelial basement membrane is critical for folliculogenesis and is controlled by endothelial cell invasion and by BMP-Smad signaling in thyrocytes."		* '''Thyroid follicle development requires Smad1/Smad5- and endothelial-dependent basement membrane assembly'''{{#pmid:27068110\|PMID27068110}} "Thyroid follicles, the functional units of the thyroid gland, are delineated by a monolayer of thyrocytes resting on a continuous basement membrane. Developmental mechanisms whereby follicles are formed by reorganization of a non-structured mass of non-polarized epithelial cells (folliculogenesis) largely unknown. Here we show that assembly of the epithelial basement membrane is critical for folliculogenesis and is controlled by endothelial cell invasion and by BMP-Smad signaling in thyrocytes."

	* '''Pyramidal lobe of the thyroid gland and the thyroglossal duct remnant: a study using human fetal sections'''{{#pmid:25458181\|PMID25458181}} "To investigate developmental changes in the thyroglossal duct, we observed serial sagittal sections of eight embryos (crown-rump length (CRL) 6-12 mm; approximately 5-6 weeks of gestation) as well as serial horizontal or cross-sections of 70 embryos and fetuses (CRL 15-110 mm; 6-15 weeks). In the sagittal sections, the thyroglossal duct was identified as a small sheet or mass of relatively large cells with vacuolization anterior, superior or inferior to the fourth pharyngeal arch artery. However, we found no continuous duct-like structure that reached the thyroid gland. Thus, previous classical schemes might have overestimated the continuity of the duct. ...Descent of the thyroid gland was not evident after the CRL 20 mm stage (6 weeks): the gland appeared to retain its position at the level of the third-sixth cervical vertebrae."

	\|}		\|}
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	\|-		\|-
	\|		\|
			* '''Pyramidal lobe of the thyroid gland and the thyroglossal duct remnant: a study using human fetal sections'''{{#pmid:25458181\|PMID25458181}} "To investigate developmental changes in the thyroglossal duct, we observed serial sagittal sections of eight embryos (crown-rump length (CRL) 6-12 mm; approximately 5-6 weeks of gestation) as well as serial horizontal or cross-sections of 70 embryos and fetuses (CRL 15-110 mm; 6-15 weeks). In the sagittal sections, the thyroglossal duct was identified as a small sheet or mass of relatively large cells with vacuolization anterior, superior or inferior to the fourth pharyngeal arch artery. However, we found no continuous duct-like structure that reached the thyroid gland. Thus, previous classical schemes might have overestimated the continuity of the duct. ...Descent of the thyroid gland was not evident after the CRL 20 mm stage (6 weeks): the gland appeared to retain its position at the level of the third-sixth cervical vertebrae."

	* '''Early thyroid development requires a Tbx1-Fgf8 pathway'''{{#pmid:19389367\|PMID19389367}} "The thyroid develops within the pharyngeal apparatus from endodermally-derived cells. ... a Tbx1->Fgf8 pathway in the pharyngeal mesoderm is a key size regulator of mammalian thyroid."		* '''Early thyroid development requires a Tbx1-Fgf8 pathway'''{{#pmid:19389367\|PMID19389367}} "The thyroid develops within the pharyngeal apparatus from endodermally-derived cells. ... a Tbx1->Fgf8 pathway in the pharyngeal mesoderm is a key size regulator of mammalian thyroid."

Z8600021 at 00:03, 3 July 2018

2018-07-03T00:03:58Z

← Older revision		Revision as of 11:03, 3 July 2018
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	\| Based on Table 3 from review on congenital hypothyroidism.{{#pmid:20537182\|PMID20537182}}		\| Based on Table 3 from review on congenital hypothyroidism.{{#pmid:20537182\|PMID20537182}}
	\|}		\|}


			{{genital}} - hypothyroidism can also impact upon male genital development, by inhibiting testicular growth, through a delay of Sertoli cell differentiation and proliferation.

