Antimicrobial activity of cobalt bis(dicarbollide) aminoderivatives

We carried out experiments focused on the determination of the antimicrobial acitivity of selected representatives of cobalt bis{dicarbollide) aminoderivates. lt was proved, that studied yeast strain C. parapsilosis DBM 2165 is not sensitive to the cobalt bis{dicarbollide) or its aminoderivatives. Gram-negative bacteria P. aeruginosa B-59188 is weakly susceptive to cobalt bis(dicarbollide), but no significant inhibition of growth by cobalt bis(dicarbollide) aminoderivatives was observed. The highest effect on inhibition of microbial growth was confirmed in the case of gram-positive bacteria 5. aureus. This observation demonstrates the real possibility of using these substances in the treatment of infection caused by gram-positive bacterial strains

Czech National Guillain-Barré Syndrome Registry

Úvod: Guillainův-Barrého syndrom je akutní zánětlivá autoimunitní polyradikuloneuropatie patřící mezi vzácnější neurologická onemocnění, nicméně po téměř úplné eradikaci poliomyelitidy je celosvětově nejčastější příčinou akutně vzniklé chabé paralýzy. Registr funguje od roku 2012 a poskytuje prospektivně zaznamenávaná data. Cíl: Cílem registru je sledování klinického profi lu, léčby a šestiměsíční prognózy nemocných s Guil lainovým-Bar rého syndromem. Metodika: Data zadávají osoby pověřené neuromuskulárními centry. Klinický průběh je hodnocen na základě GBS disability scale a svalové síly pro obličejové svalstvo a svalstvo končetin. Vyšetření je provedeno při přijetí pa cienta k hospitalizaci, před léčbou, ihned po léčbě, za 1 měsíc a za 6 měsíců od ukončení léčby. Výsledky: V registru bylo aznamenáno celkem 272 případů, u 137 z nich jsou k dispozici kompletní data za 6 měsíců. Z těchto 137 pa cientů bylo 52 léčeno intravenózním lidským imunoglobulinem a 85 výměn nou plazmaferézou. Dobrého výsledného klinického stavu po 6 měsících dosáhlo celkem 85 % pa cientů. Reziduální těžký neurologický defi cit přetrvával po 6 měsících u 11 % pa cientů. Šest pa cientů zemřelo. Nezaznamenali jsme rozdíl v účinnosti imunoglobulinu a plazmaferézy v celém souboru, v podskupině nejtěžších pa cientů či ve vztahu k pohlaví. Závěr: Centralizace péče a dodržování standardů péče vedou k dobré prognóze nemocných s Guil lainovým-Bar rého syndromem srovnatelné s relevantními zdroji.Introduction: The Guillain-Barré syndrome is an acute infl ammatory autoimmune polyradiculoneuropathy and belongs among rare neurologic diseases. Since poliomyelitis has been almost completely eliminated, it is currently the most frequent cause of acute fl accid paralysis worldwide. The registry was formed in the Czech Republic in 2012 and is an important source of prospectively recorded data. Aim: The goal of the registry is to follow up the clinical profi le, treatment and 6-month prognosis of Guillain-Barré syndrome patients. Methods: The data are collected prospectively by persons delegated by neuromuscular centres in the Czech Republic. The clinical course is assessed on the basis of the GBS disability scale and muscle strength according to the Medical Research Council sum score for facial muscles and extremity muscles. Detailed clinical investigation is done on admission, before the treatment, immediately after the treatment, 1 month and 6 months after the end of the treatment. Results: We enrolled a total 272 cases of Guillain-Barré syndrome patients in the period from 1st January 2012 to 17th August 2016. We have complete data for 6 months in 137 of them. 52 were treated with intravenous human immunoglobulin and 85 with plasma exchange. A good clinical outcome after 6 months (ability to walk unassisted) was achieved in 85% of patients. Severe residual neurological defi cit persisted after 6 months in 11% of patients. The remaining 6 patients died. We did not fi nd any diff erence in the effi ciency of immunoglobulin vs. plasma exchange in the whole group, in the subgroup of the severely disabled patients and according to sex. Conclusion: Medical care centralisation and adherence to the standard of care lead to a good clinical outcome in Guillain-Barré syndrome patients, which is comparable with relevant sources

Iron is not involved in oxidative stress-mediated cytotoxicity of doxorubicin and bleomycin

Background and purpose:The anticancer drugs doxorubicin and bleomycin are well-known for their oxidative stress-mediated side effects in heart and lung, respectively. It is frequently suggested that iron is involved in doxorubicin and bleomycin toxicity. We set out to elucidate whether iron chelation prevents the oxidative stress-mediated toxicity of doxorubicin and bleomycin and whether it affects their antiproliferative/proapoptotic effects.Experimental approach:Cell culture experiments were performed in A549 cells. Formation of hydroxyl radicals was measured in vitro by electron paramagnetic resonance (EPR). We investigated interactions between five iron chelators and the oxidative stress-inducing agents (doxorubicin, bleomycin and H(2)O(2)) by quantifying oxidative stress and cellular damage as TBARS formation, glutathione (GSH) consumption and lactic dehydrogenase (LDH) leakage. The antitumour/proapoptotic effects of doxorubicin and bleomycin were assessed by cell proliferation and caspase-3 activity assay.Key results:All the tested chelators, except for monohydroxyethylrutoside (monoHER), prevented hydroxyl radical formation induced by H(2)O(2)/Fe(2+) in EPR studies. However, only salicylaldehyde isonicotinoyl hydrazone and deferoxamine protected intact A549 cells against H(2)O(2)/Fe(2+). Conversely, the chelators that decreased doxorubicin and bleomycin-induced oxidative stress and cellular damage (dexrazoxane, monoHER) were not able to protect against H(2)O(2)/Fe(2+).Conclusions and implications:We have shown that the ability to chelate iron as such is not the sole determinant of a compound protecting against doxorubicin or bleomycin-induced cytotoxicity. Our data challenge the putative role of iron and hydroxyl radicals in the oxidative stress-mediated cytotoxicity of doxorubicin and bleomycin and have implications for the development of new compounds to protects against this toxicity.British Journal of Pharmacology advance online publication, 9 October 2006; doi:10.1038/sj.bjp.0706930