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Rising health care costs demands justifying prolonged hospitalization for syncope, yet predictors of shorter length of stay (LOS) have not been identified.The objective of this study is to identify independent predictors of LOS for syncope patients presenting to the emergency department (ED).We performed an analysis of a prospectively collected cohort of ED syncope patients. We examined risk factors from the patient's ED presentation and workup and used Spearman rank correlation to evaluate the relationship between these risk factors and LOS in a logistic regression model for prediction of hospitalization less than 1 day.Of 568 total syncope patients, 350 (61.6%) were admitted and comprise the study cohort. Mean age was 57 years (SD, ±25 years); 39.6% were male. Length of hospitalization was less than or equal to 1 in 179 patients (51.1%). The number of risk factors was associated with LOS (P.001). Most hospitalized patients with less than 1 predictor were hospitalized for less than 1 day (152/272; 55.9%). In multivariate logistic regression analysis, clear vasovagal etiology was positively correlated with LOS less than 1 day (odds ratio [OR], 1.92), whereas dysrhythmia (OR, 0.3), coronary artery disease (OR, 0.33), abnormal vital signs (OR, 0.35), implantable defibrillator/pacemaker (OR, 0.29), anemia/gastrointestinal bleeding (OR, 0.34), and central nervous system abnormalities (OR, 0.09; P.05 for all) were negatively correlated with LOS less than 1 day. Area under the curve for model accuracy was moderate: 0.70 (95% confidence interval, 0.65-0.76).Patients with less than 1 predictor of prolonged stay, who present to the ED with syncope, are unlikely to require hospitalization of more than 1 day. A set of predictors may help define which patients are appropriate for 24-hour observation rather than full hospitalization.

Purpose Global data on human papillomavirus (HPV) serological and deoxyribonucleic acid (DNA) prevalence are essential to optimize HPV prophylactic vaccination strategies. Methods We conducted a global review of age-specific HPV antibody and studies with both antibody and DNA prevalence for HPV-16, −18, −6, and −11. Results One hundred seventeen studies were included; participants' ages ranged from several hours to >90 years. HPV-16 seroprevalence was generally higher in Africa, Central and South America, and North America, more prevalent among women than among men, and peaked around ages 25–40 years. HPV-18 seroprevalence was generally lower than HPV-16 with a later age peak. Data were limited for HPV-6 and −11, both of which peaked at ages similar to HPV-18. Among 9–26-year-old females, HPV-16 seroprevalence ranged from 0%–31% in North America, 21%–30% in Africa, 0%–23% in Asia/Australia, 0%–33% in Europe, and 13%–43% in Central and South America. HPV-16/-18 DNA prevalence peaked 10–15 years before corresponding HPV-16/-18 antibody prevalence. Conclusions Females within the HPV vaccine-eligible age-group (9–26 years) had a range of dual HPV-16 DNA and serology negativity from 81%–87%, whereas 90%–98% were HPV-16 DNA negative. Serology and DNA data are lacking worldwide for females younger than age 15 years, the prime target group for vaccination.

We have reported that circulating CC erythrocytes containing HbO2 C crystals exhibit little or no Hb F suggesting that Hb F may inhibit the crystallization of Hb C. We report now that Hb F inhibits in vitro crystallization of HbO2 and HbCO C when compared to the effect of Hb A in a wide range of mixture proportions. For example, while HbCO C solutions form tetragonal C crystals within 25 min, no crystals form within 2 h with 30% Hb F, whereas 550 crystals/mm3 form with 30% Hb A. Furthermore, an increase in the percent of Hb A is correlated with a greater number of orthorhombic crystal formation rather than the tetragonal morphology observed with 100% Hb C. We also report that Hb A2 (containing delta chains that exhibit 10 sequence differences with beta chains) and Hb Lepore Boston-Washington (a fusion mutant of delta and beta chains that contains only six of these differences) both inhibit Hb C crystallization. By comparing the sequences of the three inhibitory hemoglobins, we conclude that position Gln-87 in the gamma chains is, at least partially, the cause of the inhibitory effect of Hb F on the crystallization of Hb C.