Recipients of the Bill Halpern Travel Award


Yanna Tian, Augusta University

My research has been focused on mechanisms of impaired flow induced dilation of resistance arteries in aging. Aging is considered an independent risk factor for cardiovascular diseases and associated with functional and structural changes in arteries that closely resemble vascular alterations. Dysfunction of vascular endothelial cells is one of the key mechanisms in all types of vascular complications, including aging-related phenotypic changes. The vascular endothelium is uniquely posed to sense temporal changes in blood flow and wall shear stress (WSS). It is established that changes in WSS can also affect vascular growth and morphology.

Notably, WSS sensing machinery plays a critical role in the initiation of the synthesis of endothelial mediators. The impact of aging on the endothelial WSS mechanosensing process remains elusive. Here we raise the possibility that aging-related endothelial dysfunction and the consequent abnormal vascular remodeling can be attributable to a failure of proper WSS mechanosensing by the vascular endothelial cells.

Our results demonstrate a novel role for a disintegrin and metalloproteinase 17 (ADAM17) in junctional adhesion molecule-A/F11 receptor (JAM-A/F11R) cleavage-dependent regulation of flow/WSS mechanosensing and highlight the importance of ADAM17 activation in aging-related impaired mechanosensing, which can contribute to impaired arterial dilation in aging.

The illumination of the mechanisms may provide insight into the pleiotropic effects of various cardiovascular medications or offer new therapeutic approaches using drugs that target specific signaling pathways in aging.



Mansoureh Barzegar, LSU Health Sciences Center-Shreveport

My research over the past 3 years has been in the area of neurology with a focus on

“mechanistic bases of stem cell protection in ischemic stroke”. The nature of ‘stroke’ injury is very complex with only few effective treatments available for treating this condition. Moreover, targeting only a single molecular pathway, or giving one immunosuppressing or anti-cell binding treatment in the general blood circulation is non-specific and unlikely to achieve strong protection.

Undoubtedly, stem cells are an attractive candidate for stroke treatment, since they have the potential to target multiple mechanisms and cell types and work selectively at the site of injury rather than everywhere. Among all available stem cell lineages, human placenta-derived mesenchymal stem cells (hPMSCs) appear to have many advantages, particularly their lack of immunogenicity (rejection), super-high abundance, super-low cost, ease of acquisition and lack of legal and ethical problems as well as non-tumorigenic properties.

We found that beneficial effects of hPMSCs in stroke might reflect suppression of post I/R immune, inflammatory and BBB disturbances which limit the onset and progression of stroke injury following restoration of blood flow.

We hope that better understanding of cellular interactions, subsequent mechanisms and the most potential hPMSCs -derived mediator will provide important information to enable us to identify new targets and deliver novel therapeutic strategy for stroke in future.