Spontaneous Neck Hematoma in a Patient with Fibromuscular Dysplasia: A Case Report and a Review of the Literature

Background. Fibromuscular dysplasia (FMD) is a vascular disease that may present as aneurysms in the cervical arteries. Spontaneous neck hematoma is a rare life threatening medical condition. This is the first report of neck hematoma in a patient with FMD. Methods and Results. We present a case of a 69-year-old woman, with diagnosed cervical FMD and a 3-day history of sore throat and neck pain, who presented with enlarging neck hematoma. No active bleeding was noticed on CT angiography, airway was not compromised, and patient was managed conservatively. Next day, invasive angiography was performed, and no bleeding vessel was demonstrated. Patient has improved and was discharged after 5 days of hospitalization. We have discussed the different etiology of this condition, focusing on systemic vascular diseases. Conclusion. Complaint of neck pain in a patient with a FMD should raise suspicion for possible neck hematoma. Conversely, spontaneous neck hematoma without clear etiology should raise suspicion for a systemic vascular disease

Electrochemical-chemical electron transfer in electrochromic nanoscale layers

We demonstrate here the assembly of a nanolayer of electrochromic iron complexes on top of composite layers of cobalt and ruthenium complexes. Depending on the ratio of the latter two complexes, we can tailor materials that show different elec-tron transport pathways, redox-activities, and color transitions. No redox activity of the top layer, consisting of iron com-plexes, is observable when the relative amount of the ruthenium complexes is low in the underlying composite layer because of the insulating properties of the isostructural cobalt complexes. Increasing the amount of ruthenium complexes opens an electron transport channel, resulting in charge storage both in the cobalt and iron complexes. The trapped charges can be chemically released by redox-active ferrocyanide complexes at the film-water interface, demonstrating an electrochemical-chemical electron transfer process

The Effect of Ethanol on Telomere Dynamics and Regulation in Human Cells

Telomeres (TLs) protect chromosome ends from chromosomal fusion and degradation, thus conferring genomic stability, and play crucial roles in cellular aging and disease. Recent studies have found a correlation between environmental, physiological and even mental stresses on TL dynamics in humans. However, the causal relationship between stress and TL length and the molecular mechanisms underlying that relationship are far from being understood. This study describes the effect of moderate concentrations of ethanol, equivalent to social drinking, on human TL dynamics and partially elucidates the mechanism mediating this effect. The exposure of Immortalized human foreskin fibroblast, primary human foreskin fibroblast and human hepatocellular carcinoma cells to 25 mM ethanol for one week moderately shortened telomeres in all cells. Similar TL shortening was obtained following cells’ exposure to 25 µM acetaldehyde (AcH) and to a much lower extent after exposure to 4-methylpyrazolean, an inhibitor of alcoholdehydrogenase, suggesting that AcH plays a key role in ethanol-dependent telomere shortening. Telomerase activity was not involved in this effect. TRF2 and several TRF2 binding proteins increased their binding to TLs after ethanol treatment, implying their involvement in this effect. The methylation status of several sub-telomeric regions increased in response to EtOH exposure. Gene expression profiling showed distinct patterns in cells treated with EtOH and in cells recovered from EtOH. In addition to cellular ageing, the described telomere shortening may contribute to the carcinogenic potential of acute alcohol consumption; both are associated with the shortening of TLs and provide new insights regarding the moderate consumption of alcohol referred to as “social drinking.&rdquo