Fusariosis in a Patient with Acute Myeloid Leukemia: A Case Report and Review of the Literature

Fusarium spp. causes infections mostly in patients with prolonged neutropenia. We describe the case of a disseminated Fusariumsolani infection in a patient with acute myeloid leukemia which never reached complete remission during its clinical course. The patient had profound neutropenia and developed skin nodules and pneumonia in spite of posaconazole prophylaxis. F. solani was isolated from blood and skin biopsy, being identified from its morphology and by molecular methods. By broth dilution method, the strain was resistant to azoles, including voriconazole and posaconazole, and to echinocandins. MIC to amphotericin B was 4 mg/L. The patient initially seemed to benefit from therapy with voriconazole and amphotericin B, but, neutropenia perduring, his clinical condition deteriorated with fatal outcome. All efforts should be made to determine the correct diagnosis as soon as possible in a neutropenic patient and to treat this infection in a timely way, assuming pathogen susceptibility while tests of antimicrobial susceptibility are pending. A review of the most recent literature on invasive fungal infections is reported

Clinical and epidemiological aspects of sporotrichosis: an overview of the cases reported in Europe and in Italy

Sporotrichosis is a fungal infection occurring worldwide, especially in tropical and sub-tropical areas. We present a brief review of clinical and epidemiological aspects of sporotrichosis, as well as its treatment. Sporotrichosis is rarely reported in Europe and the European Centre of Disease Control does not track its infection rate. To fill this gap, we report a survey of clinical cases described over the past forty years in Europe and in Italy

Genome-wide screening in pluripotent cells identifies Mtf1 as a suppressor of mutant huntingtin toxicity

Huntington's disease (HD) is a neurodegenerative disorder caused by CAG-repeat expansions in the huntingtin (HTT) gene. The resulting mutant HTT (mHTT) protein induces toxicity and cell death via multiple mechanisms and no effective therapy is available. Here, we employ a genome-wide screening in pluripotent mouse embryonic stem cells (ESCs) to identify suppressors of mHTT toxicity. Among the identified suppressors, linked to HD-associated processes, we focus on Metal response element binding transcription factor 1 (Mtf1). Forced expression of Mtf1 counteracts cell death and oxidative stress caused by mHTT in mouse ESCs and in human neuronal precursor cells. In zebrafish, Mtf1 reduces malformations and apoptosis induced by mHTT. In R6/2 mice, Mtf1 ablates motor defects and reduces mHTT aggregates and oxidative stress. Our screening strategy enables a quick in vitro identification of promising suppressor genes and their validation in vivo, and it can be applied to other monogenic diseases

Measurement of the ttˉZt\bar{t}Z and ttˉWt\bar{t}W production cross sections in multilepton final states using 3.2 fb−1^{-1} of pppp collisions at s\sqrt{s} =13 TeV with the ATLAS detector

A measurement of the $t\bar{t}Z$ and $t\bar{t}W$ production cross sections in final states with either two same-charge muons, or three or four leptons (electrons or muons) is presented. The analysis uses a data sample of proton-proton collisions at $\sqrt{s} = 13$ TeV recorded with the ATLAS detector at the Large Hadron Collider in 2015, corresponding to a total integrated luminosity of 3.2 fb$^{-1}$, The inclusive cross sections are extracted using likelihood fits to signal and control regions, resulting in $\sigma_{t\bar{t}Z} = 0.9 \pm 0.3$ pb and $\sigma_{t\bar{t}W} = 1.5 \pm 0.8$ pb, in agreement with the Standard Model predictions