Post-processed data and graphical tools for a CONUS-wide eddy flux evapotranspiration dataset.

Large sample datasets of in situ evapotranspiration (ET) measurements with well documented data provenance and quality assurance are critical for water management and many fields of earth science research. We present a post-processed ET oriented dataset at daily and monthly timesteps, from 161 stations, including 148 eddy covariance flux towers, that were chosen based on their data quality from nearly 350 stations across the contiguous United States. In addition to ET, the data includes energy and heat fluxes, meteorological measurements, and reference ET downloaded from gridMET for each flux station. Data processing techniques were conducted in a reproducible manner using open-source software. Most data initially came from the public AmeriFlux network, however, several different networks (e.g., the USDA-Agricultural Research Service) and university partners provided data that was not yet public. Initial half-hourly energy balance data were gap-filled and aggregated to daily frequency, and turbulent fluxes were corrected for energy balance closure error using the FLUXNET2015/ONEFlux energy balance ratio approach. Metadata, diagnostics of energy balance, and interactive graphs of time series data are included for each station. Although the dataset was developed primarily to benchmark satellite-based remote sensing ET models of the OpenET initiative, there are many other potential uses, such as validation for a range of regional hydrologic and atmospheric models.

Flavor-enhancing properties of mushrooms in meat-based dishes in which sodium has been reduced and meat has been partially substituted with mushrooms.

The effects of beef substitution with crimini or white mushrooms (Agaricus bisporus) on the flavor profiles of carne asada and beef taco blends were measured with a descriptive analysis panel. Sensory mitigation of sodium reduction through the incorporation of mushrooms was also investigated in the taco blends. The substitution of beef with mushrooms in the carne asada did not alter the overall flavor strength of the dish, but the incorporation of 50% or 80% ground mushroom in the beef taco blend did enhance its overall flavor as well as mushroom, veggie, onion, garlic and earthy flavors, and umami and sweet tastes. Overall flavor intensity of the 25% reduced-salt version of the 80% mushroom taco blend matched that of the full-salt versions of the 100% and 50% beef formulations, thus indicating that the substitution of 80% of the meat with mushrooms did mitigate the 25% sodium reduction in terms of the overall flavor impact of the dish, even if it did not quite compensate for the reduction in salty taste. This proof-of-concept study for the Healthy Flavors Research Initiative indicates that because of their flavor-enhancing umami principles, mushrooms can be used as a healthy substitute for meat and a mitigating agent for sodium reduction in meat-based dishes without loss of overall flavor.

Annotating smart environment sensor data for activity learning.

The pervasive sensing technologies found in smart homes offer unprecedented opportunities for providing health monitoring and assistance to individuals experiencing difficulties living independently at home. In order to monitor the functional health of smart home residents, we need to design technologies that recognize and track the activities that people perform at home. Machine learning techniques can perform this task, but the software algorithms rely upon large amounts of sample data that is correctly labeled with the corresponding activity. Labeling, or annotating, sensor data with the corresponding activity can be time consuming, may require input from the smart home resident, and is often inaccurate. Therefore, in this paper we investigate four alternative mechanisms for annotating sensor data with a corresponding activity label. We evaluate the alternative methods along the dimensions of annotation time, resident burden, and accuracy using sensor data collected in a real smart apartment.

Comparison of 40 milliliters of 0.25% intrapleural bupivacaine with epinephrine with 20 milliliters of 0.5% intrapleural bupivacaine with epinephrine after cholecystectomy.

To determine the influence of the volume of local anesthetic injected for intrapleural analgesia, 40 patients undergoing cholecystectomy were randomly allocated to two groups of 20 patients each. One group received 40 mL of 0.25% bupivacaine with epinephrine injected intrapleurally postoperatively. The other group received 20 mL of 0.5% bupivacaine with epinephrine. The onset time of analgesia was nearly the same in both groups and within 25 min all patients were nearly pain free. Our data demonstrate that 100 mg of bupivacaine with epinephrine elicits effective analgesia after cholecystectomy. There are only minor differences between 20 and 40 mL with regard to pain relief. The authors conclude that the volume of local anesthetic within the range of 20-40 mL in an adult has little influence on the extent or duration of intrapleural analgesia.

Distribution of bupivacaine after interpleural injection in rats.

