bluuebunny/crossref_metadata_2025_split huggingface dataset:
Measurement of Carboxyhemoglobin and Methemoglobin by Pulse Oximetry
Authors: Barker Steven J. , Curry Jeremy , Redford Daniel , Morgan Scott 
Published: October 2006

Background
A new eight-wavelength pulse oximeter is designed to measure methemoglobin and carboxyhemoglobin, in addition to the usual measurements of hemoglobin oxygen saturation and pulse rate. This study examines this device's ability to measure dyshemoglobins in human volunteers in whom controlled levels of methemoglobin and carboxyhemoglobin are induced.

Methods
Ten volunteers breathed 500 ppm carbon monoxide until their carboxyhemoglobin levels reached 15%, and 10 different volunteers received intravenous sodium nitrite, 300 mg, to induce methemoglobin. All were instrumented with arterial cannulas and six Masimo Rad-57 (Masimo Inc., Irvine, CA) pulse oximeter sensors. Arterial blood was analyzed by three laboratory CO-oximeters, and the resulting carboxyhemoglobin and methemoglobin measurements were compared with the corresponding pulse oximeter readings.

Results
The Rad-57 measured carboxyhemoglobin with an uncertainty of +/-2% within the range of 0-15%, and it measured methemoglobin with an uncertainty of 0.5% within the range of 0-12%.

Conclusion
The Masimo Rad-57 is the first commercially available pulse oximeter that can measure methemoglobin and carboxyhemoglobin, and it therefore represents an expansion of our oxygenation monitoring capability.
Recurrent Laryngeal Nerve Palsy after Anterior Cervical Spine Surgery
Authors: Audu Paul , Artz Greg , Scheid Sarah , Harrop James , Albert Todd , Vaccaro Alexander , Hilibrand Alan , Sharan Ashwini , Spiegal Joseph , Rosen Marc 
Published: October 2006

Background
Vocal fold immobility (paresis or paralysis) from recurrent laryngeal nerve injury remains an important cause of morbidity after anterior cervical spine surgery. A maneuver involving endotracheal tube (ETT) cuff manipulation has been proposed to reduce its incidence. This study is a randomized, prospective, double-blind investigation to test the hypothesis that ETT cuff manipulation reduces the incidence of postoperative vocal fold immobility after anterior cervical spine surgery.

Methods
One hundred patients scheduled to undergo anterior cervical spine surgery were randomly assigned to one of two groups. After inducing general endotracheal anesthesia, patients in the intervention group had their ETT cuff pressures maintained at 20 mmHg or less. After placement of self-retaining retractors, the ETT cuff was deflated for 5 s and then reinflated. Patients in the control group had no further manipulation of their ETT once the cuff was inflated after intubation. Cuff pressures in both groups were recorded before skin incision (baseline) and after placement of self-retaining retractors (peak). Patients' vocal fold motion was evaluated by indirect laryngoscopy performed preoperatively and postoperatively. The examination was videotaped and reviewed by a blinded otolaryngologist. Postoperative vocal fold motion was graded as normal, paretic, or paralyzed.

Results
Complete data were available in 94 patients. The incidence of vocal fold paralysis was 3.2% (95% confidence interval, 0.7-9.4%). Cuff manipulation decreased ETT cuff pressure but did not reduce the incidence of vocal fold immobility (15.4% vs. 14.5%).

Conclusion
Endotracheal tube cuff deflation/reinflation and pressure adjustment do not reduce the incidence of vocal fold immobility in anterior cervical spine surgery.
Protective Ventilation Influences Systemic Inflammation after Esophagectomy
Authors: Michelet Pierre , D’Journo Xavier-Benoît , Roch Antoine , Doddoli Christophe , Marin Valerie , Papazian Laurent , Decamps Isabelle , Bregeon Fabienne , Thomas Pascal , Auffray Jean-Pierre 
Published: October 2006

Background
Esophagectomy induces a systemic inflammatory response whose extent has been recognized as a predictive factor of postoperative respiratory morbidity. The aim of this study was to determine the effectiveness of a protective ventilatory strategy to reduce systemic inflammation in patients undergoing esophagectomy.

Methods
The authors prospectively investigated 52 patients undergoing planned esophagectomy for cancer. Patients were randomly assigned to a conventional ventilation strategy (n = 26; tidal volume of 9 ml/kg during two-lung and one-lung ventilation; no positive end-expiratory pressure) or a protective ventilation strategy (n = 26; tidal volume of 9 ml/kg during two-lung ventilation, reduced to 5 ml/kg during one-lung ventilation; positive end-expiratory pressure 5 cm H2O throughout the operative time).

