bluuebunny/crossref_metadata_2025_split huggingface dataset:
Wave dynamics of an electrojet: generalized Farley–Buneman instability
Authors: McKENZIE JAMES F. 
Published: October 2006

AbstractIn this paper we generalize the classical Farley–Buneman (FB) instability to include space-charge effects and finite electron inertia. The former effect makes the ion-acoustic wave dispersive with the usual resonance appearing at the ion plasma frequency, but other than that the structure of the FB instability remains intact. However, the inclusion of the latter, finite electron inertia, gives rise to the propagating electron-cyclotron mode, albeit modified by collisions. In the presence of differential electron streaming relative to the ions, the interaction between this mode, attempting to propagate against the stream, but convected forward by the stream, and a forward propagating ion-acoustic mode, gives rise to a new instability distinct from the FB instability. The process may be thought of in terms of the coupling between negative energy waves (electron-cyclotron waves attempting to propagate against the stream) and positive energy waves (forward propagating ion-acoustic waves). In principle, the instability simply requires super-ion acoustic streaming electrons and the corresponding growth rates are of the order of one half of the lower hybrid frequency, which are faster than the corresponding FB growth rates. For conditions appropriate to the middle day-side E-region this instability excites a narrow band of frequencies just below the ion plasma frequency. Its role in the generation of electrojet irregularities may be as important as the classical FB instability.
The anti‐amnesic and neuroprotective effects of donepezil against amyloid β25‐35peptide‐induced toxicity in mice involve an interaction with theσ1receptor
Authors: Meunier J , Ieni J , Maurice T 
Published: October 2006

Background and purpose:The acetylcholinesterase inhibitor, donepezil, is also a high affinity σ1receptor agonist. We examined the involvement of σ1receptors in its anti‐amnesic and neuroprotective properties against amyloid β25‐35peptide‐induced toxicity in mice.Experimental approach:Mice were given an intracerebroventricular (i.c.v.) injection of Aβ25‐35peptide (9 nmol) 7‐9 days before being tested for spontaneous alternation and passive avoidance. Hippocampal lipid peroxidation was measured 7 days after Aβ25‐35injection to evaluate oxidative stress. Donepezil, the σ1agonist PRE‐084 or the cholinesterase (ChE) inhibitors tacrine, rivastigmine and galantamine were administered either 20 min before behavioural sessions to check their anti‐amnesic effects, or 20 min before Aβ25‐35injection, or 24 h after Aβ25‐35injection and then once daily before behavioural sessions, to check their pre‐ and post‐i.c.v. neuroprotective activity, respectively.Key results:All the drugs tested were anti‐amnesic, but only the effects of PRE‐084 and donepezil were prevented by the σ1antagonist BD1047. Only PRE‐084 and donepezil showed neuroprotection when administered pre i.c.v.; they blocked lipid peroxidation and learning deficits, effects inhibited by BD1047. Post i.c.v., PRE‐084 and donepezil showed complete neuroprotection whereas the other ChE inhibitors showed partial effects. BD1047 blocked these effects of PRE‐084, attenuated those of donepezil, but did not affect the partial effects of the other ChE inhibitors.Conclusions and implications.The potent anti‐amnesic and neuroprotective effects of donepezil against Aβ25‐35‐induced toxicity involve both its cholinergic and σ1agonistic properties. This dual action may explain its sustained activity compared to other ChE inhibitors.British Journal of Pharmacology(2006)149, 998–1012. doi:10.1038/sj.bjp.0706927
Isoflurane Produces Delayed Preconditioning against Spinal Cord Ischemic Injury via Release of Free Radicals in Rabbits
Authors: Sang Hanfei , Cao Lin , Qiu Pengxin , Xiong Lize , Wang Rongrong , Yan Guangmei 
Published: October 2006

Background
Whether isoflurane preconditioning produces delayed neuroprotection in the spinal cord is unclear. The authors tested the hypothesis that isoflurane produces delayed preconditioning against spinal cord ischemic injury and, further, that the beneficial effect is dependent on free radicals.