The absorption and distribution of bupivacaine in several tissues was studied after interpleural injection of 14C-labelled bupivacaine through a small needle interpleurally on the right side in male rats. 14C-labelled bupivacaine 10 microCi/mmol was injected at a dose of 2.5 mg/kg. The animals, a total of 42, six at each testing time, were sacrificed at 5, 10, 20, 30, 60, 120 and 180 minutes after the interpleural injection. Bupivacaine concentration was then determined on the basis of the amount of radioactivity in tissues taken from 23 different locations. The highest concentration of bupivacaine, about 40 pmol/micrograms tissue, was found in the right lung in the middle and inferior lobes. In the inferior and dorsal aspects of the right thoracic wall, the concentrations were in the same range. In the more peripheral organs, such as the musculature in the legs, the concentration was as low as less than 5 pmol/micrograms. In the central nervous system, the concentration was less than 10 pmol/micrograms. Our conclusion is that interpleurally administered bupivacaine remains in the area of injection for a considerable time.

Side effects and complications related to interpleural analgesia: an update.

Interpleural analgesia has been successfully used for pain relief after cholecystectomy, renal surgery, breast surgery and thoracotomy. Little has been reported about side effects and complications. This article summarizes available information about adverse events collected from the literature. The survey comprises a total of 703 cases. Pneumothorax was the most frequently registered complication followed by signs of systemic toxicity and pleural effusion. Horner's syndrome, pleural infections and catheter rupture have also been reported.

Adaptive changes in alpha-2 adrenoceptor mediated responses: analgesia, hypothermia and hypoactivity.

The acute effects of the alpha-2 adrenoceptor agonists, clonidine and guanfacine, upon antinociception, hypothermia and motor activity were compared under conditions of receptor antagonism, denervation, and chronic administration of a tricyclic antidepressant compound. The analgesic actions of clonidine and guanfacine were antagonised by idazoxan, an alpha-2 receptor antagonist, but potentiated by pretreatment with the noradrenaline neurotoxin DSP4, and attenuated by chronic treatment with desipramine (DMI). Clonidine- and guanfacine-induced hypothermia was antagonised by idazoxan, potentiated by prior treatment with DSP4 and attenuated by chronic administration with DMI. Both clonidine and guanfacine produced decreases in motor activity that were attenuated by idazoxan but unaffected by prior DSP-4 treatment. Chronic DMI administration also attenuated clonidine-induced hypoactivity but potentiated guanfacine-induced hypoactivity. These diverse results describe both similar and differential adaptive mechanisms modulating the functional effect of alpha-2 receptor systems in the central nervous system.

Behavior of mother rats in conflict tests sensitive to antianxiety agents.

Previous studies of freezing and open-field activity have demonstrated that lactating rats are less fearful or less anxious than nonpregnant ones. The purpose of this investigation was to observe the behavior of mother rats in conflict tests, which are frequently used in studies on the neurobiology of anxiety. In the punished drinking test, in which licking from a water spout is punished by electric shocks, mothers (observed on Day 1 postpartum following 24 hr of water deprivation) were found to drink more than virgins. Mothers (Day 1 postpartum) also consumed more food than controls in an unfamiliar open field. In contrast, no difference between mothers (Day 5 postpartum) and virgins was present in the exploration of an electrified shock probe. The largest maternal anticonflict effects in the drinking and feeding tests were recorded when the females were tested with their pups. Increased punished drinking was also observed in virgin rats treated with the anxiolytic benzodiazepine midazolam. Water-deprived virgins and mothers did not differ in the shock titration test, a result suggesting that diminished pain reactivity was unlikely to account for the increased punished drinking in mothers. Moreover, females in late pregnancy, which are hypoalgesic (Gintzler, 1980), did not lick more than virgins in the punished drinking test. Following 24 hr of water deprivation, unpunished drinking was higher in lactating females than in virgins, so the increased acceptance of punishment by mothers might have been due to their being more thirsty than virgins.(ABSTRACT TRUNCATED AT 250 WORDS)

Noradrenergic and serotonergic involvement in brief shock-induced analgesia in rats.

