Rapamycin Reduces Arterial Mineral Density and Promotes Beneficial Vascular Remodeling in a Murine Model of Severe Medial Arterial Calcification.

Peripheral artery disease (PAD) is the narrowing of the arteries that carry blood to the lower extremities. PAD has been traditionally associated with atherosclerosis. However, recent studies have found that medial arterial calcification (MAC) is the primary cause of chronic limb ischemia below the knee.

Intimate partner violence and its correlates in middle-aged and older adults during the COVID-19 pandemic: A multi-country secondary analysis.

Intimate partner violence (IPV) may have been exacerbated during the COVID-19 pandemic. Middle-aged and older adults, ages 45 years or older, are at higher risk of COVID-19 mortality and social isolation. However, most studies on IPV during the pandemic do not focus on this important subpopulation.

Ecto-5'-nucleotidase (Nt5e/CD73)-mediated adenosine signaling attenuates TGFβ-2 induced elastin and cellular contraction.

Arterial calcification due to deficiency of CD73 (ACDC) is a rare genetic disease caused by a loss-of-function mutation in the gene encoding the ecto-5'-nucleotidase (cluster of differentiation 73, CD73) enzyme. Patients with ACDC develop vessel arteriomegaly, tortuosity, and vascular calcification in their lower extremity arteries. Histological analysis shows that patients with ACDC vessels exhibit fragmented elastin fibers similar to that seen in aneurysmal-like pathologies.

Isolation of Human Primary Valve Cells for In vitro Disease Modeling.

Calcific aortic valve disease (CAVD) is present in nearly a third of the elderly population. Thickening, stiffening, and calcification of the aortic valve causes aortic stenosis and contributes to heart failure and stroke. Disease pathogenesis is multifactorial, and stresses such as inflammation, extracellular matrix remodeling, turbulent flow, and mechanical stress and strain contribute to the osteogenic differentiation of valve endothelial and valve interstitial cells.

Dysregulation of FOXO1 (Forkhead Box O1 Protein) Drives Calcification in Arterial Calcification due to Deficiency of CD73 and Is Present in Peripheral Artery Disease.

Objective: The recessive disease arterial calcification due to deficiency of CD73 (ACDC) presents with extensive nonatherosclerotic medial layer calcification in lower extremity arteries. Lack of CD73 induces a concomitant increase in TNAP (tissue nonspecific alkaline phosphatase; ), a key enzyme in ectopic mineralization. Our aim was to investigate how loss of CD73 activity leads to increased expression and calcification in CD73-deficient patients and assess whether this mechanism may apply to peripheral artery disease calcification.

Features of Urrets-Zavalia syndrome after descemet stripping automated endothelial keratoplasty.

Purpose: To report a case series of pupil abnormalities consistent with features of Urrets-Zavalia syndrome (UZS) after Descemet stripping automated endothelial keratoplasty (DSAEK) for corneal edema secondary to corneal endothelial cell dysfunction.

Methods: Retrospective chart analysis of subjects who developed UZS after DSAEK at the University of Texas Southwestern Medical Center.

Results: We present a series of 7 eyes with features consistent with UZS, after undergoing DSAEK.

Laser in situ keratomileusis for residual refractive errors after apodized diffractive multifocal intraocular lens implantation.

Purpose: To evaluate the visual and refractive outcomes of laser in situ keratomileusis (LASIK) to correct residual refractive error after apodized diffractive multifocal intraocular lens (IOL) implantation.

Setting: University of Texas Southwestern Medical Center, Dallas, Texas, USA.

Methods: This retrospective study reviewed eyes of consecutive patients who had LASIK using the IntraLase FS60 femtosecond laser and Visx Star S4 excimer laser to correct residual refractive error after AcrySof ReSTOR IOL implantation.

Targeted inhibition of p57 and p15 blocks transforming growth factor beta-inhibited proliferation of primary cultured human limbal epithelial cells.

Purpose: To evaluate the role of cyclin-dependent kinase inhibitors p57 and p15 in transforming growth factor (TGF)-beta1 or TGF-beta2 inhibited proliferation of primary cultured human limbal epithelial cells using short interfering RNA (siRNA).

Methods: Primary cultured human limbal epithelial cells were treated with TGF-beta1 or TGF-beta2 for 6 and 24 h, and total RNA extracted for RT-PCR and real-time PCR using primers for p21, p27, and p57 (CipP/Kip family) and p15 and p19 (INK4 family). Proteins were extracted for western blot analysis of p57 and p15.

Structure of the Cul1-Rbx1-Skp1-F boxSkp2 SCF ubiquitin ligase complex.

SCF complexes are the largest family of E3 ubiquitin-protein ligases and mediate the ubiquitination of diverse regulatory and signalling proteins. Here we present the crystal structure of the Cul1-Rbx1-Skp1-F boxSkp2 SCF complex, which shows that Cul1 is an elongated protein that consists of a long stalk and a globular domain. The globular domain binds the RING finger protein Rbx1 through an intermolecular beta-sheet, forming a two-subunit catalytic core that recruits the ubiquitin-conjugating enzyme.