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  • 1
    Electronic Resource
    Electronic Resource
    Upregulated tumor necrosis factor-α gene expression in the hypoplastic lung in patients with congenital diaphragmatic hernia (1998)
    Springer
    Pediatric surgery international 14 (1998), S. 21-24 
    Details
    ISSN: 1437-9813
    Keywords: Key words Congenital diaphragmatic hernia  ; Pulmonary surfactant  ;  Tumor necrosis factor-α  ; Messenger RNA  ;  In-situ hybridization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies using animal models of congenital diaphragmatic hernia (CDH) have reported a reduction in both surfactant (SF) phospholipids and proteins in CDH lungs compared to controls, resulting in biophysical and physiologic impairment of SF function in the hypoplastic CDH lung. Furthermore, SF replacement has been shown to improve physiological function in CDH lungs. Tumor necrosis factor-α (TNF-α) is a polypeptide whose overproduction has been implicated in the pathogenesis of a number of pathological conditions, such as neonatal and adult respiratory distress syndrome. TNF-α has been shown to selectively inhibit the de-novo synthesis of SF phospholipid components in type II pneumocytes. It has been demonstrated that TNF-α is synthesized locally in lung and functions in an autocrine/paracrine mode. The aim of this study was to investigate TNF-α messenger RNA (mRNA) expression in hypoplastic CDH lung using in-situ hybridization histochemistry, to determine the molecular basis of the SF deficiency in the hypoplastic CDH lung. Lung-tissue samples were obtained at autopsy from 7 full-term newborns (age range: 1–21 days) with CDH and 4 stillborns with CDH. Normal lung tissue from eight infants with sudden infant death syndrome (age range: 5–30 days) acted as controls. In-situ hybridization was performed using TNF-α specific and digoxigenin-labeled oligonucleotide probe and visualized by nitroblue tetrazolium staining. In control lung tissue, mRNA expression of TNF-α was absent or weak in type II pneumocytes and alveolar macrophages. In contrast, mRNA expression of TNF-α was markedly increased in both type II pneumocytes and alveolar macrophages in hypoplastic CDH lung. Our findings of up-regulated TNF-α gene expression in CDH lung suggest that the SF deficiency observed in hypoplastic CDH lung may be the result of increased local production of TNF-α.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003830050427
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  • 2
    Electronic Resource
    Electronic Resource
    Comparison of the pulmonary vasculature in newborns and stillborns with congenital diaphragmatic hernia (1998)
    Springer
    Pediatric surgery international 14 (1998), S. 30-35 
    Details
    ISSN: 1437-9813
    Keywords: Key words Congenital diaphragmatic hernia  ; Persistent pulmonary hypertension  ;  Pulmonary artery  ; Pulmonary vein  ;  Stillborn  ;  Newborn
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study was to compare structural changes in the pulmonary vasculature in newborns with congenital diaphragmatic hernia (CDH) complicated by persistent pulmonary hypertension (PPH) and stillborns with CDH. Victorian blue van Gieson (VVG) staining and immunostaining with anti-alpha smooth-muscle actin (ASMA) was performed on lung tissue obtained at autopsy from 23 newborns with CDH complicated by PPH, 7 stillborns with CDH, and 11 age-matched controls with sudden infant death syndrome (SIDS). The degrees of adventitial and medial thickness and area were measured in pulmonary arteries with an external diameter (ED) of 〈75 μm, 75–100 μm, 100–150 μm, 150–250 μm, 250–500 μm, and 〉500 μm by image analyzer and compared statistically. The degrees of adventitial and medial thickness and area were measured in pulmonary veins with an ED of 〈100 μm, 100–200 μm, and 〉200 μm by image analyzer and compared statistically. In order to determine whether the characteristic structural changes were size-related, each was related to ED. There was a significant increase in adventitial thickness and area in arteries of all sizes in both newborns and stillborns with CDH compared to SIDS patients (P 〈 0.05). The degree of medial thickness in newborns and stillborns with CDH was significantly increased compared to SIDS patients (P 〈 0.01). The degree of medial area was significantly increased for arteries with ED less than 100 μm (P 〈 0.05) in newborns and stillborns with CDH compared with SIDS patients. There was a significant increase in adventitial thickness and area in veins of all sizes in newborns with CDH compared to stillborns with CDH and SIDS (P 〈 0.05). The degree of adventitial thickness and area of pulmonary veins were similar in stillborns with CDH and SIDS. There were no significant differences in medial thickness of veins between the three groups. The presence of abnormally thick-walled pulmonary arteries in stillborns with CDH suggests that the intrapulmonary arteries in CDH may become excessively muscularized during fetal life, becoming unable to adapt normally at birth. The absence of structural changes in pulmonary veins in stillborns with CDH suggests that the pulmonary venous changes observed in newborns with CDH complicated by PPH occur after birth as a result of increases in transvascular pressure or a response to release of peptide growth factors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003830050429