Methods
In experiment 1, 63 rabbits were randomly assigned to seven groups (n = 9 each): Animals in the control group only underwent spinal cord ischemia without pretreatment; animals in the Iso24h, Iso48h, and Iso72h groups received 40 min of 1.0 minimum alveolar concentration isoflurane in 100% oxygen each day for 5 consecutive days, with the last pretreatment at 24, 48, and 72 h, respectively, before spinal cord ischemia; animals in the O2 24h, O2 48h, and O2 72h groups received 40 min of 100% oxygen each day for 5 consecutive days, with the last pretreatment at 24, 48, and 72 h, respectively, before spinal cord ischemia. In experiment 2, 48 rabbits were randomly assigned into four groups (n = 12 each): Animals in the O2 and Iso groups received 3 ml/kg saline intraperitoneally 1 h before each session of oxygen pretreatment and isoflurane pretreatment, respectively. In the DMTU+Iso and DMTU+O2 groups, 10% dimethylthiourea (DMTU, a potent free radical scavenger) dissolved in saline (3 ml/kg) was administered at the same time point. Twenty-four hours after the last pretreatment, animals were subjected to spinal cord ischemia. Spinal cord ischemia was induced by an infrarenal aorta clamping for 20 min. Forty-eight hours after reperfusion, neurologic function and histopathology of the spinal cord were examined.

Results
In experiment 1, the neurologic and histopathologic outcomes in the Iso24h and Iso48h groups were better than those in the control group (P < 0.005 for each comparison); the neurologic and histopathologic outcomes in the control group showed no significant differences in comparison with the O2 24h, O2 48h, O2 72h, and Iso72h groups (P > 0.05 for each comparison). In experiment 2, the neurologic and histopathologic outcomes in the Iso group were better than those in the DMTU+Iso, O2, and DMTU+O2 groups (P < 0.01 for each comparison); there were no significant differences in the neurologic and histopathologic outcomes among the DMTU+Iso, O2, and DMTU+O2 groups (P > 0.05 for each comparison).

Conclusions
Isoflurane produces delayed preconditioning against spinal cord ischemic injury, and the beneficial effect may be dependent on the release of free radicals.
Acute Late Sepsis Attenuates Effects of a Nondepolarizing Neuromuscular Blocker, Rocuronium, by Facilitation of Endplate Potential and Enhancement of Membrane Excitability In Vitro
Authors: Niiya Tomohisa , Narimatsu Eichi , Namiki Akiyoshi 
Published: October 2006

Background
Sepsis attenuates the muscle-relaxing effects of nondepolarizing neuromuscular blockers. The authors investigated the effects of acute late sepsis on neuromuscular transmission and neuromuscular actions of rocuronium to clarify the mechanisms by which sepsis attenuates the effects of nondepolarizing neuromuscular blockers.

Methods
Sepsis was induced by cecal ligation and puncture operation. Endplate potentials, acetylcholine potentials, and electrotonic potentials were recorded from the motor endplates of isolated diaphragms from acute late septic and nonseptic rats.

Results
(1) Sepsis did not influence the effect of rocuronium to decrease endplate potential amplitude, which was increased by sepsis itself; (2) sepsis facilitated the effect of rocuronium to decrease quantal acetylcholine release, which was increased by sepsis itself; (3) sepsis did not influence the effect of rocuronium to decrease acetylcholine sensitivity, which was decreased by sepsis itself; (4) sepsis decreased critical depolarization, and rocuronium did not influence critical depolarization.

Conclusions
These results indicate that acute late sepsis facilitates endplate potentials and enhances excitability of the muscle membrane, indicated by a decrease of critical depolarization. It is thought that these elicit the sepsis-induced attenuation of the muscle-relaxing effects of rocuronium.
A Randomized Study of the Effects of Gabapentin on Postamputation Pain
Authors: Nikolajsen Lone , Finnerup Nanna B. , Kramp Steffen , Vimtrup Anne-Sofie , Keller Johnny , Jensen Troels S. 
Published: October 2006

Background
Pain after amputation is common but difficult to treat. Therefore, the authors examined whether postoperative treatment with gabapentin could reduce postamputation stump and phantom pain.

Methods
Forty-six patients scheduled to undergo lower limb amputation were randomly assigned to receive oral gabapentin or placebo. Treatment was started on the first postoperative day and continued for 30 days. The daily dose of gabapentin or placebo was gradually increased to 2,400 mg/day. The intensity of stump and phantom pain was recorded every day on a numeric rating scale (0-10) during the 30-day treatment period. Five interviews were performed after 7, 14, and 30 days and after 3 and 6 months.

