Reprint of: The impact of alpha-1-adrenergic receptor antagonists on the progression of Parkinson disease.

Background: Alpha-1-adrenergic receptor antagonists (AARAs) are used in the treatment of benign prostatic hypertrophy. Some AARAs, such as terazosin, stimulate glycolysis and increase cellular adenosine triphosphate levels through activation of phosphoglycerate kinase 1 (PGK1), which has been suggested to be of therapeutic benefit in patients with Parkinson disease (PD).

Objective: This study aimed to determine whether exposure to PGK1-activating AARAs was associated with slower PD progression.

The impact of alpha-1-adrenergic receptor antagonists on the progression of Parkinson disease.

Background: Alpha-1-adrenergic receptor antagonists (AARAs) are used in the treatment of benign prostatic hypertrophy. Some AARAs, such as terazosin, stimulate glycolysis and increase cellular adenosine triphosphate levels through activation of phosphoglycerate kinase 1 (PGK1), which has been suggested to be of therapeutic benefit in patients with Parkinson disease (PD).

Objective: This study aimed to determine whether exposure to PGK1-activating AARAs was associated with slower PD progression.

Co-stimulation of the fc receptor and interleukin-12 receptor on human natural killer cells leads to increased expression of cd25.

Natural killer (NK) cells serve a critical role in the immune response against microbes and developing tumors. We have demonstrated that NK cells produce stimulatory cytokines (e.g.

MICA-Expressing Monocytes Enhance Natural Killer Cell Fc Receptor-Mediated Antitumor Functions.

Natural killer (NK) cells are large granular lymphocytes that promote the antitumor response via communication with other cell types in the tumor microenvironment. Previously, we have shown that NK cells secrete a profile of immune stimulatory factors (e.g.

Activation of the chromosome 19q microRNA cluster in sporadic and androgenetic-biparental mosaicism-associated hepatic mesenchymal hamartoma.

Recurrent genetic alterations found in hepatic mesenchymal hamartoma include either androgenetic-biparental mosaicism or chromosomal rearrangements involving chromosome 19q13.4, in the vicinity of the chromosome 19q microRNA cluster (C19MC). Abnormal activation of C19MC, which is subject to paternal imprinting and is normally expressed only in placenta, could account for both genetic associations because androgenetic cells carry only paternal chromosomes.