bluuebunny/crossref_metadata_2025_split huggingface dataset:
Estimates of the Mean Alcohol Concentration of the Spirits, Wine, and Beer Sold in the United States and Per Capita Consumption: 1950 to 2002
Authors: Kerr William C. , Greenfield Thomas K. , Tujague Jennifer 
Published: August 2006

Background: Estimates of per capita consumption of alcohol in the United States require estimates of the mean alcohol content by volume (%ABV) of the beer, wine, and spirits sold to convert beverage volume to gallons of pure alcohol.Methods: The mean %ABV of spirits is estimated for each year from 1950 to 2002 and for each state using the %ABV of major brands and sales of sprits types. The mean %ABV of beer and wine is extrapolated to cover this period based on previous estimates. These mean %ABVs are then applied to alcohol sales figures to calculate new yearly estimates of per capita consumption of beer, wine, spirits, and total alcohol for the United States population aged 15 and older.Results: The mean %ABV for spirits is found to be lower than previous estimates and to vary considerably over time and across states. Resultant per capita consumption estimates indicate that more alcohol was consumed from beer and less from wine and spirits than found in previous estimates.Conclusions: Empirically based calculation of mean %ABV for beer, wine, and spirits sold in the United States results in different and presumably more accurate per capita consumption estimates than heretofore available. Utilization of the new estimates in aggregate time‐series and cross‐sectional models of alcohol consumption and related outcomes may improve the accuracy and precision of such models.
Heart Rate Variability and Sympathetic Skin Response in Male Patients Suffering From Acute Alcohol Withdrawal Syndrome
Authors: Bär Karl‐Jürgen , Boettger Michael Karl , Neubauer Rene , Grotelüschen Marei , Jochum Thomas , Baier Vico , Sauer Heinrich , Voss Andreas 
Published: August 2006

Background: Many symptoms of alcohol withdrawal (AW) such as tachycardia or elevated blood pressure might be explained by increased peripheral and central adrenergic activity. In contrast to many neurochemical studies of sympathetic activation during AW, only very few studies investigated autonomic balance using neurophysiological methods.Methods: We investigated heart rate variability (HRV) and sympathetic skin response (SSR) in male patients suffering from mild AW syndrome (n=20, no treatment required) and in patients with moderate to severe AW syndrome (n=20, clomethiazole treatment) in the acute stage. Sympathovagal influence was quantified using measures of time and frequency domain of HRV as well as modern nonlinear parameters (compression entropy). Furthermore, we obtained latencies and amplitudes of SSR to quantify isolated sympathetic influence. Measures were obtained during the climax of withdrawal symptomatology before treatment, 1 day after climax, and shortly before discharge from hospital. Alcohol withdrawal scores were obtained and correlated to autonomic measures.Results: Ambulatory blood pressure and AW scores revealed characteristic withdrawal symptoms in both patient groups. Apart from the nonlinear parameter compression entropy, Hc, measures of HRV revealed no sign of autonomic dysfunction in contrast to the significantly increased heart rates at the time of admission. Latencies and amplitudes of SSR did not indicate any increase of sympathetic activity. A negative correlation was found between Hc and mental withdrawal symptoms.Conclusions: We show here that classical measures for autonomic nervous system activity such as HRV and SSR are not suitable for describing the autonomic changes seen in acute AW, although a major role for the sympathetic nervous system has been proposed. This might be due to multiple dysregulation of metabolites in AWS or to subtle alcohol‐induced damage to neuronal structures, issues that should be addressed in future studies.
Smoke Exposure and Ethanol Ingestion Modulate Intrapulmonary Polymorphonuclear Leukocyte Killing, but Not Recruitment or Phagocytosis
Authors: Vander Top Elizabeth A. , Perry Greg A. , Snitily Mary U. , Gentry‐Nielsen Martha J. 
Published: August 2006