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of enterocolitis complicating Hirschsprung's disease (1994)
    Springer
    Pediatric surgery international 9 (1994), S. 237-241 
    Details
    ISSN: 1437-9813
    Keywords: Hirschsprung's disease ; Enterocolitis ; Intercellular adhesion molecule-1 (ICAM-1)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intercellular adhesion molecule-1 (ICAM-1) is a glycoprotein that is necessary for the transendothelial migration of leucocytes. This study was undertaken to elucidate the role of ICAM-1 in the pathophysiology of Hirschsprung's disease (HD)-related enterocolitis. Ganglionic and aganglionic portions of bowel from 18 patients with HD who did not have clinical or histological evidence of enterocolitis and 5 patients with HD who developed enterocolitis before or after a pull-through operation were stained using monoclonal antibody against ICAM-1. The bowel specimens obtained from 2 children with imperforate anus at the time of colostomy closure and 3 children at the time of bladder augmentation were similarly stained to act as controls. The ganglionic portion of bowel from patients with HD without enterocolitis and controls showed either no ICAM-I staining or occasional staining of the endothelial lining of submucosal vessels with no staining of the glandular crypt epithelium. In contrast, both ganglionic and aganglionic bowel from patients with enterocolitis complicating HD demonstrated strong ICAM-1 staining in the endothelium of submucosal vessels. Strong expression of ICAM-1 in the glandular crypt epithelium was seen in only 2 patients who had developed enterocolitis before pull-through operations. This study illustrates the importance of endothelial cell activation in the pathogenesis of HD-related enterocolitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00832246
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  • 4
    Electronic Resource
    Electronic Resource
    Evaluation of risk factors in the development of enterocolitis complicating Hirschsprung's disease (1994)
    Springer
    Pediatric surgery international 9 (1994), S. 234-236 
    Details
    ISSN: 1437-9813
    Keywords: Hirschsprung's disease ; Enterocolitis ; Child
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Enterocolitis remains a major cause of morbidity and mortality in patients with Hirschsprung's disease (HD). Forty-one (30%) of 135 patients treated for HD from 1975 to 1992 developed enterocolitis; enterocolitis occured preoperatively in 25. It was a presenting feature in 17 infants, including 11 neonates. The proportion of patients presenting with enterocolitis in the neonatal period increased with advancing age, 6 (11%) out of 56 presenting within the 1st week and 5 (24%) out of 21 after 1 week. Episodes of enterocolitis continued in 7 of these 25 patients after a pull-through procedure. Sixteen patients had a first episode of enterocolitis after surgery: 3 after a colostomy, and 13 after a pull-through procedure. The incidence of enterocolitis was 28% in patients with rectosigmoid involvement and 38% in patients with long-segment or total colonic aganglionosis (P= 0.1). Enterocolitis occured in 8 (47%) of 17 patients with trisomy 21 as compared to 33 of 118 (28%) other patients (P= 0.1). Four of the 41 patients died as a result of enterocolitis, 3 in the neonatal period after a colostomy performed at a mean age of 22 days, although the symptoms suggestive of HD were present since birth. Prompt diagnosis and expeditious management are necessary in patients with HD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00832245
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  • 5
    Electronic Resource
    Electronic Resource
    Hirschsprung's disease in association with trisomy 21 and duodenal obstruction (1994)
    Springer
    Pediatric surgery international 9 (1994), S. 366-367 
    Details
    ISSN: 1437-9813
    Keywords: Hirschsprung's disease ; Trisomy 21 ; Duodenal obstruction ; Child
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The association of trisomy 21 and Hirschsprung's disease (HD) is well known. In a neonate, HD characteristically presents with delayed passage of meconium and/or intestinal obstruction. However, the presence of duodenal atreasia (DA), which may present similarly, can mask the associated HD. Over an 18-year period, 17 of 135 patients with HD had trisomy 21. Three of these 17 patients presented with duodenal obstruction in the newborn period — 2 had DA and 1 a complete duodenal web. One patient developed a perforation of the jejunum 7 days after laparotomy and duodenoduodenostomy and was found to have HD while the other 2 were later investigated because of persistent unresponsive constipation and confirmed to have HD at 1 and 2 years of age. In spite of associated Down's syndrome and DA, the possibility of HD should be considered in patients who have a complicated postoperative course or persisting abnormal stooling patterns.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01686003
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