Results
Plasmatic levels of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor alpha were measured perioperatively and postoperatively. Pulmonary function and postoperative evolution were also evaluated. Patients who received protective strategy had lower blood levels of IL-1beta, IL-6, and IL-8 at the end of one-lung ventilation (0.24 [0.15-0.40] vs. 0.56 [0.38-0.89] pg/ml, P < 0.001; 91 [61-117] vs. 189 [127-294] pg/ml, P < 0.001; and 30 [22-45] vs. 49 [29-69] pg/ml, P < 0.05, respectively) and 18 h postoperatively (0.18 [0.13-0.30] vs. 0.43 [0.34-0.54] pg/ml, P < 0.001; 54 [36-89] vs. 116 [78-208] pg/ml, P < 0.001; 16 [11-24] vs. 35 [28-53] pg/ml, P < 0.001, respectively). Protective strategy resulted in higher oxygen partial pressure to inspired oxygen fraction ratio during one-lung ventilation and 1 h postoperatively and in a reduction of postoperative mechanical ventilation duration (115 +/- 38 vs. 171 +/- 57 min, P < 0.001).

Conclusion
A protective ventilatory strategy decreases the proinflammatory systemic response after esophagectomy, improves lung function, and results in earlier extubation.
No Sex Differences in Memory Formation during General Anesthesia
Authors: Stonell Christopher A. , Leslie Kate , He Cheng , Lee Leonard 
Published: October 2006

Background
Women respond differently to anesthesia than men, initially recovering more rapidly, but having more postoperative morbidity. Studies on surgical patients report evidence of memory formation during anesthesia. However, sex differences in memory formation have not been explored. Therefore, the authors investigated sex differences in the implicit and explicit memory formation during general anesthesia.

Methods
With ethics committee approval, 120 consenting adult patients scheduled to undergo surgery during general anesthesia were recruited. Intraoperatively, 16 target words were presented to patients via headphones, and the Bispectral Index was recorded. Postoperatively, memory for presented words was tested using a word stem completion test. The test was divided into inclusion and exclusion parts, to delineate implicit and explicit memory contributions.

Results
Target and distracter hit rates were similar in men and women. For the whole study group, there was a significant difference between inclusion target hit rate (0.42) and base hit rate (0.39) (P = 0.01). Buchner's model suggested that this memory formation was attributable to both implicit and explicit memory. A Bispectral Index value greater than 50 was the only significant predictor of inclusion target hit rate. None of the patients were able to consciously recall the words presented during surgery.

Conclusions
Patients showed greater memory performance for words presented during general anesthesia than for words not presented. However, sex differences in memory formation were not observed. A relation between hypnotic state and memory during sevoflurane anesthesia was also established, suggesting that memory formation is possible even at hypnotic depths considered to be adequate anesthesia.
Effects of Desflurane in Senescent Rat Myocardium
Authors: Rozenberg Sandrine , Besse Sophie , Amour Julien , Vivien Benoît , Tavernier Benoît , Riou Bruno 
Published: October 2006

Background
The myocardial negative inotropic effects of desflurane are less pronounced than those of other halogenated anesthetics, partly because of intramyocardial catecholamine store release. However, the effects of desflurane on aging myocardium are unknown, whereas aging is known to be associated with an attenuation of catecholamine responsiveness.

Methods
The effects of desflurane (1.9-9.3 vol%) were studied in left ventricular papillary muscle of adult and senescent rats (29 degrees C; 0.5 mm Ca; stimulation frequency 12 pulses/min). The inotropic effects were compared under low and high loads, using the maximum unloaded shortening velocity and maximum isometric active force, and without or with alpha- and beta-adrenoceptor blockade.

Results
Desflurane induced a moderate positive inotropic effect in adult rats but a negative inotropic effect in senescent rats. After alpha- and beta-adrenoceptor blockade, desflurane induced a comparable negative inotropic effect in adult and senescent rats. No lusitropic effect under low load was observed, whereas desflurane induced a slight but significant positive lusitropic effect under high load similar between the two groups of rats. This positive effect was abolished by adrenoceptor blockade.

