José Salvador Rodrigues de Oliveira

Fungal infections in marrow transplant recipients under antifungal prophylaxis with fluconazole

Fungal infection is one of the most important causes of morbidity and mortality in bone marrow transplant (BMT) recipients. The growing incidence of these infections is related to several factors including prolonged granulocytopenia, use of broad-spectrum antibiotics, conditioning regimens, and use of immunosuppression to avoid graft-versus-host disease (GvHD). In the present series, we report five cases of invasive mold infections documented among 64 BMT recipients undergoing fluconazole antifungal prophylaxis: 1) A strain of Scedosporium prolificans was isolated from a skin lesion that developed on day +72 after BMT in a chronic myeloid leukemic patient. 2) Invasive pulmonary aspergillosis (Aspergillus fumigatus) was diagnosed on day +29 in a patient with a long period of hospitalization before being transplanted for severe aplastic anemia. 3) A tumoral lung lesion due to Rhizopus arrhizus (zygomycosis) was observed in a transplanted patient who presented severe chronic GvHD. 4) A tumoral lesion due to Aspergillus spp involving the 7th, 8th and 9th right ribs and local soft tissue was diagnosed in a BMT patient on day +110. 5) A patient with a history of Ph1-positive acute lymphocytic leukemia exhibited a cerebral lesion on day +477 after receiving a BMT during an episode of severe chronic GvHD. At that time, blood and spinal fluid cultures yielded Fusarium sp. Opportunistic infections due to fungi other than Candida spp are becoming a major problem among BMT patients receiving systemic antifungal prophylaxis with fluconazole.

Requirement for PLCγ2 in IL‐3 and GM‐CSF‐stimulated MEK/ERK phosphorylation in murine and human hematopoietic stem/progenitor cells

Even though the involvement of intracellular Ca2+ (

Refractory angina cell therapy (ReACT) involving autologous bone marrow cells in patients without left ventricular dysfunction: a possible role for monocytes.

{\rm Ca}_{{\rm i}}^{{\rm 2 + }}

Impact of Highly Active Antiretroviral Therapy in the Treatment of HIV–Infected Patients with Systemic Non-Hodgkin‘s Lymphoma

) in hematopoiesis has been previously demonstrated, the relationship between

Diagnosis by real-time polymerase chain reaction of pathogens and antimicrobial resistance genes in bone marrow transplant patients with bloodstream infections

{\rm Ca}_{{\rm i}}^{{\rm 2 + }}

Fludarabine induces apoptosis in chronic lymphocytic leukemia - the role of P53, Bcl-2, Bax, Mcl-1, and Bag-1 proteins

signaling and cytokine‐induced intracellular pathways remains poorly understood. Herein, the molecular mechanisms integrating Ca2+ signaling with the extracellular signal‐regulated kinase 1/2 (ERK1/2) pathway in primary murine and human hematopoietic stem/progenitor cells stimulated by IL‐3 and GM‐CSF were studied. Our results demonstrated that IL‐3 and GM‐CSF stimulation induced increased inositol 1,4,5‐trisphosphate (IP3) levels and

Human leucocyte antigen and human T-cell lymphotropic virus type 1 associated diseases in Brazil

{\rm Ca}_{{\rm i}}^{{\rm 2 + }}

2-Chloro-deoxyadenosine Induces Durable Complete Remission in Castleman's Disease but may Accelerate its Transformation to Non-Hodgkin's Lymphoma

release in murine and human hematopoietic stem/progenitor cells. In addition,

Plasma levels of FL and SDF-1 and expression of FLT-3 and CXCR4 on CD34+ cells assessed pre and post hematopoietic stem cell mobilization in patients with hematologic malignancies and in healthy donors

{\rm Ca}_{{\rm i}}^{{\rm 2 + }}

N-RAS and K-RAS gene mutations in Brazilian patients with multiple myeloma.

signaling inhibitors, such as inositol 1,4,5‐trisphosphate receptor antagonist (2‐APB), PKC inhibitor (GF109203), and CaMKII inhibitor (KN‐62), blocked phosphorylation of MEK activated by IL‐3 and GM‐CSF, suggesting the participation of Ca2+‐dependent kinases in MEK activation. In addition, we identify phospholipase Cγ2 (PLCγ2) as a PLCγ responsible for the induction of Ca2+ release by IL‐3 and GM‐CSF in hematopoietic stem/progenitor cells. Furthermore, the PLCγ inhibitor U73122 significantly reduced the numbers of granulocyte‐macrophage colony‐forming units after cytokine stimulation. Similar results were obtained in both murine and human hematopoietic stem/progenitor cells. Taken together, these data indicate a role for PLCγ2 and Ca2+ signaling through the modulation of MEK in both murine and human hematopoietic stem/progenitor cells. J. Cell. Physiol. 226: 1780–1792, 2011.