Results 171 to 180 of about 1,912,173 (262)

Dental Care Needs and Treatment Priorities in a Homeless Population in Rome: An Observational Study. [PDF]

open access: yesDent J (Basel)
Lione R   +7 more
europepmc   +1 more source

A minimal cellulosome‐like system in Cellulosilyticum lentocellum

open access: yesFEBS Open Bio, EarlyView.
Cellulose‐degrading bacteria typically use cellulosomes, large multi‐enzyme complexes on a scaffold protein. In Cellulosilyticum lentocellum, we characterise a far smaller arrangement, a single scaffold bound to one cellulase through a single cohesin‐dockerin interaction.
John Allan   +2 more
wiley   +1 more source

BCG vaccination potentiates oxidative phosphorylation in neonatal myeloid‐derived suppressor cells

open access: yesFEBS Open Bio, EarlyView.
BCG vaccination enhances oxidative phosphorylation in neonatal MDSCs, impairing their immunosuppressive function. It upregulates electron transport chain genes and mitochondrial activity, increasing ATP and oxygen consumption. Pharmacological OXPHOS inhibition partially restores suppressive capacity, confirming causality.
Yingying Chen, Hui Li
wiley   +1 more source

Non-linear relationships between inflammatory indices and erectile dysfunction in a group of young men living with HIV. [PDF]

open access: yesBasic Clin Androl
Tiecco G   +11 more
europepmc   +1 more source

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

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