bluuebunny/crossref_metadata_2025_split huggingface dataset:
Minimum Local Analgesic Dose
Authors: Parpaglioni Raffaella , Frigo Maria Grazia , Lemma Anna , Sebastiani Massimo , Barbati Giulia , Celleno Danilo 
Published: November 2005

Background
This double-blind, randomized study was aimed at detecting the effect of three different volumes of intrathecal levobupivacaine on the minimum local analgesic dose in early labor.

Methods
Ninety-three nulliparous women requesting combined spinal-epidural analgesia, at more than 37 weeks gestation, with spontaneous onset of labor, cervical dilatation from 2 to 5 cm, were enrolled. Parturients received 10 ml (group 10), 5 ml (group 5), or 2.5 ml (group 2.5) of the spinal solution containing plain levobupivacaine diluted with 0.9% wt/vol saline to achieve the desired dose and volume at room temperature. A lumbar epidural catheter was then placed. The initial dose for each group was 2.0 mg, and the following doses were determined by the response of the previous patient using up-down sequential allocation. The authors required the test solution to achieve a visual analog pain score of 10 mm or less to be considered effective. The up-down sequences were analyzed using the Dixon and Massey formula and regression logistic model.

Results
The minimum local analgesic dose of spinal levobupivacaine in spontaneously laboring women was 1.35 mg (95% confidence interval, 1.25-1.45 mg) in group 10, 1.63 mg (95% confidence interval, 1.51-1.76 mg) in group 5, and 1.97 mg (95% confidence interval, 1.89-2.05 mg) in group 2.5. A unit change in volume increased the odds of an effective response multiplicatively by a factor of 1.8.

Conclusions
Analgesia can be achieved using lower doses and higher volumes even in subarachnoid space. The important role of the volume should be considered not only in epidural but also in spinal analgesia.
Ephedrine Blocks Rat Sciatic Nerve In Vivo and Sodium Channels In Vitro
Authors: Hung Yu-Chun , Kau Yi-Chuan , Zizza Anthony M. , Edrich Thomas , Zurakowski David , Myers Robert R. , Wang Ging Kuo , Gerner Peter 
Published: November 2005

Background
The sympathomimetic drug ephedrine has been used intrathecally as the sole local anesthetic for labor and delivery. Because ephedrine may be a useful adjuvant to local anesthetics, the authors investigated the local anesthetic properties of ephedrine in a rat sciatic nerve block model and the underlying mechanism in cultured cells stably expressing Na channels.

Methods
After approval of the animal protocol, the sciatic nerves of anesthetized rats were exposed by lateral incision of the thighs, 0.2 ml ephedrine at 0.25, 1, 2.5, or 5% and/or bupivacaine at 0.125% was injected, and the wound was closed. Motor and sensory/nociceptive functions were evaluated by the force achieved by pushing against a balance and the reaction to pinch, respectively. The whole cell configuration of the patch clamp technique was used to record Na currents from human embryonal kidney cells stably transfected with Nav1.4 channels.

Results
The nociception blockade was significantly longer than the motor blockade at test doses of 2.5 and 5% of ephedrine, or when 1% ephedrine was combined with 0.125% bupivacaine (analysis of variance with repeated measures, P < 0.001, n = 8/group). In vitro, the 50% inhibitory concentrations of ephedrine at -150 and -60 mV were 1,043 +/- 70 and 473 +/- 13 mum, respectively. High-frequency stimulation revealed a use-dependent block of 18%, similar to most local anesthetics.

Conclusions
Because ephedrine's properties are at least partly due to Na channel blockade, detailed histopathologic investigations are justified to determine the potential of ephedrine as an adjuvant to clinically used local anesthetics.
Spinal Muscarinic and Nicotinic Subtypes Activated by Clonidine in Postincisional Pain
Authors: Duflo Frédéric , Boselli Emmanuel , Ryvlin Philippe , Chassard Dominique 
Published: November 2005

Background
A recent model of acute incisional pain has been characterized that strongly parallels the postoperative period in patients experiencing evoked pain. In that setting, abundant literature has revealed antihypersensitive effects produced by intrathecally administered alpha2-adrenergic receptor agonists, such as clonidine, in both animals and humans. Recent reports have suggested an obligatory role of spinal acetylcholine receptors in the analgesic action of intrathecal clonidine. The authors sought to determine the involvement of spinal muscarinic and nicotinic receptor subpopulations in the antihypersensitivity effect of intrathecal clonidine in a rodent model for human postoperative pain.