	==Iodine Deficiency==		==Iodine Deficiency==

Z8600021 at 02:17, 21 Mayıs 2018

2018-05-21T02:17:34Z

← Older revision		Revision as of 13:17, 21 Mayıs 2018
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	{{Endocrine Links}} \| ~~[[Lecture - Head Development]] \| [[Abnormal Development - Iodine Deficiency\|Iodine Deficiency]]~~ \| [[Abnormal_Development_-_Drugs#Antithyroid_Drugs\|~~AbnormalDevelopment -~~ Antithyroid Drugs]]		{{Endocrine Links}}

			{{head}} \| {{iodine deficiency}} \| [[Abnormal_Development_-_Drugs#Antithyroid_Drugs\|Antithyroid Drugs]]

	==Some Recent Findings==		==Some Recent Findings==
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	* '''Pyramidal lobe of the thyroid gland and the thyroglossal duct remnant: a study using human fetal sections'''{{#pmid:25458181\|PMID25458181}} "To investigate developmental changes in the thyroglossal duct, we observed serial sagittal sections of eight embryos (crown-rump length (CRL) 6-12 mm; approximately 5-6 weeks of gestation) as well as serial horizontal or cross-sections of 70 embryos and fetuses (CRL 15-110 mm; 6-15 weeks). In the sagittal sections, the thyroglossal duct was identified as a small sheet or mass of relatively large cells with vacuolization anterior, superior or inferior to the fourth pharyngeal arch artery. However, we found no continuous duct-like structure that reached the thyroid gland. Thus, previous classical schemes might have overestimated the continuity of the duct. ...Descent of the thyroid gland was not evident after the CRL 20 mm stage (6 weeks): the gland appeared to retain its position at the level of the third-sixth cervical vertebrae."		* '''Pyramidal lobe of the thyroid gland and the thyroglossal duct remnant: a study using human fetal sections'''{{#pmid:25458181\|PMID25458181}} "To investigate developmental changes in the thyroglossal duct, we observed serial sagittal sections of eight embryos (crown-rump length (CRL) 6-12 mm; approximately 5-6 weeks of gestation) as well as serial horizontal or cross-sections of 70 embryos and fetuses (CRL 15-110 mm; 6-15 weeks). In the sagittal sections, the thyroglossal duct was identified as a small sheet or mass of relatively large cells with vacuolization anterior, superior or inferior to the fourth pharyngeal arch artery. However, we found no continuous duct-like structure that reached the thyroid gland. Thus, previous classical schemes might have overestimated the continuity of the duct. ...Descent of the thyroid gland was not evident after the CRL 20 mm stage (6 weeks): the gland appeared to retain its position at the level of the third-sixth cervical vertebrae."

	* '''Early thyroid development requires a Tbx1-Fgf8 pathway'''{{#pmid:19389367\|PMID19389367}} "The thyroid develops within the pharyngeal apparatus from endodermally-derived cells. ... a Tbx1->Fgf8 pathway in the pharyngeal mesoderm is a key size regulator of mammalian thyroid."

	* '''Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review.'''{{#pmid:19088150\|PMID19088150}} "The World Health Organization (WHO) recently increased their recommended iodine intake during pregnancy from 200 to 250 microg/d and suggested that a median urinary iodine (UI) concentration of 150-249 microg/L indicates adequate iodine intake in pregnant women. Thyrotropin concentrations in blood collected from newborns 3-4 d after birth may be a sensitive indicator of even mild iodine deficiency during late pregnancy; a <3% frequency of thyrotropin values >5 mU/L indicates iodine sufficiency."
	\|}		\|}
	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"
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	<pubmed limit=5>Thyroid Embryology</pubmed>		<pubmed limit=5>Thyroid Embryology</pubmed>
			\|}
			{\| class="wikitable mw-collapsible mw-collapsed"
			! Older papers
			\|-
			\|
			* '''Early thyroid development requires a Tbx1-Fgf8 pathway'''{{#pmid:19389367\|PMID19389367}} "The thyroid develops within the pharyngeal apparatus from endodermally-derived cells. ... a Tbx1->Fgf8 pathway in the pharyngeal mesoderm is a key size regulator of mammalian thyroid."

