bluuebunny/crossref_metadata_2025 huggingface dataset:
Surface soil acidity and fertility in the central-western wheatbelt of New South Wales
Authors: Evans C. M. , Scott B. J.
Published: January 2007

Documentation of the chemical fertility status of the soils is sparse for the western and central-western wheatbelt of New South Wales, Australia. We examined properties of the surface soils (0–10 cm) from central-western NSW by collating two published and nine unpublished datasets of soil analyses representing about 2800 soil samples. The emphasis was on the red soils used extensively for cropping. The surface soils of central-western NSW have low phosphorus (47% of soils) and sulfur (70% of soils <5 mg S/kg using KCl-40 analysis) status and commonly have organic carbon contents of about 1%. Surface soil acidity was a substantial problem with 56% of soils (0–10 cm) having a pHCa <5.0. Sodic and dispersive soils are also of concern in this area and these soils have received little attention or research. Approximately 5% of surface (0–10 cm) soils had an exchangeable sodium percentage of ≥6% (sodic). Salinity of surface soils was of minor significance compared with other soil problems in the area, although isolated areas occur. These results indicated that lime applications in this area are likely to benefit crop and pasture production. Additional use of phosphorus and sulfur fertilisers and agricultural practices which increase or maintain organic carbon will also need to be adopted to improve pasture and crop production. The use of gypsum and/or lime on sodic soils may also need to be addressed. As a priority, we suggest that the benefits of lime application to crop yield be examined. The application of lime to the 0–10 cm soil depth should ultimately arrest acidification of the subsurface soil (10–20 cm depth) through downward movement of the lime effect. Further examination of gypsum applications to dispersive sodic soils and the evaluation of sulfur deficiency in the field for pastures and canola are also priority areas of likely agricultural relevance.
Perioperative Cardiac Arrests in Children between 1988 and 2005 at a Tertiary Referral Center
Authors: Flick Randall P. , Sprung Juraj , Harrison Tracy E. , Gleich Stephen J. , Schroeder Darrell R. , Hanson Andrew C. , Buenvenida Shonie L. , Warner David O.
Published: January 2007

Background

The objective of this study was to determine the incidence and outcome of perioperative cardiac arrest (CA) in children younger than 18 yr undergoing anesthesia for noncardiac and cardiac procedures at a tertiary care center.

Methods

After institutional review board approval (Mayo Clinic, Rochester, Minnesota), all patients younger than 18 yr who had perioperative CA between November 1, 1988, and June 30, 2005, were identified. Perioperative CA was defined as a need for cardiopulmonary resuscitation or death during anesthesia care. A cardiac procedure was defined as a surgical procedure involving the heart or great vessels requiring an incision.

Results

A total of 92,881 anesthetics were administered during the study period, of which 4,242 (5%) were for the repair of congenital heart malformations. The incidence of perioperative CA during noncardiac procedures was 2.9 per 10,000, and the incidence during cardiac procedures was 127 per 10,000. The incidence of perioperative CA attributable to anesthesia was 0.65 per 10,000 anesthetics, representing 7.5% of the 80 perioperative CAs. Both CA incidence and mortality were highest among neonates (0-30 days of life) undergoing cardiac procedures (incidence: 435 per 10,000; mortality: 389 per 10,000). Regardless of procedure type, most patients who experienced perioperative CA (88%) had congenital heart disease.

Conclusion

The majority of perioperative CAs were caused by factors not attributed to anesthesia, in distinction to some recent reports. The incidence of perioperative CA is many-fold higher in children undergoing cardiac procedures, suggesting that definition of case mix is necessary to accurately interpret epidemiologic studies of perioperative CA in children.
Telescoping Tracheal Tubes into Catheters Minimizes Epistaxis during Nasotracheal Intubation in Children
Authors: Watt Stacey , Pickhardt Don , Lerman Jerrold , Armstrong James , Creighton Paul R. , Feldman Leeshy
Published: January 2007

Background

Numerous strategies have been used to reduce epistaxis after nasotracheal intubation. The authors compared the severity of epistaxis after nasotracheal intubation in children with tubes at room temperature, warm tubes, and tubes telescoped into catheters.

Methods

Children who were scheduled for elective dental surgery were randomly assigned to undergo nasotracheal intubation using a tube at room temperature (control), warmed in saline, or whose distal end had been telescoped into a red rubber catheter. After an inhalational induction and intravenous propofol, a lubricated tube or red rubber catheter was inserted into the right naris. Tracheal intubation was achieved by direct laryngoscopy and tube placement using Magill forceps. The pharynx was swabbed for blood by an observer who was blind to the treatment. The severity of bleeding was rated using reference figures. Data were analyzed using Kruskal-Wallis and Fisher exact tests. P < 0.05 was accepted.

Results

The demographics of the three groups were similar. The estimated median area of the gauze in the catheter group that was covered with blood (0%) was significantly less than the areas in the control (40%) and warm (20%) groups. The incidence of clinically relevant bleeding (>or= 40% of the gauze area covered in blood) in the catheter group (5%) was significantly less than in the control (56%) and warm (39%) groups. The incidence of no detectable blood in the catheter group (59%) was significantly greater than in the control (21%) and warm (26%) groups.