Methods
After intrathecal catheterization, rats underwent superficial plantar incision. Clonidine or a combination of clonidine and muscarinic receptor subtype antagonists (M1, M2, M3, and M4) or nicotinic receptor subtype antagonists (alpha4beta2 and alpha7) were intrathecally administered, and withdrawal thresholds to mechanical stimuli were examined.

Results
Spinal clonidine maximally reduced hypersensitivity adjacent to the wound 30 min after its injection. When animals were intrathecally pretreated with the M1 muscarinic antagonist toxin MT-7, the M3 muscarinic antagonist 4-diphenylacetoxy-N-methylpiperidine, and the M4 muscarinic antagonist toxin MT-3, clonidine lost its antihypersensitive action. When animals were intrathecally pretreated with the alpha4beta2 nicotinic receptor antagonist dihydro-beta-erythroidine, but not with the alpha7 nicotinic receptor antagonist methyllycaconitine, the antihypersensitivity action of clonidine was abolished.

Conclusions
These data indicate for the first time that the clonidine-induced increase in punctuate mechanical threshold is mediated via the activation of all but M2 muscarinic receptor subtypes, and via the activation of alpha4beta2 but not alpha7 nicotinic receptor subtypes in a rodent model for human postoperative pain.
At5PTase13 Modulates Cotyledon Vein Development through Regulating Auxin Homeostasis
Authors: Lin Wen-Hui , Wang Yuan , Mueller-Roeber Bernd , Brearley Charles A. , Xu Zhi-Hong , Xue Hong-Wei 
Published: November 2005

Abstract
Phosphatidylinositol signaling pathway and the relevant metabolites are known to be critical to the modulation of different aspects of plant growth, development, and stress responses. Inositol polyphosphate 5-phosphatase is a key enzyme involved in phosphatidylinositol metabolism and is encoded by an At5PTase gene family in Arabidopsis thaliana. A previous study shows that At5PTase11 mediates cotyledon vascular development probably through the regulation of intracellular calcium levels. In this study, we provide evidence that At5PTase13 modulates the development of cotyledon veins through its regulation of auxin homeostasis. A T-DNA insertional knockout mutant, At5pt13-1, showed a defect in development of the cotyledon vein, which was rescued completely by exogenous auxin and in part by brassinolide, a steroid hormone. Furthermore, the mutant had reduced auxin content and altered auxin accumulation in seedlings revealed by the DR5:β-glucuronidase fusion construct in seedlings. In addition, microarray analysis shows that the transcription of key genes responsible for auxin biosynthesis and transport was altered in At5pt13-1. The At5pt13-1 mutant was also less sensitive to auxin inhibition of root elongation. These results suggest that At5PTase13 regulates the homeostasis of auxin, a key hormone controlling vascular development in plants.
Heat Stability of Maize Endosperm ADP-Glucose Pyrophosphorylase Is Enhanced by Insertion of a Cysteine in the N Terminus of the Small Subunit
Authors: Linebarger Carla R. Lyerly , Boehlein Susan K. , Sewell Aileen K. , Shaw Janine , Hannah L. Curtis 
Published: November 2005

Abstract
ADP-glucose pyrophosphorylase (AGPase) is a key regulatory enzyme in starch biosynthesis. However, plant AGPases differ in several parameters, including spatial and temporal expression, allosteric regulation, and heat stability. AGPases of cereal endosperms are heat labile, while those in other tissues, such as the potato (Solanum tuberosum) tuber, are heat stable. Sequence comparisons of heat-stable and heat-labile AGPases identified an N-terminal motif unique to heat-stable enzymes. Insertion of this motif into recombinant maize (Zea mays) endosperm AGPase increased the half-life at 58°C more than 70-fold. Km values for physiological substrates were unaffected, although Kcat was doubled. A cysteine within the inserted motif gives rise to small subunit homodimers not found in the wild-type maize enzyme. Placement of this N-terminal motif into a mosaic small subunit containing the N terminus from maize endosperm and the C terminus from potato tuber AGPase increases heat stability more than 300-fold.
Induction of Thioredoxin Is Required for Nodule Development to Reduce Reactive Oxygen Species Levels in Soybean Roots
Authors: Lee Mi-Young , Shin Ki-Hye , Kim Yun-Kyoung , Suh Ji-Yeon , Gu Young-Yun , Kim Mi-Ran , Hur Yoon-Sun , Son Ora , Kim Jin-Sun , Song Eunsook , Lee Myeong-Sok , Nam Kyoung Hee , Hwang Keum Hee , Sung Mi-Kyung , Kim Ho-Jung , Chun Jong-Yoon , Park Miey , Ahn Tae-In , Hong Choo Bong , Lee Suk-Ha , Park Hong Jae , Park Jong-Sug , Verma Desh Pal S. , Cheon Choong-Ill 
Published: November 2005

