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Biomedical subjects

Jovanna Dahlgren

Publications and source records attributed to Jovanna Dahlgren.

10 recordsLinked to original sources
PubMed2006

Interleukin-6 in the maternal circulation reaches the rat fetus in mid-gestation.

Maternal systemic infection during pregnancy may expose the fetus to infectious agents and high levels of mediators of the resulting inflammatory response, such as IL-6 (IL-6). Increased fetal and maternal levels of IL-6 have been associated with adverse neonatal outcome but might also stress the fetus and contribute to cardiovascular and neuroendocrine dysfunction in adulthood. It is unclear whether interleukins cross the placental barrier, although this matter has been little studied. The aim of this study was therefore to investigate if IL-6 administered to pregnant rats in vivo is transferred to the fetus. We injected 125I IL-6 i.v. to pregnant dams at gestation day 11-13 (mid-gestation) or 17-19 (late gestation). We found 125I-IL-6 in the exposed fetuses as well as in amniotic fluids. Fetal 125I-IL-6 levels were markedly higher in animals injected in mid-gestation compared with late pregnancy (p < 0.01). This difference was mirrored in a 15-fold higher unidirectional materno-fetal clearance for 125I-IL-6 in mid-gestation (p < 0.01). We conclude that the permeability of the rat placental barrier to IL-6 is much higher in mid-gestation than in late pregnancy. Maternally derived IL-6 may directly induce fetal injury but also stimulate the release of fetal stress hormones resulting in stimuli or insults in neuroendocrine structures and hormonal axes which might lead to disease at adult age.

Animals↗
PubMed2005

The association between short stature and sensorineural hearing loss.

In order to test the Thrifty Phenotype Hypothesis on hearing, data from two cross-sectional studies on hearing were re-evaluated. The data sets comprised 500 18-year-old conscripts, and 483 noise-exposed male employees. Sensorineural hearing loss (SNHL) was over-represented among conscripts with a short stature (odds ratio=2.2) or hearing loss in the family (odds ration=4.2), but not among noise-exposed conscripts (odds ratio=0.9-1.3). Among noise-exposed short employees, hypertension and age exhibited a negative impact on high frequency hearing thresholds, while among tall employees hypertension had no effect on hearing and the influence of age was less pronounced (p<0.01 for body height; p<0.02 for age, hypertension and the interaction between body height and hypertension; p<0.05 for the interaction between body height and age). This suggests that mechanisms linked to fetal programming and growth retardation and/or insulin-like growth factor 1 levels during fetal life, such as a delayed cell cycle during the time window when the cochlea develops, may cause SNHL in adulthood.

Adolescent↗
PubMed2005

Improved final height with long-term growth hormone treatment in Noonan syndrome.

AIM: To assess whether children with Noonan syndrome on long-term growth hormone (GH) therapy improve their final height to near mid-parental height. METHODS: Twenty-five prepubertal children (13 girls) with Noonan syndrome (NS) were studied. A single clinician made the diagnosis based on clinical criteria. GH treatment started at an age ranging from 3.1 to 13.8 y and was continued for at least 2 y. Improvement or "gain" in final height (FH) was defined as either the difference between adult height SD scores (SDS) and pre-treatment height SDS (the childhood component of the Swedish reference) or height SDS compared to the Noonan reference. RESULTS: Ten children received a GH dose of 33 microg/kg/d (mean age at start 7.7+/-2.1 y, mean age at stop 17.6+/-1.7 y) and 15 received a dose of 66 microg/kg/d (mean age at start 8.6+/-3.3 y, mean age at stop 18.4+/-2.1 y). Eighteen out of 25 patients reached FH. A substantial improvement in FH of 1.7 SDS, equivalent to 10.4 cm compared to pre-treatment height, was observed. No significant difference was seen between the two GH doses. Females gained a mean height of 9.8 cm and males 1-13 cm (FH 174.5+/-7.8 cm vs mean adult height of 162.5+/-5.4 cm for males with NS) at final height. Moreover, 60% reached a mid-parental height of+/-1 SD. CONCLUSION: GH treatment improves final height in patients with Noonan syndrome, with a mean gain of 1.7 SDS. The prepubertal height gain is maintained to final height and the children achieve a height close to their mid-parental height.

