Talk:Neonatal Development - Revision history

Z8600021 at 22:40, 19 Mayıs 2020

2020-05-19T22:40:29Z

← Older revision		Revision as of 08:40, 20 Mayıs 2020
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			==2020==

			{{#pmid:32284405}}

			'''Distinct locomotor precursors in newborn babies'''

			It is commonly thought that human locomotor development stems from a single precursor behavior, consisting of alternating flexor–extensor movements, such as kicking or stepping on ground. According to this view, kicking and stepping are identical movement patterns generated by the same neural mechanisms. Here we show that the neuromuscular modules of neonatal kicking and stepping are different, presumably related to different neural mechanisms. Kicking involves an adult-like number of temporal activation patterns, whose association with specific sets of muscles varies across movements. Ground-stepping involves a limited number of activation patterns, each associated with a stable muscle synergy. Since neonatal kicking and ground-stepping seem to anticipate subsequent developmental changes of locomotion in human babies, they might represent distinct locomotor antecedents.

	==2018==		==2018==

Z8600021 at 10:06, 8 April 2018

2018-04-08T10:06:09Z

← Older revision		Revision as of 20:06, 8 April 2018
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			==2018==

			===Metrics of early childhood growth in recent epidemiological research: A scoping review===

			PLoS One. 2018 Mar 20;13(3):e0194565. doi: 10.1371/journal.pone.0194565. eCollection 2018.

			Leung M1, Perumal N1,2, Mesfin E3, Krishna A1, Yang S4, Johnson W5, Bassani DG1,2,6, Roth DE1,6.

			Abstract
			Metrics to quantify child growth vary across studies of the developmental origins of health and disease. We conducted a scoping review of child growth studies in which length/height, weight or body mass index (BMI) was measured at ≥ 2 time points. From a 10% random sample of eligible studies published between Jan 2010-Jun 2016, and all eligible studies from Oct 2015-June 2016, we classified growth metrics based on author-assigned labels (e.g., 'weight gain') and a 'content signature', a numeric code that summarized the metric's conceptual and statistical properties. Heterogeneity was assessed by the number of unique content signatures, and label-to-content concordance. In 122 studies, we found 40 unique metrics of childhood growth. The most common approach to quantifying growth in length, weight or BMI was the calculation of each child's change in z-score. Label-to-content discordance was common due to distinct content signatures carrying the same label, and because of instances in which the same content signature was assigned multiple different labels. In conclusion, the numerous distinct growth metrics and the lack of specificity in the application of metric labels challenge the integration of data and inferences from studies investigating the determinants or consequences of variations in childhood growth.
			PMID: 29558499 PMCID: PMC5860780 DOI: 10.1371/journal.pone.0194565

	==2016==		==2016==

Z8600021 at 00:00, 14 April 2016

2016-04-14T00:00:06Z

← Older revision		Revision as of 10:00, 14 April 2016
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	==2016==		==2016==

			===Effect of Kidney Function on Drug Kinetics and Dosing in Neonates, Infants, and Children===

			Clin Pharmacokinet. 2015 Dec;54(12):1183-204. doi: 10.1007/s40262-015-0298-7.

			Rodieux F1, Wilbaux M2, van den Anker JN3,4,5, Pfister M2,6.

			Abstract

			Neonates, infants, and children differ from adults in many aspects, not just in age, weight, and body composition. Growth, maturation and environmental factors affect drug kinetics, response and dosing in pediatric patients. Almost 80% of drugs have not been studied in children, and dosing of these drugs is derived from adult doses by adjusting for body weight/size. As developmental and maturational changes are complex processes, such simplified methods may result in subtherapeutic effects or adverse events. Kidney function is impaired during the first 2 years of life as a result of normal growth and development. Reduced kidney function during childhood has an impact not only on renal clearance but also on absorption, distribution, metabolism and nonrenal clearance of drugs. 'Omics'-based technologies, such as proteomics and metabolomics, can be leveraged to uncover novel markers for kidney function during normal development, acute kidney injury, and chronic diseases. Pharmacometric modeling and simulation can be applied to simplify the design of pediatric investigations, characterize the effects of kidney function on drug exposure and response, and fine-tune dosing in pediatric patients, especially in those with impaired kidney function. One case study of amikacin dosing in neonates with reduced kidney function is presented. Collaborative efforts between clinicians and scientists in academia, industry, and regulatory agencies are required to evaluate new renal biomarkers, collect and share prospective pharmacokinetic, genetic and clinical data, build integrated pharmacometric models for key drugs, optimize and standardize dosing strategies, develop bedside decision tools, and enhance labels of drugs utilized in neonates, infants, and children.