AbstractNodules are formed on legume roots as a result of signaling between symbiotic partners and in response to the activities of numerous genes. We cloned fragments of differentially expressed genes in spot-inoculated soybean (Glycine max) roots. Many of the induced clones were similar to known genes related to oxidative stress, such as thioredoxin and β-carotene hydroxylase. The deduced amino acid sequences of full-length soybean cDNAs for thioredoxin and β-carotene hydroxylase were similar to those in other species. In situ RNA hybridization revealed that the thioredoxin gene is expressed on the pericycle of 2-d-old nodules and in the infected cells of mature nodules, suggesting that thioredoxin is involved in nodule development. The thioredoxin promoter was found to contain a sequence resembling an antioxidant responsive element. When a thioredoxin mutant of yeast was transformed with the soybean thioredoxin gene it became hydrogen peroxide tolerant. These observations prompted us to measure reactive oxygen species levels. These were decreased by 3- to 5-fold in 7-d-old and 27-d-old nodules, coincident with increases in the expression of thioredoxin and β-carotene hydroxylase genes. Hydrogen peroxide-producing regions identified with cerium chloride were found in uninoculated roots and 2-d-old nodules, but not in 7-d-old and 27-d-old nodules. RNA interference-mediated repression of the thioredoxin gene severely impaired nodule development. These data indicate that antioxidants such as thioredoxin are essential to lower reactive oxygen species levels during nodule development.
Arabidopsis Calcium-Dependent Protein Kinase AtCPK32 Interacts with ABF4, a Transcriptional Regulator of Abscisic Acid-Responsive Gene Expression, and Modulates Its Activity
Authors: Choi Hyung-in , Park Hee-Jin , Park Ji Hye , Kim Sunmi , Im Min-Young , Seo Hyo-Hyun , Kim Yong-Woo , Hwang Inhwan , Kim Soo Young 
Published: November 2005

Abstract
The phytohormone abscisic acid (ABA) regulates stress-responsive gene expression during vegetative growth. The ABA regulation of many genes is mediated by a subfamily of basic leucine zipper class transcription factors referred to as ABFs (i.e. ABF1–ABF4), whose transcriptional activity is induced by ABA. Here we show that a calcium-dependent protein kinase is involved in the ABA-dependent activation process. We carried out yeast two-hybrid screens to identify regulatory components of ABF4 function and isolated AtCPK32 as an ABF4-interacting protein. AtCPK32 has autophosphorylation activity and can phosphorylate ABF4 in vitro. Mutational analysis indicated that serine-110 of ABF4, which is highly conserved among ABF family members, may be phosphorylated by AtCPK32. The serine-110 residue is essential for ABF4-AtCPK32 interaction, and transient expression assay revealed that it is also required for the normal transcriptional function of ABF4. The expression patterns and subcellular localization of AtCPK32 are similar to those of ABF4. Furthermore, its overexpression affects both ABA sensitivity and the expression of a number of ABF4-regulated genes. Together, our data demonstrate that AtCPK32 is an ABA signaling component that regulates the ABA-responsive gene expression via ABF4.
Populus euphraticaDisplays Apoplastic Sodium Accumulation, Osmotic Adjustment by Decreases in Calcium and Soluble Carbohydrates, and Develops Leaf Succulence under Salt Stress
Authors: Ottow Eric A. , Brinker Monika , Teichmann Thomas , Fritz Eberhard , Kaiser Werner , Brosché Mikael , Kangasjärvi Jaakko , Jiang Xiangning , Polle Andrea 
Published: November 2005

AbstractPopulus euphratica Olivier is known to exist in saline and arid environments. In this study we investigated the physiological mechanisms enabling this species to cope with stress caused by salinity. Acclimation to increasing Na+ concentrations required adjustments of the osmotic pressure of leaves, which were achieved by accumulation of Na+ and compensatory decreases in calcium and soluble carbohydrates. The counterbalance of Na+/Ca2+ was also observed in mature leaves from field-grown P. euphratica trees exposed to an environmental gradient of increasing salinity. X-ray microanalysis showed that a primary strategy to protect the cytosol against sodium toxicity was apoplastic but not vacuolar salt accumulation. The ability to cope with salinity also included maintenance of cytosolic potassium concentrations and development of leaf succulence due to an increase in cell number and cell volume leading to sodium dilution. Decreases in apoplastic and vacuolar Ca2+ combined with suppression of calcineurin B-like protein transcripts suggest that Na+ adaptation required suppression of calcium-related signaling pathways. Significant increases in galactinol synthase and alternative oxidase after salt shock and salt adaptation point to shifts in carbohydrate metabolism and suppression of reactive oxygen species in mitochondria under salt stress.
Protection against Photooxidative Injury of Tobacco Leaves by 2-Alkenal Reductase. Detoxication of Lipid Peroxide-Derived Reactive Carbonyls
Authors: Mano Jun'ichi , Belles-Boix Enric , Babiychuk Elena , Inzé Dirk , Torii Yoshimitsu , Hiraoka Eiji , Takimoto Koichi , Slooten Luit , Asada Kozi , Kushnir Sergei 
Published: November 2005