Adolescent↗
PubMed2004

Final height in short children born small for gestational age treated with growth hormone.

The aim of this observational study was to assess the long-term growth responses to GH treatment of children born small for gestational age (SGA). GH treatment was begun before puberty and continued to final height (FH). Seventy-seven short (height SD score below -2) prepubertal children born SGA (below -2 SD for birth weight and/or birth length), with a broad range of GH secretory capacity, were treated with GH in a daily dose of 33 microg/kg (0.1 U/kg), beginning before the onset of puberty. We observed a difference between adult and pretreatment projected height of 1.3 SD (9 cm) for the entire group. Among the children treated for >2 y before puberty, this mean gain (i.e. difference) in final height was 1.7 SD, whereas the mean gain was 0.9 SD among those in whom treatment was begun <2 y before puberty. Better catch-up growth was observed in the younger (r=-0.56, p<0.0001), shorter (r=-0.49, p<0.0001), and lighter (r=-0.46, p<0.0001) subjects. We conclude that GH treatment improves the final height of short children born SGA. The height gain attained before the onset of puberty is maintained to final height. The younger, shorter, and lighter the child at the start of GH treatment, the better the response. Moreover, most of these SGA individuals treated with GH reach their target height.

Adolescent↗
PubMed2004

Prenatal exposure to interleukin-6 results in hypertension and increased hypothalamic-pituitary-adrenal axis activity in adult rats.

During pregnancy, systemic inflammatory responses induce cytokines that may stress the fetus and contribute to cardiovascular and neuroendocrine dysfunction in adulthood. We evaluated the effects of early and late prenatal exposure to IL-6 on mean systolic arterial pressure (MSAP) and hypothalamic-pituitary-adrenal (HPA) axis regulation in male and female rats at 5-24 wk of age. MSAP and ACTH and corticosterone levels were measured basally and in response to a novel environment, immobilization stress, and stimulation with corticotropin-releasing factor (CRF) and ACTH. In addition, mRNA expression and protein levels of glucocorticoid receptor, mineralocorticoid receptor, CRF receptor type 1, and CRF were estimated in brain areas thought to mediate central effects of corticosteroids on the HPA axis and on central neuroendocrine regulation of MSAP. Both early and late prenatal IL-6 exposure led to hypertension, which was evident in females at 5 wk of age. In adult rats, basal ACTH and corticosterone levels were elevated, the responses to stress and stimulation tests were of extended duration, and circadian rhythm during the light period was flattened and reversed. Mineralocorticoid receptor and glucocorticoid receptor mRNA expression was reduced in the hippocampus, the CRF level was increased in the hypothalamus, and CRF receptor type 1 mRNA expression was increased in the pituitary. These findings suggest that fetal stress induced by prenatal exposure to IL-6 leads to hypertension and dysregulation of HPA axis activity during adulthood.

Adrenocorticotropic Hormone↗
PubMed2004

Abnormal retinal optic nerve morphology in young adults after intrauterine growth restriction.

