Region-specific delamination strength of ascending thoracic aortic aneurysm of elderly hypertensive patients with bicuspid and tricuspid aortic valves.

Both ageing and hypertension are clinical factors that may lead to a higher propensity for dissection or rupture of ascending thoracic aortic aneurysms (ATAAs). This study sought to investigate effect of valve morphology on regional delamination strength of ATAAs in the elderly hypertensive patients. Whole fresh ATAA samples were harvested from 23 hypertensive patients (age, 71 ± 8 years) who underwent elective aortic surgery.

Effect of hypertension on the delamination and tensile strength of ascending thoracic aortic aneurysm with a focus on right lateral region.

Hypertension is a major predisposing factor to initiate thoracic aortopathy. The objective of this study is to investigate effect of hypertension on delamination and tensile strength of ascending thoracic aortic aneurysms (ATAAs). A total of 35 fresh ATAA samples were harvested from 19 hypertensive and 16 non-hypertensive patients during elective aortic surgery.

Hybrid aortic arch procedure in acute type A aortic dissection with right carotid artery occlusion.

Acute type A aortic dissection complicated by carotid artery is associated with a high risk of perioperative stroke. We reported a case of application of hybrid aortic arch debranching procedure in acute type A aortic dissection complicated by right carotid artery occlusion, which resulted in no neurological complications after operation and patent carotid artery after discharging.

Nanoscale MOFs in nanomedicine applications: from drug delivery to therapeutic agents.

Metal-organic frameworks (MOFs) hold great promise for widespread applications in biomedicine and nanomedicine. MOFs are one of the most fascinating nanocarriers for drug delivery, benefiting from their high porosity and facile modification. Furthermore, the tailored components of MOFs can be therapeutic agents for various treatments, including drugs as organic ligands of MOFs, active metal as central metal ions of MOFs, and their combinations as carrier-free MOF-based nanodrug.

Hybrid repair of aberrant right subclavian artery with aortic dissection caused by Kommerell diverticulum.

Background: Aberrant right subclavian artery (ARSA) with associated Kommerell diverticulum (KD) is a rare congenital aortic disease. KD patients have a high risk of rupture, dissection, and compression of adjacent structures. Although several treatment options have been proposed (traditional surgery, hybrid operation, and endovascular intervention), a consensus regarding optimal surgical management has not yet been established.

Long noncoding RNAs in regulation of human breast cancer.

Less than 2% of the human genome DNA is composed of protein-coding genes, although the majority of the human genome is transcribed, indicating the transcripts mostly are noncoding RNAs. Those noncoding RNAs with length between 200 nt and 200 kb are categorized as long noncoding RNA (lncRNA). Around 30 000 lncRNAs have been predicted or identified, although little is known regarding the regulatory function for a vast majority of these sequences.

Effects of incremental beta-blocker dosing on myocardial mechanics of the human left ventricle: MRI 3D-tagging insight into pharmacodynamics supports theory of inner antagonism.

Beta-blockers contribute to treatment of heart failure. Their mechanism of action, however, is incompletely understood. Gradients in beta-blocker sensitivity of helically aligned cardiomyocytes compared with counteracting transversely intruding cardiomyocytes seem crucial.

miR-17/20 sensitization of breast cancer cells to chemotherapy-induced apoptosis requires Akt1.

The serine threonine kinase Akt1 has been implicated in the control of cellular metabolism, survival and growth. Herein, disruption of the ubiquitously expressed member of the Akt family of genes, Akt1, in the mouse, demonstrates a requirement for Akt1 in miRNA-mediated cellular apoptosis. The miR-17/20 cluster is known to inhibit breast cancer cellular proliferation through G1/S cell cycle arrest via binding to the cyclin D1 3'UTR.