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- All Subjects: Regulation
- All Subjects: tyrosine hydroxylase
established climb gradient minimums enforced through Federal Regulations.
Furthermore, to ensure aircraft do not accidentally impact an obstacle on takeoff due to
insufficient climb performance, standard instrument departure procedures have their own
set of climb gradient minimums which are typically more than those set by Federal
Regulation. This inconsistency between climb gradient expectations creates an obstacle
clearance problem: while the aircraft has enough climb gradient in the engine inoperative
condition so that basic flight safety is not precluded, this climb gradient is often not
strong enough to overfly real obstacles; this implies that the pilot must abort the takeoff
flight path and reverse course back to the departure airport to perform an emergency
landing. One solution to this is to reduce the dispatch weight to ensure that the aircraft
retains enough climb performance in the engine inoperative condition, but this comes at
the cost of reduced per-flight profits.
An alternative solution to this problem is the extended second segment (E2S)
climb. Proposed by Bays & Halpin, they found that a C-130H gained additional obstacle
clearance performance through this simple operational change. A thorough investigation
into this technique was performed to see if this technique can be applied to commercial
aviation by using a model A320 and simulating multiple takeoff flight paths in either a
calm or constant wind condition. A comparison of takeoff flight profiles against real
world departure procedures shows that the E2S climb technique offers a clear obstacle
clearance advantage which a scheduled four-segment flight profile cannot provide.
Premature babies are at risk of death from immature lung development. For this reason, pregnant mothers at risk for preterm delivery are administered dexamethasone (DEX), a synthetic glucocorticoid that promotes fetal lung development. However, exposure to DEX in utero is associated with low birth weight and cardiovascular development pathologies. Moreover, our lab found that DEX administration in-utero leads to a sex-specific increase in stress-induced tachycardia in female, but not male offspring. This project seeks to expand on this preliminary finding of the heart by examining local effectors of activity from the sympathetic system (tyrosine hydroxylase and catechol-o-methyltransferase). Tyrosine hydroxylase was measured as it catalyzes the rate limiting step of norepinephrine synthesis while catechol-O- methyltransferase was studied as it catalyzes the degradation of norepinephrine. Acetylcholinesterase was used to measure parasympathetic activity as it catalyzes the degradation of the primary neurotransmitter of the parasympathetic nervous system, acetylcholine. Analyses of sympathetic as well as parasympathetic activity were done to determine influences of in-utero DEX exposure on autonomic regulation in adulthood. Pregnant rats were administered DEX (0.4 mg/kg, i.p.) or vehicle (20% w/v 2-hydroxypropyl ß- cyclodextran) at gestation days 18-21, with euthanasia of offspring occurring at around the time the offspring reached 13-15 weeks of age. Left ventricles and right atria were pulverized, processed and subjected to western blot analysis to determine expression of proteins of interest. Males exposed to DEX in-utero saw a decrease in tyrosine hydroxylase expression in left ventricle and right atrium when compared to vehicle control, a difference not seen with females. In addition, catechol-o-methyltransferase expression was increased in right atria from male, but not female rats. Acetylcholinesterase expression was reduced in the right atria of female, but not male rats. The present findings suggest reduced norepinephrine signaling in the heart of male, but not female DEX-exposed offspring. Given that we have previously found that female, but not male rats exhibit exaggerated stress-induced tachycardia, our current findings suggest that males possess a sex-specific compensatory mechanism allowing the heart to resist increased sympathetic signaling from the brain, one that females do not possess. The underlying mechanics of this proposed mechanism are unclear, and further investigation is needed in this subject to determine the significance of the findings from our study.