Conclusion
The authors' study suggests that desflurane does not induce significant intramyocardial catecholamine release in senescent myocardium, a result that should be integrated in the well-known alteration in the catecholamine response during aging.
Store-operated Ca2+Influx in Airway Smooth Muscle
Authors: Prakash Y S. , Iyanoye Adeyemi , Ay Binnaz , Sieck Gary C. , Pabelick Christina M. 
Published: October 2006

Background
Volatile anesthetics produce bronchodilation in part by depleting sarcoplasmic reticulum Ca stores in airway smooth muscle (ASM). Other bronchodilatory drugs are known to act via cyclic nucleotides (cyclic adenosine 3',5'-cyclic monophosphate, cyclic guanosine 3',5'-cyclic monophosphate). Intracellular Ca regulation in ASM involves plasma membrane Ca influx, including that triggered by sarcoplasmic reticulum Ca depletion (store-operated Ca entry [SOCE]). The authors hypothesized that anesthetics and bronchodilatory agents interact in inhibiting SOCE, thus enhancing ASM relaxation.

Methods
In enzymatically dissociated porcine ASM cells imaged using fluorescence microscopy, sarcoplasmic reticulum Ca was depleted by 1 microm cyclopiazonic acid in 0 extracellular Ca, nifedipine, and potassium chloride (preventing Ca influx through L-type channels and SOCE). Extracellular Ca was rapidly reintroduced to selectively activate SOCE in the presence or absence of 1 minimum alveolar concentration (MAC) halothane, isoflurane, or sevoflurane. Anesthetic interference with SOCE regulation by cyclic nucleotides was examined by activating SOCE in the presence of (1) 1 microm acetylcholine, (2) 100 microm dibutryl cyclic adenosine 3',5'-cyclic monophosphate, or (3) 100 microm 8-bromo-cyclic guanosine 3',5'-cyclic monophosphate.

Results
SOCE was enhanced by acetylcholine, whereas volatile anesthetics and both cyclic nucleotides partially inhibited Ca influx. Preexposure to 1 or 2 MAC anesthetic (halothane > isoflurane > sevoflurane) inhibited SOCE. Only halothane and isoflurane inhibited acetylcholine-induced augmentation of Ca influx, and significantly potentiated cyclic nucleotide inhibition such that no influx was observed in the presence of anesthetics and cyclic nucleotides.

Conclusions
These data indicate that volatile anesthetics prevent sarcoplasmic reticulum refilling by inhibiting SOCE and enhancing cyclic nucleotide blunting of Ca influx in ASM. Such interactions likely result in substantial airway relaxation in the presence of both anesthetics and bronchodilatory agents such as beta agonists or nitric oxide.
Risk factors for alcoholic liver disease
Authors: Bellentani Stefano , Saccoccio Gioconda , Masutti Flora , Giacca Mauro , Miglioli Lucia , Monzoni Adriana , Tiribelli Claudio 
Published: October 2006

AbstractAlcoholic liver disease (ALD) is still a frequent disorder, even though its incidence appears to be decreasing. In spite of intense investigation, the precise mechanisms leading to ALD are still imprecisely known. This is due in part to the lack of a reliable animal model; in part to the difficulty of obtaining clinical data of adequate sample size and derived from unblased populations and finally from the lack of uniformity of the criteria used to define ALD. This paper will review what is known of the various pieces of this puzzle, with particular emphasis not only on the total amount of alcohol consumed, but also on drinking patterns and type of alcoholic beverage ingested. The other potential factors such as age, gender, genetic background, nutritional status, occupational hazards and viral diseases (especially HCV infection) will be touched upon.
Chronic dopaminergic signaling in the basal ganglia: a damage perspective on kinases and fos‐related antigens
Authors: O'Callaghan James P. , Miller Diane B. , Pennypacker Keith R. 
Published: October 2006

AbstractSpecific protein phosphorylation pathways have been shown to play a role in cellular adaptation responses underlying addiction to psychostimulants such as methamphetamine and cocaine. Transcriptional regulation through fos‐related antigens constitutes one element through which these dopaminergic agonists exert their persistent actions. In addition to their addictive properties, amphetamines are known to damage dopaminergic nerve terminals. Although not widely appreciated, protein phosphorylation cascades and fos‐related antigens also may play a role in the neurotoxic actions of substituted amphetamines such as methamphetamine. Here we document the involvement of the dopaminoceptive phosphoprotein, DARPP‐32, the fos‐related antigen, FRA‐2, and the growth associated protein kinase, MAP kinase, in the neurotoxic action of known dopaminergic neurotoxicants, including methamphetamine. The addictive and neurotoxic properties of psychostimulants may share some molecular signaling mechanisms.
NAALADase inhibition reduces alcohol consumption in the alcohol‐preferring (P) line of rats
Authors: McKinzie D. L. , Li T.‐K. , McBride W. J. , Slusher B. S. 
Published: October 2006