Conclusions

Telescoping the endotracheal tube into a catheter significantly reduces epistaxis in children undergoing nasotracheal intubation.
Risk Factors for the Occurrence of Electroencephalogram Abnormalities during Induction of Anesthesia with Sevoflurane in Nonepileptic Patients
Authors: Julliac Benjamin , Guehl Dominique , Chopin Fabrice , Arne Pierre , Burbaud Pierre , Sztark François , Cros Anne-Marie
Published: January 2007

Background

The aim of this prospective study was to determine the risk factors of epileptiform discharge during induction with sevoflurane in healthy adult patients.

Methods

Forty adult patients with American Society of Anesthesiologists physical status I were randomly allocated to one of four groups. Group A: Patients breathed 8% sevoflurane in oxygen (8 l/min) via a prefilled circuit. End-tidal sevoflurane was maintained at 4%. Tracheal intubation was performed at the third minute after cisatracurium injection. Group B: The anesthesia protocol was similar, but a vital capacity technique was performed. Group C: Patients were anesthetized as in group A but were hyperventilated. Group D: Patients were anesthetized as in group A, but end-tidal sevoflurane was maintained at 2%. An electroencephalogram was recorded before and during induction up to 11 min after the start of induction. Statistical analysis was performed with Statview 5.0 (SAS Institute Inc., Cary, NC) for multivariate analysis.

Results

Twelve patients experienced epileptiform discharges. Risk factors were female sex (odds ratio, 12.60; 95% confidence interval, 1.46-135), delay to the occurrence of beta waves (odds ratio, 0.92; 95% confidence interval, 0.86-0.99), and end-tidal sevoflurane (odds ratio, 8.78; 95% confidence interval, 1.12-69). Epileptiform discharges were not associated with significant hemodynamic or Bispectral Index variations.

Conclusion

Induction with sevoflurane may result in epileptiform electroencephalographic activity. Only electroencephalographic monitoring allows the diagnosis. Risk factors are mainly female sex, short delay to onset of anesthesia, and high alveolar sevoflurane concentration. Induction with high sevoflurane concentration is controversial mainly in women.
Sevoflurane Inhalation at Sedative Concentrations Provides Endothelial Protection against Ischemia–Reperfusion Injury in Humans
Authors: Lucchinetti Eliana , Ambrosio Sandro , Aguirre José , Herrmann Patrick , Härter Luc , Keel Marius , Meier Thomas , Zaugg Michael
Published: January 2007

Background

Endothelial cells can be protected against cytokine-induced toxicity by volatile anesthetics. The authors tested whether inhalation of sevoflurane at subanesthetic concentrations provides protection against postocclusive endothelial dysfunction induced by ischemia-reperfusion injury of the forearm in humans.

Methods

Five healthy male volunteers were enrolled in this study with crossover design. Each subject was randomly exposed to 15 min of forearm ischemia in the presence or absence of sevoflurane. Sevoflurane was inhaled at 0.5-1 vol% end-tidal concentrations from 15 min before ischemia until 5 min after the onset of reperfusion. Hyperemic reaction, an indicator of ischemic injury and endothelial function, was determined at 15 and 30 min of reperfusion using venous occlusion plethysmography. Also, markers of leukocyte activation (CD11b, CD42b) were measured by flow cytometry during reperfusion.

Results

Fifteen minutes of forearm ischemia followed by reperfusion diminished postocclusive endothelium-dependent hyperemic reaction at 15 and 30 min of reperfusion. Peri-ischemic inhalation of sevoflurane, targeted at 0.5-1 vol% end-tidal concentrations, markedly improved postocclusive hyperemic reaction. In addition, inhalation of sevoflurane attenuated activation of leukocytes, as measured by CD11b expression, after ischemia-reperfusion injury. No changes in CD42b expression were observed after ischemia-reperfusion of the forearm.

Conclusions

These data suggest that human endothelium, a key component of all vital organs, is receptive to protection by sevoflurane in vivo. Peri-ischemic administration of sevoflurane mimics a combination of pharmacologic preconditioning and postconditioning and protects at even low sedative concentrations (< 1 vol%). Inhibition of leukocyte adhesion is likely to be involved in the protection.
Intraoperative Awareness in a Regional Medical System
Authors: Pollard Richard J. , Coyle Joseph P. , Gilbert Richard L. , Beck Janet E.
Published: January 2007

Background

Intraoperative awareness in patients undergoing general anesthesia is an infrequent but well-described adverse outcome. The reported incidence of this phenomenon is between 0.1% and 0.9%.

Methods

With institutional review board approval, the authors reviewed continuous quality improvement data from 3 yr (2002-2004) at the locations where the physician group provided anesthesia. Board-certified anesthesiologists supervising certified registered nurse anesthetists in the anesthesia care team model of practice delivered all anesthetics. Brain function monitors were not used in the operating room setting. Patients were interviewed twice during a 48-h postoperative period and, as part of that process, underwent a modified Brice interview to determine intraoperative awareness. All cases that met the criteria for awareness were examined by the continuous quality improvement committee to modify anesthetic practice and were included in this study.

Results

Data from 211,842 patients undergoing anesthesia were considered. Of these, the continuous quality improvement process followed up 177,468 (83.1%). Cases were not included in the study if the patient was younger than 18 yr, did not have a general anesthetic, or had a terminal event during the hospital course. By these criteria, a total of 87,361 patients followed by the continuous quality improvement process were at risk for awareness. Six patients reported instances of recall.