Background: People who smoke and abuse alcohol are uniquely susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. The primary cellular defense against pneumococci within the lungs is the polymorphonuclear leukocyte (PMN). Cigarette smoke and ethanol (EtOH) are known to alter certain PMN functions, but little is known about their concurrent effects.Methods: Male Sprague–Dawley rats were exposed twice daily for 8 weeks to cigarette smoke (smoke‐exposed) or room air (sham‐exposed). During the final week of exposure, the rats were pair‐fed a liquid diet containing either 36 or 0% EtOH calories. Polymorphonuclear leukocytes were prerecruited into the rats' lungs by transtracheal injection of lipopolysaccharide. Five hours later, the rats were infected transtracheally with S. pneumoniae, and PMN recruitment, phagocytosis, and bactericidal activity were quantified within their lungs. Chemokine levels were also measured in bronchoalveolar lavage fluids, lung homogenates, and sera.Results: Neither PMN recruitment nor phagocytic uptake of pneumococci was altered by EtOH ingestion or smoke exposure. Killing of the organisms, however, was significantly decreased in sham‐exposed, but not smoke‐exposed, rats ingesting EtOH. Parallel results were determined for serum cytokine‐induced neutrophil chemoattractant‐1 (CINC‐1), with EtOH ingestion significantly decreasing the levels in sham‐exposed, but not smoke‐exposed, rats. Pulmonary levels of macrophage inflammatory protein‐2 (MIP‐2) and CINC‐1 were highly elevated by the combination of EtOH and smoke.Conclusions: One week of EtOH ingestion by rats impaired the ability of their PMNs to kill S. pneumoniae within their lungs. This was not due to decreased recruitment of the PMNs to the lungs or to diminished phagocytosis of intrapulmonary pneumococci. The addition of twice‐daily cigarette smoke exposure to this short‐term EtOH ingestion model restored PMN bactericidal ability to levels observed in the absence of either treatment. These EtOH‐induced and smoke‐induced alterations in PMN killing may be related to alterations in both pulmonary and systemic inflammatory chemokine levels.
Inhibition of PAR4 Signaling Mediates Ethanol‐Induced Attenuation of Platelet Function In Vitro
Authors: Kasuda Shogo , Sakurai Yoshihiko , Shima Midori , Morimura Yoshifumi , Kudo Risa , Takeda Tomohiro , Ishitani Akiko , Yoshioka Akira , Hatake Katsuhiko 
Published: August 2006

Background:Reduction in coronary heart disease morbidity in response to moderate consumption of alcoholic beverages may be partly mediated by ethanol‐induced inhibition of platelet function. However, the precise mechanisms by which ethanol modulates platelet activation induced by thrombin, which plays a central role in hemostasis, remain unclear. The goal of this study was to investigate ethanol‐induced changes in platelet function and clarify the underlying mechanisms including PAR1 and PAR4 activity and [Ca2+]idynamics in vitro.Methods:Platelet aggregation, increase in intracellular calcium ([Ca2+]i), and release of platelet factor 4 andβ‐thromboglobulin induced byα‐thrombin, PAR1‐agonist peptide (AP), or PAR4‐AP were assessed in the presence or absence of ethanol.Results:Ethanol exposure inhibited low‐dose thrombin (0.5 nM)‐induced aggregation but not an increase in [Ca2+]i. In contrast, ethanol had no effect on high‐dose thrombin (10 nM)‐induced aggregation or the [Ca2+]iincrease. Ethanol did not significantly inhibit thrombin‐induced release of platelet factor 4 andβ‐thromboglobulin. Ethanol reduced PAR1‐AP‐induced aggregation, but did not affect the spike form of [Ca2+]iincrease. In contrast, ethanol inhibited the increase in [Ca2+]ias well as the aggregation in response to PAR4‐AP and resulted in delayed [Ca2+]ipeak time. Furthermore, ethanol inhibited both PAR1‐AP‐ and PAR4‐AP‐induced platelet factor 4 andβ‐thromboglobulin release.Conclusions:These data suggest that ethanol inhibits platelet aggregation via inhibition of PAR4 signaling and subsequent inhibition of Ca2+influx and granule release. This phenomenon may contribute to the reduction in coronary heart disease morbidity in response to consumption of alcoholic beverages.
Chronic Ethanol Consumption Inhibits Hepatic Natural Killer Cell Activity and Accelerates Murine Cytomegalovirus‐Induced Hepatitis
Authors: Pan Hong‐na , Sun Rui , Jaruga Barbara , Hong Feng , Kim Won‐Ho , Gao Bin 
Published: August 2006

