Loss of Wharton's jelly and fibrosis in umbilical cord stricture area: A case report.

INTRODUCTION: Stricture of the umbilical cord, though a rare condition, is one of the critical events that can be associated with intrauterine fetal death. CASE: A 27-year-old woman, primigravida, presented with USG report of fetus mortus at 37 weeks of gestation. There were no preceding warning signs. Postmortal examination showed Grade II macerated female fetus weighing 2372 g, measuring 49 cm, with haemorrhagic fluid in the brain ventricles. Microscopically, there were signs of amniotic fluid aspiration and autolytic changes. The macroscopic placental examination was normal, while signs of intrauterine asphyxia and intrauterine fetal demise were present histologically. Umbilical cord insertion was eccentric, on the cut three-vessel cord, 49 cm long, 1 cm in diameter. Extremely narrow segment measured 3 mm, approximately 1,5 cm in length, and was located 1 cm from fetal insertion site. In the further course, hypercoiling in 12 cm of the length was present. Examination of umbilical cord in stricture area revealed loss of Wharton's jelly, replacement with extensive fibrosis and capillary vessel formation. DISCUSSION AND CONCLUSION: The causality between umbilical cord stricture and intrauterine fetal demise has been established. Etiology is still unclear, therefore postmortal examination with umbilical cord evaluation and further research are needed.

Accelerated capacity of glutamate uptake via blood elements as a possible tool of rapid remote conditioning mediated tissue protection.

Recently, the function of blood cells in remote ischemic conditioning (RIC) mediated neuroprotection was undoubtedly confirmed. In the present paper, we have focused on the role of blood elements in glutamate homeostasis. The blood of remote conditioned (tolerant) animals was incubated ex vivo with 100 µM glutamate, and the quantitative and qualitative changes of excitatory amino acid transporters (EAAT 1, 2, and 3) were determined. We confirmed RIC mediated accelerated sequestration of extracellular glutamate via EAATs and altered distribution of that amino acid between plasma and cell elements compared to non-tolerant counterparts. The activity of EAATs was elevated in erythrocytes and monocytes, while the density of transporters was not affected. Quantitative changes of EAAT1 density were detected solely in platelets where the forced scavenging was independent of EAATs inhibition. Surprisingly, the trafficking of immunovisualised EAAT2 and 3 raised at tolerant erythrocytes and monocytes. We have found that protein synthesis underlined this process. On the other hand, depletion of protein synthesis did not significantly affect the scavenging capacity of those cell populations. Our work has demonstrated that the elevated blood scavenging of glutamate overdose could be one of the potential mechanisms underlying RIC mediated tissue protection.