Conclusion

The incidence of intraoperative awareness in this large sample of patients from a regional medical center undergoing general anesthesia was 0.0068%, or 1 per 14,560 patients, substantially less than that reported in the recent literature.
Inhaled Nitric Oxide Attenuates Reperfusion Inflammatory Responses in Humans
Authors: Mathru Mali , Huda Ruksana , Solanki Daneshvari R. , Hays Stephen , Lang John D.
Published: January 2007

Background

Reduced bioavailability of endothelium-derived nitric oxide associated with reperfusion could potentially exacerbate the inflammatory response during reperfusion. Evidence suggests the pharmacologic effects of inhaled nitric oxide may extend beyond the pulmonary vasculature, and this is attributed to nitric oxide-derived complexes in blood that ultimately orchestrate antiinflammatory effects. In this study, the authors evaluated the potential for inhaled nitric oxide (80 ppm) to attenuate inflammation instigated by ischemia-reperfusion in a human model using patients undergoing knee surgery where a tourniquet was used to produce a bloodless surgical field.

Methods

Inhaled nitric oxide (80 ppm) was administered before tourniquet application and continued throughout reperfusion until the completion of surgery. Venous blood samples were collected before and after reperfusion, for the measurements of nitrate and nitrite, CD11b/CD18, soluble P-selectin, and lipid hydroperoxide. Muscle biopsies were obtained from the quadriceps muscle before skin closure and analyzed for myeloperoxide, conjugated dienes, and nuclear factor-kappaB translocation.

Results

Administration of inhaled nitric oxide (80 ppm) significantly attenuated the inflammatory response characterized by reduced expression of CD11b/CD18, P-selectin, and nuclear factor kappaB compared with the control group. This was accompanied by increased plasma levels of nitrate and nitrite and reduced oxidative stress.

Conclusions

Administration of inhaled nitric oxide at 80 ppm significantly reduces inflammation in lower extremity ischemia-reperfusion in humans. This observation supports the concept that during diseases characterized by dysfunction in nitric oxide metabolism, inhaled nitric oxide may be an effective therapy to replenish systemic nitric oxide, thus retarding inflammatory-mediated injury.
Effective Reversal of Moderate Rocuronium- or Vecuronium-induced Neuromuscular Block with Sugammadex, a Selective Relaxant Binding Agent
Authors: Suy Koen , Morias Karl , Cammu Guy , Hans Pol , van Duijnhoven Wilbert G. F. , Heeringa Marten , Demeyer Ignace
Published: January 2007

Background

Sugammadex rapidly reverses rocuronium-induced neuromuscular block. This study explored the dose-response relation of sugammadex given as a reversal agent at reappearance of the second muscle twitch after rocuronium- and vecuronium-induced block. A secondary objective was to investigate the safety of single doses of sugammadex.

Methods

In this two-center, phase II, dose-finding study, 80 patients (age >or= 18 yr, American Society of Anesthesiologists physical status I or II, surgery >or= 60 min requiring muscle relaxation for intubation) were randomly assigned to receive rocuronium (0.60 mg/kg) or vecuronium (0.10 mg/kg). Sugammadex or placebo was administered at reappearance of the second muscle twitch. The primary efficacy endpoint was time from starting sugammadex administration until recovery of the train-of-four ratio to 0.9.

Results

Compared with placebo, sugammadex produced dose-dependent decreases in mean time to recovery for all train-of-four ratios in the rocuronium and vecuronium groups. The mean time for recovery of the train-of-four ratio to 0.9 in the rocuronium group was 31.8 min after placebo compared with 3.7 and 1.1 min after 0.5 and 4.0 mg/kg sugammadex, respectively. The mean time for recovery of the train-of-four ratio to 0.9 in the vecuronium group was 48.8 min after placebo, compared with 2.5 and 1.4 min after 1.0 and 8.0 mg/kg sugammadex, respectively. Sugammadex was well tolerated.

Conclusion

Sugammadex rapidly reversed rocuronium- or vecuronium-induced neuromuscular block at reappearance of the second muscle twitch and was well tolerated. A dose-response relation was observed with sugammadex for reversal of both rocuronium- and vecuronium-induced neuromuscular block.
Effect of Combined Anticoagulation Using Heparin and Bivalirudin on the Hemostatic and Inflammatory Responses to Cardiopulmonary Bypass in the Rat
Authors: Welsby Ian J. , Jones Wilbert L. , Arepally Gowthami , De Lange Fellery , Yoshitani Kenji , Phillips-Bute Barbara , Grocott Hilary P. , Becker Richard , Mackensen G Burkhard
Published: January 2007

Background

Despite high-dose heparin anticoagulation, cardiopulmonary bypass (CPB) is still associated with marked hemostatic activation. The purpose of this study was to determine whether a reduced dose of bivalirudin, added as an adjunct to heparin, would reduce thrombin generation and circulating markers of inflammatory system activation during CPB as effectively as full-dose bivalirudin, without adversely affecting postoperative hemostasis.

Methods

Using a model of normothermic CPB in rats, the authors prospectively compared markers of thrombin generation (thrombin-antithrombin complexes) and inflammatory markers (tumor necrosis factor alpha, interleukin 1beta, interleukin 6, and interleukin 10) in three groups: conventional high-dose heparin (H), full-dose bivalirudin (B), and a combined group (standard high-dose heparin with the addition of reduced dose bivalirudin or H&B), at baseline, after 60 min of CPB, and 60 min after CPB. Postoperative hemostasis was also assessed.

Results

Groups H&B and B showed reduced thrombin-antithrombin complex formation during CPB compared with group H (P = 0.0003), and this persisted after CPB for group B (P = 0.009). Perioperative increases in interleukin 6 and interleukin 10 showed a trend toward being reduced in animals receiving bivalirudin (P = 0.06). Evidence of residual anticoagulation was found in group H&B as measured by activated clotting time (P = 0.04) and activated partial thromboplastin time (P = 0.02), but no intergroup difference in primary hemostasis was found.

