scholarly journals Significance of raised immunoglobulin M levels in cord blood of small-for-gestational-age infants.

1978 ◽  
Vol 53 (11) ◽  
pp. 895-898 ◽  
Author(s):  
T G Matthews ◽  
C O'Herlihy
Keyword(s):  
Cord Blood ◽  
Blood Group ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Intrauterine Infection ◽  
Immunoglobulin M ◽  
Hammersmith Hospital ◽  
Group B

Cord IgM values were determined in small-for-gestational-age infants born at Hammersmith Hospital during a 5 1/2-year period. 121 (12.5%) infants had levels more than 0.2 g/l; in 92 these were between 0.21 and 0.3 g/l. In only 18 (14.8%) was a level of 0.4 g/l exceeded, and 5 proved cases of intrauterine infection--rubella (2), syphilis (2), and toxoplasmosis (1)--were in this group. The factor most often associated with cord IgM more than 0.4 g/l was prolonged rupture of the membranes. There was an increased incidence of blood group B among the mothers, probably reflecting the greater number of nonCaucasian women giving birth to small-for-gestational-age infants. Determination of cord IgM did not help significantly indiagnosis.

Inflammatory Markers in Umbilical Cord Blood from Small-For-Gestational-Age Newborns

2014 ◽  
Vol 33 (2) ◽  
pp. 114-118 ◽  
Author(s):  
Ulrik Lausten-Thomsen ◽  
Marianne Olsen ◽  
Gorm Greisen ◽  
Kjeld Schmiegelow
Keyword(s):  
Cord Blood ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Inflammatory Markers

Enzymatic Determination of the Anomeric Structures of Two Blood-Group B Active Glycosphingolipids Recombined with Apolipoproteins

1978 ◽  
Vol 33 (1-2) ◽  
pp. 73-78 ◽  
Author(s):  
Peter Hanfland ◽  
Gerd Assmann ◽  
Heinz Egge
Keyword(s):  
Blood Group ◽  
Water Solubility ◽  
Erythrocyte Membranes ◽  
High Density Lipoproteins ◽  
Composition Analysis ◽  
Glycosidic Linkage ◽  
Anomeric Configuration ◽  
Enzymatic Determination ◽  
Group B

Abstract Anomeric configuration of oligosaccharides usually is established by specific glycosidases. For this purpose detergents achieving water solubility of primarily insoluble glycosphingolipids as substrates have been replaced by delipidated hum an serum high density lipoproteins. The new method, tested by several well characterized glycosphingolipids and glycosidases, finally was applied to the evaluation of anomeric structures of two blood-group B active glycosphingolipids [ceramide hexa-saccharide (B-I) and ceramide octasaccharide (B -II)] from hum an erythrocyte membranes. In both B-I and B-II, α-glycosidic linkage was dem onstrated for the term inal galactose and fucose residues. β-glycosidic linkage has been evaluated for backbone saccharides. Together with the results pre­ viously obtained by composition analysis, linkage analysis and sequence analysis the following complete structure can be established:B -I: Galα1 → 3Gal (2 ← 1αFuc)β1 → 4GlcNAcβ1 → 3Galβ1 → 4Glcβ1 → 1Cer;B-II: Galα1 → 3Gal (2 ← 1αFuc)β1 → 4GlcNAcβ1 → 3Galβ1 → 4GlcNAcβ1 → 3Galβ1 → 4Glcβ1 → 1Cer.

scholarly journals Cord blood alpha klotho is decreased in small for gestational age preterm infants with placental lesions of accelerated aging

Placenta ◽  
2019 ◽  
Vol 87 ◽  
pp. 1-7 ◽  
Author(s):  
Andrew D. Franklin ◽  
Juanita Saqibuddin ◽  
Kelli Stephens ◽  
Robert Birkett ◽  
Lily Marsden ◽  
...  
Keyword(s):  
Cord Blood ◽  
Preterm Infants ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Accelerated Aging

scholarly journals Differential DNA methylation profile in infants born small-for-gestational-age: association with markers of adiposity and insulin resistance from birth to age 24 months

2020 ◽  
Vol 8 (1) ◽  
pp. e001402
Author(s):  
Marta Diaz ◽  
Edurne Garde ◽  
Abel Lopez-Bermejo ◽  
Francis de Zegher ◽  
Lourdes Ibañez
Keyword(s):  
Insulin Resistance ◽  
Dna Methylation ◽  
Body Composition ◽  
Cord Blood ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Diabetes Risk ◽  
Metabolic Dysfunction ◽  
A Genome ◽  
Methylation Profiling

