The sky is falling: chemical characterization and corrosion evaluation of deposition produced during the static testing of solid rocket motors.

Static tests of horizontally restrained rocket motors at the ATK facility in Promontory UT, USA result in the deposition of entrained soil and fuel combustion products, referred to as Test Fire Soil (TFS), over areas as large as 30-50 mile (80-130 km) and at distances up to 10-12 miles (16-20 km) from the test site. Chloride is the main combustion product generated from the ammonium perchlorate-aluminum based composite propellant. Deposition sampling/characterization and a 6-month field corrosivity study using mild steel coupons were conducted in conjunction with the February 25th 2010 FSM-17 static test. The TFS deposition rates at the three study sites ranged from 1 to 5 g/min/m. TFS contained significantly more chloride than the surface soil collected from the test site. The TFS collected during two subsequent tests had similarly elevated chloride, suggesting that the results obtained in this study are applicable to other tests assuming that the rocket fuel composition remains similar. The field-deployed coupons exposed to the TFS had higher corrosion rates (3.6-5.0 mpy) than paired non-exposed coupons (1.6-1.8 mpy). Corrosion rates for all coupons decreased over time, but coupons exposed to the TFS always had a higher rate than the non-exposed. Differences in corrosion rates between the three study sites were also observed, with sites receiving more TFS deposition having higher corrosion rates.

Localized increases in corticotropin-releasing factor receptors in pulp after dental injury.

Corticotropin-releasing factor (CRF) binds to membrane-bound CRF receptors (CRF-Rs). Among the actions mediated by activated CRF-Rs is beta-endorphin (END) release from immune cells, increasing peripheral antinociception. For assessment of inflammatory regulation of CRF-R expression, rats underwent pulp exposure of left, first mandibular molars and recovered for 6 days. Control pulpal tissue consisted of contralateral, uninjured molars and left, first mandibular molars of uninjured animals. Pulp tissue specimens were incubated with antibodies directed against CRF-R (both isoforms), neurofilament, CD45, and END. We observed (1) increases in pulp CRF-R immunoreactivity after injury, (2) increased CRF-R immunoreactivity expressed in 3 distinct zones in relation to the injury, and (3) increased CD45 and END immunoreactivity in regions surrounding the pulpal abscess. CRF-Rs might provide an additional target for novel analgesics to treat pulpal pain.

Kv1.4 subunit expression is decreased in neurons of painful human pulp.

Kv1.4, a subunit of voltage-gated K(+) channels, plays a large role in regulating neuronal excitability. The level of Kv1.4 expression is unknown in human sensory neurons innervating healthy or painful tissue. Therefore, we examined Kv1.4 immunoreactivity in axons innervating both clinically diagnosed asymptomatic and painful symptomatic human tooth pulp. Antibodies directed against Kv1.4 and PGP9.5, a protein marker for axons, was used to determine the proportion of PGP9.5 immunopositive tissue that was also immunopositive for Kv1.4. We report that on pulpal axons innervating symptomatic teeth Kv1.4 immunoreactivity, a correlate of decreased Kv1.4 expression, is significantly decreased (p < 0.0001), suggestive of a factor responsible for facilitating chronic dental pain and decreases in currents produced, such as I(A), in neurons innervating painful pulp.

Expression of Nav1.9 channels in human dental pulp and trigeminal ganglion.

There is a higher incidence of local anesthetic failure in endodontic patients experiencing pulpal hyperalgesia. Up-regulation of Nav1.9, a voltage-gated sodium channel isoform, might play a key role in local anesthetic failure because Nav1.9 channels increase neuronal excitability and have low sensitivity to blockade by local anesthetics. Immunocytochemistry was used to examine Nav1.9 channel expression in axons of symptomatic (painful) versus asymptomatic human dental pulp and to determine Nav1.9 expression levels in neuronal somata of the human trigeminal ganglion. Nav1.9 channel immunoreactivity on pulpal axons was significantly increased in painful teeth. Nav1.9 channels were expressed in membranes and cytoplasm of human trigeminal ganglion neurons, with the highest expression in small neuronal somata. Nav1.9 expression in the trigeminal ganglion coupled with increased expression in symptomatic pulp might contribute to hypersensitivity of inflamed pulps and local anesthetic failure. Furthermore, the present study suggests that Nav1.9 channels are potential targets for novel anesthetics.

TRPM2 immunoreactivity is increased in fibroblasts, but not nerves, of symptomatic human dental pulp.

Transient receptor potential (TRP) channels function in diverse processes such as acting as second messenger systems, regulating of ionic concentrations, and aiding in thermoception. TRPM2 channels, members of the melastatin subfamily, mediate calcium influx in response to oxidative stress but during pathological states facilitate hyperexcitability and cellular necrosis via calcium excitotoxicity. We hypothesized that TRPM2 channel expression is upregulated in pulpal tissue of symptomatic teeth with signs of irreversible pulpitis. TRPM2 channel expression was significantly increased in pulp from clinically diagnosed symptomatic teeth compared with pulp from asymptomatic teeth. Additionally, increased TRPM2 expression in symptomatic pulp was the result of increased immunoreactivity in fibroblasts, whereas neural expression of TRPM2 was absent. We provide a possible mechanism explaining the association between TRPM2 channel expression with pain and necrosis. We suggest that TRPM2 channel antagonists could be administered in attempts to inhibit the progression of or even reverse pulpal degradation.

The role of the hyperpolarization-activated cationic current I(h) in the timing of interictal bursts in the neonatal hippocampus.

Under both pathological and experimental conditions, area CA3 of the adult or juvenile hippocampus generates periodic population discharges known as interictal bursts. Whereas the ionic and synaptic basis of individual bursts has been comprehensively studied experimentally and computationally, the pacemaker mechanisms underlying interictal rhythmicity remain conjectural. We showed previously that rhythmic population discharges resembling interictal bursts can be induced in hippocampal slices from first postnatal week mice, in Mg2+-free solution with GABA(A) receptor-mediated inhibition blocked. Here we show that these neonatal bursts occurred with high temporal precision and that their frequency and regularity were greatly reduced by the bradycardic agent ZD-7288 when applied at concentrations and durations that selectively block the hyperpolarization-activated, cationic current I(h). Augmenting I(h) by elevating intracellular cAMP dramatically increased burst frequency in a protein kinase A-independent manner. Burst amplitudes were strongly correlated with the preceding, but not the following, interburst intervals. The experimentally observed distribution of interburst intervals was modeled by assuming that a burst was triggered whenever the instantaneous rate of spontaneous EPSPs (sEPSPs) exceeded a threshold and that the mean sEPSP rate was minimal immediately after a burst and then relaxed exponentially to a steady-state level. The effect of blocking I(h) in any given slice could be modeled by decreasing only the steady-state sEPSP rate, suggesting that the instantaneous rate of sEPSPs is governed by the level of I(h) activation and raising the novel possibility that interburst intervals reflected the slow activation kinetics of I(h) in the neonatal CA3.