Academic Response to Storm-Related Natural Disasters-Lessons Learned.

On 30 October 2017, selected faculty and administrators from Research Centers in Minority Institutions (RCMI) grantee institutions gathered to share first-hand accounts of the devastating impact of Hurricanes Harvey, Irma, and Maria, which had interrupted academic activities, including research, education, and training in Puerto Rico, Florida, and Texas. The presenters reviewed emergency response measures taken by their institutions to maintain community health care access and delivery, the storm-related impact on clinical and research infrastructure, and strategies to retain locally grown clinical expertise and translational science research talent in the aftermath of natural disasters. A longer-term perspective was provided through a comparative review of lessons learned by one New Orleans-based institution (now more than a decade post-storm) in the aftermath of Hurricane Katrina. Caring for the internal and external communities associated with each institution and addressing the health disparities exacerbated by storm-related events is one key strategy that will pay long-term dividends in the survival of the academic institutions and the communities they serve.

Stress During Development of Experimental Endometriosis Influences Nerve Growth and Disease Progression.

PURPOSE: We have previously shown that stress prior to induction worsens clinical presentation and inflammatory parameters in a rat model of endometriosis. This study was designed to examine whether stress during the development of endometriosis can affect the growth of endometriotic implants through nerve growth and immune alterations. METHODS: Endometriosis was surgically induced in female Sprague-Dawley rats by suturing uterine horn implants onto the small intestine mesentery. Two weeks later, one group of rats (endo-stress) was subjected to a 10-day swim stress protocol. Controls had no stress (endo-no stress) or sutures only and stress (sham-stress). On day 60, all rats were killed and examined for the presence of endometriotic vesicles. The size of each vesicle was measured. The uterus and colon were removed and assessed for damage, cell infiltration, and expression of nerve growth factor (NGF), its receptors (p75 and Tropomyosin receptor kinase A (Trk-A)/pTrk-A), and calcitonin gene-related peptide, a sensory fiber marker. A differential analysis of peritoneal fluid white blood cell count was performed. RESULTS: Stress significantly increased endometriotic vesicle size but not colonic damage and increased infiltration of mast cells. Significantly increased expression of NGF and its receptors was found in the uterus of animals with endometriosis receiving stress. CONCLUSIONS: Stress stimulates the development of ectopic endometrial vesicles in an animal model of endometriosis and increases inflammatory cell recruitment to the peritoneum. In addition, stress promotes nerve fiber growth in the uterus.

Glutamate transporters are differentially expressed in the hippocampus during the early stages of one-day spatial learning task.

INTRODUCTION: Uptake of glutamate in the hippocampus by specialized transporters appears to be important for the prevention of glutamate-induced neurotoxicity. However, the role of these transporters in synaptic plasticity and learning is still unclear. We examined the expression pattern of glutamate transporters at different stages of spatial learning using a one-day (three blocks) version of the Morris Water Maze. METHODS: Male rats (Sprague Dawley, 3 months old) were divided into three groups (learner, swim control, or naïve control) and animals were sacrificed after the first, second, or third block of training. The hippocampi were immediately extracted and flash frozen for RNA analysis. Real time polymerase chain reaction was employed to examine the expression of glutamate transporter 1 (Glt-1), Glt1b, glutamate-aspartate transporter (GLAST) and excitatory amino acid carrier-1 (EAAC1) in whole hippocampi. RESULTS: EAAC1 and GLAST RNA were downregulated in the learner and swimmer groups (compared to naïve) after the first two blocks of training during the one-day protocol but EAAC1 returned to control levels by the end of the third block. GLAST levels were upregulated by the third block of training. Glt-1b expression was downregulated during the second block of training but returned to control by the third block. CONCLUSIONS: The observed decreases in glutamate transporter expression may be important during the early stages of spatial learning as a possible mechanism to enhance glutamatergic availability during critical stages of learning. However, similar decreases in glutamate transporter expression in both the learner and swimmer groups indicate that the observed differences may be task-induced. Additional experiments are currently underway to examine this possibility.