Management of paroxysmal nocturnal hemoglobinuria in CALR mutated post-essential thrombocythemia myelofibrosis: A case report.

Paroxysmal nocturnal hemoglobinuria (PNH) results from the loss of erythrocyte surface proteins, leading to complement activation and its spectrum of effects. We explore this case of a 57-year-old man with post-essential thrombocythemia (ET) myelofibrosis (MF) who developed symptomatic anemia with evidence of hemolysis on lab work. While hemolysis was localized to be intramedullary based on workup, the exact diagnosis was undetermined, leading to a prolonged course of steroid therapy to control anemia.

De novo acute myeloid leukemia with 20-29% blasts is less aggressive than acute myeloid leukemia with ≥30% blasts in older adults: a Bone Marrow Pathology Group study.

It is controversial whether acute myeloid leukemia (AML) patients with 20-29% bone marrow (BM) blasts, formerly referred to as refractory anemia with excess blasts in transformation (RAEBT), should be considered AML or myelodysplastic syndrome (MDS) for the purposes of treatment and prognostication. We retrospectively studied 571 de novo AML in patients aged >50 years, including 142 RAEBT and 429 with ≥30% blasts (AML30), as well as 151 patients with 10-19% BM blasts (RAEB2). RAEBT patients were older and had lower white blood count, but higher hemoglobin, platelet count, and karyotype risk scores compared to AML30, while these features were similar to RAEB2.

Molecular genetic characterization of lymphoma: application to cytology diagnosis.

Mature B- and T-cell lymphomas are increasingly being associated with specific genetic alterations; characterization of these changes can sometimes be crucial to both diagnosis and prognosis. Molecular testing encompasses fluorescence in situ hybridization (FISH) and polymerase chain reaction (PCR)-based assays, as well as classical cytogenetics. FISH and PCR-based assays can be performed on cytology material without the need for advanced planning for testing with fresh tissue.

Primary and secondary drug screening assays for Friedreich ataxia.

Friedreich ataxia (FRDA) is an autosomal recessive neuro- and cardiodegenerative disorder for which there are no proven effective treatments. FRDA is caused by decreased expression and/or function of the protein frataxin. Frataxin chaperones iron in the mitochondrial matrix for the assembly of iron-sulfur clusters (ISCs), which are prosthetic groups critical for the function of the Krebs cycle and the mitochondrial electron transport chain (ETC).

Comparison of air-fluidized therapy with other support surfaces used to treat pressure ulcers in nursing home residents.

To provide empirical evidence comparing pressure ulcer healing rates between different support surfaces, data were analyzed from eligible residents with pressure ulcers (N = 664) enrolled in the National Pressure Ulcer Long-Term Care Study, a retrospective pressure ulcer prevention and treatment study. Support surfaces were categorized as: Group 1 (static overlays and replacement mattresses), Group 2 (low-air-loss beds, alternating pressure, and powered/non-powered overlays/mattresses), and Group 3 (air-fluidized beds). Calculation of healing rates, using the largest ulcer from each resident, found mean healing rates greatest for air-fluidized therapy (Group 3) (mean = 5.