Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019270 (hernia)
 15,856 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuroendocrine cells (NEC) are abundant in fetal and neonatal lungs, but reduced in infants with hyaline membrane disease. Perinatal neuroendocrine cell hyperplasia (NCH) has been reported in the hypoplastic lung in diaphragmatic hernia, bronchopulmonary dysplasia, and Wilson-Mikity syndrome. Since we are unaware of any reports on NCH in fetal inflammatory conditions, this report addresses the NEC in fetuses with congenital pneumonia. Twenty-one fetuses/neonates with congenital pneumonia, autopsied between 1995 and 2001, were compared to 21 fetuses without a congenital infection matched for gestational age. Lung sections were immunostained for chromogranin, bombesin, calcitonin, and synaptophysin. Proportions of immunopositive cells lining 20 consecutive bronchioles calculated from digital images were significantly higher in the study than the control group for chromogranin (1.8 vs. 0.8%, P = 2.4 E-06), calcitonin (1.2 vs. 0.7%, P = 0.005), and bombesin (1.1 vs. 0.7%, P = 0.005). There was no difference in synaptophysin (11.7% vs. 12.6%, P = 0.07). The absence of significant differences in the synaptophysin ratio excludes simple NCH in the study group. The synchronous increase in three neurohormones is indicative of NEC hyperfunction, due to either altered enzymatic inactivation by neutral endopeptidase, known to be reduced in adult lung inflammation, or by an increase in expression of the neurohormone genes. These data indicate that NEC hyperfunction may be responsible for the deranged fetal/neonatal lung function and circulatory adaptation, and contribute to the lethality of the amniotic sac infection syndrome.
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PMID:Amniotic sac infection syndrome features fetal lung neuroendocrine cell hyperfunction. 1501 48

The purpose of this study is to determine and to compare histopathologic alterations of hernia sacs obtained from patients with inguinal hernia with those of the peritoneal tissue from patients operated on for other abdominal disorders. Samples were obtained from 42 pediatric patients with uni- or bilateral hernias, and from 30 pediatric control patients without hernia. Sections were stained with hematoxylin-eosin, Gomori's trichrome, and Gomori's reticulin. Furthermore, they were immunohistochemically stained with anti-synaptophysin for the quantification of neural structures. All the slides were examined for six parameters, including variations in tissue and collagen types, the presence of inflammation and proliferation of vessels, neural plexus, and mesothelial cells. The results were evaluated statistically using the independent T-test and the Mann-Whitney-U test. Parametric tests revealed a higher presence of large neural plexus (p = 0.003), increased proliferation of mesothelial cells (p = 0.009), and hypervascularization (p = 0.003) in sacs of the hernia group. There were also major changes that were dependent on the sex of the patients. Most part of hernia sacs tissue was found to be fibrous and adipose in most boy patients, but was fibro-muscular in girls with inguinal hernia (male/female p = 0.03), while the tissues were fibro-adipose in both sexes in the control group (inguinal hernia/control p = 0.016). Similarly, vascular proliferation was mainly encountered in hernia sacs of girls (p = 0.013). These features were not observed in the control groups. Therefore, on the basis of sex, we determined whether or not these findings could indicate the difference between the etiopathologic mechanisms of inguinal hernias. Furthermore, we went into the question of whether or not the comprehensive examination of hernia sacs sufficed to enlighten the etiology of hernias.
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PMID:A comparative histopathological evaluation of sacs from boys and girls with inguinal hernia. 1546