Conclusions

Bivalirudin attenuates hemostatic activation during experimental CPB with potential effects on markers of the inflammatory response. However, with this dosing regimen, the combination of heparin and bivalirudin does not seem to confer any measurable advantages over full-dose bivalirudin anticoagulation.
Propofol Modulates Na+–Ca2+Exchange Activity via Activation of Protein Kinase C in Diabetic Cardiomyocytes
Authors: Wickley Peter J. , Shiga Toshiya , Murray Paul A. , Damron Derek S.
Published: January 2007

Background

The authors' objective was to identify the role of the Na+-Ca2+ exchanger (NCX) in mediating the contractile dysfunction observed in diabetic cardiomyocytes before and after exposure to propofol.

Methods

Freshly isolated ventricular myocytes were obtained from normal and diabetic rat hearts. Intracellular concentration of Ca2+ and cell shortening were simultaneously measured in electrically stimulated, ventricular myocytes using fura-2 and video-edge detection, respectively. Postrest potentiation (PRP) and sarcoplasmic reticulum Ca2+ load were used to assess propofol-induced changes in the activity of the NCX.

Results

Propofol (10 microM) increased PRP in diabetic cardiomyocytes but had no effect on PRP in normal cardiomyocytes. Removal of sodium enhanced and KB-R7943 (reverse mode NCX inhibitor) blocked PRP in both normal and diabetic cardiomyocytes. In the absence of sodium, propofol enhanced PRP in diabetic cardiomyocytes but had no additional effect in normal cardiomyocytes. KB-R7943 completely blocked propofol-induced potentiation of peak intracellular concentration of Ca2+ and shortening in both cell types. Propofol increased sarcoplasmic reticulum Ca2+ load and prolonged removal of cytosolic Ca2+ in diabetic cardiomyocytes, but not in normal cardiomyocytes. Removal of sodium enhanced propofol-induced increases in sarcoplasmic reticulum Ca2+ load and further prolonged removal of cytosolic Ca2+, whereas KB-R7943 completely blocked propofol-induced increase in sarcoplasmic reticulum Ca2+ load. Protein kinase C inhibition with bisindolylmaleimide I prevented the propofol-induced increase in PRP and prolongation in Ca2+ removal.

Conclusions

These data suggest that propofol enhances PRP via activation of reverse mode NCX, but attenuates Ca2+ removal from the cytosol via inhibition of forward mode NCX in diabetic cardiomyocytes. The actions of propofol are mediated via a protein kinase C-dependent pathway.
Opioid Self-administration in the Nerve-injured Rat
Authors: Martin Thomas J. , Kim Susy A. , Buechler Nancy L. , Porreca Frank , Eisenach James C.
Published: January 2007

Background

Neuropathic pain is associated with several sensory abnormalities, including allodynia as well as spontaneous pain. Opioid intake in neuropathic pain patients is motivated by alleviation of both pain and allodynia. However, laboratory animal studies rely almost exclusively on reflexive withdrawal measures of allodynia. The authors examined the pharmacology of self-regulated intake of opioids in rats with or without nerve injury and compared the rate of drug intake to reversal of allodynia.

Methods

Rats were implanted with intravenous catheters, and the L5 and L6 spinal nerves were ligated in half of these animals. Rats were then trained to self-administer a commonly abused opioid (heroin) and commonly prescribed opioids (morphine, fentanyl, hydromorphone, and methadone). In addition, rats trained to self-administer heroin were given either clonidine or adenosine spinally before self-administration sessions to assess opioid-sparing effects.

Results

Nerve injury significantly decreased the reinforcing effects of low doses of opioids, and only doses of each opioid that reduced mechanical hypersensitivity maintained self-administration after spinal nerve ligation. The rate of drug consumption was correlated with the duration of the antiallodynic effect for each dose of opioid. Intrathecal administration of clonidine or adenosine reversed mechanical hypersensitivity, but only clonidine reduced heroin self-administration in rats with spinal nerve ligation.

Conclusion

Opioid self-administration is significantly altered by nerve injury, with rate of drug intake being correlated with reversal of allodynia. Intrathecal clonidine, but not adenosine, produces opioid-sparing effects in self-administering rats. The neurobiologic mechanisms that regulate opioid consumption in rats therefore seem to be altered after nerve injury.
A Computer Model of Electrical Stimulation of Peripheral Nerves in Regional Anesthesia
Authors: Johnson Chad R. , Barr Roger C. , Klein Stephen M.
Published: January 2007

Background

Nerve stimulation for regional anesthesia can be modeled mathematically. The authors present a mathematical framework to model the underlying electrophysiology, the development of software to implement that framework, and examples of simulation results.

Methods

The mathematical framework includes descriptions of the needle, the resulting potential field, and the active nerve fiber. The latter requires a model of the individual membrane ionic currents. The model geometry is defined by a three-dimensional coordinate system that allows the needle to be manipulated as it is clinically and tracked in relation to the nerve fiber. The skin plane is included as an electrical boundary to current flow. The mathematical framework was implemented in the Matlab (The MathWorks, Natick, MA) computing environment and organized around a graphical user interface. Simulations were performed using an insulated needle or an uninsulated needle inserted perpendicular to the skin with the nerve fiber at a depth of 2 cm. For each needle design, data were obtained with the needle as cathode or anode. Data are presented as current-distance maps that highlight combinations of current amplitude and tip-to-nerve distance that evoked a propagated response.