Background: Chronic alcohol drinking accelerates the progression of liver disease in patients with hepatitis viral infection; however, the underlying mechanisms are not fully understood.Methods: Here, we examined the effects of chronic ethanol feeding on hepatic natural killer (NK) cells and liver injury in 2 murine models of liver injury: injection of synthetic double‐stranded RNA polyinosinic‐polycytidylic acid (poly I:C), which mimics viral infection, and infection with murine cytomegalovirus (MCMV). Mice were fed the Lieber‐DeCarli liquid diet containing 5% (vol/vol) ethanol for 8 weeks, resulting in a significant decrease in the percentage and total number of NK cells in the liver.Results: In control, pair‐fed mice, poly I:C injection induced NK cell accumulation in the liver and activated hepatic NK cell cytotoxicity, whereas such induction and activation were diminished in ethanol‐fed mice. Treatment with poly I:C also induced expression of NKG2D, granzyme B, perforin, Fas L, TRAIL, and IFN‐γ on liver lymphocytes, which were delayed or reduced in ethanol‐treated mice compared with pair‐fed mice. In contrast, chronic ethanol feeding did not affect poly I:C–induced mild liver injury. Furthermore, MCMV infection activated hepatic NK cells and induced hepatic inflammation and injury. Chronic ethanol consumption inhibited hepatic NK cell activation during MCMV infection, but enhanced MCMV‐induced liver injury, viral titer, and inflammation in the liver.Conclusions: Taken together, these findings suggest that chronic ethanol consumption decreases hepatic NK activity, thereby accelerating MCMV‐induced hepatitis and liver injury.
Using the Internet and Email for Health Purposes: The Impact of Health Status*
Authors: Goldner Melinda 
Published: August 2006

Objective. Increasingly, people use the Internet and email for health purposes; however, we know little about whether this varies by health status. This study examines whether sick or healthy people are more likely to access the Internet, conduct online health searches, and exchange emails regarding health issues.Methods. We conduct multivariate analysis on a random sample of 2,038 adults.Results. Despite greater Internet access, respondents in excellent/good health are less likely to say they conduct online health searches because they have no health concerns or are satisfied with other health sources. In contrast, sick and disabled respondents are more likely to seek medical information online, and do so more frequently. They are also more likely to exchange health emails with friends and physicians.Conclusions. Practitioners especially need to educate their sicker patients about the uneven quality of online health information since they are more likely than healthier patients to conduct online health searches.
Inappropriate ICD Therapy: Does Device Configuration Make a Difference
Authors: SOUNDARRAJ DWARAKRAJ , THAKUR RANJAN K. , GARDINER JOSEPH C. , KHASNIS ATUL , JONGNARANGSIN KRIT 
Published: August 2006

