The Role of the Independent in Alaska\u27s Mineral Development

In 68 years of oil industry history in Alaska, the independent has already played a substantial role. Eighty-three independent oil companies or operators have participated in drilling 82 exploratory wells or stratigraphic tests. Their activities extended from the discovery of first commercial oil at Katalla in 1902, to the extension of the Prudhoe Bay field in 1970. The success ratio for wildcat wells in Alaska is considerably higher than “outside,” and fields have all been major in statute, thereby reducing the cost per barrel of finding oil. The most immediate deterrent to the success of the independent in Alaska is the land freeze resulting from the lack of settlement of the claims of Alaska natives. The hoped for lifting of the freeze will afford success to those operators prepared to take advantage of the opportunities

EXPERIMENTAL THERAPEUTICS Structure-Activity Relationship for Substance P Inhibition of Carbamylcholine-Stimulated 22Na Flux in Neuronal (PCi 2) and Non Neuronal (BC3H1 ) Cell Lines1

ABSTRAC

AM-251, A Cannabinoid Antagonist, Modifies the Dynamics of Sleep–Wake Cycles in Rats

Study objectives: a) To describe the microarchitecture of wakefulness and sleep following administrations of 5 and 10 mg/kg AM-251 in rats. b) To develop a new statistical method to follow bout-to-bout dynamics. Method: Wistar rats (n = 6) had been equipped with electroencephalography (EEG) and electromyography (EMG) electrodes. Following their recovery and habituation after the surgery, the animals were injected with vehicle and 5 and 10 mg/kg AM-251 intraperitoneally and EEG, EMG and motor activity was analyzed for the subsequent three hours. Results: AM-251 induced a dose- and time-dependent increase in the number of bouts in active wake (AW) and it decreased this number in all other vigilance states except in passive wake (PW). In contrast, the bout duration in PW compensatory decreased. The effect of AM-251 on the sleep transition dynamics was monitored with a new tool we call "transition heatmap". The analysis of bout trajectories with transition heatmaps reveals a highly organized pattern. Conclusion: AM-251 selectively influences the frequency of vigilance state transitions, but it has no direct impact on the state lengths. AM-251 markedly changed the state transition dynamics, which was visualized with the help of state transition heatmaps

Foreign bodies in the ears causing complications and requiring hospitalization in children 0-14 age: results from the ESFBI study

The occurrence of foreign bodies (FBs) in otorhinolaryngological practice is a common and serious problem among patients in paediatric age. The aim of this work is to characterize the risk of complications and prolonged hospitalization due to foreign bodies in ears in terms of the characteristics of the injured patients (age, gender), typology and features of the foreign bodies, the circumstances of the accident and the hospitalization's details

Role of Homer Proteins in the Maintenance of Sleep-Wake States

Sleep is an evolutionarily conserved process that is linked to diurnal cycles and normal daytime wakefulness. Healthy sleep and wakefulness are integral to a healthy lifestyle; this occurs when an organism is able to maintain long bouts of both sleep and wake. Homer proteins, which function as adaptors for group 1 metabotropic glutamate receptors, have been implicated in genetic studies of sleep in both Drosophila and mouse. Drosophila express a single Homer gene product that is upregulated during sleep. By contrast, vertebrates express Homer as both constitutive and immediate early gene (H1a) forms, and H1a is up-regulated during wakefulness. Genetic deletion of Homer in Drosophila results in fragmented sleep and in failure to sustain long bouts of sleep, even under increased sleep drive. However, deletion of Homer1a in mouse results in failure to sustain long bouts of wakefulness. Further evidence for the role of Homer1a in the maintenance of wake comes from the CREB alpha delta mutant mouse, which displays a reduced wake phenotype similar to the Homer1a knockout and fails to up-regulate Homer1a upon sleep loss. Homer1a is a gene whose expression is induced by CREB. Sustained behaviors of the sleep/wake cycle are created by molecular pathways that are distinct from those for arousal or short bouts, and implicate an evolutionarily-conserved role for Homer in sustaining these behaviors

Potassium channel blockers have minimal effect on repolarization of spontaneous action potentials in rat pituitary lactotropes

Patch-clamp techniques were used in primary cultures of rat lactotropes and the rat pituitary clonal cell line GH3 to determine the population characteristics of spontaneous action potentials and the nature of the currents responsible for repolarization of spontaneous action potentials. Spontaneous action potentials were observed in 75% of lactotropes (74/99) and 80% of GH3 cells (42/51). Lactotropes exhibited broad and shallow action potentials (average duration 460 ms, peak -17 mV, slope of upstroke 0.5 mV/ms) compared to the GH3 cells which displayed narrow and tall action potentials (average duration 177 ms, peak -10 mV, slope of upstroke 1.6 mV/ms). Blockers of potassium currents were used to determine the role of specific potassium currents in the repolarization process. Spontaneous action potentials in lactotropes were largely unaffected by 4-aminopyridine (4AP), charybdotoxin, and apamin. Tetraethylammonium (TEA) caused only an small increase in peak amplitude and, in a subset of cells, a small increase in duration. In contrast, in GH3 cells, TEA, 4AP, charybdotoxin, and apamin all caused a significant increase in duration, while TEA and charybdotoxin also caused an increase in peak amplitude. Further, apamin caused a positive shift in the afterhyperpolarization voltage. In lactotropes, strong buffering of intracellular calcium with calcium chelators (EGTA or BAPTA) caused a profound increase in action potential duration. Thus, repolarization of action potentials in lactotropes is a calcium-dependent process, but unlike GH3 cells, is not mediated by calcium-dependent potassium currents, nor is it strongly influenced by voltage-dependent potassium currents

