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candidiasis invasive/phosphatase

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СтатииКлинични изследванияПатенти
5 резултата

Protection from systemic Candida albicans infection by inactivation of the Sts phosphatases.

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Вход / Регистрация
The human fungal pathogen Candida albicans causes invasive candidiasis, characterized by fatal organ failure due to disseminated fungal growth and inflammatory damage. The suppressor of TCR signaling 1 (Sts-1) and Sts-2 are two homologous phosphatases that negatively regulate signaling pathways in a

Ppg1, a PP2A-type protein phosphatase, controls filament extension and virulence in Candida albicans.

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Candida albicans, a major human fungal pathogen, is the primary cause of invasive candidiasis in a wide array of immunocompromised patients. C. albicans virulence requires the ability to undergo a reversible morphological transition from yeast to filaments in response to a variety of host

A Multicenter, double-blind trial of a high-dose caspofungin treatment regimen versus a standard caspofungin treatment regimen for adult patients with invasive candidiasis.

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BACKGROUND The standard caspofungin treatment regimen (50 mg/day after a 70-mg dose on day 1) is effective and well tolerated for the treatment of invasive candidiasis, but experience with higher doses of caspofungin is limited. We evaluated the safety and efficacy of caspofungin at 3 times the

Fluconazole prophylaxis in extremely low birth weight infants: association with cholestasis.

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BACKGROUND Extremely low birth weight (ELBW) infants are at increased risk for invasive candidiasis and associated morbidity and mortality. The use of fluconazole prophylaxis in this population has raised a benefit versus risk concern among clinicians. OBJECTIVE To evaluate the effectiveness and

Overview of safety experience with caspofungin in clinical trials conducted over the first 15 years: a brief report.

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Safety experience is available from 32 completed clinical studies (17 Phase I and 15 Phase II-III) of caspofungin (CAS) conducted between 1995 and 2010 in adult and paediatric patients. Clinical and laboratory adverse events (AEs) were collected from all enrolled subjects and patients. Investigators
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