Introduction: Inappropriate implantable cardioverter defibrillator (ICD) therapy (IT) is a common complication in patients with ICD. IT is commonly triggered by supraventricular tachycardias (SVT). Dual chamber ICDs (D‐ICDs) may distinguish SVT from ventricular tachycardia/ventricular fibrillation better than single chamber ICDs (S‐ICDs) and may be associated with a smaller incidence of IT.
Methods: We reviewed the charts of 386 patients who had an ICD implanted for an AHA class I indication. Intracardiac electrograms were used to classify shocks as either appropriate or inappropriate.
Results: Of 295 patients with an S‐ICD, 66 (22.3%) received IT, compared to 5 (5.4%) of 91 patients with a D‐ICD. The likelihood of being event‐free at 1, 2, 3, and 4 years was 96.1%, 96.1%, 96.1%, and 89% for patients with D‐ICD and 80.7%, 72.7%, 69.6%, and 66.4%, respectively, for patients with S‐ICD (P < 0.001). Multivariate analysis showed no significant association with age, sex, history of atrial fibrillation, history of hypertension, or ejection fraction. SVTs were the commonest cause of IT in our patients.
Conclusion: Patients with D‐ICD are less likely to receive IT as compared to patients with S‐ICD.
Seasonal Variations of Ventricular Arrhythmia Clusters in Defibrillator Recipients
Authors: STUBER THOMAS , EIGENMANN CHRISTA , DELACRÉTAZ ETIENNE 
Published: August 2006

Background: Clustering ventricular arrhythmias are the consequence of acute ventricular electrical instability and represent a challenge in the management of the growing number of patients with an implantable cardioverter‐defibrillator (ICD). Triggering factors can rarely be identified.
Objectives: Several studies have revealed seasonal variations in the frequency of cardiovascular events and life‐threatening arrhythmias, and we sought to establish whether seasonal factors may exacerbate ventricular electrical instability leading to arrhythmia clusters and electrical storm.
Methods: Two hundred and fourteen consecutive defibrillator recipients were followed‐up during 3.3 ± 2.2 years. Arrhythmia cluster was defined as the occurrence of three or more arrhythmic events triggering appropriate defibrillator therapies within 2 weeks. Time intervals between two clusters were calculated for each month and each season, and were compared using Kruskal‐Wallis test and Wilcoxon‐Mann‐Whitney test with Bonferroni adjustment.
Results: During a follow‐up of 698 patient years, 98 arrhythmia clusters were observed in 51 patients; clustering ventricular arrhythmias were associated with temporal variables; they occurred more frequently in the winter and spring months than during the summer and fall. Accordingly, the time intervals between two clusters were significantly shorter during winter and spring (median and 95% CI): winter 16 (5–19), spring 11.5 (7–25), summer 34.5 (15–55), fall 50.5 (19–65), P = 0.0041.
Conclusion: There are important seasonal variations in the incidence of arrhythmia clusters in ICD recipients. Whether these variations are related to environmental factors, change in physical activity, or psychological factors requires further study.
Evidence for Increased Atrial Sympathetic Innervation in Persistent Human Atrial Fibrillation
Authors: GOULD PAUL A. , YII MICHAEL , MCLEAN CATRIONA , FINCH SAMARA , MARSHALL TANNEALE , LAMBERT GAVIN W. , KAYE DAVID M. 
Published: August 2006

Objective: In this study, we aimed to compare the level of atrial sympathetic innervation in human atrial fibrillation (AF) to that in sinus rhythm (SR).
Background: Histological studies of atrial tissue obtained from animals with experimentally induced AF indicate that sympathetic hyperinnervation could play a role in the pathogenesis of AF.
Methods: In 24 patients (12 in SR and 12 in AF) undergoing bypass surgery, we collected right atrial appendage tissue. In AF patients, left atrial appendage tissue was also acquired. The degree of sympathetic innervation was quantified by measuring the amount of staining for tyrosine hydroxylase (TH) and tissue norepinephrine (NE). In conjunction, nerve growth factor (NGF) mRNA expression was assessed by real‐time polymerase chain reaction (PCR). Growth‐associated protein 43 (GAP43) immunostaining was used to assess degree of new neural growth.
Results: When corrected for differences in tissue fibrosis, the expression of both TH (AF 0.45 ± 0.1%, SR 0.09 ± 0.03%, P = 0.02) and tissue NE (AF 358 ± 49 pg/mg, SR 225 ± 39 pg/mg, P = 0.04) was greater in atrial tissue of the AF cohort. The degree of atrial TH staining (P = 0.01) and NE content (P < 0.001) was also significantly greater in the right compared with left atrial samples in the AF cohort. There were no differences in NGF mRNA expression or GAP43 staining.
Conclusion: This study provides evidence for the presence of heightened atrial sympathetic innervation in patients with persistent AF, suggesting autonomic remodeling may be part of atrial substrate for AF.
QRS Duration in High‐Resolution Methods and Standard ECG in Risk Assessment After First and Recurrent Myocardial Infarctions
Authors: KORHONEN PETRI , HUSA TERHI , TIERALA ILKKA , VÄÄNÄNEN HEIKKI , MÄKIJÄRVI MARKKU , KATILA TOIVO , TOIVONEN LAURI 
Published: August 2006