			PMID 26138291

	===Microvillus inclusion disease===		===Microvillus inclusion disease===

Z8600021 at 23:20, 13 March 2016

2016-03-13T23:20:20Z

← Older revision		Revision as of 09:20, 14 March 2016
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	===Microvillus inclusion disease===		===Microvillus inclusion disease===

	:(MVID) A postnatal gastrointestinal tract disease due to the shortening or absence of epithelial cell (enterocytes) apical microvilli. Infants have life-threatening watery diarrhoea and mutations in myosin VB gene (MYO5B). Other forms of congenital diarrhea include congenital secretory chloride diarrhoea, an autosomal recessive form of severe chronic ~~diarrhea~~ .		:(MVID) A postnatal gastrointestinal tract disease due to the shortening or absence of epithelial cell (enterocytes) apical microvilli. Infants have life-threatening watery diarrhoea and mutations in myosin VB gene (MYO5B). Other forms of congenital diarrhea include congenital secretory chloride diarrhoea, an autosomal recessive form of severe chronic diarrhoea. International Classification of Diseases - XVI Perinatal Period Noninfective neonatal diarrhoea Neonatal diarrhoea NOS Excl.: neonatal diarrhoea NOS in countries where the condition can be presumed to be of infectious origin (A09).

	:(More? [[Neonatal Development]] \| [[Gastrointestinal Tract Development]] \| [http://omim.org/entry/251850 OMIM 251850] \| [http://omim.org/entry/606540 OMIM MYO5B] \| PMID 20186687 \| PMID 26830108)		:(More? [[Neonatal Development]] \| [[Gastrointestinal Tract Development]] \| [http://omim.org/entry/251850 OMIM 251850] \| [http://omim.org/entry/606540 OMIM MYO5B] \| PMID 20186687 \| PMID 26830108)

Z8600021 at 23:17, 13 March 2016

2016-03-13T23:17:51Z

← Older revision		Revision as of 09:17, 14 March 2016
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			==2016==

			===Microvillus inclusion disease===

			:(MVID) A postnatal gastrointestinal tract disease due to the shortening or absence of epithelial cell (enterocytes) apical microvilli. Infants have life-threatening watery diarrhoea and mutations in myosin VB gene (MYO5B). Other forms of congenital diarrhea include congenital secretory chloride diarrhoea, an autosomal recessive form of severe chronic diarrhea .

			:(More? [[Neonatal Development]] \| [[Gastrointestinal Tract Development]] \| [http://omim.org/entry/251850 OMIM 251850] \| [http://omim.org/entry/606540 OMIM MYO5B] \| PMID 20186687 \| PMID 26830108)



	==2009==		==2009==

Z8600021 at 01:30, 6 February 2013

2013-02-06T01:30:18Z

← Older revision		Revision as of 11:30, 6 February 2013
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	PMID 18846389		PMID 18846389
	<pubmed>18846389</pubmed>		<pubmed>18846389</pubmed>

			==2001==

			NHMRC - [http://www.nhmrc.gov.au/guidelines/publications/exclusion NHMRC Infectious Diseases School Exclusion recommendations] This table has been revoked, and no longer represents the advice of NHMRC. It is included here only for historical reference purposes.


	==Ageing==		==Ageing==

Z8600021 at 23:40, 15 July 2012

2012-07-15T23:40:44Z

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 {{Talk Page}}
 ==Ageing==
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 Melamine is commonly used to manufacture strong and durable laminates, plastics, adhesives, and flame-resistant textiles. It also has been deliberately added to food and animal feed, sometimes in high amounts, to boost the appearance of protein content based on nitrogen analysis.
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2799490/?tool=pubmed
+http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2799490/?tool=pubmed

Z8600021: /* Neonatal progeria: increased ratio of progerin to lamin A leads to progeria of the newborn */

2012-06-12T02:53:36Z

Neonatal progeria: increased ratio of progerin to lamin A leads to progeria of the newborn

← Older revision		Revision as of 12:53, 12 Haziran 2012
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	==Ageing==		==Ageing==

	~~===Neonatal progeria: increased ratio of progerin to lamin A leads to progeria of the newborn===~~
	~~Eur J Hum Genet. 2012 Mar 14. doi: 10.1038/ejhg.2012.36. [Epub ahead of print]~~

	~~Reunert J, Wentzell R, Walter M, Jakubiczka S, Zenker M, Brune T, Rust S, Marquardt T.~~
	~~Source~~
	~~Universitätsklinikum Münster, Klinik für Kinder- und Jugendmedizin - Allgemeine Pädiatrie, Münster, Germany.~~

