A postdoctoral fellow position is available in the laboratory of Dr. Qing Yang in the Department of Neuroscience, Cell Biology and Anatomy at the University of Texas Medical Branch at Galveston. The successful candidate in collaboration with the mentor and her team will be responsible for designing and utilizing in vitro and in vivo methodologies, especial electrophysiology to investigate the pathophysiology of chemotherapy-induced peripheral neuropathy (CIPN) with an emphasis on identifying the role of specific molecules and pathways that regulate neuroprotective effect in the CIPN. Applicants should have a Ph.D. degree in biological sciences preferably with a strong neuroscience/pharmacology background. The position requires a minimum of 4-5 years of graduate research experience and a strong publication record. The candidate must be highly motivated and have extensive experience in electrophysiology, molecular biology, animal (mice or rat) handling, experimental planning, and data interpretation. Excellent communication skills and the ability to work as a team member are essential. The position requires the ability to lead projects, and work co-operatively with others. Ideal candidates will have excellent organizational, time management, and multitasking skills. To apply, please send the following to Dr. Qing Yang (qiyang@utmb.edu). A full CV with publication list; Cover letter including the names and contact details of 3 references; PDF copies of 2 of your most recent publications.

The research background of Dr. Yang’s Lab:

My long-term research interest is to understand mechanisms underlying chemotherapy and traumatic injuryinduced neuropathy with a major goal to identify potential therapeutic targets that can be used to effectively treat chemotherapy- and traumatic injury-induced complications. At present, I seek to deconstruct the role of ion channels in spinal cord injury (SCI)-induced secondary degeneration and chemotherapy-induced peripheral neuropathy (CIPN) to gain new insight on the treatment.

1. One research in lab focus on the identifying molecular mechanism underlying CIPN, as well as a potential therapeutic target to prevent the development of CIPN, including chronic pain. Excessive neuronal excitation is a primary source of CIPN. My goal is to identify the channelopathy that involved in CIPN-induced over-excitation of primary sensory neurons, and try to identify novel targets for therapeutic development.

2. Another research focus on the contribution of ion channels in neuroprotection and axon regeneration after spinal cord injury (SCI). Traumatic injury to the spinal cord results in acute necrosis and secondary degeneration of spinal tissues, followed by a chronic stage with cavities and scar tissue formed, leaving the individual living with paralysis, and sensory dysfunction. Mild or strong neuronal excitations are at the core of injury evoked by various insults, necrotic neuronal damage often is a fee paid for excessive excitation. Thus, decreasing neuronal excitability by modulating some ion channels would be a useful strategy to treat SCI-induced complications in both acute and chronic phases.

[打 印] [关 闭]