Role of Transient Receptor Potential Channels in Cholecystokinin-Induced Activation of Cultured Vagal Afferent Neurons

Cholecystokinin (CCK), an endogenous brain-gut peptide, is released after food intake and promotes the process of satiation via activation of the vagus nerve. In vitro, CCK increases cytosolic calcium concentrations and produces membrane depolarization in a subpopulation of vagal afferent neurons. However, the specific mechanisms and ionic conductances that mediate these effects remain unclear. In this study we used calcium imaging, electrophysiological measurements, and single cell PCR analysis on cultured vagal afferent neurons to address this issue directly. A cocktail of blockers of voltage-dependent calcium channels (VDCC) failed to block CCK-induced calcium responses. In addition, SKF96365, a compound that blocks both VDCC and the C family of transient receptor potential (TRP) channels, also failed to prevent responses to CCK. Together these results suggest that CCK-induced calcium influx is not subsequent to the membrane depolarization. Ruthenium red, an inhibitor of the TRPV family and TRPA1, blocked both depolarizing responses to CCK and CCK-induced calcium increases, but had no effect on the KCl-induced calcium response. Selective block of TRPV1 and TRPA1 channels with SB366791 and HC030031, respectively, had minor effects on the CCK-induced response. Application of 2-aminoethoxydiphenyl borate, an activator of select TRPV channels but a blocker of several TRPC channels, either had no effect or enhanced the responses to CCK. Further, results from PCR experiments revealed a significant clustering of TRPV2-5 in neurons expressing CCK1 receptors. These observations demonstrate that CCK-induced increases in cytosolic calcium and membrane depolarization of vagal afferent neurons are likely mediated by TRPV channels, excluding TRPV1

Novel analysis of sleep patterns in rats separates periods of vigilance cycling from long-duration wake events

Rats are polyphasic sleepers. However, a formal definition of when one sleep episode ends and another begins has not been put forth. In the present study we examine the distribution of wake episode durations and based on this distribution conclude there are multiple components of wake. If the wake episode exceeds 300 sec the wake episode is assigned to long duration wake (LDW), if the episode is less than 300 sec it is assigned to brief wake (BW). Further support for this separation was found in close analysis of the EEG power spectrum in BW versus LDW. We then used LDW episodes to separate one sleep episode from another. We term the sleep episodes vigilance cycling (VC) because the rat is cycling between the vigilance states of brief wake (BW), slow-wave sleep (SWS), and rapid-eye movement sleep (REMS). We find that the characteristics of VC are different in the light period versus the dark period. We further find that as VC episodes progress, SWS pressure lessens, but the amount of time spent in REMS increases. These findings suggest that VC episodes are regulated and meaningful to the sleep behavior of rats. The use of the concepts of LDW and VC provides additional insights into the description of sleep patterns in rats that may be important in the development of a complete description of sleep behavior in this animal

Chronic alcohol treatment in rats alters sleep by fragmenting periods of vigilance cycling in the light period with extended wakenings

Studies have shown that disturbed sleep produced by chronic alcohol abuse in humans can predict relapse drinking after periods of abstinence. How alcohol produces disturbed sleep remains unknown. In this study we used a novel analysis of sleep to examine the effects of alcohol on sleep patterns in rats. This analysis separates waking into multiple components and defines a period labeled vigilance cycling (VC) in which the rat rapidly cycles through various vigilance states. These VC episodes are separated by long duration wake periods (LDW). We find that 6 weeks of alcohol (6% in a liquid diet) caused fragmentation of extended VC episodes that normally occur in the light period. However, total daily amounts of slow-wave sleep (SWS) and rapid-eye movement sleep (REMS) remained constant. The daily amount of wake, SWS, and REMS remained constant because the alcohol treated rats increased the amount of VC in the dark period, and the sleep nature of VC in the dark period became more intense. In addition, we observed more wake and less REMS early in the light period in alcohol treated rats. All effects completely reversed by day 16 of alcohol withdrawal. Comparison of the effects of chronic alcohol to acute alcohol exposure demonstrated the effects of chronic alcohol are due to adaptation and not the acute presence of alcohol. The effects of chronic alcohol treatment in rats mimic the effects reported in humans (REMS suppression, difficulty falling asleep, and difficulty remaining asleep)