Results

With the needle tip positioned 2 mm proximal to the depth of the nerve, an insulated needle required a current greater than 0.457 mA for impulse propagation when attached to the cathode; when attached to the anode, the minimal current was 2.354 mA. In the same position, an uninsulated needle attached to the cathode required a current greater than 2.395 mA to generate a response. However, when an uninsulated needle was attached to the anode, currents up to 7 mA were inadequate to produce a propagated response. Of particular interest were combinations of current amplitude and needle position that activated the fiber but blocked impulse propagation for cathodal stimulation.

Conclusions

Mathematical modeling of nerve stimulation for regional anesthesia is possible and could be used to investigate new equipment or needle designs, test nerve localization protocols, enhance clinical and experimental data, and ultimately generate new hypotheses.
Neosaxitoxin as a Local Anesthetic
Authors: Rodriguez-Navarro Alberto J. , Lagos Nestor , Lagos Marcelo , Braghetto Italo , Csendes Attila , Hamilton James , Figueroa Cristian , Truan Dominique , Garcia Carlos , Rojas Andres , Iglesias Veronica , Brunet Luis , Alvarez Francisco
Published: January 2007

Background

Neosaxitoxin is a phycotoxin that reversibly blocks the voltage-gated sodium channels at the neuronal level. Its activity results in blocking the axonal conduction, stopping the propagation of the nerve impulse. The objective of the present work was to evaluate neosaxitoxin as a local anesthetic in a human trial.

Methods

The authors conducted a randomized, double-blind, placebo-controlled trial with 10 healthy volunteers. Subcutaneous injections were made in the middle posterior skin of the calf: one leg received 50 microg neosaxitoxin, and the contra-lateral leg received placebo. The anesthetic effect was evaluated using a standardized human sensory and pain model. TSA II Neurosensory Analyzer (Medoc Ltd, Minneapolis, MN) and von Frey technique were used to evaluate five parameters: sensory threshold for warm and cold, pain thresholds for heat and cold, and mechanical touch perception threshold. Measurements were made 0, 1, 3, 6, 9, 12, 16, 24, and 48 h after the injections.

Results

For all the patients, effective and complete blocking of the evaluated parameters was obtained. As the blocking began to revert gradually, heat pain was the first to return to normal values after 3 h. Cold pain was the longest sensation abolished, achieving 24 h of blockade. The toxin was undetected in blood and urine samples. No adverse reactions to neosaxitoxin were detected.

Conclusions

Neosaxitoxin showed an effective local anesthetic effect when injected in the subcutaneous plane. The efficacy of a 50-microg dose of neosaxitoxin was shown. This is the first report of neosaxitoxin as a local anesthetic in a human trial.
Influence of Patient and Hospital Characteristics on Anesthesia Time in Medicare Patients Undergoing General and Orthopedic Surgery
Authors: Silber Jeffrey H. , Rosenbaum Paul R. , Zhang Xuemei , Even-Shoshan Orit
Published: January 2007

Background

Procedure time is a clinically important variable that is often analyzed when studying quality and efficiency. Norms for procedure length have not been reported from Medicare data sets, nor has the influence of patient and hospital characteristics on procedure time been estimated using Medicare data.

Methods

The authors obtained Medicare claims on all patients aged 65-85 years who underwent general surgical and orthopedic surgical procedures in Pennsylvania. Anesthesia procedure time was estimated from anesthesia time units bills supplied from Medicare on 20 common general and orthopedic surgery procedures, and models to determine the influence of hospital and patient characteristics were developed.

Results

Of the 77,638 patients, 31,472 had general surgery and 46,166 underwent orthopedic procedures. The median anesthesia time for general surgery was 133 min, and for orthopedic surgery it was 146 min. After adjusting for principal procedure, hospital, and physiologic severity, covariates associated with increased anesthesia time included: multiple procedure on same day + 18.3 min (P < 0.0001); transfer-in + 6.7 min (P = 0.0002); black race + 5.5 (P < 0.0001); coagulation disorders + 4.9 (P = 0.0012); and paraplegia + 4.5 (P = 0.0006). Lower-income black patients had significantly longer procedure times than lower-income white patients (+ 7 min; P < 0.0001). Among the 15 hospitals with the largest black surgical populations, 5 hospitals had statistically significant procedure lengths for black versus white patients, ranging from + 9 to + 16 min.

Conclusions

In addition to variation by patient comorbidities and procedure, anesthesia procedure time varies with hospital, medical history, and sociodemographic characteristics.
General Anesthetics and Vascular Smooth Muscle
Authors: Akata Takashi , Warltier David C.
Published: January 2007

General anesthetics threaten cardiovascular stability by causing changes in cardiac function, vascular reactivity, and cardiovascular reflexes and significantly alter distribution of cardiac output to various organs. Their overall impact is often systemic hypotension, which is attributable to myocardial depression, peripheral vasodilation, and attenuated sympathetic nervous system activity. However, one could be more causative than the others, depending on anesthetic agents and cardiovascular factors inherent in patients (e.g., coexisting heart disease). It is generally believed that most general anesthetics attenuate sympathetic nervous system outflow from the central nervous system, thereby decreasing vascular resistance in peripheral circulations. Indeed, in previous in vivo studies, during administration of various general anesthetics, vascular resistance was decreased in most peripheral circulations; however, it was unaffected or increased in some peripheral circulations. General anesthetics may act directly on vascular smooth muscle and/or endothelial cells in various vascular beds, influencing total peripheral and/or regional vascular resistance, and hence organ blood flow. This article reviews previously reported direct (i.e., nonneural) vascular actions of general anesthetics and discusses their underlying mechanisms, their in vivo relevance, and the future of research for general anesthetic vascular pharmacology.
The psychological science of addiction
Authors: Gifford Elizabeth , Humphreys Keith
Published: January 2007

Aim  To discuss the contributions and future course of the psychological science of addiction.