	~~Abstract~~

	Hutchinson-Gilford progeria syndrome (HGPS) is an important model disease for premature ageing. Affected children appear healthy at birth, but develop the first symptoms during their first year of life. They die at an average age of 13 years, mostly because of myocardial infarction or stroke. Classical progeria is caused by the heterozygous point mutation c.1824C>T in the LMNA gene, which activates a cryptic splice site. The affected protein cannot be processed correctly to mature lamin A, but is modified into a farnesylated protein truncated by 50 amino acids (progerin). Three more variations in LMNA result in the same mutant protein, but different grades of disease severity. We describe a patient with the heterozygous LMNA mutation c.1821G>A, leading to neonatal progeria with death in the first year of life. Intracellular lamin A was downregulated in the patient's fibroblasts and the ratio of progerin to lamin A was increased when compared with HGPS. It is suggestive that the ratio of farnesylated protein to mature lamin A determines the disease severity in progeria.European Journal of Human Genetics advance online publication, 14 March 2012; doi:10.1038/ejhg.2012.36.

	~~PMID 22419169~~

	==Immunity==		==Immunity==

Z8600021 at 02:23, 12 Haziran 2012

2012-06-12T02:23:49Z

← Older revision		Revision as of 12:23, 12 Haziran 2012
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			{{Talk Page}}

			==Ageing==

			===Neonatal progeria: increased ratio of progerin to lamin A leads to progeria of the newborn===
			Eur J Hum Genet. 2012 Mar 14. doi: 10.1038/ejhg.2012.36. [Epub ahead of print]

			Reunert J, Wentzell R, Walter M, Jakubiczka S, Zenker M, Brune T, Rust S, Marquardt T.
			Source
			Universitätsklinikum Münster, Klinik für Kinder- und Jugendmedizin - Allgemeine Pädiatrie, Münster, Germany.

			Abstract

			Hutchinson-Gilford progeria syndrome (HGPS) is an important model disease for premature ageing. Affected children appear healthy at birth, but develop the first symptoms during their first year of life. They die at an average age of 13 years, mostly because of myocardial infarction or stroke. Classical progeria is caused by the heterozygous point mutation c.1824C>T in the LMNA gene, which activates a cryptic splice site. The affected protein cannot be processed correctly to mature lamin A, but is modified into a farnesylated protein truncated by 50 amino acids (progerin). Three more variations in LMNA result in the same mutant protein, but different grades of disease severity. We describe a patient with the heterozygous LMNA mutation c.1821G>A, leading to neonatal progeria with death in the first year of life. Intracellular lamin A was downregulated in the patient's fibroblasts and the ratio of progerin to lamin A was increased when compared with HGPS. It is suggestive that the ratio of farnesylated protein to mature lamin A determines the disease severity in progeria.European Journal of Human Genetics advance online publication, 14 March 2012; doi:10.1038/ejhg.2012.36.

			PMID 22419169

	==Immunity==		==Immunity==

S8600021 at 06:41, 23 October 2010

2010-10-23T06:41:59Z

← Older revision		Revision as of 16:41, 23 October 2010
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	* Neonatal innate immunity to infectious agents. Maródi L. Infect Immun. 2006 Apr;74(4):1999-2006. Review. No abstract available. [http://www.ncbi.nlm.nih.gov/pubmed/16552028 PMID: 16552028]		* Neonatal innate immunity to infectious agents. Maródi L. Infect Immun. 2006 Apr;74(4):1999-2006. Review. No abstract available. [http://www.ncbi.nlm.nih.gov/pubmed/16552028 PMID: 16552028]
	* Passive immunity to vaccinia in newborns. I. Placental transmission of antibodies. KEMPE CH. Yale J Biol Med. 1952 Feb;24(4):328-33. No abstract available. [http://www.ncbi.nlm.nih.gov/pubmed/14914000 PMID: 14914000]		* Passive immunity to vaccinia in newborns. I. Placental transmission of antibodies. KEMPE CH. Yale J Biol Med. 1952 Feb;24(4):328-33. No abstract available. [http://www.ncbi.nlm.nih.gov/pubmed/14914000 PMID: 14914000]


			===Melamine===
			Melamine is commonly used to manufacture strong and durable laminates, plastics, adhesives, and flame-resistant textiles. It also has been deliberately added to food and animal feed, sometimes in high amounts, to boost the appearance of protein content based on nitrogen analysis.

			http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2799490/?tool=pubmed