Living with Chronic Kidney Disease and Type 2 Diabetes Mellitus: The Patient and Clinician Perspective.

Comorbid type 2 diabetes mellitus (T2D) and chronic kidney disease (CKD) is associated with poor health outcomes and a high economic burden. Management of these conditions remains a significant challenge for current healthcare systems. The objective of this article is to describe the experiences of patients living with T2D and CKD and their thoughts on how communication between patients and their clinicians could be improved despite the multiple comorbidities that need to be addressed.

The potential role of DNA methylation in abdominal aortic aneurysms.

Abdominal aortic aneurysm (AAA) is a complex disorder that has a significant impact on the aging population. While both genetic and environmental risk factors have been implicated in AAA formation, the precise genetic markers involved and the factors influencing their expression remain an area of ongoing investigation. DNA methylation has been previously used to study gene silencing in other inflammatory disorders and since AAA has an extensive inflammatory component, we sought to examine the genome-wide DNA methylation profiles in mononuclear blood cells of AAA cases and matched non-AAA controls.

MicroRNA expression signature in human abdominal aortic aneurysms.

Background: Abdominal aortic aneurysm (AAA) is a dilatation of the aorta affecting most frequently elderly men. Histologically AAAs are characterized by inflammation, vascular smooth muscle cell apoptosis, and extracellular matrix degradation. The mechanisms of AAA formation, progression, and rupture are currently poorly understood.

Endothelin stimulates sis-inducing factor-like DNA binding activity in CHO-K1 cells expressing ETA receptors.

ET-1, a member of the family of peptides known as endothelins, binds to a G-protein-coupled receptor, ET(A), and stimulates a variety of cellular responses, including contraction, growth, and mitogenesis. ET-1 stimulation of a chinese hamster ovary cell line stably transfected with the ET(A) receptor (CHO/ET(A)) induced formation of SIF (sis-inducing factor), a key component of the STAT (Signal Transducers and Activators of Transcription) pathway, in a concentration-dependent manner. SIF induction was blocked by a specific inhibitor of ET(A), BQ610, and by genistein, a tyrosine kinase inhibitor.