Cyclooxygenase (COX) is a key enzyme in prostanoid synthesis. It exists in two isoforms, COX-1 and COX-2. COX-1 is referred to as a ‘constitutive isoform’, and is considered to be expressed in most tissues under basal conditions. In contrast, COX-2 is referred to as an ‘inducible isoform’, which is believed to be undetectable in most normal tissues, but can be up-regulated during various conditions, many of them pathological. Even though the role of COX in homeostasis and disease in now well appreciated, controversial information is available concerning the distribution of COX isoforms in normal human tissues. There is mounting evidence that it is much more complex than generally believed. Our aim was therefore to analyse the expression and distribution of COX isoforms in normal human tissues, using immunohistochemistry, Western blotting and real-time RT-PCR. Autopsy samples from 20 healthy trauma victims and samples from 48 biopsy surgical specimens were included. COX-1 was found in blood vessels, interstitial cells, smooth muscle cells, platelets and mesothelial cells. In contrast, COX-2 was found predominantly in the parenchymal cells of many tissues, with few exceptions, for example the heart. Our results confirm the hypothesis that the distribution of COX isoforms in healthy tissues is much more complex than generally believed. This and previous studies indicate that both isoforms, not only COX-1, are present in many normal human tissues, and that both isoforms, not only COX-2, are up-regulated in various pathological conditions. We may have to revise the concept of ‘constitutive’ and ‘inducible’ COX isoforms.

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BackgroundMediastinal fetal teratoma can be detected as a mass in the chest during a routine prenatal ultra-sound screening. Because of the pressure on mediastinal structures it can be the cause of non-immune hydrops fetalis and polyhydramnion. The development of hydrops fetalis leads to fetal death or premature delivery in most reported cases. Early surgical removal is important, but, the result of treatment depends on the stage of development of mediastinal organs and complications in the postoperative period.Case report.A 31-year-old gravida carrying twins, with spontaneous membrane rupture at 32 weeks gestation underwent urgent caesarean section after antenatal ultrasound revealed severe polyhydramnion and hydrops fetalis in geminus A. The child was intubated immediately after birth due to severe respiratory distress. Ultrasound and X-ray revealed a tumour mass in the right hemithorax. Tumour resection was performed at the age of 7 days. Histology examination revealed an encapsulated immature teratoma. The postoperative course was complicated with respiratory insufficiency which turned into chronic at the age of eight months.ConclusionThis is the fifth reported child with fetal mediastinal teratoma and severe hydrops fetalis that survived the neonatal period. Additional diagnostic search revealed abnormal course of both pulmonary arteries, which was probably one of the main causes of respiratory insufficiency.

The heart is the first organ to function in the developing embryo. MicroRNAs (miRNAs) are small non-coding RNAs involved in the translational regulation of gene expression, which is beside transcriptional regulation crucial for the morphologic development of muscle tissue. The aim of our study was to test the hypothesis that the expression of miR-1, miR-133a/b, and miR-208a correlates with gestational age as well as with an apoptotic and proliferative index in the developing human heart. Our study included normal heart tissue samples obtained at autopsy from 46 fetuses, 12 children, and 15 adults. Proliferation and apoptosis were measured by the immunohistochemical detection of Ki67 and cleaved-CK18. Expression of miR-1, miR-133a, miR-133b, and miR-208a was measured using real-time PCR. We found a similar level of expression of miR-133a/b in fetal and children hearts that was different from the levels in healthy adults. We also found a correlation between a miR-208a expression to the gestational age of fetuses. We observed an inverse correlation between Ki67 expression and gestational age. Expression of Ki67 was positively correlated to the expression of miR-208a and miR-1, but inversely correlated to the expression of miR-133a/b. Expression of cleaved-CK18 was also inversely correlated to the expression of miR-133a/b. Our results showed a general decrease in the expression of miR-1 and an increase of miR-133a/b with increasing gestational age. We also found a general decrease in the expression of miR-208a, mimicking the expression of its host gene. Our results also suggest the involvement of miR-208a and miR-1 in the proliferation as well as anti-proliferative and anti-apoptotic roles of miR-133a/b.