Intrauterine growth restriction (IUGR) is a recognized risk factor for neurologic deficits later in life. Abnormal fetal blood flow in the presence of fetal growth retardation helps to distinguish true fetal growth impairment from small but normally grown infants. The present study aimed to investigate the influence of IUGR with abnormal fetal blood flow on retinal optic nerve morphology at 18 y of age. A prospective study was performed in 19 subjects with IUGR [abnormal fetal aortic blood flow velocity; median birth weight deviation of -31% (-22 to -42%; median (range)] and in 23 subjects with a normal birth weight for gestational age [normal fetal aortic blood flow velocity; median birth weight deviation of -2% (-10 to 22%)]. All subjects were previously examined concerning minor neurologic dysfunction (MND) at 7 y of age. The ocular fundus was examined by ophthalmoscopy, and the optic nerve morphology was evaluated by digital image analysis. Decrease in neuroretinal rim area at 18 y of age was associated with increasing negative birth weight deviation (r = 0.71, p < 0.0001). The subjects with severe MND at 7 y had a reduced neuroretinal rim area [median (range), 1.57 mm(2) (1.37-1.78 mm(2))] compared with those with less severe MND [1.94 mm(2) (1.33-2.71 mm(2))] and with those with normal neurologic function [2.18 mm(2) (1.75-2.70 mm(2)); p < 0.05 and p < 0.0001, respectively]. A decrease in neuroretinal rim area reflects either a reduction in axonal volume or a decrease in the number of axons in the optic nerve. It is yet unclear whether this finding represents neuronal changes within other cerebral regions in subjects with IUGR.

Adolescent↗
PubMed2004

Abnormal retinal vascular morphology in young adults following intrauterine growth restriction.

OBJECTIVE: Intrauterine growth restriction (IUGR) resulting in low birth weight for gestational age may predispose one to development of cardiovascular disease later in life. Abnormal fetal blood flow in the presence of fetal growth restriction helps to distinguish infants with true fetal growth impairment from small but normal infants. Our goal was to investigate associations between IUGR with abnormal fetal blood flow and abnormal retinal vascular morphology at 18 years of age. METHODS: A prospective study was performed with 21 subjects with IUGR (abnormal fetal aortic blood flow velocity; birth weight small for gestational age; median birth weight deviation from the population mean of -31% [range: -22% to -42%] and in 23 subjects with birth weight appropriate for gestational age [normal fetal aortic blood flow velocity; median birth weight deviation of -2% (range: -10% to 22%)]). The retinal vessel morphology was evaluated by digital image analysis. RESULT: Subjects with IUGR (n = 21) had significantly less retinal vascularization as evidenced by a lower number of vascular branching points (median: 26; range: 20-31) as compared with the subjects who were born appropriate for gestational age (median: 28; range: 26-32). Within the entire group (N = 44), increasing negative birth weight deviation was associated with a reduced number of vascular branching points (r = 0.36. CONCLUSION: Our findings show that IUGR with abnormal fetal blood flow is associated with abnormal retinal vascular morphology in young adult life.

Adolescent↗
PubMed2003

Association between insulin-like growth factor I (IGF-I) polymorphisms, circulating IGF-I, and pre- and postnatal growth in two European small for gestational age populations.

The purpose of this study was to assess the association of IGF-I and birth size by studying small for gestational age (SGA) subphenotypes and undertaking more detailed analysis of IGF-I genetic markers. SGA subjects from Haguenau, France (n = 113), and Gothenburg, Sweden (n = 174), were studied. The Swedish subjects were subphenotyped according to postnatal growth (114 short SGA and 60 SGA catch-up). IGF-I dinucleotide repeat and single nucleotide polymorphism (SNP) markers were studied, and haplotypes were generated in the Swedish short SGA group by identity of state. Association analysis was undertaken using the Monte Carlo method of association analysis of multiallelic markers for dinucleotide repeat markers, by exact chi(2) analysis for SNPs and by ANOVA for serum IGF-I levels. IGF-I genotype was associated with the SGA phenotype, in particular with symmetrical SGA and low birth weight, and with IGF-I levels in SGA subjects. Association with postnatal growth was different in the two populations, which may reflect the power of the smaller subphenotype groups. Haplotype analysis in the Swedish short SGA subjects showed that the region of association lay between the promoter and intron 2 of the IGF-I gene. These studies validate the association of the IGF-I gene with birth size and refine the region of association in Swedish short SGA subjects.

Adolescent↗