Embolization of ruptured intracranial aneurysms with detachable coils: case series

Purpose  

We present a series of patients with subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms who were treated with endovascular embolization by detachable coils.     

In vitro evaluation of the clastogenicity of fumagillin

Fumagillin, an antibiotic compound produced by Aspergillus fumigatus, is effective against microsporidia and various Amoeba species, but is also toxic when administered systemically to mammals. Furthermore, a recent in vivo study by Stanimirovic Z et al. 2007: (Mutat Res 628:1-10) indicated genotoxic effects of fumagillin. The aim of the present study was to investigate and explain the clastogenic effects of fumagillin (in the form of fumagillin dicyclohexylamine salt) on human peripheral blood lymphocytes in vitro by sister-chromatid exchanges (SCE), chromosome aberrations (CA), and micronucleus (MN) tests. The mitotic index (MI), proliferation index (PI), and nuclear division index (NDI) were calculated to evaluate the cytotoxic potential of fumagillin. Five concentrations of fumagillin (0.34, 0.68, 1.02, 3.07, and 9.20 microg/ml) were applied to lymphocyte cultures. All the tested concentrations of fumagillin increased the frequency of SCE per cell significantly (P < 0.001 or P < 0.01) compared with the negative control. A significant (P < 0.001) increase in frequency of structural CA was observed at the three highest concentrations in comparison with the negative control. In addition, the three highest test concentrations increased MN formation and decreased MI, PI, and NDI significantly compared with the negative control. The present results indicate that fumagillin is clastogenic and cytotoxic to cultured human lymphocytes.     

„Negative pressure wound therapy“ bei sternalen Wundinfektionen

Zeitschrift für Herz-,Thorax- und Gefäßchirurgie - Die mediane Sternotomie ist in der Herzchirurgie der am häufigsten durchgeführte chirurgische Zugang. Gleichwohl treten...     

Dramatic response of chronic ulcerating necrobiosis lipoidica to ultraviolet A1 phototherapy

We report on a 52-year-old female patient with chronic, ulcerating necrobiosis lipoidica (NL) who dramatically responded to ultraviolet A1 (UVA1) phototherapy. The patient had NL on her right shin for more than 30 years without evidence of diabetes mellitus. Treatment with a variety of local and systemic agents failed to prevent progression into ulceration, which necessitated repeated surgical interventions in the past. When the patient presented again with torpid ulcers at the periphery of previously grafted skin, high-dose UVA1 phototherapy was initiated. Improvement occurred rapidly and after 22 irradiations and a total exposure dose of 1480 J/cm2, the ulcers had healed completely. During a follow-up period of 6 years,two minor recurrences were successfully retreated with UVA1 phototherapy.     

Reactivating and protective effects of Pro-2-PAM in mice poisoned with paraoxon

Acute toxicity of N-methyl-1,6-dihydropyridine-2-carbaldoxime hydrochloride (Pro-2-PAM) in mice, its concentrations in blood and brain and its protective and reactivating effects in diethyl p-nitrophenyl phosphate (paraoxon) poisoning were determined. Comparative studies with N-methylpyridinium-2-aldoxime chloride (PAM-2 Cl) and a mixture of two oximes were also performed. Pro-2-PAM was much less toxic than was PAM-2 Cl. In contrast to this, the Pro-compound penetrates well into central nervous system (CNS), and effectively reactivates brain acetylcholinesterase (AChE) in vivo inhibited by paraoxon. The two oximes were equally effective in reactivating blood AChE. However, protective effects of Pro-2-PAM were unexpectedly lower than those of PAM-2 Cl. The observation suggests that there is no correlation between brain AChE reactivating power and protective effects of Pro-2-PAM. Contrary to the present belief, it seems that Pro-2-PAM undergoes slow conversion in vivo into its active form PAM-2 Cl. The possible use of Pro-2-PAM as a model oxime for penetration into CNS requires further evaluation with regard to therapy of organophosphorus poisoning.