Background: Prolonged QRS duration (QRSd) is associated with increased mortality after myocardial infarction (MI). Only little data exist about its predictive ability and relationships to clinical variables in the present era of active treatment of myocardial ischemia and cardiac dysfunction. We investigated whether QRSd in high‐resolution methods and standard ECG predict arrhythmic events and cardiac death in post‐infarction patients with cardiac dysfunction and how it relates to clinical variables, with a special emphasis on history of previous MI.
Methods and Results: Patients (n = 158) with acute MI and cardiac dysfunction had magnetocardiography (MCG), signal‐averaged ECG (SAECG), and ECG registered at discharge. Patients with a previous MI had significantly longer QRSd although their left ventricular function was almost similarly impaired. During the mean follow‐up of 50 ± 15 (range 1–72) months, 32 patients died and 17 (53%) of the deaths were classified as cardiac. Eighteen patients had an arrhythmic event. QRSd >121 ms in MCG and >114 ms in SAECG were significant predictors of arrhythmic events and cardiac death, whereas QRSd in ECG predicted only cardiac death. In multivariate analysis, QRSd in MCG (hazard ratio (HR) = 3.6, P = 0.007) and SAECG (HR = 4.6, P = 0.016) predicted only arrhythmic events, whereas QRSd in ECG was an independent predictor of cardiac death.
Conclusions: Prolonged QRSd in MCG and SAECG are powerful indicators of the arrhythmia substrate in post‐infarction patients with cardiac dysfunction, whereas prolonged QRSd in standard ECG associates with increased risk of cardiac death.
Magnetic Resonance Imaging Abnormalities in Right Ventricular Outflow Tract Tachycardia and the Prediction of Radiofrequency Ablation Outcome
Authors: KRITTAYAPHONG RUNGROJ , SAIVIROONPORN PAIRASH , BOONYASIRINANT THANANYA , NAKYEN SUPAPORN , THANAPIBOONPOL PRAJAK , WATANAPRAKARNCHAI WIPAWIN , RUKSAKUL KRONGKARN , KANGKAGATE CHARUWAN 
Published: August 2006