Background  The psychology of addiction includes a tremendous range of scientific activity, from the basic experimental laboratory through increasingly broad relational contexts, including patient–practitioner interactions, families, social networks, institutional settings, economics and culture. Some of the contributions discussed here include applications of behavioral principles, cognitive and behavioral neuroscience and the development and evaluation of addiction treatment. Psychology has at times been guilty of proliferating theories with relatively little pruning, and of overemphasizing intrapersonal explanations for human behavior. However, at its best, defined as the science of the individual in context, psychology is an integrated discipline using diverse methods well‐suited to capture the multi‐dimensional nature of addictive behavior.

Conclusions  Psychology has a unique ability to integrate basic experimental and applied clinical science and to apply the knowledge gained from multiple levels of analysis to the pragmatic goal of reducing the prevalence of addiction.
Predictors of mortality among injecting and non‐injecting HIV‐negative drug users in northern Thailand
Authors: Quan Vu Minh , Vongchak Tasanai , Jittiwutikarn Jaroon , Kawichai Surinda , Srirak Namtip , Wiboonnatakul Kanokporn , Razak Myat Htoo , Suriyanon Vinai , Celentano David D.
Published: January 2007

Aims  To estimate mortality rates among HIV‐negative injecting drug users (IDUs) and non‐injecting drug users (non‐IDUs), and to assess predictors for mortality among the IDUs.

Design  Prospective cohort study in northern Thailand with 2‐year follow‐up.

Setting  IDUs and non‐IDUs who were admitted for detoxification treatment for opiate or amphetamine dependence in a regional drug treatment center were screened. After discharge, HIV‐negative individuals were followed‐up in the community.

Participants  A total of 821 HIV‐negative drug users [346 IDUs (42%) and 475 non‐IDUs, median age = 32; 51% were ethnic minorities].

Measurements  All‐cause mortality.

Findings  There were 33 deaths over 1360 person‐years of follow‐up. The all‐cause mortality rate was 39 per 1000 person‐years among IDUs [standardized mortality ratio (SMR) = 13.9], and was 14 per 1000 person‐years among non‐IDUs (SMR = 4.4). Among male IDUs, the hazards for all‐cause deaths were ethnic minority status [adjusted hazard ratio (HR) = 2.9, 95% CI = 1.2–7.2], incident HIV infection (HR = 2.8, 95% CI = 1.1–7.7) and longer duration of drug injection (HR = 1.07, 95% CI = 1.01–1.14).

Conclusions  The mortality among IDUs is high. Being from an ethnic minority, recent HIV acquisition, and a greater number of years of drug injection are predictors of mortality among the IDUs in this region.
Seed dispersal and recruitment limitation are barriers to native recolonization of old‐fields in western Australia
Authors: STANDISH R. J. , CRAMER V. A. , WILD S. L. , HOBBS R. J.
Published: January 2007

Native recolonization of abandoned farmland in the wheat‐growing region of western Australia is slow to non‐existent, even 45 years after abandonment. Instead, old‐fields tend to be dominated by non‐native annual grasses. The native vegetation in the region is highly fragmented. We predicted that recovery is limited by seed availability and recruitment failure.

We compared the seed rain, soil seed bank and extant vegetation of three old‐fields and three adjacent native woodland remnants to test our predictions.

Seed dispersal limitation was evident at two old‐fields: species richness of the native seed in the soil seed bank declined at 50‐m increments (i.e. 0 m, 50 m and 100 m) into the old‐fields. Species richness of recolonizing native vegetation also declined along this transect.

Recruitment limitation was evident at one old‐field, probably linked to the few abundant non‐native species that dominated the vegetation. These non‐natives dominated the seed supply, and tended to germinate more rapidly than the native seeds.

In contrast, seed dispersal and recruitment had not limited native recolonization of the third old‐field: 91% of the species present in the adjacent remnant had recolonized this old‐field. Species richness and abundance of non‐natives in the seed supply and extant vegetation were minor compared with that of the other old‐fields. Therefore an adequate seed supply of natives, the lack of non‐natives and chance natural disturbance events (i.e. cyclone and fire) had probably contributed to this result.

Synthesis and applications. Native recolonization of wheatbelt old‐fields is contingent upon the unusual coincidence of seed availability, favourable conditions for recruitment and an absence of competitive non‐natives. Grasses, annual herbs and Acacia shrubs are dominant among the few native species that have consistently recolonized these old‐fields. In most cases, direct seeding and control of non‐natives are the minimum requirements for restoration of wheatbelt old‐fields to species‐rich eucalypt woodlands.
One‐year adherence to clinic visits after highly active antiretroviral therapy: a predictor of clinical progress in HIV patients
Authors: Park W. B. , Choe P. G. , Kim S.‐H. , Jo J. H. , Bang J. H. , Kim H. B. , Kim N. J. , Oh M. , Choe K. W.
Published: January 2007

Objective.  To determine whether adherence to clinic visits early after initiation of highly active antiretroviral therapy (HAART) is predictive of long‐term clinical outcome.

