Congratulations to Brittany Martinez, who was awarded a Ruth L. Kirschstein F31 Diversity Award:

Brittany Martinez

Congratulations to Pharmacology Graduate Student Brittany Martinez (Bland Lab) who was awarded a Ruth L. Kirschstein Individual Predoctoral Fellowship to Promote Diversity in Health-Related Research from the National Institute of Diabetes and Digestive and Kidney Diseases.

According to the NIH, the purpose of this particular F31 program is to enhance the diversity of the health-related research workforce by supporting the research training of predoctoral students from population groups that have been shown to be underrepresented in the biomedical, behavioral, or clinical research workforce. The proposed mentored research training is expected to clearly enhance the individual’s potential to develop into a productive, independent research scientist.

Brittany will be exploring “Mechanisms underlying peripheral insulin resistance and metabolic dysfunction caused by chronic immune activation.” She is the first predoctoral student in Pharmacology to receive the F31 Diversity Fellowship Award.

(by Antoinette Reid)

 

Congratulations: 2018 Wagner Fellowship Awardees

Please join us in congratulating the 2018 Robert R. Wagner Fellowship awardees. We are thrilled that the Wagner Fellowship fund was able to support 14 BIMS students this year due to the incredible generosity of Dr. Robert Wagner and his wife, Mary.


 
Rising 3rd year students (left to right)

Erin Weddle
Robbie Cornelison
Saad Hussain
Mitch Granade
Adam Borne
Eric Wengert
Michaela Rikard

 
 
 


 
Rising 4th/5th year students (left to right)

Brooke Sauder
Olivia Sabik
Katrina McNeely
Becky Stanhope
Ben Holloway
Greg Medlock
Laura Dunphy

 

 


 

Congratulations to Alex Keller, who was awarded an American Heart Association Predoctoral Fellowship:

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Alex Keller

Alex Keller, a Pharmacology Ph.D. candidate in Brant Isakson’s laboratory has received a pre-doctoral fellowship from the American Heart Association to research “Mechanisms of ATP release from Pannexin 1 in Red Blood Cells in response to hypoxia.” Regulation of blood flow to supply oxygen at an appropriate rate to meet the metabolic demand of tissues across the body is an imperative homeostatic process. Red blood cells have been shown to release ATP in response to hypoxic conditions, resulting in arteriolar dilation in a manner that could contribute to increased perfusion of hypoxic tissues. However, the details of the ATP release mechanism from red blood cells in this context are unclear. Pannexin 1, a channel believed to be involved in this ATP release pathway, is of particular interest to the Isakson lab. By studying the activation of Pannexin 1 in this context, Alex seeks to elucidate the molecular pathway underlying ATP release from red blood cells in response to hypoxia. In addition, he plans to use modern techniques to study the broader pathway in more physiologically relevant contexts than those in which it has previously been examined. Overall, this research will improve our understanding of an important mode of blood flow regulation while simultaneously offering an opportunity to learn more about under-studied red blood cell signaling mechanisms.


 

Congratulations to Steven Keller, who was awarded an American Heart Association Predoctoral Fellowship:

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Steven Keller

A Molecular Physiology and Biological Physics graduate student co-mentored by Linda Columbus and Brant Isakson has received an American Heart Association Pre-Doctoral Fellowship. “Increasing nitric oxide (NO) via an alpha globin mimetic peptide as a treatment for sickle cell-induced pulmonary hypertension.” Endogenously produced NO is one of the most potent mechanisms to maintain blood pressure homeostasis. A recently discovered regulator of NO production in vascular endothelium is the direct interaction of endothelial nitric oxide synthase (eNOS) and the alpha chain of hemoglobin, putting a sink for NO in complex with its source. We are using a peptide mimicking the binding sequence of alpha globin to disrupt alpha globin/eNOS complex formation and increase NO availability, thus lowering blood pressure. Structural aspects of this interaction are being investigated in the context of hypertensive pathologies, especially pulmonary hypertension, a common condition in sickle cell disease that is associated with high mortality.