Results
Results from 41 patients were included in the data analysis. The risk of phantom pain (gabapentin vs. placebo) was 55.0% versus 52.6% (risk difference, 2.4%; 95% confidence interval, -28.9 to 33.7%; P = 0.88; 30 days) and 58.8% versus 50.0% (risk difference, 8.8%; 95% confidence interval, -23.3 to 40.9%; P = 0.59; 6 months). The median intensity of phantom pain (gabapentin vs. placebo) was 1.5 (range, 0-9.0) versus 1.2 (range, 0-6.6) (P = 0.60; 30 days) and 1.0 (range, 0-6.0) versus 0.5 (range, 0-5.0) (P = 0.77; 6 months). The median intensity of stump pain was 0.85 (range, 0-8.2) versus 1.0 (range, 0-5.4) (P = 0.68; 30 days) and 0 (range, 0-8.0) versus 0 (range, 0-5.0) (P = 0.58; 6 months).

Conclusion
Gabapentin administered in the first 30 postoperative days after amputation does not reduce the incidence or intensity of postamputation pain.
Experimental heart muscle damage in alcohol feeding is associated with increased amounts of reduced‐ and unreduced‐acetaldehyde and malondialdehyde–acetaldehyde protein adducts
Authors: Worrall Simon , Richardson Peter J. , Preedy Victor R. 
Published: October 2006

AbstractChronic and excessive alcohol consumption induces defined myocardial lesions characterized by impaired structural, mechanical and biochemical features. The pathogenic mechanisms are unknown, although it is possible that protein adduct formation by reactive metabolites of ethanol may be a contributory process. Hitherto, this has only been tested with respect to antibodies against reduced‐acetaldehyde protein adducts in clinical studies, despite the fact that during alcohol toxicity the formation of reduced‐acetaldehyde, unreducedacetaldehyde, malondialdehyde, malondialdehyde‐acetaldehyde and hydroxyethyl protein adducts have been reported in non‐cardiac tissues. It was our hypothesis that the heart is particularly sensitive to the formation of protein adducts in alcohol toxicity.Totest this hypothesis, we analysed hearts from rats fed nutritionally complete liquid diets containing ethanol as 35% of total calories for 6 weeks, using the Lieber‐DeCarli pair‐feeding protocol. Control rats were treated identically and fed the same diet in which ethanol was replaced by isocaloric glucose. At the end of the feeding period, the hearts were dissected and ventricular muscle analysed. After 6 weeks' ethanol feeding, ELISA analysis showed increased amounts of reduced‐acetaldehyde protein adducts (p < 0.01) unreduced‐acetaldehyde (p < 0.01) and malondialdehyde‐acetaldehyde (p= 0.01) protein adducts. However, malondialdehyde and α‐hydroxyethyl‐protein adducts were not significantly increased in hearts of ethanol‐fed rats compared to pair‐fed control (p > 0.1 in both instances). This is the first report of acetaldehyde adduct formation in alcoholic cardiomyopathy. This suggests that either immune process may develop or functional impairment of affected proteins may occur.
Changes in cigarette smoking among alcohol and drug misusers during inpatient detoxification
Authors: Harris Jennifer , Best David , Man Lan‐Ho , Welch Sarah , Gossop Michael , Strang John 
Published: October 2006

AbstractSmoking prevalence and changes during inpatient detoxification were examined among 135 admissions to an inpatient alcohol and drug detoxification unit, of whom 83 (61.5%) were re‐interviewed one week later. Ninety‐two per cent of the initial sample were currently smokers; 87% of alcohol misusers, 97% of drug misusers and 100% of drug/alcohol misusers. Smokers consumed a daily mean of 27 cigarettes before admission. Those classified as heavy smokers (smoking 40 or more cigarettes prior to admission) decreased their smoking levels by an average of 10.5 cigarettes during detoxification. Light smokers (1–19 cigarettes per day) increased by a daily average of 8.6 cigarettes and intermediate smokers (20–39 cigarettes) by 4.9 cigarettes. The findings suggest a dose‐dependent relationship between cigarette smoking and inpatient detoxification that requires further study. Over three‐quarters of the sample expressed a desire to change their smoking behaviour, many of whom felt they would like help to tackle this change. Given the high smoking prevalence and reported interest in smoking cessation/reduction, there is an opportunity to address the smoking behaviour of drug and alcohol misusers entering inpatient care, whether during or after their detoxification.
CLINICAL STUDY: Quantification of breath carbon disulphide and acetone following a single dose of disulfiram (Antabuse) using selected ion flow tube mass spectrometry (SIFT‐MS)
Authors: Bloor Roger N. , Španěl Patrick , Smith David 
Published: October 2006

