Allergol Int 2010, 59:161–166.PubMedCrossRef Competing interests The authors declare no competing interests concerning this work. Authors’ contributions SKu and SKa conceived and designed the experiments. SKu and TO performed animal experiments. SKu and HY performed real time PCR procedures. SKu, SKa and HT analyzed the data. TO, HY and KA contributed reagents/materials/analysis tools. All authors
read and approved the final manuscript.”
“Erratum to: Int J Clin Oncol (2010) DOI 10.1007/s10147-010-0111-4 During the editorial production process, an error was inadvertently created LY2606368 order in the title of this article. The correct version is “Successful long-term remission following repeated salvage surgery in a patient with chemotherapy-resistant metastatic non-seminomatous germ cell tumor: an additional report to Int J Clin Oncol 2007; 12:485–487”. The publisher sincerely apologizes for the error.”
“Background The ubiquitous saprophytic mould Aspergillus fumigatus is known to cause a spectrum of diseases in humans, including allergic syndromes, noninvasive infections, and invasive aspergillosis, a condition associated with significant morbidity and mortality [1]. A. fumigatus is one of the human pathogenic fungi that have a natural habitat in the environment, including soil and plants
[2]. Some members of the azole drug class, which includes voriconazole (VRC) and posaconazole (POS), have been shown to be effective in the treatment of invasive aspergillosis [3], and for a long time, azole resistance among clinical A. fumigatus isolates was considered to be an uncommon Cyclin-dependent kinase 3 finding. Seliciclib However, multiazole resistance is emerging and is increasingly recognized as a
cause of treatment failure [4, 5]. In agriculture, thousands of tons of azoles are sold annually for the purpose of plant protection, either to prevent or to control fungal growth that can cause extensive loss of crops or to ease the problem of postharvest spoilage of plants and fruits [6]. The mechanism of action of all azoles – irrespectively of their chemical structure and variable biological properties – is based on its interference with the activity of fungal lanosterol 14 alpha-demethylase, an enzyme encoded by Cyp51A gene in A. fumigatus that is responsible for the transformation of lanosterol in ergosterol, an essential component of the fungal cytoplasmatic membrane. The inhibition of ergosterol formation results in cell membrane disorganization and impairment of fungal growth. Therefore, azoles are considered fungistatic rather than fungicidal, and it is well known that a strong and persistent antimicrobial pressure can lead to the selection of resistant clones, particularly if the drug effect is static rather than microbicidal [7]. Since azoles are the mainstay treatment for both human and agricultural fungal diseases, a major concern is the predictable emergence of cross-resistance to clinical A.