			* '''Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review.'''{{#pmid:19088150\|PMID19088150}} "The World Health Organization (WHO) recently increased their recommended iodine intake during pregnancy from 200 to 250 microg/d and suggested that a median urinary iodine (UI) concentration of 150-249 microg/L indicates adequate iodine intake in pregnant women. Thyrotropin concentrations in blood collected from newborns 3-4 d after birth may be a sensitive indicator of even mild iodine deficiency during late pregnancy; a <3% frequency of thyrotropin values >5 mU/L indicates iodine sufficiency."
	\|}		\|}
	== Reading ==		== Reading ==

Z8600021 at 01:43, 21 Mayıs 2018

2018-05-21T01:43:06Z

← Older revision		Revision as of 12:43, 21 Mayıs 2018
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	===Reviews===		===Reviews===
			{{#pmid:29767691}}

	{{#pmid:28153799}}		{{#pmid:28153799}}

Z8600021 at 01:37, 21 Mayıs 2018

2018-05-21T01:37:45Z

← Older revision		Revision as of 12:37, 21 Mayıs 2018
Line 8:		Line 8:
	This pathway forms a temporary duct (thyroglossal duct). There are abnormalities of incomplete or excessive descent of these thyroid precursor cells. The thyroid is one of the earliest endocrine organs to differentiate and has an important hormonal role in embryonic development. The early bundle of cells then forms the thyroid by first dividing to form 2 lobes separated by a narrow connecting isthmus.		This pathway forms a temporary duct (thyroglossal duct). There are abnormalities of incomplete or excessive descent of these thyroid precursor cells. The thyroid is one of the earliest endocrine organs to differentiate and has an important hormonal role in embryonic development. The early bundle of cells then forms the thyroid by first dividing to form 2 lobes separated by a narrow connecting isthmus.

			In the first trimester, the developing fetus is initially dependent upon maternal thyroid hormone crossing the placental barrier.{{#pmid:17574007\|PMID17574007}} Around week 16 ({{GA}} week 18) the fetal thyroid becomes active enough to support the fetal requirements for neural development.

	* '''Maternal thyroid hormone''' - required for early stages of brain development ([[#Maternal Thyroid\|Maternal Thyroid]] recent studies show both high and low thyroid hormone impact)		* '''Maternal thyroid hormone''' - required for early stages of brain development ([[#Maternal Thyroid\|Maternal Thyroid]] recent studies show both high and low thyroid hormone impact)
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	[[#Maternal Thyroid\|Maternal thyroid]] function also changes in early pregnancy, through pituitary changes, resulting in thyroid stimulating hormone (TSH) levels decreasing during the transition from pre-pregnancy to early pregnancy.{{#pmid:22436200\|PMID22436200}} This change in TSH was less predictable in women with thyroid antibodies. ~~Maternal thyroid hormone crosses~~ the ~~placenta~~.~~{{#pmid:17574007\|PMID17574007}}~~		[[#Maternal Thyroid\|Maternal thyroid]] function also changes in early pregnancy, through pituitary changes, resulting in thyroid stimulating hormone (TSH) levels decreasing during the transition from pre-pregnancy to early pregnancy.{{#pmid:22436200\|PMID22436200}} This change in TSH was less predictable in women with thyroid antibodies. Generally maternal TSH and free T4 are maintained within the same range as those in nonpregnant women.


	Hyperthyroidism in adults is generally treated with antithyroid drugs (ATDs), some of these drugs have been identified as teratogens during pregnancy. (More? [[Abnormal_Development_-_Drugs#Antithyroid_Drugs\|Antithyroid Drugs]])		Hyperthyroidism in adults is generally treated with antithyroid drugs (ATDs), some of these drugs have been identified as teratogens during pregnancy. (More? [[Abnormal_Development_-_Drugs#Antithyroid_Drugs\|Antithyroid Drugs]])


	Iodine deficiency disorders (IDD) is the single most common cause of preventable mental retardation and brain damage in the world. Iodine (Greek, ioeides = violet) is required for the synthesis of thyroid hormone, a key regulator of neurological development. IDD causes goiters and decreases the production of hormones vital to growth and development. (More? ~~[[Abnormal Development - Iodine Deficiency\|Iodine Deficiency]]~~)		Iodine deficiency disorders (IDD) is the single most common cause of preventable mental retardation and brain damage in the world. Iodine (Greek, ioeides = violet) is required for the synthesis of thyroid hormone, a key regulator of neurological development. IDD causes goiters and decreases the production of hormones vital to growth and development. (More? {{iodine deficiency}})