Four experiments were performed to investigate the effects of different techniques causing noradrenergic and serotonergic depletions in the brain and spinal cord on brief shock-induced analgesia. Newborn pups were administered N-2-choloroethyl-N-ethyl-2-bromobenzylamine systemically (2 x 50 mg/kg, ip) and 6-hydroxydopamine administered either systemically (100 micrograms/g, sc) or directly (8 micrograms in 1 microliter, bilaterally) into the locus coeruleus region, or intrathecally (20 micrograms in 10 microliter) into the lumbar subarachnoidal space, caused notable and consistent attenuations of the analgesia caused by brief shock. These treatments reduced noradrenaline concentrations in the spinal cord drastically. A potentiation of brief shock-induced analgesia was caused by the administration of p-chlorophenyl-alanine, whereas administration of 5,7-dihydroxytryptamine, into the nucleus raphe magnus or intrathecally into the subarachnoidal space, produced attenuation of the analgesic effect. Biochemical analyses revealed marked 5-hydroxytryptamine depletions in the spinal cord. The present findings are discussed with regard to the role of spinal noradrenaline and 5-hydroxytryptamine involvement in brief shock-induced analgesia and in reactions to stressful events.

Evidence for crosstolerance to the analgesic effects between morphine and selective alpha 2-adrenoceptor agonists.

Rats were injected subcutaneously (s.c.) with morphine (5 mg/kg) until tolerance developed to its antinociceptive action, or with 0.9% saline which was used as vehicle for morphine. Subsequently, both groups of animals were given an intrathecal (i.th.) dose of either noradrenaline (2 micrograms), clonidine (12.5 micrograms) or guanfacine (12.5 micrograms), that had been found previously to be reliably antinociceptive. In the saline-treated animals, these doses of noradrenaline, clonidine or guanfacine induced clear antinociceptive effects, but not in the morphine-group. It is therefore concluded that cross-tolerance to the antinociceptive effects of systemic morphine and the alpha-adrenoceptor agonists was obtained. The cross-tolerance between morphine on one hand, and noradrenaline, clonidine and guanfacine on the other, implies that a substantial opiate-adrenoceptor interaction exists in antinociceptive processes.

Intrathecal noradrenaline restores 5-methoxy-N,N-dimethyltryptamine induced antinociception abolished by intrathecal 6-hydroxydopamine.

Intrathecal administration of 6-hydroxydopamine (6-OHDA) abolished the antinociceptive effects of acute administration of 5-methoxy-N,N-dimethyltryptamine (5-MeODMT, 1 mg/kg, s.c.) in the hot-plate, tail-flick and shock titration tests of nociception. The antinociceptive effects of 5-MeODMT, abolished by the prior intrathecal 6-OHDA treatment, were restored by intrathecal administration (2 or 1 microgram) of noradrenaline (NA), immediately prior to 5-MeODMT, in all three tests of nociception. Biochemical analysis confirmed severe NA depletions (95 percent loss) in the lumbar and thoracic regions of the spinal and much lesser dopamine depletions (25-35 percent loss). Intrathecal 5,7-dihydroxytryptamine (5,7-DHT) attenuated 5-MeODMT induced antinociception in the tail-flick test and combined NA + 5-MeODMT induced antinociception in the hot-plate and tail-flick tests. Intrathecal administration of 5,7-DHT caused a severe depletion of 5-hydroxytryptamine in the lumbar region of the spinal cord. The present findings demonstrate further the modulatory role of NA upon serotonergic systems in nociception and indicate the necessity of NA availability for induction of 5-MeODMT analgesia.

Lack of effects of prenatal exposure to lidocaine on development of behavior in rats.

The objective of this investigation was to study the effects of lidocaine upon postnatal development of the rat. Lidocaine, 6 mg/kg (21 mumol/kg), was given to a group of 12 rats. Injections were administered intramuscularly, bilaterally in the masseter muscles, once a day on days 10 and 11 of pregnancy. Twelve control rats were given physiologic saline. Clinical signs, mortality, body weight, and food consumption were recorded during pregnancy and lactation. The duration of gestation was also recorded. The development of the offspring was monitored by tests of spontaneous activity, nociception, learning ability, and physical development. No clinical signs of adverse reactions were seen in any of the groups. In the majority of the learning ability tests, the control and lidocaine-treated groups showed similar results. However, in the schedule of differential reinforcement of low rates of responding (DRL 20), the lidocaine-exposed males received more reinforcements than the controls and made fewer responses. In the tests of nociception, a significant difference between sexes was recorded, in that the females were more sensitive than the males in the shock-titration test. Physical development, as monitored by swimming ability and spontaneous activity, showed no inter-group difference. The present results indicate that prenatal exposure to lidocaine fails to result in postnatal impairment of the development of behavioral performance of a wide range of tasks.

Increased antinociception by alpha-adrenoceptor drugs after spinal cord noradrenaline depletion.