Abstract
Degradation of lipid peroxides leads to the formation of cytotoxic 2-alkenals and oxenes (collectively designated reactive carbonyls). The novel NADPH-dependent oxidoreductase 2-alkenal reductase (AER; EC 1.3.1.74) from Arabidopsis (Arabidopsis thaliana), which is encoded by the gene At5g16970, catalyzes the reduction of the α,β-unsaturated bond of reactive carbonyls, and hence is presumed to function in antioxidative defense in plants. Here we show that Arabidopsis AER (At-AER) has a broad substrate spectrum to biologically relevant reactive carbonyls. Besides 2-alkenals, the enzyme recognized as substrates the lipid peroxide-derived oxenes 9-oxo-octadeca-(10E),(12Z)-dienoic acid and 13-oxo-octadeca-(9E),(11Z)-dienoic acid, as well as the potent genotoxin 4-oxo-(2E)-nonenal, altogether suggesting AER has a key role in the detoxification of reactive carbonyls. To validate this conclusion by in vivo studies, transgenic tobacco (Nicotiana tabacum) plants that had 100- to 250-fold higher AER activity levels than control plants were generated. The engineered plants exhibited significantly less damage from either (1) the exogenously administered 4-hydroxy-(2E)-nonenal, (2) treatment with methyl viologen plus light, or (3) intense light. We further show that the At-AER protein fused with the Aequorea victoria green fluorescent protein localizes in cytosol and the nucleus in Bright-Yellow 2 cells. These results indicate that reactive carbonyls mediate photooxidative injury in leaf cells, and At-AER in the cytosol protects the cells by reducing the α,β-unsaturated bond of the photoproduced reactive carbonyls.
The clients’ perspective on change during treatment for an alcohol problem: qualitative analysis of follow‐up interviews in the UK Alcohol Treatment Trial
Authors: Orford Jim , Hodgson Ray , Copello Alex , John Bev , Smith Melanie , Black Rachel , Fryer Kate , Handforth Linda , Alwyn Tina , Kerr Cicely , Thistlethwaite Gill , Slegg Gary ,   UKATT Research Team
Published: November 2005

ABSTRACTAim  To develop a model of change during and following professional treatment for drinking problems, grounded in clients’ accounts.Participants  Subsets of consecutively selected clients of the UK Alcohol Treatment Trial (UKATT), followed‐up at 3 months (n = 211) and 12 months (n = 198) after randomization.Location  Five statutory and non‐statutory alcohol problems treatment agencies in three areas of England and Wales.Data  Open‐ended interviews conducted according to a brief interview guide, leading to 400–800‐word post‐interview reports used for analysis (tape‐recordings used for auditing purposes).Analysis  Reports analysed by a team according to grounded theory principles, involving an iterative process with successive refinement of interviewing and analysis with each successive batch of data.Findings  A model of change from the clients’ perspective was developed. Treatment was seen by clients as facilitating various changes in ways of thinking and/or increased support of various kinds from family and friends, along with new ways of acting in relation to drinking or more generally. For many those changes had led to an appreciation of the benefits accruing to them. Treatment was seen as part of a broader treatment system which included pretreatment assessment, forms of help additional to the trial treatment, plus an element of self‐directed change during and following treatment. Taken with awareness of worsening alcohol‐related harms, triggering events and external influence to seek treatment (the catalyst system), to which clients continued to refer following treatment, the change process is depicted as a complex, ongoing set of systems in which a trial treatment is embedded.Conclusions  Models of change should be broadened so that treatment is seen as a complex system of parts, facilitating a nexus of cognitive, social and behavioural changes, embedded within a broader system of events and processes catalysing change. Such a model helps explain the relative absence of between‐treatments outcome differences in UKATT and in the alcohol problems treatment and more general psychotherapy research literatures.
Financial stress, smoking cessation and relapse: results from a prospective study of an Australian national sample
Authors: Siahpush Mohammad , Carlin John B. 
Published: November 2005