Design.  Observational cohort study.

Setting.  A tertiary referral hospital.

Subjects.  A total of 387 adult HIV patients who were followed for at least 1 year after initiation of HAART between January 1998 and December 2004.

Main outcome measurements.  The effect of 1‐year adherence to clinic visits on the occurrence of new AIDS‐defining illness or death was assessed using Kaplan–Meier survival estimates, and hazard ratios were estimated using Cox proportional hazards regression model.

Results.  Multivariate analysis revealed that advanced clinical stage, fewer new drugs in HAART, and longer total elapsed time without clinical visits for 1 year after HAART were all significant risk factors for the occurrence of new AIDS‐defining illnesses or death. Compared with no missed visits, the hazard ratio adjusted by clinical stage and number of new drugs in HAART was 2.87 (95% confidence interval [CI], 1.34–6.16, P = 0.007) for one missed appointment, 4.37 (95% CI: 1.74–10.98, P = 0.002) for two, and 8.19 (95% CI: 2.95–22.78, P < 0.001) for three or more.

Conclusion.  Adherence to clinic visits early after initiation of HAART is an independent predictor for long‐term clinical progression in HIV patients.
Effects of rotating shift work on biomarkers of metabolic syndrome and inflammation
Authors: Sookoian S. , Gemma C. , Fernández Gianotti T. , Burgueño A. , Alvarez A. , González C. D. , Pirola C. J.
Published: January 2007

Objective.  The major function of the circadian system is the internal cycling of physiological and metabolic events. The present study sought to explore the effect of rotating shift work schedule on leucocyte count and its relationship with risk factors of metabolic syndrome (MS).

Design and participants.  From a population‐based design, 1351 men of self‐reported European ancestry were included in a cross‐sectional study: 877 day workers were compared with 474 rotating shift workers. Medical history, health examination including anthropometric and arterial blood pressure measurements, a questionnaire on health‐related behaviours and biochemical determinations was given to all participants.

Results.  In comparison with day workers, rotating shift workers had elevated (mean ± SE) body mass index (27.1 ± 0.3 vs. 26.3 ± 0.2, P < 0.0154), waist‐hip ratio (0.95 ± 0.01 vs. 0.93 ± 0.01, P < 0.00024), diastolic arterial blood pressure (78 ± 1 vs. 76 ± 1, P < 0.033), fasting insulin (65.5 ± 2.9 vs. 55.9 ± 1.9 pmol L−1, P < 0.017), Homeostasis Model Assessment index (2.12 ± 0.11 vs. 1.77 ± 0.07, P < 0.0027), triglycerides (1.71 ± 0.1 vs. 1.5 ± 0.1 mmol L−1, P < 0.002), uric acid (292.7 ± 2.8 vs. 282 ± 3.4 μmol L−1, P < 0.01) and leucocyte count (7030 ± 84 vs. 6730 ± 58, P < 0.0094). In multiple regression analysis, leucocyte count was correlated with rotating shift work independently of age, smoking, education and components of MS.

Conclusion.  The odds ratio for MS in rotating shift workers compared with day workers was 1.51 (95% CI 1.01–2.25), independently of age and physical activity. Increased leucocyte count, a biological marker of systemic inflammation, was associated with rotating shift work.
Loss of cell wall alpha(1‐3) glucan affects Cryptococcus neoformans from ultrastructure to virulence
Authors: Reese Amy J. , Yoneda Aki , Breger Julia A. , Beauvais Anne , Liu Hong , Griffith Cara L. , Bose Indrani , Kim Myoung‐Ju , Skau Colleen , Yang Sarah , Sefko Julianne A. , Osumi Masako , Latge Jean‐Paul , Mylonakis Eleftherios , Doering Tamara L.
Published: January 2007

Yeast cell walls are critical for maintaining cell integrity, particularly in the face of challenges such as growth in mammalian hosts. The pathogenic fungus Cryptococcus neoformans additionally anchors its polysaccharide capsule to the cell surface via α(1‐3) glucan in the wall. Cryptococcal cells disrupted in their alpha glucan synthase gene were sensitive to stresses, including temperature, and showed difficulty dividing. These cells lacked surface capsule, although they continued to shed capsule material into the environment. Electron microscopy showed that the alpha glucan that is usually localized to the outer portion of the cell wall was absent, the outer region of the wall was highly disorganized, and the inner region was hypertrophic. Analysis of cell wall composition demonstrated complete loss of alpha glucan accompanied by a compensatory increase in chitin/chitosan and a redistribution of beta glucan between cell wall fractions. The mutants were unable to grow in a mouse model of infection, but caused death in nematodes. These studies integrate morphological and biochemical investigations of the role of alpha glucan in the cryptococcal cell wall.
Shaping the Borrelia burgdorferi genome: crystal structure and binding properties of the DNA‐bending protein Hbb
Authors: Mouw Kent W. , Rice Phoebe A.
Published: January 2007