Animals depleted of the bulbospinal NA fiber tracts have been reported to be supersensitive to antinociceptive effects of intrathecally administered noradrenaline (NA) in vivo. In the present investigation, the antinociceptive effects were determined after systemic or intrathecal injections of noradrenergic agents. NA and the selective alpha 2-adrenoceptor agonists guanfacine and clonidine were used. NA depletion was performed by treatment neonatally with 6-hydroxydopamine (6-OHDA), or in adult animals by intrathecal 6-OHDA administration or systemic N-2-chloroethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP4). The neurotoxins were found to cause a severe depletion of spinal NA without affecting dopamine (DA) or 5-hydroxytryptamine (5-HT) levels. The antinociceptive effects of intrathecal injection of NA, clonidine and guanfacine were more strongly enhanced in the depleted than in the control rats. It was also found that clonidine and guanfacine given systemically had a stronger effect in depleted than in control animals. In conclusion, depletion of descending NA pathways induces functional supersensitivity both to intrathecally administered NA and to the selective alpha 2-adrenoceptor agonists clonidine and guanfacine. It was also found that systemically administered clonidine and guanfacine had a stronger effect in NA-depleted than in control animals.

Antinociceptive effects and spinal cord tissue concentrations after intrathecal injection of guanfacine or clonidine into rats.

In the present study, the antinociceptive effects of intrathecal injections of the alpha 2-adrenoceptor agonists clonidine and guanfacine in rats was determined to establish their dose-response curves. Spinal cord tissue concentrations were also determined in a separate group of animals. Guanfacine was found to be more potent than clonidine and had a considerably longer duration of action. Thus, whereas the analgesic effect of clonidine declined to baseline by 4 hr after injecting doses of up to 50 micrograms, guanfacine still showed a considerable effect 18 hr after injecting both 25 and 50 micrograms. With both compounds, concentration gradients existed within the spinal cord. In the experiments with guanfacine, the region in the spinal cord tissue with the highest concentrations 10 min after injection contained around 30 pmol/mg wet weight. At 3 hr, this figure was around 20 pmol/mg. With clonidine, on the other hand, the concentration decreased from the maximal level of 200 pmol/mg at 10 min to 10 pmol/mg at 3 hr. On all occasions, except 10 min after injecting clonidine, it was found that the maximal tissue concentrations for both drugs remained below the cervical spinal cord, i.e., the rostral spread was less than expected, especially with drugs with such a long duration of action. The present investigation demonstrates analgesic effects of both clonidine and guanfacine after intrathecal administration, with guanfacine proving more potent and longer acting; the difference in duration of action is probably attributable to differences in rates of elimination of the drugs from spinal cord tissue.

Chronic treatment with antidepressant drugs and ECT differentially modifies the hypothermic action of clonidine and guanfacine.

The hypothermia inducing action of clonidine and guanfacine was abolished by yohimbine and idazoxan pretreatment which suggests an alpha 2-adrenoceptor involvement in this effect. The effects of acute and chronic treatment with the antidepressant drugs desipramine (DMI), amitriptyline (AMI), maprotiline (MAP), mianserin (MIAN), iprindol (IPR), alaproclate (ALA) and electroconvulsive treatment (ECT) on the hypothermic action of the alpha 2-adrenoceptor agonists clonidine and guanfacine were studied. Acute administration of MIAN potentiated clonidine induced hypothermia whereas acute MIAN, IPR and ALA potentiated guanfacine induced hypothermia. Repetitive DMI, AMI and MAP treatment attenuated clonidine-induced hypothermia whereas guanfacine-induced hypothermia was potentiated by chronic treatment with DMI, AMI, MAP and MIAN, ECT applied without anaesthesia attenuated both clonidine and guanfacine hypothermia, however, under ethyl ether anaesthesia ECT was effective only towards guanfacine hypothermia. This discrepancy is discussed in terms of the relative selectivity of the agonists used, the reliability of agonist studies for indexing receptor function, and possible pharmacokinetic interaction.

(+)-8-OH-DPAT and 5-MeODMT induced analgesia is antagonised by noradrenaline depletion.