ABSTRACTAims  Our aim was to examine the association between financial stress and subsequent smoking cessation among smokers, and relapse among ex‐smokers.Design and participants  Data came from the first two waves of the Household Income and Labour Dynamics in Australia (HILDA) survey. The size of the subsample of smokers was 2076, and that of ex‐smokers was 2717. Data collection was based on face‐to‐face interviews.Measurement  Eight questionnaire items (e.g. difficulty paying electricity, gas or telephone bills and going without meals due to shortage of money) were used to construct a nine‐point financial stress index.Findings  Smokers with more financial stress were less likely to quit, with the odds of quitting reducing by 13% (95% CI: 4–21%; P = 0.008) per unit of the financial stress index. Ex‐smokers with more financial stress were more likely to relapse (P < 0.001).Conclusions  Special programmes may have to be implemented to counter the potentially adverse effects of tobacco price increases on smokers who have financial stress and fail to quit smoking.
Prospective prediction of children's smoking transitions: role of parents’ and older siblings’ smoking
Authors: Bricker Jonathan B. , Peterson Jr Arthur V. , Leroux Brian G. , Andersen M. Robyn , Rajan K. Bharat , Sarason Irwin G. 
Published: November 2005

ABSTRACTAims To use a novel social epidemic probability model to investigate longitudinally the extent to which parents’ and older siblings’ smoking predict children's smoking transitions.Design Parents’ and older siblings’ smoking status was assessed when children were in 3rd grade (baseline). Three smoking transitions were assessed over the period of child/adolescent smoking acquisition (up to 12th grade): (1) transition from never smoking to trying smoking, (2) transition from trying to monthly smoking and (3) transition from monthly to daily smoking. Setting Forty Washington State school districts participating in the long term Hutchinson Smoking Prevention Project (HSPP).Participants and measurements Participants were the 5520 families for whom data on both parents’ and older siblings’ baseline smoking status, as well as on children's smoking transitions, were available. Findings The probability that a smoking parent influenced their child to make the first transition to trying smoking was 32% (95% CI: 27%, 36%); to make the second transition from trying to monthly smoking, 15% (95% CI: 10%, 19%); and to make the third transition from monthly to daily smoking, 28% (95% CI: 21%, 34%). The probability that an older sibling influenced a child to make the first transition to trying smoking was 29% (95% CI: 17%, 39%); to make the second transition from trying to monthly smoking, 0% (95% CI: 0%, 8%); and to make the third transition from monthly to daily smoking, 20% (95% CI: 4%, 33%).Conclusions In contrast to previous research, the results provide new evidence suggesting that family smoking influences both initiation and escalation of children's smoking. Results also quantify, in terms of probabilities, the importance of parents’ and older siblings’ smoking on children's three major smoking transitions. Parents’ smoking, as well as older siblings’ smoking, are important behaviors to target in preventing adolescents from making smoking transitions.
Longitudinal trajectories of heavy drinking in adults in the United States of America
Authors: Karlamangla Arun , Zhou Kefei , Reuben David , Greendale Gail , Moore Alison 
Published: November 2005

ABSTRACTAims  To estimate age, period, cohort and other demographic influences on heavy alcohol consumption and trajectories of heavy drinking in American adults.Design  Prospective cohort of 14 127 participants, aged 25–74 years at baseline. Generalized estimating equations to model longitudinal change in the probability of heavy drinking and its association with demographic factors.Setting  National, population‐based sample of non‐institutionalized civilians.Measurements  Heavy alcohol consumption (usual number of drinks per occasion ≥ five for men; ≥ four for women) at baseline (1971–74) and three follow‐ups until 1992.Findings  Heavy alcohol consumption declined with increasing age (age effect) and tracked national average consumption (period effect). There was no cohort effect. Higher probability of heavy drinking was associated with male gender (relative risk: RR = 2.4), being not married (RR = 1.4), having less than high school education (RR = 1.7), having annual income below the median (RR = 1.5), not living in the South‐east (RR = 1.7), and smoking (RR = 3.4). Getting married and quitting smoking during the study were each associated with reduction in heavy drinking (RR = 0.55 and 0.61, respectively). Slower age‐related decline in the probability of heavy drinking was seen in men (P < 0.0001), married individuals (P = 0.03), and smokers (P = 0.05).Conclusions  Demographic predictors of trends in heavy drinking are different from those for trends in average alcohol consumption. The likelihood of heavy drinking declined more slowly with increasing age in men and smokers, suggesting that the negative health effects of alcohol in older ages may be greatest in these groups.