As a result of progress in the modern treatment of burns, systemic candidosis (CA), in the sense of "surviving mycoses", has become increasingly frequent. The site of entry is not usually the wound, but the intestinal tract, which becomes overgrown by the yeasts as a consequence of the requisite therapy with antibacterial antibiotics in high dosage. Passage of the organism into the circulation occurs by persorption. In view of the bad prognosis of systemic CA, it is essential to recognize its incipient development and counteract by timely prophylactic measures, primarily sterilization of the intestine. In a developed case os systemic CA, the chances of cure improve with rapidity of recognition of the infection and initiation of treatment. Early diagnosis of the infection is achieved by the regular quantitative determination of the organism in the faeces, in urine and blood, as well as in swabs of mucous membranes and the wounds and, above all, by serological examination (movement of titre). The practical problems of the disease are demonstrated and discussed on the basis of 2 cases treated in this department.
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is a growing health concern as the leading causal agent of systemic candidiasis, a life-threatening fungal infection with a mortality rate of ∼40% despite best available therapy. Yck2, a fungal casein kinase 1 (CK1) family member, is the cellular target of inhibitors YK-I-02 (YK) and MN-I-157 (MN). Here, multiplexed inhibitor beads paired with mass spectrometry (MIB/MS) employing ATP-competitive kinase inhibitors were used to define the selectivity of these Yck2 inhibitors across the global proteome.
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M.M. Shemyakin and Yu.A. Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia.
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Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Wuhan University, Wuhan, China.
is an opportunistic human fungal pathogen that causes superficial mucosal and life-threatening bloodstream infections in immunocompromised individuals. Remodeling in cell wall components has been extensively exploited by fungal pathogens to adapt to host-derived stresses, as well as immune evasion. How this process contributes to pathogenicity is less understood.
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