In experiments with both rats and mice the 5-HT agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and 5-methoxy-N,N-dimethyl-tryptamine (5-MeODMT) were shown to produce reliable analgesic effects after acute administration (1 mg/kg SC) in the tail-flick, hot-plate and shock-titration tests of nociception. Prior treatment with the noradrenaline neurotoxin, N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4), systemically administered to both rats and mice abolished the analgesic effects of both the 5-HT agonist compounds in all the tests of nociception used. Intrathecal 6-hydroxydopamine (6-OHDA) treatment also abolished the analgesic effects of 8-OH-DPAT and 5-MeODMT; in the tail-flick test the analgesia induced by 8-OH-DPAT was reversed to an hyperalgesia. Biochemical analyses confirmed notable noradrenaline depletions in the spinal cord. It is concluded that an important interaction between presynaptic noradrenergic terminals and serotonergic receptor sites, possibly 5-HT1A, mediates spinal nociception processes.

Selective attention and place navigation in rats treated prenatally with methylazoxymethanol.

Prenatal treatment of rats on gestation day 15 with methylazoxymethanol (MAM) caused forebrain microencephaly. The behavioral analyses included measures of spontaneous motor activity and tests for cognitive deficits, and were performed when the rats had reached adult age. Female MAM-treated rats failed to demonstrate contextual control of latent inhibition, which confirms earlier findings with male rats. Male MAM-treated rats demonstrated a notable impairment of place navigation in a swim-maze, but showed as strong sensory preconditioning as the control animals. Biochemical analyses indicated considerable increases in catecholamine levels in the cerebral cortex, hippocampus and striatum. The cognitive deficits, characterised by the various conditioning (taste-aversion) and instrumental learning (swim-maze) tasks, suggested that the MAM rats are deficient in their capacity to attend selectively to the relevant stimulus in complex arrangements of the stimulus situation.

5-Methoxy-N,N-dimethyltryptamine-induced analgesia is blocked by alpha-adrenoceptor antagonists in rats.

The effects of the alpha-adrenoceptor antagonists prazosin, phentolamine and yohimbine upon 5-methoxy-N,N-dimethyltryptamine (5-MeODMT)-induced analgesia were tested in the hot-plate, tail-flick and shock-titration tests of nociception with rats. Intrathecally injected yohimbine and phentolamine blocked or attenuated the analgesia produced by systemic administration of 5-MeODMT in all three nociceptive tests. Intrathecally administered prazosin attenuated the analgesic effects of 5-MeODMT in the hot-plate and tail-flick tests, but not in the shock titration test. Intrathecal yohimbine showed a dose-related lowering of pain thresholds in saline and 5-MeODMT-treated animals. Phentolamine and prazosin produced normal dose-related curves in the hot-plate test and biphasic effects in the shock titration and tail-flick tests. These results demonstrate a functional interaction between alpha 2-adrenoceptors and 5-HT agonist-induced analgesia at a spinal level in rats.

Chronic treatment with antidepressant drugs and the analgesia induced by 5-methoxy-N,N-dimethyltryptamine: attenuation by desipramine.

The effect of chronic and acute oral or intraperitoneal treatment with the antidepressant drugs, desipramine, amitriptyline, alaproclate and iprindole, upon pain thresholds in the tail flick, hot plate and shock titration tests of nociception in saline- and 5-MeODMT-treated rats was studied. Chronic desipramine treatment increased the pre-test tail flick latencies. In the saline-treated rats, chronic oral desipramine treatment increased tail flick latencies, whereas chronic oral amitriptyline treatment decreased tail flick latencies. In 5-MeODMT-treated rats, chronic oral desipramine treatment attenuated the effects of 5-MeODMT (1 mg/kg) in all three tests of nociception, whereas chronic amitriptyline caused a potentiation in the tail flick and hot plate tests. Chronic oral iprindole treatment attenuated 5-MeODMT-induced analgesia in the hot plate test. Chronic intraperitoneal desipramine treatment attenuated 5-MeODMT analgesia in the tail flick and shock titration tests. In a different chronic treatment experiment, oral desipramine treatment attenuated 5-MeODMT analgesia in the tail flick test and zimeldine did for both the tail flick and hot plate tests, whereas mianserin potentiated 5-MeODMT-induced analgesia in both the tail flick and hot plate tests. In the saline-treated rats, acute treatment with all four drugs, desipramine, amitriptyline, iprindole and alaproclate, elevated the shock thresholds, whereas in 5-MeODMT-treated rats, desipramine and amitriptyline elevated shock thresholds. Two main conclusions can be drawn: chronic desipramine caused a quite consistent attenuation of 5-MeODMT-induced analgesia and the effects of acute treatment differed strongly from that of the chronic treatment. The effects of chronic administration with these antidepressants were compared with other findings using different measures of behavioural and receptor function.