Background: Recent reports have shown abnormalities on cardiac magnetic resonance imaging (MRI) in patients with right ventricular outflow tract (RVOT) tachycardia.
Objectives: Objectives of this study were to demonstrate abnormalities on MRI and signal‐averaged ECG (SAECG) in patients with RVOT tachycardia and their correlation with the outcome of radiofrequency (RF) ablation.
Methods: We studied 41 patients with symptomatic RVOT tachycardia and 15 controls. SAECG and cardiac MRI were performed on every subject. An evaluation of structural abnormality, chamber size, function, and wall motion abnormality of the left and right ventricle was performed by MRI. Focal wall thinning was evaluated by the black blood technique and fatty infiltration was evaluated by the T1 image with and without fat suppression.
Results: MRI abnormalities were demonstrated in 24 (58.5%) patients with RVOT tachycardia. The abnormalities included localized wall bulging in 22 (53.7%), focal wall thinning in 10 (24.4%), and fatty replacement in 9 (22%) patients. MRI abnormality was found in only one patient in the control group (P < 0.001). Late potentials from SAECG were demonstrated in six (10.7%) patients but none in the controls (P = 0.117). Among 29 patients who underwent RF ablation, 3 patients had a failed procedure and 3 having arrhythmia recurrence needed repeated ablation. MRI abnormalities and late potentials were associated with an unfavorable outcome of RF ablation.
Conclusions: MRI abnormalities were frequently found in patients with RVOT tachycardia. MRI abnormalities and late potentials can predict outcomes of RF ablation.
Predictors of Response to the Head‐Up Tilt Test in Patients with Unexplained Syncope or Presyncope
Authors: KAZEMI BABAK , HAGHJOO MAJID , ARYA ARASH , SADR‐AMELI MOHAMMAD ALI 
Published: August 2006

Background: Unexplained syncope is a relatively frequent symptom, mostly caused by a neurocardiogenic reaction. The purpose of this study was to determine predictors of response to head‐up tilt testing (HUTT) in patients with unexplained syncope or presyncope.
Methods: HUTT was done in 640 consecutive patients with unexplained syncope or presyncope (393 men, mean age 45±19 years) after initial workup including history, physical examination, and appropriate laboratory evaluation.
Results: Three hundred and forty‐four (54%) patients had a positive result. The most common type of response was mixed type (46%) followed by vasodepressor (39%) and cardioinhibitory (15%) types. Age, gender, presence of structural heart disease, baseline heart rhythm, and the presenting symptom before the test failed to predict a positive response to HUTT, but among patients with a positive response to the test, age (OR: 1.54, CI = 1.04–2.47, P = 0.016) and presyncope (OR: 2.16, CI = 1.2–3.85, P = 0.008) as the presenting symptom predicted a vasodepressor type of response. The age (OR: 1.58, CI = 1.29–3.94, P = 0.01) and presyncope (OR: 4.6, CI = 1.74–12.24, P = 0.001) were also predictors for test positivity in the active stage.
Conclusions: There is an age‐related gradient in hemodynamic response during neurocardiogenic syncope. The elderly patients more commonly had a vasodepressor and late response, in the active stage, but young subjects more commonly experienced an earlier and cardioinhibitory or mixed responses in the passive stage.
Ultrasound‐Guided Venous Access for Permanent Pacemaker Leads
Authors: JONES DAVID G. , STILES MARTIN K. , STEWART JAMES T. , ARMSTRONG GUY P. 
Published: August 2006

Background: Existing methods of venous access for permanent pacemaker leads have disadvantages. We documented learning times for ultrasound‐guided lead implantation and compared them with cephalic venotomy technique.
Methods: Two implanters learnt ultrasound‐guided technique by implanting consecutive pacemaker patients. When procedural times stabilized, we reverted to our normal cephalic approach. We measured lead placement time and screening time from skin incision until all leads were placed in superior vena cava were measured.
Results: Initial strategy adopted was ultrasound for 60, then cephalic for 38 patients. There were no significant differences between groups in baseline characteristics or number of leads implanted. Lead placement and screening times were significantly shorter for ultrasound, despite inclusion of all learning cases. There was a high success rate for both strategies (88% ultrasound, 87% cephalic). There was significantly greater use of pressure dressings with ultrasound, but no difference in pocket hematoma or pneumothorax. There was a trend for more predictable lead implant times with ultrasound and fluoroscopy times were shorter and more predictable. Independent predictors of lead placement time were body mass index, operator, initial strategy (ultrasound vs cephalic), and procedure number.
Conclusion: Ultrasound‐guided venepuncture for placement of permanent pacing leads is quick to learn and achieves faster lead placement times with shorter and more predictable fluoroscopy time when compared with the cephalic venotomy technique.