The genome of the Lyme disease‐causing spirochete Borrelia burgdorferi encodes only a single polypeptide from the integration host factor (IHF)/HU or ‘DNABII’ family of nucleoid‐associated proteins – Hbb. DNABII proteins induce large bends in DNA and serve as architectural factors in a variety of prokaryotic cellular processes. We have solved the crystal structure of an Hbb–DNA complex in which the DNA is bent by over 180°. We find that like IHF, Hbb relies exclusively on indirect readout to recognize its cognate site. Additional binding studies show that the sequence preferences of Hbb are related to, yet distinct from those of IHF. Defining these binding characteristics may help to uncover additional roles for Hbb in Borrelia DNA metabolism as well as further our understanding of the mechanism of indirect readout.
Plasmodium falciparum var gene expression is developmentally controlled at the level of RNA polymerase II‐mediated transcription initiation
Authors: Kyes Sue , Christodoulou Zóe , Pinches Robert , Kriek Neline , Horrocks Paul , Newbold Chris
Published: January 2007

The Plasmodium falciparum var gene family codes for a major virulence factor in this most lethal of human malaria parasites. A single var protein variant type is expressed on each infected red blood cell, with antigenic variation allowing progeny parasites to escape host immune detection. The control of mutually exclusive var gene expression in the parasite relies on in situ epigenetic changes. Whether control of expression occurs at transcription initiation or post transcription, however, remains to be established. Recent evidence supports existence of a unique var transcription site at the nuclear periphery containing the dominantly expressed var gene, although silent var genes can colocalize to the same region. We demonstrate here that exclusive var gene expression is controlled at the level of transcription initiation during ring stages and that var genes are transcribed by RNA polymerase II. This represents another example where P. falciparum differs from the paradigm for antigenic variation, Trypanosoma brucei.
Artificial regulation of ospC expression in Borrelia burgdorferi
Authors: Gilbert Michael A. , Morton Elizabeth A. , Bundle Sharyl F. , Samuels D. Scott
Published: January 2007

Outer surface lipoprotein (Osp) C is a virulence factor required for transmission of the Lyme disease agent, Borrelia burgdorferi. We have constructed an inducible promoter system to study the function and regulation of OspC by integrating regulatory elements from the Escherichia coli lac operon into the B. burgdorferi genome. An inducible promoter (flacp) was constructed by inserting a synthetic lac operator sequence between the transcriptional start site and the ribosomal binding site of the B. burgdorferi flgB promoter; flacp was then used to replace the native ospC and rpoS promoters in B. burgdorferi derivatives that constitutively express the E. coli Lac repressor protein (LacI). In vitro, the expression of ospC and rpoS from flacp was dependent on the inducer isopropyl β‐D‐thiogalactopyranoside and was unaffected by temperature or pH, conditions commonly used to mimic different aspects of the B. burgdorferi life cycle. Our results suggest that OspC is essential immediately upon injection into a mouse and OspC expression must be maintained during the early stages of infection. In addition, the mouse infectivity experiment indicates that this system can be used to regulate B. burgdorferi genes in vivo, within the context of an experimental tick–mouse infectious cycle. RpoS is an alternative sigma factor that is required for ospC transcription. However, the role of other temperature‐dependent factors has not previously been addressed. Our results with the inducible rpoS strain demonstrate that RpoS alone is sufficient to activate OspC expression, even at 23°C. This is the first functional inducible promoter system developed for use in B. burgdorferi and, for the first time, will provide researchers with the ability to artificially regulate the expression of genes in this pathogenic spirochaete.
Mutational and expression analysis of CDK1, cyclinA2 and cyclinB1 in epilepsy‐associated glioneuronal lesions
Authors: Schick V. , Majores M. , Fassunke J. , Engels G. , Simon M. , Elger C. E. , Becker A. J.
Published: January 2007

Gangliogliomas and focal cortical dysplasias (FCDs) constitute glioneuronal lesions, which are frequently encountered in biopsy specimens of patients with pharmacoresistant focal epilepsy and relate to impaired differentiation and migration of neural precursors. However, their molecular pathogenesis and relationship are still largely enigmatic. Recent data suggest several components of the insulin‐pathway, including TSC1 and TSC2 mutated in tuberous sclerosis complex (TSC), to be altered in gangliogliomas and FCD with Taylor type balloon cells (FCDIIb). The proteins tuberin (TSC2) and hamartin (TSC1) constitute a tumour suppressor mechanism involved in cell‐cycle control. Hamartin and/or tuberin were reported to colocalize and/or interact with CDK1, cyclinB1 and cyclinA2 that are critically involved in cell‐size and cell‐growth control. Here, we have carried out mutational and expression analyses of CDK1, cyclinB1 and cyclinA2 in gangliogliomas and FCDIIb. Mutational screening was performed by single‐strand conformation polymorphism analysis in gangliogliomas (n = 20), FCDIIb (n = 35) and controls. CyclinB1 revealed a polymorphism (G to A, cDNA Position 966, GenBank: NM_031966) in exon 7 with similar frequencies in FCDIIb, gangliogliomas and control specimens (FCD n = 9/35; gangliogliomas n = 5/20; control n = 20/100). We used real‐time reverse transcription polymerase chain reaction to determine expression levels of CDK1, cyclinB1 and cyclinA2 in 10 FCDIIb and nine gangliogliomas compared with unaffected adjacent control tissue of the same patients. We observed significantly lower expression of CDK1 and cyclinA2 in FCDIIb vs. controls whereas no significant expression differences were present for CDK1, cyclinB1 and cyclinA2 in gangliogliomas. Our data strongly argue against mutational events of CDK1, cyclinB1 and cyclinA2 to play a role in gangliogliomas or FCDIIb. However, a potential functional significance of lower expression for the cell‐size and cell‐cycle regulators CDK1 and cyclinA2 in FCDIIb composed of large dysplastic neurones and balloon cells needs to be further resolved.