ABSTRACTSelected ion flow tube mass spectrometry (SIFT‐MS) has been used to measure simultaneously the concentrations of both carbon disulphide and acetone in exhaled breath following the ingestion of a single dose of disulfiram (Antabuse). Carbon disulphide is a product of the metabolism of disulfiram and is excreted mainly through the lungs. Acetone is a product of normal metabolism and appears in the breath of all individuals. These breath analyses were performed in single exhalations and the results were available in real time. The levels of breath acetone and carbon disulphide were compared with levels obtained from a control subject who had not ingested disulfiram. Breath carbon disulphide was seen to increase from 15 p.p.b. to 618 p.p.b. over a 28‐hour period, in the single individual tested, following ingestion of disulfiram, while acetone levels increased from 300 p.p.b. (normal) to over 4000 p.p.b. (greatly elevated). No such increases were seen in the breath of the control subject over the same period. An obvious positive correlation between breath carbon disulphide and acetone concentrations following disulfiram ingestion is seen and discussed.
REVIEW: The genetics of alcoholism: identifying specific genes through family studies
Authors: Edenberg Howard J. , Foroud Tatiana 
Published: October 2006

ABSTRACTAlcoholism is a complex disorder with both genetic and environmental risk factors. Studies in humans have begun to elucidate the genetic underpinnings of the risk for alcoholism. Here we briefly review strategies for identifying individual genes in which variations affect the risk for alcoholism and related phenotypes, in the context of one large study that has successfully identified such genes. The Collaborative Study on the Genetics of Alcoholism (COGA) is a family‐based study that has collected detailed phenotypic data on individuals in families with multiple alcoholic members. A genome‐wide linkage approach led to the identification of chromosomal regions containing genes that influenced alcoholism risk and related phenotypes. Subsequently, single nucleotide polymorphisms (SNPs) were genotyped in positional candidate genes located within the linked chromosomal regions, and analyzed for association with these phenotypes. Using this sequential approach, COGA has detected association withGABRA2,CHRM2andADH4; these associations have all been replicated by other researchers. COGA has detected association to additional genes includingGABRG3,TAS2R16,SNCA,OPRK1andPDYN, results that are awaiting confirmation. These successes demonstrate that genes contributing to the risk for alcoholism can be reliably identified using human subjects.
REVIEW: The alcohol‐preferring AA and alcohol‐avoiding ANA rats: neurobiology of the regulation of alcohol drinking
Authors: Sommer Wolfgang , Hyytiä Petri , Kiianmaa Kalervo 
Published: October 2006

ABSTRACTThe AA (alko, alcohol) and ANA (alko, non‐alcohol) rat lines were among the earliest rodent lines produced by bidirectional selection for ethanol preference. The purpose of this review is to highlight the strategies for understanding the neurobiological factors underlying differential alcohol‐drinking behavior in these lines. Most early work evaluated functioning of the major neurotransmitter systems implicated in drug reward in the lines. No consistent line differences were found in the dopaminergic system either under baseline conditions or after ethanol challenges. However, increased opioidergic tone in the ventral striatum and a deficiency in endocannabinoid signaling in the prefrontal cortex of AA rats may comprise mechanisms leading to increased ethanol consumption. Because complex behaviors, such as ethanol drinking, are not likely to be controlled by single factors, system‐oriented molecular‐profiling strategies have been used recently. Microarray based expression analysis of AA and ANA brains and novel data‐mining strategies provide a system biological view that allows us to formulate a hypothesis on the mechanism underlying selection for ethanol preference. Two main factors appear active in the selection: a recruitment of signal transduction networks, including mitogen‐activated protein kinases and calcium pathways and involving transcription factors such as Creb, Myc and Max, to mediate ethanol reinforcement and plasticity. The second factor acts on the mitochondrion and most likely provides metabolic flexibility for alternative substrate utilization in the presence of low amounts of ethanol.
Subinsular vascular lesions: an analysis of 119 consecutive autopsied brains
Authors: Tomimoto H. , Lin J. , Ihara M. , Ohtani R. , Matsuo A. , Miki Y. 
Published: October 2006