IntroductionPrenatal growth restraint followed by rapid postnatal weight gain increases lifelong diabetes risk. Epigenetic dysregulation in critical windows could exert long-term effects on metabolism and confer such risk.Research design and methodsWe conducted a genome-wide DNA methylation profiling in peripheral blood from infants born appropriate-for-gestational-age (AGA, n=30) or small-for-gestational-age (SGA, n=21, with postnatal catch-up) at age 12 months, to identify new genes that may predispose to metabolic dysfunction. Candidate genes were validated by bisulfite pyrosequencing in the entire cohort. All infants were followed since birth; cord blood methylation profiling was previously reported. Endocrine-metabolic variables and body composition (dual-energy X-ray absorptiometry) were assessed at birth and at 12 and 24 months.ResultsGPR120 (cg14582356, cg01272400, cg23654127, cg03629447), NKX6.1 (cg22598426, cg07688460, cg17444738, cg12076463, cg10457539), CPT1A (cg14073497, cg00941258, cg12778395) and IGFBP 4 (cg15471812) genes were hypermethylated (GPR120, NKX6.1 were also hypermethylated in cord blood), whereas CHGA (cg13332653, cg15480367, cg05700406), FABP5 (cg00696973, cg10563714, cg16128701), CTRP1 (cg19231170, cg19472078, cg0164309, cg07162665, cg17758081, cg18996910, cg06709009), GAS6 (N/A), ONECUT1 (cg14217069, cg02061705, cg26158897, cg06657050, cg15446043) and SLC2A8 (cg20758474, cg19021975, cg11312566, cg12281690, cg04016166, cg03804985) genes were hypomethylated in SGA infants. These genes were related to β-cell development and function, inflammation, and glucose and lipid metabolism and associated with body mass index, body composition, and markers of insulin resistance at 12 and 24 months.ConclusionIn conclusion, at 12 months, abnormal methylation of GPR120 and NKX6.1 persists and new epigenetic marks further involved in adipogenesis and energy homeostasis arise in SGA infants. These abnormalities may contribute to metabolic dysfunction and diabetes risk later in life.

scholarly journals Racial disparities in cord blood vitamin D levels and its association with small-for-gestational-age infants

2016 ◽  
Vol 36 (8) ◽  
pp. 623-628 ◽  
Author(s):  
T L Seto ◽  
M E Tabangin ◽  
G Langdon ◽  
C Mangeot ◽  
A Dawodu ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cord Blood ◽  
Racial Disparities ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Vitamin D Levels

scholarly journals Association between Soluble (Pro)Renin Receptor Concentration in Cord Blood and Small for Gestational Age Birth: A Cross-Sectional Study

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e60036 ◽  
Author(s):  
Noriyoshi Watanabe ◽  
Satoshi Morimoto ◽  
Takeo Fujiwara ◽  
Tomo Suzuki ◽  
Kosuke Taniguchi ◽  
...  
Keyword(s):  
Cord Blood ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Cross Sectional ◽  
Receptor Concentration

scholarly journals Small for Gestational Age and Magnesium in Cord Blood Platelets: Intrauterine Magnesium Deficiency May Induce Metabolic Syndrome in Later Life

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Junji Takaya ◽  
Kazunari Kaneko
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Cord Blood ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Magnesium Deficiency ◽  
Blood Platelets ◽  
Later Life ◽  
Intracellular Magnesium ◽  
Increased Risk

Magnesium deficiency in pregnancy frequently occurs because of inadequate or low intake of magnesium. Magnesium deficiency during pregnancy can induce not only maternal and fetal nutritional problems, but also consequences that might last in offspring throughout life. Many epidemiological studies have disclosed that small for gestational age (SGA) is associated with an increased risk of insulin resistance in adult life. We reported that intracellular magnesium of cord blood platelets is lower in SGA groups than that in appropriate for gestational age groups, suggesting that intrauterine magnesium deficiency may result in SGA. Taken together, intrauterine magnesium deficiency in the fetus may lead to or at least program insulin resistance after birth. In this review, we propose that intrauterine magnesium deficiency may induce metabolic syndrome in later life. We discuss the potential contribution of aberrant magnesium regulation to SGA and to the pathogenesis of metabolic syndrome.

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