ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Reduced fetal growth is known to be associated with a reduced ovarian fraction of primordial follicles, with ovarian hyperandrogenism and anovulation in late adolescence. In this study, we examined whether adolescent girls born small for gestational age also present an abnormality in uterine or ovarian size. Standardized ultrasound measurements of the internal genitalia were performed in 36 healthy post-menarcheal girls (mean age 14 y) born with a size that was either appropriate for gestational age (AGA) or small (SGA), birth weight averaging 0.1 and −3.0 SD, respectively; clinical and endocrine characteristics were documented concomitantly. Compared with AGA girls, the SGA girls had a smaller uterus (mean difference of 20%;p< 0.006) and a reduced ovarian volume (mean difference of 38%;p< 0.0002). In conclusion, the gynecological correlates of prenatal growth restriction are herewith extended to include a reduced size of the uterus and the ovaries.

ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Normative body composition during the first 2 y of life was derived from a prospective study of 76 children. We present1) fat free mass (FFM) and its components, and fat mass (FM),2) incremental growth rates partitioned into chemical components, and3) age-specific and gender-specific constants for converting chemical and physical components into FFM for children during the first 2 y of life. A multicomponent model based on measurements of total body water (TBW), total body potassium (TBK) and bone mineral content (BMC) was used to estimate FFM and FM at 0.5, 3, 6, 9, 12, 18, and 24 mo of age. TBW was determined by deuterium dilution, TBK by whole body counting, and BMC by dual energy x-ray absorptiometry. FFM was higher in boys than girls between 0.5–18 mo of age (p≤ 0.05). Percent FM increased on average from 13 to 31% between 0.5 and 3–6 mo, and then gradually declined. Percent FM was significantly higher in girls than in boys at 6 and 9 mo of age (p≤ 0.02). The components of FFM on a percentage basis changed with age (p= 0.001), but not gender. The protein content of FFM increased gradually with age, while TBW declined (p= 0.001). As a percentage of FFM, osseous mineral increased from 2.0 to 3.4% in boys and from 2.1 to 3.3% in girls between 0.5 and 24 mo (p= 0.001). Density and potassium content of FFM increased gradually with age (p= 0.001). These normative body composition data provide an updated reference upon which to assess normal growth and nutritional status of pediatric populations representative of mixed feeding groups during the first 2 y of life.

ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Cranial irradiation in prepubertal children with leukemia or brain tumors can lead to precocious or in high doses to late puberty. To unravel the underlying mechanisms, we developed a rat model with selective cranial Co60-irradiation technique. Infantile (12–16 d old) or juvenile (21–23 d old) female Sprague-Dawley rats received a single dose of 4, 5, 6, 9 or 2 × 9 Gy (at days 21 and 23). Each group consisted of 7–20 animals. High radiation doses (9 Gy and more) caused retardation of sexual development, whereas low radiation doses (5 or 6 Gy) led to accelerated onset of puberty in 20% of infantile irradiated rats animals as determined by vaginal opening. Interestingly, at peripubertal age (postnatal day 32–34), 5 or 6 Gy infantile irradiated rats had significantly higher serum LH levels stimulated by GnRH and estradiol levels (p< 0.05). 2 × 9 Gy irradiated rats had at the age of 3 mo a marked growth retardation and significantly lower GH levels than the controls (p< 0.05) whereas prolactin, FSH, TSH, T4, and corticosterone levels were comparable with controls. These studies demonstrate that the GnRH-pulse generator is very radiosensitive as precocious activation occurred after low dose irradiation (5 or 6 Gy) of infantile rats without any other endocrine disorder. High radiation doses (9 or 2 × 9 Gy) induced retardation of sexual maturation and later on growth hormone deficiency. Moreover this model of cranial irradiation seems to be suitable to study the molecular mechanisms of radiation induced pubertal changes.

ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

The allergy-preventing effect of breast-feeding remains controversial, possibly because of individual variations in the composition of the breast milk. Recently, we showed that allergic mothers had higher concentrations of IL-4 and lower concentrations of ovalbumin-specific IgA in their breast milk than nonallergic mothers. The aim of this study was to investigate the concentrations of chemokines and cytokines that are chemotactic to cells involved in allergic reactions in breast milk from allergic and nonallergic mothers. Cytokine and chemokine concentrations were determined with ELISA in colostrum and mature milk samples from 23 mothers with and 25 mothers without atopic symptoms. IL-8 was detected in all milk samples. RANTES (regulated on activation, normal T cell expressed and secreted), eotaxin, and IL-16 were detected in 50%, 76%, and 48%, respectively, in colostrum and less commonly in mature milk. Macrophage inflammatory protein-1&agr;, however, could not be detected in any of the samples. The concentrations of IL-8 and RANTES were higher in breast milk from allergic, compared with nonallergic, mothers. In conclusion, the presence of chemoattractant factors in breast milk may be responsible for the traffic of leukocytes from the maternal circulation to the breast milk. The higher concentrations of RANTES and IL-8 in allergic mothers may partly explain the controversy regarding the protective effect of breast-feeding against the development of allergy by stronger chemotaxis and activation of cells involved in allergic diseases, and possibly by elevated IgE production.

ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Polychlorinated biphenyls (PCB) and hexachlorobenzene (HCB) are ubiquitous compounds that have tumor-promoting properties if applied together with tobacco-specific carcinogens. It was the purpose of the present study to investigate whether parental smoking by itself will increase the prenatal uptake of such organochloric compounds. With the informed consent of the parents, blood samples were taken from 80 full-term neonates before the first oral feeding. Six PCB congeners (PCB 28, 52, 101, 138, 153, and 180) and HCB were analyzed with capillary gas chromatography. Information about parental smoking behavior, the geographic origin of the parents, and their actual and previous working places was recorded. We composed three study groups for statistical analyses: active smoking mothers (n= 12), passive smoking mothers (n= 33), and nonsmoking families (n= 35). Neonates born to active smoking mothers had the highest PCB and HCB concentrations compared with children of passive or nonsmoking mothers. These differences were statistically significant (p< 0.01) in the cases of PCB 138, total PCB, and HCB. Newborns of passive smoking mothers had higher PCB and HCB concentrations than children of nonsmoking families but lower values than those of active smoking mothers. These differences were statistically significant for all compounds with the exception of PCB 180. It is concluded that active and passive maternal smoking increases the neonatal burden with PCB and HCB.

ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Cyclooxygenases-1 and -2 are the key enzymes in the conversion of arachidonic acid to prostanoids. Cyclooxygenase-2 (COX-2) takes part both in inflammation and in control of cell growth. COX-2 immunohistochemistry was performed on lung tissues from autopsies, with four groups included: fetuses (n= 4, GA = 16.0 to 32.0 wk), preterm infants (n= 10, GA = 23.0 to 29.9 wk), term infants (n= 6, GA = 38.7 to 42.0 wk), and infants with bronchopulmonary dysplasia (BPD) (n= 4, GA = 28.9 to 30.7 wk). COX-2 staining occurred exclusively in the epithelial cells resembling type II pneumocytes in the alveolae, and in ciliated epithelial cells in the bronchi. In fetuses, moderate intensity alveolar staining was seen in 90–100% cells lining the alveolar epithelium. In preterm infants, high intensity alveolar staining was seen in a scattered pattern. In term infants, the alveolar staining was also scattered, but with a lower proportion of positive cells. In BPD no staining appeared in alveolar epithelial cells. The most intense bronchial staining was found in fetuses and the least intense in term infants; staining was also seen in BPD. COX-2 is present in human perinatal lung from the gestational age of 16 wk, in a changing pattern. We suggest that COX-2 may, in addition to participating in inflammation, also play a developmental role in the perinatal lung.

ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Although the endothelial cell is the most abundant cell type in the differentiated lung, little is known about regulation of lung developmental vasculogenesis. Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen and angiogenic factor that has putative roles in vascular development. Mitogenic actions of VEGF are mediated by the tyrosine kinase receptor KDR/murine homologue fetal liver kinase Flk-1. HLF (hypoxia-inducible factor-like factor) is a transcription factor that increases VEGF gene transcription. Dexamethasone augments lung maturation in fetal and postnatal animals. However,in vitrostudies suggest that dexamethasone blocks induction of VEGF. The objectives for the current study were to measure VEGF mRNA and Flk-1 mRNA in developing mouse lung and to measure the effects of dexamethasone treatmentin vivoon VEGF and Flk-1 in newborn mouse lung. Our results show that VEGF and Flk-1 messages increase in parallel during normal lung development (d 13 embryonic to adult) and that the distal epithelium expresses VEGF mRNA at all ages examined. Dexamethasone (0.1–5.0 mg·kg−1·d−1) treatment of 6-d-old mice resulted in significantly increased VEGF, HLF, and Flk-1 mRNA. Dexamethasone did not affect cell-specific expression of VEGF, VEGF protein, or proportions of VEGF mRNA splice variants. These data suggest that the developing alveolar epithelium has an important role in regulating alveolar capillary development. In addition, unlike effects on cultured cells, dexamethasone, even in relatively high doses, did not adversely affect VEGF expressionin vivo. The relatively high levels of VEGF and Flk-1 mRNA in adult lung imply a role for pulmonary VEGF in endothelial cell maintenance or capillary permeability.

ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Angiotensin II (Ang II) and basic fibroblast growth factor (bFGF/FGF-2) play relevant roles in renal development. Since the signaling pathways modulating the mitogenic effects of Ang II and bFGF in human fetal mesangial cells (HFMc) are not clearly defined, we carried out experiments to determine whether they would exert their mitogenic effects by modulating the activity of the mitogen-activated protein kinases (MAPK) [extracellular signal-regulated kinase-2 (ERK-2)] and cAMP signaling pathways. In confluent HFMc, bFGF (20 ng/mL) induced a significant 4-fold increase in ERK-2 activity and [3H]-thymidine incorporation (6-fold). In contrast, under similar tissue culture conditions, Ang II (10−6M) induced a more modest increase in ERK-2 activity (2-fold) and [3H]-thymidine incorporation (35 ± 4%). The mitogen-activated protein kinase kinase-1 (MEK-1) inhibitor PD098059 (25 &mgr;M) almost completely abolished the bFGF-induced proliferation in HFMc but did not significantly affect Ang II proliferative effects. In the presence of the cAMP elevating agent isoproterenol, Ang II and bFGF induced opposite changes in cAMP accumulation and cell growth. Isoproterenol inhibited the basal and bFGF-induced proliferation of HFMc through a MEK-1/2–independent pathway that included the accumulation of cAMP. In contrast, isoproterenol increased Ang II mitogenic effects in correlation with a reduction in cAMP accumulation. We conclude that Ang II and bFGF modulate the proliferation of HFMc through the stimulation of different MEK-1/2–dependent and independent signaling pathways. Activation of MEK-1/2 is required but not sufficient for mitogenesis in HFMc. The accumulation of cAMP in HFMc counteracts the mitogenic effects of bFGF by a MEK-1/2–independent pathway.

ISSN:0031-3998    

出版商:OVID    

年代:2000

数据来源: OVID