The insula of Reil constitutes a functionally intriguing complex of the brain related to multifunctional activities. We examined the subinsular region in 119 consecutively autopsied patients, as T2 hyperintense lesions are frequently observed in magnetic resonance diagnosis of this region. The patients were admitted in neurology wards and were diagnosed as having cerebrovascular disease in 55 patients (46%), other neurological diseases in 57 patients (48%) and non‐neurological diseases in seven patients (6%). Demyelination of the white matter was semi‐quantified as a fiber density score (percent stained area/total area) with computer‐assisted image analysis on Klüver–Barrera‐stained sections. Astrogliosis was assessed by immunohistochemistry for glial fibrillary acidic protein.The lesion analysis showed a dilated perivascular space in 29 patients (24%), demyelination (fiber density score less than the mean − 1 SD) in 27 patients (23%), slit‐shaped lesion in six patients (5%), lacunar infarction in one patient (1%) and cerebral hemorrhage in one patient (1%). A histologic–radiologic comparison in two patients with subcortical ischemic vascular dementia showed correspondence between subinsular hyperintensities, and demyelination, gliosis and a dilated perivascular space. These results indicate that subinsular lesions rarely signifies focal vascular lesions, and are consisted of demyelination, gliosis and a dilated perivascular space.
Antithrombin is as effective as heparin and hirudin to prevent formation of microvascular thrombosis in a murine model
Authors: Sorg Heiko , Hoffmann Johannes , Menger Michael , Lindenblatt Nicole , Goehring Peter , Vollmar Brigitte 
Published: October 2006

SummaryA recently published post-hoc analysis of a trial using high-dose antithrombin (AT) in septic patients (KyberSept) revealed significant reduction of lethality when no concomitant heparin was administered, whereas patients with the combination of heparin and AT did not benefit in terms of survival. Therefore, it seems feasible to study the capability of AT in prevention of microvascular thrombus formation to avoid concomitant application of heparin and AT. Using fluorescence microscopy and a light/dyeinjury mouse ear model, the kinetics of thrombus formation were analyzed quantitatively in vivo upon single iv bolus of saline (control), heparin (100 IU/kg), hirudin (1 mg/kg) or AT (25, 50, 100 or 250 IU/kg) (N=7 animals per group each). In controls, light/dye-injury induced complete thrombotic occlusion in all arterioles and venules studied. Heparin and hirudin prevented thrombotic vessel occlusion in 62% and 43% of arterioles and 11% and 28% of venules. AT-250 was found to be more effective than heparin and hirudin, because thrombus formation was completely banned in all arterioles and venules. AT-100 and AT-50 were also capable of significantly blocking thrombus formation in both arterioles and venules. In blood vessels, which finally clogged, the time for development of complete vessel occlusion was delayed after heparin, hirudin and AT-25, but in particular after AT-50 and AT-100. In conclusion, AT-mediated antithrombotic activity has been characterized in a model of phototoxicity-induced microvascular thrombosis formation, demonstrating thatAT delays and prevents thrombus formation in arterioles and venules at least comparably effective as heparin and hirudin.
Emerging anticoagulants for the treatment of venous thromboembolism
Authors: Weitz Jeffrey 
Published: October 2006

SummaryAnticoagulant therapy is the cornerstone of treatment of venous thromboembolism (VTE). Such treatment is divided into two stages. Rapid initial anticoagulation is given to minimize the risk of thrombus extension and fatal pulmonary embolism, whereas extended anticoagulation is aimed at preventing recurrent VTE, thereby reducing the risk of postphlebitic syndrome. With currently available drugs, immediate anticoagulation can only be achieved with parenteral agents, such as heparin, low-molecular-weight heparin, or fondaparinux. Extended treatment usually involves the administration of vitamin K antagonists,such as warfarin. Emerging anticoagulants have the potential to streamline VTE treatment. These agents include idraparinux, a long-acting synthetic pentasaccharide that is given subcutaneously on a once-weekly basis, and new oral anticoagulants that target thrombin or factor Xa. This paper i) reviews the pharmacology of these agents, ii) outlines their potential strengths and weaknesses, iii) describes the results of clinical trials with these new drugs, and iv) identifies the evolving role of new anticoagulants in the management of VTE.