AbstractN‐acetyl‐aspartyl‐glutamate (NAAG) is a major peptide component of the brain, with millimolar tissue levels of 0.1–5 nmol/mg wet weight. NAAG is hydrolyzed by the enzyme N‐acetylated alpha‐linked acidic dipeptidase (NAALADase; glutamate carboxypeptidase II; EC no. 3.4.17.21) to N‐acetyl‐aspartate (NAA) and glutamate. Recently, a potent and selective NAALADase inhibitor termed 2‐(phosphonomethyl)pentanedioic acid (2‐PMPA) was identified that has a 300 pM Ki for NAALADase inhibition. Given the accumulating evidence indicating an important role of the glutamate system in alcoholism and dependence, the objective of this study was to evaluate the effects of systemic administration of 2‐PMPA (50, 100 and 200 mg/kg; i.p.) upon the ethanol intakes of alcohol‐preferring (P) rats. Female P rats (n = 8) received daily 1‐hour scheduled access to a 10% (v/v) ethanol. In a within‐subjects design, 2‐PMPA treatments were tested once a week. Baseline ethanol drinking consisted of the mean of the 3 days prior to testing in which saline injections were given. Results indicated that, whereas the 200 mg/kg dose of 2‐PMPA had no effect on ethanol intake, both the 50 and 100 mg/kg doses significantly reduced ethanol consumption by approximately 25% (p< 0.05) during the 1‐hour access period. Body weights and 24‐hour water intakes were not altered at any of the doses. These data suggest that the NAAG/NAALADase system may be involved in neuronal systems regulating alcohol‐drinking behavior.
The dopamine D2 receptor (DRD2) gene–a genetic risk factor in heavy smoking?
Authors: Batra Anil , Gelfort Gisbert , Bartels Mathias , Smoltczyk Hanna , Buchkremer Gerhard , Riess Olaf , Schöls Ludger 
Published: October 2006

AbstractIndications of a genetic predisposition to nicotine dependence have been derived from numerous epidemiological data and from individual genetic studies suggesting the involvement of the dopaminergic D2 receptor. Previous association studies defined the TaqlA polymorphism as a risk factor for addiction, in particular for alcoholism and tobacco dependence. Results of investigations into this polymorphism in 110 severely addicted smokers and a control group of 60 population‐matched German non‐smokers did not support these findings. However, our results indicate an association between the DRD2‐Fokl‐1 allele and the onset and intensity of smoking.
REVIEW: Non‐human primate models of inheritance vulnerability to alcohol use disorders
Authors: Barr Christina S. , Goldman David 
Published: October 2006

ABSTRACTMany animal species have been used to model certain aspects of alcohol use and addiction. However, there are complex behavioral and social features of alcohol use disorders that are not easily modeled in animal species. This review considers both the limitations and advantages of using a non‐human primate to model alcohol use disorders and discusses how non‐human primates can be particularly useful for studying how genetic variants interact with social factors, temperament and alcohol response as motivating factors for alcohol consumption and abstinence. Genetic variants in rhesus macaques (Macaca mulatta) that are functionally equivalent to those increasing addiction vulnerability in humans influence temperament, stress reactivity and alcohol response in addition to voluntary alcohol consumption. Non‐human primate models may also have translational value for understanding of how variants within addiction and abuse vulnerability genes influence alcohol‐induced neuroadaptation, neuropathology and treatment response.
PRECLINICAL STUDY: Ghrelin stimulates locomotor activity and accumbal dopamine‐overflow via central cholinergic systems in mice: implications for its involvement in brain reward
Authors: Jerlhag Elisabet , Egecioglu Emil , Dickson Suzanne L. , Andersson Malin , Svensson Lennart , Engel Jörgen A. 
Published: October 2006

ABSTRACTIt is becoming increasingly apparent that there is a degree of neurochemical overlap between the reward systems and those regulating energy balance. We therefore investigated whether ghrelin, a stomach‐derived and centrally derived orexigenic peptide, might act on the reward systems. Central ghrelin administration (1 µg/µL, to the third ventricle) induced an acute increase in locomotor activity as well as dopamine‐overflow in the nucleus accumbens, suggesting that ghrelin can activate the mesoaccumbal dopamine system originating in the ventral tegmental area, a system associated with reward and motivated behaviour. The cholinergic afferents to the ventral tegmental area have been implicated in natural reward and in regulating mesoaccumbal dopamine neurons. The possibility that nicotinic receptors are involved in mediating the stimulatory and dopamine‐enhancing effects of ghrelin is supported by the findings that peripheral injection of the unselective nicotinic antagonist mecamylamine (2.0 mg/kg) blocked these ghrelin‐induced effects. Tentatively, ghrelin may, via activation of the acetylcholine–dopamine reward link, increase the incentive values of signals associated with motivated behaviours of importance for survival such as feeding behaviour. It will be important to discover whether this has therapeutic implications for compulsive addictive behaviours, such as eating behaviour disorders and drug dependence.
GENETIC STUDY: Analysis of variations in the tryptophan hydroxylase‐2 (TPH2) gene in cocaine dependence
Authors: Dahl John P. , Cubells Joseph F. , Ray Riju , Weller Andrew E. , Lohoff Falk W. , Ferraro Thomas N. , Oslin David W. , Kampman Kyle M. , Dackis Charles , Tang Yilang , Gelernter Joel , Kranzler Henry R. , O’Brien Charles P. , Berrettini Wade H. 
Published: October 2006

ABSTRACTWhile the exact physiological mechanisms underlying cocaine dependence remain unclear, a growing body of evidence indicates a role for the serotonergic neurotransmitter system in the pathology of this substance use disorder. The focus of the present study is to determine whether genetic variation in the tryptophan hydroxylase‐2 (TPH2) gene, which encodes the enzyme responsible for synthesis of the majority of the serotonin contained in neurons of the central nervous system, contributes to the pathophysiology of cocaine dependence. To examine this hypothesis, we used a case–control study design in which the genotype and allele distributions for six single nucleotide polymorphisms (SNPs) in the TPH2 gene were compared between cocaine‐dependent (n = 299) and control individuals (n = 208) of African descent. The results indicate that none of the SNPs in the TPH2 gene examined in this study associate with the cocaine‐dependent phenotype. This work suggests that variations in the TPH2 gene are not a risk factor for the development of cocaine dependence, but these findings require confirmation in larger, independent samples of cocaine‐dependent and control subjects.
CLINICAL AND IMAGING STUDY: Enhanced cue‐elicited brain activation in African American compared with Caucasian smokers: an fMRI study
Authors: Okuyemi Kolawole S. , Powell Joshua N. , Savage Cary R. , Hall Sandra B. , Nollen Nicole , Holsen Laura M. , McClernon F. Joseph , Ahluwalia Jasjit S. 
Published: October 2006

ABSTRACTCurrent evidence indicates that, although African Americans (AA) are more likely to attempt to quit smoking than Caucasians (CC) in any given year, success rates are lower for AA. However, factors contributing to these differences are not well known. In order to explore potential factors, this study assessed differences in attention to smoking cues between ethnic groups. Participants underwent morning functional magnetic resonance imaging scanning while viewing images of AA models and CC models who were either smoking (smoking cues) or engaging in everyday activities (neutral cues), interspersed with a fixation baseline period. The study was conducted at the Hoglund Brain Imaging Center of the University of Kansas Medical Center in Kansas City, KS. We studied 17 smokers (eight AA, nine CC) after 12‐hour abstinence and 17 non‐smokers (eight AA, nine CC) matched by age, gender, years of education, and handedness. The AA and CC smoking groups were also matched for number of cigarettes smoked per day. All results are P < 0.01, corrected for whole brain. There was a strong ethnicity by condition interaction among smokers in several a priori regions of interest. AA smokers showed a greater increase in response to smoking (versus neutral cues) than CC smokers in the medial prefrontal cortex, right lateral orbitofrontal cortex, and bilateral ventrolateral prefrontal cortex. In smoking versus baseline contrasts, additional areas of greater activation were found in AA, including the right amygdala and left caudate nucleus. No significant differences in cue‐elicited brain activation were found between AA and CC non‐smokers. These preliminary findings demonstrate variation in brain activation in response to smoking cues between AA and CC smokers in structures known to be associated with nicotine addiction. Differences in neural response may reflect fundamental differences in attention to smoking cues, which may in turn contribute to differences in effectiveness of nicotine dependence treatments among ethnic populations.